Muscle fiber neurogenic

Diseases affecting skeletal muscle are not always primary diseases of muscle, and it is necessary first to determine whether a particular disorder is a primary disease of muscle, is neurogenic in origin, is an inflammatory disorder, or results from vascular insufficiency. A primary disease of muscle is one in which the skeletal muscle fibers are the primary target of the disease. Neurogenic disorders are those in which weakness, atrophy, or abnormal activity arises as a result of pathological processes in the peripheral or central nervous system. Inflammatory disorders may result in T-cell mediated muscle damage and are often associated with viral infections. Vascular insufficiency as a result of occlusion in any part of the muscle vasculature can cause severe disorders of muscle, especially in terms of pain, metabolic insufficiency, and weakness. 

Insulin is a powerful anabolic hormone but it is unlikely that insulin deficiency causes skeletal muscle atrophy by direct action on muscle fibers (as opposed to neurogenic atrophy) except in chronic untreated cases. There is however a close parallel between the catabolic states induced by glucocorticoid excess and by insulin deficiency. Moreover, impaired insulin action is implicated in other endocrine myopathies as a contributory cause of muscle wasting. Both acromegaly and thyrotoxicosis are associated with insulin resistance due to a postreceptor defect, and secondary hyperparathyroidism due to hypophosphatemia also gives rise to insulin insensitivity. 

Skeletal muscle is neurogenic and requires stimulation from the somatic nervous system to initiate contraction. Because no electrical communication takes place between these cells, each muscle fiber is innervated by a branch of an alpha motor neuron. Cardiac muscle, however, is myogenic, or self-excitatory this muscle spontaneously depolarizes to threshold and generates action potentials without external stimulation. The region of the heart with the fastest rate of inherent depolarization initiates the heart beat and determines the heart rhythm. In normal hearts, this "pacemaker region is the sinoatrial node. 

Number of phases indicates the complexity of the MUP and the degree of misalignment between SFAPs. In neurogenic diseases, polyphasic MUPs arise due to slow conduction velocity in immature nerve sprouts or slow conduction velocity in reinnervated but still atrophied muscle fibers. Variation in muscle fiber size also causes polyphasic MUPs in myopathic diseases. To prevent noisy baseline fluctuations from affecting the count of MUP phases, a valid baseline crossing must exceed a minimum absolute amplitude criterion. 

Denervation and dysinnervation abnormalities are usually neurogenous (but, atypically, sometimes can be myogenous see Chapter 1). Conceptually, denervation is a complete loss of neural influence on the muscle fiber (which initially can be reversible by... 

As a result of vascular or neurogenic alteration, amyotrophies and osteopathies have been observed in diabetes. The muscle atrophy involves the individual fibers and is usually not associated with an inflammatory reaction. The electron microscope may reveal a marked increase in the granular osmiophilic material between myofibrils. Frequently, the basement membrane of the capillaries nourishing the muscle is greatly thickened. Abnormalities of motor end plates resulting in a soap bubble appearance have been described in diabetes. 

The biological actions of capsaicin are primarily attributable to release of the neuropeptide substance P, calcitonin gene-related peptide (CGRP), and neurokinin A from sensory neurons. These transmitters from primary sensory neurons communicate witir other cell types. They produce alterations in the airway mucosa and neurogenic inflammation of the respiratory epithelium, airway blood vessels, glands, and smooth muscle. Alterations in multiple effector organs lead to bronchoconstriction, increased vascular permeability, edema of the tracheobronchial mucosa, elevated mucosal secretion, and neutrophil chemotaxis (Tominack and Spyker, 1987). Capsaicin-induced effects of bronchoconstriction, vasodilation, and plasma protein extravasation are mediated by substance P. In addition, substance P can cause bronchoconstriction through stimulation of c-fibers in pulmonary and bronchial circulation. 

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