200 Section - An approach to Slimmer's palsy

A 22-year-old woman presented with a 4-month history of progressive weakness in her right lower leg leading to falls and mobility issues. Her habits included prolonged sitting, often in a cross-legged position. Additionally, familial disharmonies led her to episodes of depression, resulting in anorexia, anhedonia and weight reduction. Her Body Mass Index (BMI) measured at 20 kg/m². There was mild atrophy in her right leg. She struggled to stand on her right heel. The strength of her right toe extensors and foot evertors were diminished. The sciatic nerve stretch test was negative. Her investigations revealed iron deficiency anemia and axonopathy of right CPN with reduced sensory nerve action potential amplitude in superficial peroneal nerve. Other tests for spine MRI, blood sugar, inflammatory markers, thyroid function, vitamin B12, and folate were all normal.

Discussions:

The CPN is enveloped only by skin and subcutaneous tissue around the neck of the fibula. Significant weight loss results in superficial fat depletion, making it vulnerable to injury or compression, particularly from prolonged or cross-legged sitting. Peroneal palsy presents with sensory deficits and weakness in the toe extensors, ankle dorsiflexors, and foot evertors.

Treatment strategies includes short course steroid, vitamin B1,B12,B6 and pregabalin. Electrical stimulation therapy, avoiding prolonged or cross-legged sitting and a protective pad around the fibula are helpful. An ankle-foot orthosis and elbow crutch improves mobility. Nutritional guidance and weight gain goals are required. Psychiatric support is needed for depressive symptoms.

Conclusions:

Slimmer's palsy is considered once other common causes of CPN neuropathy have been ruled out. It often occurs following significant weight loss and subsequent nerve compression. Underlying causes for weight loss and nerve compressions should be focused along with rehabilitation process.