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556 - Vitamin Deficiency Neuropathy

Friday, February 28, 2025

5:00 PM - 6:30 PM MST

Presenting Author(s)

MS

Mollie Schear, MS

Medical Student
Touro College of Osteopathic Medicine
New York, New York, United States

Corresponding Author(s)

Laura J. Malmut, MD

Medical Director of Transplant Rehabilitation, Assistant Professor, Associate Clerkship Director
MedStar National Rehabilitation Hospital and Georgetown University School of Medicine
Washington, District of Columbia, United States

Co-Author(s)

KP

Kelly Pellegrino, MD

Resident Doctor
MedStar National Rehabilitation Hospital
Washington, District of Columbia, United States

Case Diagnosis: Peripheral neuropathy

Case Description: A 45-year-old female with a history of alcohol use disorder, anxiety, and depression presented with neuropathic pain, gait instability, and weight loss. Physical examination showed length-dependent weakness, numbness, and hyporeflexia. She was diagnosed with alcoholic neuropathy and discharged to an inpatient rehabilitation facility for comprehensive care. Additional workup revealed vitamin E deficiency with low levels of vitamin D and vitamin A. She was started on nutritional supplementation and her symptoms improved with gabapentin and nortriptyline. She was referred to gastroenterology for evaluation of fat-soluble vitamin deficiency.

Discussions: Alcoholic neuropathy is caused by chronic alcohol consumption and presents with pain, numbness, tingling, and weakness. It results from a combination of direct alcohol-induced nerve damage, oxidative stress, and metabolic disturbances. It is a diagnosis of exclusion and may coexist with other causes of neuropathy. This patient was found to concomitantly have vitamin E deficiency, which presents with hyporeflexia, impaired vibratory sensation, ataxia, and weakness. Symptoms of vitamin E neuropathy overlap with those of alcoholic neuropathy and necessitates high suspicion for other contributing factors when considering alcoholic neuropathy. In North America, vitamin E deficiency is unlikely to occur due to diet and often stems from fat malabsorption or genetic disorders. Patients with suspected cases of vitamin E neuropathy should receive a full neurologic workup and evaluation for other deficiencies. Treatment involves dietary management, nutritional supplementation, and addressing the underlying cause. Rehabilitation is recommended if neuropathy affects ADLs.

Conclusions: Peripheral neuropathy is common and has various etiologies. Alcoholic neuropathy is a diagnosis of exclusion and may overlap with other causes of neuropathy. When vitamin E deficiency is identified, clinicians should evaluate for deficiencies in other fat-soluble vitamins. Proper diagnosis of the underlying cause is essential for effective management.