From the Guidelines
Acute nutritional axonal neuropathy requires immediate treatment with thiamine supplementation, particularly in patients presenting with rapid weight loss, poor dietary intake, vomiting, alcohol abuse, oedema, or symptoms of neuropathy, without delay pending blood results. This condition is a nerve disorder caused by severe nutritional deficiencies that damage the axons, which are the parts of nerve cells that transmit signals. The typical development of this condition is from inadequate intake of essential vitamins, particularly B vitamins (B1/thiamine, B6/pyridoxine, B12/cobalamin), vitamin E, and copper.
- Key factors that contribute to the development of acute nutritional axonal neuropathy include:
- Inadequate dietary intake
- Alcohol abuse
- Rapid weight loss
- Vomiting
- Oedema
- Treatment involves immediate nutritional supplementation, with high-dose vitamin B complex, and patients should also receive a balanced diet rich in proteins, healthy fats, and micronutrients, as suggested by guidelines such as those from the British Obesity and Metabolic Surgery Society 1.
- In severe cases, hospitalization for intravenous supplementation may be necessary, and recovery can take months to years as nerves heal slowly.
- The condition is preventable through adequate nutrition, and those at risk (alcoholics, those with malabsorption disorders, or on restrictive diets) should be monitored closely, with a focus on preventing thiamine deficiency, as emphasized in the 2020 update of the British Obesity and Metabolic Surgery Society guidelines on perioperative and postoperative biochemical monitoring and micronutrient replacement for patients undergoing bariatric surgery 1.
From the Research
Definition and Causes of Acute Nutritional Axonal Neuropathy
- Acute nutritional axonal neuropathy (ANAN) is a severe axonal polyneuropathy that develops in patients with acute nutritional deficiency, often in the setting of alcoholism, bariatric surgery, or anorexia 2.
- The condition is characterized by sensory ataxia, areflexia, variable muscle weakness, poor nutritional status, and weight loss, often with prolonged vomiting and normal cerebrospinal fluid protein 2.
- Vitamin deficiencies, particularly thiamine and vitamin B6, are common in patients with ANAN 2, 3.
Clinical Spectrum and Prognosis
- The clinical spectrum of ANAN is wide, ranging from pure sensory neuropathy to pure motor neuropathy, and mixed sensorimotor axonal polyneuropathy 3.
- The prognosis of ANAN is guarded, with residual neuropathic pain and slow recovery of independent ambulation 3.
- Early recognition of patients at risk is important, and vitamin supplementation may serve as an effective therapeutic strategy 3, 4.
Role of Vitamins in Neuropathy
- Vitamin deficiency is a risk factor in the development of peripheral neuropathy, and vitamin supplementation may help alleviate symptoms 4, 5.
- Deficiencies of almost all vitamins are associated with diabetic neuropathy, and vitamin supplementation may serve as an effective therapeutic strategy 4.
- B-vitamins, particularly B12, have been shown to be associated with peripheral neuropathy, and treatment with B-vitamins may improve symptoms 5.
Nutritional Neuropathies
- Nutritional neuropathies are routinely encountered by practicing neurologists, and most are length-dependent, sensory axonopathies 6.
- Cobalamin deficiency neuropathy is an exception, often presenting with a non-length-dependent sensory neuropathy, and patients with cobalamin and copper deficiency neuropathy characteristically have concomitant myelopathy 6.
- Deficiencies occur in the context of malnutrition, malabsorption, increased nutrient loss, autoimmune conditions, and with certain drugs that inhibit nutrient absorption 6.