ACUTE SPINAL CORD LESSION
MEITI FRIDA
DEPARTMENT OF NEUROLOGY FACULTY OF
MEDICINE ANDALAS UNIVERSITY
ANATOMY OF SPINE AND SPINAL
CORD
The spine has three major components:
 the spinal column (bones and discs)
 neural elements (the spinal cord and nerve roots)
 supporting structures (muscles and ligaments)
The spinal column consists of:
 seven cervical vertebrae (C1–C7) i.e. neck
 twelve thoracic vertebrae (T1–T12) i.e. upper back
 five lumbar vertebrae (L1–L5) i.e. lower back
 five bones (that are joined, or "fused," together in
adults) to form the bony sacrum
 three to five bones fused together to form the
coccyx or tailbone
Adult spinal cord:

Inside vertebral canal

31 segments, each
associated with a pair
of dorsal root ganglia

Extends to L1/ L2
(Conus medularis)

Cauda equina - origin
of spinal nerves
extending inferiorly
from conus medullaris
Spinal Meningen
Three membranes
surround all of CNS
3) Pia mater
1) Dura mater - "tough
2) Arachnoid
mother", strong
2) Arachnoid - spidery
looking, carries blood
vessels, etc.
Subarachnoid space
3) Pia mater - adheres
tightly to surface of spinal
cord
1) Dura mater
Organization of Cord Cross Section
Gray matter
posterior - somatic and visceral sensory nuclei
anterior (and lateral) gray horns – somatic and visceral motor control
gray commissures - axons carrying information from side to side
White matter
posterior white column anterior white column
lateral white column
anterior white commissure
Functions
ascending tracts - sensory toward brain
descending tracts - motor from brain
White Matter: Pathway
Generalizations
Vascular anatomy - Anterior spinal
artery
Anterior spinal artery originates in upper
cervical region, from anterior spinal branches
of vertebral artery.
 6-10 anterior radicular arteries contribute to
it throughout its length.
 Supplies anterior two thirds of cord, via
central branches and penetrating branches of
pial plexus

Vascular anatomy – posterior spinal
artery
Run along posterolateral cord
 Sometimes discontinuous
 Originates from verterbral artery
 Has contribution from 10-23 posterior
radicular a.
 Supplies posterior one third of cord

Vascular anatomy - arteries and venous
Acute lession of spinal cord
 Traumatic
spinal cord injury
 Vascular Myelopathies
 Infectious Myelopathies
 Inflammatory Myelopathies
Traumatic spinal cord injury
Mechanism of injury
 Flextion and flextion-rotation injury
 Compression injury
 Hyperextention injury
Level of injury
 Quadriplegia :
injury in cervical region
all 4 extremities affected
 Paraplegia :
injury in thoracic, lumbar or sacral segments
2 extremities affected
Complete and Incomplete
Spinal Cord Syndromes can be classified into either
complete or incomplete categories
 Complete – characterized as complete loss of
motor and sensory function below the level of the
traumatic lesion

Incomplete – characterized by variable neurological
findings with partial loss of sensory and/or motor
function below the lesion
Spinal Shock
An immediate loss of reflex function, called
areflexia, below the level of injury
 Signs:

◦
◦
◦
◦
◦
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Slow heart rate
Low blood pressure
Flaccid paralysis of skeletal muscles
Loss of somatic sensations
Urinary bladder dysfunction
Spinal shock may begin within an hour after
injury and last from several minutes to several
months, after which reflex activity gradually
returns
Brown-Sequard Syndrome
(Special Form of Spinal Cord Injury)






Results from an injury to only half of the
spinal cord and is most noticed in the
cervical and thoracal region
Often caused by spinal cord penetrating
trauma
Motor loss is evident on the same side as the
injury to the spinal cord
Sensory loss is evident on the opposite side
of the injury location (pain and temperature
loss)
Bowel and bladder functions are usually
normal
Person is normally able to walk although
some bracing or stability devices may be
required
ASIA Impairment Scale of spinal cord
injury
ASIA – American Spinal Injury Association :
A – Complete: no sensory or motor function
preserved in sacral segments S4 – S5
B – Incomplete: sensory, but no motor function in
sacral segments
C – Incomplete: motor function preserved below
level and power graded < 3
D – Incomplete: motor function preserved below
level and power graded 3 or more
E – Normal: sensory and motor function normal
ATLS principles







A irway; protect spine
B reathing
C irculation
D isability
E xpose patient
Treat
Secondary survey
Pharmacologic Therapy

