Arachnoiditis

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SPINAL ARACHNOIDITIS

Clinical syndrome

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

Causes

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

Systemic

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
1-Bromopropane (n-propyl bromide)
Konzo
Lathyrism
Zinc

Direct

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 & Neuropathy ⁵

General
- Disease presence: Dose related (> 4,000 rads)
- Disease onset: Weeks to Decades after treatment
- Weakness pattern: Asymmetric; Patchy
- EMG with nerve damage: Myokymia common
Clinical: 4 syndromes
- Sensory symptoms: Transient
  - Onset: 2 to 37 weeks after treatment
  - Lhermitte sign: Shock-like sensation after neck flexion
  - Course: Resolution common after 2 to 36 weeks
- Myelopathy: Chronic progressive
  - Onset: Mean 17 months after Rx; Range 3 months to Decades
  - Asymmetric; Brown-Séquard syndrome
  - Course: Progression over months
  - Treatment: ? Anticoagulation
  - Pathology: Vasculopathy; White matter > Grey
- Transverse myelopathy: Acute
- Amyotrophy +, Local
  - Lesion Locations
    - Spinal cord: Myelopathy
    - Radiculopathy
    - Plexopathy
      - Brachial
      - Lumbosacral
    - Neuropathy: Phrenic; Sciatic
  - Syndromes: Vary with onset timing
    - Early: < 6 Months after treatment
      - Pain: Common
      - MRI: T2 hyperintensity; Nerve large; Contrast +
      - Nerve pathology: Axon loss, patchy; Inflammation,Perivascular, Epineurial; Perineurium thick; Hemosiderin
      - Treatment: May improve incompletely with prednisone
      - May have monophasic course with improvement but not to normal
    - Chronic: Months to Decades after treatment
      - Pain: Some patients; Less severe
      - Progression: Slow
      - Nerve pathology: Axon loss; Epineurial vessel fibrosis

ELECTRICAL INJURY

Clinical
- Lesion location: Most often cervical
- Intensity
  - < 1,000 volts: Predominantly anterior horn cell damage
  - > 1,000 volts, or with burns near spinal cord: Lateral & posterior column damage
- Course
  - Acute: Associated encephalopathy
  - Progressive for few months or static
Pathology
- Perivascular & petechial hemorrhages

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

HEROIN TOXICITY

Myelopathy
Neuropathy
Rhabdomyolysis

General

Drug route: Intravenous; Intranasal

Myelopathy¹

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

Rhabdomyolysis

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

Neuropathy³

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

1-Bromopropane (n-propyl bromide) ⁴

Source: Solvent
- Substitute for ozone-depleting chloro-fluorocarbons
- Vapor & immersion degreasing operations
- Aerosol-applied adhesives.
- Dry cleaning: Substitute for perchloroethylene (tetrachloroethylene)
Epidemiology: US; Aerosol exposure
Clinical: Myelopathy+
- Onset: After exposure of 3 months to years; Ages 16 to 46 years
- Systemic: Headache; Dizziness
- Myelopathy
  - Spasticity: Legs
  - Gait disorder
  - Weakness: Legs
  - Reflexes
    - Tendon: Increased in legs
    - Plantar: Extensor
  - Sensory: Panmodal distal loss; Paresthesias & Pain
- CNS (50%): Reduced memory; Altered mood; Cognitive change
- Course: Partial improvement after exposure discontinued
Laboratory
- Serum Chloride & Bromide: High
- Nerve conduction testing: Normal or Borderline slow

Konzo ²

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

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References
1. Neurology 2000;55:316-317
2. Disability Rehabilitation 2001;23:731-736, Clinical Neurophysiology 2002;113:10–15
3. Journal of Peripheral Nervous System 2006;11:304–309
4. Clin Toxicol (Phila) 2007;45:270-276
5. Neurology 2023;101:e1455-e1460

2/4/2024