Place of the brainstem in the somatomotor coordination
• Posture regulation
• Integration and
comparison of various
sensory inputs
– -visual
– -vestibular
– -somatosensory
Regulation of posture and muscle tone
Studying the role of the brain stem in the motor coordination: transection experiments
Sir Charles Scott
Lower decerebration (cut caudally from the red nucleus); Sherrington
1857-1952
decerebration rigidity = increased tone of the extensor
muscles, inhibitory areas are excluded, the animal is
not able for locomotion
Higher decerebration (cut frontally from the midbrain);
decerebration rigidity develops but ceases in a few days
Decortication in animals does not cause decerebration
rigidity, the subcortical areas facilitate the functions of
the mid-brain centers responsible for the regulation of
the posture
The role of cerebellum in
movement regulation
The cerebellum
• Major functions:
• Maintaining balance
• Coordination of movements – especially
that of rapid movements (corrections)
• Motor learning
• Cognitive function
Electrical stimulation of the cerebellum does not evoke conscious sensation,
and it is not followed by noteworthy movement(s)
• Although it receives sensory inputs from many sources, these
do not reach conscious level
• Although it has significant roles in the actual execution of the movements, it does
not participate DIRECTLY in their completion
Cerebellar modules
+
Cerebellar cortex
+ Interneurons Purkinje- +
cell
-
+ deep
+
nuclei
Mossy fiber OUTPUT Climbing fiber
(brainstem nuclei, spinocerebellar tracts) (oliva inferior)
(sensory information from the periphery and cortex) (somatosensory, visual and
cortical information)
Cerebellar modules
Functional parts of the cerebellum
• Vestibulocerebellum (the flocculo-nodular lobe)
– Archicerebellum
– Coordination of the trunk muscles
• Maintaining balance, reflex movements of the head
– Coordination of the extraocular muscles (eye movements)
• Spinocerebellum (vermis and the related cortical areas)
– Paleocerebellum
– Tracking and correction of movements using the proprioceptive inputs
• Trunk and limb movements – walking (gait)
• “inner feed-back loop” – motor pathway collaterals (desired result) – ventral spinocerebellar tract
• “outer feed-back loop” – proprioceptors, sensory information (actual result) – dorsal and ventral
spinocerebellar tract
• Cerebrocerebellum (cerebellar hemispheres)
– Neocerebellum
– Planning and tracking of skilled movements, and cognitive function
• Highly skilled, learned, voluntary movements
Lesions of the vestibulo- and spinocerebellum
– Trunk- and walking ataxia (towards the injured side)
– Nystagmus (more pronounced when looking towards the injury
side)
Consequences of lesions affecting the
cerebrocerebellum
– Ataxia
– Dysmetria
– Intention tremor
– Dysarthria (scanning speech)
– Dysdiadochokinesis
– Adiadochokinesis
– Alteration of muscle tone
– Dyssynergia (decomposition of
movements)
– Rebound phenomenon
Consequences of lesions affecting the
cerebrocerebellum
– Ataxia
– Dysmetria
– Intention tremor
– Dysarthria (scanning speech)
– Dysdiadochokinesis
– Adiadochokinesis
– Alteration of muscle tone
– Dyssynergia (decomposition of
movements)
– Rebound phenomenon
Consequences of lesions affecting the
cerebrocerebellum
– Ataxia
– Dysmetria
– Intention tremor
– Dysarthria (scanning speech)
– Dysdiadochokinesis
– Adiadochokinesis
– Alteration of muscle tone
– Dyssynergia (decomposition of
movements)
– Rebound phenomenon
Consequences of lesions affecting the
cerebrocerebellum
– Ataxia
– Dysmetria
– Intention tremor
– Dysarthria (scanning speech)
– Dysdiadochokinesis
– Adiadochokinesis
– Alteration of muscle tone
– Dyssynergia (decomposition of
movements)
– Rebound phenomenon
Consequences of lesions affecting the
cerebrocerebellum
– Ataxia
– Dysmetria
– Intention tremor
– Dysarthria (scanning speech)
– Dysdiadochokinesis
– Adiadochokinesis
– Alteration of muscle tone
– Dyssynergia (decomposition of
movements)
– Rebound phenomenon
Consequences of lesions affecting the
cerebrocerebellum
– Ataxia
– Dysmetria
