CENTRAL NERVOUS SYSTEM (CNS)

- Dr Vivek Nalgirkar
Professor, Physiology

Table of contents
 Section 1: Introduction to nervous system: Hierarchical organization of nervous
system. Neuron: The basic functional unit.
 Section 2: Synapse: Types of synapses, structure of a synapse, Physiology of
synaptic transmission, properties of synapse. REFLEX:- Classification of reflexes,
reflex arc, properties of reflex.
 Section 3: Sensory system: Encoding of sensory information, Receptors ~ Classification,
properties, Receptor adaptation. Ascending tracts ~ Dorsal column system,
anterolateral system. Physiology of Pain.
 Section 4: Motor system: Introduction ~ Upper v/s lower motor neuron; organization
of motor system. Pyramidal tract ~ Origin, course, functions, effects of lesions.
Cerebellum ~ Connections, functions, effects of lesions. Basal ganglia ~
Connections/circuits, functions, effects of lesions. Spinal cord ~ Lower motor neuron,
proprioceptors in muscle. Stretch reflex, muscle tone. Injuries to spinal cord. Postural
reflexes ~ Experimental animal preparations, postural reflexes. Equilibrium ~ Vestibular
apparatus.
 Section 5: Higher functions of brain: Hypothalamus ~ Connections, functions, and
effects of lesions. Cerebral cortex ~ Regions, functions. Limbic system ~ Components,
functions. Higher functions of cerebrum ~ concept of hemispheres, speech, learning &
memory. EEG & sleep ~ Waves of EEG; types of sleep. Cerebrospinal fluid (CSF) ~
Formation, CSF pressure, functions, lumbar puncture. Blood-brain barrier.

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 Section 1

Introduction to nervous system

Learning objectives:

- To understand the hierarchy of nervous system functioning.

Introduction

- The nervous system and the endocrine system are the two regulatory
systems in the body.
- Nervous system has the following divisions:-

nervous
system
central peripheral
nervous nervous
system system
brain spinal autonomic
cord somatic
nervous
nervous
system
system
cranial spinal
parasy
nerves nerve sympathetic
nerves mp
s
athetic
nerves

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On the basis of the organizational pattern, the nervous system is subdivided into central and
peripheral nervous systems. The central nervous system includes the brain and the spinal cord.
The peripheral nervous system consists of 31 pairs of spinal and 12 pairs of cranial nerves
(which are destined to innervate somatic structures), and the sympathetic and parasympathetic
nerves of the autonomic nervous system (which innervate viscera).

This chapter is mostly about the central nervous system (CNS).

Nervous system receives millions of bits of information from the different sensory
organs and then integrates all these to determine the responses to be made by
the body. Discussion on the nervous system can be divided into 3 parts: (a)
Sensory system – Sensory stimuli are received by the body and are transmitted to
the brain for processing, (b) Motor system – Based on the sensory inputs,
appropriate responses are made by the body, and (c) Higher functions – Learning
processes in the brain, memory storage, sleep & arousal, emotions, etc.

Cells in the nervous system:

[Ratio of neurons to glia is in the range of 1:4 to 1:10.]

(A)Neurons: The basic structural & functional unit

(B) Glia: Non-neural cells;
1. Macroglia:
 Astrocyte – (star-shaped glial cell)

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  Supports and protects neurons
 Provides nutrition to neurons
 It surrounds blood vessels in CNS; it reinforces the blood-brain
barrier (BBB)
 Other functions ~ Takes up neurotransmitters (released at
synapses) and redistributes them among neurons; regulates K +
levels around neurons
 Oligodendrocyte –
 Causes myelination of neurons in CNS
2. Microglia: (The only cell that is born outside of CNS and then migrates
into CNS)
 It is derived from monocyte (in bone marrow)
 It is ‘scavenger cell’;
 Performs phagocytic function; e.g., removal of debris after
injury to some part of CNS.

 Neuron: The basic functional unit

The CNS contains more than 100 billion neurons. The neurons are connected to one
another by the synapses.

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[Fig: Structure of a neuron. Dendrites are the receptor zones where impulse is received from
another neuron. Impulse then travels electrotonically up to axon hillock. First AP is generated
at the axon hillock; impulse is then transmitted down the axon, up to the axon terminal.]

Sensory division:

Most activities of the nervous system are initiated by sensory inputs coming
from the periphery. These sensory signals are processed, so as to produce an
immediate motor response, and/or, they are stored in the memory for future
reference.

Motor division – the effectors:

Based on the sensory input (or, even in the absence of inputs, at times),
motor division designs and executes voluntary movements of the body. This is
achieved by causing contraction of appropriate skeletal muscle groups. This is the
motor function of the CNS, and the muscles are called effectors.

Processing of information – “integrative” function of the nervous system

- One of the most important functions of the nervous system is to process

incoming information in such a way that appropriate motor responses will
occur.
- More than 99% of all sensory information is discarded by the brain as
irrelevant and unimportant. (For instance, one is ordinarily unaware of the
parts of the body that are in contact with clothing, or, the seat pressure while
sitting.)
- When important sensory information excites the mind, it is immediately
channeled into proper integrative and motor regions of the brain to cause
desired responses. This channeling and processing of information is called
the integrative function of the nervous system.

~ Hierarchical organization of nervous system:

The three major levels of nervous system: (functional organization in relation

to anatomical levels of CNS)

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 1. The spinal cord level,
2. The lower brain level,
3. The higher brain or cortical
level. The spinal cord level-

Two functions are performed at this level – (1) Integrate the reflex
responses:- Reflex is an automatic and instantaneous response to a sensory input,
without the involvement of cortex (i.e., occurs without conscious involvement).
(2) Offer to-and-fro passage for neural signals:- Sensory signals coming from
periphery enter the spinal cord, which are then relayed to higher centers. Motor
signals regarding voluntary movements come from the higher centers, descend
through the spinal cord, to be conveyed to the effectors (muscles).

The lower brain level/sub cortical level-

- Spinal cord continues upward into the lower most part of the brain – the
medulla.
- Hind brain: It comprises of medulla, pons, and cerebellum.
- Brain stem: It is made up of medulla, pons, and mid brain.
 Medulla and pons consist of centers for involuntary functions, viz.,
vasomotor center, respiratory center, swallowing center, micturition
center.
 Midbrain has nuclei involved in regulation of motor activities.
 Cerebellum co-ordinates muscle contractions during voluntary
movements.
- Basal ganglia:- Subcortical masses of grey matter; help the cortex in
selecting a purposeful voluntary movement
- Diencephalon: (di ~ two) Two structures – Thalamus & hypothalamus.
Thalamus is the relay station for all the sensations coming from periphery;
these sensations are conveyed to sensory cortex. Hypothalamus controls all
the vegetative and visceral functions.

The higher brain or cortical level-

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 90% of the cortex is neocortex. The four lobes of the brain – frontal, parietal,
temporal, and occipital. Each lobe houses a cortex.

Motor cortex in frontal lobe, somatosensory cortex in parietal lobe, auditory

cortex in temporal lobe, and visual cortex in occipital lobe.

The remaining 10% is archicortex. It includes limbic system which is associated with
emotions and behavioral patterns.

Cortex is also the seat of higher functions like speech, thought, intelligence, social
behavior, etc.

————————————————————————————————————

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 Section 2

SYNAPSE, REFLEX

THE INTERNEURONAL COMMUNICATION

Learning objectives:

- Humans continue to learn new things throughout life; the brain capacity
goes increasing after birth. This occurs due to formation of new synapses
and the neurotransmitters. This section deals with the interneuronal
communication.
- Many of our activities occur “reflexly”. How are these reflex acts co-
ordinated? This section discusses the basis for for our reflex actions.

Definition-

A synapse is a junction between two neurons which participate in a one-way

flow of information.

Or

It is the junctional region between two neurons, where the impulse is

transmitted from one neuron to another neuron (although there is no structural
continuity/protoplasmic connection between the two neurons).

[Note:- Junction between nerve and muscle is also considered a synapse; it is

commonly referred to as neuromuscular junction. The term ‘synapse’ is generally
indicative of the junction between a nerve and another nerve.]

Synapses are of two types: (1) electrical, (2) chemical.

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 There are very few electrical synapses in the CNS (of mammals). Hence, a
synapse would generally mean a chemical synapse, where there is release of a
chemical or transmitter.

Types of chemical synapses:

- The axon of the presynaptic neuron may end on different parts of the
postsynaptic neuron; based on this, there are three varieties of the
synapses-

(1) Axo-dendritic (commonest type; almost 98% synapses in brain are of

this type):
 axon of the first neuron ends on the dendrite of the next
neuron;
 E.g., synapses in cerebral cortex, cerebellum
 Note: These are excitatory synapses
(2) Axo-somatic (inhibitory synapse):
 Axon of the first neuron ends on the soma of the next
neuron;
 E.g., (i) Renshaw cell ending on the cell soma of the anterior
motor neuron in spinal cord, (ii) Granule cell axon ending
on cell soma of Purkinje cell in cerebellum
(3) Axo-axonal:
 axon of the first neuron ends on the axonal terminal of the
next neuron; very few synapses are of this type.
 These synapses are meant for presynaptic facilitation &
presynaptic inhibition.
 E.g., pain inhibitory synapses of the descending analgesia
system

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Structure of a synapse:

- The neuron which sends or transmits the impulse is called the presynaptic
neuron.
- The neuron which receives the impulse is called the postsynaptic neuron.

[Fig: Structure of a synapse. It shows a presynaptic neuron, whose axon ends on postsynaptic
neuron. Bouton or bulb is the expanded axon terminal of the presynaptic neuron. The bulb
contains neurotransmitter (NT) vesicles and mitochondria. The presynaptic membrane has
voltage-gated Ca++ channels (VGCCs) and the release sites for transmitter release. The
postsynaptic membrane has NT receptors, which are coupled with ligand-gated ion channels.]

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 - The ends of the presynaptic fibers are generally enlarged to form round or
oval knobs, called as synaptic knobs, or terminal buttons, or end-feet, or
simply presynaptic terminals.
- The membrane of the postsynaptic neuron is called the postsynaptic
membrane. Between the presynaptic terminal and the postsynaptic
membrane there exists a gap called synaptic cleft. Width of the synaptic cleft
is about 20 to 30 nm.
- The presynaptic terminal has two internal structures: (i) the synaptic vesicles,
and (ii) the mitochondria.
- The synaptic vesicles contain a transmitter substance (neurotransmitter).
The mitochondria provide ATP, to synthesize the neurotransmitter.
- The postsynaptic membrane bears receptors for neurotransmitter.
The Physiology of synaptic transmission

[Fig: It shows sequence of events in synaptic transmission. Refer to text for details.]

(1) THE ARRIVAL OF THE IMPULSE:

- The impulse (A.P.) arrives at the presynaptic terminal.
(2) INFLUX OF Ca++ INTO THE TERMINAL:

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 - Depolarization, being a voltage change, is sensed by voltage-gated Ca++
channel (VGCC).
- VGCC opens, allowing Influx of Ca++ into the terminal.
(3) NT vesicle MIGRATES TOWARD PRESYNAPTIC MEMBRANE:
- Neurotransmitter (NT) vesicle now moves toward the presynaptic
membrane.
(4) TRANSMITTER RELEASE BY EXOCYTOSIS:
- The NT vesicle fuses with the presynaptic membrane; it releases its
contents (transmitter, co-transmitter, etc) into the synaptic cleft.
(5) TRANSMITTER COMBINES WITH RECEPTOR ON POSTSYNAPTIC MEMBRANE:
- The neurotransmitter traverses the gap, reaches the postsynaptic
membrane where it combines with its receptor.
(6) INFLUX OF CATIONS; POSTSYNAPTIC MEMBRANE DEPOLARIZED:
- As transmitter combines with the receptor, the associated channel opens,
allowing influx of cations into the postsynaptic neuron. This results in
development of the synaptic potential, called excitatory postsynaptic
potential (EPSP). If multiple EPSPs summate, threshold is reached. AP is
generated and it propagates down the post synaptic neuron.

The postsynaptic potentials: (EPSPs and IPSPs)

Stimulation of a neuron, forming a synapse with another neuron, does not

always produce a propagated action potential in the postsynaptic neuron. It may
cause a transient partial depolarization or hyperpolarization, in the postsynaptic
neuron. The transient partial depolarizing change is called excitatory postsynaptic
potential (EPSP), and the hyperpolarizing change would be called inhibitory
postsynaptic potential (IPSP).

The initial depolarizing response produced by a single stimulus begins about

0.5 msec after the impulse arrives at the synapse; it reaches its peak 1 to 1.5 msec
later and then declines exponentially over next 15 msec. During this potential, the
excitability of the neuron to other stimuli is increased, hence it is called an

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excitatory postsynaptic potential (EPSP). The EPSP is a depolarizing change;
however it is a localized change of potential.

Mechanism of development of EPSP

When the synaptic transmitter combines with its receptors on the

postsynaptic membrane, it causes opening of cation channels (Na + / Ca++) in the
membrane. The influx of cations reduces the membrane potential to a less negative
value. However, the area of the cation influx is so small that it does not allow
enough positivity to flow in, and a propagated AP does not result. It only causes a
small potential change to develop locally. These localized EPSPs may summate to
produce a propagated AP. An EPSP is a precursor of an AP.

EPSP v/s AP:

(1) An EPSP is strictly a localized change; it does not propagate. An AP is

propagated.
(2) An EPSP is a graded change; stronger the stimulus greater will be the EPSP.
It does not obey all-or-none law. An AP obeys all-or-none law.
(3) An EPSP is monophasic; an AP is biphasic.

EPSP AP
- Localized potential - Propagated potential

- Graded potential - Obeys “all-or-none” law (no

gradations)

- Monophasic - Biphasic

Properties of synaptic transmission:

(1) One way conduction

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 Synapses allow conduction of impulses in one direction only, from the
presynaptic to the postsynaptic neurons. The chemical transmitter is in the
presynaptic terminal only.

(2) Synaptic delay

- All the events involved in synaptic transmission need some time. This lapse
of time during the impulse transmission at the synapse is the synaptic
delay; it is about 0.5 msec at every synapse. (This information can be used
for estimating the number of synapses involved in a polysynaptic
reflex/pathway.)
- More the number of synapses in a pathway, longer is the time taken by the
impulse to travel and reach its destination.

(3) Fatigue:
When excitatory synapses are repetitively stimulated for prolonged period,
the postsynaptic response becomes progressively less. This is called fatigue
of synaptic transmission. It is due to exhaustion of the neurotransmitter
caused by repetitive stimulation.
Significance:
The development of fatigue is a protective mechanism against excess
neuronal activity. For example, the excess excitability of the brain during an
epileptic seizure is finally subdued so that the seizure ceases.

(4) Post-tetanic potentiation

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 If a synapse is stimulated at a tetanic frequency (high frequency), followed
by a brief pause, then a subsequent stimulation will produce an enhanced
response at the synapse. This is called post-tetanic potentiation.
It is thought to be due to accumulation of calcium ions in the presynaptic
terminal during the high frequency stimulation. (Each impulse causes influx
of calcium ions into the presynaptic terminal. Rapid stimulation causes
calcium to enter and accumulate in the presynaptic terminal.) The amount
of neurotransmitter released by the presynaptic neuron is proportional to
the amount of calcium in the terminal. Thus, more neurotransmitter is
released, and the synaptic response is potentiated.

(5) Summation: (spatial & temporal)

Addition of the postsynaptic potentials is called summation. It is of two
types:-

(A) Spatial summation: (spatial = space)

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 - If a number of fibers converging on a single neuron are stimulated
individually with weak (subthreshold) stimuli the postsynaptic neuron does
not fire A.P. However, if all the fibers are stimulated simultaneously, the
postsynaptic neuron may fire. All the fibers create EPSPs on the
postsynaptic membrane at different points. These EPSPs get added
(summated) so that the postsynaptic membrane potential reaches
threshold, and fires A.P. This

is called spatial summation.

[Fig: Diagrammatic representation of spatial summation. 3 neurons make synaptic contacts

with a single post synaptic neuron. Impulse arrives in each of the presynaptic neuron; it
causes influx of cations and development of EPSP at different points on the post synaptic
membrane. Due to the passive flow of cations, these EPSPs get added and the post synaptic
neuron reaches threshold for firing an AP.]

(B) Temporal summation: (temporal = time)

- If a subthreshold stimulus is repeated several times in quick succession, the
postsynaptic neuron may eventually fire an AP. Each impulse in the
presynaptic neuron is creating an EPSP on the postsynaptic membrane.
Before this EPSP decays, if the next impulse arrives at the synapse, it
creates another EPSP which gets added (summated) to the previous
one. Thus,

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 successive EPSPs get added so that postsynaptic membrane potential
reaches threshold, and fires A.P. This is called temporal summation.

[Fig: Representative diagram. Let’s say, the post synaptic neuron needs 15 mV depolarization
to reach threshold. 3 impulses arrive in the presynaptic neuron, each creating a 5 mV
depolarization on the post synaptic membrane. If these EPSPs are occurring within 15 msec of
each other, they will get added and the post synaptic neuron will reach threshold.]

(6) Inhibition at synapses:

Inhibition of transmission in CNS can occur in one of the following ways:

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(A) Presynaptic inhibition:

[Fig: Presynaptic inhibition. Neuron A makes an excitatory synaptic contact with

neuron B; impulse is transmitted from A to B. Another neuron C makes contact with
the presynaptic neuron A. Neuron C releases inhibitory transmitter which is thought to
close the Ca++ channels in the terminal of neuron A. Decreased Ca ++ in the A’s terminal
leads to decreased release of excitatory transmitter by A on to B.]

(B) Post synaptic inhibition:

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 [Fig: Neuron A makes an excitatory synaptic contact with neuron B. Neuron C makes
synaptic contact with B; it releases inhibitory transmitter which causes
hyperpolarization of neuron B. Thus, even when impulse arrives in A, it will not excite
B as membrane of B is less excitable.]

Two special types of synaptic inhibition: (1) Autogenic inhibition or recurrent

inhibition, (2) Feedforward inhibition.

(1) Recurrent inhibition: (executed by Renshaw cell)

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 [Fig: Renshaw cell inhibition. Alpha-motor neuron has nerve cell body in the anterior horn.
Axon of the alpha-motor neuron, before leaving the spinal cord, gives off a collateral which
ends on the Renshaw cell (shown in red). Axon of the Renshaw cell turns back and ends on
the soma of the same motor neuron.]

- The anterior motor neuron gives off a collateral that excites the
Renshaw cell.

- Renshaw cell is an inhibitory interneuron. Its axon terminates on – (i)

soma of the motor neuron that gave off the collateral, (ii) soma of the
other neurons in the motoneuron pool in the anterior horn, and (iii)
Ia inhibitory interneurons. NT for Renshaw cell is glycine.

Functional significance:

(i) “Dampening”: (Renshaw cell axon ending on the soma of the same
motor neuron that gave off collateral) An overexcited motor neuron
may send repetitive, high frequency signals to the muscle innervated by
it, resulting in tetanic contraction of the muscle. This kind of signaling is

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 dampened by the recurrent inhibition exerted by the Renshaw cell.
Explanation:The alpha-motor neuron is bombarded by impulses from
various sources – Ia afferents involved in reflex arc, descending tracts,
and so on. Each impulse passing in the alpha-motor neuron will also
excite, via collateral, the Renshaw cell. The Renshaw cell will exert
inhibitory influence on the motor neuron, thus preventing excessive
signaling to the concerned muscle. It will prevent tetanic contractions; it
may delay the onset of fatigue.

(ii) “Sharpening”: (Influence of Renshaw cell on other neurons in the

motoneuron pool) Renshaw cell innervates other motor neurons in the
motoneuron pool. It may hence inhibit some weakly firing motor
neurons, thus sharpening the signal in the parent motor neuron (that
gave off the collateral for the Renshaw cell).

(iii) Recurrent facilitation: (Renshaw cell influence on the Ia inhibitory

interneuron) As Ia afferent, coming from a muscle (agonist), enters the
spinal cord, it gives a branch that ends on an inhibitory interneuron.
This inhibitory interneuron, in turn ends on the motor neurons that
innervate the antagonist muscle. Thus, even as Ia afferent excites the
motor neuron to the agonist (i.e., forming stretch reflex pathway), it
inhibits the motor neuron innervating the antagonist. This inhibition of
the antagonist, via the Ia inhibitory interneuron, is inhibited by the
Renshaw cell. It is termed ‘recurrent facilitation’.

(2) Feedforward inhibition: (an important mechanism in

cerebellar learning)

- Granule cell, in cerebellum, excites the Purkinje cell. However, via

the short inhibitory interneurons (such as, basket cell and stellate
cell) granule cell can inhibit the Purkinje cell. This is termed
“feedforward inhibition”.

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 [Figure: It shows feedforward inhibition. Granule cell gives out short
axons which run to the surface, and forming a ‘T’, run parallel – the so-
called parallel fibers. The granule cell excites the Purkinje cell; however,
via basket cell and stellate cell, it can also inhibit the Purkinje cell.]

Significance:

Cerebellar learning involves feedforward inhibition. It creates checks and

balances on cerebellar outputs going to agonist and antagonist muscles.

(7) Occlusion and subliminal fringe:

{Occlusion and subliminal fringe are two different properties of synaptic
transmission. Here, they are explained together just to understand the
contrast between them.}
(a) Occlusion:
Consider two presynaptic neurons A and B. They are making synaptic
contacts with 4 neurons each.

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[Fig: Diagrammatic representation. Occlusion of the synaptic response.]

When impulse comes in neuron A, it excites 4 postsynaptic neurons (say, 4 units

response is produced). When impulse comes in neuron B, it excites 4 postsynaptic
neurons (say, another response of 4 units response is produced). However, when
A & B are firing together, it will excite only 7 neurons (or, produces 7 units
response instead of 8). This is because, one postsynaptic neuron (the shaded
neuron in the diagram) is common to both A and B neurons. This lesser response
is said to be the “occlusion” of the responses.

(b) Subliminal fringe:

Now consider another situation; two presynaptic neurons A and B.
They make synaptic contact with 4 neurons each.

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 [Fig: Subliminal fringe. When impulse arrives in neuron A, it excites 3 post synaptic
neurons. When impulse arrives in B, it excites another post synaptic neurons. When
impulse arrives simultaneously in A & B, it excites 7 neurons instead of (3 + 3 =) 6.
Neuron 4 in the figure is in the subliminal fringe of both A & B. Refer to text for
details.]

When impulse comes in the neuron A, it excites 3 postsynaptic neurons (say,

produces 3 units response), but 4 th neuron is stimulated only subliminally (it does
not fire). When impulse comes in the neuron B, it too excites 3 neurons (say,
another 3 units response produced), but 4 th neuron is stimulated subliminally. The
postsynaptic neuron which is subliminally excited, is common to both A and B. Now,
if both A and B are stimulated simultaneously, 3+3=6 neurons fire, plus the 7 th
neuron fires now. This is because subliminal excitations (EPSPs) produced by the A
and B on the 7th (common) neuron get added/summated, so that this neuron
reaches the threshold and starts firing. Thus, there will be 7 units response
instead of 6. The 7th (common) neuron is said to be in the “subliminal fringe” of A
and B.

The neurotransmitters:

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 Whether a transmitter will cause excitation or inhibition is determined by
the nature of the transmitter, the nature of the receptor in the postsynaptic
membrane, and the channel it acts upon.

(I) Excitatory transmitters:

- A transmitter will be ‘excitatory’ if it opens Na+ or Ca++ channel in the post
synaptic membrane.
- Influx of these cations will result in depolarization of the post synaptic
neuron.
- Glutamate and aspartate are the most common excitatory transmitters in
CNS. Note:- Almost 90% transmission in the CNS is caused by glutamate.
(II) Inhibitory transmitters:
- A transmitter will be ‘inhibitory’ if it opens K+ or Cl- channels in the post
synaptic membrane.
- Opening of K+ channel (K+ efflux) or Cl- channel (Cl- influx) results in
hyperpolarization.
- GABA and glycine are the commonest inhibitory transmitters in the CNS.
(GABA more common in brain; glycine more common in spinal cord)

Classification of neurotransmitters:

There are two broad categories of synaptic transmitters-

(A)Small molecule, rapidly acting transmitters [Low-molecular-weight (LMW)

transmitters]
Class I
Acetylcholine
Class II: The amines
Norepinephrine
Epinephrine
Dopamine
Serotonin
Histamine
Class III: Amino acids
Gamma-aminobutyric acid (GABA)

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 Glycine
Glutamate
Aspartate
Class IV:
Nitric oxide (NO)
(B) Neuropeptides, slowly acting transmitters: [High-molecular-weight (HMW)
transmitters]
- Neuropeptide Y (NPY)
- Opioids
- CART
- Endocannabinoids

————————————————————————————————————

REFLEX

Definition:

(1) It is a process in which a sensory stimulus is automatically converted

into a motor response/effect without the involvement of the conscious
higher centers of the brain.
(2) It is an involuntary response to a sudden, adequate stimulus.
{Explanation of the definition-

- There has to be an adequate sensory stimulus.

- It produces an immediate motor response. It could be in the form of muscle
contraction or secretion by a gland.
- The motor response is automatic or involuntary; it does not occur as a
conscious response.}

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 Example:- If our hands touch upon a hot vessel, we withdraw the limb instantly
and subconsciously. Here, the sensory stimulus was the heat, and the motor
response was the muscle contractions that caused withdrawal of the limb.

Classification of reflexes-

Reflexes can be classified in various ways.

REFLEXES

ANATOMICAL PHYSIOLOGICAL CLINICAL INBORN OR ACQUIRED

[1] segmental [1]flexor [1] superficial [1] conditioned

(withdrawal)
[2] intersegmental [2] extensor [2] deep [2] unconditioned

[3] suprasegmental [3] visceral

[4] pathological

(A) Anatomical classification-

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 (i) A segmental reflex is the one in which the sensory and the
motor neuron belongs to the same segment of the spinal cord
(a single segment is involved in the reflex).
(ii) In an intersegmental reflex, sensory and the motor neurons
belong to different segments (more than one segment of the
spinal cord are involved).
(iii) In suprasegmental reflexes, the center for a reflex is in the
spinal cord and the structures above the spinal cord (such as
the brain stem).
(B) Physiological classification-
(i) Flexor withdrawal reflexes: sometimes also called nociceptive
reflexes. When a nociceptive (i.e. painful) stimulus is applied to
some body part such as a limb, there is reflex flexion of the
limb and it withdraws from the source of the stimulus. These
reflexes are protective in nature.
(ii) Extensor reflexes: when a muscle is stretched suddenly, it
responds by a brief contraction. This is called the stretch
reflex. Stretch reflex forms the basis for muscle tone and posture
of the body.
As per the number of synapses involved in a reflex, the reflexes can also be
classified as:

- Monosynaptic reflexes: a single synapse is involved; which means only two

neurons – a sensory and a motor – participate in the reflex. E.g. knee jerk
- Polysynaptic reflexes: many synapses are involved; which means number
of neurons involved is also more than two. E.g. flexor reflexes.
(C) Clinical classification-
This classification is based on the area of the body from which the
reflex arises.
(i) Superficial reflexes:
These are elicited by stimulating the superficial parts of the
body – skin or mucous membrane. E.g. plantar reflex, abdominal
reflex, corneal and conjunctival reflexes, etc.

