0071643192.pdf

PATHOPHYSIOLOGY

■ Antecedent illness (viral or Campylobacter jejunigastroenteritis, URI) →
autoimmune response →damage to myelin sheath →symptoms.

SYMPTOMS/EXAM

■ Antecedent illness followed by latent period of days to weeks
■ Classic presentation is ascending symmetric paresthesias and motor
weaknesswith peak symptoms within 3 weeks of onset.
■ Relatively acute onset
■ Decreased deep tendon reflexes
■ Variable sensory loss
■ Normal rectal tone
■ May progress to ventilatory failure
■ Less common findings (seen in half of patients):
■ Autonomic dysfunction (eg, urinary retention)
■ Cranial nerve involvement (including 7th nerve palsy)

DIFFERENTIAL

■ Tick paralysis (examine thoroughly for ticks)
■ Lyme disease

DIAGNOSIS

■ Suspect based on clinical presentation.
■ Electrodiagnostic testing
■ Cerebrospinal fluid analysis
■ Classic picture = markedly elevated protein with up to 100 lymphocytes/ μL.
■ Often normal, when early

NEUROLOGY

TABLE 15.15. Grouping of Neuromuscular Disorders Based on Location of Pathology

LOCATION OFPATHOLOGY COMMONDISEASES

Anterior horn cells Spinal muscular atrophies

Peripheral nerve Demyelinating polyneuropathies (eg, Guillain-Barré syndrome, diphtheria)

Distal symmetric polyneuropathies (eg, diabetic, alcoholic)

Radiculopathies and plexopathies (eg, brachial plexopathy)

Mononeuropathies (eg, Saturday night palsy)

Mononeuropathy multiplex

Amyotrophic lateral sclerosis

Neuromuscular junction Myasthenia gravis

Lambert-Eaton myasthenic syndrome

Botulism

Tick paralysis

Skeletal muscle Myopathies

Muscular dystrophies

Periodic paralysis

The classic CSF finding in GBS

is a markedly elevated

protein with up to

100 lymphocytes/uL.