Acute Myelopathy

Talha Nazir (1), Awais Khan (2)
1 King Edward Medical University, Lahore, Pakistan
2 Assistant Professor, Department of Neurology, University of Arizona


Introduction

  • The incidence of acute myelopthy vary based on etiologies e.g., Transverse myelitis (1400 new cases each year), Spinal epidural abscess (1.2 per 10,000 people) and Multiple Sclerosis (>100/100,000 people).
  • The traumatic spinal cord injury often results from a gunshot wound (10.4%), accidental trauma to head, neck and back region (31.5%), falling (25.3%) and spinal sports injuries (4.3%).
  • Non-traumatic spinal cord injuries can have a range of etiologies like degenerative changes, infections (Staph. Aureus and Mycobacterium tuberculosis), malignancy of spine (Primary: multiple myelomas, Metastasis: prostate in male and breast in females are common etiologies), inflammation or congenital abnormalities

Acute Myelopathy

Pathology of spine and meninges covering the spinal cord is termed as myelopathy. Acute myelopathies can be classified as

Compressive Myelopathies

Abscess related myelopathy

  • The common causative organisms are staphylococcus aureus and mycobacterium tuberculosis
  • Risk factors include IV drug abuse, diabetes, alcohol
  • Fever and local tenderness that may progress to neurological deficit.
  • Commonly involve thoracic and lumbar regions
  • MRI is diagnostic (well-defined enhancement of perilesional area and edema)
  • Treat with antimicrobial therapy and surgery

Vascular malformation

  • Vascular malformation can lead to compressive or non-compressive myelopathy
  • Etiology
  • Thrombosis of Aortic surgery, spinal angiography, embolism, and coagulative disorders
  • Occlusion of arteries such as anterior spinal artery (Anterior spinal cord syndrome), posterior spinal artery (posterior spinal cord syndrome) and sub-commissural artery (brown Sequard syndrome) can lead to different presentations.
    • AV fistula
    • Venous infarct
    • Spinal aneurysm
    • Hemangioblastoma and cavernous malformation
  • Imaging Findings
    • MRI
      • Serpent like images
      • Absence of flow signals
  • CSF Findings
    • CSF is normal, but protein concentration may be higher in AV fistulas.
    • Low cell content and absent oligoclonal bands
Management of compressive myelopathy
  • Immobilization
  • IV methylprednisolone
  • Urgent surgical intervention

Non-compressive myelopathies

Transverse myelitis

  • Bilateral spinal cord dysfunction with a well-defined area of sensory loss during the first four weeks of presentation without any compression or disease and evidence of spinal inflammation (CSF pleocytosis, raised IgG)
  • Peak incidence is during the 2nd and 4th decade of life.
  • Perivascular and medullary infiltration of monocytes, lymphocytes (acute) and macrophages (subacute).
  • MRI Findings
    • Central and focal high signal areas
    • Involvement of three to four segments (thoracic spine is the most common)
    • Diffuse enhancement on contrast medium (differentiate from other intramedullary tumors)
  • Management
    • IV corticosteroids (methylprednisolone, dexamethasone)
    • Plasma exchange
    • Immunosuppressive therapy for relapses

Infections related myelopathy

  • Associated with blood-borne infections of lungs, skin and genitourinary system.
  • Etiologies can be classified and based on the causative organism (Table 3)
  • CSF Findings
    • Pleocytosis
    • Neutrophilia
    • Increased protein
    • Absent oligoclonal bands
  • MRI Findings
    • Central high signal areas
    • Spinal edema
    • Management
    • Appropriate antibiotics
    • Surgical intervention (epidural abscess, subdural empyema etc.)