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 (ii) Deep reflexes:
The tendon jerks are the deep reflexes. Tendon jerks or stretch
reflexes are elicited by stroking a tendon of a muscle (by a
reflex hammer); it stretches the muscle suddenly and there is a
brief contraction of the muscle which shows up as a jerk at the
joint.
(iii) Visceral reflexes:
These reflexes occur at the viscera. At least a part of the reflex
arc involves autonomic nerves. E.g. G.I.reflexes, baroreflexes,
etc.
(iv) Pathological reflexes:
They are not present normally; their presence indicates some
pathology. E.g. Babinski’s sign.

(D)Depending on whether the reflex is present at birth or acquired in later life:

(i) Inborn or unconditioned reflexes-
These reflexes are present generally in all individuals, and they
are present naturally since birth. (it’s not present because of
some training/conditioning) e.g. blink reflex, papillary reflexes,
many G.I. reflexes, etc.
(ii) Acquired or conditioned reflexes-
The individuals acquire these reflexes after
training/conditioning. They may be specific for the individual
as the individual acquired them after some kind of training.
[It was demonstrated by Pavlov’s classical experiment: A dog is
presented with some food; there is reflex salivation in the dog.
This is an innate or inborn reflex. Now, a bell is rung and
immediately food is presented. This is repeated several times.
The dog now “learns” that whenever the bell is rung, food is
presented. A new reflex is established in the dog now; only the
ringing of the bell produces reflex salivation.]

30
  The reflex arc-

[Fig: Components of a reflex arc.]

Components of a reflex arc-

(1) A receptor: a reflex is initiated by stimulation of a receptor (say, in the
skin).
(2) An afferent limb: an afferent nerve that arises from the receptor, takes
the signal towards the center.
(3) A center: a part of the CNS, it is here that the afferent nerve ends and
efferent nerve begins. Reflex is said to be integrated at the center
(4) An efferent limb: an efferent nerve that arises from the center, and
takes the proposed response to the periphery i.e. to the effector organ
(5) Effector organ: it could be a muscle or a gland. It finally demonstrates
the response to the sudden sensory stimulation; it could be muscle
contraction or secretion by a gland.

 Properties of the reflexes:

31
{Since the reflex involves at least a single synapse or even more synapses,
hence many of the properties of a synapse are applicable to the reflexes.}
1. Delay
2. Summation: (i) spatial, (ii) temporal
3. Fatigue
4. Occlusion
5. Subliminal fringe
In addition to these properties (which have been already described in the
“synapse”), there are some additional properties of the reflexes.
6. Localization-
A specific stimulus applied to a particular locus (part) causes a specific
reflex response. A sharp tap on the ligamentum patellae leads to reflex
contraction of quadriceps femoris muscle (knee jerk); or touching the
eyeball causes reflex closure of the eye.
7. Reciprocal innervation-
If an afferent nerve is stimulated, the protagonists contract and the
antagonists relax. This is due to reciprocal innervation of the neurons
from the spinal cord.
8. Facilitation-
If a receptor or a sensory neuron, i.e. afferent path of a reflex arc is
stimulated, a reflex response is obtained. If immediately after the first
stimulus, a second stimulus is applied, the reflex response occurs
quicker than the time taken by the first response.
9. Fractionation-
When a motor nerve to a muscle forming a reflex arc is stimulated, we
get a maximal response. When the corresponding sensory nerve in this
reflex arc is stimulated, the response is only a fraction of the total
response obtained from the motor nerve stimulation. This is known as
“fractionation”. Explanation: the afferent neurons enter into different
levels of spinal cord, and ultimately converge upon a final common
path. And, a particular reflex response is due to sum total of inhibitory
and excitatory effects produced by the converging fibers in the spinal
cord.
10.Rebound-
32
 This phenomenon is observed in connection with reflex inhibition.
Sometimes it is seen that with cessation of reflex inhibition, the reflex
response returns with greater magnitude. This is called rebound. It is
possibly due to overexcitation following a transient inhibition.
11.Irradiation-
It is observed that if a painful stimulus is applied to the toes, there is not
only flexion of the toes, but also contraction of flexor muscles of the
foot, ankle, and the entire limb is withdrawn from the source of the
stimulus. This is thought to be due to “irradiation” of the impulse. When
an incoming signal enters the spinal cord at a particular level, it will
excite the motor neuron involved in the reflex arc, and also may
irradiate or spread to adjacent motor neurons and even to the motor
neurons in other segments of the cord.
12.Recruitment-
If an afferent neuron is stimulated repeatedly, initially there is some
response, and then the response gradually increases and becomes
maximum. This is thought to be due to phenomenon of “recruitment”.
Initially, the stimulation excites the motor neurons in the reflex arc, and
gradually the other neurons in the motoneuron pool start to fire. Since
more and more motoneurons are recruited in the reflex process, it
becomes stronger gradually and reaches maximum.
13.After discharge-
In many polysynaptic reflexes, the reflex path involves reverberating
circuits. That is, the neurons/interneurons in the reflex pathway give out
branches; these branches turn backwards and end on some previous
neuron in the arc. Thus, when there is stimulation of the reflex arc, the
response will be elicited plus the impulse will continue to reverberate
through the pathway for some time. Due to this, the motor neurons
continue to fire and muscles will continue to contract even after the
original stimulus has ceased. This is called “after discharge”.

33
 Section 3

THE SENSORY SYSTEM

Learning objectives:

- To learn the receptor Physiology; How various forms of energy are detected
by sensory receptors, and signals sent to cortex.
- To understand pathways involved in sending of sensory signals to cortex.
- To study the mechanisms involved in transmission of pain signals, and the
analgesia systems in the body.

Introduction:

The sensory system brings information from the periphery into the CNS.
These are sensations which are channeled into the CNS for an immediate
involuntary reflex response and a conscious voluntary motor response.

 Sensation-
It is a conscious feeling evoked by a stimulus. Stimulus is a disturbance in
the environment.
(Sensory modality ~ A sensation with all its related aspects is called a
sensory modality. For instance, touch is a sensory modality having
dimensions like quality, location, intensity, discriminative sense.)
Classification of sensations:

Sensations can be broadly categorized into two types: (I) General, and (II)
Special.

{General sensations can arise from any part of the body. Special senses arise from
specialized end-organs only. General sensations are conveyed spinal as well as
cranial nerves. Each special sense is conveyed by a specific designated cranial
nerve only. Special senses are described in a separate chapter. General senses are
discussed in the present chapter.}

34
(1) General sensations- (such as touch, pain, etc.)
- The general sensations can arise from any part of the body.
- The general sensations are further subdivided into: (i) superficial, (ii) deep,
and (iii) visceral sensations, depending on the body area from which they
arise. {superficial sensations arise from the skin or mucus membranes, deep
sensations arise from deeper structures such as a muscle, visceral
sensations arise from viscera.}
Head’s classification of superficial sensations: Head and his colleagues have
further classified superficial sensations into: (a) epicritic sensations, and (b)
protopathic sensations

- Deep sensations: these include muscle & joint sensations, sense of position
or proprioception, deep pressure and deep pain.
- Visceral sensations: arise from the organs, e.g. thirst, hunger, visceral pain

 “Encoding” of the sensory information:

35
Following principles govern the coding of the sensory information:
(1) Dale’s principle:

‘Same neurotransmitter is released by all the axonal branches of a

neuron.’

(2) Doctrine of specific nerve energies: (Muller’s law)

No matter what form of energy is applied, to excite a particular
sensory pathway, the pathway will convey the same form of energy
(which it always conveys).
Each sensory pathway is distinct, from receptor to cortex. A receptor is
specialized to convey a particular modality of sensation because, there is
a very clear, specific, and distinct pathway that carries the information
from this receptor to a specific area in the brain. No matter how this
particular pathway is stimulated, it will always evoke the sensation
which it is specialized for. This principle was first put forward by Muller,
and is called “doctrine of specific nerve energies”. For example, a visual
pathway leads to the occipital cortex and specializes for vision. Even if it
is stimulated by, say touch, the sensation evoked will be of light/vision
and not touch.
(3) Law of projection:
If a particular sensory pathway is stimulated anywhere in its course,
from the receptor to the cortex, the conscious sensation will be evoked
as though it is arising from the receptor. That is, the sensation will be
referred or projected onto the receptor, no matter where that pathway
is stimulated. This is called “law of projection”. An example of this is
phantom limb. In some cases of amputation of limb, even years after a
limb has been surgically removed, the patient might complain of pain
sensation in that absent limb (phantom limb). The nerve fibers in the
remaining portion of the limb may get stimulated intermittently; the

36
 impulses that are generated are in nerve fibers that previously came
from receptors in the amputated limb, and the sensations evoked are
‘projected’ to where the receptors used to be.

(4) Intensity discrimination:

How do we understand the intensity of a stimulus? For example, how do
differentiate between light touch and heavy touch?
There are two ways in which information about intensity of stimuli is
transmitted to the brain:
(i) By variation in the frequency of the action potentials generated
by the activity in a given receptor, and
(ii) By variation in the number of receptors activated.
Intensity discrimination by the CNS is expressed by the following
laws:

(a) Weber-Fechner law:

Magnitude of the sensation felt is proportionate to the log of the intensity
of the stimulus.

R = K × log
Where R is the sensation felt; S is the intensity of the stimulus, and, K & A
are constants for any specific sensory modality.
{For instance, if the intensity of the applied stimulus (S) is 10 units, and K is
1 (the constant); then the sensation felt (R) will be 1 unit. And, if S is 100
units then the sensation felt will be 2 units. [Log of 10 = 1 and log of 100 =
2]. It means, when the stimulus intensity is increased 10 times, the
perception of the sensation got only doubled. Or, when perception of the
sensation felt

37
 gets doubled, the stimulus intensity is actually increased by 10 times. That is
how we understand the stimulus intensity.}

(b) Steven’s power law function:

It now appears that a power function more accurately describes this
relation, rather than the log function.

R = K × SA
[That is, the frequency of the action potentials generated by a stimulus
is related to the intensity of the stimulus by a power function.]

(5) Stimulus location:

It is encoded primarily by the location of the sensory projection to the

cerebral cortex. This mechanism of encoding is called “topographic
representation”.
Each sensory neuron receives information from a particular sensory area
called its receptive field. The smaller the receptive field, more precise
the encoding of stimulus localization. If two stimuli are applied to the
skin, the sensory task is to indicate whether one or two stimuli are
present. The closest that two stimuli can be to each other and still be
distinguished as separate stimuli is called two-point threshold. The two
stimuli are recognized as separate only if they are placed in receptive
fields that are separated from each other by a nonstimulated receptive
field.
Stimulus localization can be made more precise by lateral inhibition.
Lateral inhibition can decrease the two-point threshold by reducing the
discharge of the neuron innervating the receptive field in the center.
(6) The most sophisticated mechanism of sensory coding uses feature
detectors. These are neurons within the brain that integrate information

38
 from a variety of sensory fibers and fire to indicate the presence of a
complex stimulus.

————————————————————————————————————

 SENSORY RECEPTORS:
Definition:

The receptors are biological “transducers” that convert various forms of

energy in the environment into action potentials (“electrical” impulses) in
the neurons.

The sensory receptor may be part of a neuron, or a specialized cell that

generates action potentials in neurons. The receptor is often associated with
non-neural cells that surround it, forming a sense organ.

 Classification of sense organs-

(A) According to the location of the source of stimulus:
(1) Telereceptors – {“tele” = distance”} They detect the stimuli for
which the source is at a distance from the body. For example,
receptors for vision (light) – rods & cones; receptor for sound –
hair cell in the organ of Corti, receptor for smell.
(2) Exteroceptors – They detect the stimuli applied to the external
surface of the body. Receptors for touch, pain, temperature in the
skin.
(3) Interoceptors – They are concerned with internal environment.
Sensations that arise from internal organs are initiated in the
interoceptors.

39
  Proprioceptors are the receptors that detect proprioception, i.e.
body position in space; they collect information from muscles,
tendons, and joints. E.g., muscle spindle, Golgi tendon organ
 Visceroceptors are the receptors that collect information from
the viscera/organs, e.g., stretch receptors in hollow organs,
baroreceptors, chemoreceptors, osmoreceptors, pain receptors

(B) According to the stimulus energy:

Receptors can be classified into five basic types according to the
stimulus energy detected by them-
(1) Mechanoreceptors: which detect the mechanical energy
(compression or stretching of the receptor or of tissues adjacent
to the receptor); e.g., touch, pressure, vibration
(2) Thermoreceptors: which detect changes in temperature; receptors
for warmth and cold
(3) Nociceptors: (pain receptors), which detect damage occurring in
the tissues
(4) Electromagnetic receptors: which detect light on the retina of the
eye
(5) Chemoreceptors: which detect chemical energy; chemical senses
are taste, smell, oxygen level in the arterial blood, osmolality of
body fluids

 Transduction of sensory stimuli into nerve impulses:

Local electrical currents at nerve endings – RECEPTOR POTENTIALS
Whatever the type of stimulus energy that excites the receptor, its
immediate effect is to change the resting membrane potential of the
receptor. This change in potential is called a receptor potential.
Mechanism of receptor potential or generator potential
Let us consider the example of pacinian corpuscle. It is an encapsulated nerve
fiber terminal.

40
A receptor has two regions: (a) a transducer region, and (b) a spike generator
region.

[Fig: It shows a mechanoreceptor and the sensory neuron associated with it. The transducer
region has mechanically-gated Na+ channels. When a mechanical stimulus (say, touch) is
applied to the receptor, the Na+ channel opens, and the Na+ causes a local depolarization of
the receptor membrane. If this depolarization is more than 10 mV, spike is generated at the
first node of Ranvier. Refer to text for details.]

i. The transducer region of the receptor is responsible for converting the

stimulus energy into an electrical signal called the receptor potential or
generator potential. For instance, in a mechanoreceptor, when the
mechanical energy is applied, it deforms the nerve terminal. The
deformation opens Na+ channels. Influx of sodium causes the membrane to
depolarize. The receptor potential is this small, transient depolarization.
ii. The spike generator region of the receptor is responsible for converting the
receptor potential into train action potentials. The receptor potential
spreads passively from the transducer region to the spike generator region.
It is generally the first node of Ranvier. If the spike generator is depolarized

41
 to threshold, an action potential is generated. The AP then propagates
through the sensory neuron starting from the receptor.

RECEPTOR POTENTIAL:
(i) It is a graded change. That is, if the strength of the stimulus is
increased, the magnitude of the receptor potential also increases
proportionately. {It does not obey all-or-none law like an AP.}
(ii) It is a non-propagated change. It is localized to the receptor
membrane.
Thus, a weak stimulus will elicit a small change in membrane potential; as the
stimulus strength is increased, the amplitude of receptor potential also increases.
When the amplitude of the receptor potential is about 10 mV an action potential
is generated and propagated through the sensory neuron.

The amplitude and duration of receptor potential is directly proportional to the

intensity and duration of the applied stimulus and determines the frequency of
firing (number of impulses per second) of the sensory neuron.

 Properties of receptors-
(1) Excitability:
Each receptor is an excitable unit which can be stimulated by any form
of energy, applied in the form of a stimulus. The receptor shows
electrical “excitation” due to ionic fluxes, resulting in depolarization.
(2) Specificity:
Each receptor is excitable only by a specific stimulus. (For instance,
pacinian corpuscle is stimulated by deformity caused by pressure.) Thus,
specific stimulus would excite a particular receptor. (The specificity is
not

42
 absolute, though. A receptor can be stimulated by other forms of stimuli
as well.)
(3) Adaptation/accommodation:
When a stimulus of constant strength is applied continuously to a
receptor, initially the action potentials are generated at a certain
frequency in the sensory neuron. However, with continued application
of that stimulus, the AP frequency in the neuron declines after some
time. This phenomenon is known as adaptation (or desensitization).
The most obvious function of adaptation is to decrease the amount of
sensory information to the brain. If the receptor adapts, it means it
stops sending signals to the brain about that particular sensation. (We
don’t feel the touch sensation of our clothes after some time of wearing
them because a particular touch receptor adapts to the touch stimulus;
thus unimportant sensory information is not sent to the brain).
There are two types of sensation based on this property:
i. Rapidly adapting (phasic) receptors or velocity receptors – e.g. Pacinian
corpuscle
ii. Slowly adapting (tonic) receptors or intensity receptors – e.g. pain
receptors

(4) Localization:
By stimulation of a particular receptor, the localization of the particular
sensation is possible. This is because of the topographic representation.
The nerve pathways starting from a particular receptor on the body end
in a particular area of the sensory cortex in the brain.

Examples of receptors:

1) Mechanoreceptors: (i) Merkel’s discs, (ii) Meissner’s corpuscle, (iii) Pacinian

corpuscle, (iv) Ruffini corpuscle, (v) Iggo dome receptor

43
 2) Thermoreceptors: They belong to the TRP superfamily of receptors. [TRP =
Transient receptor potential.] E.g., Cold- and menthol-sensitive receptor
(CMR).
3) Chemoreceptors: Taste receptors in taste buds, smell receptors, glomus cell
in carotid body.
4) Electromagnetic receptors: Rods & cones in retina
5) Nociceptors: They belong to TRP superfamily. E.g., TRP-V1. [V = vanilloid]

Sensory units-

A single sensory axon and all its peripheral branches are collectively called
as a “sensory unit”.

The receptive field of a sensory unit is the area from which a stimulus produces a
response in that unit.

“Recruitment” of sensory units:

As the strength of a stimulus is increased, it tends to spread over a large

area and generally not only activates the sense organs immediately in contact with it
but also “recruits” those in the surrounding area. Furthermore, weak stimuli
activate the receptors with the lowest thresholds, whereas stronger stimuli also
activate those with higher thresholds. Because of overlap and interdigitation of
one sensory unit with another, receptors of many sensory units get stimulated
with a stronger stimulation. Consequently, more units fire, more afferent
pathways are activated, and this is interpreted in the brain as an increase in
intensity of the sensation.

44
 Ascending tracts in spinal cord

[Transmission of sensations in the CNS]

General organization:

A sensory stimulus is detected by receptor and it generates signal in the

peripheral sensory neuron. This neuron enters the spinal cord. Sensory signal will
now ascend upward in the spinal cord, and will eventually reach the sensory
cortex.

A 3-neuron path conveys any sensation from periphery to cortex:

(i) First-order neuron [from receptor to spinal cord]-

The cell body of the first-order neuron is located in the dorsal root
ganglion of a spinal nerve. The axon carries signals from the somatic
receptor into the spinal cord by way of the dorsal root of the spinal
nerve.
(ii) Second-order neuron [spinal cord to thalamus]-
Axons of the second order neurons carry signals from the spinal cord or
brain stem to the thalamus. The axons cross the midline (decussate) in
the spinal cord or in the brain stem and ascend to the contralateral
thalamus, where they synapse with third-order neurons located in the
thalamic nuclei.
(iii) Third-order neuron [thalamus to cortex]-
Axons of the third-order neuron transmit signals from the thalamus to the
sensory cortex (parietal lobe); conscious perception of somatic
sensation occurs in the cortex.

 Sensory pathways (ascending tracts) in the CNS:

The sensory information from the periphery enters the spinal cord through
the dorsal roots of the spinal nerves. From the entry point of the cord to
45
the

46
 brain, the sensory signals are carried through one of two sensory (ascending)
pathways:
(1) The dorsal column-medial lemniscal system (or posterior columns);
(2) The anterolateral system

[Fig: The transverse section of spinal cord, at one segment. It shows the grey matter at the
center; it divides the remaining portion into 3 white columns – the anterior, lateral, and
posterior/dorsal white columns.]

The dorsal column-medial lemniscal system carries signals in the dorsal white
columns of the cord. Signals of the anterolateral system ascend through the
anterior and lateral white columns of the cord.

(I) Dorsal columns carry the following sensations:

 Fine touch

47
  Pressure
 Vibration
 Proprioception and kinesthetic sensation
(II) Anterolateral system carries following sensations:
 Crude touch
 Pain
 Temperature
 Tickle and itch
 Sexual sensations

Dorsal columns Anterolateral system

(1) Composed of large, myelinated Composed of smaller myelinated
fibers; rapid velocity of signal fibers; slower velocity of signal
transmission (30-110 m/sec) transmission (max. upto 40 m/sec)
(2) Fibers have high degree of spatial Lesser degree of spatial orientation of
orientation (causes accurate nerve fibers (point-to-point
point-to-point transmission) transmission of information is not so
accurate)

{If there is a sensation of pain or temperature due to some object, we would

perceive the touch of that object first, and pain or temperature is felt a fraction of
a second later. Touch is transmitted faster in the CNS, by dorsal columns. Pain and
temperature are carried slower, by the anterolateral system.

Localization of fine touch is more accurate; localization of pain and temperature

may not be so accurate.}

Dorsal column system:

48
(Transmission of fine touch)

[Fig: Transmission of touch from periphery to cortex. Note:- In the dorsal columns, fibers
coming from lower limb are pushed to the midline by fibers coming from upper limb. Refer to
text for further details.]

- Receptors in the skin : Meissner’s corpuscle, Merkel’s disc

I. First order neuron: A type of nerve fiber starts from the receptors and
enters the spinal cord through the dorsal horn.
- On entering the spinal cord, the fibers divide into two branches. The lateral
branch enters the dorsal horn, divides many times, and synapses with local
neurons. This provides the pathway for local spinal cord reflexes.
- The medial branch turns upward in the dorsal white matter; the dorsal
columns then ascend upwards toward the brain.
- In the dorsal columns, the fibers located near midline are coming from
lower extremities and abdomen. They form the fasciculus gracilis. The
fibers

49
 located laterally in the dorsal columns are the fibers coming from upper body
parts (except face); they form the fasciculus cuneatus. Together, the
fasciculus gracilis and fasciculus cuneatus are called the dorsal columns.
- These fibers continue uninterrupted up to the upper medulla, where they
synapse with dorsal column nuclei – nucleus gracilis and nucleus cuneatus
– respectively.
II. Second order neuron:
Fibers from the dorsal column nuclei cross midline to run on the opposite
side as medial lemniscus. While medial lemniscus runs through the brain
stem, it is joined by trigeminal nerve fibers (V N.) that carry touch
sensation from the face.
These fibers reach the thalamus on the opposite side. The trigemino-
thalamic tract synapses with the VPM nucleus and fibers coming from
nucleus gracilis & cuneatus synapse with the VPL nucleus of thalamus.
III. Third order neuron: Neurons from the thalamic nucleus then project to the
sensory cortex, mainly to the postcentral gyrus, called somatic sensory
area I (or S I).

The somatosensory cortex:

50
[Fig: Sensory cortex in parietal lobe, behind central sulcus.]

- Located mainly in the post central gyrus; in the parietal lobe.

- There are two sensory areas in the anterior parietal lobe: somatic sensory
area I (S I), and somatic sensory area II (S II). S I also projects to S II.
- S I corresponds to Broadmann’s areas 3, 1, and 2.
- Body representation is contralateral. (left half of the body is represented in
the right cortex, and right half in the left cortex)
- Body parts are represented in an inverted manner (legs are represented on
top and the head is represented at the bottom of the gyrus). Map of the body
parts is called somatotopic organization. There is detailed localization of the
fibers from the various body parts in the post central gyrus; parts of the
body that have the greatest density of receptors are represented by a
greater proportion of the cortex. Cortical areas for sensation from the trunk
and back are small, whereas very large areas are designated for impulses
coming from lips and face. The map of the entire body created in the
somatosensory cortex is called the sensory homunculus.
- S II is located in the superior wall of the sylvian fissure, the fissure that
separates the temporal from the frontal and parietal lobes. It corresponds
to

51
 Broadmann’s areas 5 and 7. The representation of the body parts is not
complete or very detailed.

In the somatosensory areas, the complete meaning of a particular sensation is

understood, such as (i) appreciation of the size, shape, texture, and weight of
the objects – stereognosis. (ii) appreciation of relative intensity of the different
stimuli. (iii) tactile localization, two-point discrimination.

Function of S II: Stereognosis

It combines information arriving from multiple points in the area S I to

decipher its meaning.

Cortical plasticity:

If a limb or a finger is amputated, now the cortical area representing that part
will become dormant. Then, neurons from the neighboring areas of the cortex
will converge onto this area.

Conversely, if the cortical area representing a limb or a finger is removed, the

sensory map of that body part will move to the surrounding cortex.

~ Transmission of vibration sense:

- Receptor: pacinian corpuscle

- Peripheral (sensory) nerve: A type of fiber
- It enters the spinal cord and then transmitted toward brain in the dorsal
columns

~ Transmission of proprioception:

- Receptor: muscle spindle and Golgi tendon organ

- Peripheral nerve: A type or type Ia, type Ib, and type II (from the
“annulospiral” and “flower spray” endings)

52
 - It enters the spinal cord. Then conscious proprioception is transmitted
mainly via the dorsal columns to the sensory cortex. Subconscious
proprioception is also sent in dorsal columns to the cortex, and to cerebellum
via spinocerebellar tracts.

 Anterolateral pathway- (transmission of crude touch, pain, temperature)

[Fig: Lateral spinothalamic tract. Note:- In the lateral white column, arrangement of fibers,
from lateral to medial aspect is – Lower limb (LL), abdomen, upper limb (UL).]

i. Receptors:
- Pain & Temperature receptors:- TRP superfamily;
- Tickle & itch:- Free nerve endings (of C-type unmyelinated nerve fibers)
ii. First order neuron: (primary afferents)

53
 - A- (fast pain, temperature) and C-fibers (slow pain) carry the impulses into
the spinal cord.
- On entering the spinal cord, these fibers end in the laminae in the dorsal
horn.
iii. The second order neuron: It crosses the midline via the anterior commissure,
and reach the lateral white column of the opposite side.
It then runs upward as lateral spinothalamic tract. (Crude touch is carried
in anterior white column.) Axons of the spinothalamic tracts from sacral
and lumbar segments are pushed laterally by axons entering in at
successively higher levels.
- Thus, in lateral spinothalamic tract, the arrangement of fibers from lateral
to medial is – lower limb, abdomen, upper limb.
- The second order neuron relays in VPL nucleus of thalamus. In addition, the
fibers are also relayed to:
 To the reticular nuclei of the brain stem, and
 Ventrobasal complex and intralaminar nuclei of thalamus.

