1543 - Axonal Neuropathy Linked to Nutritional Deficiency

Thursday, February 19, 2026

5:00 PM - 6:30 PM AST

Presenting Author(s)

KS

Kush H. Shah, DO

Resident
UPMC Community Osteopathic
Kendall Park, New Jersey, United States

Co-Author(s)

AA

Alexis Aiman, DO

Fellow
UPMC Community Osteopathic
Harrisburg, Pennsylvania, United States
MB

Micheal Bishara, DO

Resident
UPMC Community Osteopathic
Harrisburg, Pennsylvania, United States
AB

Aaron Barasch, DO

Associate Program Director
UPMC Community Osteopathic
Harrisburg, Pennsylvania, United States

Submitter(s)

ks

kush H. shah, DO

UPMC Community Osteopathic
Kendall Park, New Jersey, United States

Case Diagnosis: Axonal neuropathy secondary to nutritional deficiency

Case Description: A 53-year-old female with a history of chronic pancreatitis post-Whipple surgery (2014), and fatty liver disease from alcohol abuse presented from an acute rehab facility due to worsening hallucinations and edema. Exam revealed significant muscle weakness in the neck, deltoids, triceps, ankle movements, and hip flexors. Sensation was decreased in the feet, and vibration sense was reduced in the toes. Coarse fasciculations were observed in the left deltoid, biceps, and triceps, along with absent Achilles reflexes bilaterally. EMG showed moderately severe generalized sensorimotor axonal peripheral neuropathy, with no radiculopathy in the left extremities. Labs indicated normal cobalamin, folic acid, and iron but deficiencies in zinc, copper, selenium, niacin, and undetectable vitamin D (7 ng/mL).

Discussions:

This case highlights the importance of vitamin D in peripheral nerve health and the consequences of its deficiency. The patient's vitamin D level of 7 ng/mL strongly correlates with her symptoms of pain, weakness, and fatigue. Severe vitamin D deficiency impairs calcium homeostasis and nerve conduction, causing neuronal damage, inflammation, and neuropathic symptoms. Previous literature has shown drastic improvements in axial neuropathy when patients are started on Vitamin D supplementation.

This case also highlights how EMG testing can differentiate between axonal and demyelination neuropathy. This can impact rehabilitation strategies as axonal injuries often benefit from targeted strength training and neuromuscular re-education, while demyelinating conditions prioritize proprioceptive retraining and balance-focused therapy. Nerve conduction studies in this case revealed the presence of reduced conduction velocities and f-wave latencies in this patient. Thus, help confirm the diagnosis of axonal sensorimotor polyneuropathy.

Conclusions:

EMG was an instrumental diagnostic tool in this case by confirming sensorimotor axonal peripheral neuropathy that can help guide diagnostic and rehabilitation planning. This case also highlights the role of nutritional deficiencies as a reversible yet often overlooked cause of peripheral neuropathy.