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SPINAL ARACHNOIDITIS

• Pain: Low back & radiating down both legs
• Weakness: One or multiple lumbar or sacral root distribution
• Sensory loss: One or multiple lumbar or sacral root distribution

• Spinal surgery: Especially multiple
• Chemical
  • Oil based radiographic contrast agents
  • Spinal drugs: Anesthetics; Steroids; Amphotericin B; Methotrexate
• Infections: Tuberculosis; Cryptococcosis; Syphilis; Viral
• Trauma: Vertebral injuries; Disc herniation
• Spinal subarachnoid hemorrhage

TOXIC MYELOPATHIES

• Organophosphates: TOCP
  • Source: Contaminants in cooking oil or flour; Alcohol substitute
  • Myelopathy & Polyneuropathy
  • Pathology: Distal axonal degeneration: CNS & PNS
• Iodochlorhydroxyquinoline (Clioquinol)
• Nitrous oxide
• Substance abuse
  • Heroin; ? Cocaine
  • Anterior spinal artery syndrome
• Hexacarbons: Occasional delayed myelopathy
• Muzolimine
  • Use: Diuretic
  • Toxicity especially with renal insufficiency
  • Myelopathy
  • Polyneuropathy: Demyelination
• Konzo
• Lathyrism
• Zinc

• Angiographic contrast agents
• Myelographic contrast agents
  • Acute onset spinal cord irritability: Often transient
  • Arachnoiditis
• Chymopapain: Used to treat herniated discs
• Spinal anesthesia: ? direct toxic vs. vascular
• Chemotherapeutic agents: Methotrexate; Cytosine arabinoside
  • Often in patients treated with both systemic & intrathecal drugs
  • Onset: Acute (Hours) to Subacute
  • Risk increased
    • More frequent treatments;
    • High cumulative dose
    • Concurrent methotrexate & cytarabine
    • Spinal radiotherapy
  • Pathology: 2 types
    • Spinal white matter: Peripheral cord; Lateral & posterior funiculi
    • Grey matter lesions
• Amphoterecin B
  • Focal myelopathy
  • Diffuse radiculopathy

RADIATION MYELOPATHY

• Transient sensory symptoms
  • Onset: 2 to 37 weeks after treatment
  • Lhermitte sign: Shock-like sensation after neck flexion
  • Course: resolution after 2 to 36 weeks
• Chronic progressive myelopathy
  • Onset: Mean 17 months after Rx; Range 3 months to 5 years
  • Asymmetric; Brown-Séquard syndrome
  • Course: Progression over months
  • Treatment: ? Anticoagulation
  • Pathology: Vasculopathy; White matter > Grey
• Acute transverse myelopathy
• Local amyotrophy: ? spinal lesion vs. radiculopathy

ELECTRICAL INJURY

• Most often cervical
• < 1,000 volts: Predominantly anterior horn cell damage
• > 1,000 volts, or with burns near spinal cord: Lateral & posterior column damage
• Acutely: Associated encephalopathy
• Course: Progressive for few months or static

• Perivascular & petechial hemorrhages

Heroin myelopathy Increased T2 signal (Arrow) in cervical spinal cord

HEROIN TOXICITY

• Drug route: Intravenous; Intranasal

• Onset
  • Acute, within hours after drug administration, after awakening from sleep
  • Often related to single dose after period of abstinence
• Spinal cord syndrome
  • Weakness: Paraplegia or Quadriplegia
  • Tendon reflexes: Reduced or absent
  • Urinary retention
  • Prominent recovery may occur over weeks to months
• Laboratory
  • CSF: Usually normal, Occasional pleocytosis or increased protein
  • MRI: Transverse myelitis-like findings
    • T2 imaging: Cord swelling; Enhancement, patchy, over several levels
    • Gadolinium enhancement: Acute
• Mechanism of disease: ? Hypersensitivity
• Treatment: ? Corticosteroids; Plasma Exchange

• Several mechanisms of drug-toxin related rhabdomyolysis
  • Direct muscle toxicity
  • Adulterants (Quinine)
  • Compression: ? Most common for heroin
    • Inactivity for long period: Prolonged compression
    • Compartment syndromes
      • Leg: Gluteal
        • Associated with sciatic or lumbo-sacral plexus palsy
      • Arm: Associated with brachial plexus, especially upper, lesions
  • Ischemic necrosis due to direct arterial injection: Common mechanism for tamazepam
  • Exacerbating factors: Dehydration; Poor nutrition
• Heroin-associated rhabdomyolysis may occur in association with acute myelopathy

• Local involvement: Compressive neuropathy
• Non-compressive neuropathy
  • Onset
    • Time: 3 to 36 hours after heroin administration
    • Progression: Acute
  • Patient age: 22 to 42 years
  • Clinical syndromes
    • Plexopathy
      • Onset: Pain; Allodynia
      • Weakness: Distribution
        • Lumbosacral or Brachial
        • Proximal
        • Single extremity
        • Asymmetric
      • Course
        • Persistent proximal weakness
        • Pain resolution over months
    • Sensory-Motor Neuropathy
      • Onset: Acute
      • Clinical
        • Symmetric
        • Distal
        • Legs > Arms
  • Course: Mild or no improvement
  • Electrophysiology: Axon loss
  • Nerve pathology: Axon loss
  • Associated syndrome: Rhabdomyolysis

Iodochlorhydroxyquinoline (Clioquinol) Myelopathy

• Source: Used as anti-diarrheal drug
• Epidemiology: Predominantly in Japan
• Clinical features
  • Myelopathy
    • Dose: Oral intake of 2 g/day for >3 weeks
    • Onset: Numbness & pain in legs
    • Clinical
      • Sensation loss: Especially vibration
      • Hyperesthesia
      • Leg weakness & stiffness (50%)
  • ± Optic neuropathy: Especially children
  • Course: Rapid onset; Slow recovery

Konzo²

• Epidemiology
  • Poor rural communities in Africa: Zaire, Mozambique, Tanzania & Central African Republic
  • Epidemics: Occur during dry season, especially in drought years
  • High risk: Women of child-bearing age; Children 3-13 years old
  • Lower risk: Men; Breast-fed children
  • Familial clustering
• Etiology
  • Probable cyanide toxicity
  • Source: Cassava plant (Manihot esculenta esculenta)
    • Consumption of food processed from starchy roots
    • Roots have high cyanide levels: Patients exposed with poor removal of toxin during processing
    • Higher risk: Protein-deficient diet with low intake of sulphur amino acids
      • Sulphur substrates needed for conversion (detoxification) of cyanide to thiocyanate
• Onset
  • Sudden: Less than 1 day
  • Leg weakness
  • Occasional: Low back pain; Paresthesias
• Clinical
  • Spasticity: Paraparesis or Tetraparesis
    • Legs > Arms
    • Symmetric
    • Hip adductor spasms
    • Hands: Reduced fine movements
    • Tendon reflexes: Brisk
    • Plantar responses: Extensor
    • Strength: May be normal in spastic extremities
    • Course
      • Partial improvement over months
      • Then permanent & Non-progressive gait disability
      • Occasional patients with 2nd exacerbation
      • Contractures
  • Other transient features: May persist in severe cases
    • Eye: Blurred vision; Nystagmus
    • Speech difficulties: Spasticity
  • Normal: Mental status; Hearing; Sensation; Bladder, Bowel & Sexual functions
• Laboratory
  • Somatosensory evoked potentials: Prolonged cortical responses & central sensory delay