– Intention tremor
– Dysarthria (scanning speech)
– Dysdiadochokinesis
– Adiadochokinesis
– Alteration of muscle tone
– Dyssynergia (decomposition of
movements)
– Rebound phenomenon
Consequences of lesions affecting the
cerebrocerebellum
– Ataxia
– Dysmetria
– Intention tremor
– Dysarthria (scanning speech)
– Dysdiadochokinesis
– Adiadochokinesis
– Alteration of muscle tone
– Dyssynergia (decomposition of
movements)
– Rebound phenomenon
Consequences of lesions affecting the
cerebrocerebellum
– Ataxia
– Dysmetria
– Intention tremor
– Dysarthria (scanning speech)
– Dysdiadochokinesis
– Adiadochokinesis
– Alteration of muscle tone
– Dyssynergia (decomposition of
movements)
– Rebound phenomenon
The role of the basal ganglia and the cortex in the motor
regulation
Basal ganglia
http://www.neuroanatomy.wisc.edu/coursebook/motor2.pdf
The essential facts
• Basal ganglia receive little information from the
spinal cord
• The most important input device: neostriatum
(putamen and caudate nucleus)
• The source of the incoming information: cortex,
hypothalamus, subthalamic nucleus, substantia nigra
• Output element: globus pallidus (int):
• Target: motor thalamus – motor cortex
Basic functions of the basal ganglia
• Genesis of basic movement patterns
– To select motor programs in response to the
information arriving from the association cortex
• Regulation of muscle tone and movements
• Initiation of movements based on emotional
changes
• Cognitive and affective functions
Symptoms of basal ganglia disorders
• Positive (or hyperkinetic) symptoms
– TREMOR
– RIGIDITY
– CHOREA
– ATHETOSIS
– BALLISMUS
• Negative (or hypokinetic) symptoms
– HYPO- or AKINESIA
James Parkinson Parkinson’s disease
1755 – 1828
(a.k.a. paralysis agitans)
• Parkinson’s trias:
– Akinesia
– Rigidity
– Tremor (resting)
• Reason:
– Damage of the dopaminergic
nigrostriatal pathways
(1817)
• Histology:
– Lewy Bodies – degenerating nigral
dopaminergic cells accumulate
deposits of protein
• Therapy:
– Administration of L-DOPA
– transplants of dopaminergic cells into the striatum of patients
(EXPERIMENTAL)
– Deep brain stimulation
Parkinson’s disease
(a.k.a. paralysis agitans)
• Parkinson’s trias:
– Akinesia
– Rigidity
– Tremor (resting)
• Reason:
– Damage of the dopaminergic
nigrostriatal pathways
• Histology:
– Lewy Bodies – degenerating nigral
dopaminergic cells accumulate
deposits of protein
• Therapy:
– Administration of L-DOPA
– transplants of dopaminergic cells into the striatum of patients
(EXPERIMENTAL)
– Deep brain stimulation
George Huntington
1850-1916
Huntington’s chorea
Involuntary choreiform movements which show up as
rapid, involuntary and purposeless jerks of irregular
and variable location on the body. They are
spontaneous and cannot be inhibited, controlled, or
directed by the patient.
• Incidence: 5-10/100 000
• Autosomal dominant
• Short arm of the 4th chromosome
(1872)
Non-motor symptoms
• Depression, Anxiety, Irritability, Apathy,
Psychotic state
There is no way to prevent the onset of the disease,
to alleviate the symptoms or to delay the onset.
Cortical areas involved in the motor function
• Primary motor cortex
• Precentral gyrus
• Brodmann’s 4
• Praemotor area
• „Non-primary” motor cortex
• Brodmann’s 6
• „True” praemotor area
• Supplementary motor area
Significance of the cortical motor areas
• Primary motor cortex
– Actual performance of the motoric tasks
• Premotor cortex
– The activity of this region always preceds that recorded
from the primary motor cortex
– Involved in the „preparation” phase of the voluntary
movements
– Isolated lesion: apraxia (inability to perform complex
motor tasks)
The corticospinal (pyramidal) tract
• Voluntary fine movements
• Targets
– Grey matter of the spinal cord
on the contralateral side
α-motoneurons
– Direct – monosynaptic
– Indirect – polysynaptic
γ-motoneurons
– polysynaptic
The “extrapyramidal system”
Partially or fully automatic movements
Reticular formation lateral and medial reticulospinal tract
Vestibular nuclei vestibulospinal tract
Red nucleus rubrospinal tract
Tectum tectospinal tract
