Spinal Cord Lesions

Jia Yan-jie M.D Ph.D

贾 延劼
Department of Neurology, the First
Affiliated Hospital, Zhengzhou University
 Introduction

CNS
Brain
Spinal Cord
 Introduction

Brain Spinal Cord

Vascular Trauma or mechanical
Degenerative Tumor
Inflammatory Inflammatory
Trauma Infectious
Infectious Vascular
 Introduction

Major cause of disability in spinal

cord due to effects on motor,
sensory and autonomic pathways.
Most common causes are
compression due to trauma and
metastatic cancer.
 Introduction
Causes
Anatomy and Physiology
 Spinal cord
Dorsal root
ganglion
Meninges
(protective
Spinal coverings)
nerve

Vertebra

Intervertebral
disk
Sympathetic
ganglion
chain
Cervical Cervical
cord nerves Vertebra

Thoracic
Thoracic
cord
nerves

Lumbar
Lumbar
nerves
cord
Cauda
equina
Sacral
Sacral nerves
cord
Coccygeal
nerve
Anatomy and Physiology

C1—C4

C5-T4 +1

T5—T8 +2

T9—12 +3

L1—5 T10 、 11 、 1
2
 L2

L5

S2

Medullary anaesthesia Spinal puncture

A region of the body surface innervated by sensory fibers
from the dorsal roots of a single spinal cord segment is
a dermatome.
Anatomy and Physiology
Anatomy and Physiology
Anatomy and Physiology
Anatomy and Physiology
Anatomy and Physiology

Corticospinal tract, anterior

Corticospinal tract, lateral

Anatomy and Physiology

Motoneuron in spinal cord

 Anatomy and Physiology

Somatosensory modalities = bodily sensations of touch, pain,

temperature, vibration, and proprioception
The somatosensory pathways are 2 long sensory tracts
1. Posterior column – medial lemniscus system
Proprioception, vibration, fine discriminative touch
2. Anterolateral system (including the spinothalamic tract)

Pain, temperature, crude touch

 Dorsal root entry zone
Anatomy and Physiology
Posterior (dorsal) columns
Posterior (dorsal) column nuclei
Gracile fasciculus
Cuneate fasciculus
Nucleus gracilis
Nucleus cuneatus
Internal arcuate fibers
Medial lemniscus
Ventral posterior lateral nucleus
of thalamus
Posterior limb of internal capsule
Thalamic radiations
Primary somatosensory cortex

Trigeminal sensory fibers go to

Dorsal column
ventral–posterior medial nucleus
medial lemniscus
of thalamus
system
 Dorsal root entry zone
Some axons ascend/descend
Anatomy and Physiology
a few segments in Lissauer’s
tract
Lamina I and lamina 5
Spinal cord anterior commissure
Ascend diagonally over 2-3 cord
segments and enter the
Contralateral spinothalamic tract
Ventral posterior lateral nucleus of
thalamus
Primary somatosensory cortex

Trigeminal fibers go to ventral

posterior
medial nucleus of thalamus
Spinoreticular tract (old pain path)
Spinomesencephalic tract (PAG)

Anterolateral
(spinothalamic) system
Anatomy and Physiology
Anatomy and Physiology
 Poliomyelitis

Acute infectious disease, in severe

form, affects the central nervous
system with destruction of lower
motor neurons in spinal cord resulting
in flaccid paralysis.
History
 Associated with man since
ancient times
 Egyptian hieroglyph indicates
presence since 1400 BC
 1840 - Heinle characterizes
poliomyelitis
 Poliomyelitis – “grey marrow”
in Greek
 1954 - Salk vaccine
 1960 - Sabin vaccine
 1991 – Molla produces polio in
vitro from virus RNA
 2002 – completele synthetic
production
History

Summer of 1916:
epidemic struck New
York City
-27,000 people paralyzed
-9,000 people dead
 Structure
 Small; 28 – 30 nm in diameter
 Structure is intersection of icosahedron and dodecahedron
 3 external capsid proteins (VP1, VP2, and VP3) with
conserved antiparallel beta barrel cores
 Capsid structural stability extremely temperature sensitive
 B – C loop of VP1 important for antigenic site
 Sequence canyon formed between proteins important for
immunological reasons and receptor binding
Structure
 Cell Binding and Entry