(The crude touch signals are then transmitted from here, with the fibers of dorsal
column system, to the sensory cortex.)
Pain and temperature signals mostly terminate in the reticular nuclei; they
activate reticular activating system, which in turn maintains the cortex in the alert
state.

The anterolateral system transmits the crude sensations which do not require exact
localization and discrimination.

Some other important aspects of the ascending tracts:

54
 (a) If there is a lesion of the cortex, finer discriminative senses (fine touch,
two-point discrimination, etc) are lost, but crude touch and other crude
sensations are not lost.
(b) Sense of pain and temperature are felt at the level of thalamus, brain
stem, and other lower brain centers (intact cortex isn’t necessary).

————————————————————————————————————

PHYSIOLOGY OF PAIN

Introduction:

PAIN IS AN UNPLEASANT SENSORY EXPERIENCE.

- Many diseases of the body cause pain; it is one of the commonest symptoms.
- Pain is mainly a protective mechanism for the body; it occurs whenever any
tissues are being damaged, and it causes the individual to react to remove
the pain stimulus.
(for instance, sitting for a long time can cause tissue destruction because of
lack of blood flow to the skin where the skin is compressed by the weight of
the body. When the skin becomes painful as a result of ischemia, the
person subconsciously changes position and shifts weight.)

 Types of pain: (fast v/s slow)

There are two major types of
pain-
(1) Fast pain:- also described as sharp pain, acute pain, pricking pain. E.g.
pain felt when the skin is cut with a sharp object. It is felt within 0.1
second after a pain stimulus is applied. This type of pain mostly arises
from superficial parts of the body

55
 (2) Slow pain:- also described as dull pain, chronic pain, aching pain. It
begins only after 1 second or more (after stimulus application) and then
increases slowly over many seconds or minutes. It is usually associated
with tissue destruction (thus arising, generally, from deeper parts), it can
also occur in the skin.

Pain receptors and their stimulation:

- Earlier, free nerve endings were thought to be nociceptors.

- Now it is known that the pain receptors belong to the TRP superfamily.
TRP- V1 (V = vanilloid).
- They are widespread in the superficial layers of the skin, and in some
internal tissues. Many deep tissues, however, are NOT supplied extensively
with pain receptors.
- Three types of stimuli excite pain receptors:- mechanical, thermal, and
chemical. In general, fast pain is elicited by the mechanical and thermal types
of stimuli, and slow pain can be elicited by all three types.
- Pain receptors are nonadapting receptors. They continue to send the pain
signals as long as the stimulus continues.

 Dual transmission of pain signals into the CNS:

Pain signals arise from vanilloid receptors, and then two separate pathways
transmit the signals into the CNS:- the fast pain pathway, and the slow pain
pathway.

- The fast pain is transmitted from the periphery in A type of fibers

(velocity: 5 to 30 m/sec) toward the spinal cord; the slow pain is
transmitted in C type of fibers (velocity: 0.5 to 2 m/sec).

56
 - On entering the spinal cord, the A fibers (fast pain) terminate mainly in
lamina I (lamina marginalis) of the dorsal horns, and C fibers (slow pain)
terminate in laminae II and III (together called substantia gelatinosa) of the
dorsal horns.

[Fig: It shows transmission of fast & slow pain. A fibers and C fibers (primary afferents for
fast and slow pain, respectively) enter the spinal cord. They release glutamate and substance
P, respectively, on the nerve cell bodies of the 2nd order neuron.]
Glutamate is the neurotransmitter secreted by A fibers carrying fast pain to the
spinal cord. Substance P is the neurotransmitter secreted by C fibers carrying slow
pain to the spinal cord.

Neospinothalamic tract for fast pain-

- The fibers carrying fast pain cross to the opposite side of the cord through
the anterior commissure and then pass upward as NEOSPINOTHALAMIC
TRACT.
- Some fibers of this tract terminate in the reticular areas of the brain stem,
most other fibers reach thalamus and end in the ventrobasal complex of
thalamus. From the thalamus, the third-order neurons project to the
sensory cortex.

Paleospinothalamic tract for slow pain-

57
 - From the laminae II and III of the spinal cord, the fibers carrying slow pain
cross to the opposite side, and then second-order neuron runs upward in
paleospinothalamic tract.
- The paleospinothalamic fibers give collaterals in these areas: (i) reticular
nuclei of the brain stem, (ii) tectum of the midbrain, and (iii) periaqueductal
gray.
- Then, the fibers relay in the thalamus; in the nonspecific (midline and
intralaminar) nuclei of the thalamus. Some fibers are also relayed into
portions of hypothalamus.
- Eventually, the fibers are projected to the sensory cortex.

 Pain sensitive and insensitive structures of the body-

Pain sensitive Pain insensitive

(1) Skin, mucous membranes,
(cornea is particularly sensitive
to irritants)
(2) Blood vessels and sinuses in the Brain substance totally insensitive;
cranium; muscle around the dura and pia mater insensitive
cranium
(3) Parietal pleura; heart (sensitive Lung, visceral pleura, pericardium
to chemical stimuli)
(4) Parietal peritoneum, liver Liver parenchyma, spleen, kidney,
capsule, bile ducts, mesenteric visceral peritoneum. (intestines have
arteries sparse sensory innervations)
(5) Pelvis of kidney, ureter, base of
the bladder, urethra
(6) Cervix of uterus Uterus (not sensitive to cutting or
cauterization)
(7) Testis

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  Types of pain:
(A) Physiologic pain-
(B) Pathologic pain-
Neuropathic pain

(A)Physiologic pain:

Stimulation of pain receptors (nociceptors) causes pain sensation. This is

physiologic pain.

(a) Allodynia: A non-noxious stimulus (like, touch) causing pain sensation

(b) Nociceptive pain: A noxious stimulus causing corresponding degree of pain
(c) Hyperalgesia: A noxious stimulus causing exaggerated or excessive pain
Inflammatory conditions cause hyperalgesia. Inflammation of a tissue
causes release of chemical mediators and cytokines. These chemicals
sensitize the receptors and nerve fibers (which become hypersensitive);
hence, there is excessive pain signal even with modest stimulus.
Two types of hyperalgesia: - (i) Primary hyperalgesia ~ When stimulus is
applied at the site of injury/inflammation. (ii) Secondary hyperalgesia ~
When stimulus is applied away from the site of injury, anywhere along the
path to CNS.

(B) Neuropathic pain:

- Pain sometimes occurs in the absence of nociceptor stimulation.
- Pain caused due to damage to nerves or damage to parts of the CNS that
are involved in pain transmission.
- Peripheral neuropathic pain is caused by damage to a peripheral nerve.
(E.g. causalgia, and phantom limb pain). Central neuropathic pain occurs
after damage to CNS structures.
- Neuropathic pain may be relieved by surgical procedure such as
anterolateral cordotomy (spinothalamic tracts are carefully cut).

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 Referred pain:

- Irritation of a viscus or a deep organ frequently produces pain which is felt

not in the organ but in some superficial structure that may be well away from
that organ. Such pain is said to be a referred pain.
- The best known example is of cardiac pain. The pain due to angina (that is,
cardiac origin) is “referred” to the inner aspect of the left arm. It is felt in
the left arm and left shoulder.
- Inflammation of the appendix usually produces pain around the umbilicus.
Disease of the gall bladder may irritate the diaphragm and the pain is
referred to tip of the shoulder.

Explanation:
The common point between the site of the referred pain and the diseased
organ is that both are innervated by the same segment of the spinal cord.
Since the brain is usually trained to receive information about painful
stimuli only from the superficial parts of the body, it interprets the painful
stimulus arising from a deep organ also as originating from superficial part.
Dermatomal rule:
When pain is referred, it is usually to a structure that developed from
the same embryonic segment or dermatome as the structure in which the
pain originates. This principle is called the dermatomal rule. For example,
during embryonic development, the diaphragm migrates from the neck
region to its adult location (between the chest and the abdomen), and
takes its nerve supply, the phrenic nerve, with it. Afferent fibers in the
phrenic nerve enter the spinal cord at the level of C-2 to C-4 , the same
location at which afferents from the tip of the shoulder enter. Similarly, the
heart and the arm have the same segmental origin.

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Mechanism of referred pain:

[Fig: Fiber coming from heart and fiber coming from left upper limb ‘converge’ on the same
segment of spinal cord. Their second-order neurons are carried together in the spinothalamic
tract. When signals reach a particular cortical area, cortex makes the person ‘believe’ that the
pain is arising from the left upper limb, whereas actual source of pain is the heart.]
The main cause of referred pain appears to be plasticity in the CNS
coupled with convergence of peripheral and visceral pain fibers on the
same second-order neuron that projects to the brain. Peripheral and
visceral neurons converge in lamina VII of the dorsal horn. The peripheral
pain fibers normally do not fire the second-order neurons, but when the
visceral stimulus is prolonged there is facilitation of the peripheral fibers.
They now stimulate the second-order neurons, and of course the brain
cannot determine whether the stimulus came from the viscera or from the
area of referral.
Theory of convergence:
Because the number of fibers in the spinothalamic tract is less than
the sensory fibers in the peripheral nerves, there is convergence of fibers
from somatic and visceral structures.
Theory of facilitation:
Owing to a subliminal fringe effect, the incoming fibers from the
visceral structures lowers the threshold for incoming fibers from somatic
structure.

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 Causes of visceral pain:
(1) Ischemia-
Lack of oxygen supply would result in anaerobic metabolism; the acidic
metabolic end products (lactic acid) or tissue degenerative products
(bradykinin, etc) may irritate the pain nerve endings.
(2) Chemical stimuli-
For instance, proteolytic acidic gastric juice may come in contact with a
gastric or duodenal (peptic) ulcer.
(3) Spasm of a hollow organ-
Spasmodic contractions of hollow structures (gut, bile duct, ureter, etc)
may cause mechanical stimulation of the pain nerve endings, or the
spasm may cause diminished blood flow to the muscle. It results in
cramps.
(4) Overdistention of a hollow organ-
It may cause pain due to overstretch of the tissues.

 Endogenous pain relief system: (analgesia systems in the brain and spinal
cord)
The body has an in-built system for reducing the intensity of pain. The body’s
pain control system or analgesia system has following components-
(A) The brain’s opiates system (endorphins, enkephalins, and dynorphin)
Opioids or “morphine-like” substances have been found in different
parts of the brain. And, there are opioid receptors present in these
parts of the brain, on which the opioids act. The three major opiates
found in the brain are: -endorphin, enkephalin, and dynorphin. The
receptor subtypes for these opioid peptids are: mu (, kappa (,
and delta (. Opioids inhibit neurons in the brain involved in the
perception of pain. (They may also elevate the pain threshold. Thus,
intensity of pain sensation is reduced.)

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 (B) Descending pain-inhibitory system-

[Fig: Components of the descending analgesia system. Refer to text.]

- It starts in the brain and descends onto the spinal cord.

- It has 3 components: (i) periaqueductal grey, (ii) nucleus raphe magnus, (iii)
pain inhibitory complex of the spinal cord.
- Activation of the periaqueductal grey (enkephalinergic) neurons sends the
signals to the nucleus raphe magnus. The neurons of this nucleus are
serotonergic; they project onto the pain inhibitory complex in the dorsal
horn of the spinal cord. This complex has enkephalinergic neurons. These
neurons cause pre-synaptic and post-synaptic inhibition of the incoming pain
fibers into the spinal cord.

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 (C) Gate control theory: (acupressure therapy is based on gate control)

[Fig: “Gate” control mechanism. The pain afferent, coming from periphery, synapses in the
substantia gelatinosa (laminae II & III in the dorsal horn). Pressure-carrying fiber (shown in
green) enters spinal cord and gives off a collateral that excites an inhibitory interneuron
(shown in red). The inhibitory interneuron inhibits the pain afferent, thereby closing the gate
for pain signals.]

- The “gate” is in the laminae II & III or substantia gelatinosa of the dorsal
horn. Dorsal horn neurons that transmit painful stimuli to the brain can be
inhibited by simultaneous application of non-noxious stimuli (touch or
pressure). The touch fiber (a large myelinated afferent) gives off a collateral
which excites an inhibitory interneuron. This interneuron inhibits the pain
fiber presynaptically. The interneuron acts as a gate. When the
touch/pressure stimulus excites the inhibitory interneuron, the gate is
closed, that is, pain impulses cannot ascend upwards.
- A medical therapy designed to activate the gate control mechanism is
Transcutaneous Electrical Nerve Stimulation (TENS). In this procedure,
application of electric shocks to the skin in the painful area reduces pain.

64
Applied physiology:

- Analgesic medication commonly used to alleviate pain belongs to the

category called NSAIDs (non-steroidal anti-inflammatory drugs).
- NSAIDs have one or more of the following properties – analgesia, anti-
pyretic, anti-inflammatory.
- Some drugs in this category have strong anti-inflammatory action, e.g.
ibuprofen, diclofenac. The others have weak anti-inflammatory action but
strong analgesic and anti-pyretic action, e.g. paracetamol.

65
 Section 4
MOTOR SYSTEM

Learning objectives:
- Motor system is about making voluntary movements in a smooth,
precise, and well co-ordinated manner. First objective is to understand
the organization of motor system.
- This section discusses the components of motor system, viz.,
descending tracts, cerebellum, and basal ganglia. It is imperative to
understand the circuitry and neural paths that constitute these parts.
- Vestibular system, postural reflexes allow a person to maintain
equilibrium and desired background posture on the basis of which
any voluntary movement is possible.
- Lower motor neuron (LMN) is the final common path involved in
execution of voluntary movements. This section explains the
mechanisms underlying the functions of muscle proprioceptors and LMN.

Introduction:

All the information gathered from the external environment by sensory

systems is used by the brain to organize and execute an appropriate motor
response. This motor response is in the form of muscle contractions that produce
movements. (For instance, ringing of a cell phone at some distance would be the
sensory information sent into the brain. Then, an appropriate response is
designed by the brain, and it is executed by causing appropriate muscle group
contractions, so as to walk up to the phone, pick it up, switch it on, and speak.)

What regions of the brain are involved in motor function?

- Various areas of the cerebral cortex organize and interpret

complex sensory input and program the responding movements.
- The brain stem controls spinal cord output in maintaining posture
and balance of the body.

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 - The cerebellum and the basal ganglia also plan, program, and
coordinate specific types of motor responses.

Motor responses may be automatic, involuntary reflex actions (such as knee

jerk); or they may be complex, voluntary activities, such as those needed to play a
piano. The final common pathway for all these actions is the alpha motor
neuron, which originates in the anterior horn of the spinal cord. These neurons
innervate skeletal muscle. Activation of these neurons cause contraction of
skeletal muscles, which results in either movement or tension development to
stabilize the body parts.

- Motor system functioning is based on a 2-neuron path:- (1) Upper motor

neuron [UMN] – It starts from motor cortex and other higher centers
(cerebellum, basal ganglia) and descends down to end in the spinal cord
(or, in some instances, in the brain stem nuclei), and (2) Lower motor
neuron [LMN] – It starts from the spinal cord (or brain stem) and
reaches the muscles.

[Fig: Upper motor neuron (cortex-to-spinal cord) and lower motor neuron (spinal cord-to-
muscle).]

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  Upper motor neuron (UMN) exerts both excitatory and inhibitory
influences on the lower motor neuron (LMN); however, inhibitory
influence predominates.
- In the lesion of UMN: The predominently inhibitory influence on the LMN
is lost. It results in unchecked, excessive impulses in the LMN. It is
manifested as excessive muscle tone (spasticity/rigidity) and exaggerated
tendon reflexes.
- In the lesion of LMN: Lower motor neuron (LMN) is the final common
path reaching muscles. Hence, in the lesion of LMN, no signals reach
muscles. It is manifested as loss of muscle tone (flaccidity) and diminished
tendon reflexes.

Organization of motor system: (Refer to the diagram below while reading the
text)

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[Fig: Organization of motor system. Refer to text for detailed explanation.]

 The thought for a movement is generated in premotor

and supplementary motor areas (area 6).
 Then, the thought is transferred to basal ganglia, where the
thought is converted into voluntary movement. [Also, basal ganglia
select the desired movement and suppress other movements.
Purpose of the movement is determined; proportion of the
movement is decided.]
 Next, cerebellum is signaled about the movement. Sequence of
muscle contractions is set (by neocerebellum).
 As per the sequence decided, the command for the
concerned muscles is generated in the primary motor cortex
(area 4); the

69
 command is then sent down for execution, via the descending tracts,
on to the spinal cord.
 The descending fibers: Arising from the cortex, the fibers descend
down in two sets ~ (i) One set of fibers starts from the cortex and
directly reaches the spinal cord uninterrupted. This is corticospinal
tract. (While passing through medulla, these fibers make
appearance of a pyramid, for which reason, it is also referred to as
“pyramidal
tract”.) (ii) The other set of fibers, starting from the cortex, end in
the brain stem. These are corticobulbar and corticonuclear fibers
(cortex- to-brain stem nuclei). From the brain stem, a fresh set of
fibers arises and descends down on to the spinal cord. These are
conventionally called “extrapyramidal tracts” (any descending tract
other than the pyramidal tract).
 The dual arrangement:
 Corticospinal tract initiates the voluntary movement and
control smaller muscle groups.
 Extrapyramidal tracts control axial musculature; they provide
postural support and maintain equilibrium of the body
during the movement.

[From brain stem nuclei to spinal cord, the extrapyramidal tracts are:- (1)
Vestibulospinal tract – From vestibular nuclei to spinal cord, (2) Reticulospinal
tract – From reticular nuclei to spinal cord, (3) Rubrospinal tract – From red
nucleus of midbrain to spinal cord, and (4) Tectospinal tract – From tectum
(superior & inferior colliculi) to spinal cord.]

 The spinal cord contains the final common pathways through which
a movement is executed. By selecting the proper motoneurons for a

70
 particular task and by reflexly adjusting the amount of motoneuron
activity, the spinal cord plays an important role in the coordination of
motor activity.
 Once the movement is initiated (by corticospinal tract), cerebellum starts
playing a major role. As the muscle contractions begin, proprioceptive
information, arising from those muscles, is sent back to spinal cord
(moment-to-moment changes in muscle length). From the spinal cord, this
information is sent to cerebellum (spinocerebellar tracts). Cerebellum
compares this information with the intention of cortex. Accordingly, it
sends the signals back to spinal cord, and thereby to those contracting
muscles, to make adjustments in contractions; thus, the movement will
be performed precisely, in a smooth and well coordinated manner.
 Sensory feedback to the motor cortex:
- Neurons in the motor cortex are informed of the consequences of
movement through sensory feedback pathways. They receive input from
either the muscles they project to or from areas of skin surrounding the
muscle. This long loop of sensory feedback results in the alteration of
information from the motor cortex to the spinal cord to correct any
deviations from the intended movement. Sensory feedback to the
motor cortex occurs by the way of the somatosensory cortex.
- The nerve cells in the sensory cortex are connected to those in the motor
cortex in a topographic manner. Cells in the sensory cortex receiving
proprioceptive input from muscles in the thumb, for example, are
connected with cells in the motor cortex responsible for the contraction
of these same muscles. In this way, feedback is provided by the sensory
system to inform the cells in the motor cortex whether the instructions
they have transmitted for the muscular contraction have been faithfully
executed.
 The posterior parietal cortex integrates sensory stimuli for
purposeful movement:
The posterior parietal cortex is located immediately behind the
somatosensory cortex. This cortex receives both somatic and visual sensory
information and transmits it to the supplemental and premotor areas. This

71
 area is responsible for the processing of sensory stimuli leading to
purposeful movement.

The upper motor neuron [UMN]

(The descending tracts and pathways that end on brain stem or spinal cord; the
pyramidal and extrapyramidal tracts)

Pyramidal system:

Corticospinal and corticobulbar tracts:

 Origin: THE MOTOR CORTEX:

Anterior to the central sulcus (the precentral gyrus), occupying the

posterior one third of the frontal lobes is the motor cortex. The motor
cortex is further divided into 3 areas: (i) the primary motor cortex, (ii) the
premotor area, and (iii) the supplementary motor area.
(i) Primary motor cortex: (area 4)

 Located in the precentral gyrus, in the frontal

lobe; Broadmann’s area 4;
 There is topographic representation of body muscles; the
face is represented laterally, near the lateral fissure, and the
lower extremity is represented on the medial aspect of the
hemisphere. The entire body map drawn on the cerebral
cortex is called motor homunculus.
 Most medial parts control toes/lower limbs; most lateral
parts represent face/jaw. Area for thumb has a
disproportionately large area in the motor cortex. Also,
muscles for mastication and muscles for vocalization have a
very large representation in the motor cortex.

72
  More than 50% of the entire primary cortex is occupied by
the neurons controlling the hands and muscles of speech.
 Body representation is contralateral, that is, right
hemisphere motor cortex controls the left half of the body
and vice versa.

[Fig: Motor cortex in frontal lobe. Refer to text.]

(ii) Premotor area: (area 6)

 Lies immediately anterior to the primary motor cortex; Area

6 of Broadmann;
 Topographical representation is roughly the same as that of
the primary cortex, with mouth and face areas located most
laterally and then, moving upward, the hand, arm, trunk,
and leg areas.
 Nerve signals generated in the premotor area cause
much more complex “patterns” of movement than the
discrete patterns generated in the primary motor cortex.

(iii) Supplementary motor area:

Lies mainly in the longitudinal fissure, extends onto the superior
frontal cortex.
Contractions elicited by stimulating this area are often bilateral
rather than unilateral.

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Pyramidal tract: (Corticospinal tract plus corticobulbar & corticonuclear fibers)

[Fig: Pyramidal tract. Note a few points. The fibers converge and start running down; they
pass through the anterior 2/3rd of the posterior limb of internal capsule. Corticobulbar &
corticonuclear fibers end on the brain stem nuclei. There is crossing over of the fibers,
creating motor decussation in lower medulla. Refer to text for more details.]
 Origin:
- 30% fibers arise from area 4, 30% fibers arise from area 6, and 40%
fibers arise from somatosensory cortex (post central gyrus; parietal
lobe).
- Area 4 of the Broadmann, that is, the primary motor cortex, contains
giant pyramidal cells or Betz cells. Axons of these Betz cells are very

74
 broad, heavily myelinated, and rapidly conducting. However, only 3% of
the fibers of the pyramidal tract are axons of these cells. The other 97%
fibers of the pyramidal tract are small diameter fibers that conduct the
signals slowly; mainly background tonic signals to the motor areas of the
spinal cord.
 Course:
From all the cortical areas (mentioned above) fibers converge and descend
downwards through the subcortical structures-
- Corona radiata - Fibers converging from the various cortical areas make
an appearance that is described as corona radiata.
- Internal capsule - It is a V-shaped structure having two limbs, anterior
and posterior. Fibers of the pyramidal tract are closely packed in the
internal capsule; they occupy the genu and the anterior 2/3 rd of the
posterior limb of the internal capsule. {It is important to note that
while descending through the internal capsule, fibers of the pyramidal
tract intermingle with extrapyramidal fibers. Hence, lesions of the
internal capsule invariably involve extrapyramidal fibers along with
pyramidal fibers.}
- Midbrain – Some cranial nerve nuclei are present in the midbrain. Some
of the pyramidal fibers (coming from the appropriate area of the
cortex) end on these cranial nerve nuclei; they are corticonuclear fibers.
Corticobulbar fibers are the fibers ending on the brain stem nuclei,
such as, vestibular & reticular nuclei)
All the other fibers descend down.
- Pons – Compactness of the bundle (of pyramidal fibers) is
loosened here.
- Medulla - Fibers are again assorted into a compact bundle. The
compact bundle now produces an elevation on the ventral aspect of the
medulla (the so-called “pyramids”), one on each side. These are called
medullary pyramids. Hence the name, pyramidal tract.
Further lower down, near the lower end of the medulla, 80-85% fibers
cross to the opposite side. This creates the “motor decussation”
(created by crossing of pyramidal fibers to the opposite sides).

75
 Remaining 15-20% fibers remain on the same side. Thus, there will now
be two pyramidal tracts entering the spinal cord – the crossed pyramidal
tract and the uncrossed pyramidal tract.
- Spinal cord - On entering the spinal cord, the crossed fibers run
downward in the lateral funiculus of the cord, hence called
lateral corticospinal tract.
The uncrossed fibers descend through the anterior funiculus of the
spinal cord and hence known as anterior corticospinal tract. Eventually,
most of these fibers also will cross to the opposite side at successive
segments of the cord as they descend. (Mostly they cross to the
opposite side of the cord in the neck or in the upper thoracic region).
Distribution of fibers in relation to body parts:
55% of the corticospinal fibers pass to the upper limb, 20% to the trunk,
and 25% to the lower limb.
 Termination:

- Fibers of the corticospinal tracts terminate principally on the

interneurons, in the intermediate regions of the cord grey
matter.
- Some of the fibers end on sensory relay neurons in the dorsal horn
of the spinal cord.
- Some fibers end directly on the anterior motor neurons that cause
muscle contraction. These fibers are concerned with the movements of
the fine muscles of the fingers (muscles which require delicate
control).

 Functions:
(i) It initiates voluntary movements.
(ii) It controls skillful activity and fine movements
(iii) It controls the distal musculature of the extremities (especially
of upper limbs).
(iv) It gives precision, accuracy, and fineness to the motion.

Clinical application:
Effects of pyramidal lesion:
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 (i) Paralysis of contralateral half of the body, due to lesion on one
side; loss of voluntary movements
(ii) Loss of superficial reflexes (such as abdominal and
cremasteric reflexes)
(iii) Presence of Babinski’s sign (extensor plantar response)
 If there is also extrapyramidal lesion present, it will lead to
(iv) rigidity, (v) exaggerated deep reflexes.

A pure pyramidal lesion produces hypotonia/flaccidity of muscles. This is

because, due to the lesion of the corticospinal fibers, there is loss of facilitatory
impulses to the spinal cord and muscles. This may occur if, particularly, the lesion
is at medullary pyramids. However, anatomic arrangement of the descending
tracts is such that, in humans, lesion of only the corticospinal fibers is rare. It will
also involve lesion of the posture-regulating (extrapyramidal) pathways. For
instance, a lesion in the internal capsule will not only damage corticospinal fibers,
but also those fibers from the cortex which are sending inhibitory influences to
the lower neurons. If these inhibitory influences are lost due to the lesion, then
the lower motor neurons will become hyperactive. This will lead to exaggerated
deep reflexes and hypertonia.

