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PubMed2002

[Anesthesia in neuromuscular disorders. Part 2: specific disorders].

The neuromuscular disorders described are divided into four groups: motoneuron diseases, peripheral neuropathies, disturbances of neuromuscular transmission and myopathies. In motoneuron diseases problems mainly result from respiratory insufficiency and the predisposition for aspiration caused by progressive muscular weakness. Depolarising muscle relaxants may elicit myotonic reaction and massive hyperkalemia. In contrast to non-depolarising muscle relaxants there may be an extreme hypersensitivity. In peripheral neuropathies the cardiac function is often limited whereby dysautonomia may enhance cardiovascular instability. The negative inotropic effect of anaesthetic agents must be observed with care and patients with higher degree of AV blocks may need a cardiac pacemaker during general anaesthesia. The Charcot-Marie-Tooth-Syndrome is characterized with a high sensitivity to thiopental. Disturbances of neuromuscular transmission frequently cause respiratory problems The fluctuating weakness of bulbar and respiratory muscles may impair swallowing and can lead to recurrent aspirations. Due to the reduced number of acetylcholine receptors the sensitivity to non-depolarizing muscle relaxants is elevated and the response to succinylcholine is reduced. Drugs reducing neuromuscular transmission such as antibiotics and beta-blockers may enhance these symptoms and should be avoided. In progressive muscular dystrophies the anaesthetic risk is mainly dependent on cardiac and respiratory impairment. Administration of succinylcholine leads to the risk of hyperkalmic cardiac arrest. Patients with metabolic myopathies are also at risk due to the involvement of cardiac muscle but respiratory problems are less frequent. Muscle metabolism should be supported by administration of substrates depending on the underlying disorder. In membrane disorders muscle rigidity (myotonic reactions) or weakness may lead to respiratory insufficiency. In addition to the depolarising muscle relaxants also anticholinesterase drugs, hypothermia and dyskalaemia can evoke myotonic reactions.

Anesthesia↗
PubMed1992

A large inbred Palestinian family with two forms of muscular dystrophy.

This paper reports the results of a clinical, genetic and histopathological study of 19 patients belonging to a large inbred Palestinian family living in Um-El-Fahem, a town located in Israel, which is solely inhabited by Arabs. Their custom of marrying only among relatives has kept the genetic homogeneity of the families intact. There were ten cases of congenital muscular dystrophy (CMD) and nine cases of adult limb-girdle muscular dystrophy (LGMD) belonging to two generations of the same family. Both forms showed autosomal recessive inheritance. The patients with congenital muscular dystrophy had generalized muscular weakness and hypotonia at birth without arthrogryposis or CNS involvement and then had a relatively benign evolution with stabilization of the clinical picture at different ages and variable degree of severity. Muscle biopsy showed a dystrophic pattern. The other nine patients presented with the picture of adult limb-girdle muscular dystrophy but with an unusual tendency to the stabilization of symptoms.

Adolescent↗
PubMed1979

The otolaryngologic presentation of myasthenia gravis.

Myasthenia gravis is a neuromuscular disease of insidious onset, characterized by weakness and fatigability of voluntary muscles. Most patients present with symptoms relating to the head and neck and thus may be seen first by the otolaryngologist. Predominant symptoms may be ocular (ptosis or diplopia) or related to fatigue of the oropharyngeal or laryngeal musculature (dysarthria, dysphonia, or dysphagia). Alleviation of muscular weakness and fatigability after administration of anticholinesterase drugs is pathognomonic of myasthenia gravis.

Adolescent↗
PubMed1992

[Therapy of neuropathies with a vitamin B combination. Symptomatic treatment of painful diseases of the peripheral nervous system with a combination preparation of thiamine, pyridoxine and cyanocobalamin].

STUDY DESIGN: In an open, multicentric observational study involving 234 doctors in private practice, the evolution of symptoms and the tolerability of a vitamin B preparation (Neurotrat forte) used as treatment in 1,149 patients with polyneuropathy, neuralgia, radiculopathy and neuritis associated with pain and paresthesias, were observed. The form of administration (ampoules, dragées), dosage and duration of treatment were left to the individual care-providing physician. The target symptoms evaluated were intensity of pain, muscle weakness affecting the legs, and paresthesia. RESULTS: Under treatment, there was a clear improvement in these symptoms. At a second examination approximately three weeks after initiation of treatment, a positive effect on pain in particular was observed in 69% of the cases. Similar observations were also made for paresthesias and muscular weakness in the legs.

