Myopathy paralysis

Rhabdomyosarcoma outlined by many vertical rows of muscle fiber that is gathered from muscle cells. Nervous system through the anterior horn cells of the nerve axon terminals of each muscle fiber membrane structure of the special-motor end plates, and the formation of synapses. Synaptic from the peripheral motor neurons and motor end boards. Campaign nerve endings within mitochondria and many synaptic vesicles, vesicles containing acetylcholine (ACh). Campaign nerve endings at the end of a membrane structure, known as the presynaptic membrane, and when the motor excitement, synaptic vesicles within the acetylcholine after this break into the synaptic membrane between the cavity. Synaptic cavity between the rear of the motor end plates after the film, acetylcholine can cause the membrane wife in a change of the balance (depolarization) have endplate potential and muscle contraction. Immediately acetylcholinesterase decomposition and outside of the membrane ion balance is complex (depolarization), the muscle to relax. In nerve-muscle connections or muscle himself obstacles that cause myopathy. Cause pathogenesis according to the pathogenesis of these may relate to the normal muscle contraction different segments : presynaptic membrane lesions caused by the synthesis or release of Ach, there was a reduction in botulism, hypermagnesemia type of cancer and myasthenia syndrome. Synaptic gap cholinesterase activity by inhibiting too, where the role of excessive Ach extended enable nerve-muscle transmission excited to extend the polarization, blocked depolarization and re-excited acceptance, as organophosphate poisoning. Postsynaptic membrane lesions, including various mechanisms caused by the reduction in the number of ACh receptors (eg, myasthenia gravis) and Ach Ach receptor on the VCR flu, as found in the Americas application Arrow toxin, sugar-sticky, polymyxin, neomycin, streptomycin and other kanamycin. Muscle cell membrane permeability abnormal, endplate potential not yet occurred, such as periodic paralysis. Muscle cells within the supply system diseases, as some patients with glycogen storage disease, hyperthyroidism myopathy, muscle disease, lysosomal, will enable the sarcoplasmic reticulum calcium ion transporters adverse where muscle relaxation time. Muscle disease itself as muscular dystrophy, muscle fiber inflammation, myofibrils structural damage, fracture, degeneration, will reduce the ability of muscle contraction. Clinical manifestations neuromuscular junction of acetylcholine secretion or reduce the formation of obstacles, or its receptor, Choline-enzyme inhibition or motor endplates the damage and muscle cells outside the abnormal distribution of ions, can cause paralysis. But most are temporary and its paralysis when the level changes, like lower motor neuron paralysis have the same muscle tone and reduce or tendon reflexes disappear, but in general no muscle atrophy and muscle fibrillation. no pathological reflexes, and sensory impairments. Diseases caused by muscle paralysis, and often not by nerve distribution. Muscle atrophy, amyotrophic focus on paralysis, proximal to the more serious damage may have muscle tension and reduce tendon reflexes. In addition, there are various myositis pain and tenderness, but without feeling diminish or disappear without pathological reflex. Differential diagnosis (1) periodic paralysis (periodic paralysis) is a recurrent episodes of muscle relaxation paralysis characteristic of the disease. Onset hurried, often in the middle of the night or early morning, bilateral or limbs, paralysis and bilaterally symmetrical, proximal to the distal weight. Paralysis of limbs to reduce muscle tension, reduced tendon reflexes or disappeared, along with muscle and solid, electrical stimulation is not reactive, feeling normal, as the diaphragm, intercostal muscle involvement, which can cause breathing difficulties, purple Guitar. If myocardial involvement, there arrhythmia, ECG changes have hypokalemia. Most seizures associated with changes in serum potassium levels. By the change of potassium divided into low potassium, potassium and normal hypokalemic periodic paralysis to hypokalemic to see the most. (2) of myasthenia gravis (myadthenia gravis) is a nerve-muscle transmission of obstacles autoimmune diseases. Clinical features of systemic or local extreme muscle fatigue, short-term contraction strength diminishes, will be able to resume after the break. Extraocular myasthenia most often Post to ptosis to see the most, with strabismus, diplopia, unable to turn a blind eye. If swallowing masticatory muscle with muscle involvement, there were stop chewing difficulty swallowing. Physically less muscle involvement, the Pull often precede lower limbs, distal to the proximal weight. Symptoms in the evening or tired after heavier, and the rest after the morning alleviate. Course with ease and tend to relapse. Respiratory muscles and diaphragm involvement can cause difficulty in breathing, cyanosis, accelerated heart rate, coma can be serious and even death, called myasthenic crisis. Fatigue tests and neostigmine drug testing will contribute to the diagnosis.