a neurodegenerative disease with upper and lower motor neuron dysfunction.

Epidemiology

  • Mean age of onset is 65 years.

Etiology


Pathophysiology

  • Classically affects the entire motor neuron system at two or more levels (both upper and lower motor neuron degeneration).
    • Upper motor neurons in the precentral gyrus and, frequently, prefrontal cortex
    • Lower motor neurons in the anterior horn of the spinal cord and brainstem
  • Pathology
    • UMN: degeneration & atrophy of lateral corticospinal tracts, precentral gyrus
    • LMN: degeneration of anterior horn (thin anterior roots) & cranial nerve motor nuclei
    • Muscle: denervation atrophy (angular fibers with crowded nuclei)

Clinical features

General disease characteristics

Early symptoms

  • Symptoms are highly variable and potentially non-specific (e.g., subtle vocal changes or difficulties grasping objects)
  • Asymmetric limb weakness, often beginning with weakness in the hands and feet
  • Bulbar symptoms such as dysarthria, dysphagia, and tongue atrophy (20% of cases at disease onset)
  • Pseudobulbar palsy with pseudobulbar affect may develop.
  • Fasciculations, cramps, and muscle stiffness
  • Weight loss
  • Split hand sign: a wasting pattern in which the muscles of the thenar eminence atrophy due to degeneration of the lateral portion of the anterior horn of the spinal cord

Late symptoms

  • Cognitive impairment (approx. 15% of ALS patients meet the criteria for frontotemporal dementia)
  • Autonomic symptoms (e.g., constipation, bladder dysfunction) may develop; the mechanism of development is unclear.
  • Life-threatening symptoms
    • Respiratory failure due to paralysis of respiratory muscles
    • Dysphagia due to bulbar weakness or pseudobulbar palsy

Diagnosis

  • Electromyography
    • Denervation: fibrillations, positive sharp waves, and large amplitudes
    • Fasciculations

Differential Diagnosis

  • Myasthenia gravis
    • Weakness improves with acetylcholinesterase inhibitors
    • No UMN or LMN signs

Treatment

  • Riluzole
    • A sodium-channel blocker that inhibits glutamate release in the CNS and decreases glutamate excitotoxicity
    • Prolongs survival and slows functional decline in patients with ALS (on average, for 3 months)
  • Edaravone
    • A free radical scavenger
    • Has been shown to slow functional decline in some patients with ALS