Diabetic Neuropathies↗
PubMedDate not supplied

Environmental toxicology and health effects associated with dinitrotoluene exposure.

Dinitrotoluenes (DNTs) are nitroaromatic compounds appearing as pale yellow crystalline solids at room temperature. Dinitrotoluenes exist as a mixture of 2 to 6 isomers, with 2,4-DNT, and 2,6-DNT being the most significant. About 500 persons are estimated to be potentially exposed yearly to 2,4-DNT and 2,6-DNT during the production of munitions and explosives. The main route of human exposure at ammunition facilities is inhalation, but dermal contact and inadvertent ingestion can also be substantial. In factory workers, exposure to DNTs has been linked to many adverse health effects, including cyanosis, vertigo, headache, metallic taste, dyspnea, weakness and lassitude, loss of appetite, nausea, and vomiting. Other symptoms including pain or parasthesia in extremities, abdominal discomfort, tremors, paralysis, chest pain, and unconsciousness have also been reported. The primary targets of DNT toxicity are the hematopoietic system (pallor, cyanosis, anemia, and leukocytosis), the cardiovascular system (ischemic heart disease), the nervous system (muscular weakness, headache, dizziness, nausea, insomnia, and tingling pains in the extremities) and the reproductive system (reduction of sperm counts, alteration of sperm morphology, and aspermatogenesis). An association between DNT exposure and increased risk of hepatocellular carcinomas and subcutaneous tumors in rats, as well as renal tumors in mice, has been established. Epidemiologic studies of DNT toxicity have been limited to small groups of workers who had been occupationally exposed at various ammunitions production facilities. Clearly defining the health effects of DNTs with a high degree of confidence has therefore been difficult because of the multigenic nature of occupational exposure. In an attempt to update the toxicologic profile of the DNTs, we hereby provide a critical review of the environmental and toxicologic pathology of DNTs, with a special emphasis on their potential implications for public health.

Air Pollutants, Occupational↗
PubMed1999

[Imported trichinellosis with severe myositis--report of a case].

A 38-year-old Japanese male who had traveled in China from September 13 to October 5, 1997, developed fever and severe conjunctivitis from October 20. After he was hospitalized in Kyoto City Hospital for persistent high fever on October 29, he developed muscular weakness and dysphagia which continued for two weeks. An electromyogram showed a myogenic pattern, and laboratory findings showed significant elevation of serum enzyme levels of muscle origin: CPK, 3,095 IU/l; aldorase, 195 IU/l; myoglobin, 7,570 ng/ml, and myoglobinuria, 94,700 ng/ml. The WBC was 10,800/microliter with 45% eosinophils. Muscular biopsy showed degeneration of muscle fibers with infiltration of macrophages and lymphocytes. On further inquiry, it was revealed that the patient had eaten smoked bear meat in China on September 30, three weeks prior to the onset of symptoms. A dot-ELISA serologic test for parasites was positive for Trichinella. Further, a coiled 1.2 mm long Trichinella larve was recovered from approximately 100 mg of frozen biopsied muscle by an enzyme digestion method. Mebendazole was given to the patient at a dosage of 200 mg/day for seven days. CPK levels were normalized within 3 days of the beginning of the treatment, and he was discharged without any symptoms. Physicians must be aware of trichinellosis and should include it in their differential diagnosis when examining patients with myositis and eosinophilia of unknown origin.

Adult↗
PubMedDate not supplied

Myasthenia gravis: dental treatment considerations.

Myasthenia gravis is an autoimmune neuromuscular disorder that presents challenges for the dental practitioner. Facial and masticatory muscles may be involved and complicate dental treatment. Exacerbations of the skeletal muscle weakness and fatigability that characterize this disorder can be precipitated by certain medications used in dentistry. A review of 47 dental treatment episodes in 16 patients with myasthenia gravis was undertaken to identify neuromuscular responses to dental treatment and post-dental treatment medical therapy required for control of resultant exacerbations of muscular weakness. Neuromuscular sequelae occurred in 5 treatment episodes for four different patients. Management considerations and drug precautions are discussed.

