Acute and subacute inflammatory demyelinating polyneuropathy

Acute and subacute inflammatory demyelinating polyneuropathy encompasses a group of immune-mediated disorders that attack the peripheral nervous system by damaging the myelin sheath — the protective insulating layer surrounding peripheral nerves. The acute form is widely known as Guillain-Barré syndrome (GBS), specifically the acute inflammatory demyelinating polyneuropathy (AIDP) variant, while the subacute form represents a clinical course that progresses over 4 to 8 weeks before stabilizing, bridging the gap between acute GBS and chronic inflammatory demyelinating polyneuropathy (CIDP). The condition typically presents with rapidly progressive, symmetrical muscle weakness that often begins in the legs and ascends to involve the arms, trunk, and sometimes the facial and respiratory muscles. Patients frequently experience tingling, numbness, and pain in the extremities, along with diminished or absent deep tendon reflexes (areflexia). Sensory symptoms such as paresthesias are common. In severe cases, respiratory failure may occur, requiring mechanical ventilation. Autonomic dysfunction — including blood pressure instability, cardiac arrhythmias, and bladder dysfunction — can also develop and may be life-threatening. The disease is often preceded by an infectious trigger, most commonly respiratory or gastrointestinal infections (notably Campylobacter jejuni), which is thought to provoke an aberrant autoimmune response through molecular mimicry. Diagnosis is supported by clinical findings, nerve conduction studies showing demyelinating features, and cerebrospinal fluid analysis revealing elevated protein with normal cell counts (albuminocytologic dissociation). Treatment includes intravenous immunoglobulin (IVIg) and plasma exchange (plasmapheresis), both of which have demonstrated efficacy in hastening recovery. Supportive care, including respiratory monitoring and rehabilitation, is essential. Most patients with the acute form recover substantially, though residual weakness and fatigue may persist in a proportion of cases. The subacute variant may require prolonged immunomodulatory therapy.

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