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At least 307 records · Page 17Linked to original sources
PubMed1989

[A case of amyotrophic lateral sclerosis associated with clinical features of progressive supranuclear palsy].

A 64-year-old male patient of amyotrophic lateral sclerosis (ALS) with frozen gait, axial rigidity and supranuclear upper gaze palsy was reported. We have followed this patient more than four years. He was well until November 1982, when he noticed weakness of left arm. In March 1983, he noticed hypogeusia and in July, he developed dysarthria and frozen gait. On admission, he was alert and oriented. Neurological examination revealed dysarthria, dysphagia and muscular weakness and atrophy in bilateral upper extremities, dominantly in left side. He showed remarkable frozen gait, retropulsion and could not walk. Brain CT showed mild dilatation of the third ventricle. In August 1988, he showed tongue atrophy, and weakness and atrophy of the extremities progressed during these four years. He also showed axial rigidity and frozen gait. Brain CT showed severe third ventricular dilatation and atrophy of tegmentum of the midbrain and cerebellum that were compatible with progressive supranuclear palsy (PSP). Six months later, he developed upper gaze palsy. From these findings, we concluded that this patient had a quite unique clinical features of both ALS and PSP.

Amyotrophic Lateral Sclerosis↗
PubMedDate not supplied

Facioscapulohumeral type spinal muscular atrophy: report of a case.

A case of muscular weakness and atrophy with a facioscapulohumeral distribution is described in this report. The neurogenic origin, as judged from the results of laboratory studies, is discussed. The diagnosis and classification of the spinal muscular atrophy syndrome are also discussed. Facioscapulohumeral type spinal muscular atrophy is thought to constitute a distinct form of spinal muscular atrophy.

Adolescent↗
PubMed1990

[Cardiomyopathy in Becker muscular dystrophy].

In 6 patients with dystrophin-verified Becker muscular dystrophy (BMD), 3 patients had dilated cardiomyopathy (DCM group). The other 3 patients (non-DCM group) also had ECG abnormalities including incomplete right bundle branch block, left ventricular enlargement and intraventricular conduction defect. Between DCM and non-DCM group, there was no prominent difference in ages at onset, mean duration and severity of muscular weakness. Serum CK levels, and molecular weight and amount of dystrophin also showed no significant difference between two groups. On reviewing 14 BMD patients, including 3 present patients with cardiomyopathy, the cardiac symptoms appeared from 4 to 41 years, averaging 17.1 years of age. The mean duration of muscle symptoms was 9 years, ranging from 0 to 33 years. There was no correlation between severity of muscle weakness and cardiomyopathy. Six patients died of heart failure and 3 received cardiac transplantation. Thus there was no characteristic clinical feature in BMD patients with cardiomyopathy except for very poor prognosis. Since the myocardial involvement is not related with clinical severity and duration of the disease, careful observation for cardiac function should be carried out in all BMD patients even in the early stage of muscle weakness.

Adolescent↗
PubMed1978

Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss.

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.

Animals↗
PubMed1989

Distal infantile spinal muscular atrophy associated with paralysis of the diaphragm: a variant of infantile spinal muscular atrophy.

We report the clinical, electrophysiological, and morphological observations of five infants with an unusual form of spinal muscular atrophy (SMA). In these infants muscular weakness and atrophy were initially restricted to the distal limbs and this pattern was associated with paralysis of the diaphragm. The difference between the clinical manifestations of this syndrome and the classical form of infantile spinal muscular atrophy (SMA type 1) as well as other congenital hereditary neuropathies is discussed.

Atrophy↗
PubMed1995

Duplication of dystrophin gene and dissimilar clinical phenotype in the same family.

We report here three related patients with a duplication of exons 19-41 of the dystrophin gene, having dissimilar clinical phenotype and dystrophin immunohistochemistry. Two brothers aged six and three years had myalgia, proximal muscular weakness and hypertrophic calves, with 10- 20-fold increase of serum creatine kinase. Muscle biopsy showed dystrophic changes and reduced, patchy binding of dystrophin. The clinical and laboratory findings were consistent with a diagnosis of Becker muscular dystrophy with early onset. Their 14-year-old cousin had only mild hyperCKemia. His muscle biopsy was normal with only mild reduction of dystrophin immunostaining. At follow-up, he is still without symptoms and signs at age 19. All three patients had the same gene duplication and an increased dystrophin size of 507 kDa. Expression of the dystrophin-associated glycoproteins adhalin, alpha-dystroglycan, and beta-dystroglycan were normal in the three patients. An intrafamilial variability in patients carrying a partial duplication of the dystrophin gene may be related to a quantitative difference in mRNA.