Adult↗
PubMed1986

Breathlessness and exercise in patients with cardiorespiratory disease.

Previous studies have led to the revival of the hypothesis that breathlessness is the perception of respiratory muscle effort and is present when the tension developed by muscles increases, when the muscles are weak, or when both conditions are present simultaneously. Using a category scale, the intensity of breathlessness was measured in 20 subjects (2 normal subjects and 18 patients) undergoing an incremental exercise test (50 to 100 kpm/min) to maximal capacity. The patients were selected to provide a heterogeneous group of pulmonary diseases, obesity, muscular weakness, and cardiac disease, with a wide variability in exercise capacity (250 to 1,900 kpm/min) and severity of dyspnea. Maximal inspiratory pressure (MIP), pleural pressure (Ppl), the extent of shortening of the inspiratory muscles as indicated by the tidal volume expressed as a percent of vital capacity (VT/VC), the rate of shortening as indicated by flow rate, the frequency of contraction as indicated by breathing frequency (fb), and the duty cycle (TI/Ttot) were measured throughout exercise to assess their relative contribution to the intensity of breathlessness. Using multifactorial analysis, the perception of breathlessness was significantly (p less than 0.01) related to the Ppl, inspiratory flow rate (VI), VT/VC, TI/Ttot, and fb. A multiple linear regression equation that included all these variables explained 69% of the variance, with no single factor being identified as uniquely predominant: Breathlessness = 3.0 (Ppl/MIP) + 1.2 (VI) + 4.5 (VT/VC) + 0.13 (fb) + 5.6 TI/Ttot) - 6.2 (R = 0.83). The intensity of effort required to produce a given pressure increases when the muscle is weak, when the velocity of contraction increases, or when the muscle shortens.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Congenital muscular dystrophy. Apropos of 4 cases].

Four cases of congenital muscular dystrophy are reported. Muscular weakness and hypotonia, with different clinical severity, was present from birth in three patients; in the fourth one, it began at two months old. Three cases had joint contractures. One patient died by respiratory infection. Serum CK level was very high in all of them. Muscle biopsies showed pathologic changes consistent with muscular dystrophy with endomysial and perimysial fibrosis and fatty infiltration. Authors analysed this illness emphasizing clinical and biochemical (CK) data so that an early diagnosis can be suspected.

Biopsy↗
PubMed1972

Diabetic amyotrophy: a follow-up study.

A clinical follow-up study of 12 patients with diabetic amyotrophy is reported. Re-examination after an interval indicated that improvement had occurred in all but one instance, and had been maintained over an average follow-up period of four and a half years. Improvement in the neurological syndrome appeared to follow improvement in diabetic control or institution of treatment in those whose diabetes had not previously been diagnosed.Seven patients made a good functional recovery, three no longer having any muscular weakness. Five showed significant residual disability.

Action Potentials↗
PubMed2004

[Cerebral embolism associated with Becker muscular dystrophy-related dilated cardiomyopathy].

A 65-year-old man with previous history of congestive heart failure and genetically proven Becker muscular dystrophy (BMD) was suddenly suffered from aphasia and right hemiplegia. Physical examination showed severe motor aphasia, right hemiplegia, and signs of left heart failure. An echocardiogram before the onset of aphasia showed markedly dilated left ventricle and decreased ventricular contraction. Intracardiac thrombus was not detected. Although his electrocardiogram on admission showed sinus rhythm, atrial fibrillation was noted at the time of neurological deterioration. MRI of the brain revealed acute infarction in the territory of the left middle cerebral artery and the left anterior inferior cerebellar artery. MR angiography showed vascular occlusion at the left M2 segment. Cerebral embolism due to atrial fibrillation associated with BMD-related DCM was diagnosed. While an administration of anti-coagulant, diuretics, and dopamine relieved his respiratory distress and right hemiplegia, severe motor aphasia persisted. Cerebral embolism may be a notable complication in patients with BMD presenting with late-life expression of skeletal muscular weakness and antecedent cardiac involvement.

Aged↗
PubMedDate not supplied

Parenteral magnesium sulfate fails to control electroshock and pentylenetetrazol seizures in mice.