 Binds only to poliovirus

receptor (Pvr)
 Pvr is a transmembrane
glycoprotein with three
extracellular
immunoglobulin like
domains
 Pvr is involved with actin
skeleton
 Poor viral entry
probability
( 0.1 - 1%)
Cell Binding and Entry
 Poliovirus Genome
 Single RNA molecule ~7500 nucleotides
 3 sub-regions with 10 protein products
 IRES (internal ribozyme entry site)important for virulence
 Anti-Host Activity
 Shuts off host transcription
 2B, 2BC, and 3A interfere with apoptotic pathways
 3A causes tumor necrosis receptor depletion, making cell

resistant to TNFα necrosis

 2BC, 3A interfere with antiviral cytokine secretion

 Many transcription factors bound rather than proteolysed

 Increases cell membrane lipid composition, leads to
membrane rupture
 5’ UTR determines if the virus will by lytic or nonlytic
 RNA Replication
 RNA polymerase (3D)
 RNA is copied into –RNA template for further RNA
replication; no free -RNA
 50:1 ratio +RNA: -RNA
 Vpg is used as primer for both + RNA synthesis and –RNA
synthesis
 Quality control proteins to maintain only intact RNA is used
for replication
 Mutation prone synthesis, ~1 mutation/ replication
 Serotypes
 Specificity to receptor restricts mutation rate; slow genetic drift
 Occur because of immunological reasons, vary at sequence canyon
 Three serotypes with no cross immunity
 Type 1 polio 90%
Weakest, only 1% causes neuroparalysis
 Type 2 polio 9% (Eliminated)
 Type 3 polio 1%
Greater temperature stability
 Requires trivalent polio vaccine
 Polioviruses can also vary in phenotype of virulence, host cell lysis, and
ability to raise host defense triggers
Summary
 Pathogenesis
 Symptoms of poliomyelitis always CNS specific
 Neurological symptoms found in 1-2% of infected individuals
 Three possible routes of entry into CNS
 Retrograde axonal transport

 Transport across blood – brain barrier

 Transport via infected macrophages (Trojan Horse)

 Specific to CD155 (Pvr) receptor

 Tropic to lower spinal cord and alimentary tract

 5’ NTR key to neurovirulence, especially IRES( internal

ribozyme entry site)
 Virus with rhinovirus analogue IRES fails to propagate in neuronal cells
 Provocation Poliomyelitis
Pathogenesis
 Vaccines
 Salk or Inactivated Polio Vaccine (IPV) –1954
 Formalin killed virus
 Balance between killing virus and antigenicity (Cutter Incident)
 Difficult to produce in mass quantities
 Does not work in tropical climates because of interference from other entric
viruses
 Sabin or Oral Polio Vaccine (OPV) – 1960
 Alters IRES function
 Reduces virus efficiency, replication rate, neuronal invasion
 Risk of reversion to more virulent form through mutation
1 in 1.2 million vaccinations produces neuronal effects
Vaccines
 Eradication
 Historically, 0.5% of population became paralyzed by
poliomyelitis
 Easily transmissible, less than 1% clinically recognizable
 1988 – World Health Assembly calls for global polio
eradication by 2005
Decline in Poliomyelitis
World Polio Map
World Polio Map
World Polio Map
World Polio Map
 GOAL

The World Health

Organization hopes to
completely wipe out
polio by 2005.
Subacute combined degeneration
of the spine cord

Vitamin B12 is needed for integrity of

myelin. In severe deficiency, insidious,
diffuse, uneven demyelination – clinically
manifested:
peripheral neuropathy
Spinal cord degeneration affecting both
posterior and lateral columns
Cerebral degeneration (dementia)
Optic atrophy
Subacute combined degeneration
of the spine cord
 Subacute combined degeneration
Vit B12 Deficiency of the spine cord

Dietary
- Vegans
- Breastfed offspring of vegans
Gastric disorders
Pernicious anaemia
Small Bowel disorders
 Subacute combined degeneration
of the spine cord

Microscopically, spongy changes and foci of myelin and

axon destruction are seen in the white matter of the spinal
cord. The most severely affected areas include the posterior
and lateral columns of the cervical and upper thoracic spinal
cord. In the peripheral nervous system, axonal degeneration,
without significant demyelination, is seen. In some cases,
involvement of the optic nerve and cerebral white matter
can be seen.
 Clinical features

Neurologic manifestations
- proprioceptive and vibratory sensation, spinal ataxia
- megaloblastic madness or psychosis
symptoms of anemia
gastrointestinal compraints
- loss of appetite
- glosstis (red, sore, smooth tongue)
- diarrhea or constipation
 Treatment

