Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Muscle Rigidity”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed2003

Effects of a 5HT(2) receptor agonist on anaesthetized pigs susceptible to malignant hyperthermia.

BACKGROUND: The pathophysiology of the serotoninergic system in malignant hyperthermia (MH) is not completely understood. The serotonin-2 (5HT(2A)) receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI) induces typical MH symptoms, including skeletal muscle rigidity, an increase in body temperature, hyperventilation and acidosis in conscious MH-susceptible (MHS) pigs. Whether these symptoms are directly generated in skeletal muscle, result from central serotonergic overstimulation or from a porcine stress syndrome remains unresolved. In this study the in vivo effects of DOI on anaesthetized (and thus stress-protected) MHS and MH-normal (MHN) pigs were investigated. METHODS: and results. DOI 1 mg kg(-1) was administered three times at 40-min intervals to five MHS and five MHN anaesthetized pigs. Body temperature, heart rate, muscle tone, arterial carbon dioxide pressure (Pa(CO(2))), pH and creatine kinase concentrations were measured. The clinical occurrence of MH was defined by Pa(CO(2)) above 70 mm Hg and an increase in body temperature of more than 2 degrees C. Intragroup differences were analysed with the Friedman test as an overall non-parametric ANOVA and, in case of significance, with the Wilcoxon test. Intergroup comparisons were performed with the Mann-Whitney U-test (statistical significance P<0.05). MHS and MHN pigs developed muscle fasciculations, significant increases in body temperature and Pa(CO(2)) and a significant decrease in pH after the administration of DOI. These changes were comparable in both groups until the third dose of DOI, when in MHS pigs heart rate and Pa(CO(2)) rose significantly and pH fell significantly compared with MHN pigs. All MHS pigs fulfilled the MH criteria. Body temperature increased by more than 2 degrees C in all MHN pigs and Pa(CO(2)) exceeded 70 mm Hg in two. Thus, two MHN pigs fulfilled the criteria of MH. CONCLUSIONS: The comparability of the clinical presentation following DOI administration in MHS and MHN animals and the order of the development of MH-like symptoms favour the hypothesis of a central serotonergic overstimulation, leading to a serotonin syndrome.

Amphetamines↗
PubMed2005

Heat- and anesthesia-induced malignant hyperthermia in an RyR1 knock-in mouse.

Malignant hyperthermia (MH) is a life-threatening disorder characterized by skeletal muscle rigidity and elevated body temperature in response to halogenated anesthetics such as isoflurane or halothane. Mutation of tyrosine 522 of RyR1 (the predominant skeletal muscle calcium release channel) to serine has been associated with human malignant hyperthermia. In the present study, mice created harboring this mutation were found to represent the first murine model of human malignant hyperthermia. Mice homozygous for the Y522S mutation exhibit skeletal defects and die during embryonic development or soon after birth. Heterozygous mice, which correspond to the human occurrence of this mutation, are MH susceptible, experiencing whole body contractions and elevated core temperatures in response to isoflurane exposure or heat stress. Skeletal muscles from heterozygous mice exhibit increased susceptibility to caffeine- and heat-induced contractures in vitro. In addition, the heterozygous expression of the mutation results in enhanced RyR1 sensitivity to activation by temperature, caffeine, and voltage but not uncompensated sarcoplasmic reticulum calcium leak or store depletion. We conclude that the heterozygous expression of the Y522S mutation confers susceptibility to both heat- and anesthetic-induced MH responses.

Anesthesia↗
PubMed1982

Malignant hyperthermia.

A report is made of a 65-year-old male who died of a malignant hyperthermia of 42 degrees C. Symptoms included muscle rigidity at the termination of operation for neck-clipping of an aneurysm of the anterior communicating artery. Latent myopathy was observed in skeletal muscle, and a bleeding focus was present in the left anterior region of the hypothalamus, coinciding with the temperature regulation center. The mechanism of onset of this disease is still poorly understood, but it seems that this disease occurred due to synergic effects of the hypothalamic hemorrhage and the pre-existing myopathy. The serum CPK level at the time of death was abnormally high (250 U), and 3.4% of isozyme CPK1 was detected. The serum myoglobin was 204, 850 ng/ml, a markedly high level, and myoglobinuric nephrosis was present as a result.

Aged↗
PubMed1995

Neuroleptic malignant-like syndrome: a complication of acute organophosphate poisoning.

