Polyneuropatiaa

Polyneuropatiaa is a disorder characterized by damage to multiple peripheral nerves, usually in a symmetric, distal-predominant pattern. It can be acutely or chronically progressive and may affect sensory, motor, and autonomic fibers.

Common causes include diabetes mellitus, nutritional deficiencies (notably vitamin B12), chronic alcohol use, toxins (such as certain chemotherapy agents and heavy metals), autoimmune neuropathies (CIDP), acute Guillain-Barré syndrome, infectious diseases (HIV, hepatitis C, Lyme disease), hereditary neuropathies (Charcot‑Marie‑Tooth), and kidney or liver disease.

Pathophysiology may involve axonal degeneration, demyelination, or both. The process is often length-dependent, with symptoms starting in the toes and fingers. Mechanisms are varied: metabolic, inflammatory, toxic, or immune-mediated.

Clinical features include numbness, tingling, or burning pain (sensory) and weakness with decreased reflexes (motor); autonomic symptoms such as orthostatic intolerance, abnormal sweating, or gastrointestinal issues may occur.

Diagnosis relies on history and examination, supported by nerve conduction studies and electromyography to distinguish axonal versus demyelinating forms. Laboratory tests screen for diabetes and glucose control, vitamin B12 and other deficiencies, thyroid disease, kidney and liver function, and infectious or inflammatory markers. Genetic testing is considered when hereditary neuropathy is suspected.

Management targets the underlying cause when possible and may include optimized glucose control, nutritional supplementation, cessation of toxin exposure, and immunotherapy for immune-mediated forms. Symptom management includes analgesics (e.g., anticonvulsants, antidepressants), physical therapy, and occupational therapy. Prognosis varies; some causes are reversible, while others are chronic or progressive.