•Vitamin B12 administration intramuscular in dose 1000 μg

per day for a week , then 100 μg 2x per week for 2 weeks,
1 x per week 100μg for month
•Reticulocytosis begins 2 or 3 days after therapy started and
maximal number reached on day 5 to 8.
•Serum iron monitoring, after 7-10 days of vit.B12 treatment,
if Fe deficiency is diagnosed we should start iron substitution
•100 ug vit.B12 i.m. every month, regimen that must be
maintained for the rest on the patients life.
 KEY CLINICAL CONCEPTS
SPINAL CORD LESIONS

 A sensory level and motor dysfunction

 Abnormal sphinocteric function
 Spinal shock
 Myelitis
 Nerve Roots or Peripheral Nerves
Distal symmetrical polyneuropathies cause bilateral sensory loss
in a "glove and stocking" distribution in all modalities. Specific
nerve or nerve root lesions cause sensory loss in specific
territories. Associated deficits of lesions of the peripheral nerves
or nerve roots often include LMN-type weakness.
 KEY CLINICAL CONCEPTS
SPINAL CORD LESIONS

 Transverse Cord Lesion

All sensory and motor pathways are either partially
or completely interrupted. There is often a sensory
level.The pattern of weakness and reflex loss can
also help determine the spinal cord level. Common
causes of transverse cord lesions include trauma,
tumors, multiple sclerosis, and transverse myelitis.
 KEY CLINICAL CONCEPTS
SPINAL CORD LESIONS

 Hemicord Lesions: Brown-Sequard Syndrome

Damage to the LCST causes ipsilateral UMN-type
weakness. Interruption of the posterior columns
causes ipsilateral loss of vibration and joint position
sense. Interruption of the ALS (anterolateral
sclerosis) causes contralateral loss of pain and
temperature sensation.
 KEY CLINICAL CONCEPTS
SPINAL CORD LESIONS

 Central Cord Syndrome

Spinothalamic fibers causes bilateral regions of suspended
sensory loss to pain and temperature. Lesions of the cervical
cord: the classic cape distribution;
With larger lesions, the anterior horn cells are damaged,
producing LMNS
UMN when CST(corticospinal tract) are affected
Spinal cord contusion, posttraumatic syringomyelia, and
spinal cord tumors.
 KEY CLINICAL CONCEPTS
SPINAL CORD LESIONS

 Posterior Cord Syndrome

loss of vibration and position sense below the level
of the lesion.
With larger lesions, there may also be
encroachment on the LCST causing UMN-type
weakness. Common causes include trauma,
compression from posteriorly located tumors,
multiple sclerosis vitamin B12 deficiency and tabes
dorsalis.
 KEY CLINICAL CONCEPTS
SPINAL CORD LESIONS

 Anterior Cord Syndrome

Damage of: ALS(anterolateral sclerosis) pathways;
loss of pain and temp. sensation below the level of
the lesion;to the anterior horn cells produces LMNS
at the level of the lesion; larger lesions, the LCST
causing UMN signs. Incontinence is common
Causes include trauma, multiple sclerosis, and
anterior spinal artery infarct.
 KEY CLINICAL CONCEPTS
SPINAL CORD LESIONS

 Bladder, Sexual Lubrication, Erectile and

Ejaculatory Function
 Acontractile (flaccid, atonic) or hyperreflexic
(spastic) bladder include trauma, tumors,
transverse myelitis, and multiple sclerosis.
 Lesions of the peripheral nerves, or of the spinal
cord at S2 to S4, usually cause a flaccid areflexic
bladder; overflow incontinence.
 Upper Motor Neuron Lesion 

 Following a bilateral lesion of the entire spinal cord at C2

the detrussor initially becomes flaccid (like arm and leg
muscles following a lesion of the LCST) resulting in
urinary retention. 
 With time spasticity develops and the bladder contracts
with small degrees of stretch: urinary frequency and
urgency.
 In acute lesions of the spinal cord rostral to the sacral cord
(UMNL), two things occur.  First there is a flaccid bladder
(acute), then later there is a spastic bladder (chronic). 
 Lower Motor Neuron Lesion

 LMNL results in weakness, atrophy, and hyporeflexia.  The

bladder does not contract and, if the sensory afferents are
affected, no sensation of a full bladder will be perceived. 
 Remember, lesions of the spinal cord rostral to the sacral
cord result first in a flaccid (atonic; acute) bladder,
followed by a spastic (chronic) bladder.  Lesions from S1
down, and involving all of the various nerves, result in
ONLY a flaccid bladder.
 Term definition