We report a 60-yr-old woman with schizophrenia, who manifested a neuroleptic malignant (NM)-like syndrome after acute organophosphate poisoning (OPP). She attempted suicide by ingesting 40% emulsions of DMTP (S-2,3-dihydro-5-methoxy-2-oxo-1,3,4-thiadizol-3-yl-methyl O,O-dimethyl phosphorodithioate) 100 ml. On admission, she was unconscious and demonstrated convulsions, depressed respiratory movements, miosis and profuse salivation. Plasma cholinesterase concentration (842 IU.L-1) was very low and OPP was diagnosed. She was treated with gastric lavage, atropine and pralidoxime (PAM). By the seventh day after admission, symptoms of OPP disappeared and serum ChE had recovered to a sub-normal level. On the 13th day, she demonstrated coma, high fever (41.0 degrees C) and lead-pipe rigidity. Serum CPK was increased (1631 IU.L-1). Dantrolene sodium iv was administered for three days. Body temperature began to decrease in 24 hr, and her consciousness, muscle rigidity and other neurological symptoms returned to normal by the 16th day after admission. She was discharged from the hospital without sequelae 55 days after admission. We conclude that OPP can predispose to an NM-like syndrome and that dantrolene may be effective in the management.

Atropine↗
PubMed1986

[Symptoms of acute cerebral hernia following induction of anesthesia in hydrocephalus--malignant hyperthermia in reality].

We report the case of a 4.9-year-old boy with congenital hydrocephalus and obstruction of his shunt who just after the induction of anaesthesia suddenly developed generalized muscle rigidity that made intubation impossible. Because of temporary mydriasis the situation could hardly be differentiated from acute cerebral herniation. The lack of any decrease in muscle tone after emergency trephination and drainage of the right lateral ventricle and the immediate improvement following intravenous dantrolene left no doubt about the diagnosis of malignant hyperthermia. The diagnosis was confirmed by the increase in serum creatine phosphokinase and the documentation of massive myoglobinuria. Reconstruction of the course of the first anaesthetic necessary for shunt implantation at the age of 62 days revealed that the same symptoms already had occurred. However, they then were not attributed to malignant hyperthermia but interpreted as symptoms of acute herniation. A detailed description of this first anaesthetic is given which again elucidates the problems associated with the abrupt onset of muscular hypertonus in a patient with neurologic disorder; moreover this may well be the first published case report of malignant hyperthermia at the age of just 2 months.

Anesthesia, General↗
PubMed1999

The dropped head sign in parkinsonism.

We describe seven patients who exhibited the dropped head sign in parkinsonism. These included six females and one male between the ages of 53 and 74. Three patients were clinically diagnosed as probable Parkinson's disease and four were diagnosed with probable multiple system atrophy. None had weakness in the posterior neck muscles or spasms in the anterior neck muscles. When the patients attempted to extend the head voluntarily or passively muscle contraction that was not seen in the dropped-head condition appeared. Surface electromyography of the neck indicated that the anterior neck muscles had rigidity. A gamma-block of the SCM muscles reduced the muscle activity when the head was elevated and improved the dropped-head condition slightly. These findings seem to indicate that the dropped head sign in parkinsonism could be associated with anterior neck muscle rigidity. Although the severity of the dropped head condition was affected by medication or by the clinical course in three patients, there was no clear relationship between the severity of the dropped head condition and the parkinsonism. We suspected that unbalanced muscle rigidity between the anterior and the posterior neck muscles could cause the dropped head sign.

Aged↗
PubMed1998

Parkinsonian syndrome as a neurological manifestation of Behçet's disease.

BACKGROUND: The central nervous system is often involved in Behcet's disease. Most common are meningoencephalitic and brain stem syndromes. Although basal ganglia involvement is not an uncommon finding on necropsy, there are only single reports on extrapyramidal syndromes-dyskinesia, chorea and Parkinsonism in patients with Behcet's disease. CASE STUDY: We report a patient fulfilling the criteria of the International Study Group for Behcet's disease. He had recurrent oral ulcerations, bilateral posterior uveitis and retinal vasculitis, skin papules and pustules, and recurrent monoarthritis. Neurologic examination revealed pseudobulbar palsy, slight and asymmetric bilateral pyramidal syndrome, muscle rigidity involving the four limbs, bradykinesia, masked face, and impaired postural reflexes. There was postural tremor in the extremities and myoclonic jerks involving the tongue and face muscles. Magnetic resonance imaging demonstrated small bilateral multifocal hyperintense lesions, with right predilection, involving the periventricular white matter, brain stem and basal ganglia. CONCLUSIONS: The Parkinsonian syndrome found in our patient might be due to involvement of both substantia nigra and basal ganglia. This case further emphasizes the wide spectrum of the neurological manifestations of Behcet's disease.