Babinski’s sign: (extensor plantar response)

When a child is born, its plantar response is extensor plantar response.

When the sole of the foot is stimulated firmly, it will give an extensor plantar
response in the newborn infant; that is, the toes will move upwards, moving away
from the stimulus. (It is also called “upgoing great toe” or “dorsiflexion of the
great toe and fanning of the other toes”). This is because; pyramidal tract is not
myelinated and hence not yet fully functional. By the age of 18 months (1 and ½
yrs) the pyramidal tract is myelinated and starts functioning. Now the pyramidal
tract becomes predominant and supersedes the function of extrapyramidal
system. Now on, the stimulation of the sole of the foot will produce plantar

77
flexion of the toes. This reflex will now help in walking. When the foot is placed on
the ground, stimulation of the sole will cause reflex plantar flexion of the toes
(towards ground) so as to grip the surface.

In later life, if there is lesion of the pyramidal tract, the reflex will revert to
extensor plantar response (since now again pyramidal tract is not functioning).
This is called BABINSKI’S SIGN.

- Removal of the primary motor cortex (the area pyramidalis) causes

paralysis of varying degrees (of the opposite half of the body), loss of
voluntary control of discrete movements of the distal segments of
the limbs, and hypotonia.

Other descending pathways: Extrapyramidal tracts

(Lateral v/s medial motor systems)
This terminology is based on the sites of termination of the descending
pathways in the spinal cord. The descending motor tracts that end on
the lateral parts of the spinal cord gray matter are called lateral motor
system of the cord. They include lateral corticospinal tracts and
rubrospinal tracts.

 Lateral corticospinal tract:- Controls distal muscle groups (hands

& feet); executes skilled voluntary movements
 Rubrospinal tract:- (from red nucleus of mesencephalon to
spinal cord) It controls proximal muscle groups.

The other descending fiber pathways that end on the medial aspect of
the spinal cord constitute the medial motor system of the cord. It
mainly includes:

 Vestibulospinal tracts: Concerned with posture

and equilibrium of the body
 Reticulospinal tracts: Control the axial (central, large)
muscles

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  Tectospinal tract: Controls movement in response to
visual & auditory inputs.

[Corticospinal tract and corticobulbar & corticonuclear pathways constitute

pyramidal system. Vestibulospinal, reticulospinal, rubrospinal, and tectospinal
tracts are called extrapyramidal tracts; extrapyramidal system = basal ganglia,
extrapyramidal tracts, and the cortical areas controlling these tracts.]

 Rubrospinal tract:

The red nucleus serves as an alternative pathway for transmitting cortical

signals to the spinal cord:

 Origin: The red nucleus, located in the mesencephalon, functions in close

association with the corticospinal tract. It receives a large number of direct
fibers from the primary cortex (the corticorubral tract) as well as branching
fibers from the corticospinal tract as it passes through the mesencephalon.
The large neurons of the red nucleus then give rise to the rubrospinal
tract.
 Course: The rubrospinal tract crosses to the opposite side and runs in
close association with the lateral corticospinal tract.
 Termination:The rubrospinal fibers terminate on the interneurons of
the cord grey matter.
 Function:

Red nucleus has a somatographic representation of all the muscles of

the body (as in the motor cortex). The corticorubrospinal pathway
serves as an accessory route for transmission of discrete signals from
the motor cortex to the spinal cord. Thus, in association with the
corticospinal tract, the rubrospinal tract is involved in the fine
discrete movements of the hands and fingers. It also controls
proximal muscle groups, so as to provide stability to those
movements of hands and fingers.

 Reticulospinal tracts:
- There are two major groups of reticular nuclei: (i) pontine reticular
nuclei (in the pons), and (ii) medullary reticular nuclei (in the
79
medulla).

80
 They send the signals to the spinal cord via the reticulospinal tracts. The
pontine reticulospinal tracts excite the antigravity muscles and
medullary reticulospinal tracts inhibit them.
- The medullary reticular nuclei receive strong input from the
motor cortex and descending motor pathways.
 Vestibulospinal tracts:
- Vestibular nuclei in the brain stem function in close association with
the pontine reticular nuclei to excite the antigravity muscles.
- They send vestibulospinal tracts on the spinal cord. Vestibular nuclei
receive signals from the vestibular apparatus (inner ear) in response to
head movements and then they selectively excite antigravity muscles
to maintain equilibrium of the body.

[Fig: Vestibulospinal tract. Upon head movement, the vestibular apparatus is stimulated. It
sends signals to vestibular nuclei. Vestibular nuclei, via vestibulospinal tracts, send impulses
to spinal cord. From spinal cord, signals will be sent to posture-regulating muscles.]

 Tectospinal tract:

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 [Roof of the midbrain is called tectum. It has corpora quadrigemina – 4 bodies:
2 superior colliculi and 2 inferior colliculi. Superior colliculi are connected to
visual pathway; inferior colliculi relay in auditory pathway.]

[Fig: Tectospinal tract. It controls movements in response to visual and auditory inputs.]

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 CEREBELLUM
The master co-ordinator for voluntary movements
Introduction:
Cerebellum is more extensively folded and fissured than the cerebral
cortex; the cerebellum weighs only 10% as much as the cerebral cortex,
but its surface area is about 75% of that of the cerebral cortex; it contains
50% of the total population of neurons in brain.
~ Role of cerebellum in voluntary movements of the body:

[Fig: Role of cerebellum in voluntary movements. Refer to text for explanation.]

Read the numbers in the figure above, and follow the arrows along with the
numbers.

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1. Intention of the cortex: Cerebral motor cortex plans a particular voluntary
movement. It sends the signals about this intended movement to the
cerebellum.
2. Cerebellum helps in the programming: Cerebellum sends the signals back
to the cerebral cortex. These signals are meant to help the cortex to
design, plan the movement, with proper sequence of muscle contractions.
3. Execution initiated by the motor cortex: Cerebral motor cortex then sends
the signals, via spinal cord, to the specific muscle groups to initiate the
programmed voluntary movement. (This is via the corticospinal tract.)
4. Proprioceptive signals from contracting muscles: Once the movement
begins, the contracting muscles send continuous signals about moment-to-
moment changes in the length of the muscle, intensity of contraction, etc.
These signals are sent into the cerebellum. Thus, cerebellum already
knows what is the plan (intention of the cortex), and now it also knows
how it is being executed at the level of the concerned muscle groups.
5. (Not shown in the figure) Cerebellum compares intention of cortex with
proprioceptive feedback from muscles; then orders the muscles
accordingly: Knowing both, the plan and its implementation, cerebellum
can control and coordinate between various muscle groups involved in
the movement. It can also take corrective action, if the movement is not
going according to the plan. E.g. if the muscles are contracting too rapidly,
and the limbs are likely to go past the target, cerebellum will damp the
contraction so that they precisely stop at the target.

Functional divisions:

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[Fig: Functional divisions of cerebellum.]
1. Vestibulocerebellum: (or archicerebellum)
- The flocculonodular lobe of the cerebellum houses
the vestibulocerebellum.
- This part is mainly concerned with equilibrium of the body; it
functions in concert with the vestibular apparatus. Hence, it is
called vestibulocerebellum.
- Phylogenetically, it is the oldest part to evolve. Hence, it is also
called “archicerebellum”.
- Since this division is concerned with the equilibrium and posture
regulation of the body, mainly the axial musculature is
represented or controlled from here – neck, shoulders, hip, and
the axial body.
2. Spinocerebellum: (or paleocerebellum)
- The cerebellum has central vermis, which joins the two cerebellar
hemispheres. Each hemisphere has an intermediate zone (on either
side of vermis) and the lateral zone. Vermis plus the intermediate
zone is the functional division called spinocerebellum. It is
connected mainly with the spinal cord.

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 - It is concerned with muscle contractions in the distal portions of
the upper and lower limbs, particularly the hands and fingers, feet
and toes.
- In phylogeny, this part is newer in evolution; developed in
those animals which require more than just body equilibrium,
that is, control of finer movements. Hence, it is also called the
paleocerebellum.
3. Cerebrocerebellum: (or neocerebellum)
- The lateral zone of cerebellar hemisphere is functionally called
cerebrocerebellum, because it functions in concert with the
cerebral cortex.
- When the motor cortex decides on a particular voluntary motor
activity, this zone of cerebellum helps the cortex in planning
and programming of the activity, so that the movement is
executed smoothly and precisely.
- It is, phylogenetically, the newest part to evolve. Hence, it is
also called the neocerebellum.
- Note that: This part of the cerebellum does not represent or
control any of the body’s musculature. It only helps in overall
control of the body’s voluntary movements. {The body’s
musculature is represented in vermis – the axial muscles, and
intermediate zone – distal muscles.}

Connections of the cerebellum:

A. Afferent connections (inputs) to the cerebellum:

{Let us consider the inputs according to the divisions of the cerebellum.}
1. Inputs into vestibulocerebellum: {concerned with head
movements and posture/equilibrium}
a. Vestibulocerebellar tract-

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[Fig: Vestibulocerebellar pathway. Vestibular apparatus detects head orintation and head
movement; it sends signal to cerebellum, via vestibulo-cerebellar tract. Fibers reach
vestibulocerebellum. This division of the cerebellum then sends signals to vestibular nucleus.
Vestibulospinal tract then adjusts the posture and maintains balance.]

- Fibers from the vestibular apparatus go to the vestibular nucleus.

From there, the fibers are sent into the vestibulocerebellum. Some
fibers from the vestibular apparatus are directly sent into the
vestibulocerebellum. All these fibers are vestibulocerebellar fibers.
- Function: They convey the position of head in space and its sudden
movements or rotation. {The vestibulocerebellum will then send
the fibers to axial and postural muscles of the body, to maintain
body’s equilibrium.}
b. Reticulocerebellar tract-
- Fibers arise from brain stem reticular formation and go into
the vestibulocerebellum.

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 - Function: They are also concerned with the postural or antigravity
muscles.
2. Inputs into spinocerebellum: (proprioceptive and audio-visual inputs)
a. Spinocerebellar tracts-
o Dorsal spinocerebellar
o Ventral spinocerebellar
- Signals regarding the momentary status of (i) muscle contraction,
(ii) muscle length and its tension, (iii) positions of body parts, are
conveyed from the muscles to the spinal cord. From there, dorsal
spinocerebellar tracts convey these signals to the cerebellum.
- Signals of the cortex, reaching the anterior motor neurons of
the cord, are taken back from there to the spinal cord via
ventral spinocerebellar tracts.
b. Cuneocerebellar tracts-
- Spinocerebellar tracts carry proprioceptive information from whole
body; the same information from the head and neck is carried by
the cuneocerebellar tract.
c. Tectocerebellar tracts-
- Tectocerebellar pathway takes auditory and visual impulses into
the cerebellum.
- It is concerned with voluntary movements in response to
auditory and visual inputs.
3. Inputs into the cerebrocerebellum: (inputs regarding the intended
movement)
a. Corticopontocerebellar pathway-
- An extensive pathway that starts from various parts of the cortex
(motor and premotor cortices, and sensory cortex), passes
through the ponitne nuclei, and eventually enter the lateral
cerebellar hemispheres.
- The voluntary movement that is intended by the cortex is
informed to the cerebellum via this pathway.
4. Olivocerebellar pathway:

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 This pathway is mentioned separately because: from various parts of
CNS mentioned above, tracts enter the cerebellum separately, or the
fibers first converge on “inferior olive” and then a single bundle –
“olivocerebellar pathway” – enters all parts of the cerebellum.

Afferent tract Transmits

vestibulocerebellar Vestibular impulses, directly
from labyrinth and via
vestibular
nuclei
Dorsal spinocerebellar Proprioceptive impulses from
body
ventral spinocerebellar Impulses reaching the spinal
motor neurons, from the
descending tracts
Cuneocerebellar Proprioceptive impulses,
especially from head and neck
Tectocerebellar Auditory and visual impulses via
inferior and superior colliculi
Corticopontocerebellar Impulses from motor and
other parts of cerebral cortex
via
pontine nuclei
Olivocerebellar Proprioceptive input from whole
body via relay in inferior olive

B. Efferents (outputs) from the cerebellum:

Outputs from the cerebellum can also be considered according to the 3
functional divisions of the cerebellum. Output pathways from the
cerebellum, from each division, mainly go to the same area from where the
inputs have come into that division. (For example, vestibulocerebellum:

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 receives input from vestibular and reticular nuclei, and sends output to the
same.)
Consider two important points here:
(i) All outputs from the cerebellum start from the deep cerebellar
nuclei. These are the nuclei located deep into the cerebellar
mass. For each division, there is one deep nucleus.
Vestibulocerebellum: Nucleus
fastigius Spinocerebellum: Nucleus
interpositus Cerebrocerebellum:
Dentate nucleus
(Nucleus interpositus has two parts – Globose nucleus &
emboliform nucleus)
(ii) All outputs from the cerebellum will eventually end on the anterior
motor neurons of the spinal cord. Because, cerebellum is
concerned with coordinating and correction of the muscle
contractions, it controls the muscle groups via anterior motor
neurons.

[Fig: Outputs from cerebellum. Deep into the mass of cerebellum, there is deep nucleus; all
outputs from cerebellum arise from deep nucleus. Also note:- Purkinje cell exerts an
anhibitory influence (-) on the deep nuclear output.]

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[Fig: Efferents from cerebellum. Refer to text for details.]
1. Outputs from the vestibulocerebellum:
- The outputs start from the nucleus fastigius.
- Fibers are projected to vestibular nuclei and reticular nuclei.
- From these nuclei:- the vestibulospinal and reticulospinal tracts
are sent onto the spinal cord.
- These fibers will control the axial muscles; and will help in
equilibrium and posture maintenance during a voluntary
movement.
2. Outputs from the spinocerebellum:
- The outputs start from the nucleus interpositus.
- Fibers are projected to cortex, basal ganglia, and red nucleus mainly.
- From these structures, the descending tracts will be sent onto
the spinal cord (e.g. rubrospinal cord).
- These fibers will mainly control the muscle groups of the extremities,
mainly the distal musculature, during a voluntary movement.
3. Outputs from the cerebrocerebellum:
- The outputs start from the dentate nucleus.
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 - Fibers are sent to the ventroanterior and ventrolateral nuclei of
the thalamus.
- From here, the fibers are sent to the cerebral motor cortex.
- From the cortex, the corticospinal tract is sent onto the spinal cord.
- These fibers help the cerebral cortex in planning and programming
of a voluntary movement, and sequencing of muscle contractions in
a movement.

Neuronal circuit in the cerebellum:

{The cerebellum has following layers: from superficial to deep: molecular

(surface) layer, Purkinje cell layer, granule cell layer, deep nuclear cell layer.
Inputs into the cerebellum make synaptic connections with the cerebellar
neurons; and after signal processing, the cerebellar neurons send output signals.
Thus, a functional unit of neuronal circuit is established. The cerebellum has
nearly 30 million such functional units.}

- The functional unit of the cerebellum is centered on a very large

Purkinje cell, and a corresponding deep nuclear cell.

[Fig: The two cells central to cerebellar circuit. Purkinje cell exerts inhibitory influence
on the deep nuclear output.]

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  The afferent inputs to the cerebellum are mainly of two types: (1)
the climbing fiber type, and (2) mossy fiber type.
{The inputs into the cerebellum are from two sources: from various parts of the
brain and the spinal cord fibers enter the cerebellum discretely, or from these
sources fibers converge on “inferior olive”and then from the olive, fibers enter
the cerebellum.}

[Fig: cerebellar circuit. Refer to text for details.]

(1) The climbing fibers: They originate from the inferior olive. After entering
the cerebellum, they send a collateral to excite the deep nuclear cell. The
deep nucleus will send excitatory output. Then, the fibers project
(“climb”) on the Purkinje cell to excite it. This will cause the Purkinje cell
to exert its inhibitory influence on deep nuclear cell; deep nuclear output
will be suppressed.

(2) The mossy fibers: From all other sources, mossy fibers enter cerebellum.
These fibers send collaterals to excite the deep nuclear cell directly. Then
the mossy fibers proceed further to synapse with the granule cells.
Granule cells send short axons upto the outer surface; here they divide
into two branches which run in each direction, parallel to the surface.
These

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 “parallel fibers” then synapse with dendrites of Purkinje cells to excite
those cells. Purkinje cell will then send inhibitory fibers to deep nuclear
cell.
Thus, the theme of cerebellar circuit is:- Output signals from cerebellum are
facilitated by the incoming signals directly; and, via Purkinje cell’s influence, the
output signals are held in check.

Other inhibitory cells in cerebellum:

[Fig: Inhibitory interneuron in cerebellum. Basket cell inhibits (-) Purkinje cell. This removes
the inhibitory check of Purkinje cell on deep nuclear output. The deep nuclear output will be
facilitated, as a result.]

- Purkinje cell, an inhibitory neuron, keeps an inhibitory check on

the cerebellar output. Inhibiting the Purkinje cell will thus result in
disinhibition. That is, the inhibitory check on the cerebellar output
will be lifted. The deep nuclear cell will then be facilitated to send
outputs (mainly to contracting muscles).
- Purkinje cell is not only under excitatory influences from the inputs
to the cerebellum.
- There are 3 short neurons in the cerebellum – (i) Golgi cell, (ii)
Basket cell, and (iii) Stellate cell.
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 - All these neurons have short axons that are inhibitory to the
Purkinje cell.

Thus, there are various checks-and-balances of excitatory and inhibitory signals

that form the functional basis of cerebellum.

Significance: “turn-ON/turn-OFF” and “turn-OFF/turn-ON” output signals from

the cerebellum –

At the onset of a voluntary, purposeful movement, turn-on signals to the

agonist muscles and simultaneous turn-off signals to the antagonist muscles, will
cause the movement to be started and carried out in a smooth manner. Then, on
approaching the termination of the movement, turn-off signals to the agonists
and turn-on signals to the antagonists will cause the movement to be terminated
at the precise moment and point. This is possible because of the checks-and-
balances provided by the cerebellar circuit. The movements are smooth, precise,
well-executed, with proper coordination between various muscle groups
involved in the movement.

~ Functions of the cerebellum:

1. Vestibulocerebellum –
(i) It functions in association with the vestibular apparatus
to maintain the body’s equilibrium.
(ii) During a voluntary movement, the body’s desired posture
is regulated by this part of the cerebellum.
2. Spinocerebellum –
(i) Feedback control of distal limb movements is achieved by this part
of the cerebellum.
(ii) Coordination between various muscle groups involved in a
particular movement, so that the movement is precise, smooth, and
properly executed.

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 3. Cerebrocerebellum –
(i) This part of the cerebellum functions in association with the
cerebral cortex. When the cortex decides on a voluntary movement,
cerebellum helps the cortex in planning of the movement.
(ii) It helps the cortex in “timing” of the muscle contractions. The
muscle contractions, in a goal-oriented movement, occur in a
sequential manner. This sequence of contractions of particular
muscles, and the timing of their contractions, is decided with the
help of cerebellum.
4. Damping function:
When a movement is started, due to the momentum of the limbs, there
may be overshoot. Cerebellum damps the contractions so that the
movement stops precisely at the target.
5. Smooth progression of movements: In a continuous, goal-oriented
movement, the proper timing and intensity of muscle contractions helps a
smooth progression from one movement to the next.
6. Alternate rapid movements: Cerebellum can precisely turn-off one type of
movement and then turn-on the opposite movement, in a continuous
manner. This is possible because of the turn-on/turn-off type of signals
from the cerebellar circuit.
7. Maintenance of muscle tone: Regulation of muscle tone helps to attain
or maintain a desired posture or attitude of limbs during a movement.

Applied Physiology:

Clinical abnormalities of the cerebellum:

(Disorders due to cerebellar lesions)

1. Ataxia:
Loss of coordination between muscle groups during a movement is called
ataxia. It will cause the movement to be jerky and off-the-target.
2. Dysmetria and past-pointing:
Due to cerebellar lesion, the movements cannot be executed smoothly, and
the limbs do not stop precisely at the target. It causes overshoot, since the
96
 damping function of the cerebellum is lost. The hands go past the intended
target. This is called past pointing.
Since the motor control system cannot predict how far movements will go,
the movements overshoot the target. The conscious control centers of the
motor cortex then overcompensate in the opposite direction. Thus,
correction overshoots to the other side. This is called dysmetria.
3. Intentional tremor:
Due to the cerebellar lesion, the damping of the movement at the precise
target does not happen. There is overshoot, correction on the backward,
again overshoot. This causes oscillation in the movement, especially near
intended target. This is called intention tremor or action tremor.
4. Dysdiadochokinesia: (failure to perform alternate rapid movements,
such as alternate rapid pronation and supination.)
When the motor control system fails to predict where the different parts of
the body will be at a given time, during a continuous movement, there will
not be orderly “progression of movement”. Thus, in cerebellar lesions, the
patient “loses” all perception of the instantaneous position of the hand
during any portion of the movement.
5. Dysarthria: (difficulty in speech due to loss of proper articulation of
the organs of the speech)
Formation of words depends on rapid and orderly succession of individual
muscle movements in the larynx, mouth, and respiratory system. Lack of
coordination in these will lead to jumbled vocalization and slurred
speech.
6. Decomposition of movement:
Patients with cerebellar disease have difficulty performing actions that
involve simultaneous motion at more than one joint. They dissect such
movement and carry them out one joint at a time. This is “decomposition
of movement”.
7. Cerebellar nystagmus:
It is tremor of the eyeballs that occurs usually when one attempts to fixate
eyes on a scene to one side of the head.
8. Hypotonia:

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 It results from loss of feedback cerebellar facilitation of the motor cortex
and brain stem motor nuclei by tonic discharge of the deep cerebellar
nuclei.
Function of cerebellum Effect of lesion
Co-ordination between Ataxia
muscle groups
“Damping” of Past pointing
movement
Maintains muscle tone Hypotonia
Eye fixation and rotation Nystagmus
Perform alternate rapid Dysdiadochokinesia
movements

Tests to detect the coordination –

A. For upper limb:

(i) Finger-nose test
(ii) Finger-to-finger test
B. For lower limb:
(i) Knee-heal test
(ii) Rhomberg’s test
(iii) Tandom walking test

Rhomberg’s test:

The patient of suspected cerebellar lesion is asked to stand upright, with

feet close together. He should do this with eyes open first, and then with eyes
closed.

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If the patient fails to stand like this, he has ataxia. Standing with feet close
together requires coordination among muscle groups of the lower limbs; ataxia is
loss of coordination.

Ataxia is of two types:

(1) Sensory ataxia, and

(2) Cerebellar/motor ataxia

Coordination of muscle groups requires two components of the nervous system.

(i) proprioceptive sensory input from the concerned muscles, and (ii) cerebellum.

The proprioceptive information from the muscles and joints is continuously sent,
at a subconscious level, to the cerebral cortex and the cerebellum. Then,
cerebellum achieves the proper coordination by sending appropriate signals to
the muscles.

If the patient is able to perform the test when eyes are open, but fails when eyes
are closed, it is sensory ataxia.

Explanation: In sensory ataxia, there is loss of proprioceptive sensory input from

the muscles and joints. When the eyes are open, there is vision to aid the muscle
movement. So, even if the prorioceptive input is not there, patient is able to
perform the test. However, when the eyes are closed, this visual “aid” is no
more there. Patient will not be able to perform the test.

In cerebellar ataxia, patient will not be able to perform the test at all. Eyes open
or closed will not matter in cerebellar ataxia. This is because, cerebellum is the
coordinator for the muscles. If there is a lesion of cerebellum, coordination will
not be possible in any which way (eyes open or closed).

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 Basal ganglia

Introduction:

The basal ganglia are the interconnected nuclei at the base of the brain.

The basal ganglia, like the cerebellum, are another accessory motor system
that functions in close association with the cerebral cortex and corticospinal
motor system.

The basal ganglia receive virtually all their input signals from the cortex itself and
also return almost all their output signals back to the cortex.

The basal ganglia do not make direct connections with the spinal cord. It appears
that the major function of the basal ganglia is to aid the motor cortex in
generating commands concerned with controlling proximal muscle groups during
a movement. For example, when the hand is used to write on a blackboard, the
large muscles of the arm and shoulders are used to hold the hand in its proper
position for writing. The coordination of these muscle groups is under the control
of the basal ganglia.

Physiologic anatomy:

The basal ganglia are subcortical masses of grey matter, or interconnected

nuclei beneath the cortex, near base of the brain.

{Three important structures – caudate nucleus, putamen & globus pallidus – lie
alongside the internal capsule (V).}

The five structures universally considered to constitute basal ganglia are:

1. Caudate nucleus
2. Putamen

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 3. Globus pallidus (GP)
4. Substantia nigra
5. Subthalamic nucleus (body of Luys)

Caudate nucleus

Putamen
striatum
Lentifor
Globus pallidus ——— —Pallidum
m

According to appearance and connections:

- Caudate nucleus and putamen have striated appearance, hence

are together called striatum; and globus pallidus called pallidum.
As per location:
- Caudate nucleus on one side of the internal capsule; and {putamen
+ globus pallidus} on the other side, together are called lentiform
nucleus.

 Globus pallidus is divided into two parts: globus pallidus externum

(GPE), and globus pallidus internum (GPI).
 Substantia nigra is divided into two parts: pars compacta (PC), and
pars reticularis (PR).

~ Connections and circuits of the basal ganglia:

- Basal ganglia have exclusive connections with motor cortex. They

receive afferents from motor cortex; they send efferents back to
motor cortex.

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 - Since the main role of the basal ganglia is to help the motor cortex
in executing a voluntary movement, its inputs start from the motor
cortex. The intended movement, thought by the cortex, is conveyed
to the basal ganglia.
- And, the outputs of the basal ganglia go back to the cortex. The
output signals will help the motor cortex in the execution of the
voluntary movement, in terms of the purpose, intensity,
proportion of the desired movement.
- The inputs into the basal ganglia terminate in the striatum
(mainly, the caudate nucleus).
- The outputs from the basal ganglia start from the pallidum (or,
globus pallidus internum – GPI).
Efferent neurons that emerge from GPI have a background tonic
activity. These are inhibitory neurons; they project to thalamus. It
means, when there is no motor activity, the pallidal neurons keep
the specific thalamic neurons inhibited.
There are two circuitous connections between motor cortex and basal ganglia ~
(1) Direct circuit, (2) Indirect circuit.

(1) Direct circuit:

(Note:- Excitatory fiber comes in from the cortex into basal ganglia;
excitatory fiber goes back to the cortex. The remaining fibers of the circuit
are inhibitory.)

