ArticleCureus2026
Necrotizing Myopathy Presenting With Guillain-Barré-Like Areflexic Paraparesis, Severe Rhabdomyolysis, and Dialysis-Requiring Acute Kidney Injury.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Necrotizing myopathy typically presents with subacute symmetric proximal weakness and marked creatine kinase elevation. Acute areflexic paraparesis with sensory abnormalities may instead suggest Guillain-Barré syndrome and create uncertainty regarding neuromuscular localization. A man in his 50s presented after collapse with abrupt bilateral lower-extremity paralysis. Examination demonstrated 0/5 strength across proximal and distal lower-extremity muscle groups, marked rigidity and hypercontracture, areflexia, and sensory impairment, with preserved upper-extremity function. Early laboratory abnormalities included serum sodium 164 mmol/L, potassium peaking at 6.5 mmol/L, creatinine 4.96 mg/dL, blood urea nitrogen 194 mg/dL, creatine kinase greater than 60,000 IU/L, and marked aminotransferase elevations. Lumbar puncture on hospital day (HD) 3 showed cerebrospinal fluid protein 70 mg/dL, glucose 66 mg/dL, and fewer than one nucleated cell/mm3. Guillain-Barré syndrome remained an early consideration; intravenous immunoglobulin was administered, and hemodialysis was initiated for severe hyperkalemia in the setting of acute renal failure. Inpatient electromyography and nerve conduction studies were unavailable; therefore, a concurrent neuropathic process could neither be confirmed nor excluded. Bilateral thigh magnetic resonance imaging demonstrated diffuse intramuscular edema, and right-thigh biopsy subsequently established a necrotizing myopathic pattern with frequent necrotic and regenerating myofibers and sparse inflammation. The biopsy pattern was etiologically nonspecific, and the underlying cause remained unresolved. This case illustrates that areflexia and cerebrospinal fluid albuminocytologic dissociation should not override substantial biochemical, radiographic, and histopathologic evidence of muscle injury. In patients with acute paralysis and massive creatine kinase elevation, neuropathic and myopathic processes should be evaluated in parallel.
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