Most at-risk patients have a length-dependent, sensorimotor and an axonal-predominant neuropathy; unfortunately, most do not regain independent ambulation.

Neuropathies associated with nutritional deficiencies are commonly encountered by neurologists and general practitioners. To study associated factors, investigators retrospectively identified 40 patients (age range, 16 to 72 years; 83% female) with new-onset nutritional neuropathy and poor oral intake and weight loss. Risk factors included alcohol use disorder, bariatric surgery, dietary modification, gastrointestinal disturbance and eating disorders. The most common deficiencies were vitamin B1, vitamin B6 and folate. Vitamin E, copper and vitamin B12 levels were normal in most. Two-thirds of patients required hospitalisation. Only one patient had abnormal cerebrospinal fluid (elevated protein). Associated conditions included Wernicke encephalopathy (18%), optic atrophy (10%) and myopathy (10%).

Most patients (23/40) presented with a symmetric, length-dependent polyneuropathy with distal weakness, large- and small-fibre sensory loss and greater leg than arm hyporeflexia. An additional 14 patients had features of a symmetric, length-dependent sensory polyneuropathy, and three patients had a length-dependent motor neuropathy. Neuropathy type was not associated with a particular vitamin deficiency. Motor physiology was predominantly axonal, and needle electromyography showed distal-predominant denervation.

Only 35% could walk independently at follow up (mean, 22 months). All patients with pure motor involvement, and only one of 12 with sensory neuropathy, regained independent ambulation.

Just one of 12 patients who received intravenous immunoglobulin or corticosteroid treatment for presumed immune-mediated neuropathy regained the ability to walk independently. Most required pain medications.

Comment: Patients screened and treated earlier by outpatient doctors, and those with small-fibre neuropathies, may not have been identified due to selection bias. However, education on risk factors and prompt recognition and treatment are mandatory in preventing potentially irreversible disability from nutritional neuropathies. The pathogenic role of direct toxic effects of alcohol and the interaction with other key mediators such as genetic predisposition, are unknown. Besides vitamin supplementation, other targets for nerve repair are needed.

Leana Doherty, MD, Assistant Professor, Department of Neurology, University of Pittsburgh Medical Center, Pittsburgh, USA.

Hamel JI, Logigian EL. Clinical spectrum and prognosis in patients with acute nutritional axonal neuropathy. Neurology 2023 Mar 27; e-pub (https://doi. org/10.1212/WNL.0000000000207215).

This summary is taken from the following Journal Watch title: Neurology.