Muscle & nerve
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Six patients with chronic pain, mechanical and thermal hyperalgesia/allodynia, and cutaneous vasodilatation starting distally in their extremities, were evaluated using clinical and neurophysiological methods and microneurography. Evidence of small-fiber polyneuropathy was documented in all, but the etiology remained cryptogenic in several. ⋯ The clinical and electrophysiological profiles of these patients resemble the experimental syndrome evoked by application of capsaicin to the skin. This similarity, and the striking heat dependence of the spontaneous pain, suggest that a common feature may be altered expression or modulation of vanilloid 1 receptor, provoking abnormal nociceptor discharges.
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Review Comparative Study
Comparing the function of the corticospinal system in different species: organizational differences for motor specialization?
An appreciation of the comparative functions of the corticospinal tract is of direct relevance to the understanding of how results from animal models can advance knowledge of the human motor system and its disorders. Two critical functions of the corticospinal tract are discussed: first, the role of descending projections to the dorsal horn in the control of sensory afferent input, and second, the capacity of direct cortico-motoneuronal projections to support voluntary execution of skilled hand and finger movements. We stress that there are some important differences in corticospinal projections from different cortical regions within a particular species and that these projections support different functions. ⋯ Insights into corticospinal function in different animal models are of direct relevance to understanding the human motor system, providing they are interpreted in relation to the functions they underpin in a given model. Studies in non-human primates will continue to be needed for understanding special features of the human motor system, including feed-forward control of skilled hand movements. These movements are often particularly vulnerable to neurological disease, including stroke, cerebral palsy, movement disorders, spinal injury, and motor neuron disease.
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Published databases of quantitative sensory testing (QST) for sensory thresholds provide a means for detecting deficits of the thermonociceptive sensory nervous system. These databases, however, do not assist in the assessment of neuropathic pain, which is characterized by pain or hyperalgesia, or both. We utilized the method of levels for innocuous thermal stimuli, warm and cool, and the method of limits for noxious thermal stimuli, hot pain and cold pain, to determine QST thresholds. ⋯ Thresholds for innocuous and noxious stimuli in this study were similar to previously published results. The mean pain rating across all sites at thresholds for noxious heat and cold stimuli was 4.10, as rated on a 0-10 numeric scale. Suggestions are provided for combining threshold information for innocuous and noxious stimuli and related pain ratings for the evaluation of sensory nervous system function and, specifically, neuropathic pain.
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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.