1/11. Specific muscle EMG biofeedback for hand dystonia.Currently available therapies have only limited success in patients having hand dystonia (writer's cramp). We employed specific muscle EMG biofeedback (audio feedback of the EMG from proximal large muscles of the limb that show abnormally high activity during writing) in 10 of 13 consecutive patients (age, 19-62 years; all males) with a duration of illness from 6 months to 8 years. In three patients, biofeedback was not applicable due to lack of abnormal EMG values. Nine patients showed dystonic posture during writing and had hypertrophy of one or more large muscles of the dominant hand. The remaining four patients showed either involvement of small muscles or muscle wasting. Ten patients were given four or more sessions of EMG audio biofeedback from the proximal large limb muscles, which showed maximum EMG activity. They also practiced writing daily with the relaxed limb for 5 to 10 min. Nine patients showed improvement from 37 to 93% in handwriting, alleviation of discomfort, and pain (assessed on a visual analogue scale). One patient did not show any improvement. Thus EMG biofeedback improved the clinical and electromyographic picture in those patients with hand dystonia who showed EMG overactivity of proximal limb muscles during writing. This specific type of EMG biofeedback appears to be a promising tool for hand dystonia and might also be applied to other types of dystonias.- - - - - - - - - - ranking = 1keywords = hypertrophy (Clic here for more details about this article) |
2/11. A congenital dermal sinus presenting the muscle fasciculation and hypertrophy.OBJECTIVE: To report unique and unknown clinical features of muscle fasciculation and muscle hypertrophy in a case of congenital dermal sinus. patients: A 16-year-old girl presented with continuous fasciculation, often cramp, and hypertrophy of the left calf muscle. The radiography showed spina bifida of L4, L5 and S1. MRI revealed dermal sinus tract from the skin dimple of the back to the dura mater, and connected to the intradural inclusion tumor. At surgery the inclusion tumor contained many short hairs, and the cauda equina were severely adherent. microdissection of the tumor and the adhesion was performed. At 2 years after surgery fasciculation decreased but continued; however, painful cramps of the calf muscle do not occur. CONCLUSIONS: Short hairs of dermoid and the adherence might be irritative to the cauda equina. The hyperactivity of the stimulated motor neuron may cause the muscle fasciculation leading to hypertrophy of the calf muscle.- - - - - - - - - - ranking = 7keywords = hypertrophy (Clic here for more details about this article) |
3/11. Neurologic and cardiac progression of glycogenosis type VII over an eight-year period.Little is known about the progression of phosphofructokinase deficiency (glycogenosis type VII, Tarui's disease). We describe a 66-year-old woman who had this disease diagnosed in 1997. Initial manifestations had included simple partial seizures since 1977, anginal chest pain since 1982, and muscle cramps since 1983. To prevent recurrent myocardial infarction, anticoagulation therapy with phenprocumon was initiated. Cardiac involvement progressed over an 8-year period, manifesting as low-voltage electrocardiogram (ECG), ectopic supraventricular tachycardia, thickened mitral valve, mitral valve insufficiency, enlarged left atrium, left ventricular hypertrophy, and diastolic dysfunction. Progression of neurologic involvement manifested as complex partial seizures, double vision, reduced tendon reflexes, central facial palsy, bradydiadochokinesia, and distal weakness of the upper extremities. Discontinuance of oral anticoagulation after 19 years, initiation of enalapril therapy, and administration of carbamazepine markedly improved the patient's condition.- - - - - - - - - - ranking = 1keywords = hypertrophy (Clic here for more details about this article) |
4/11. Hereditary neuropathy with liability to pressure palsies (HNPP) in a toddler presenting with toe-walking, pain and stiffness.The typical clinical presentation of hereditary neuropathy with liability to pressure palsies is an adult-onset recurrent, painless monoparesis. Electrophysiological abnormalities--decreased nerve conduction velocities and delayed distal latencies--can be detected even in asymptomatic patients. We describe a toddler, who presented with asymmetric toe walking, painful cramps and stiffness in the legs. He had calf hypertrophy, brisk tendon reflexes and bilateral Babinski signs and the electrophysiological examination was normal. The unlikely diagnosis of hereditary neuropathy with liability to pressure palsies was reached 5 years later, when the boy started to complain of episodic numbness and weakness in the upper extremities. His father, paternal aunt and grandmother had similar symptoms, but they had never been investigated. The typical 1.5 Mb deletion on chromosome 17p11.2-12 was found in our patient and his affected relatives.- - - - - - - - - - ranking = 1keywords = hypertrophy (Clic here for more details about this article) |
