Muscle & nerve
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Clinically, phenol is used often as a neurolytic agent to treat pain and spasticity. The purpose of this study was to examine the time course of denervation and recovery in several hindlimb muscles following application of a 5% aqueous solution of phenol to the sciatic nerve. Phenol was applied to the sciatic nerve of adult female rats either by intraneural or perineural injection. ⋯ Following denervation, the soleus became slower in that all of the fibers expressed the slow myosin heavy chain (MHC). At 5 months, maximum tension of the soleus was 74% of control and the muscle consisted of more fast fibers on average, some of which expressed IIx MHC. These data suggest that 5% phenol causes an injury to the nerve that is more severe than a crush injury, and that reinnervation of denervated muscles may be by motoneurons other than those that originally innervated the muscles.
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Nondepolarizing neuromuscular blocking agents (NMBA) are being used with increasing frequency in critically ill patients. Recently, many centers have described patients with prolonged muscle weakness after long-term use of these agents, either alone or in combination with other agents or disorders. Brief weakness lasting several hours to several days is probably the result of prolonged neuromuscular blockade, while more prolonged weakness lasting several weeks to months is, in all likelihood, caused by a myopathy. ⋯ Muscle biopsy findings include atrophy of type I and type II fibers, myofiber necrosis, and selective loss of thick myofilaments. The myopathy is believed to be related to the prolonged use of NMBA either alone or in combination with other disorders or medications, particularly corticosteroids. The weakness experienced by these patients leads to additional respiratory compromise, difficulty weaning from the ventilator, and prolonged hospitalization.
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To determine which sensory nerve conduction studies (S-NCS) are helpful in detecting supraclavicular axon loss brachial plexopathies, we selected 53 cases (of 417 reviewed) in whom complicating factors were absent and which, by needle electrode examination findings, involved only a single "truncal" element (upper, middle, or lower) of the brachial plexus. Extensive S-NCS included: median, recording thumb (Med-D1), index (Med-D2), and middle fingers (Med-D3); ulnar, recording fifth finger (Uln-D5); dorsal ulnar cutaneous, recording dorsum of the hand (DUC); radial, recording base of thumb; and both medial and lateral antebrachial cutaneous (MABC, LABC), recording forearm. Except for the median sensory fibers, the "cord" elements traversed by the sensory fibers assessed during the S-NCS listed above are anatomically defined (i.e., the sensory fibers enter the brachial plexus at only one cord). ⋯ With upper trunk brachial plexopathies, in contrast, only the "uncommon" S-NCS (Med-D1; LABC) are consistently affected. The "routine" median S-NCS recording digit 2 (Med-D2) is far less reliable than the median S-NCS recording digit 1 (Med-D1) in detecting upper trunk axon loss brachial plexopathies. Additionally, the various pathways traversed by the fibers contributing to the individual S-NCS responses can be predicted, an important point when the full extent of a brachial plexus lesion is sought.
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Streptozotocin-induced diabetes mellitus is known to cause a reduction of both conduction velocity and axon caliber in sciatic nerves and also a decrease in muscle fiber size. The present study investigates whether the distal parts of the peripheral nervous system, including extra- and intrafusal muscle fibers, are more severely affected than the proximal segments in the diabetic state. Proximal and distal sensory nerve conduction velocities were monitored during a period of 3 months in rats rendered diabetic by injection of streptozotocin. ⋯ Fibers of the intrafusal nerve segments appeared to be equally affected compared to the fibers in the sciatic nerve, although no quantitative comparison was made. The increase of small caliber skeletal muscle fibers in experimental streptozotocin-induced diabetes was confirmed. These findings indicate that proximal and distal segments of peripheral nerves are affected equally in the early stages of experimental diabetic neuropathy.
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Case Reports
Prolonged paralysis due to nondepolarizing neuromuscular blocking agents and corticosteroids.
The long-term use of nondepolarizing neuromuscular blocking agents (ND-NMBA) has recently been implicated as a cause of prolonged muscle weakness, although the site of the lesion and the predisposing factors have been unclear. We report 3 patients (age 37-52 years) with acute respiratory insufficiency who developed prolonged weakness following the discontinuation of ND-NMBAs. Two patients also received intravenous corticosteroids. ⋯ A muscle biopsy in this patient showed loss of thick, myosin filaments. The weakness in these patients is due to pathology at both the neuromuscular junction (most likely due to ND-NMBA) and muscle (most likely due to corticosteroids). Hepatic dysfunction and acidosis are contributing risk factors.