 Paresis Weakness (partial paralysis)

Hemiparesis Weakness of one side of body (face, arm, and leg)
 -plegia No movement
Hemiplegia No movement of one side of body (face, arm, and leg)
 Paralysis No movement
 Palsy Imprecise term for weakness or no movement
 Facial palsy Weakness or paralysis of face muscles
 Term definition

 Hemi- One side of body (face, arm, and leg)

Hemiparesis Weakness of one side of body (face, arm, and leg)
 Para- Both legs
Paraparesis Weakness of both legs
 Mono- One limb
Monoparesis Weakness of one limb (arm or leg)
 Di- Both sides of body equally affected
Facial diplegia Symmetrical facial weakness
 Quadri- or Tetra- All four limbs
Quadriplegia (tetraplegia) Paralysis of all four limbs
Transverse Cord Lesion
all sensory and motor
pathways
partially or completely
interrupted.
Dermatomes affected
will give localization

causes:
trauma, tumors, MS,
transverse myelitis
Central Cord Syndrome
 Central Cord Syndrome

 Small lesion gives sensory loss in cape distribution due to

damage to anterior white commissure fibers.
 Large lesions often include ventral horn neurons giving
LMN symptoms.
 Corticospinal tracts can be damaged giving UMN deficits.
 Dorsal columns are also often damaged.
 Sacral sparing can occur due to somatotopic organization of
spinothalamic tract.
Causes include cord contusion, posttraumatic syringomyelia,
and intrinsic cord tumors.
Syringomyelia
 Anterior cord syndrome

 Compression of the ant. Cord, usually a flexion

injury
 Sudden, complete motor paralysis at lesion and
below; decreased sensation (including pain) and
loss of temperature sensation below site.
 Touch, position, vibration and motion remain
intact.
 Posterior cord syndrome

 Assocciated with cervical hyperextension

injuries
 Dorsal area of cord is damaged resulting in
loss of proprioception
 Pain, temperature sensation and motor
function remain intact.
 Brown-Sequard syndrome

 Damage to one half of the cord on either side.

 Caused by penetrating trauma or ruptured disk. ischemia
(obstruction of a blood vessel), or infectious or
inflammatory diseases such as tuberculosis, or multiple
sclerosis(MS) BSS may be caused by a spinal cord tumor,
trauma (such as a puncture wound to the neck or back),.
 a rare SCI syndrome which results in
 weakness or paralysis (hemiparaplegia) on one side of

the body and

 a loss of sensation (hemianesthesia) on the opposite side.
 acute (developing over hours to
Acute myelitis
several days)
subacute (developing over 1 to
2 weeks).

Concept
Acute transverse impairments caused by
demyelination or necrosis on white matter of
the myeline.
Such as:
myelitis following infection,
myelitis following vaccine inoculation,
demyelinative myelitis, necrosis myelitis,
para-tumor myelitis.
 Myelinated nerve fibers in SC

• Similar to Myelinated nerve fibers in PNS;

• No neurolemma, no incisures of Schmidt-Lanterman;
Myelin sheath is formed by processes of
oligodendrocytes.
 Acute myelitis

• Researchers are uncertain of the exact causes of transverse

myelitis
auto-immune reaction in association with a viral
infection or vaccine inoculation 1~4 weeks ago.
But there were no detective virus in nervous tissues,
also no antibodies in CSF(cerebrospinal fluid)
detected.
 Acute myelitis

 Every segment may be involved, Range:

T3~5, cervical or lumbar segment.Focal
or transverse lesions,
 Findings under naked eyes
 Findings under microscope
 Clinical features

 The youth & post adolescent,

 No difference between the two sex.
 Infection or vaccine inoculation history
 Inducement of cold, overfatigue,
trauma
 Clinical features

Acute onset, gets to the peak after several

hours or 2~3 days.
The initial symptoms:
Numbness and weakness
Backache and girdle sensation
The most frequent sites: T3-5,
 Clinical features

• Dyskinesia: spinal shock 2~4weeks

upper motor neuron paralysis
• Sensory disturbance
• Autonomic nerves dysfunction
 Clinical features

• From this wide array of symptoms, four

classic features of transverse myelitis emerge:
(1) weakness of the legs and arms, (2) pain,
(3) sensory alteration, and (4) bowel and
bladder dysfunction.
 Clinical features