Multiple sclerosis

  • Autoimmune demyelination of nerves in brain and spinal cord. Associated with HLA-DR2. Symptoms include
  • Relapsing and remitting symptoms. Common in women of 20 and 30 years old.
  • Immune-mediated inflammation may lead to demyelination of axons in CNS (brain and spinal cord)
  • Optic neuritis (associated with Marcus Gun pupil)
  • Brainstem and cerebellar involvement (bilateral involvement is more common)
  • Demyelination of pyramidal tract (spasticity)
  • MRI Findings
    • Gold standard
    • Periventricular plaques
    • Multiple lesion in white matter
👆
McDonald’s criteria:
  • Space: One or more than one lesion in two areas with or without enhancement (periventricular, infratentorial, juxtacortical and spinal cord)
  • Time: One new white matter lesion as compared to the previous MRI with or without enhancement.
  • CSF Findings
    • Raised IgG levels
    • Oligoclonal bands (diagnostic)
  • Management
    • IV steroids for acute flares
    • Prevent relapses by disease-modifying therapy (beta-interferon)
    • Catheterization and anticholinergic drugs for neurogenic bladder
    • Baclofen for spasticity
    • TCAs (Tricyclic antidepressants) for pain
 

Neuromyelitis Optica

  • Incidence is 0.4 per million in western population with a male to female ratio of 1:3
  • Acute myelitis and optic neuritis along with two or more than two of the following
  • Spinal cord lesion involving more than three segments
  • IgG positive (aquaporin four antibodies)
  • CSF Findings
    • Raised protein
    • Pleocytosis
    • Absent oligoclonal bands
  • MRI Findings
    • Central longitudinal lesion (confluent) involving more than three segments
    • Spinal expansion in T1 (low signals) and T2 (high signals)
    • Periventricular lesion in more than 60% of the patients (high aquaporin four concentration)
    • Optic nerve lesion
  • Management
    • Acute
      • IV methylprednisolone (100mg for 3-5days)
      • Plasmapheresis (5-7 cycles)
    • Chronic
      • Immunosuppression (Rituximab, Mycophenolate mofetil, azathioprine)
      • Change the drug or optimize the dose if patient relapses.

Workup for acute myelopathy

Step 1: Confirm the diagnosis of acute myelopathy
  • History and physical examination
  • Neurological deficit and involvement of bladder and bowel
Step 2: MRI (Gadolinium enhancement)
  • To rule out a compressive myelopathy
Step 3: CSF analysis and confirm the presence of the lesion
  • Step 3a: Define the infectious causes of myelopathy
    • Pleocytosis
    • Neutrophilia
    • Increased protein
    • Absent oligoclonal bands
  • Step 3b: Define the inflammatory causes of myelopathy
    • Raised IgG and oligoclonal bands (MS)
    • IgG against aquaporin 4, raised proteins, pleocytosis and absent oligoclonal bands (Neuromyelitis Optica)
  • Step 3c: Determine the location of the lesion
    • Brain and spinal cord (MS)
    • Spinal cord only (Transverse myelitis)
    • Optic nerve and spinal cord (Neuromyelitis Optica)

Table 1: Etiologies of Compressive and Non-compressive Myelopathies

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Table 2: Tumors causing Compressive Myelopathy

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Table 3: Infections of Spinal cord

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Further Reading

  • Marignier R. Acute and subacute myelopathy. Rev Neurol (Paris). 2021 May;177(5):557-566. doi: 10.1016/j.neurol.2020.08.003. Epub 2020 Oct 21. PMID: 34024334.
  • Hays, Angela & Chalela, Julio. (2010). Acute Myelopathy. 10.1007/978-1-4419-6842-5_19.

Bibliography

  • Ana María Granados Sánchez, L. M. G. P., César Andrés Ortega Toscano, Alejandra López López. (2011). DIAGNOSTIC APPROACH TO MYELOPATHIES Rev. Colomb. Radiology, 22(3), 1-21.
  • Walker, J. (2009). Spinal cord injuries: acute care management and rehabilitation. Nursing Standard, 23(42), 47-56. doi: 10.7748/ns2009.06.23.42.47.c7055
 
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