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[Fig: Diagrammatic representation of direct circuit. Cortex —> striatum —> pallidum (GPI) —>
thalamus —> back to cortex. NOTE: The internal globus pallidus (GPI) has background tonic
inhibitory activity; thus, pallido-thalamic projection will keep the thalamic neurons inhibited,
when there is no motor activity being designed. When motor activity is being planned, cortex
will start exciting the striatal neurons; striatal neurons will start inhibiting the pallido-
thalamic inhibitory projections. Excitatory fibers are shown in green and with a (+) sign;
inhibitory fibers are shown in red and with a (-) sign. P = Putamen, GPE & GPI = external and
internal globus pallidus, respectively. The 3 thalamic nuclei:- VA = ventro-anterior, VL = ventro-
lateral, CM = centro-medial. Refer to text for more details.]

When cortex starts thinking about making a voluntary movement:

 Cortex to striatum: (“striatum, please start your activity”)
- Cortico-striate projections DO NOT have any tonic activity at rest.
- When cortex starts thinking of a voluntary movement, the cortico-
striate projections become active. That is, cortex now starts
exciting the striatal neurons.
 Striatum to pallidum: (“pallidum, please stop your activity”)
- Striatal neurons now start inhibiting the pallidal neurons in GPI.
 Pallidum to thalamus: (“thalamus, I can’t inhibit you now”)

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 - Even when no movement was thought of, the pallidal neurons were
active; that is, they were continuously keeping an inhibitory check
on the thalamic nuclei.
- As a movement is being thought of now, and striatal neurons start
inhibiting the pallidal neurons, the tonic inhibitory activity of
pallidal neurons will be inhibited. This is called disinhibition
(‘inhibition of inhibition’).
 Thalamus to cortex: (“cortex, it’s a ‘go-ahead’ for the movement)
- Since thalamic neurons are now no more inhibited by pallidal
neurons, the thalamic neurons (which are excitatory) will start
sending excitatory signals to the relevent areas of motor cortex. In
a way, motor cortex gets a ‘go-ahead’ signal in the context of the
particular movement.

Function of the direct circuit: facilitation of the movement.

(2) Indirect circuit:

- There is an addition to the direct circuit – subthalamic nucleus.
- There is an excitatory projection – from subthalamic nucleus to GPI.
This is in addition to the two already discussed facilitatory
projections, i.e., fiber coming in from the cortex, and fiber going
back to the cortex.
- Just as pallido-thalamic fibers are inhibitory, so are pallido-
subthalamic fibers.
Refer to figure and the text given below.

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[Fig: Diagrammatic representation of indirect circuit. Also, refer to the direct circuit and the
text given below.]

When cortex starts thinking about making a voluntary movement:

 Cortex to striatum:
- Cortex starts exciting the striatal neurons.
 Striatum to pallidum: (but in this case, to the GPE)
- Striatum now starts inhibiting the pallidal neurons, in external
globus pallidus (GPE).
 GPE to subthalamic nucleus: (GPE was already inhibiting the neurons
in subthalamic nucleus, before cortex started signaling)
- As striatal neurons start inhibiting the GPE neurons, the
GPE inhibition of subthalamic nucleus will stop.
 Subthalamic nucleus to pallidum (GPI): (excitatory projection)

105
 - Since inhibition of subthalamic nucleus is now lifted, neurons
of subthalamic nucleus now start faciltating the GPI neurons.

[GPI —> thalamus —> cortex] Remaining path is the same as in the direct circuit.
That is, faciltation of GPI neurons will exert inhibitory influence on the thalamic
nuclei. Since thalamic nuclei are inhibited, they will NOT give cortex a “go
ahead” via their excitatory fibers. End result:- CORTEX DOES NOT GET A “GO-
AHEAD” signal.
Function of the indirect circuit: Inhibition of movement. (The unpurposeful,
undesirable movements will be suppressed.)

Role of substantia nigra:

- Substantia nigra is not a constituent of the cortex-to-basal ganglia
circuits (direct or indirect).
- Substantia nigra modulates activity of the striatal neurons involved
in direct and indirect circuits.
- Nigro-striatal tracts: Substantia nigra projects dopaminergic neurons
on to the nerve cells in the striatum.

[Dopamine receptor is of 5 types: D1, D2, D3, D4, D5.]

- Nigrostriatal tract has D1 & D2 receptors for dopamine.
- D1 receptors mediate excitatory effects of dopamine; D2 receptors
mediate inhibitory effects of dopamine.
1. D1 dopaminergic neurons end in the striatal nerve cells that are
part of direct circuit. Thus, they facilitate the direct circuit.
2. D2 dopaminergic neurons end in the striatal nerve cells that are
part of indirect circuit. Thereby, they inhibit the indirect circuit.

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[Fig: Role of substantia nigra. Figure shows only the relevent part of the circuits. The
nigrostriatal tract has dopaminergic fibers that act via D1 and D2 receptors present on striatal
nerve cells. D1 dopaminergic neurons have excitatory influence on direct pathway; D2
dopaminergic neurons have inhibitory influence on indirect pathway. Also note the
cholinergic projection from striatum to substantia nigra. Refer to text.]

[Fig: Effect of influence of substantia nigra on voluntary movement. Nigro-striatal tracts have
two influences ~ (1) facilitation of direct circuit. Direct circuit is involved in facilitation of the
movement. Thus, movement will be facilitated by this nigro-striatal projection; (2) Inhibition
(x) of the indirect circuit. Indirect circuit functions for suppression of movement; thus,
inhibiting the indirect circuit will facilitate the movement.]

Functions of the basal ganglia:

(1) Neurons in the basal ganglia start discharging before a voluntary

movement begins. This observation suggests that, the basal ganglia are
involved in the planning and programming of voluntary movement.

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 (2) Basal ganglia help the motor cortex in controlling the proximal
postural muscle groups during a voluntary movement.
(3) Basal ganglia are involved in the processes by which an abstract thought
is converted into voluntary action.
(4) Cognitive control of motor activity –
The term “cognition” means the thinking processes of the brain, using both
the sensory input to the brain and the information already stored in
memory. Most of our voluntary motor activities occur as a consequence of
thoughts generated in the mind, a process called “cognitive control of
motor activity”. The caudate nucleus and the caudate circuit play a major
role in this cognitive control of motor activity.
(5) Basal ganglia provide the proper purpose to the movement.
(6) Basal ganglia can scale the intensity of movements. They can also change
the timing of the movement. For instance, if a person is writing on a
small piece of paper, or on a large chalkboard, there will be a sense of
proportion.
(7) Basal ganglia are involved in production of automatic associated
movements. For example, swinging of arms during walking is an
automatic movement associated with walking.
(8) Basal ganglia determine the proportion of the movement.

The neurotransmitters in the basal ganglia circuits: {Only the important pathways
mentioned below}

a. There is the dopaminergic pathway from the substantia nigra to the

caudate nucleus and putamen. The neurons in this nigro-striatal
pathway secrete dopamine.
b. GABAergic pathway from the caudate nucleus and putamen to the globus
pallidus. The neurons in these tracts secrete GABA – gamma amino
butyric acid.
c. Acetyl choline pathway from the cortex to striatum; and, from striatum
to substantia nigra.

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Note that: GABA is an inhibitory transmitter. GABA neurons in the feedback
loops from the cortex through the basal ganglia and then back to the cortex
make all these loops “negative feedback loops”. They lend stability to the motor
control systems.

Applied Physiology:

Clinical syndromes resulting from damage to the basal ganglia:

(Disorders of the basal ganglia)

Lesions in the basal ganglia produce characteristic deficits in motor behavior.

A. Lesions within the striatum (caudate N. and putamen):

The pathways arising from the striatum are GABAergic pathways, that is,
inhibitory pathways. Hence, lesions in the striatum produce variety of
motor syndromes related to release of inhibition of the motor control
system; loss of inhibition allows spontaneous outbursts of globus pallidus
and substantia nigra activity that cause distortional movements.
1. Huntington’s chorea – It is characterized by continuous,
uncontrollable, quick movements of the limbs. There are unpurposeful
movements involving muscles of face and limbs.
2. Athetosis – The limbs, fingers, and hands perform continuous, irregular,
twisting motions.
3. Torsion spasm or dystonia – Twisting movements of the trunk and neck.
B. Lesions in the subthalamic nucleus:
The lesions in the subthalamic nucleus cause spontaneous, wild, flinging,
and ballistic movements of the limbs. This syndrome is called
hemiballismus.

- The feedback loop between subthalamic nucleus and the globus

pallidus is inhibitory in function. The release of this inhibition,
caused by the lesion, leads to these movements.
- Because the movements appear to be like those performed when
an individual is thrown off balance, the subthalamic nucleus is
believed

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 to be involved with controlling the centers that issue the motor
commands for balance.

C. Parkinson’s disease: (paralysis agitans)

- It is a neurodegenerative disorder; occurs mostly in 7th or 8th decade

of life.
- There is degeneration or destruction of the dopaminergic neurons
in the nigro-striatal tract. Or, the lesion of the substantia nigra.
- The triad of symptoms: tremor, rigidity, and akinesia (hypokinesia)
1. Tremor:

 Tremor due to the lesion of the basal ganglia or particularly

the substantia nigra, is a tremor at rest. (Compare this with
cerebellar tremor: it is the action tremor, that is, no tremor at
rest, but tremor appears when a voluntary movement is
performed.) Tremor of Parkinson’s disease is the tremor at
rest, and usually disappears during voluntary activity.
 The tremor has a frequency of about 4 to 7 cps.

2. Rigidity:

 The rigidity in Parkinson’s disease involves all of the muscles

at a joint. Thus, it is different from spasticity that is associated
with cortical lesions (which involves group of muscles on one
side of a joint).
 The rigidity may be due to release of inhibition of the
motor command systems.
 It is described as “lead-pipe” rigidity. Because, the rigid
limb, when moved passively, remains where it is placed.
 Sometimes, it appears as cog-wheel rigidity. When an
examiner tries to move a limb of the patient, there is rigidity
– then limb gives way – then again rigidity, type of pattern. It
is due to appearance of hypertonia alternately in agonists and
antagonists around a joint.

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 3. Hypokinesia or akinesia:

The movement patterns normally associated with motor

activity are reduced. For example, the arms do not swing
during walking; facial expressions do not change during
conversation.

D. Some other symptoms related to the basal ganglia lesions: micrographia –

the written letters will be small, because the sense of proportion is lost.

Loss of drive or motivation for purposeful voluntary activity is seen in

basal ganglia lesions.
Treatment of Parkinsonism –

- Since there is degeneration of dopaminergic neurons, giving

dopamine is the mainstay of treatment. However, dopamine
does not cross the blood-brain barrier (BBB) readily or
consistently.
 L-DOPA is the precursor of dopamine; it acts as a prodrug. It
crosses BBB, enters brain and forms dopamine.
 Recently, dopamine-loaded PLGA nanoparticles have
been developed that deliver dopamine into the brain.
- Since there is degeneration of inhibitory neurons in the nigro-striatal
tract, it causes hyperactive cholinergic neurons in the striato-nigral
pathway. This is responsible for some of the symptoms. Anti-
cholinergic drugs are given to block the excess activity of ACh.
- Surgical treatment – Stereotactic thalamotomy.

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 LOWER MOTOR NEURON (LMN)
MOTOR FUNCTIONS OF THE SPINAL CORD
Introduction:

[Fig: Bell-Magendie law. Sensory neurons enter the spinal cord through dorsal horn; motor
neurons emerge from anterior horn.]

Apart from the sensory relay neurons, each segment of the spinal cord has two
other types of neurons: (1) the anterior motor neurons, and (2) the interneurons.

 Anterior motor neuron:

[Fig: Anterior motor neuron. It is of two types ~ (1) -motor neuron, and (2) -motor neuron.]

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 - Located in each segment; in the anterior horns of the grey matter;
several thousand anterior motor neurons. They leave the cord
and innervate the skeletal muscle fibers.
- They are of two types: (i) alpha motor neuron, and (ii) gamma
motor neuron.

(i) Alpha motor neuron: large A type of nerve fibers. They

innervate large skeletal (extrafusal) muscle fibers. These motor
neurons are responsible for muscle contraction
(ii) Gamma motor neuron: small A type of nerve fibers arising
from the anterior horn; they innervate small intrafusal fibers in
the skeletal muscle which are NOT responsible for muscle
contraction; the intrafusal fibers constitute the muscle spindle.
(Discussed later)

 Interneurons:
- Small, highly excitable interneurons are present in all areas of the cord
grey matter (dorsal and ventral horns, and intermediate areas). They are
30 times as numerous as anterior motor neurons.
- They have many interconnections with one another and with
the anterior motor neurons.

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 - They are responsible for most of the integrative functions of the spinal
cord. Most of the incoming sensory signals are first transmitted through
the interneurons, they are appropriately processed by interneurons.
(Most of the fibers of the corticospinal tract fibers too end on the
interneurons, instead of anterior motor neurons.)

[Fig: It shows sensory & motor neurons, and an interneuron between the two.]

 Renshaw cell inhibition- (refer to discussion on “properties of synapse”)

Located in the anterior horns of the spinal cord, in close association with
the motor neurons, are small interneurons called Renshaw cells.
Immediately as the axon emerges from cell body of the anterior motor
neuron, collateral branches from the axon are given off. These
collaterals end on the adjacent Renshaw cells.
Renshaw cells are inhibitory neurons. They terminate on the cell body
of the motor neuron that gave off the collateral, and also of other
adjacent neurons of the motor neuron pool.
Impulses generated in the motor neuron activate the collateral that then
activates the Renshaw cell. Renshaw cell, in turn, secretes inhibitory
transmitter and it slows or stops the discharge of the motor neurons in the
motor neuron pool of that segment.

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 This is also called as “recurrent inhibition”.

 Proprioceptors in the muscle:

(Recall from the chapter on muscle ~ When a muscle contracts, two things
happen in the muscle: (a) Tension is generated in the muscle, and (b)
shortening of the muscle, i.e., change of length. To detect these two things,
there are two proprioceptors in a muscle.)
(i) Muscle spindle: (for length)

 Situated in the belly of a muscle

 Made up of intrafusal fibers
 It detects ~ (a) length of the muscle (when muscle is
stationary), (b) rate of change of length of the
muscle (when muscle is in a continuous contraction)

(ii) Golgi tendon organ: (for tension)

 Situated in the tendon of a muscle

 Built up of tendon fibers
 It detects ~ (a) tension in the muscle (when muscle is static),
and (b) rate of change of tension in the muscle (when muscle
is contracting)

[Fig: Proprioceptors in muscle. Muscle spindle at the belly of muscle; Golgi tendon organ
(GTO) in the tendon of muscle.]

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  Muscle spindle:

[Fig: muscle spindle structure and innervation. Refer to text for details]

- Each muscle spindle is built up of about 10-12 very small intrafusal

fibers. These fibers are attached to the glycocalyx of the surrounding
large extrafusal skeletal muscle fibers. (extrafusal fibers are the regular
contractile units of the muscle. That is, muscle contraction is
contraction of extrafusals.)
- The central region of intrafusal fibers has no contractile elements.
It functions as a sensory receptor.
- There are two types of intrafusal fibers in a muscle spindle- (1) NUCLEAR
BAG FIBERS, in which many nuclei are contained in a dilated central area
or “bag”; and (2) NUCLEAR CHAIN FIBERS, which are thinner and nuclei
are aligned in a chain throughout the receptor area.
- In a muscle spindle, there are about 10-12 intrafusal fibers, of which, 2-3
are nuclear bag type and remaining are nuclear chain type.

There are two types of sensory endings in each spindle:

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  Annulospiral endings are the terminations of rapidly conducting type
Ia afferent fibers. They encircle the very center of each intrafusal
fiber
 Flower–spray endings are terminations of type II sensory fibers
and are located nearer the ends of the intrafusal fibers, but only
on nuclear chain fibers.
Thus, nuclear chain fiber is innervated by both types of afferents.

(i) Response of both the primary and the secondary endings to the
length of the receptor – the “STATIC” response:
When there is a sustained stretch on the skeletal muscle, (the muscle is
stretched slowly and the joint is held in the same position- joint/muscle
is static), both the primary and secondary endings continue to transmit
the signals regarding the length to the spinal cord and from the spinal
cord to higher centers.
Because the nuclear chain type of intrafusal fiber is innervated by both
the primary and secondary endings, it is believed that these fibers are
mainly responsible for the static response.
(ii) Response of the primary ending (only) to the rate of change of
receptor length – the “DYNAMIC” response:
When the muscle is suddenly stretched, that is, its length is changed
rapidly, length of the spindle receptor increases rapidly. The primary
ending (but not the secondary ending) is stimulated powerfully. This is
called the dynamic response, which means that the primary ending
responds extremely actively to a rapid rate of change in spindle length.
Because only the primary endings transmit the dynamic response and
the nuclear bag fibers have only primary endings, it is assumed that the
nuclear bag fibers are responsible for the dynamic response.
Tendon jerk (discussed later) is a classic example of dynamic response.

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Effects of gamma motor neuron discharge:

- The spindles have a motor nerve supply of their own. These nerves
constitute about 30% of the fibers arising from anterior horn of
the spinal cord.
- They are of A type. They are called the gamma () efferents of Leksell
or the -motor neuron, or the fusimotor neuron.
- The endings of the  efferent fibers are of two histologic types: there
are motor end plates (plate endings) on the nuclear bag fibers, and
there are endings that form extensive networks (trail endings) primarily
on the nuclear chain fibers.

Stimulation of the  efferent system is not meant to cause contraction of

the muscles because the intrafusal fibers are not strong enough or plentiful
enough to cause contraction. However, stimulation does cause the contractile
ends of the intrafusal fibers to shorten and therefore stretches the nuclear bag
portion of the spindles, deforming the annulospiral endings and initiating
impulses in the Ia (primary) fibers. This in turn can lead to reflex contraction of
the muscle. Thus, muscle can be made to contract via stimulation of the  motor
neurons that innervate the extrafusal fibers or the -efferent neurons that initiate
contraction indirectly via the stretch reflex.

Although  motor neurons do not cause muscle contraction, they increase

sensitivity of the muscle spindle. Muscle spindle becomes more excitable when
 motor neuron is discharging.

Control of intensity of the static and dynamic responses by the  motor nerves:-
the  motor nerves to the muscle spindle are of two types – gamma-dynamic
(gamma-d) and gamma- static (gamma-s). The gamma-d excites mainly the
nuclear bag fibers and the gamma-s excites mainly the nuclear chain fibers.
When the gamma-d fibers excite the nuclear bag fibers, the dynamic response of
the muscle spindle becomes tremendously enhanced. Stimulation of the gamma-
s fibers enhances the static response.

 co-activation or  linkage:

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  When continuous voluntary motor activity is being initiated, there is
simultaneous activation of both - and -motor neurons. This is 
co- activation or  linkage.
 Contraction and shortening of the extrafusal fibers causes the central
region of the intrafusal fibers to be compressed. This reduces the
deformation of the primary (Ia) endings, causing the Ia fiber to reduce its
firing rate. The reduction of firing rate that occurs during muscle
contraction, called unloading, is functionally disadvantageous because
the CNS stops receiving information about the rate and extent of muscle
shortening. Unloading can be prevented by the activity of the gamma
motor neurons.
 During a continuous voluntary movement, the motor command system
coactivates both  and  motor neurons. As the alpha motor neuron
causes the muscle to contract, simultaneously activated gamma motor
neuron causes muscle spindle to remain excitable by stretching the
receptor portion. Thus, unloading of muscle spindle during muscle
contraction is prevented, and the higher centers (mainly cerebellum) will
continue to get information regarding the changing length of the muscle.

Gamma loop: The CNS is theoretically capable of initiating movements directly by

stimulating just the gamma motor neurons, using a pathway called the gamma
loop. Increasing gamma motor neuron activity causes the stretching of the central
portion of the intrafusals and activation of the Ia fiber. Firing of Ia fibers causes
alpha motor neuron activity to increase, resulting in an increased amount and
force of skeletal muscle activity. (Although the gamma loop can elicit movement
on its own, it normally does not do so. However, because of coactivation, the
gamma loop is activated during all movements and thus contributes to the
excitability and firing rate of the alpha motor neuron.)
Brain areas for control of the gamma motor system:

The gamma efferent system is excited especially by signals from the

bulboreticular facilitatory region of the brain stem and, secondarily by impulses

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transmitted into the bulboreticular area from (i) the cerebellum, (ii) the basal
ganglia, and (iii) the cerebral cortex.

Influencers of gamma motor neuron discharge:

- The gamma motor neuron discharge is regulated by descending tracts

from the brain. Via these pathways the sensitivity of the muscle
spindles can be adjusted.
- Anxiety causes an increased  efferent discharge. (This explains
the hyperactive tendon reflexes in anxious patients.)
- An unexpected movement causes greater  efferent discharge.
- Stimulation of the skin, especially by painful stimuli, increases  efferent
discharge to ipsilateral flexor muscle spindles while decreasing that to
extensors and produces the opposite pattern in the opposite limb.
- Jendrassik’s maneuvre: Trying to pull the hands apart when the
flexed fingers are hooked together, or, clenching of teeth facilitates
the knee jerk reflex (Jendrassik’s maneuvre). Hooking of the fingers
would initiate afferent impulses from the hands; it results in  motor
neuron discharge.

 Muscle stretch reflex:

The simplest manifestation of muscle spindle function is the muscle

stretch reflex, also called myotatic reflex.

Definition: Whenever a muscle is stretched suddenly, excitation of the

spindles causes reflex contraction of the same muscle and also of closely
allied synergistic muscles.

Neuronal circuitry/mechanism of the stretch reflex:

STRETCH REFLEX IS A MONOSYNAPTIC REFLEX.

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When the muscle is stretched suddenly, the spindle of the muscle is stimulated.
Ia (primary) afferents arising from the spindle then transmit the signal into the
spinal cord. On entering through the dorsal horn, a branch of this fiber passes
directly to the ventral/anterior horn and synapses directly with the anterior
motor neuron that send nerve fibers back to the same muscle from whence the
spindle fiber originated. The motor neuron causes a brief contraction of the
muscle.

Clinical example of stretch reflex: THE TENDON JERKS

Knee jerk is an example of stretch reflex. Tapping the patellar tendon
causes reflex contraction of quadriceps femoris muscle and manifested
in the form of knee jerk. Biceps jerk, triceps jerk, jaw jerk are all the
examples of stretch reflex.

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[Fig: Process of tendon jerk. (I) When clinician strikes hammer over a tendon, entire muscle is
stretched. (II) Intrafusals are stretched; muscle spindle is stimulated. Signals are sent via
primary (Ia) afferents which enter spinal cord and excite alpha-motor neuron. The alpha-
motor neuron, going back to the muscle, causes brief contraction of extrafusals. That is, the
muscle contracts briefly, manifesting as ‘jerk’ at the joint.]

Note a few points:

 Hammer used by clinicians, to elicit a tendon jerk, is called reflex

hammer, or, clinicians’s hammer, or percussion hammer.
 Receptor for a tendon jerk is ~ muscle spindle (although hammer is struck
over the tendon).
 Tendon jerk is:- (i) Physiologically, a stretch reflex, (ii) Clinically, a
deep reflex, (iii) Structurally, a monosynaptic reflex.

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Dynamic stretch reflex v/s static stretch reflex-

- When a muscle is stretched suddenly, a strong signal arises

instantaneously from its spindle and sent to the spinal cord, it leads to
a brief, strong, reflex contraction of the muscle. This is dynamic stretch
reflex. All the tendon jerks are dynamic stretch reflexes. This reflex
actually functions to oppose sudden changes in the muscle length
because the muscle contraction opposes the stretch.
- If a muscle is held “static” at a particular length, signals from its spindle
cause a continuous contraction of the muscle. This is called static
stretch reflex.

{An especially important function of the stretch reflex is its ability to prevent
oscillation or jerkiness of body movements. This is a damping, or smoothing
function. The primary input or signals from spinal cord to a muscle transmitted in
an unsmooth, jerky fashion. Muscle spindle damps the signals so that muscle
contractions are smooth. This is called a signal averaging function of the muscle
spindle reflex.}

Supraspinal regulation of stretch reflexes:

- The brain areas that would inhibit stretch reflexes are: (i) motor cortex,
(ii) basal ganglia, (iii) cerebellum, (iv) reticular inhibitory area.
- The brain areas that would facilitate stretch reflexes are: (i)
reticular facilitatory area, (ii) vestibular nuclei.
- These areas generally act by increasing or decreasing the muscle
spindle sensitivity.
- The large facilitatory area in the brain stem reticular formation
discharges spontaneously. However, the smaller brain stem area that
inhibits  efferent discharge is driven instead by fibers from the cerebral
cortex and cerebellum. The inhibitory area in the basal ganglia may act
through descending connections or by stimulating the cortical
inhibitory center.
- When the brain stem is transected at the upper border of pons,
the effects of two of the three inhibitory areas that drive the
reticular
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 inhibitory center are removed. Discharge of the facilitatory area
continues, but that of the inhibitory area is decreased. Consequently,
the balance of facilitatory and inhibitory impulses converging on the 
efferent neurons shifts toward facilitation. Gamma efferent discharge is
increased, and stretch reflexes become hyperactive.
- The vestibulospinal and some related descending pathways are also
facilitatory to stretch reflexes and promote rigidity. This rigidity is due
to a direct action on the  motor neurons.

Applied Physiology:

- In upper motor neuron (UMN) lesions, the stretch reflexes (tendon

jerks) will be exaggerated. Reason: In UMN lesion, there is loss of
inhibitory influence of UMN on the LMN; hence, the excessive firing
of LMN causes exaggerated stretch reflexes. E.g., pyramidal tract
lesion, lesion of basal ganglia, etc.
- In lower motor neuron (LMN) lesions, the stretch reflexes
are diminished or absent.

Muscle tone:

(I) Physiological definition-

Muscle tone may be defined as the partial tension/contraction in the

muscle even when the muscle is in relaxed state. (Even when the muscle is in a
resting state, there is some amount tension or contraction present in the muscle.
This is called tone.)

(II) Clinical definition-

It is the resistance encountered when a joint is moved is passively.

(Because there is some contraction present in a muscle, when a joint is moved
passively, there will be some resistance to this passive movement.)

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Cause of the tone:

There is asynchronous gamma motor neuron discharge to the muscles;

this discharge is there even when there is no active muscle contraction. The
gamma discharge excites the muscle spindle. The signals from the spindle are
transmitted in Ia afferents to the spinal cord, which end on the alpha motor
neurons. These alpha motor neurons in turn send impulses back to the extrafusal
muscle fibers, creating tension in the muscle. Thus, tone can be said to be a
stretch reflex.

