Skeletal muscle dysfunction

Skeletal muscle dysfunction can cause myalgia, bone pain, weakness, and potentially fatal rhabdomyolysis. Respiratory muscle weakness and diaphragmatic contractile dysfunction can cause acute respiratory failure. 

Myoadenylate deaminase (or AMP deaminase) deficiency is a relatively benign muscle disorder characterized by fatigue and exercise-induced muscle aches. This disorder is presumably inherited as an autosomal recessive trait. The relationship between the exercise-induced skeletal muscle dysfunction and AMP deaminase deficiency is explained by an interruption of the purine nucleotide cycle. 

Symptoms of cardiac or skeletal muscle dysfunction pose problems, particularly for patients with long-chain fatty acid oxidation disorders. 

Exercise limitation and functional disability in COPD have a complex, multifactorial basis. Ventilatory limitation is caused by increased airways resistance, static and dynamic hyperinflation, increased elastic load to breathing, gas exchange disturbances, and mechanical disadvantage and/or weakness of the respiratory muscles (4-6). Car-diocirculatory disturbances (7,8), nutritional factors (9), and psychological factors, such as anxiety and fear, also contribute commonly to exercise intolerance. Skeletal muscle dysfunction is characterized by reductions in muscle mass (10,11), atrophy of type I (slow twitch, oxidative, endurance) (12,13) and type Ila (fast twitch) muscle fibers (14), altered myosin heavy chain expression (15), as well as reductions in fiber capillarization (16) and oxidative enzyme capacity (17,18). Such a dysfunction is another key factor that contributes... 

American Thoracic Society/European Respiratory Society. Skeletal muscle dysfunction in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999 159 S1-S40. 

Autoantibodies are directed against nicotinic acetylcholine receptors in myasthenia gravis, resulting in receptor loss, skeletal muscle paralysis, and dysfunction (100). In addition, antibodies directed against voltage-gated Ca " channels produce similar neuromuscular dysfunction of Lambert-Eaton... 

HMG-CoA REDUCTASE INHIBITORS AND FlBRIC ACID DERIVATIVES. The antihyperlipidemic drugp, particularly die HMG-CoA reductase inhibitors, have been associated with skeletal muscle effects leading to rhab-domyolysis. Rhabdomyolysis is a very rare condition in which muscle damage results in die release of muscle cell contents into die bloodstream. Rhabdomyolysis may precipitate renal dysfunction or acute renal failure The nurse is alert for unexplained muscle pain, muscle tenderness, or weakness, especially if tiiey are accompanied by malaise or fever. These symptoms should be reported to die primary health care provider because the drug may be discontinued. 

Birch-Machin, M.A., Jackson, S., Singh Kler, R.S., Turnbull, D.M. (1993). Smdy of skeletal muscle mitochondrial dysfunction. Methods Toxicol. 2, 51-69. 

Measuring muscle-evoked responses to repetitive motor nerve electrical stimulation permits detection of presyn-aptic neuromuscular junction dysfunction. In botulism and the Lambert-Eaton syndrome, repetitive stimulation elicits a smaller than normal skeletal muscle response at the beginning of the stimulus train, due to impaired initial release of acetylcholine-containing vesicles from presyn-aptic terminals of motor neurons followed by a normal or accentuated incremental muscle response during repeated stimulation. This incremental response to repetitive stimulation in presynaptic neuromuscular disorders can be distinguished from the decremental response that characterizes autoimmune myasthenia gravis, which affects the postsynaptic component of neuromuscular junctions. 

Physical therapists may encounter the use of local anesthetics in several patient situations because of their various clinical applications. For example, therapists may be directly involved in the topical or transdermal administration of local anesthetics. As discussed earlier, repeated topical application of local anesthetics may help produce long-term improvements in motor function in patients with skeletal muscle hypertonicity, so therapists may want to consider incorporating topical anesthetics into the treatment of certain patients with CNS dysfunction. Therapists may also administer local anesthetics transdermally, using the techniques of iontophoresis and phonophoresis. Agents such as lido-caine can be administered through this method for the treatment of acute inflammation in bursitis, tendinitis, and so on. 

Diabetes mellitus Exocrine dysfunction Skeletal muscle Myopathy Fatigue Weakness Other... 

Local application of concentrated sodium channel blockers can provide complete pain relief through nerve conduction block (local anesthetics). This approach to pain relief is limited to a few applications involving short-term treatment of acute pain, since sodium channels are also vital to conduction in the heart, CNS, skeletal muscle, and non-nociceptive sensory neurons. However, some types of chronic pain signaling appear to be sensitive to sodium channel blockers at concentrations that do not cause conduction block. In particular, neuropathic pain, defined as chronic pain resulting from a primary lesion or dysfunction of the peripheral nervous system by the International Association for the Study of Pain (IASP) [58], is thought to originate from aberrant signaling in the nervous system and can be ameliorated by sodium channel blockers. 

---