Magnesium sulfate has been used as an anticonvulsant in the treatment of eclampsia, but efficacy of magnesium in other types of seizure disorders is poorly documented. We examined the effects of magnesium sulfate (MgSO4) on seizures produced in mice by maximal electroshock (MES) and pentylenetetrazol (PTZ), MgSO4 injection (6.7 mEq/kg i.p.) caused weakness in all animals. With suprathreshold electroshock, 10/10 controls and 11/12 treated animals had seizures with tonic hind limb extension (P = NS). Electroshock threshold was unaltered by magnesium treatment (n = 48; P = 0.47). PTZ induced clonic seizures in 12/12 controls and 5/14 treated animals (P less than 0.05). This difference was likely due to muscular weakness because frequency of EEG spikes was the same in PTZ and PTZ + MgSO4 groups. Mean serum magnesium levels were 2.3 +/- 0.3 mEq/l in animals not given MgSO4; 10.9 +/- 1.4 mEq/l and 12.8 +/- 2.2 mEq/l in treated animals with and without seizures (P = NS). We conclude that magnesium sulfate had no significant anticonvulsant activity in mouse MES and PTZ models for epilepsy. The relevance of these findings to the possible efficacy of magnesium sulfate in eclamptic seizures and other types of epilepsy remains to be determined.

Animals↗
PubMed1986

Pathogenesis of experimental thyrotoxic myopathy.

Focal degenerative changes of skeletal muscle fibers (decrease in mean diameter, excessive axonal branching and a decrease in the mean diameter of motor end-plates together with a reduction of their acetylcholinesterase levels) were found by means of the experimental model thyrotoxic myopathy in mice compared to controls. A decrease in protein kinase affinity to cAMP and an increase in the number of nucleotide binding sites were revealed with a simultaneous decrease in cAMP level. The weakening of hormonal control of cAMP-dependent processes is probably the basic cause of muscular weakness and structural changes in skeletal muscles in thyrotoxic myopathy.

Acetylcholinesterase↗
PubMed1992

Nephrotoxicity of germanium compounds: report of a case and review of the literature.

A 55-year-old woman was admitted to our hospital, complaining of general malaise, muscular weakness, anorexia and weight loss. She had a history of ingesting of a certain germanium (Ge) compound over the preceding 19 months, with a total dose of 47 g as Ge element. She was found to have renal failure (blood urea nitrogen, 44 mg/dl; serum creatinine, 2.6 mg/dl) without abnormal findings in urinalysis, and muscular and nervous damage. Initially, polymyositis was diagnosed and prednisolone administered. However, no improvement was seen, and neuromuscular symptoms and signs steadily worsened, ending in death. Microscopic study of the kidney showed that lipofuscin granules increased in the cells of the thick ascending limb of Henle's loop to the distal convoluted tubule accompanying mild tubular atrophy and that some of the tubules of these segments had vacuolar degeneration or desquamation. No apparent glomerular and vascular changes were observed. High Ge content was found in serum, urine and various tissues, e.g., spleen, liver, kidney, adrenal gland and myocardium, while in controls Ge could not be detected in sera, urine or tissues. We also review case reports about Ge toxicity, and discuss the pathogenesis of renal failure induced by Ge compounds.

Acute Kidney Injury↗
PubMed1989

[Critical observation of selected exercises of power training in relation to prevention of postural damage and physical handicaps].

Prevention of and compensation for muscular weaknesses in postural disorders and physical disability are priority tasks of physiotherapy. A range of typical exercises are therefore being used to strengthen weakened groups of muscles, some of them traditionally already included in school sports. Most therapy concepts primarily focus on muscle strengthening, without taking into consideration that it is crucial to redress muscular imbalances by stretching contracted muscle groups as well. Based on this experience, the effectiveness of several specifically modified exercises was tested, derived from the usual range of physiotherapy activities in strengthening very commonly weakened muscle groups, i.e. the abdominal, gluteal, sacrospinalis and shoulder-blade affixing musculature. To increase exercise effectiveness, training machines were used in addition. Stretching exercises were carried out initially, in terms of passive stretching with isometric pre-tension. The following muscle groups were stretched: rectus femoris m., iliopsoas m., pectoralis m., and lumbar sacrospinalis m. Altogether, 64 patients between age 16 and 27 were examined following training therapy, 58 patients presented pure postural disorders, 6 had slight cerebral movement disorders. Two almost equal study groups were formed, one (31 patients) receiving only gymnastic exercises, the other (33 patients) using training machines. The muscular situation was tested after 6 months by means of Janda's semiquantitative muscle-testing. For further objective assessment of therapy outcome, Neugebauer's 'back-index' was determined. Muscular harmony and spinal balance were found to have significantly improved in the second group who had used the training machines. A slight reduction of muscle spasticity in addition was found in the patients with cerebral movement disorders.

