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At least 325 records · Page 18Linked to original sources
PubMed2001

Parkinsonism and neck extensor myopathy: a new syndrome or coincidental findings?

BACKGROUND: Dropped head in parkinsonism has been attributed to dystonia or unbalanced muscle rigidity. To our knowledge, isolated neck extensor myopathy with parkinsonism has been described in only one patient. OBJECTIVES: To assess the occurrence of neck extension weakness resulting in dropped head in patients with parkinsonism and to explore whether the head drop might be the consequence of neck extensor myopathy. PATIENTS AND METHODS: All patients who were evaluated because of parkinsonism in the Department of Neurology in our hospital between January 1, 1997, and December 31, 1999, and were found to have both parkinsonism and neck extension weakness resulting in head drop were studied. The patients underwent clinical examination, blood tests including the levels of creatine kinase and myoglobin and neurophysiological evaluation with needle electromyography and autonomic tests. Open biopsy on a neck muscle was performed in the patients who could cooperate. RESULTS: Of 459 patients evaluated because of parkinsonism, 7 were found to have neck extensor weakness resulting in head drop. Needle electromyography revealed myopathic changes in all 7 patients. Muscle biopsy, which was performed in 5 patients, disclosed myopathic changes in all 5 patients. Electron microscopy revealed mitochondrial abnormalities in 2 of these 7 patients. Three of the patients had concomitant neck rigidity that could contribute to the neck position. All 7 patients had autonomic dysfunction and 6 responded poorly to levodopa therapy, making a diagnosis of multiple system atrophy probable. CONCLUSION: Parkinsonism may be associated with isolated neck extensor myopathy resulting in dropped head, and this condition should be suggestive of multiple system atrophy.

Aged↗
PubMed1992

Malignant hyperthermia.

Malignant hyperthermia is a rare syndrome that occurs in genetically susceptible individuals who are exposed to frequently used inhalation anesthetics. The disorder is most common in children and young adults. It is triggered through a defect in the ability of skeletal muscles to concentrate and release calcium. Signs of malignant hyperthermia include hypercarbia, muscle rigidity and tachycardia. Temperature elevation is often a late sign of the syndrome. Treatment begins with stopping all inhaled anesthetics at the earliest sign of the syndrome. The use of dantrolene has significantly reduced mortality from malignant hyperthermia. No simple screening test exists. Family members or those with a suspicious history need to be counseled and should consider muscle biopsy and testing prior to surgery.

Adult↗
PubMed1978

[Malignant hyperthermia in a black child. A case report].

A case of malignant hyperthermia in a Black boy is presented. He developed this condition during repair of a cleft palate, with halothane as the triggering agent. The importance of the high incidence of malignant hyperthermia in patients with certain musculoskeletal abnormalities is stressed. Despite a cool and well air-conditioned theatre, the patient's temperature was 41 degree C when the condition was suspected. At that stage general muscle rigidity was present. The patient was successfully treated with procainamide, sodium bicarbonate and hydrocortisone; surface cooling (with ice packs) was instituted and the stomach was washed out with ice-cold Ringer's solution. Over a period of 14 days serum creatine phosphokinase values decreased from 630 IU (on the day of the incident) to 12 IU. A muscle biopsy showed variation in muscle fibre size. Electron microscopical studies showed myofibrillar disruption and folding of the basement membrane. A modified version of Denborough's technique was used for the in vitro exposure of muscle strips to halothane and suxamethonium. Isometric contraction was measured and recorded. A severe contraction followed the exposure of muscle strips to halothane, which confirmed the diagnosis.

Child↗
PubMed2006

Neuroleptic malignant syndrome with delayed onset of fever following risperidone administration.

