Acute non-alcoholic nutritional neuropathies in high-income countries - a systematic review

We determined the semiology, causes, risk factors and outcomes of patients with acute nutritional neuropathies requiring hospitalisation in high-income countries.

We searched PubMed, Cochrane Library and Embase for non-alcoholic malnutrition neuropathy cases published since 1990.

Thirty-six studies were identified, including 83 patients (mean age 39.8 years; 70% women) with deficient levels of thiamine (54%), pyridoxine (16%), copper (11%) or folate (7%). Common clinical signs were lower extremity weakness (100%), hypesthesia (63%), hypo-/areflexia (54%) and cranial nerve deficits (27%). Thirty-two (39%) patients also had Wernicke's encephalopathy. The mean time from symptom onset to hospitalisation was 4.2 weeks (range: 1-12). Ten (12.1%) patients required intensive care. Risk factors were weight loss (60%), vomiting (51%) and diarrhoea (11%). Aetiologies included bariatric surgery (n = 60, 72%), psychiatric disorders (n = 15, 18%) and hyperemesis gravidarum (n = 4, 5%). Electrophysiology showed axonal polyneuropathy in 60 (72.3%) patients, typically with sensorimotor involvement (n = 42). Besides nutritional supplements, 19 (23%) patients also received IVIG, plasmapheresis or steroids. Forty-nine patients had a one-year follow-up, with a good outcome (modified Rankin Scale Score ≤ 2) in 25 (51%).

Nutritional neuropathies may mimic axonal Guillain-Barré syndrome. Early recognition is crucial to avoid lasting deficits and unnecessary therapy like IVIG or plasmapheresis.