Diagnosis and Management of Muscle Disease by Albert P. Galdi M.D. (auth.)

By Albert P. Galdi M.D. (auth.)

Neurologists and non-neurologists alike can now not forget about illnesses of the neuromuscular process. The outdated dogma that those problems are either unusual and untreatable has misplaced its validity. fresh technological advances have enabled us to review extra accurately muscle and nerve anatomy, body structure and biochem­ istry. due to this growth, we're now spotting new neuromuscular di­ seases in addition to diagnosing extra sophisticated situations of myasthenia gravis, myotonia, and metabolic myopathies. remedy of the neuromuscular illnesses has additionally un­ dergone dramatic switch in response to new discoveries within the fields of immunology and pharmacology. now not are myotonia, periodic paralysis, and malignant hyperthermia untreatable clinical curiosities. now not are situations of steroid-un­ responsive myositis given up as hopeless. as a result of most of these advances, non-sur­ gical physicians and particularly neurologists needs to replace their wisdom regard­ ing the neuromuscular issues. This e-book, it's was hoping, can assist such clinicians in facing this job. Emphasis has been put on the prognosis and administration of those problems instead of on their pathophysiology. The extra unusual illnesses and people of doubtful life were passed over purposely and left to the bigger and extra encyclopedic reference works. bankruptcy 1 discusses the medical indicators and symptoms of muscle sickness and is designed to let the reader to formulate a differential prognosis at the foundation of the patient's historical past and actual examination.

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Example text

The conduction velocity is calculated by determining the difference in the latencies between two points of stimulation along a single nerve and dividing this number into the distance between these same two points (see Figure 24). , velocities reduced by less than thirty percent of normal) can be seen with axonal disorders, decreased nerve conduction velocities usually indicate disease of the peripheral nerve myelin. Nerve conduction velocities are normal with primary myopathic and junctional disorders.

These biochemical distinctions are directed by the innervating lower motor neuron. When a type I motor neuron inneravates a cluster of embryonic muscle fibers (myotubes) it influences their biochemical and physiologic properties (via "trophic factors") so that they all become type I muscle fibers. Type II motor neurons, by similar mechanisms, influence the development of myotubes to type II muscle fibers. As a result, fibers of the same motor unit are of a uniform histochemical type. If the neural supply of a motor unit is disrupted, the "orphaned" muscle fibers will either degenerate or will be reinnervated by nerve twigs from neighboring axons.

If the patient has botulism, the pretreated group of animals will survive while the former group will die within 48 hours of receiving the patient's serum. Laboratory Studies Serum muscle enzymes and muscle biopsy Determination of serum levels of muscle enzymes is of no value in the diagnosis or management of botulism. Muscle biopsy shows changes compatible with structurally deinnervated muscle. This is presumably the result of physiologic deinnervation of the fibers secondary to disrupted neuromuscular transmission.

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