Blotting, Southern↗
PubMed2002

Correction of blepharoptosis in oculopharyngeal muscular dystrophy.

Oculopharyngeal muscular dystrophy is a hereditary, autosomal dominant, slowly progressive disorder with onset that occurs during middle age. Major symptoms are ptosis and dysphagia resulting primarily from selectively involved levator palpebrae and the pharyngeal muscles. Progressive, usually symmetrical blepharoptosis, with or without dysphagia, appears during middle age. Muscular weakness in the limbs can be noted in some patients. The guidelines for surgery in myopathic ptosis are conservative in view of the increased risk of postoperative corneal complications. However, orbicularis function remains intact in oculopharyngeal muscular dystrophy; therefore, corrective surgery is performed in most patients. This report describes four cases of ptosis correction in patients with oculopharyngeal muscular dystrophy in one family. The frontalis action was very poor to qualify for frontalis transfer; therefore, the authors performed moderate to large levator resection in all patients. The follow-up results 5 years postoperatively are promising to date and all the patients are satisfied with the results.

Adult↗
PubMed1981

Periodic paralysis complicating malaria.

Episodic muscular weakness, commonly associated with alterations of serum potassium, is the cardinal feature of periodic paralysis. The combination of transient hyperkalaemia and rigors occurring during febrile episodes of malaria is suggested as the underlying cause which precipitated the muscular paralysis. Three patients with malaria who developed a similar paralysis during the paroxysms of fever are described to illustrate this.

Adult↗
PubMed1976

Muscular dystrophy of mink: a new animal model.

Muscular dystrophies comprise an important group of inherited disorders of man. Although the disease has been studied extensively, little is known about the underlying primary pathomechanisms. Consequently, treatment of patients is difficult and prognosis is poor. An animal model of muscular dystrophy is a useful research tool for approaching the basic problems of pathogenesis in muscle diseases. An inherited progressive muscular dystrophy of mink which resembles the amyotonic forms of human muscular dystrophy is currently under study. Clinically, the earliest sign is progressive muscular weakness and atrophy. Muscle enzyme activities in serum are usually elevated to pathologic levels. Urinary creatine/creatinine ratio is elevated. Pathologic changes are limited to skeletal muscle and are typical of those seen in amyotonic forms of human muscular dystrophy. These changes include variation in diameter size of muscle fibers, centralized nuclei, floccular and hyaline degeneration of scattered muscle fibers, increase in connective tissue in endomysial and perimysial areas, and regenerative attempts. Both type I and type II muscle fibers are involved in the disease process. Genetic studies indicate an autosomal recessive mode of inheritance. Although the primary defect in muscular dystrophy is traditionally thought to reside in skeletal muscle, recent studies have produced theories of primary involvement of other tissues and organ systems. These theories are presented and relationships to the traditional theory are discussed.

Animals↗
PubMed1983

Potentiation of magnesium-induced neuromuscular weakness by gentamicin.

A term neonate with hypermagnesemia secondary to maternal administration of MgSO4 for pre-eclampsia had a respiratory arrest after receiving gentamicin im. The neuromuscular tracings and sequential physician exams done before and after administering gentamicin suggest aminoglycosides may potentiate a magnesium-induced impairment of neuromuscular transmission and cause muscular weakness in neonates.

Critical Care↗
PubMed1971

Haemodialysis in poisoning by sea-snake venom.

Myoglobinuria, renal failure, and muscular weakness or paralysis were noted in two patients following sea-snake bite. A pathological study by biopsy showed renal tubular necrosis and myonecrosis. Both patients were treated by haemodialysis, and there was a remarkable improvement in the muscular symptoms. Recovery was complete in both cases. It is believed that muscular paralysis was the effect of hyperkalaemia and uraemia on the muscles sensitized by the toxic effect of the sea-snake venom. Removal of potassium and uraemic factors by dialysis thus led to the rapid improvement of the muscular activity. Haemodialysis seems to be a useful alternative method to sea-snake antivenom in the treatment of sea-snake bite poisoning.