• Pain is the primary presenting symptom of

transverse myelitis in approximately one-third
to one-half of all patients. The pain may be
localized in the lower back or may consist of
sharp, shooting sensations that radiate down
the legs or arms or around the torso.
 Clinical features

• Patients who experience sensory disturbances often

use terms such as numbness, tingling, coldness, or
burning to describe their symptoms. Up to 80 percent
of those with transverse myelitis report areas of
heightened sensitivity to touch, such that clothing or a
light touch with a finger causes significant discomfort
or pain (a condition called allodynia). Many also
experience heightened sensitivity to changes in
temperature or to extreme heat or cold. .
 Clinical features

• Bladder and bowel problems may involve

increased frequency of the urge to urinate or
have bowel movements, incontinence,
difficulty voiding, the sensation of incomplete
evacuation, and constipation. Over the course
of the disease, the majority of people with
transverse myelitis will experience one or
several of these symptoms.
 Clinical features

Acute ascending myelitis

Demyelinative myelitis
 Investigation

1. Blood routine test

Rule out various disorders such as systemic lupus
erythematosus, HIV infection, and vitamin B12
deficiency.
2. Examination of the CSF:
normal pressure,
Thenormal or increased
cerebrospinal fluid thatwhite
bathescell
the count,
spinal cord
and brain contains
slightly moreprotein
increased protein than usual and an
concentration,
increased number of leukocytes (white blood
normal glucose and chloride
cells), indicating possible infection.
 Investigation

3.Electro-physiologic examination: VEP(visual

evoked potential) 、 SEP(sensory evoked
potential) 、 MEP 。
4. Iconographic examination
Investigation
Investigation
 Diagnosis

Physicians diagnose transverse myelitis by taking a

medical history and performing a thorough
neurological examination.
If none of all tests suggests a specific cause, the
patient is presumed to have idiopathic transverse
myelitis.
 Diagnosis

Diagnose:
• Acute onset
• The history of infection and vaccine inoculation
• The symptoms of cord transverse or focal
impairment
 The examination of CSF \ Electro-physiologic
examination\MRI (magnetic resonance imaging)
 Differential diagnosis

Acute epidural abscess

Spinal hemorrhage
Carcinomatous metastases
 Differential diagnosis

Neuromyelitis optica
A subtype of multiple sclerosis,
neuritis optica: decline of eyesight
signs reflecting multiple focus, such as:

nystagmus, diplopia, ataxia.

 Treatmment

As with many disorders of the spinal cord, no

effective cure currently exists for people with
transverse myelitis.
Treatments are designed to manage and alleviate
symptoms and largely depend upon the severity of
neurological involvement.
 Treatmment

Therapy generally begins when the patient first experiences

symptoms. Physicians often prescribe corticosteroid therapy
during the first few weeks of illness to decrease
inflammation. Although no clinical trials have investigated
whether corticosteroids alter the course of transverse
myelitis, these drugs often are prescribed to reduce immune
system activity because of the suspected autoimmune
mechanisms involved in the disorder.
 Treatmment

The principle of treatment in the acute stage:

Corticosteroids are often prescribed
• Proper antibiotics to prevent infection
• Emphasis of nutrition,
• Emphasis of nursing, prevent complications.
 Treatmment

Following initial therapy, the most critical part of

the treatment for this disorder consists of keeping
the patient’s body functioning while hoping for
either complete or partial spontaneous recovery
of the nervous system.
 Treatmment

Treatment in recovery phase

Physical Therapy
Occupational Therapy
Vocational Therap
 Prognosis

 Recovery from transverse myelitis usually begins

within 2 to 12 weeks of the onset of symptoms and
may continue for up to 2 years
 About one-third of people affected with transverse
myelitis experience good or full recovery from their
symptoms
 Prognosis

 Another one-third show only fair recovery

and are left with significant deficits such
as spastic gait, sensory dysfunction, and
prominent urinary urgency or incontinence
 The remaining one-third show no recovery
at all, remaining wheelchair-bound or
bedridden with marked dependence on
others for basic functions of daily living.
 Prognosis

 The majority of people with this disorder

experience only one episode although in rare
cases recurrent or relapsing transverse
myelitis does occur.
 In all cases of relapse, physicians will likely
investigate possible underlying causes such
as MS or systemic lupus erythematosus
 Compression myelopathies