Option: Methylprednisolone

NASCIS II (1992)
◦ 30mg/kg IV loading dose + 5.4 mg/kg/hr (over 23hrs)
effective if administered within 8 hours of injury

NASCIS III (1997)
◦ If initiated < 3hrs continue for 24 hrs, if 3-8 hrs after
injury, continue for 48hrs (morbidity higher increased sepsis and pneumonia)
Vascular Myelopathies
Spinal Cord Ischemia
 Spinal Hemorrhage

Spinal Cord ischemia
 In most cases Sensory features ( pain ) emerge first ,
followed by weakness within minutes or hours
 Pain often follows radicular pattern ( common presentation )
 Maximum weakness is observed within 12 hrs of onset
 Lower thoracic and lumbar spinal levels are most commonly
affected
 Urinary retention : in acute phase
Involuntary voiding or defecation : associated with onset of
ischemic insult
STROKE SYNDROME
FEATURE
ANTERIOR SPINAL ARTERY INFARCT
Bilateral motor deficit with Spinothalamic
sensory deficit
ANTERIOR UNILATERAL INFARCT
Hemiparesis with Contralateral
spinothalamic sensory deficit
POSTERIOR UNILATERAL INFARCT
Hemiparesis with Homolateral lemniscal
sensory deficit
CENTRAL INFARCT
Bilateral Spinothalamic sensory deficit
without motor deficit
POSTERIOR SPINAL ARTERY INFARCT
Bilateral motor deficit with lemniscal
sensory deficit
TRAVERSE INFARCT
Bilateral motor deficit with complete
sensory deficit
Spinal Cord Hemorrhage
 Spinal cord dysfunction – due to hemorrhage
into
Sub arachnoid space
Sub dural space
Epidural space
 Onset : Sudden & Painful
 Triggers : Trauma
Bleeding diatheses
Vascular malformations
Investigations :
 CSF Analysis : usually normal
can be xanthochromic
raised protein
 MRI
 Contrast enhanced CT scan with sagittal / coronal reformatting is useful in
pts who cannot undergo MRI
 MR Angiography
 Selective Spinal Angiography using Digital Substraction Techniques
Treatment :
 SCH is surgical emergencies
 Immediate surgery
 Laminectomy and clot evacuation
 Angiographically directed embolization of vascular malformation
Infectious Myelopathies
Virus
 Enteroviruses (poliovirus, coxsackie virus, and enterovirus
71), Flaviviruses (West Nile virus and Japanese encephalitis
virus) have been known to target the gray matter
(Anterior horn cells) producing acute lower motor neuron
disease
 CMV,VZV, HSV I &II, HCV, and EB
 HIV
Bacterial
 Mycoplasma (acute and post infectious), Listeria
monocytogenes
 TB
 Lyme disease
Schistosomiasis (in endemic areas)
Clinical features of infectious
process
Fever
 Meningismus
 Encephalopathy
 Rash
 Lymphadenopathy
 Known systemic infection
 Immunocompromised status
 Known exposure to infectious agent

Inflammatory Myelopathies
Acute Disseminated Encephalomyelitis
 Transverse Myelitis

Acute Disseminated Encephalomyelitis
 Characterized by acute to subacute onset of fever,
meningismus, encephalopathy and multifocal symptoms
& signs of CNS dysfunction
 More common in children
 Recent vaccination or systemic infection is noted in ½
of cases
 Brain MRI reveals numerous medium to large size ,
fairly symmetrical subcortical white matter lesions
often with involvement of deep gray matter
Transverse Myelitis (TM)
Immune-mediated process results
in neural injury to the spinal cord
 Varying degrees of weakness,
sensory alterations and autonomic
dysfunction
 Up to half of idiopathic cases will
have a preceding respiratory or
gastrointestinal illness

TM Diagnostic Criteria
Treatment of Myelitis
Acute myelitis attacks are typically treated
with
IV Corticosteroids
Methyl prednisolone
 Resistant cases : Plasmapheresis
 Very severe attacks : combination of
Corticosteroids, Plasmapheresis,
Cyclophosphamide
 No evidence supports use of IV Ig in
inflammatory myelitis

Neoplastic & Paraneoplastic
Myelopathies
Most primary tumors of cord do not cause
acute myelitis syndromes
 Lymphoma is the only exception – causes a
subacute myelopathy
- corticosteroid responsive
 Breast carcinoma : antiamphiphysin
antibodies and severe spastic myelopathy
 Ovarian and Non small cell lung cancer :
glutamic acid decarboxylase 65
autoantibodies causing stiff man like
syndrome with brain stem features and
ataxia
