ACUTE SPINAL CORD LESSION MEITI FRIDA DEPARTMENT OF

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 (C 1–C 7) i. e. neck � twelve thoracic vertebrae (T 1–T 12) i. e. upper back � five lumbar vertebrae (L 1–L 5) 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 L 1/ L 2 (Conus medularis) � Cauda equina - origin of spinal nerves extending inferiorly from conus medullaris

Spinal Meningen Three membranes surround all of CNS 1) Dura mater - "tough mother", strong 3) Pia mater 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

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 S 4 – S 5 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

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) ◦ 30 mg/kg IV loading dose + 5. 4 mg/kg/hr (over 23 hrs) effective if administered within 8 hours of injury � NASCIS III (1997) ◦ If initiated < 3 hrs continue for 24 hrs, if 3 -8 hrs after injury, continue for 48 hrs (morbidity higher increased sepsis and pneumonia)

Vascular Myelopathies � Spinal Cord Ischemia 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

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