 The symptoms and signs of spinal cord compression

consists of sensory (pain, numbness and paresthesia),
motor and autonomic disturbances, the nature and
extend of which is related to: 
 The level that is compressed
 The direction from which the compression originates
 The speed with which the compression is
accomplished 
 Compression myelopathies

 Extra-medullary tumors
The loss of pain and temperature appears first,
and is most complete, in the sacral dermatomes. 
As the tumor expands, the sensory loss
ASCENDS TOWARD THE LESION.
 Compression myelopathies

Intra-medullary tumors  
 Compression myelopathies

 The pain and temperature loss starts near the level of

the tumor
 As the tumor grows laterally within the
ALS(anterolateral sclerosis),deficit DESCENDS
LOWER to the location of the lesion,(sacral sparing)
before the sensory loss is complete.
 Lesions within the center of the spinal cord cause a
symmetrical loss of pain and temperature, usually with
sparing of other sensory modalities,ex. Syringomyelia.
Lesions within the spinal cord
 The dorsal columns  

 Dorsally situated tumors compress the dorsal or posterior

column first, and cause paresthesia (funny sensations),
numbness and impairment of 2-point discrimination, vibration
and conscious proprioception on the side of the tumor. 
 The "Lhermitte sign." an electric shock like sensation running
through the back and limbs upon flexion of the neck. 
 Lesions in the cervical cord (compression, multiple sclerosis,
subacute combined degeneration from B12 deficiency). 
Figure: The dorsal (posterior) columns  
MRI
MRI
MRI
THANKS!
 Spinal Cord Injuries

Incidence
–40/million
–10,000 new cases per year
–Does not include those who die at scene
4/million or 1,000 per year
Prevalence
–200,000 – 400,000 in US
 Spinal Cord Injuries

Life expectancy greatly increased

since WW II.
–Intermittent catheterization

–Medications, equipment, etc

Cause of premature death is usually

related to COMPROMISED
RESPIRATORY FUNCTION
 Spinal Cord Injuries

 Age at injury increasing

 Mean 32 years
 More people 60 years+ at time of injury
 80% male
 Neurologic level and completeness (ASIA)
 Cervical 50.7%
 Thoracic35.1%
 Lumbosacral 11%
 C5 > C4 > C6 > T12 > C7 > L1
 Spinal Cord Injuries

 Causes (in order of frequency)

 MVA
 Gunshot wounds/acts of violence
 Falls
 Sports injuries
 Spinal and Neurogenic Shock

 Below site of injury:

 Total lack of function
 Decreased or absent reflexes and flaccid
paralysis
 Lasts from a week to several months after onset.
 End of spinal shock signaled by muscular
spasticity, reflex bladder emptying, hyperreflexia
 Spinal and Neurogenic Shock

In acute trauma of spinal cord there is often initially a period of spinal

shock characterized by flaccid paralysis below the level of the lesion,
loss of tendon reflexes, decreased sympathetic activity to vascular
smooth muscle causing reduced blood pressure, and absent
sphincter reflexes and tone.
Over several weeks or months spasticity and other upper motor neuron
signs typically develop.Some sphincter and erectile reflexes may
return, although often w/o voluntary control.
Acute spinal cord trauma patients may have improved outcome if
treated in the first 8 hrs with high doses of steroids. New
experimental drugs are being tested that will block the effects of
glutamate release following injury.
 Classification of SCI

 Mechanism of injury
 Flexion (bending forward)
 Hyperextension (backward)
 Rotation (either flexion- or extension-rotation)
 Compression (downward motion)
 Pathophysiology of SCI

 Insert stuff here

 Insert picture here
 Classification of SCI

 Level or Injury
 Cervical (C-1 through ??)
 Thoracic (T-1through ??)
 Lumbar (L-1through ??)
 Degree of Injury
 Complete
 Total paralysis and loss of sensory and motor function although
arms or rarely completely paralyzed
 Incomplete or partial
 Degree of Injury

 Complete transection
 Total paralysis and loss of sensory and motor function
although arms or rarely completely paralyzed
 Incomplete (partial transection)
 Mixed loss of voluntary motor activity and sensation
 Four patterns or syndromes
 Incomplete cord patterns

 Central cord syndrome More common in older

clients
 Frequently from hyperextension of spine
 Weakness in upper and lower ext, but greater in

upper.
 Anterior cord syndrome
 Posterior cord syndrome
 Brown-Sequard syndrome
 Clinical manifestations of SCI

 Depend on the LEVEL and DEGREE of the injury!