Acute Kidney Injury↗
PubMed1987

[Nemaline myopathy. General review apropos of 3 cases].

Three cases of nemaline myopathy are reported. The first one was characterized by delayed motor milestones, hypotonia and proximal weakness in a 2-year-old girld. The second case was diagnosed at 19 in a boy who suffered from a severe scoliosis without any neurological sign. The third patient was a 31 year-old man who had a progressive muscular weakness of limb girdles. Muscle biopsy revealed rods in muscle fibers with Gomori trichrome staining in two cases, and by electron microscopy in one case only. Variations of fiber calibration, fiber I predominance and a myofibrillar disorganization were seen in two cases. Clinical, histopathological and physiopathological of nemaline myopathy are discussed.

Adult↗
PubMed1979

[Lipidic myopathy with severe cardiomyopathy caused by a generalized carnitine deficiency. Favourable course during carnitine hydrochloride treatment].

The case of a girl who presented with gastrointestinal upsets with nausea, vomiting and occasional hypoglycaemic attacks during childhood is reported. At about 5 years of age generalised muscular weakness with severe amyotrophy, cardiomegaly with a cardiothoracic ratio of 0,63, left ventricular hypertrophy on electrocardiography and left ventricular dilatation with hypokinesis on echocardiography were observed. A few weeks later she developed severe cardiac failure. Muscle biopsy showed muscular dystrophy with lipid infiltration due to carnitine deficiency )serum carnitine 9 nmoles/ml, normal values: 46 +/- 6,9 nmoles/ml; muscle carnitine 0,27 nmoles/mg, normal values: 3,0 +/- 0,79 nmoles/mg fresh frozen weight). She improved rapidly with carnitine chlorhydrate and a diet low in lipids and high in medium chain triglycerides. Regression of muscular symptoms and cardiac failure was observed. After 13 months follow-up with no tonicardiac therapy she is much improved; the signs of heart failure have disappeared, the cardiothoracic ratio is now 0,55 and the electrocardiogramme and echocardiogramme are normal.

Biopsy↗
PubMed2005

Post-poliomyelitis syndrome.

Post-poliomyelitis syndrome (PPS) is a common neurological disorder that occurs in a large proportion of individuals who have recovered from paralytic poliomyelitis. The main clinical features are new weakness, muscular fatigability, general fatigue, and pain. The primary criteria necessary for the diagnosis of PPS are a history of paralytic poliomyelitis, partial or complete recovery of neurological function followed by a period of stability (usually several decades), persistent new muscle weakness or abnormal muscle fatigability, and the exclusion of other causes of new symptoms. The cause of PPS remains unclear, but is likely due to a distal degeneration of enlarged post-poliomyelitis motor units. Contributing factors to PPS may be aging (with motor neuron loss), overuse, and disuse. PPS is usually a slowly progressive neuromuscular disease. Although there is no specific treatment for PPS, an interdisciplinary management program can be useful in controlling symptoms.

Humans↗
PubMed1986

Comparative behavioral effects of anticholinergic agents in cats: psychomotor stimulation and aggression.

The effect on behavior of eight anticholinergic agents: atropine, scopolamine, trihexyphenidyl, biperiden, homatropine, eucatropine, hexocyclium and propantheline, injected into the cerebral ventricle (ICV) of the cat was investigated and compared. The anticholinergic agents evoked: (1) psychomotor stimulation such as miaowing, loud calling, restlessness, impelling locomotion, jumping, vacant staring, apprehension and loss of interest of the surroundings; (2) aggression, hissing, threat, attack, defense, fighting with paws and flight; (3) autonomic responses including mydriasis, tachypnea, dyspnea, licking, vomiting, salivation, micturition and defection; and (4) motor phenomena comprising scratching, ataxia, rigidity, tremor, weakness with adynamia or myoclonic jerks. Convulsions appeared only after ICV injections of atropine and homatropine. The most characteristic behavioral effect of anticholinergic agents was psychomotor stimulation accompanied by mild aggressive responses. The only exception was propantheline which caused a muscular weakness and adynamia. Atropine and scopolamine alone induced a dose-dependent impelling locomotion as well as fighting behavior. Carbachol and eserine injected intracerebroventricularly reversed the locomotion autonomic and motor phenomena produced by anticholinergic agents administered similarly. It is suggested that anticholinergic agents acting as partial agonists, can produce their behavioral effects through central cholinoceptive sites.