OBJECTIVE: To report and discuss a case of neuroleptic malignant syndrome (NMS) with delayed onset of fever in a patient taking risperidone. CASE SUMMARY: A 59-year-old white female presented with progressive weakness, confusion, and disorientation 10 days after restarting risperidone 2 mg/day therapy for bipolar disorder. She had taken risperidone for several years prior to this episode and had stopped it for approximately 3 weeks; risperidone was discontinued on admission. The patient's creatine kinase (CK) level was elevated (901 IU/L; reference range 39-162) on admission and increased to 1991 IU/L the following day. She was initially afebrile and had no muscular rigidity. Elevated temperature (38.1 degrees C) did not occur until hospital day 2. The patient was successfully treated with diazepam, bromocriptine, and dantrolene and suffered no long-term sequelae. DISCUSSION: Other clinicians have reported atypical presentations of NMS in patients taking newer neuroleptic agents. Although this patient met diagnostic criteria for NMS, the hallmark symptoms of fever and muscle rigidity were delayed in onset. Also, the patient never remained febrile for more than 24 hours and her maximum temperature was only 38.6 degrees C. An objective causality assessment suggests that this case of NMS was probably related to restarting risperidone. CONCLUSIONS: Because of the life-threatening nature of this syndrome, clinicians should consider NMS in afebrile patients presenting with diaphoresis, changes in level of consciousness, mutism, tremors, tachycardia, leukocytosis, and elevated CK levels.

Female↗
PubMed1981

Malignant hyperthermia: current perspectives.

The incidence, etiology, clinical manifestations, and management of malignant hyperthermia (MH) are reviewed. The syndrome of MH is recognized as one of the causes of anesthesia-related deaths. It is considered pharmacogenetic because both an abnormal gene and precipitating environmental factors are necessary to produce an acute reaction. Metabolic defects, involving a derangement of calcium dynamics, appear to be the common characteristic of susceptible individuals. Calcium release and uptake from the sarcoplasmic reticulum is altered when an individual with MH is exposed to certain anesthetic agents or triggering physical and emotional stresses. Muscle rigidity, tachycardia, tachypnea, and high fever can lead to other complications and death. Management of an acute reaction of MH includes cooling methods to lower body temperature, hyperventilation, sodium bicarbonate control of acidosis, maintenance of fluid and electrolyte balance, and the administration of dantrolene sodium. A thorough family history, baseline CPKs, caffeine-halothane contracture tests, and ultramicroscopic examination of muscle biopsy specimens are recommended as screening techniques. The early administration of dantrolene sodium in acute reaction of MH has been shown to rapidly alleviate the symptoms and ensuing severe complications. Individuals with a strong family history of MH or previous episodes may be treated with oral dantrolene sodium before surgery to effectively prevent a crisis, and after surgery to prevent recurrence.

Creatine Kinase↗
PubMed2002

[Neuroleptic malignant syndrome].

The neuroleptic malignant syndrome (NMS) is a rare but potentially lethal form of neuroleptic drug-induced hyperthermia, altered level of consciousness, extrapyramidal effects, autonomic instability and muscle rigidity. The present review describes pathophysiology, frequency, course, outcome, mortality and management of NMS in prehospital care and emergency department care. Review discusses clinical features, diagnosis differentiation of this hyperpyretic-rigidity syndrome from other disorders and prevention of this serious iatrogenic condition as life-threatening disorder.

Acute Kidney Injury↗
PubMed2001

An autopsy case of neuroleptic malignant syndrome (NMS) and its immunohistochemical findings of muscle-associated proteins and mitochondria.

Neuroleptic malignant syndrome (NMS) is a rare but potentially fatal disorder. In forensic cases, post-mortem diagnosis of NMS is sometimes difficult if ante-mortem information, such as neuroleptic ingestion or signs and symptoms, cannot be obtained. A 39-year-old Japanese male on a neuroleptic treatment regimen suddenly became agitated and died. Autopsy revealed muscle rigidity and hyperthermia. Post-mortem examination of blood revealed elevation of creatine phosphokinase-MM (CK-MM) and lactate dehydrogenase-4 and dehydrogenase-5 (LDH-4 and LDH-5). In renal glomeruli and tubules, myoglobin was stained immunohistochemically. From these findings, the cause of death was considered to be NMS. To support the diagnosis of NMS, both skeletal and cardiac muscles were stained with actin, myoglobin, desmin and mitochondria antibodies immunohistochemically. Actin, myoglobin, desmin, and mitochondria had been lost from skeletal, but not from the cardiac muscle, which suggested that only the skeletal muscle was damaged. Moreover, because mitochondria had disappeared only from the skeletal muscle, it was considered that skeletal muscle degeneration was caused by mitochondrial damage. Therefore, it is suggested that immunostaining of skeletal muscle by antibodies for muscle-associated proteins and mitochondria is useful to corroborate a diagnosis of NMS.

Adult↗
PubMed2006

Parkinson's disease-like syndrome in rats induced by 2,9-dimethyl-beta-carbolinium ion, a beta-carboline occurring in the human brain.