 Quadriplegia occurs with C-1 through C-8 injuries.
 Paraplegia occurs with T-1 thru L-4.
 Clinical Manifestations of SCI

 Respiratory
 C1 – C3: Absence of ability to breathe

independently.
 C4 – poor cough, diaphragmatic breathing,

hypoventilation
 C5 – T6: decreased respiratory reserve

 T6 or T7 – L4: functional respiratory system

with adequate reserve.

 What is the phrenic nerve?

 The phrenic nerve stimulates the diaphragm to contract.

 Two phrenic nerves (right and left) - injury to one or the
other paralyzes contraction of only one half of the
diaphragm but even hemi- (half) paralysis can significantly
interfere with breathing for patients with lung disease.
 The nerve arises from branches of the C3,4, and 5 nerve
roots.
 The phrenic nerve can be damaged by procedures
exploring the neck & upper back
 Loss of the phrenic nerve on either side
results in paralysis of the diaphragm on that
side. 
 Paralysis of the diaphragm on one side
results in less inflation of the lung on that
side. 
 Whether this is physiologically significant
(producing respiratory distress,
hypoventilation/hypercapnia) depends on
other aspects of a patient's pulmonary
physiology (namely underlying chronic
obstructive pulmonary disease
[emphysema, bronchitis], pneumonia, etc.). 
 Cardiovascular system

 C1 – T5 shows decreased or absent SNS

influence.
 BRADYCARDIA AND HYPOTENSION (due
to vasodilation)
 What is the VAGUS nerve?

 The longest of the cranial nerves- exits out of the

medulla and ends in the abdomen
 It supplies sensory and motor function to the
pharynx
 Supplies motor function to the muscles of the
abdominal organs
 Provides parasympathetic activity to the heart,
lungs, and most of the digestive system
 Urinary System

 Atonic bladder with RETENTION in spinal shock.

 Post acute phase – irritability causing dribbling or
frequent urination.
 Urinary infection and calculi from retention and
distention.
 INTERMITTENT CATHETERIZATION!
 GI system

 Decreased motility
 Paralytic ileus
 Gastric distention – intermittent NG suctioning
 Increased H2 – administer H2 inhibitors such as
Zantac or Pepcid in initial stages
 Carafate and antacids later as prophyaxis
 Intra-abdominal bleeding! Remember, no pain or
tenderness to warn you.
 Watch for H/H decrease and impactions
 Skin System

 Pressure ulcers!
 Muscle atrophy in flaccid paralysis
 Contractures in spastic paralysis
 Poikilothermism – the adjustment of body temp to
room temperature
 Decreased ability to sweat below lesion
 Peripheral vascular system

 DVT common but not detected easily

 Pulmonary embolism a significant cause of death.
 Doppler studies, measurement of extremity girth,
impedance plethysmography
 Post Injury Assessment

 Goals are to
 Sustain life
 Prevent further cord damage
 Assessment of muscle groups; motor status
 Against gravity
 Against resistance
 Both sides of the body
 Ask to move legs, hands, fingers, wrists, then shrug
shoulders
 Post injury assessment

 Thorough motor examination including position

sense and vibration.
 Sensory examination
 Pinprick starting at toes and working upward

 ALWAYS HAVE CLIENT CLOSE EYES OR

LOOK AWAY! If he can see what you’re

doing, he will answer accordingly.
 Assess for head injury and ICP
 X-ray, CT scan, EMG
 Surgical Therapy

 Reduces injury and stabilizes the SC

 Done for
 Compression

 Bony fragments in the cord

 Compound fracture

 Penetrating trauma
 Drug Therapy

 Vasopressors (Dopamine) to keep mean arterial

pressure greater than 80mm to 900mm/Hg so that
PERFUSION TO CORD is improved.
 Methylprednisolone

 Increases the recovery of function and is the SOC!

IV bolus then continuous IV over a 23 hour period.