[Fig: Neuronal circuit responsible for muscle tone. (1) There is asynchronous gamma-motor
neuron discharge from spinal cord to muscle; it excites the muscle spindle, (2) Signals from
muscle spindle are sent back to spinal cord; these signals excite the alpha-motor neuron, (3)
alpha-motor neuron sends the signals to the extrafusals; muscle remains in a partially
contracted state.]

Importance of muscle tone:

 Muscle tone sets the bias for efficient voluntary movement. Background tone
in a muscle group keeps those muscles prepared to start a particular
movement at any given moment.

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 Muscle tone is important for acquiring, maintaining, and changing of body
posture. Body posture is acquired by reflex redistribution of tone in different
muscle groups. Thus, in the upright posture, tone will be high in the
antigravity muscles of the body.

Applied Physiology:
 Hypotonia: (flaccidity)
- Reduction in tone is hypotonia or flaccidity. It results from LMN lesions.
- Destruction of the afferent limb (e.g. by tabes dorsalis) or the efferent
limb (e.g. poliomyelitis, trauma) of the reflex arc abolishes tone.
 Hypertonia: (spasticity, rigidity)
- Excessive tone in muscles; it occurs due to UMN lesions.
- Two types: Spasticity and rigidity.
- Spasticity results from pyramidal tract lesion; rigidity is seen
in extrapyramidal lesions.

 Golgi tendon organ: (GTO) (proprioceptor in muscle)

- The Golgi tendon organ is an encapsulated sensory receptor situated
in tendon of the muscles.
- About 15-20 muscle fibers are connected in series with each Golgi
tendon organ. (Note: muscle spindle is in parallel with the
extrafusal muscle fibers; Golgi tendon organ is in series with the
extrafusals.)
- GTO is stimulated by tension in the muscle. Thus, it detects tension and
rate of change of tension of a muscle.

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[fig: Neural circuit for lengthening reaction. Refer to text.]

- The sensory fibers arising from the GTO are Ib type of fibers. These fibers
enter the spinal cord and end on inhibitory interneurons, which, in turn
terminate directly on the -motor neuron going back to the muscle.
(The same Ib fiber also makes excitatory connections with motor
neurons supplying antagonists to the muscle.)

The reflex initiated by the GTO will always be inhibitory to the agonist muscle
from which the GTO is sending signals about its tension.

* Inverse stretch reflex-

Up to a point, the harder a muscle is stretched, the stronger is the reflex

contraction. However, when the tension becomes too high, contraction suddenly
ceases and the muscle relaxes. This relaxation in response to strong stretch is
called the inverse stretch reflex or autogenic inhibition. This inverse stretch
reflex is initiated by the Golgi tendon organ.

Lengthening reaction: (Clasp-knife reflex, or, spasticity seen in pyramidal lesion)

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 - When the tension on the muscle, and therefore, on the tendon
becomes extreme, the sequence of moderate stretch —> muscle
contraction, strong stretch —> muscle relaxation is clearly seen.
- Passive flexion of the elbow, for example, meets immediate resistance
as a result of the stretch reflex in the triceps muscle. Further stretch
activates the inverse stretch reflex. The resistance to flexion suddenly
collapses, and the joint gives way completely, and the elbow flexes.
This sequence of resistance followed by complete relaxation when a
limb is moved passively is known clinically as the clasp-knife reflex
because of its resemblance to the closing of a pocket knife. The
physiological name for it is the lengthening reaction because it is the
response of a spastic muscle to lengthening.

Importance of lengthening reaction:

 It is a protective mechanism to prevent tearing of the muscle or avulsion of
the tendon from its attachments to the bone. When there is already
excessive tension on the muscle (and hence on the tendon), further
stretch and contraction may damage the muscle. Hence, GTO, which is
stimulated by the tension of the muscle, initiates this reflex which inhibits
further development of tension and thus relaxes the muscle completely.

Applied Physiology:

(1) Spasticity:
 Hypertonia seen in pyramidal tract lesion is
termed spasticity. It elicits the clasp-knife reflex.
 There is already an excess tone in the muscles. It elicits
as the initial high resistance to a passive stretch.
 Further stretching of the muscle initiates GTO reflex, which
relaxes the muscle completely. Thus, after initial resistance,
the joint suddenly collapses.
(2) Rigidity:
 Hypertonia seen in extrapyramidal lesions is termed rigidity.

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  When a joint is moved passively, there is high
resistance throughout the movement.
 Lead-pipe rigidity: Resistance throughout the movement (as
may be encountered while bending a lead pipe). Where the
passive movement is stopped, the joint will remain in that
bent position (just like a bent lead pipe). Explanation: The
GTOs of both agonist & antagonist muscles fire
simultaneously. (Recall, the GTO of a muscle initiates the reflex
that relaxes that muscle while it contracts the antagonist
muscle. If both GTOs fire together, both the muscle groups will
remain contracted.)
 Cog-wheel rigidity: During the passive movement of a joint,
the movement is interrupted intermittently (resistance comes,
then goes, and appears again; like, cogs in a wheel).
Explanation: GTOs of agonists and antagonists fire alternately.

Clonus:

- Increased gamma motor neuron discharge is responsible for

a neurological manifestation called clonus.
- This neurologic sign is the occurrence of regular, rhythmic
contractions of a muscle subjected to sudden, maintained stretch.
Ankle clonus is a typical example. It is initiated by brisk, maintained
dorsiflexion of the foot, and the response is rhythmic plantar flexion at
the ankle. The stretch reflex-inverse stretch reflex sequence may
contribute to this response.
- The spindles of the tested muscle are hyperactive, and the burst of
impulses from them cause discharge in all the motor neurons
supplying
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 the muscle at once. The consequent muscle contraction stops spindle
discharge. However, the stretch has been maintained, and as soon as
the muscle relaxes it is again stretched and the spindles are stimulated.

The decerbrate rigidity:

(In experimental animals, an operative procedure isolates hindbrain and spinal
cord from rest of the brain; it is called ‘decerebration’.)

[Fig: Mechanism of decerebrate rigidity. Vestibular nuclei have intrinsic activity;

vestibulospinal tract causes contraction of anti-gravity extensor muscles. Cortical inhibitory
influences on brain stem nuclei will be lost after transection. Excess firing of vestibulospinal
tract, after transection, will result in excessive contraction (rigidity) of the anti-gravity
muscles.]

- When a section is made below the midlevel of the midbrain, leaving

reticular and vestibular nuclei intact, the animal develops a condition
called decerebrate rigidity. The rigidity occurs in the antigravity
muscles (the muscles of the neck and trunk and the extensors of the
legs).

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 - Because of the section, the cortical input to the medullary reticular
nuclei is lost. Thus, inhibition of the antigravity muscles is lost. And,
overactivity of the pontine reticulospinal tract and vestibulospinal
tracts causes overexcitation of these muscles.

Mechanism of decerebrate rigidity-

Decerebrate rigidity is the spasticity due to diffuse facilitation of stretch

reflexes. The facilitation is due to two factors: increased general excitability of the
motor neuron pool and an increase in the rate of discharge in the  efferent
neurons.

 Significance of decerebrate rigidity:

In cats and dogs, the spasticity produced by decerebration is most marked
in the extensor muscles, the muscles with which the cat and dog resist
gravity. In humans, the pattern in true decerebrate rigidity is extensor in all
four limbs, like that in cats and dogs (even though the main antigravity
muscles of the arms in the upright position are flexors). However,
decerebrate rigidity is rare in humans, and the defects that produce it are
usually incompatible with life. The more common pattern is extensor
rigidity in the legs and moderate flexion in the arms. It is called decorticate
rigidity, and is due to lesions of the cerebral cortex, with most of the brain
stem intact.

* POLYSYNAPTIC REFLEXES: THE FLEXOR WITHDRAWAL REFLEX

When a painful stimulus is applied to a limb, there is reflex flexion of the

limb, and the limb is withdrawn from the stimulating object. This is called flexor
reflex. (If some body part other than a limb is stimulated similarly, the similar
reflex response is observed, but the reflex may not be confined to flexor muscles.
Hence, all such reflexes are called as withdrawal reflexes.)

Importance of the withdrawal reflex:

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 Nociceptive or painful stimuli may be potentially harmful. Hence, flexion of
the stimulated limb gets away from the source of noxious stimulation.

- Since this type of reflex is elicited by painful stimuli, it is also called

nociceptive reflex or pain reflex.

Properties of flexor withdrawal reflexes:

 Withdrawal reflexes are prepotent. They preempt the spinal
pathways from any other reflex activity taking place at the
moment.
 These reflexes are polysynaptic; that is the reflex path involves a
number of synapses. In such polysynaptic pathways, there is
prolonged bombardment of the motor neurons from a single
stimulus and consequently prolonged responses in these
reflexes.
 The withdrawal reflex has a relatively long latency because the
afferent pathway uses small, slowly conducting fibers and
involves many synapses.
 Some of the neurons involved in these reflexes give out
collaterals which turn back and end on a neuron in the same
pathway. This creates reverberating circuits in such polysynaptic
pathways, and the reflex activity continues to occur in a
reverberating fashion.
 Afterdischarge: The pathways for eliciting the flexor reflex do not
pass directly to the anterior motor neurons but instead pass first
into the spinal cord interneuron pool and then to the motor
neurons. These pathways involve the following types of circuits:
(i) diverging circuits to spread the reflex to the necessary muscles
for withdrawal; (ii) circuits to inhibit the antagonist muscles,
called reciprocal inhibition circuits; and (iii) circuits to cause
afterdischarge lasting many fractions of a second after the
stimulus is over.
- A weak stimulus causes one quick flexion movement; a strong stimulus
causes prolonged flexion and sometimes a series of flexion
movements. This prolonged response is due to prolonged, repeated
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firing of the motor neurons. The repeated firing is called
afterdischarge. It is due to

133
continued bombardment of motor neurons by impulses arriving by
complicated and circuitous polysynaptic paths. The afterdischarge
causes the response to outlast the stimulus. This keeps the affected limb
away from the painful stimulus while the brain determines where to put
it.
 Irradiation: When the hind limb of a spinal cat is pinched, the
stimulated limb is withdrawn, the opposite limb is extended, and
the ipsilateral forelimb extended, and the contralateral forelimb
flexed. This spread of excitatory impulses up and down the spinal
cord to more and more motor neurons is called irradiation of the
stimulus, and the increase in the number of active motor units is
called recruitment of motor units.
 Local sign: The exact flexor pattern of the withdrawal reflex in a limb
varies with the part of the limb that is stimulated. If the medial
surface of the limb is stimulated, for example, the response will
include some abduction, whereas stimulation of the lateral surface
will produce some adduction with flexion. The reflex response in
each case generally serves to effectively remove the limb from the
irritating stimulus. This dependence of the exact response on the
location of the stimulus is called the local sign.
 Crossed extensor response:
 When a strong stimulus is applied to a limb, the response
includes not only flexion and withdrawal of that limb but also
extension of the opposite limb. This is part of the withdrawal
reflex. The interneurons form pathways that cross the spinal cord
to innervate the extensor motorneurons on the contralateral
side. The crossed extensor reflex, in the lower limbs, allows the
contralateral limb to support the body while the other limb is
raised off the ground.
 Fractionation and occlusion:
 Supramaximal stimulation of any of the sensory nerves from a
limb never produces as strong a contraction of the flexor
muscles as that elicited by direct electrical stimulation of the
muscles
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 themselves. This indicates that the afferent inputs fractionate the
motor neuron pool; ie, each input goes to only part of the motor
neuron pool for the flexors of that particular extremity.

On the other hand, if all the sensory inputs are dissected out and
stimulated one after the other, the sum of the tension developed by
stimulation of each is greater than that produced by direct electrical
stimulation of the muscle or stimulation of all inputs at once. This
indicates that the various afferent inputs share some of the motor
neurons and that occlusion occurs when all inputs are stimulated at
once.
Other properties of reflexes:

 Adequate stimulus-
 The stimulus that triggers a reflex is generally very precise.
This stimulus is called the adequate stimulus for that
particular reflex.
 Final common path-
 The motor neurons that supply the extrafusal fibers in
skeletal muscles are the efferent side of many reflex arcs.
All neural influences affecting muscular contraction
ultimately funnel through them to the muscles, and they
are therefore called the final common paths. Numerous
inputs converge on them. There are at least five inputs
from the same spinal segment to a typical spinal motor
neuron. In addition, there are excitatory and inhibitory
inputs, generally relayed via interneurons, from other levels
of the spinal cord and multiple long descending tracts from
the brain. All of these pathways converge on and determine
the activity in the final common paths.
 Central excitatory & inhibitory states-
 The spinal cord also shows prolonged changes in
excitability, possibly because of activity in reverberating
circuits or prolonged effects of synaptic mediators. There

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 may be a prolonged state in which excitatory influences
overbalance inhibitory influences (central excitatory state)
and vice versa (central inhibitory state).

{In chronically paraplegic humans, a mild noxious stimulus may cause, in

addition to prolonged withdrawal-extension patterns in all four limbs,
urination, defecation, sweating, and blood pressure fluctuations (mass
reflex).}

 Effects of spinal cord injury:

(I) Complete transection of spinal cord:-
- It may be caused by gunshot wounds or motor bike accidents.
- When there is complete transection of the spinal cord, it is followed by
a period of spinal shock during which all spinal reflex responses are
profoundly depressed. It usually lasts for about 2 weeks.
- Subsequently, reflex responses return and become relatively
hyperactive.
3 succesive stages are seen after transection of cord:-
1. Spinal shock: Stage of flaccidity-
- Motor function: The muscles are completely paralyzed; all the
reflexes are abolished and muscle tone is lost.
- Sensory function: There is complete loss of sensation below the level
of lesion; cramp-like pains at the level of lesion
- Visceral function: The bladder and rectum are generally paralyzed.
The sphincter vesicae, however, frequently retains its function, or
recovers very rapidly, resulting in retention of urine.
- ANS function: As the vasoconstrictor fibers leave the cord between the
T-1 and L-2 segments, a transection below the level of L-2 produces
very little fall of blood pressure, while section at the T-1 causes a fall of
BP equal to that resulting from destruction of the vasomotor center,
i.e., to a level of 40 mm Hg. As the legs are immobile, venous return is
reduced.

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 This temporary state is called spinal chock.
Normally, the descending pathways send tonic excitatory impulses on to the
spinal neurons. These impulses are interrupted by transection of spinal cord;
hence, the spinal reflexes are depressed initially.

2. Stage of reflex activity: Reflexes return

- As the stage of shock passes off, functional activity returns first in
smooth muscle. The bladder sphincter (if it was paralyzed) recovers
very soon, but the detrusor of the bladder regains its power more
slowly.
Blood pressure is restored to about its normal level.
- The first reflex response to appear as spinal shock wears off is
frequently a slight contraction of the leg flexors and adductors in
response to a noxious stimulus.
- Skeletal muscle tone: Tone in the skeletal muscle returns after 2-3
weeks. (Note: The isolated cord ‘favors’ the flexor neurons and
muscles.) The limbs tend to adopt a position of slight flexion, and
the paralysis is therefore referred to as “paraplegia in flexion”.
- In case only the pyramidal tract was damaged, leaving extrapyramidal
tracts relatively intact, it may lead to ‘paraplegia in extension’.
- Reflex movements:
 FLEXOR REFLEX- The reflex movement that returns first is
the flexor reflex. In this stage, there is BABINSKI’S SIGN
PRESENT (Dorsiflexion of great toe and fanning of the other
toes).
 MASS REFLEX- A very widespread reaction is elicited by scratching
any point on the lower limbs or the anterior abdominal wall
below the level of lesion. The response obtained consists of:

o Flexor spasms of both lower extremities and contraction of the

anterior abdominal wall.
o Evacuation of the bladder; this may be partly due to
the abdominal compression raising intravesical
pressure to threshold level.
137
o Profuse sweating below the level of the lesion.

138
  COITUS REFLEX- This is produced by stimulation of the glans
penis, or the skin around the genitals, anterior abdominal wall, or
anterior and inner surface of the thighs. The response consists of
swelling and stiffening of the penis, withdrawal of the testes
because of contraction of the cremaster muscles and curling up of
the scrotal skin from the action of the dartos. The recti abdominis,
flexors of the hip, and adductors of the thighs also contract.
Seminal emission may occur.
 DEEP REFLEXES- The knee jerk returns about one to five
weeks later than the flexor responses. Ankle clonus may be
present.
 Autonomic reflexes:

Reflex evacuation of the bladder is gradually established; reflex

defecation also occurs.

The recovery of reflex excitability and eventual hyperactivity of these reflexes

may be due to the development of denervation hypersensitivity to the chemical
transmitters released by the remaining spinal excitatory endings. Another
possibility is the sprouting of collaterals from existing neurons, with the
formation of additional excitatory endings on interneurons and motor neurons.

3. Stage of reflex failure:

If general infection or toxemia occurs, failure of reflex function occurs.
The threshold for all reflexes is raised. There is muscle wasting.

Complications of cord transection:

- Because of the paralysis of muscles, the patient is immobilized. Hence,

they develop negative nitrogen balance as there is breakdown of large
amounts of body protein.
- The tissues that are broken down include the protein matrix of bone,
and this plus the immobilization cause Ca++ to be released from bones in
large amounts. This leads to hypercalcemia and hypercalciuria, and

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 calcium stones are formed in the urinary tract. Also, there is
urinary tract infection due to stones and paralysis of bladder
function.
- Since the patient is immobilized, the weight of the body compresses the
circulation to the skin over bony prominences, so that unless the
patient is moved frequently the skin breaks down at these points and
decubitus ulcers (bed sores) form.

(II) Incomplete transection (hemisection) of the spinal cord: Brown-

Sequard syndrome
- Bike accidents, gun shot injuries may some times result in
hemisection of the spinal cord involving a particular segment. It
results in Brown- Sequard syndrome.

[Fig: Hemisection of spinal cord at one particular segment (shown as shaded region). {X}
shows the sensations that can not ascend upward beyond the level of lesion. Hence, they can
not reach cortex and can not be felt. Refer to text for further discussion.]

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Sensory loss below the level of lesion -

- There will be loss of fine touch from the same side, below the level
of lesion.
- Pain & temperature will be lost from the opposite side, below the
level of lesion. Pain & temperature from the same side will be spared,
below the level of lesion.

Explanation: Refer to diagram above

(For sensations to be felt, they have to reach cortex.)
- Fine touch-carrying fibers enter spinal cord and ascend upward on the
same side, in dorsal column. Let’s say, the lesion is at the level of T-10,
and right half of the segment, at this level, is damaged. Fibers carrying
fine touch from the right lower limb will enter spinal cord and start
ascending upward on the same side. The impulses will be interrupted
at the level of T-10 (won’t be able to reach cortex).
- Pain-carrying fibers from right lower limb will enter spinal cord; 2 nd
order neuron will cross midline (below T-10), and ascend upward in
lateral white column of the left half of the spinal cord. These signals will
ascend uninterrupted up to cortex. However, pain-carrying fibers from
left lower limb will enter spinal cord; 2nd order neuron will cross midline
(below T-10) and ascend upward in lateral white column of the right
side. These signals will be interrupted at the level of T-10 (won’t reach
thalamus/cortex).

Motor defects:
(a) Below the level of lesion -
- Fibers of the descending tracts, on the side of lesion, cannot send
impulses below the level of lesion. Hence, it will be a UMN type lesion
for below the level of damage. There will be hypertonia and
exaggerated tendon jerks.
(b) At the level of lesion –

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 - Anterior motor neuron is damaged at the level of lesion. Hence, it
will be an LMN type lesion, on the side of the damage. There will be
hypotonia and diminished tendon jerks.

————————————————————————————————————

Posture and equilibrium

Introduction:

- The term posture means ‘stance’. For instance, standing posture, sitting
posture, etc.
- A particular posture is attained through one or more reflexes. In a
particular posture, some muscles are in a state of contraction and
others are relaxed. For instance, in upright posture, there is more tone
in the antigravity muscles of lower limbs. When the posture is changed
to that of sitting, now tone in some muscles of the legs will reduce and
some other group (flexors of leg) will have more tone.

Therefore, posture may be defined as “reflex redistribution of tone in various

muscle groups in order to attain and maintain a particular body
position/stance”.

Another definition of tone is: “active muscular resistance to displacement of body

by gravity and/or acceleration”.

A particular body posture is attained in a reflex manner. Various body postures

are attained through “postural reflexes”.

Study of postural reflexes: Experimental animal preparations

Posture is attained through “postural reflexes”. These reflexes involve muscle

groups, and the reflexes have centers in the CNS. To study the postural reflexes,

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sections are taken at various levels in the CNS to make experimental animal
preparations. These sections achieve two objectives:

(i) When a section is made at a particular level in the CNS, it leaves the
parts of the CNS below the section intact. But it removes influences of
higher centers of CNS on these lower parts. Since the cortex is
removed in experimental animals, it removes the inhibitory influences
of the cortex on the lower levels of CNS. The centers for postural
reflexes are present in these lower levels; removal of cortical inhibitory
influences will make the postural reflexes more prominent (that is,
they are unmasked now).
(ii) Experimental animal preparations are made by taking sections at
different levels in the CNS. This helps in finding out the centers for the
various postural reflexes. For instance, some reflexes are present in
spinal animals (animals in which only the spinal cord is present). If some
reflexes are present in such animal, it means the centers for those
reflexes are in the spinal cord. But, some other postural reflexes are not
present in such spinal preparation. Now, in another animal, section is
made higher in the CNS to retain spinal cord and brain stem. Now, if
the reflexes absent in the spinal animal are present in this preparation,
the centers for those reflexes must be the brain stem nuclei.

The experimental animal preparations-

(1) Spinal animal: When the spinal cord is sectioned at the highest level, all
the higher brain centers and their influences on the spinal cord are
removed. The highest neural center for this animal is the spinal cord; and it
will have no inhibitory influences coming from the brain. The (postural)
reflexes which have their centers in the spinal cord will be observed
prominently.

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(2) Decerebrate animal: Transection of the midbrain between the superior and
inferior colliculi causes decerebrate rigidity. In decerebrate preparation,
vestibular nuclei are retained. Some postural reflexes that were not
present in spinal animal will be present in decerebrate preparation.
Obviously, the centers for such reflexes will be above the spinal cord
(vestibular and reticular nuclei). The decerebrate animal cannot actively
assume upright posture by itself, but if it is placed in upright posture it can
remain insecurely in upright posture (it will somehow maintain the posture
in which it is placed).
(3) Thalamic animal: If the section is taken further higher up, and the whole
of the midbrain is left intact, such an animal is called thalamic animal (or
midbrain preparation). Some postural reflexes are not elicited by
decerebrate animal but are present in the thalamic animal (e.g. righting
reflexes). Centers for such reflexes will be present in the midbrain,
particularly, the red nucleus. The midbrain animal can actively assume
upright posture and can even walk a few steps.
(4) Decorticate preparation: If the section is taken further higher up, and the
cerebral cortex is removed but basal ganglia and the brain stem is left
intact, such preparation is called decorticate preparation. All postural
reflexes (except those that require cortex) are present in decorticate
animal. The animal can assume erect posture and can even walk
awkwardly.

144
[Fig: A schematic diagram to show experimental animal preparations, by making transections
at various levels in CNS. The red line indicates level of transection. Parts above the
transection are removed. Refer to text for details.]

Some postural reflexes require an intact cortex. (Optical righting reflexes, and
placing & hopping reactions). These reflexes will not be present in any of the
abovementioned experimental animals, since cortex is removed in these animals.

THE POSTURAL REFLEXES:

The basic postural reflex is the stretch reflex. (The basis for attaining/maintaining
a posture is stretch reflexes in various muscle groups.) Recall:- Muscle tone is a
stretch reflex.

By altering the discharges through the extrapyramidal system of fibers, the

stretch reflex in some muscle groups is increased and in some other
muscle groups decreased; thus, redistribution of tone is achieved.

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Postural reflexes are initiated by sensory organs located in various body parts.
Five important areas (receptors or their locations) that initiate postural responses
are: (i) the visual system, (ii) the vestibular apparatus, (iii) receptors in muscles,
tendons, and joints of the limb, (iv) pressure receptors in the toe pad and in other
parts of the body, and (v) stretch receptors of the muscles and joints of the neck.

Postural reflexes can be classified into two categories:

(1) Static reflexes: Gravity is acting on the body, and the postural reflexes
prevent the displacement of the body posture. (the body is
stationary)
(2) Statokinetic reflexes: Gravity and/or acceleration are acting to displace
the body, and the reflexes maintain the posture. (the body is moving)

(1) Static postural reflexes:

 Local static reactions
 Segmental static reactions
 General static reactions: (attitudinal reflexes, righting reflexes)

(a) Local static reactions-

{They involve a segment of the spinal cord, and only one side of the
segment. Thus, they will be present in spinal animals.}
(i) Positive supporting reaction: (magnet reaction)
When pressure is applied to footpad (as in, while standing on
ground), there is strong contraction of agonists and antagonists of
the limb. The limb stiffens and becomes rigid like a pillar to support
the body weight. This is called positive supporting reaction. The locus
of the pressure on the pad of the foot determines the direction in
which the limb will extend; pressure on one side causes extension in
that direction, an effect called the magnet reaction. This helps keep
an animal from falling to that side.
(ii) Negative supporting reaction:
(Relaxation of limbs to move to a new position due to passive flexion
of the limb). Stretch of the muscles during positive supporting

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 reaction causes release of positive supporting reaction. This is called
negative supporting reaction.
(b) Segmental static reactions-
{They involve an entire segment of the spinal cord, that is, both sides
of a segment. They will be present in spinal animal.}
When a limb is flexed and the foot is raised above ground, the
opposite limb extends (crossed extension), which helps support the
body when change in body position occurs. It has also been called
crossed extensor reflex or Phillipson’s reflex.
(c) General static reactions- (Attitudinal reflexes, righting reflexes)

- Whole body is involved (unlike in local and segmental reactions in

which only the hind limbs are involved)
- Center is above the level of spinal cord; hence, these reactions are
not elicited by spinal animals

 ATTITUDINAL REFLEXES: (shown by decerebrate animal)

In decerebrate animal the posture of the trunk and limbs can be
adjusted:
o In accordance with alterations in the position of the head
in space;
o By changing the position of the head relative to the trunk.

In the first case the afferent impulses arise solely from the otolith
organ of the vestibule (tonic labyrinthine reflexes); in the second
case additional afferent impulses come from the neck muscles
(tonic neck reflexes). The new position reflexly imposed on the
body persists for as long as the new position of the head is
maintained.
{The animal takes a certain “attitude” of limbs to maintain the posture. Hence,
these are called attitudinal reflexes.}

(i) Tonic neck reflexes- These reflexes are set up by alterations of

the position of the head relative to the body.