Regarding the pathogenesis of Parkinson's disease, a neurotoxin hypothesis was proposed following the discovery that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces a Parkinson-like syndrome in humans and primates. Since then, researchers have searched for endogenous and exogenous compounds that are structurally similar to this neurotoxin. Such compounds include beta-carbolines, formed from tryptophan and its derivatives. beta-carbolines are present naturally in the human brain and cerebrospinal fluid. The present study examined the effect of bilateral, intranigral administration of 2,9-dimethyl-beta-carbolinium ion on muscle tone, electromyographic activity, dopamine metabolism in the striatum, and the number of tyrosine hydroxylase-immunoreactive neurons and volume of the substantia nigra in rats. We found that the beta-carbolinium ion (15 or 40 nmol per side) caused a significant decrease in the striatal levels of dopamine and its metabolites, which was accompanied by an enhancement of muscle tone and electromyographic activity. Stereological counting revealed that the beta-carbolinium caused a significant decrease in the total number of tyrosine hydroxylase-immunoreactive neurons and shrinkage of the substantia nigra. The findings suggest that the methylated beta-carbolinium ion produces a dose-dependent degeneration of nigrostriatal neurons, leading to deficits in dopaminergic neurotransmission and an increase of muscle resistance and electromyographic activity, a syndrome equivalent to muscle rigidity in Parkinson's disease.

Animals↗
PubMed2000

The use of halothane gas to identify turkeys prone to developing pale, exudative meat when transported before slaughter.

Halothane screening has been used in the swine industry to identify animals susceptible to stress and prone to developing pale, soft, exudative (PSE) meat. This study evaluated the ability of halothane to identify stress-susceptible turkeys prone to developing PSE meat when reared to market age and transported before slaughter. Male Nicholas turkeys (n = 1,286) were exposed to 3% halothane for 5 min at 4 wk of age in two trials. Birds were classified as halothane sensitive (HAL+) or halothane nonresponder (HAL-), in which HAL+ birds showed signs of muscle rigidity in the legs upon removal from halothane gas, and HAL- birds showed no stiffness response. Approximately 3.5% (45) of the turkeys were HAL+. All HAL+ birds and an equal number of HAL- birds were grown until 20 wk of age. Immediately prior to slaughter, all birds were transported in coops on a flatbed trailer for 2 h and then immediately slaughtered upon arrival at the processing plant. Breast muscle pH (0, 1.5, and 24 h postmortem) and L* value (1.5 h and 24 h postmortem) were measured on the fillets. Drip loss and cook loss were also determined on marinated and nonmarinated breast fillets from each carcass. There were no significant mean differences in any parameter measured between the HAL+ and HAL- turkeys. However, the HAL+ turkeys had a greater percentage of fillets with L* values >51 compared with the HAL- turkeys. These results suggest that either halothane response is only a limited predictor of PSE meat in turkeys or that transportation is not an appropriate stressor to induce the PSE condition.

Anesthetics, Inhalation↗
PubMed1991

The muscle findings in the neuroleptic malignant syndrome associated with lysergic acid diethylamide.

A detailed pathological description of the muscle findings in a case of the neuroleptic malignant syndrome (NMS) following ingestion of lysergic acid diethylamide (LSD) is given, including the first ultrastructural analysis. Focal necrosis, oedema, and hypercontraction of fibres with glycogen and lipid depletion, were identified, all of which had resolved completely a year later. The findings are compared with those in malignant hyperthermia. It is suggested that the results support the view that in NMS, the muscle rigidity is due to central mechanisms and, in both this disorder and malignant hyperthermia, it is responsible for the hyperpyrexia and its life-threatening complications.

Adult↗
PubMed2005

Malignant hyperthermia: update on susceptibility testing.

Malignant hyperthermia (MH) is a pharmacogenetic clinical syndrome that manifests as a hypermetabolic crisis when a susceptible individual is exposed to an anesthetic triggering agent. Clinical signs include unexplained elevation of end-tidal carbon dioxide, muscle rigidity, acidosis, tachycardia, tachypnea, hyperthermia, and evidence of rhabdomyolysis. This process is a result of an abnormally increased release of calcium from the sarcoplasmic reticulum, which is often caused by an inherited mutation in the gene for the ryanodine receptor (RYR1) that resides in the membrane of the sarcoplasmic reticulum. The gold standard for determination of MH susceptibility is the caffeine-halothane contracture test. However, it is invasive, requiring skeletal muscle biopsy and is not widely available. Researchers have begun to map mutations within the ryanodine receptor gene (chromosome 19q13.1) responsible for conferring MH susceptibility. Ryanodine receptor mutations are found in at least 25% of known MH susceptible individuals in North America. Mutation analysis has recently become available in the United States and is expected to play an integral role in the diagnosis of MH susceptibility in the future.