Aggression↗
PubMed1987

Evaluation of information-processing speed and neuropsychological functioning in patients with myotonic dystrophy.

Patients with myotonic dystrophy (MD) were compared to a control group, matched to the patients in important demographic variables including IQ, on the Sternberg Memory Scanning procedure, to investigate the hypothesis of a selective change in speed of information processing in MD patients. The neuropsychological functioning of these MD patients was also compared to normative data to provide a descriptive picture of their abilities; these results were correlated to the factors of age of onset and duration of the disease. Finally, the MD patients were also compared to the defined control group on the neuropsychological measures. There was little evidence of selective slowness of information processing or particular deficit independent of overall IQ. Neuropsychologically, the MD patients as a group performed at the low average level. There was, however, a wide range of abilities, suggesting that MD patients are not a unitary group in terms of neuropsychological functioning. Age of onset of the disease was important, at least for certain results. Further research of the neuropsychological functioning of MD patients must account for the wide range of results, with more precise measures of actual onset of the disease and muscular weakness, in a longitudinal evaluation.

Attention↗
PubMed2003

Recent advances in the rehabilitation of isolated and combined anterior cruciate ligament injuries.

The rehabilitation process begins immediately following ACL injury, with emphasis on reducing swelling and inflammation; improving motion; regaining quadriceps control; allowing immediate weight-bearing; and restoring full passive knee extension and, gradually, flexion. The goal of preoperative rehabilitation is to prepare the patient mentally and physically for surgery. Once the ACL surgery is performed, it is important to alter the rehab program based on the type of graft used and any concomitant procedures performed. This will aid in preventing several postoperative complications, such as loss of motion, patellofemoral pain, graft failure, and muscular weakness. The goal of this article has been to provide an overview of the application and the scientific basis for formulating a rehabilitation protocol following ACL surgery. For an athlete to return to competition, it is imperative that he or she regain muscular strength and neuromuscular control in their injured leg while maintaining static stability. In the past, rehabilitation programs attempted to prepare the athlete for return to sports by using resistance exercise alone. Current rehabilitation programs focus not only on strengthening exercises, but also on proprioceptive and neuromuscular control drills in order to provide a neurologic stimulus so that the athlete can regain the dynamic stability needed in athletic competition. We believe that it is important to use this approach not only possible causes that might predispose the individual to future injury.

Anterior Cruciate Ligament↗
PubMed1995

Expression of transforming growth factor-beta 1 in dystrophic patient muscles correlates with fibrosis. Pathogenetic role of a fibrogenic cytokine.

Duchenne muscular dystrophy is a fatal disorder characterized by progressive muscular weakness, wasting, and severe muscle contractures in later disease stages. Muscle biopsy reveals conspicuous myofiber degeneration and fibrosis substituting muscle tissue. We quantitatively determined mRNA of the potent fibrogenic cytokine transforming growth factor-beta 1 by quantitative PCR in 15 Duchenne muscular dystrophy, 13 Becker muscular dystrophy, 11 spinal muscular atrophy patients, and 16 controls. Higher transforming growth factor-beta 1 expression was greater in Duchenne muscular dystrophy patients than controls (P = 0.012) and Becker patients (P = 0.03). Fibrosis was significantly more prominent in Duchenne muscular dystrophy than Becker muscular dystrophy, spinal muscular atrophy, and controls. The proportion of connective tissue in muscle biopsies increased progressively with age in Duchenne muscular dystrophy patients, while transforming growth factor-beta 1 levels peaked at 2 and 6 yr of age. Transforming growth factor-beta 1 protein was also detected by immunocytochemistry and immunoblotting. Our findings suggest that transforming growth factor-beta 1 stimulates fibrosis in Duchenne muscular dystrophy. Expression of transforming growth factor-beta 1 in the early stages of Duchenne muscular dystrophy may be critical in initiating muscle fibrosis and antifibrosis treatment could slow progression of the disease, increasing the utility of gene therapy.

Age Factors↗