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HIV-associated myelopathy

Summary

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  • Progressive spastic paraparesis and sensory ataxia in HIV patients
  • Vacuolar myelopathy of the spinal cord, predominantly affecting thoracic region
  • MRI shows cord atrophy and T2 hyperintensity in posterior and lateral columns

Pathophysiology

  • Exact mechanism unclear, but likely multifactorial:
    • Direct HIV infection of spinal cord cells
    • Immune-mediated damage to myelin and axons
    • Metabolic disturbances, including vitamin B12 deficiency
  • Vacuolar changes in white matter, predominantly in lateral and posterior columns
  • Axonal degeneration and demyelination

Demographics

  • Occurs in 5-10% of HIV-infected individuals
  • More common in advanced stages of HIV infection (CD4 count <200 cells/μL)
  • Typically affects adults aged 30-50 years
  • No significant gender or racial predilection

Diagnosis

  • Clinical presentation:
    • Gradual onset of lower limb weakness and spasticity
    • Sensory ataxia and impaired vibration sense
    • Urinary and bowel dysfunction
  • Exclusion of other causes of myelopathy (e.g., compression, infection)
  • CSF analysis: may show mild pleocytosis and elevated protein
  • Serum vitamin B12 levels should be checked

Imaging

  • MRI findings:
    • Spinal cord atrophy, particularly in thoracic region
    • T2 hyperintensity in posterior and lateral columns
    • Symmetrical involvement, typically extending over multiple segments
    • No contrast enhancement
  • Differential diagnosis:
    • Vitamin B12 deficiency myelopathy
    • HTLV-1-associated myelopathy
    • Primary progressive multiple sclerosis

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  • 45-year-old patient presented with weakness and brisk upper limb reflexes. The patient had a recent diagnosis of HIV with a CD4 count of 10.
  • MRI showed an "inverted V" pattern of high signal in the dorsal columns.

Treatment

  • Antiretroviral therapy (ART) is the mainstay of treatment:
    • May slow progression but rarely leads to complete resolution
    • Early initiation of ART may prevent or delay onset
  • Symptomatic management:
    • Physiotherapy and occupational therapy
    • Antispasticity medications (e.g., baclofen, tizanidine)
    • Management of neurogenic bladder and bowel dysfunction
  • Vitamin B12 supplementation if deficient
  • Experimental therapies:
    • L-methionine supplementation
    • Intravenous immunoglobulin in selected cases

Differential diagnosis

Differential Diagnosis Distinguishing Feature
Vitamin B12 deficiency Normal serum B12 levels in HIV myelopathy; elevated methylmalonic acid and homocysteine in B12 deficiency
Multiple sclerosis Absence of brain lesions on MRI in HIV myelopathy; presence of oligoclonal bands in CSF for MS
Syphilitic myelopathy Negative serum VDRL/RPR and CSF VDRL in HIV myelopathy; positive in syphilis
HTLV-1 associated myelopathy Negative HTLV-1 serology in HIV myelopathy; positive in HTLV-1 myelopathy
Spinal cord compression Normal spinal MRI in HIV myelopathy; visible compression on imaging in compressive myelopathy
Neuromyelitis optica Absence of optic neuritis in HIV myelopathy; presence of aquaporin-4 antibodies in NMO
Copper deficiency myelopathy Normal serum copper and ceruloplasmin levels in HIV myelopathy; low levels in copper deficiency
Primary progressive MS Slower progression and less severe disability in HIV myelopathy; more aggressive course in PPMS
Lyme disease Negative Lyme serology in HIV myelopathy; positive in Lyme disease
Radiation myelopathy No history of radiation exposure in HIV myelopathy; history of radiation therapy in radiation myelopathy