Adult↗
PubMed1987

Postoperative neuroleptic malignant syndrome. A case report.

A case of postoperative neuroleptic malignant syndrome is presented. A healthy 23-year-old male underwent a shoulder repair under uneventful fentanyl, halothane, nitrous oxide and oxygen anaesthesia. He received droperidol 5 mg IV and metoclopramide 10 mg IV intraoperatively to prevent postoperative nausea. Postoperatively, the patient developed autonomic instability, fever and generalized muscle rigidity. His level of consciousness was depressed. These findings were consistent with the diagnosis of neuroleptic malignant syndrome. The supportive treatment of the patient included active cooling measures, muscle relaxation and mechanical ventilation. The ability of anti-dopaminergic agents, including metoclopramide and droperidol, to precipitate the neuroleptic malignant syndrome is discussed. Treatment of the neuroleptic malignant syndrome is briefly discussed.

Adult↗
PubMed2004

Motor output characterizing thanatosis in the cricket Gryllus bimaculatus.

The cricket Gryllus bimaculatus displays a sudden rigid immobility (thanatosis) when voluntary leg movements are forcibly restrained. The tibial joints in all legs are stiffly immobilized for several minutes. The flexed-leg posture typical of thanatosis is maintained by the flexor tibiae muscle. To characterize thanatosis at the motor output level, the mechanical and physiological properties of the metathoracic tibia muscle were investigated. The accessory flexor muscle, especially well-developed in the cricket, acts to stably maintain the tibial flexion driven by the main flexor muscle. Extracellular recordings from the flexor muscle of tethered crickets revealed that activity of intermediate- and fast-excitatory units was almost completely suppressed, while slow-excitatory units persisted in firing tonically during thanatosis. The firing rate of slow-excitatory units progressively increased as the tibia flexed, but remained less than the firing rate seen in the quiescent state. Common inhibitory motor neurones that fire sporadically in the quiescent state were suppressed during thanatosis, especially in the beginning, and showed a large excitation immediately after arousal. These findings suggest that the entire motor neuronal pool is held under active suppression during thanatosis, and that flexor muscle rigidity is maintained by a weak discharge of the slow exciters together with suppression of the inhibitors.

Animals↗
PubMed1990

Pathogenesis and treatment of neuroleptic malignant syndrome.

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.

Antipsychotic Agents↗
PubMed1997

Pure akinesia manifested neuroleptic malignant syndrome: a clinical variant of progressive supranuclear palsy.

An autopsy case of pure akinesia (PA) is reported. The patient manifested L-dopa-unresponsive akinesia without accompanying rigidity, tremor, eye movement disorder or dementia from the age of 58 years. Brain magnetic resonance T2-weighted imaging at the age of 63 showed high intensity areas in the subthalamic regions, but brain atrophy was not observed. She received amantadine-HCl and L-threo-3,4-dihydroxyphenylserine (L-DOPS) for 5 years. At the age of 66, she died of the severe illness accompanied by consciousness disturbances, hyperthermia, muscle rigidity, abnormal blood pressure and elevated serum enzymes which were derived from the muscle. We considered her condition to be neuroleptic malignant syndrome (NMS). Pathologically the brain revealed degeneration in the subthalamic nucleus, globus pallidus and substantia nigra. Neurofibrillary tangles were detected in the temporal cortex, hippocampus, amygdaloid body and spinal cord, as well as in the basal ganglia, thalamus and brain stem. These findings were consistent with that of progressive supranuclear palsy (PSP); the change in the ventral pons was insignificant, suggesting that PA may have minimum involvement in the ventral pons. The skeletal muscle showed scattered necrosis that was compatible with NMS. As far as we know, this is the first report of NMS accompanied with PA.

Brain↗
PubMed2001

The anesthetic propofol modulates gating in paramyotonia congenita mutant muscle sodium channels.

We examined the effects of propofol on a paramyotonia congenita mutant skeletal muscle sodium channel in vitro, because life-threatening complications resulting from severe muscle rigidity during induction of anesthesia have been observed using other anesthetics in patients with hereditary sodium channel myopathies. Our hypothesis was that propofol might interact directly with mutant channels, causing enhanced muscle excitability in affected patients. Whole-cell voltage-clamp experiments were performed on HEK 293 cells expressing R1448H mutant sodium channels. Propofol blocked sodium inward current at clinical concentrations (5 micromol/L) when depolarizing pulses were started from holding potentials close to the physiological resting potential (-70 mV). Higher propofol concentrations (>/=25 micromol/L) accelerated pathologically delayed inactivation kinetics and delayed pathologically enhanced recovery from inactivation. Our in vitro results show that inactivation-deficient sodium channels are specifically targeted and blocked by propofol. This might reduce enhanced muscle excitability experienced by affected patients in vivo.

