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Extractions: It is possible that the main title of the report Neuromyotonia is not the name you expected. Please check the synonyms listing to find the alternate name(s) and disorder subdivision(s) covered by this report. Neuromyotonia is a rare neuromuscular disorder characterized by abnormal nerve impulses from the peripheral nerves. These impulses cause continuous muscle fiber activity that may continue, even during sleep. The disorder, which has both inherited and acquired forms, is characterized by muscular stiffness and cramping, particularly in the limbs. Continuous fine vibrating muscle movements (myokymia) can be seen. Muscle weakness may also be present. Muscle relaxation may be difficult especially after physical activity involving the particular muscle(s). NIH/National Arthritis and Musculoskeletal and Skin Diseases Information Clearinghouse
Baylor Neurology Case Of The Month The syndrome has also been called a variety of other names such as QuantalSquander , The syndrome of continuous motor activity , Pseudomyotonia and http://www.bcm.edu/neurology/challeng/pat2/summary.html
Extractions: The patient was admitted to the hospital and received 6 courses of plasma exchange. He was subsequently started on oral prednisone and cyclophosphamide and during his hospital stay noticed a marked improvement in the myokymia and muscle strength. The myotonia improved as well. The patient was then discharged and was to be followed in clinic. The condition is extremely rare and has therefore never been studied in a controlled fashion. A recent review of all reported cases by Jamieson and Katiriji in 1994 suggests an equal incidence in both sexes. The disease appears to present earlier in life with most patients being less than 40 years of age at the time of symptom onset. A study of 3 families by Ashizawa et al in 1983 suggested a dominant mode of inheritance in the familial form of the disease. The etiology of the disease remains unclear. Isaacs in 1961 was the first person to localize the disorder to the peripheral nerves. Pharmacological localization of the generator of the myokymia seems to confirm the initial observations of Isaacs. More exact localization has been less fruitful. The electrical activity appears to originate from multiple sites in the axon. There is some evidence to suggest the role of autoimmunity and, specifically, antibodies against the potassium channel in motor nerve terminals. The potential importance of circulating antibodies is supported by the fact that plasma exchange is effective in treatment of some patients with this disease. A recent case has been reported in which a patient met criteria for both Isaacs' syndrome and CIDP, another potential autoimmune disease.
Extractions: It is possible that the main title of the report is not the name you expected. Please check the synonyms listing to find the alternate name(s) and disorder subdivision(s) covered by this report. Information on the following diseases can be found in the Related Disorders section of this report: Isaacs' Syndrome is a peripheral motor neuron disorder characterized by muscular stiffness and cramping, particularly in the limbs. Continuous fine vibrating muscle movements (myokymia) can be seen. Muscle relaxation may be difficult especially after physical activity involving the particular muscle(s). These symptoms persist even during sleep. In Isaacs' Syndrome, involuntary continuous muscle fiber activity may cause stiffness and delayed relaxation in the affected muscles. Continuous fine vibrating muscle movements (myokymia) may occur along with these symptoms. Affected individuals may have episodes of the inabilitiy to coordinate voluntary muscle movement and difficulty walking (ataxia). Other symptoms may include staggering and reeling (titubation), stiffness, and lack of balance in response to starle. There may be diminished spontaneous gross motors activity.
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