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 (C1C7) i.e. neck
twelve thoracic vertebrae (T1T12) i.e. upper back
five lumbar vertebrae (L1L5) 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
2) Arachnoid

3) Pia mater

1) Dura mater "tough mother",

strong
2) Arachnoid spidery looking,
carries blood vessels,
etc.
Subarachnoid space
3) Pia mater adheres tightly to

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:

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 38 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 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

THANK
YOU