Algorithms↗
PubMed1992

Malignant hyperthermia and neuromuscular disease.

Malignant hyperthermia (MH) is a rare clinical syndrome characterized by hypermetabolism and triggered by specific anesthetic agents. The mechanism of this abnormal reaction is due to uncontrolled calcium flux in the skeletal muscles resulting in a variable clinical syndrome of muscle rigidity, respiratory and metabolic acidosis, and elevation of temperature. The specific genetic defect underlying this condition has not been identified in humans, though in susceptible swine a mutation of the gene for the ryanodine receptor, a large protein which comprises the calcium channel in the sarcoplasmic reticulum, has been identified recently. Inheritance in humans appears to be autosomal dominant with variable penetrance. Patients with MH rarely have physical or laboratory signs of muscle disease. However, scattered case reports and investigations of individuals with known myopathies and other muscle related problems, such as acute rhabdomyolysis or idiopathic persistently elevated creatine kinase, suggest a possible association of MH with a variety of neuromuscular diseases and stress syndromes. This association is very strong in the case of central core disease (CCD) where it is supported by clinical and laboratory evidence, including the proximity of the CCD gene to the ryanodine receptor gene on chromosome 19. A variety of other diseases have been implicated and can be classified as possibly associated (King-Denborough syndrome, Duchenne muscular dystrophy) or unlikely to be associated (myotonia congenita, sudden infant death syndrome, limb girdle dystrophy, neuroleptic malignant syndrome, etc.).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Experimental comparison of ketamine with a combination of ketamine, butorphanol and medetomidine for general anaesthesia of the Eurasian badger (Meles meles L.).

The refinement of anaesthetic regimes is central to improving the welfare of captured wildlife. The Eurasian badger (Meles meles) has been the subject of an intensive long-term ecological and epidemiological study at Woodchester Park, Gloucestershire, England. During routine trapping operations (June 21st, 2000-January 23rd, 2001) an experimental trial was conducted on 89 badgers to compare the physiological effects of anaesthesia using ketamine hydrochloride alone, and in conjunction with medetomidine hydrochloride and butorphanol tartrate. The mixture induced a significantly longer period of anaesthesia, and either substantially reduced or eliminated the adverse effects associated with ketamine anaesthesia (e.g., excessive salivation, bouts of sneezing, rough recoveries, and muscle rigidity). In a sub-sample of badgers given the mixture, anaesthesia was reversed using atipamezole hydrochloride. Under ketamine anaesthesia, heart rates were initially significantly higher and respiration rates were consistently higher, than in badgers given the mixture. In all badgers heart rates declined and respiration rates increased during anaesthesia, but the rate of change was greatest in animals given only ketamine. Overall, the mixture provided a more balanced anaesthesia characterised by muscle relaxation and complete unconsciousness.

Anesthesia, General↗
PubMed2001

Spasticity in kids. An intrathecal option.

The painful muscle rigidity and severe spasms suffered by patients with brain and spinal injury can be managed even more successfully than in the past with intrathecal baclofen. For many, it's provided effective relief and improved levels of function.

Baclofen↗
PubMed2004

The use of halothane and succinylcholine to identify broilers prone to developing pale, soft, exudative meat.

