Transverse Myelopathy Spin7 Transverse Myelopathy

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Transverse Myelopathy Spin7 ()

Transverse Myelopathy

Last updated: September 5, 2017

Etiology 1

Idiopathic acute transverse myelitis 2

Etiology 2

Clinical Features 2

Diagnosis 3

Treatment 4

Surfer's Myelopathy 4

Transverse Myelopathy - syndrome of spinal cord segment damage across greater part of sectional area.


  1. Trauma - most frequent cause of complete lesions.

  1. Demyelinating & inflammatory processes (transverse myelitis) - most commonly incomplete lesions (although there is evidence of involvement of entire cross-section of cord):

  1. MS, neuromyelitis optica

  2. infection – enteroviruses (esp. poliomyelitis*, enterovirus 70-71), herpesviruses (HSV-2**, VZV***, EBV, CMV), mumps, measles, mycoplasma, acute meningovascular syphilis, HIV, HTLV-I.

*prototypical acute infectious myelitis

**recurrent sacral myelitis in association with outbreaks of genital herpes

***most common cause of acute viral myelitis

  1. collagenoses - SLE (!), Sjögren's syndrome, Behçet's disease.

  2. sarcoidosis (subacute transverse myelopathy with severe cord swelling).

  1. Spinal cord ischemia - complete or incomplete lesion (e.g. anterior 2/3 anterior spinal artery syndrome).

  1. Hemorrhage into spinal cord.

  1. Intraparenchymal abscess.

  1. Idiopathic acute transverse myelitis

Idiopathic acute transverse myelitis


- frequently after nonspecific viral infectiondirect viral invasion into cord or autoimmune mechanisms.

Pathology - inflammatory demyelination which involves several segments (usually thoracic).

  • may progress to necrosis and cavitation.

Clinical Features

- lost all motor & sensory functions below level of transverse myelopathy.

N.B. sensory & motor findings tend to be symmetric (vs. MS – asymmetric)!

    • onset – (sub)acute back pain, ascending leg weakness, paresthesias below level of lesion, sphincter dysfunction.

  • pathological process may be acute - initially produces spinal shock, but hyperreflexia soon supervenes; persistent areflexic paralysis indicates necrosis over multiple spinal segments (differentiate from Guillain-Barré syndrome).

    • common additional features:

      • band of disagreeable dysesthesia above uppermost border of sensory loss.

      • radicular pain at lesion level.

      • tender (on percussion) spinous processes - in epidural abscess, vertebral metastasis.

    • spontaneous complete recovery (over weeks ÷ months) occurs in 60% cases.


CT / MRI - mild fusiform swelling in affected region.

    • diffuse / multifocal abnormal bright signal on T2-MRI.

    • contrast enhancement (BBB disruption) in acute cases.

    • brain MRI for all cases - to assess for of MS.


  1. normal

  2. pleocytosis (up to several hundred mononuclears; in severe acute cases, PMNs may be present), protein normal or mildly elevated.

T2-MRI: mild expansion of upper spinal cord and signal change (white) within it:

Most important differentiation (must be done rapidly with MRI!) - compressive myelopathy:

  1. spinal or epidural abscess / hematoma

  2. tumor, especially metastatic (may present acutely even though tumor has been present for weeks or longer)

  3. herniated intervertebral disk (central herniation may cause acute compression without local pain).


Corticosteroids (e.g. IV methylprednisolone 500 mg q 12 hours for 3 days → tapering with prednisone) - reduce edema and lead to earlier function restitution.

Surfer's Myelopathy

Freedman, Brett A “Surfer's Myelopathy: A Rare Form of Spinal Cord Infarction in Novice Surfers: A Systematic Review” Neurosurgery: May 2016 - Volume 78 - Issue 5 - p 602–611

  • rare (64 cases reported), acute, atraumatic thoracic/conus medullaris myelopathy that occurs in young, healthy, novice surfers who have no pre-existent spinal disease.

  • most definitive support is for a vascular cause (angiogram may show the absence of radicular artery and no artery of Adamkiewicz).

  • altered venous return that occurs from lying prone for prolonged periods of time on a surfboard can contribute to vascular insufficiency.

  • occlusion by embolus or vasospasm induced by prolonged hyperextension; there have been no reported cases of a similar acute myelopathy in novice or elite butterfly stroke swimmers, who repetitively and violently hyperextend their flexible trunks for brief periods of time, often while performing a Valsalva maneuver; therefore, it is more likely that prolonged hyperextension plays the putative role.

  • clinically start with back pain and rapidly progress to complete / incomplete myelopathy.

  • diagnosis: T2 signal in the central cord within 24-72 hours; gadolinium enhancement and DWI are not helpful; at follow up – cord atrophy at involved levels.

  • treatment - patients receiving steroids improved 55% of the time; optional – lumbar drain.

  • prognosis:

  • incomplete cases improve within 24 hours of onset

  • no improvement has been reported for ASIA A cases (>50% of reported cases)

  • overall neurological recovery rate - 42%;

Bibliography for ch. “Spinal Disorders” → follow this link >>

Viktor’s Notes for the Neurosurgery Resident

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