Secondary muscle atrophy

Secondary, or neurogenicmuscle atrophy in contrast to the simple develops affection of peripheral motor neuron, i.e. motor cells in the anterior horns of the gray matter of the spinal cord, which is at the same time and trophic centre for the relevant muscles. It was also observed during peripheral nerves. In the latter case, atrophic syndrome accompanied by frustration of sensitivity. Neurogenic muscle atrophy appear not earlier than two weeks after the development of paralysis is characterized by qualitative changes of elektrovozoremontnij. There is a partial or complete response rebirth. The muscle becomes newsradio to faradic current in safe or even increased in the beginning of excitability to direct current. Distorted normal formula elektrovozoremontnij: with the closure of the cathode, reducing become weaker, than with the closure of the anode, and instead lightning reduction typical of normal muscle, appears slow sluggish type of cuts ("worm"). Characteristic of atrophy of this type of fibrillar twitching, pointing to defeat the motor cells.
Histologically for secondary (neurogenic) A. M. characterized by the distribution of atrophic fibers in the form of changed beams or fields along with a well-preserved groups fibers. This "beam atrophy of muscle fibers", opened the first Century K. room, is the result of what each nerve cell or nerve fiber nerviruet certain group of muscle fibers, whose functions fall together in pathological process.
In secondary muscle atrophy General disorders currency is expressed less, than at the primary, but often joined by a variety of disorders of sensitivity - parestesia, pain, Hypo - or anesthesia without distinct boundaries. Amyotrophic the process is localized mainly in the distal extremities and gradually extends to the proximal departments, not grasping usually trunk muscles. Retraction, end atrophy and pseudohypertrophy when A. M. neurogenic type are not observed. On the contrary, sometimes there is a true compensatory hypotrophy of the proximal limbs.
The pathogenesis of neurogenic form of amyotrophic process is yet unknown. In some cases the disease is hereditary, but not yet clear metabolic disorder that causes the system peripheral motor neuron and peripheral nerve trunk. In other cases, the cause of A. M. neurogenic type may be, as with primary muscular atrophy, harmfulness of the external environment nonspecific character. In these cases, A. M. for the first time can develop after nutritional depletion, prolonged fatigue, excessive exercise, cooling, but mainly in connection with acute and chronic infections. From the recent past in the first place stood acute poliomyelitis. In connection with the mass vaccination in the USSR against polio this infection may not be accepted now in the calculation. However, one must keep in mind some pathogenic strains of viruses ECHO and Coxsackie with myotropic properties. Muscle atrophy may occur for tick-borne encephalitis, epidemic encephalitis, amyotrophic form of syphilis, brucellosis, and when amyotrophic lateral sclerosis, those of syringomyelia, trauma and tumors of the spinal cord. The defeat of the front roots and peripheral nerve trunks as radiculitis, plexitis, neuritis and polyneuritis infectious and toxic and traumatic nature leads to development A. M. secondary character. Atrophic process can be observed in ischemic neuropathy developing in the wound of the main arteries of the leg.