Lower‐Limb‐Predominant Axonal Sensorimotor Polyneuropathy With Severe Proximal Weakness and Possible Myopathic Involvement After Sleeve Gastrectomy: A Case Report of Delayed Recognition

ABSTRACT Bariatric surgery is increasingly performed in adolescents and young adults. Although sleeve gastrectomy preserves intestinal continuity and is often regarded as nutritionally low‐risk, it can still precipitate micronutrient deficiency, and obesity itself predisposes to thiamine deficiency, which can cause both Wernicke encephalopathy and a peripheral neuropathy. Peripheral neuromuscular complications after sleeve gastrectomy are less well characterized than those after malabsorptive procedures. An 18‐year‐old woman with class II obesity (body‐mass index 39.2 kg/m 2 ) underwent laparoscopic sleeve gastrectomy and, about 10 weeks later, developed progressive lower‐limb weakness, distal paresthesiae, myalgia, cognitive fatigue, and loss of independent ambulation, with rapid weight loss (30 kg in three months) but no vomiting and no structured supplementation. Early nerve‐conduction studies were non‐diagnostic, and the presentation was attributed to a functional disorder, for which olanzapine was started; specialist reassessment was delayed until after objective progression. Repeat studies showed a lower‐limb‐predominant axonal sensorimotor polyneuropathy with preserved tibial and upper‐limb responses and no demyelinating features. The decisive finding was a discrepancy: Medical Research Council grade 1/5 proximal weakness out of proportion to the modest distal axonal loss, pointing to an unlocalized proximal process—lumbosacral radiculoplexus neuropathy or myopathy—for which needle electromyography of proximal and paraspinal muscles was the highest‐yield missing test. Vitamin B12, creatine kinase, and albumin were normal; thiamine, the wider micronutrient panel, and cerebrospinal fluid were never obtained. After rehabilitation, without documented micronutrient repletion, strength recovered to grade 3/5, and assisted walking returned. Nutritional deficiency was suspected but neither confirmed nor treated, so the etiology remains unresolved. The transferable lesson is diagnostic: severe neuromuscular injury can evolve within weeks of a restrictive procedure, nondiagnostic early tests do not exclude it, and objective signs should override a functional label.

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Journal
Clinical Case Reports
Published
2026-10-30
DOI
https://doi.org/10.1002/ccr3.73813
Primary Topic
Peripheral Neuropathies and Disorders
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article

Lower‐Limb‐Predominant Axonal Sensorimotor Polyneuropathy With Severe Proximal Weakness and Possible Myopathic Involvement After Sleeve Gastrectomy: A Case Report of Delayed Recognition

Erand Llanaj, Altin Kuqo, Floreta Kurti
Clinical Case Reports
Peripheral Neuropathies and Disorders
article

Lower‐Limb‐Predominant Axonal Sensorimotor Polyneuropathy With Severe Proximal Weakness and Possible Myopathic Involvement After Sleeve Gastrectomy: A Case Report of Delayed Recognition

Erand Llanaj, Altin Kuqo, Floreta Kurti
article en

Abstract

ABSTRACT Bariatric surgery is increasingly performed in adolescents and young adults. Although sleeve gastrectomy preserves intestinal continuity and is often regarded as nutritionally low‐risk, it can still precipitate micronutrient deficiency, and obesity itself predisposes to thiamine deficiency, which can cause both Wernicke encephalopathy and a peripheral neuropathy. Peripheral neuromuscular complications after sleeve gastrectomy are less well characterized than those after malabsorptive procedures. An 18‐year‐old woman with class II obesity (body‐mass index 39.2 kg/m 2 ) underwent laparoscopic sleeve gastrectomy and, about 10 weeks later, developed progressive lower‐limb weakness, distal paresthesiae, myalgia, cognitive fatigue, and loss of independent ambulation, with rapid weight loss (30 kg in three months) but no vomiting and no structured supplementation. Early nerve‐conduction studies were non‐diagnostic, and the presentation was attributed to a functional disorder, for which olanzapine was started; specialist reassessment was delayed until after objective progression. Repeat studies showed a lower‐limb‐predominant axonal sensorimotor polyneuropathy with preserved tibial and upper‐limb responses and no demyelinating features. The decisive finding was a discrepancy: Medical Research Council grade 1/5 proximal weakness out of proportion to the modest distal axonal loss, pointing to an unlocalized proximal process—lumbosacral radiculoplexus neuropathy or myopathy—for which needle electromyography of proximal and paraspinal muscles was the highest‐yield missing test. Vitamin B12, creatine kinase, and albumin were normal; thiamine, the wider micronutrient panel, and cerebrospinal fluid were never obtained. After rehabilitation, without documented micronutrient repletion, strength recovered to grade 3/5, and assisted walking returned. Nutritional deficiency was suspected but neither confirmed nor treated, so the etiology remains unresolved. The transferable lesson is diagnostic: severe neuromuscular injury can evolve within weeks of a restrictive procedure, nondiagnostic early tests do not exclude it, and objective signs should override a functional label.

Clinical Case ReportsVol. 14(11)
University of Medicine Tirana (AL), Bielefeld University (DE), Mother Teresa Hospital (AL)
Good health and well-being
Openalex Percentile: Top 14%
Peripheral Neuropathies and Disorders
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