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  Ventroflex the head: the fore limbs flex and the hind
limbs become extended. (“as if looking under a shelf”)
 Dorsiflex the head: the fore limbs extend and the hind limbs
flex. (“as if looking above a cupboard”)

[The purpose of these responses seems obvious; the position of the

body is being adopted, so as to maintain a certain posture.]

 Press ventralwards on the lower part of the cervical vertebral

column: all four limbs flex (vertebra prominens reflex), as ‘in
an animal crawling into a hole’.
 Rotate or incline the head in various directions: to simplify
description, the limbs on the side to which the jaw is turned
are called ‘jaw limbs’; the limbs to which the vertex is turned
are
called ‘skull limbs’. In general the jaw limbs extend (to support the
weight of the head) and the skull limbs flex.

The receptors for the neck reflexes are the proprioceptors in the
neck (neck muscle spindles and pacinian corpuscles in the ligaments
of the cervical vertebral joints.
Centers for these reflexes are in the cervical region of the spinal cord.
(ii) Tonic labyrinthine reflexes-
{These reflexes are studied after section of the dorsal nerve roots of
C1,2,3 or after immobilizing the head, neck, and upper thorax by
means of a plaster jacket (to prevent neck reflexes from coming into
play).} The labyrinthine reflexes are due to alterations in the position of
the head relative to the horizontal plane.

 If the animal is placed in the supine position, maximum tone

is present in the antigravity muscles.
 In the prone position, with the snout 45 degrees below the
horizontal plane, tone in the extensor muscles is reduced to a
minimum; in intervening positions intermediate grades of
tone are present.

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 These reflexes are initiated by the action of gravity on the otolithic
organs (vestibular apparatus). The centers for labyrinthine reactions are
the vestibular and reticular nuclei; and they are effected by
vestibulospinal and reticulospinal tracts. (The purpose of these reactions
is not very clear.)

 RIGHTING REFLEXES-
 These reflexes are NOT shown by decerebrate animal,
but they are shown by midbrain animal. It means, the
centers for these reflexes are in the midbrain.
 By means of the righting reflexes the animals can rise to
the standing position, walk, and right themselves. That is, a
midbrain animal or a decorticate animal can bring its head
right way up and get the body into the erect position under
all circumstances. If the animal is laid on its side or on its
back, the head at once rights itself, the body follows suit,
and finally the animal resumes the upright posture.

The decerebrate animal can never actively assume the upright position; it has
no righting reflexes. It can only remain insecurely in the upright posture if
put there. Midbrain or decorticate animal can actively go into upright
posture.

The righting reflex consists of a chain of reactions following one another in

an orderly sequence as each reaction produces the next one.
(i) Labyrinthine righting reflex-
When the animal’s head is in the lateral position, or if the animal is
held by its body and tipped from side to side, the head stays level
because of an immediate righting of the head. The stimulus is tilting
of the head, which stimulates the otolithic organs; the response is
compensatory contraction of the neck muscles to keep the head
level.

149
 (ii) Body-on-head righting reflex-
If the animal is laid on its side, the side of the trunk in contact with
the bench is undergoing constant stimulation, while the other side in
contact with air is not. This asymmetric stimulation of the deep
structures in the body wall also reflexly rights the head. (The head
can thus be righted even if the labyrinths have been destroyed.)
(iii) Neck righting reflex-
If the head is righted by either of the two above reflexes, and the
body remains tilted, the neck muscles are stretched. (The head is
righted but the body is still in lateral position, so neck is twisted.) This
evokes a further reaction- the neck righting reflex- which rights the
thorax and initiates a wave of similar stretch reflexes that pass down
the body, which bring the lumbar region and hind limbs, successively,
into the upright position.
(iv) Body-on-body righting reflex-
Even if the head is prevented from righting, pressure on the body
surface may cause righting of the body directly.
(v) Optical righting reflexes- {These reflexes require an intact cortex,
the visual cortex. Hence they are not present in any of the
experimental animal preparations as cortex is removed in such
animals.} In the normal animals with intact visual cortex, visual cues
can initiate optical righting reflexes. In man, the optical righting
reflexes are far more important than the other righting reflexes. If an
intact animal (or a normal human) is falling due to gravity, there will
be alterations in visual impulses for him (tilting of the erect
structures in front of him). The image in the cortex will provide the
cue, and there will be reflex righting of the head. Thus, the center
for these reflexes is in the visual cortex.
Grasp reflex: When a primate in which the brain tissue above the thalamus has
been removed lies on its side, the limbs next to the supporting surface are
extended. The upper limbs are flexed, and the hand on the upper side grasps
firmly any object brought in contact with it (grasp reflex). This whole response is

150
probably a supporting reaction that steadies the animal and aids in pulling it
upright. (Thus, it is sometimes considered a righting reflex.)

(2) STATOKINETIC REFLEXES-

These reflexes are evoked by acceleration/movements of the body.

That is, when the body is moving, the upright posture is
maintained by these reflexes. These reflexes also require an intact
cortex.

 Hopping and placing reactions:

When a standing animal is pushed laterally, there are hopping
movements that keep the limbs in position to support the body.

When a standing animal is pushed laterally, the animal places the

foot firmly on a supporting surface, at a little distance away.

{Vestibular placing reaction: If a blindfolded animal is lowered rapidly, its forelegs

extend and its toes spread. This response to linear acceleration is a vestibular
placing reaction that prepares the animal to land on the foot. It does not need an
intact cortex. However, animal is in acceleration; hence, it can be considered a
type of statokinetic reflex.}

151
Reflex Stimulus Response Receptor Integrated
in
Stretch Stretch Contraction Muscle spindles Spinal cord,
reflexes of muscle medulla
Positive Contact Foot Proprioceptors in Spinal cord
supporting with sole extended to distal flexors
(magnet) or palm support body
reaction
Negative Stretch Release of Proprioceptors in Spinal cord
supporting positive extensors
reaction supporting
reaction
Tonic Gravity Contraction Otolithic organs Medulla
labyrinthine of limb (Vestibular
reflexes extensor apparatus)
muscles
Tonic neck Head Change in Neck Medulla
reflexes turned: pattern of proprioceptors
extensor
contraction
1. to side 1.extension
of limbs on
side to which
head is
turned
2. up
2.hind legs
3.down flex
3.forelegs
flex

152
Reflex Stimulus Response Receptor Integrated
in
Labyrinthine Gravity Head kept Otolithic organs Midbrain
righting level (Vestibular
reflexes apparatus)
Neck righting Stretch of Righting of Muscle spindles Midbrain
reflexes neck thorax
muscles and
shoulders,
then pelvis
Body on head Pressure Righting of Exteroceptors Midbrain
righting on side of head
reflexes body
Body on body Pressure Righting of Exteroceptors Midbrain
righting on side of body even
reflexes body when head
held
sideways
Optical Visual Righting of Eyes Cerebral
righting cues head cortex
reflexes
Placing Various Foot placed Various Cerebral
reactions visual, on cortex
extero- supporting
ceptive, surface in
and position to
proprio- support
ceptive body
clues
Hopping Lateral Hops, Muscle spindles Cerebral
reactions displace- maintaining cortex
ment limbs in
while position to
standing support
body

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  Locomotion generator- (walking)
- There are two pattern generators for locomotion (walking) in the spinal
cord: one in the cervical and one in the lumbar region. The pattern
generator has to be turned on by tonic discharge of a discrete area in
the midbrain – the mesencephalic locomotor region.
- The act of walking requires the coordinated contraction and relaxation
of flexor and extensor muscles of the legs. This rhythmic alteration
between flexion and extension is produced entirely by the
interconnections of neurons in the spinal cord. These neurons and
their interconnections compose the locomotion generators for walking.
- During the walking process, the locomotion generators coordinate the
flexor and extensor leg muscles to carry out the stance phase and the
swing phase of walking. In the stance phase, the leg is fully extended,
with the foot on the ground, supporting the weight of the body. In the
swing phase, the leg is flexed and the foot is off the ground and
swinging forward.

Vestibular system

{Equilibrium of the body during static position and movements}

Though the vestibular system & equilibrium involves cranial nerve, and can be considered a special sense,
it is discussed here. Since motor system had mention of labyrinth/vestibular apparatus at many places, it
would serve a better correlation if this system discussed along side the motor system.

~ Vestibular system reflexes are responsible for:

 Maintaining tone in antigravity muscles, to maintain the

upright posture

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  Coordinating the adjustments made by the limbs and eyes
in response to changes in body position.
 Functional anatomy:
 In the petrous part of the temporal bone, there is bony labyrinth.
 Within the bony labyrinth, there is a system of coiled tubes
and sacs, called membranous labyrinth.
 Membranous labyrinth has two distinct functional parts:

1. Cochlea – It is the organ for hearing.

2. Vestibular apparatus – It is the organ for equilibrium; that
is, body’s balance under all circumstances – static and
moving.

[Fig: The membranous labyrinth. It has two parts:- (1) Cochlea – The organ for hearing, and
(2) vestibular apparatus – The organ for equilibrium. Vestibular apparatus has two
components:- (a) Utricle & saccule, and (b) semicircular canals.]

Vestibular apparatus:

It consists of two functional components –

A. Otolith organs:- utricle & saccule

B. Three semicircular canals

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{The saccule communicates directly with the cochlea, which is beneath it, and the
utricle, which is above it.

Both ends of all three semicircular canals emerge from the utricle.}

A. Utricle & saccule: (detect orientation of head with respect to gravity, and
maintain balance during linear movement)

 There is a small sensory area located on the inside surface of the utricle
and saccule. This sensory area, about 2 mm diameter, is called a
macula.
 Macula of the utricle lies in the horizontal plane. It plays the role
in equilibrium when the person is upright. It detects horizontal
linear acceleration (e.g., while sitting in a moving train).
 Macula of the saccule is vertical. It detects vertical linear acceleration
(e.g., while standing in a moving elevator). It also plays a role in
equilibrium when person is lying down.

[Fig: Maculae inside utricle and saccule, in a person with upright head. ]

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  Each macula is covered by a gelatinous layer. In this layer, there are many
small calcium carbonate crystals are imbedded. These are called otoconia
or statoconia.
 In the macula, there are thousands of hair cells. These hair cells
have hair/cilia which project up into the gelatinous layer.
 The bases and sides of the hair cells synapse with the vestibular
nerve ending (that is, vestibular division of the VIII cranial nerve).

[Fig: Constituents in a macula. It shows receptor cells – hair cells, otoconia, and VIII nerve
fibers.]

 The bases and sides of the hair cells synapse with the vestibular nerve
fibers (VIII nerve). And the stereocilia (the hair) project from the hair
cells into the gelatinous layer covering macula.

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  The gelatinous layer has otoconia/statoconia. The calcified statoconia have
a higher specific gravity compared to surrounding tissues. Therefore, the
weight of the statoconia bends the cilia in the direction of gravitational
pull.

[Fig: A hair cell in the labyrinth. Note: It shows neurotransmitter vesicles; glutamate is the
transmitter released by hair cells, on to vestibular nerve fibers.]

Directional sensitivity of the hair cells – THE KINOCILIUM:

 Each hair cell has 50 to 70 small cilia called stereocilia; and
one large cilium called kinocilium, located at one side.
 The stereocilia become progressively longer toward the
kinocilium end. The tip of each stereocilium is connected to
the tip of the next longer stereocilium by filamentous
attachment. Thus, when stereocilia bend, they all bend in one
direction.
 When stereocilia bend toward the kinocilium side, it results in
opening of channels that allow influx of positive charges into
the hair cell. The hair cell will be depolarized.
 When the stereocilia bend to the opposite side, away from
the kinocilium, it causes closure of channels. The hair cell will
be hyperpolarized.

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  Under normal conditions, the vestibular nerve fibers send
continuous signals to the vestibular nuclei. When the hair
cells are depolarized, this impulse traffic also increases. And,
when the hair cells are hyperpolarized, this impulse traffic is
diminished. Thus, appropriate signals are sent to the brain
regarding orientation of the head.

Mechanism that detects linear acceleration:

When the body is suddenly thrust forward, the statoconia fall behind as
they have greater specific gravity and greater inertia.

Head thrust forward:

[Fig: It shows bending of stereocilia due to head movement. Refer to text.]

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 - Let’s say, a person is seated in a train. The train suddenly starts, and
the person’s head is thrust forward.
- The vestibular apparatus will also move forward, and so will the
macula inside the utricle. Thus, hair cells will move instantly in that
direction.
However, statoconia, having greater weight, will have a certain inertia;
hence, they do not start moving instantly.
- This will cause bending of the stereocilia in the opposite direction.
- Bending of stereocilia opens K+ channels at the top of the hair cells.
- K+ influx results in depolarization of hair cells. As a result, the hair cells
will release neurotransmitter (glutamate) on to the vestibular nerve
fibers.
- The impulse traffic in the vestibular nerve fibers is altered. The signals
sent to the vestibular nuclei and from there to other parts of the brain,
then cause appropriate anti-gravity muscles to contract. This
maintains the body’s equilibrium and the desired posture.
- Macula of the utricle will be stimulated when there is horizontal
movement of the head; e.g. in a moving car. Macula of the saccule
will be stimulated when the person’s movement is vertical; e.g. as in
an elevator.

B. Semicircular canals: (detection of head rotation or angular acceleration)

 There are 3 semicircular canals in each ear: anterior vertical, posterior

vertical, and horizontal. They all are perpendicular to each other so
that, they represent all 3 planes in space. Hence, rotation of head in any
angle, in any direction, can be detected by the canals.

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[Fig: It shows interior of a semicircular canal. One end of the semicircular canal is dilated; it’s
called ampulla. The canal is filled with endolymph. Refer to text for more details.]

 Each semicircular canal has an enlargement at one end, called

ampulla. The canals and ampulla are filled with a fluid called
endolymph.
 Inside the ampulla, there is a small crest, called “crista ampullaris”.
On the top of this crista, there is a loose gelatinous tissue mass, called
the cupula.

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  Within the crista, there are hair cells. Stereocilia of the hair cells
are projected into the cupula. Bending of the cupula to one side
causes depolarization of the hair cells.

[Fig: It shows how hair cells are stimulated upon head rotation. Refer to text.]

 The diagram shows direction of the head rotation. As the head rotation
begins, the semicircular canal starts moving in the same direction.
However, endolymph inside the semicircular canal has inertia. Hence, it
does not start moving immediately. Thus, canal moves but endolymph
is stationary. This is “relative opposite movement” of endolymph.
 See the direction of the arrow inside the canal. The stationary endolymph
will cause bending of the cupula in the opposite direction. It results in
bending of the stereocilia, and depolarization of the hair cells. It increases
the impulse discharge in the vestibular nerve fibers. These impulses, via
the fibers, are sent to vestibular nuclei and other brain areas. These nuclei
and motor areas then will control the appropriate muscles to maintain
equilibrium of the body.
 This will happen in the beginning of the rotation. As the head/body
continues to rotate, now the endolymph also begins to move slowly in
the same direction. Endolymph catches up the speed of canal movement.

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 Now, bending of the cupula will stop. Hair cell discharge will return to
original level.
 When the head rotation stops suddenly, exactly opposite effects will take
place. The canal has stopped but because of inertia of endolymph,
endolymph will continue to move in the direction of the rotation. The
cupula will bend this time in the opposite direction. This will stop the
hair cell discharge for some time, as long as endolymph continues to
move even after head rotation has stopped. Again the signals for
equilibrium will be generated. Eventually endolymph movement will
stop, and the hair cell signals will return to normal.

Predictive function of the semicircular canal system in the maintenance of

equilibrium:
When a person is running forward rapidly and then suddenly
begins to turn to one side, he may fall off balance. However,
semicircular canal system can predict this possible loss of equilibrium
due to sudden turn. It “predicts” this sudden loss of equilibrium
ahead of the actual turn. And, it then causes the equilibrium centers
to make appropriate anticipatory preventive adjustments.

~ Neuronal connections of the vestibular apparatus with CNS:

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[Fig: Neural circuit connected to vestibular apparatus.]

- The primary pathway for the equilibrium reflexes begins in the

vestibular nerves. Head position is detected by the vestibular
apparatus, and the signals are sent via vestibular nerve fibers to the
vestibular nuclei in the brain stem. (Signals are also sent to the reticular
nuclei of brain stem.)
- From there, the descending fibers are sent to the spinal motor neurons
via the vestibulospinal and reticulospinal tracts. These tracts control
the antigravity muscles that regulate equilibrium and posture.
- From the vestibular nuclei, the fibers are also sent into the
cerebellum; to the vestibulocerebellum. Cerebellum sends the signals
back to the vestibular nuclei. This connection will help in the dynamic
equilibrium; that is, control and coordination between muscle groups
during a voluntary movement, to maintain equilibrium.
- Signals from the vestibular nuclei and cerebellum to the brain stem
are also passed via medial longitudinal fasciculus. These fibers are
concerned with corrective movements of the eyes every time the head
rotates, so that the eyes remain fixed on a specific visual target.

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Applied physiology:

 Nystagmus –
- They are the oscillatory jerky movements of the eyeballs.
- During the head rotation, if the eyes move along in the same
direction with head, the images will move across the retina
quickly; images will be blurred because eyes are not “fixed” on
each object long enough. To have a stable image on the retina
during head rotation, the eyes will have to be fixed on a visual
target/object. This happens automatically by the reflexes
arising from the semicircular canals.
- The vestibular nerves transmit the signals as the head rotation
begins. It causes the eyes to slowly rotate in a direction equal and
opposite to the rotation of head. When the eyes reach extreme
of the orbit, they quickly return to the center of the orbit, to have
new visual fixation. This fast movement is due to signals in the
medial longitudinal fasciculus to the oculomotor nerve nuclei. If
the head rotation continues, eyes again slowly rotate in the
opposite direction and then quickly return to the center. Thus,
eyes oscillate, in an attempt to stabilize the image.
- Vestibular nerve signals are due to bending of the cupula, as the
endolymph has not started to move but the canal is moving in
the direction of the head rotation.
- When the head rotation stops suddenly, now the endolymph
continues to move in the direction of head rotation for some
time even after rotation has stopped. This will again bend the
cupula, now in the opposite direction. Now, again the eyes will
oscillate. But, the slow movement will be in the direction of the
head rotation and fast movement will be opposite. This is called
post- rotatory nystagmus.

 Vertigo –
- Abnormal perception of spinning of head, or rotation of world
around head (when head and world both aren’t actually
rotating).
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 - Origin of this abnormal perception is vestibular apparatus.
- Due to some factors, endolymph pressure becomes abnormal.
This results in spontaneous bending of cupula, giving rise to
the sensation of spinning.

————————————————————————————————————

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 Section 5

HIGHER FUNCTIONS OF BRAIN

Learning objectives:

 Apart from receiving sensory inputs from periphery, and

performing motor activities based on such inputs, brain performs
certain functions that require complex neural mechanisms.
These higher functions, such as, speech, learning, memory,
emotional basis of behaviour are discussed in this section.
 Hypothalamus, having connections with limbic system, is also
involved in emotions. Hence, it is discussed in this section. An
important learning objective is to understand hypothalamic
mechanisms that regulate vegetative & visceral functions.

Hypothalamus:

Introduction:

Hypothalamus controls the vegetative/visceral functions of the body. It is

an integrating center where several neural and endocrine influences
originating throughout the brain converge. After due processing, the neural
and endocrine outputs of the hypothalamus diverge to all parts of the body.

Hypothalamus consists of a large number of nuclei and also fiber tracts.

 Connections and functions:

- The main afferent connections of the hypothalamus are with the limbic
system and the midbrain tegmentum.
- The main efferents from the hypothalamus are projected to the
limbic system, midbrain, thalamus, pituitary, and the medulla.

(1) Regulation of activity of the anterior pituitary gland –

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  The hypothalamus regulates the activity of the anterior pituitary; it
releases the “releasing factors” and “inhibiting factors” for the
hormones of the anterior pituitary gland. {For example: the
growth hormone (GH) of the anterior pituitary is controlled by
GH.RH and GH.IH secreted by the hypothalamus.}
(2) Regulation of the posterior pituitary hormone secretion –
 Hormones of the posterior pituitary gland (ADH & oxytocin)
are synthesized in the hypothalamic nuclei: the supra-optic
and paraventricular nuclei of the hypothalamus.
 Then, via the axons of those nerve cells (of nuclei), the hormones
are transported into the posterior pituitary. The hormones are then
released by the posterior pituitary into the circulation.
(3) Control of the circadian rhythm –
- The body has internal “biological clock”; it follows the 24-hour cycle.
This cycle is circadian rhythm.
- Variations in the body functions during daytime and nighttime are
called diurnal variations.
- For example: cortisol levels are highest at 6 A.M. (morning),
and lowest at 6 P.M. (evening).
 Hypothalamus is the link between external environmental
changes and the body’s internal biological rhythm.
 Visual impulses (about day and night) are transmitted from the
retina into the optic tract (II cranial nerve). The optic nerve gives out
collateral fibers that reach the hypothalamus. These fibers synapse in
the suprachiasmatic nucleus (SCN) of hypothalamus.
 From the SCN, the signals about light and darkness are forwarded to
the pineal gland. Pineal gland secretes the hormone melatonin.
This secretion increases in the darkness (or nighttime). Thus, it forms
a signal mechanism for body functions to be altered as the darkness
sets in.

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[Fig: Neural circuit for circadian rhythm. Retino-hypothalamic neurons relay in
suprachiasmatic nucleus (SCN) of hypothalamus. From SCN, signals are sent, via superior
cervical ganglion, to pineal gland.]

(4) Regulation of body temperature –

 In anterior hypothalamus, there are “warm-sensitive” neurons; in
posterior hypothalamus, there are “cold-sensitive” neurons.
 When blood temperature begins to fall (as a result of entering cold
environment), it is sensed by nerve cells in posterior hypothalamus.
These neurons induce shivering of the body, thereby raising the
body temperature.
 In hot environments, body temperature begins to rise. Temperature
of circulating blood, upon reaching hypothalamus, is sensed by nerve
cells in anterior hypothalamus. These neurons send signals to VMC
in medulla. The resulting cutaneous vasodilation and sweating will
decrease the body temperature.

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 [Regulation of body temperature by hypothalamus.]

(5) Regulation of body water and osmolality of body fluids -

Osmolality of the plasma (and body fluids) is linked to its water
content. Nerve cells in the hypothalamus can act as “osmoreceptors”;
they can sense the osmolality of plasma.
If the plasma water is decreased, the plasma will become hypertonic.
Hypothalamus then regulates it in two ways:
- When the plasma water is decreased, plasma becomes hypertonic.
Blood circulates, and reaches the brain.
- Hypothalamic neurons sense this increased osmolality of the plasma.
Now, (1) the thirst center in the hypothalamus gets activated; and
(2) neurons in the supraoptic nucleus of hypothalamus, projecting
onto posterior pituitary, release ADH hormone from the posterior
pituitary.

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 - Water will be consumed and will be absorbed from GIT into blood.
ADH will cause water reabsorption from kidney. Water content and
osmolality of the body fluids/plasma returns to normal.

[Fig: The flow chart shows regulation of body water and plasma osmolality.]
(6) Regulation of hunger and feeding –
 There are two hypothalamic centers concerned with hunger
and feeding:
a. Ventromedial nucleus of hypothalamus: It acts as satiety
center. When the neurons of this center fire, it limits the food
intake (it gives the feeling of “satiety” at the end of food intake).
The neurotransmitter C.A.R.T. (Cocaine- and amphetamine-
regulated transcript) plays the central role in satiety.
b. Lateral hypothalamic area: It acts as hunger center.

o The neurons in the “satiety center” are said to be

“glucostats” or “glucoreceptors”; they can sense the blood
glucose level.
o When the blood glucose level falls, satiety center lifts the
inhibition of the hunger center. The person will feel the
hunger. When food intake occurs, and glucose level in blood
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 rises, the satiety center becomes active, and it inhibits the
hunger center.

(7) Cardiovascular regulation –

The hypothalamus acts as the relay station; there are corticohypothalamic
descending pathways which discharge by emotions. Emotional effects on
the CVS are executed by these fibers.
(8) Control of the ANS –
The hypothalamus is called the “head ganglion of the autonomic nervous
system (ANS)”. Areas in hypothalamus are said to control sympathetic and
parasympathetic nerve responses.
(9) Control of emotional responses –
Stimulation of the periventricular nuclei in hypothalamus leads to fear and
punishment reactions.
(10) Sexual drive -

 Preoptic area in hypothalamus is known to control the sexual function.

 Anterior neurons are androgen-sensitive; posterior neurons are estrogen-
sensitive. They regulate sexual function in males and females,
respectively.

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Nucleus/Area in Connection/Neurotransmitter Function Effect of
hypothalamus lesion

Supra-optic Connected to osmoreceptors Synthesis of Diabetes

nucleus ADH insipidus

Paraventricular Neuroendocrine reflex Synthesis of Delayed

nucleus oxytocin labour

Suprachiasmatic Retina/visual pathway Circadian Jet lag-like

nucleus (SCN) rhythm symptoms

Anterior Warm-sensitive neurons; Temperature Hyperthermia

hypothalamus stimulation results in regulation
cutaneous vasodilation, (by heat
sweating loss)

Posterior Cold-sensitive neurons; Temperature Hypothermia

hypothalamus stimulation results in shivering regulation
(by heat
generation)

Preoptic area Contains Androgen-sensitive Sexual Loss of libido

and estrogen-sensitive function
neurons

Ventromedial Neurotramitter = C.A.R.T Satiety Hyperphagia

nucleus and obesity

Lateral Contains orexigenic neurons Hunger Loss of

hypothalamic appetite
area

Lateral superior Connected to osmoreceptors Thirst Adipsia

hypothalamic
area

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[Table:- Hypothalamic nuclei and their functions. NOTE: Lesions are taken to be ‘loss of
function’ type. Orexigenic = hunger-producing. (Anorexia = loss of appetite.)]

~ Effects of hypothalamic lesions: (refer to the table above)

- Lesion of the lateral hypothalamic area: It leads to decreased

drinking and eating. There may be lethal starvation. Also, the
animal becomes extremely passive.
- Lesion of the ventromedial nucleus of hypothalamus: It will produce
opposite effects. There will be excessive drinking and eating. And,
there will be hyperactivity.