5/11. Familial X-linked myalgia and cramps: a nonprogressive myopathy associated with a deletion in the dystrophin gene.We report a family with an X-linked recessive disorder characterized by muscle cramps and myalgia. Nine affected male family members had high resting serum levels of creatine kinase, and well-developed musculature with calf hypertrophy but no evidence of muscular weakness. Symptoms began in childhood and did not progress. Electromyographic findings were consistent with myopathy while muscle biopsies showed nonspecific myopathic changes without evidence of storage of glycogen or lipid. Analysis of dna revealed a deletion in the 1st third of the dystrophin gene. Western blot analysis revealed that dystrophin was smaller than that in normal samples, with no reduction in the amount of the protein present. This disorder represents a new clinical phenotype associated with a deletion in the dystrophin gene. This deletion affects a portion of the dystrophin molecule that clinically does not appear to significantly alter its function. Other patients with deletions in this region may have truncated dystrophin without clinical signs of progressive muscle disease.- - - - - - - - - - ranking = 1keywords = hypertrophy (Clic here for more details about this article) |
6/11. myxedema myopathy: a case report.A classical case of myxedema, demonstrating the typical Hoffmann syndrome (muscle weakness, hypertrophy, pseudomyotonic phenomena) and the usual rise in serum creatine phosphokinase (CPK), is discussed. Assuming that there is a CPK loss in the muscle fiber, the pseudomyotonic phenomena may be due to an increase in ADP, which in turn inhibits the calcium pump. Furthermore, light-microscopic and electron-microscopic findings are reported.- - - - - - - - - - ranking = 1keywords = hypertrophy (Clic here for more details about this article) |
7/11. insulin resistance with acanthosis nigricans and acral hypertrophy.Two patients are described with obesity, acanthosis nigricans, acral hypertrophy, basal hyperinsulinism and exaggerated insulin responses to oral glucose. One patient, a diabetic female showed features of virilisation due to polycystic ovarian disease and underwent gonadectomy with some resolution of her androgenisation and acanthosis nigricans. Binding of labelled insulin to erythrocytes was significantly decreased in both patients compared with normal or obese control subjects. In contrast, the receptor concentration in adipose tissue obtained from the patient undergoing gonadectomy was higher than seen in obese control subjects. Thus, somatic growth may be stimulated by insulin in some tissues in these hyperinsulinaemic patients due to relative preservation of receptor numbers.- - - - - - - - - - ranking = 5keywords = hypertrophy (Clic here for more details about this article) |
8/11. Isaacs' syndrome with muscle hypertrophy reversed by phenytoin therapy.A 16-year-old boy was seen for severe episodic muscle cramps and generalized myokymia, consistent with Isaacs's syndrome. Bilateral calf hypertrophy (46-cm calf circumference) and ankle areflexia were noted. He was treated with phenytoin sodium, 300 mg/day. Within three months there was marked decrease in myokymia, total relief of cramps, return of ankle reflexes, and 6-cm reduction in calf circumference. We suggest that the excess muscle activity in Isaacs's syndrome may be responsible for the associated phenomena of muscle hypertrophy and areflexia.- - - - - - - - - - ranking = 6keywords = hypertrophy (Clic here for more details about this article) |
9/11. Severe muscle cramps relieved by transcutaneous nerve stimulation: a case report.The case is described of a 51-year-old man with a 21 year history of severe, long-lasting and widespread muscle cramps. physical examination revealed muscle hypertrophy and fasciculation; electromyography showed spontaneously active motor units which disappeared during sleep. Cramps could be aborted by ice or mechanical vibration but the most effective management was achieved using transcutaenous nerve stimulation.- - - - - - - - - - ranking = 1keywords = hypertrophy (Clic here for more details about this article) |
10/11. A benign motor neuron disorder: delayed cramps and fasciculation after poliomyelitis or myelitis.Two patients had a delayed syndrome of benign fasciculation after complete recovery from paralytic poliomyelitis and a third had the syndrome after an attack of purely motor myelitis. myalgia was prominent in all three, and two had frequent cramps. denervation hypertrophy occurred in two. The patients were observed for at least three years, and no new weakness was seen. These cases suggest that some chronic diseases of motor neurons may be benign.- - - - - - - - - - ranking = 1keywords = hypertrophy (Clic here for more details about this article) |
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