Amino Acid Substitution↗
PubMed2004

Rhabdomyolysis and paraneoplastic stiff-man syndrome with amphiphysin autoimmunity.

Stiff-Man syndrome (SMS) is a rare disease of the central nervous system characterized by chronic muscle rigidity and autoimmunity directed against synaptic antigens. In a subset of patients, generally positive for antiamphiphysin autoantibodies, SMS has an autoimmune paraneoplastic origin. Amphiphysin isoforms are expressed at high levels in brain and skeletal muscle and often are overexpressed in breast cancer. We report here the occurrence of rhabdomyolysis in a patient with SMS, breast cancer, and antibodies that recognize both brain and muscle amphiphysin isoforms. Immunotherapy induced a remission of both rhabdomyolysis and SMS symptoms. Autoimmune rhabdomyolysis may represent a paraneoplastic complication of cancer patients with amphiphysin autoimmunity.

Animals↗
PubMed1993

[Anesthetic-induced heart arrest. A case report of 2 infants with previously unrecognized muscular dystrophy].

We report two boys aged 4 and 10 months who suffered cardiac arrests after induction of anaesthesia. Both infants had no personal or family history of myopathy. In both cases anaesthesia was induced by inhalation with halothane and N2O/O2 (70/30). To facilitate tracheal intubation both were given succinylcholine after the administration of atropine. The 4-month-old developed muscle rigidity and cardiac arrest occurred immediately after tracheal intubation. Resuscitation was unsuccessful. Laboratory findings during resuscitation showed elevated serum potassium levels of more than 10 mmol/l and serum creatine phosphokinase 17.700 IU/l. Histopathologic examination of the skeletal muscle revealed congenital muscular dystrophy. In the older boy no muscle contractures were noted after administration of succinylcholine. He developed bradycardia that progressed to asystole 15 min after induction of anaesthesia. After 1 h of resuscitation a sinus rhythm could be established. The boy developed myoglobinuria and his serum creatine phosphokinase reached a maximum level of 45,000 IU/l on the 2nd day. The child survived and made a complete recovery. Two months later a muscle biopsy taken from the quadriceps showed marked muscular dystrophy. Duchenne's muscular dystrophy could be excluded. The most likely underlying reasons for these complications are discussed: anaesthesia-induced acute rhabdomyolysis or malignant hyperthermia.

Anesthesia↗
PubMed1995

Dopamine receptors in the substantia nigra are involved in the regulation of muscle tone.

The aim of the present study was to localize the dopamine receptors involved in the regulation of muscle tone. A strategy was used whereby the effects on muscle tone of injecting the irreversible dopamine receptor antagonist N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) in discrete brain regions were assessed. Increases in muscle tone were measured as changes in electromyographic activity of the gastrocnemius and tibialis muscles of conscious, unrestrained rats. No increases in muscle tone were found after injections of EEDQ into the anterior and posterior striatum, which produced marked reductions in dopamine receptor concentration. The effects of muscle tone of injecting EEDQ into the substantia nigra pars reticulata were also assessed. Large increases in muscle tone were observed associated with inactivation of either D1 or D2 dopamine receptors in the substantia nigra. The increased muscle tone was not reduced by subcutaneous administration of apomorphine, despite the presence of a normal population of striatal dopamine receptors. These findings provide evidence that dopamine receptors in the substantia nigra play an important role in the regulation of muscle tone. Further, they challenge the hypothesis that the muscle rigidity of Parkinson disease results primarily from loss of striatal dopamine receptor stimulation.

Animals↗
PubMed1992

Malignant hyperthermia.

In humans genetically predisposed to malignant hyperthermia, anesthesia can induce skeletal muscle rigidity, hypermetabolism, and high fever, which, if not immediately reversed, can lead to tissue damage or death. The corresponding condition in swine leads to stress-induced deaths and devalued meat products. Abnormalities in the Ca2+ release channel of skeletal muscle sarcoplasmic reticulum (the ryanodine receptor) have been implicated in the cause of both the porcine and human syndromes by physiological and biochemical studies and genetic linkage analysis. In swine, a single founder mutation in the ryanodine receptor gene (RYR1) can account for all cases of malignant hyperthermia in all breeds, but a series of different RYR1 mutations are likely to be uncovered in human families with MH. Moreover, lack of linkage between malignant hyperthermia and RYR1 in some families indicates a heterogeneous genetic basis for the human syndrome.

Animals↗