The cerebral cortex

Physiologic anatomy:

 There are two cerebral hemispheres; they are connected with

each other by a bundle of nerve fibers called the corpus callosum.
 The most superficial part of each cerebral hemisphere is the
“cerebral cortex” (or cerebral grey matter). It is 2 to 4 mm thick. Its
total surface area is about 2200 cm2.
 Beneath the cerebral cortex lies the subcortical white matter in
which embedded are masses of the grey matter. These subcortical
masses of grey matter or masses of nuclei mainly include the
thalamus, hypothalamus, and the basal ganglia.
 The entire cerebral hemisphere is marked by ridges called gyri,
and the fissures called sulci.
 Because of the major sulci, the entire cerebral hemisphere is
divided into 4 lobes:
1. Frontal lobe – It lies in front of the central sulcus. Motor cortex
is located here. It is concerned with initiation and control of the
voluntary movements of the body.
2. Parietal lobe – It lies between the central sulcus and
parieto- occipital sulcus. Somatosensory cortex is located
here. It is

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 concerned with perception of general sensations (such as touch,
pressure, etc) from all over the body.
3. Temporal lobe – It lies below the lateral sulcus. Auditory cortex
is located here. Sound perception occurs here.
4. Occipital lobe - It lies behind the parieto-occipital sulcus.
Visual cortex is located here. Visual sense starting from the
eyes is perceived here.
~ The typical cortex has 6 layers, numbered I to VI from outside to inside.

 In the region called neocortex (or isocortex), all 6 layers are present. 90%
of the cerebral cortex has all 6 layers of cells. (Visual, auditory,
somatosensory, and motor cortices are constituents of neocortex.)
 10% of the cortex is “allocortex”. It includes parts of the limbic system.
(It does not have all 6 layers.)

In all the lobes, the cortex has two functional divisions: (a) primary cortex, and (b)
secondary cortex or association areas.

{Primary cortex in each lobe performs the primary function of that particular
cortex; secondary or association areas perform the “analytical” function. For
instance, primary sensory areas detect specific sensations – visual, auditory, or
somatic – transmitted from periphery. Secondary sensory areas analyze the
meanings of the specific sensory signals. Primary motor cortex has direct
connections with muscles so as to cause specific muscle contractions. Association
or supplementary motor areas provide “patterns” of motor activity.}

(1) Frontal lobe: (mainly the motor areas)

- Located in front of the central sulcus; it is mainly concerned with
the motor functions.
- It is subdivided into two main areas: (a) precentral cortex, and
(b) prefrontal cortex.
(a) Precentral cortex: (immediately in front of the central sulcus)
 Area 4: Primary motor cortex. It is the area for initiation
of the voluntary motor activity.

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  Area 6: Premotor areas. In front of the primary motor
cortex, thought/idea of the voluntary movement
begins here. It provides the “pattern” for the motor
activity.
 Area 8: frontal eye field. Situated in front of the area 6.
It controls the conjugate movements of the eyeballs to
the opposite side.
 Area 44: Broca’s area for speech. Situated in the
dominant hemisphere; it is the motor area for speech.
(b) Prefrontal cortex/prefrontal lobe: (remainder of the frontal
lobe, situated most anteriorly, in front of areas 4,6, & 8)
 It is also called orbito-frontal cortex.
 It has to and fro connections with the thalamus,
hypothalamus, and many other regions of the
cerebral cortex.
 Area 24: of the cingulate gyrus; is connected with
hippocampus. It forms a part of “Papez circuit”; involved in
genesis of emotions
 Areas 9, 10, 11, & 12: “Seat of intelligence”.
 Functions of the prefrontal cortex:
 Control of some of the higher intellectual activities
 Control of personality
 Control of behavior and social consciousness
(2) Parietal lobe: (somatosensory cortex)
- Areas 3, 1, & 2: primary sensory area [S1]. Situated just behind
the central sulcus (in the post central gyrus).
 It is concerned with appreciation of general sensations such
as touch, pain, temperature, etc.
 Body representation is upside down. That is, sensations
from the face reach the lower aspect.
- Areas 5 & 7: sensory association areas [S2].
 It analyzes the sensations perceived by primary sensory areas.

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  Recognition of the objects placed in the hand, without
looking at them – “stereognosis”. This is by analyzing the
touch, pressure, texture of the object.
 Tactile localization, two-point discrimination, and recognition
of spatial relationship are the functions assigned to this
cortex.
- Posterior parietal cortex: This area provides continuous analysis of
the spatial coordinates of all parts of the body as well as of the
surroundings of the body.
(3) Temporal lobe: (auditory cortex)
- Areas 41 & 42: in the Heschl’s gyrus. Auditosensory area I & II.
These areas are concerned with perception of sound.
- Areas 20, 21, & 22: auditopsychic areas. They are
auditory association areas.
- Area planum temporale: large in musicians; recognition of pitch
of the sound
- Wernicke’s area: area for language comprehension; behind
the primary auditory cortex.
 It is the area where somatic, visual, and auditory
association areas meet.
 It is also called general interpretive area.
(4) Occipital lobe: (visual cortex)
- Area 17: the primary visual cortex; areas 18 & 19: secondary or
visual association areas.
- Primary visual cortex perceives an image; visual association areas
(visuopsychic areas) interpret the exact meaning of a visual
image.
- Area for recognition of faces; area for naming objects. These
areas are located in the occipital lobe.

 Angular gyrus:
 Lies in the posterior parietal lobe; it fuses with the visual areas in
the occipital lobe.

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 It is concerned with interpretation of visual information.

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  Lesion of this area results in “dyslexia” or word blindness – The
person may be able to see words and even know that they are,
but not be able to interpret their meanings.

Applied Physiology:
 Parietal ‘hemineglect’ syndrome:
- Spatial orientation of body parts with each other and with the
surroundings is located in posterior parietal cortex (PPC) of
non- dominant hemisphere.
- Lesion of parietal lobe, in non-dominant hemisphere, results in
hemineglect. The person neglects the opposite half of the body and
the immediate surrounding.

The limbic system:

{Limbus means a ring; the term limbic system is applied to the parts of the cortical
and subcortical structures that form a ring around the brain stem.}

- The limbic system consists of the limbic lobe or limbic cortex and
the related subcortical nuclei.
- The limbic cortex includes cingulated gyrus, isthmus,
hippocampal gyrus, and uncus.
- The related subcortical nuclei include: (i) amygdala (the group
of nuclei on the tip of the temporal lobe), (ii) septal nuclei, (iii)
hypothalamus, and (iv) anterior thalamic nuclei.

 This area was formerly called as ‘rhinencephalon’ (rhino = related to nose)

because of its relation to olfaction (smell); however, only a small part of it
is actually concerned with smell.
 The limbic cortex is phylogenetically the oldest part of the cerebral
cortex. Histologically, it is made up of a primitive type of cortical tissue,
called “allocortex”.
 Functions:

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[Fig: Limbic system structures and relations.]

1. The limbic system represents the primary area for the control
of autonomic functions (heart rate, BP, G.I. movements, etc).

2. Amygdala: The emotional window through which a person sees

external world. It is known to regulate the emotional behavior of an
individual. The emotions of rage and fear are elicited on stimulation
of the limbic system.
3. It plays an important role in the motivational drive of the individual.
4. It is also concerned with olfaction.
5. Hippocampus: The seat of long-term memory. Hippocampus
converts working memory into a long-term memory.

 Papez circuit: (named after neuroanatomist James Papez)

- It gives the emotional basis of human behavior.

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 [Fig: Papez circuit. MMT = Mammillo-thalamic tract.]

Role of the hypothalamus:

- The non-hypothalamic parts of the limbic system receive

information from cortical association areas, particularly those in the
frontal lobe. This information is sent directly to the hypothalamus.
The emotional meaning of the external stimuli, information gathered
from memory and understanding, is passed on to the hypothalamus.
- The hypothalamus then integrates the endocrine, autonomic,
and some other motor activities that form appropriate emotional
behavior.

Higher functions of the cerebrum

 The concept of the dominant hemisphere:

- There are two cerebral hemispheres: the left and the right.

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 In general, higher functions of the nervous system are developed on one
side of the brain or one cerebral hemisphere than the other.

(I) Dominant hemisphere or categorical hemisphere:

 Higher functions, such as language (speech), are developed in one
hemisphere. This hemisphere is called the dominant or
categorical hemisphere.
(II) Non-dominant hemisphere or representational hemisphere:
 This hemisphere is specialized in “spatio-temporal coordinates”; that
is, orientation/relation of body parts with each other, and
orientation of the body with respect to the surrounding.

~ About 90% or more of the human population is right-handed. For them, the
left cerebral hemisphere is the dominant hemisphere.

The individuals who are left-handed: in about 30% left handed individuals –
right hemisphere is dominant; in the remaining 70% - left hemisphere is
dominant.

Speech: (The language function)

Definition:

Speech is the production of articulate sounds which bear a definite

meaning.

The speech requires formation of the proper words and expression of those
words verbally.

Speech has two components –

1. Proper word formation in the brain. The centers in the brain that cause
this are collectively called “central speech apparatus”.
2. Production of the words verbally. This would require respiratory system,
vocal cords, and organs of the oral cavity. This is called “peripheral
speech apparatus”.

(I) Central speech apparatus: (Brain mechanism for speech)

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  For the proper speech to be executed, following
neural mechanisms/centers will be necessary:

a. We must be able to hear sounds. This requires an intact auditory

pathway, from the ears to the auditory cortex (area 41).
b. We must be able to understand the sounds/spoken words. This
requires the audio-psychic area (or auditory association area; areas 20,
21).
c. We must be able to express the thoughts in spoken words. This
process involves the activity of the Wernicke’s area.

[Fig: Central speech apparatus. Wernicke’s area (W) receives inputs from somatosensory,
auditory, and visual cortices. Based on inputs, it decides what is to be spoken. It sends
impulses, via arcuate fasciculus, to Broca’s area (B). Broca’s area then sends signals to
muscles of speech and thus executes the speech.]
 Wernicke’s area is located in the superior temporal gyrus; in the
dominant (categorical) hemisphere. It is concerned with interpretation
and understanding of auditory and visual informations. It is called the
“sensory area of speech”.
Wernicke’s area integrates the auditory, visual, and other sensory
information necessary to form the speech.
It then sends the information to another area, the “Broca’s area”.
 Broca’s area: It is located in the inferior frontal gyrus, in the
dominant (categorical) hemisphere. It processes the information
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received from

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 Wernick’e area, to form a detailed and coordinated pattern for
vocalization (speech). This pattern is then projected to the motor cortex
which initiates the appropriate movements of the lips, tongue, and larynx
to produce.
Thus, Broca’s area is the “motor area of speech”.

(II) Peripheral speech apparatus:

The signals initiated by the Broca’s area are sent to the peripheral speech
apparatus for execution (that is, production of spoken words).

It involves two processes: (a) phonation – means production of sound, and (b)
articulation – means conversion of that sound into the specific words.

Phonation: As the expired air is coming out of lungs, it causes vibrations of the
vocal cords. This will produce a sound.

Articulation: The organs of the mouth (lips, tongue, palate) articulate in a specific
manner while the sound is coming out; so that the sound is converted into a
specific word.

Applied physiology:

 Aphasia:
Defect of speech that results from lesions of the central speech apparatus
(speech centers of the brain).
Types of aphasias –
a. Wernicke’s aphasia:
Spoken or written word can be understood, but inability to interpret
the thought that is expressed. It results from a lesion of the Wernicke’s
area (superior temporal gyrus).
b. Motor aphasia:
The person may be capable of deciding what he or she wants to say
but cannot make the vocal system emit the decided words.

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 Neurophysiology of learning & memory:

Definition:

“Learning” is acquisition of new information.

“Memory” is the retention and storage of that information.

 Learning:

 Learning is due to “synaptic plasiticty”. That is, there are changes in

the synaptic function; the modification of the synaptic transmission is
the basis for learning.
 Learning is mainly of two types – (1) non-associative learning: in this
form of learning, the animal learns about a single stimulus, and (2)
associative learning: in this form of learning, the animal learns
about the relation of one stimulus to another.

(1) Non-associative learning:

In this form of learning, the animal learns about a single stimulus.
Examples of this type of learning are habituation & sensitization.
a. Habituation:
 It is a simple form of learning in which a neural stimulus is
repeated many times. Initially, it evokes a reaction. However,
as the stimulus is repeated, it evokes less and less response.
 Eventually, the subject becomes habituated to the stimulus,
and learns to ignore it. E.g. ticking of a clock may not allow
a person to fall asleep initially. But, later on, the person’s
nervous system learns to ignore it so that he/she can sleep.
 Mechanism: With repeated stimulation, there will be
decreased release of neurotransmitter from the presynaptic
terminal.
b. Sensitization: (opposite of habituation)

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  A repeated stimulus produces a greater response if it is
coupled with an unpleasant or a pleasant stimulus.
 E.g. the mother who sleeps through many kinds of noise
but wakes promptly when her baby cries.
 Mechanism: augmented postsynaptic responses.
(2) Associative learning:
This type of learning is based on observing repeatedly the association
between two events. For example, observing repeatedly that dark
clouds are followed by rain makes us learn that dark clouds lead to rain
(a ‘cause-effect’ relationship). As a result, the next time we observe dark
clouds while leaving home, we carry an umbrella (change in behavior).
This type of learning occurs by the “conditioning” of the animal to paired stimuli.

a. Classical conditioning: (a reflex or passive process)

- This type of learning was studied by Pavlov in dogs. {It is also
called Pavlov’s conditioned reflex.}
- If a dog is presented with food, there is reflex salivation in the dog.
This is innate reflex, and food is the “unconditioned stimulus”
(US).
- Ringing of a bell does not produce salivary secretion normally. In the
experiment, a bell is rung and then immediately food is presented to
the dog. This is done repeatedly. The dog ‘learns’ to expect food
after the ringing of bell. Then, only ringing of bell will cause reflex
salivation in the dog. Sound of the bell is called the “conditioned
stimulus” (CS). The reflex response to the CS is called “conditioned
reflex”.
- Thus, pairing of two stimuli (CS & US) will cause the animal to
learn. CS should be immediately followed by the US. If the CS is
presented repeatedly without the US, the conditioned reflex
eventually dies out. This is called “extinction” or “internal
inhibition”. If there is external stimulus causing disturbance,
between CS and US, the conditioned response may not occur. This
is called “external inhibition”.
b. Operant conditioning: (animal operates “actively” on the environment)

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 - It is a form of conditioning in which the animal is taught to
perform some task (“operate on the environment”), in order to
obtain a reward or avoid punishment.
- The US is the pleasant or unpleasant event. For example, an animal
is taught that by pressing a bar it can prevent an electric shock to the
feet.
- This type of learning is an “active” form. (compare with
classical conditioning which is a reflex or passive process)

 Memory:
- Memory is retention and storage of the learned information.
- It is the ability to recall past events at the conscious or
unconscious level.
It is also due to the synaptic plasiticity or modulation of the synaptic
transmission.

(I) Declarative or explicit memory –

It involves conscious recall of

events.

(II) Non-declarative or implicit memory – (reflexive memory)

It includes classical conditioning, skills, habits; it is generally unconscious.

Types of declarative memory:

Depending on how long a conscious memory lasts, it is divided into

following types – (1) short-term memory, (2) intermediate-term memory, and
(3) long-term memory.

(1) Short-term or recent memory:

- It involves mechanisms that can cause immediate recall of
events that occurred some time ago (seconds/minutes/hours).
- E.g. remembering and recalling a phone number for some time
by repeatedly going through the digits.

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 - Mechanism: POST TETANIC POTENTIATION
If a particular synapse in the brain is stimulated tetanically (repeated
quick successive stimuli for short duration), the transmission at that
synapse is enhanced for some time thereafter. This is “post tetanic
potentiation”.
Repeated quick successive stimuli will cause Ca++ to accumulate in
the presynaptic neuron. Neurotransmitter release by this neuron will
be greater as long as the Ca++ content in it is high. Hence, the
response at this synapse is also potentiated.

- Another probable mechanism is presynaptic facilitation.

(2) Intermediate-term memory:

- It may last for several minutes or even upto weeks.
- Eventually it will be lost unless converted into long-term memory.
- Mechanism: (cAMP mediated activation of protein kinase in
the neurons)
 There is facilitation at the synapses of brain. The
postulated neurotransmitter at these synapses is
serotonin.
 Serotonin acts on its receptors on the presynaptic terminal.
This leads to activation of adenylyl cyclase enzyme, and
formation of cAMP in the neuron. cAMP activates protein
kinase enzyme. This leads to prolonged facilitation of
synaptic transmission.
(3) Long-term memory:
In this type, the events and information can be recalled even after years.
- Long-term memory is believed to result from actual structural
changes at the synapses. Structural and functional changes lead
to facilitation of synaptic transmission on a long-term basis.
- Structural changes:
 Increase in the number of presynaptic terminals
 Changes in the dendritic geometry
 Increase in the number of transmitter vesicles

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 - There is evidence which suggests that activation of genes and
new protein synthesis is involved in the processes responsible for
memory.
- Molecular or biochemical basis of long-term memory: (long-term
potentiation)
 The synaptic facilitation that occurs on a long-term basis is
postulated to be due to the phenomenon called “long-
term potentiation” (LTP) at the synapses.
 Role of hippocampus in long-term memory:
LTP is known to occur at the synapses in the hippocampus.
The neurons projecting from other parts of the brain to
the hippocampus release glutamate as the transmitter.
Glutamate acts on its receptors, the NMDA receptors. This
leads to increased entry of Ca++ in the post- synaptic neurons.
There is long-term potentiation of the hippocampal neurons.

[Fig: Long-term memory circuit. A working memory of event is first formed in cortex. Cortical
projection on hippocampus then converts it into long term memory. CA 1 region of
hippocampus is of particular importance in this. Eventually, this memory will be consolidated
in neocortex.]
Consolidation and storage of memory:
Hippocampus converts working memory into long-term memory.
This memory will then be consolidated in neocortex.

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Applied physiology: (AMNESIA)

- Loss of memory is called amnesia.

- Bilateral lesion of hippocampus leads to anterograde amnesia. That
is, person is not able to establish new long-term memories after
hippocampal lesion because hippocampus is the storage site for
memory.
- Retrograde amnesia: Inability to recall memories from the past.

Electroencephalogram (EEG) and sleep

 Electroencephalogram (EEG):
- The background electrical activity of the brain can be recorded
from the scalp. Record of these brain potentials is called
electroencephalogram (EEG).

- These potentials are recorded by placing electrodes on the scalp.

- These potentials are NOT ACTION POTENTIALS of the neurons; they
are post-synaptic potentials (EPSPs & IPSPs) of the synapses in the
brain.
- German psychiatrist Hans Berger introduced the term EEG; hence
the waves of the EEG are also called “Berger rhythm”.
- EEG record may be useful in the diagnosis of functional
brain diseases, e.g., epilepsy.
 Waves of EEG –
(1) Alpha waves: (waves of quiet wakefulness)
 When an adult human is awake but mind is at rest eyes
closed and mind is wandering, his EEG record will mainly
show these () waves.
 Frequency of these waves: 8 – 12 Hz.
 These waves are recorded mainly from the parieto-occipital
area.
(2) Beta waves: (waves of alert wakefulness)

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  When the person is awake and mentally alert, with
eyes open, his EEG record will mainly show these ()
waves.
 Frequency: 15 – 30 Hz; low amplitude
 These waves are generally recorded over the parieto-
frontal region of the brain.
 Paradoxically, these waves are also seen in REM type
of sleep.
(3) Theta waves: (large amplitude, slower frequency)
 These waves are generally recorded in children;
recorded from temporo-parietal region
 Frequency: 4 – 7 Hz; large amplitude
 They are also known to be generated in the hippocampus.
 These waves are seen in the EEG when the person
falls asleep; in stage 2 & 3 of the sleep.
(4) Delta waves: (large amplitude, slowest frequency)
 These waves have the slowest frequency: less than 4 Hz.
 They are recorded in very deep sleep, deep coma,
deeper planes of anesthesia, and in organic brain
disease.
 These waves do not require activity of the lower
brain regions.
~ Gamma oscillations:

- Very high frequency: 30 – 80 Hz

- These rapid oscillations in EEG are seen when the individual
is aroused and focuses attention on something.
 Changes in EEG pattern at different states of wakefulness and sleep: (note
that: when the person is awake, the waves are high frequency and low
amplitude. As the person falls asleep, and goes into deeper sleep,
progressively the waves become low frequency and high amplitude.)

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 Sleep

Definition:

It is the unconsciousness from which the person can be aroused by sensory

or other stimuli.

(Compare with coma; the unconsciousness from which the person cannot be
aroused.)

 Two types of sleep:

During each night, a person goes through stages of two types of sleep: (1)
slow-wave sleep (the brain waves are very large but very slow), and (2)
rapid eye movement sleep (“REM sleep”) (there are rapid eye
movements during this type of sleep)
o When a person falls asleep, about 90 minutes of slow-wave sleep
(non-REM sleep) and then a bout of REM sleep for 5 to 30
minutes. This pattern will occur throughout the sleep duration.

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Normal sleep architecture:

 When a person goes to sleep, there are 90 minutes of n-REM sleep. It goes
through successive stages, i.e., sleep becomes deeper & deeper. Then, it
goes through reversed sequence of stages (becomes superficial). At the
end of these 90 minutes, the sleep enters its 1st episode of REM sleep (5-30
minutes).
 At the end of 1st REM episode, the nREM sleep starts again.
 This pattern will occur throughout sleep duration. There will be 4-5
episodes of REM sleep in a night’s sleep duration.

(1) Slow-wave sleep: (or nREM sleep)

- As the person falls asleep, it begins with the nREM sleep. And,
except for the bouts of REM sleep intermittently, the major
proportion of the sleep is slow-wave sleep.
- The person goes through 4 stages of slow-wave sleep, which
becomes deeper and deeper with these stages.
 Stage 1: low voltage waves in the EEG
 Stage 2: sleep spindles and large “K-complexes” are seen in
the EEG

 Stage 3: theta waves

 Stage 4: delta waves (slowest waves, deepest sleep)

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 - Sleepwalking (“somnambulism”), bed-wetting, and nightmares occur
during slow-wave sleep.
- Although dreams may occur during slow-wave sleep, there is no
consolidation of those dreams in the memory. Hence, those
dreams are not likely to be remembered when the person wakes
up.
(2) REM sleep: (or paradoxical sleep)
- In a night, bouts of REM sleep (5 to 30 minutes each) occur every
90 minutes. There may be 5 to 6 episodes of REM sleep every night.
- In young adults, it may occupy 25% of the total sleep duration.
- There are ‘Rapid Eye Movements’ during this type of sleep, hence
it is called REM sleep.
- During the episode of REM sleep, the brain is highly active. EEG
record of this sleep shows predominance of beta () waves which
are the waves of alert wakefulness. Hence, it is called “paradoxical
sleep”.
- This type of sleep is associated with active dreaming. There may
also be consolidation of dreams into the memory, so that the person
can remember the dreams (which occurred during REM sleep).
Along with this, there may be tooth-grinding (“bruxism”) in some
individuals.
- The muscle tone is throughout the body is depressed.
- Heart rate and respiratory rate become irregular.
 Probable cause: (genesis of REM sleep)
There are cholinergic neurons in the reticular formation of the pons.
Discharge of these neurons is thought to initiate the REM sleep.

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Applied physiology:

- Insomnia:
It generally means inability to fall asleep normally. (Sleep latency will
be more; there may be intermittent awakening during sleep, and
total duration of sleep reduced.)

- Somnolence:
Excessive sleepiness; it may be due to hormonal disorders (e.g.,
hypothyroidism – there is decreased synaptic excitability)

Cerebrospinal fluid [CSF]

Introduction:

It is the fluid circulating around the brain and the spinal cord. It is found the
ventricles of the brain, in the cisterns around the outside of the brain, and in the
subarachnoid space around the brain and the spinal cord.

Composition of the CSF:

 It is a clear, colorless alkaline fluid; specific gravity: 1005 – 1008

 Volume: about 150 ml
 Daily secretion: about 500 ml
 It is almost cell-free and protein-free
 It contains less glucose than plasma; (glucose: about 50 mg% in CSF)
~ Formation, flow, and absorption of CSF:

- About 2/3rd of CSF is formed as a secretion from the choroid plexuses

in the ventricles, mainly the two lateral ventricles.
- Additional amounts are secreted by the ependymal surfaces of
the ventricles. Some amount is also secreted by blood vessels of
the brain and the spinal cord.

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 - After its formation, it passes from the lateral ventricle into the 3 rd
ventricle. Some fluid gets added here. Then, along the aqueduct of
Sylvius it comes into the 4th ventricle. from here, it passes out via
foramina of Luschka and foramen of Magendie, and via cisterna
magna it comes into the subarachnoid space. CSF then circulates
in the subarachnoid space around the brain and the spinal cord.
- It is mainly absorbed by the subarachnoid villi into the venous
(dural) sinuses.
~ CSF pressure:

About 130 mm of water; in lateral lying position

130 mm of water = 13 cm of water

13 cm of water = 10 mm of Hg {1 mm Hg = 1.3 cm of water}

In seated posture:- CSF pressure is (130 + 130 =) 260 mm of water.

 Functions of CSF:
1. CSF serves as a fluid buffer that provides optimum environment to
neurons of the CNS.
2. Protective function: CSF provides the cushioning effect to the delicate
structures of the cranial vault.
3. Regulates contents of the cranium: CSF acts as a reservoir and
regulates contents of the cranium. For example, if the blood volume of
brain increases, then CSF drains away the excess amount of fluid.
4. It helps in transfer of metabolic waste products of brain into the blood.
5. It may serve as a medium for nutrient supply to the CNS.
Applied physiology:

- Lumbar puncture:

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 It is the procedure by which CSF can be accessed through the lumbar
segments of the spinal cord. A needle is inserted between the two
lumbar vertebrae (L2-3), to reach the subarachnoid space.
For diagnosis:
CSF is collected by lumbar puncture; it is then analyzed for infections
of the CNS, or malignancies.
For therapeutic purpose:
Drugs can be instilled into the CSF, for the purpose of anesthesia or
antibiotics against CNS infections

Blood-brain barrier (BBB)

- Many substances from blood cannot enter the brain easily due to the
presence of blood-brain barrier (BBB). Similarly, there is also blood-
CSF barrier.
- This barrier is primarily formed due to the tight junctions
between adjacent endothelial cells that line the cerebral
capillaries.
- The barrier is further reinforced by a glial cell – Astrocyte.
- Water and Lipid soluble substances (CO2, O2, alcohol, anesthetic
agents, etc) can cross the BBB easily.
- Ionic forms (such as H+) and water-soluble substances (such as
plasma proteins) cross the BBB poorly or slowly (or do not cross
at all).
- BBB acts as a protective barrier that prevents entry
harmful substances into brain or CSF.
- Blood-brain barrier is deficient in some areas of brain collectively
called as circumventricular organs (CVOs). These CVOs comprise of:
 Area postrema (chemoreceptor trigger zone – CTZ)
 Organum vasculosum
 Pineal gland

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  Some areas of hypothalamus (median eminence)

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