 Improves blood flow and reduces edema in the SC

 Other drug therapy

 Symptom-reducing drugs for

 GI problems - zantac, tagamet, pepcid

 Bradycardia - atropine

 Hypotension - vasopressors

 bladder spasticity - anticholinergics

 autonomic dysreflexia – blood pressure

reduction
 Function of Motor Neurons

 Upper motor neurons

 Function of Motor Neurons

 Lower motor neurons

 Diagnoses and Interventions

 Impaired Gas Exchange r/t muscle fatigue and

weakness
 Decreased PaO , increased PaCO
2 2
 Fatigue
 Diminished breath sounds
 Impaired gas exchange

 Maintain patent airway

 Assess respiratory status q 2 hours
 Monitor ABGs
 Provide aggressive pulmonary toilet; chest PT and
quad-assist coughing
 Assess strength of cough
 Suction secretions
 Inability to sustain spontaneous
ventilation

 Related to diaphragmatic fatigue or paralysis

evidenced by
 Dyspnea
 Use of accessory muscles
 Abnormal ABGS
 Provide chest PT
 Assist with mechanical ventilation
 Provide emotional support
 Decreased cardiac output

 Related to venous pooling of blood and

immobility as evidenced by
 Hypotension
 Tachycardia
 Restlessness
 Oliguria
 Decreased pulmonary artery pressures
 Decreased cardiac output

 Monitor blood pressure, pulse and cardiac rhythm

 Administer vasopressors to maintain MAP at
80mm/Hg or above
 Apply pneumatic compression boots or stockings
 Perform ROM at least q8h to aid in muscle
contraction and venous return
 Impaired skin integrity

 Related to immobility and poor tissue perfusion

 Inspect skin and areas around pins or tongs
 Turn at least q2h and use kinetic table or other
specialty care devices.
 Insure adequate nutritional intake
 INFORM family and client about risk of pressure
ulcers
 Constipation

 Related to location of injury,  fluid intake,

diet, immobility AEB
 Lack of BM in over 2 days
  bowel sounds
 Palpable impaction
 Hard stool or incontinence
 Constipation

 Auscultate bowel sounds and monitor abdominal

distention
 Note and report any nausea and vomiting
 Begin bowel program when BS return and teach to
client and family
 Administer suppositories and stool softeners
 Ensure appropriate fluid and fiber intake
 Bowel program for SCI

 Needs to be consistent
 Give suppository after meal and place on toilet
approx 30 minutes after.
 Do this at same time each day!
 Fiber, fluids and activity are important
 Constipation leads to AUTONOMIC
DYSREFLEXIA!!!
 Urinary Retention

 Related to injury and limited fluid intake as

evidenced by
 Decreased output

 Bladder distention

 Involuntary emptying of bladder

 Urinary Retention

 Palpate bladder every shift

 During acute phase, insert indwelling catheter
 Begin intermittent cath program when appropriate
 Keep I and O and end fluids
 Monitor BUN and creatinine
 Crude (pronounced croo-DAY) manuever when
voiding/cathing
 Risk for autonomic dysreflexia

 Assess for HTN, bradycardia, headache, sweating,

blurred vision, flushing, nasal stuffiness/congestion
 Reduce or eliminate noxious stimuli such as
impaction, urine retention, tactile stimulation and
skin lesions or pain!
 Autonomic dysreflexia

 Elevate HOB 43 degrees

 Identify cause and eliminate
 Take BP and pulse
 Administer antihypertensives as ordered if
hypertensive.
 Call physician if interventions not effective
 TEACH CLIENT AND CARGIVERS HOW TO
PREVENT THIS!
 Other diagnoses

 Impaired physical mobility

 Altered nutrition: < body requirements
 Sexual dysfunction
 Risk or injury r/t sensory deficits
 Altered family processes
 Risk for ineffective individual coping
 Body image disturbance
 Acute intervention

 Immobilization
 Crutchfield tongs

 Halo vest

 Stryker bed

 Roto-rest bed (side to side)

 Motion sickness a problem with these.

 Respiratory dysfunction

 Intubation if injury is high

 Decreased tidal volume and shallow breathing
lead to pneumonia and atelectasis
 pain management
 Prone position may be risky
 Count to 10 test
 COUGH technique to assist with ineffective
abdominal muscles
 Fluids and nutrition

 Paralytic ileus common in 48-72 hours

 When bowel sounds return:
 High calorie, high protein, high fiber diet

 Evaluate SWALLOWING before feeding!

 EATING CAN BECOME A POWER

STRUGGLE!
 Bowel and Bladder mgmt.

 Indwelling catheter initially

 Intermittent catheterization when able
 Monitor pH of urine (should be acetic!)
 Ascorbid acid and Mandelamine (an antiseptic)
given to keep down bacteria
 Temperature control

 NO vasoconstriction, piloerection or heat loss

through sweating below level of injury
 Do not over cool or over heat client. They only
have the remaining upper portion of their bodies,
generally, for temperature adjustment