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DDx of Rapidly progressive limb weakness

DDx of Acute Peripheral Neuropathy
  • Guillain–Barré syndrome is the likely diagnosis in the majority of patients. 
  • Other consideration includes:
    • V
      • vasculitic neuropathy (check erythrocyte sedimentation rate); 
    • I
      • diphtheria (early oropharyngeal disturbances); 
      • Lyme polyradiculitis and other tick-borne paralyses; 
      • poliomyelitis (fever and meningismus common); 
      • West Nile virus; 
      • CMV polyradiculitis (in immunocompromised patients); 
      • poisonings with organophosphates, thallium, or arsenic; 
      • paralytic shellfish poisoning; or 
      • severe hypophosphatemia (rare).

    • T
      • neuromuscular junction disorders such as myasthenia gravis and botulism (pupillary reactivity lost early); 

    • M
      • beriberi, 
      • toxic neuropathy,
      • neuromuscular junction disorders such as myasthenia gravis and botulism (pupillary reactivity lost early); 
    • I
      • acute myelopathies (especially with prolonged back pain and sphincter disturbances); 
      • critical illness neuropathy or myopathy; 
    • N
    • C
  • Ref
  • A common misconception holds that there should always be albuminocytologic dissociation. However, albuminocytologic dissociation is present in no more than 50% of patients with the Guillain–Barré syndrome during the first week of illness, although this percentage increases to 75% in the third week.  Some patients with human immunodeficiency virus infection and the Guillain–Barré syndrome have pleocytosis. 
  • mono phasic course and typically does not recur; but two or more episodes have been reported in 7% of patients
  • Although hyporef lexia or areflexia is a hallmark of the Guillain–Barré syndrome, 10% of patients have normal or brisk reflexes during the course of the illness. Thus, the possibility of the Guillain–Barré syndrome should not be excluded in a patient with normal or brisk reflexes if all other features are supportive of the diagnosis 
  • Clinical deterioration after initial improvement or stabilization with immunotherapy suggests that the treatment had a transient effect or that chronic inflammatory demyelinating polyneuropathy is present 
  • The presence of distal paresthesia increases the likelihood that the correct diagnosis is the Guillain–Barré syndrome. If sensory involvement is absent, disorders such as poliomyelitis, myasthenia gravis, electrolyte disturbance, botulism, or acute myopathy should be considered. Hypokalemia shares some features with the Guillain–Barré syndrome but is commonly overlooked in the differential diagnosis. In patients with acute myopathy, tendon jerks are preserved and serum creatine kinase levels are increased. If paralysis develops abruptly and urinary retention is prominent, magnetic resonance imaging of the spine should be considered, to rule out a compressive lesion. 
  • Ref