Muscle & nerve
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The pathophysiology of oxaliplatin-induced neurotoxicity remains unclear, although in vitro studies suggest involvement of voltage-gated Na+ channels. In the present study, clinical assessment was combined with nerve conduction studies (NCS) and nerve excitability studies in 16 patients after completion of oxaliplatin therapy. Chronic neuropathic symptoms persisted in 50% of patients. ⋯ Refractoriness was significantly greater in patients (symptomatic group, 56.3 +/- 24.9%; entire patient group, 46.3 +/- 12.5%; controls, 27.1 +/- 1.9%; P < 0.05). Thus, although positive sensory symptoms of oxaliplatin-induced neuropathy improved, negative sensory symptoms and abnormalities of sensory nerve conduction persisted. Differences in nerve excitability measures, particularly refractoriness, support in vitro studies indicating involvement of voltage-gated transient Na+-channel dysfunction in the development of oxaliplatin-induced neurotoxicity.
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Case Reports
Acute exertional compartment syndrome in the setting of anabolic steroids: an unusual cause of bilateral footdrop.
Acute exertional compartment syndrome is the result of muscle ischemia within a tight fascial compartment. We report a 22-year-old boxer, with recent intake of anabolic steroids, who developed acute exertional compartment syndrome of the lower legs following an assault from which he had to run away. ⋯ Nerve conduction studies (NCS) and electromyography (EMG) were consistent with bilateral deep and superficial peroneal neuropathies, but magnetic resonance imaging (MRI) demonstrated hemorrhagic necrosis of the pretibial muscles. This case illustrates that the differential diagnosis for footdrop includes not only central and peripheral nervous system and muscle causes, but also compartment syndromes.