Within the last several years, the poultry industry has seen a dramatic increase in the occurrence of pale, soft, and exudative (PSE) meat. This problem is known to be associated with a rapid decline in postmortem (PM) muscle pH, which results in inferior protein functionality similar to that found in PSE pork. Many factors such as seasonal changes have been known to influence the occurrence of PSE meat in poultry and swine. Halothane and succinylcholine have been used within the pork industry to identify animals susceptible to stress and prone to developing PSE meat. The mechanism for the triggering of the PSE gene in poultry has not been fully understood. Therefore, a study was conducted to determine the effectiveness of screening broilers with halothane to identify those prone to developing PSE meat. Succinylcholine was used before slaughter to serve as a triggering agent for the PSE condition. At 4 wk of age, broilers from 4 commercial strains (n = 1,000) were subjected to 3% halothane gas and classified as either halothane positive (HAL+) or negative (HAL-) based on muscle rigidity within the legs. Although halothane sensitivity varied slightly among the strains, approximately 14% of the birds overall were classified as HAL+. All HAL- birds (n = 163) and an equal number of HAL-birds (n = 163) in each strain were grown to market age (7 wk) and were commercially processed. At the time of processing, half of the HAL+ and HAL- birds were injected intravenously with succinylcholine and were slaughtered at 0.25 h postinjection. Pectoralis muscle samples were collected at 0.25, 2, 5, and 24 h PM for the evaluation of rigor development (muscle pH) and meat quality (L* value, moisture, drip loss, and cook loss). Halothane sensitivity had no effect on rigor development, muscle color, or water-holding capacity in the 4 broiler strains. Although birds exhibited reactions to the halothane gas, the halothane sensitivity, along with the use of succinylcholine, was not able to identify birds prone to developing PSE meat.

Animals↗
PubMed2001

Abnormal elevation of resting pressure at the upper esophageal sphincter of Parkinson's disease patients.

We investigated the oral and pharyngeal swallowing function in seven Parkinson's disease (PD) patients, using videomanofluorometry, which is videofluorographic and manometric evaluation conducted simultaneously. Abnormal elevations of resting pressure were found at the upper esophageal sphincter (UES) in three of the seven cases, when they were asked to hold a bolus in the mouth and initiate swallowing. One of these three cases showed an abnormal elevation of resting pressure, intermingled with a normal pressure pattern. Since the UES showed complete relaxation in these three cases, it is inappropriate to suppose that irreversible pathophysiological changes at the level of peripheral nerves had occurred. Our results suggested that altered resting pressure resulted from dysfunction at a more central level, such as a lack of dopaminergic stimulation at the supramedullary level causing skeletal muscle rigidity. Since a tonic abnormality of the UES cannot be measured by only videofluorography, both videofluorographic and manometric evaluation will be necessary to assess the pharyngeal phase of swallowing in PD patients.

Aged↗
PubMed1991

Neurobehavioral evidence for kappa agonist activity of the morphinan derivative 14-beta-methyl 8-oxacyclorphan [BC (3016)].

The purpose of the present study was to determine if the in vivo neurobehavioral effects of the morphinan 14-beta-methyl 8-oxacyclorphan, [BC (3016)], would reflect the kappa agonist activity found in our previous in vitro studies. The effects of intracisternal administration of various doses (10-80 micrograms) of BC (3016) on body temperature, muscle rigidity, nociception of thermal, chemical and mechanical stimuli as well as its ability to induce catalepsy were examined. The effects of intrathecal administration of the same doses of the compound on reactivity of animals to a thermal stimulus were also assessed. Finally, the ability of BC (3016) to antagonize well known neurobehavioral effects of morphine was investigated. Results indicate that the analgesic properties of BC (3016) resemble those of typical kappa agonists: Intracisternal administration of the drug failed to affect nociception to an aversive thermal stimulus but markedly reduced the reactivity of animals subjected to noxious chemical or mechanical stimuli. On the other hand, intrathecal administration of BC (3016) significantly attenuated nociception of animals to a thermal stimulus. The in vivo neurobehavioral effects of BC (3016) appear to be kappa selective since the drug did not decrease body temperature, increase muscular tone or induce catalepsy, three effects generally attributed to mu agonists. Furthermore, BC (3016) antagonized the immobility, trunk rigidity, catalepsy and analgesia induced by morphine. In summary, the present results reveal that BC (3016) displays a profile of neurobehavioral effects similar to that of well known kappa agonists.

Animals↗
PubMed1997

[Intraoperative malignant hyperthermia: apropos of a case].

Malignant hyperthermia (MHS) is a rare potentially fatal complication of general anesthesia. Anesthetic agents most frequently incriminated are succinylcholine and halogenated agents. Respiratory acidosis is the most specific and sensitive sign. Hyperthermia per se may occur secondarily or may stay totally absent. Tachycardia and/or arrhythmias often develop due to hyperkalemia and metabolic acidosis. Muscle rigidity whenever present is pathognomonic The "gold standard" test for the diagnosis of MHS is the halothane-caffeine contracture test. Dantrolene is the treatment of choice and prognosis depends on the early administration of this agent.

Dantrolene↗