Adult↗
PubMed2001

Transgenic mice with an expanded CAG repeat controlled by the human AR promoter show polyglutamine nuclear inclusions and neuronal dysfunction without neuronal cell death.

We generated transgenic mice that expressed a highly expanded 239 polyglutamine (polyQ) repeat under the control of the human androgen receptor promoter. These transgenic mice developed progressive neurological phenotypes of muscular weakness and ataxia, small body size and short life-span. PolyQ nuclear inclusions (NIs) were remarkable and widespread but found in selective regions of the central nervous system (CNS) such as the spinal cord, cerebrum and cerebellum as well as in selective peripheral visceral organs. This distribution pattern resembled that of spinal and bulbar muscular atrophy somewhat, but was more widespread. In neuronal tissues, NIs were present in astrocytes as well as neurons. Cytoplasmic and axonal inclusions were not observed. In the CNS regions with abundant NIs, neuronal populations were well-preserved, and neither neuronal cell death, reactive astrogliosis nor microglial invasions were detected. These findings suggest that polyQ alone can induce the neuronal dysfunction that precedes gross neuronal degeneration and provides a clue for investigating molecular mechanisms that underly the pathway to neuronal dysfunction from polyQ expansion.

Animals↗
PubMed2003

Duchenne muscular dystrophy with associated growth hormone deficiency.

A patient with Duchenne muscular dystrophy (DMD) and growth hormone (GH) deficiency is described who had no clinical evidence of muscular weakness before initiation of GH replacement therapy. Treatment with human GH resulted in appearance of symptoms of easy fatigability and proximal muscle weakness. Thorough investigations including serum creatinine phosphokinase (CK) levels is recommended in every patient with GH deficiency before starting GH replacement therapy.

Child↗
PubMed2004

[An autopsy case of systemic vasculitis associated with hepatitis C virus-related mixed cryoglobulinemia presenting severe peripheral neuropathy].

A 75-year-old man, previously diagnosed as having chronic hepatitis C virus (HCV) infection, suddenly developed left foot drop, followed by progressive motor weakness and sensory disturbance in all of the extremities. Because of an elevated level of the rheumatoid factor (RF), he had been treated with antirheumatic drugs three years before the onset of his neurological symptoms. Within two months, he became unable to walk any more, and was transferred to our hospital. Neurologic examination showed asymmetrical severe muscular weakness and atrophy of all the limbs, and a sensory deficit under the level of the wrists and knees. Livedo reticularis was also noted in bilateral legs. Nerve conduction study revealed severe sensorimotor axonal neuropathy, and muscle biopsy specimens showed necrotizing vasculitis of small arteries in the perimysium. Serological tests indicated type II cryoglobulinemia (monoclonal IgAkappa + polyclonal IgG). A diagnosis of vasculitic neuropathy associated with HCV-related mixed cryoglobulinemia was made. A high-dose intravenous immunoglobulin therapy (IVIg) and a high-dose steroid therapy were not effective, and he died of alveolar hemorrhage probably due to pulmonary vasculitis. Postmortem pathological examination revealed severe vasculitis, accompanied by fibrinoid degeneration and the infiltration of predominant mononuclear cells into the small and medium-sized vascular walls of multiple organs such as the liver, kidney, pancreas and intestine as well as the peripheral nerves and skeletal muscles. A severe loss of myelinated fibers were also observed in the multiple peripheral nerves examined. We emphasize that patients with HCV infection and mixed cryoglobulinemia may develop severe systemic vasculitis resembling polyarteritis nodosa leading to often life-threatening polyvisceral failure, particularly in patients showing progressive mononeuropathy multiplex.

Aged↗