ACUTE SPINAL CORD LESSION

MEITI FRIDA

DEPARTMENT OF NEUROLOGY FACULTY OF MEDICINE ANDALAS UNIVERSITY

ANATOMY OF SPINE AND SPINAL CORDThe 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. necktwelve thoracic vertebrae (T1–T12) i.e. upper

backfive lumbar vertebrae (L1–L5) i.e. lower backfive 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

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

Adult spinal cord:

Spinal Meningen

3) Pia mater

2) Arachnoid

1) Dura mater

Three membranes surround all of CNS

1) Dura mater - "tough mother", strong

2) Arachnoid - spidery looking, carries blood vessels, etc.

Subarachnoid space

3) Pia mater - adheres tightly to surface of spinal cord

Organization of Cord Cross Section

Gray matter posterior - somatic and visceral sensory nucleianterior (and lateral) gray horns – somatic and visceral motor controlgray commissures - axons carrying information from side to side

White matter posterior white column - anterior white columnlateral white columnanterior 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 cordSometimes discontinuousOriginates from verterbral arteryHas contribution from 10-23

posterior radicular a.Supplies posterior one third of cord

Vascular anatomy - arteries and venous

Acute lession of spinal cordTraumatic spinal cord injuryVascular MyelopathiesInfectious MyelopathiesInflammatory Myelopathies

Traumatic spinal cord injuryMechanism of injuryFlextion and flextion-rotation injuryCompression injuryHyperextention injury

Level of injuryQuadriplegia :

injury in cervical regionall 4 extremities affected

Paraplegia :injury in thoracic, lumbar or sacral segments2 extremities affected

Complete and Incomplete

Spinal Cord Syndromes can be classified into either

complete or incomplete categoriesComplete – 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 ShockAn 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 injuryASIA – 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 segmentsC – Incomplete: motor function preserved below level and power graded < 3D – Incomplete: motor function preserved below level and power graded 3 or moreE – 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 TherapyOption: 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 HemorrhageSpinal 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 MyelopathiesVirus

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 processFeverMeningismus Encephalopathy Rash LymphadenopathyKnown systemic infection Immunocompromised statusKnown 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 : PlasmapheresisVery severe attacks : combination of

Corticosteroids, Plasmapheresis, CyclophosphamideNo 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 responsiveBreast 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

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