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 181 records · Page 10Linked to original sources
PubMed1997

Pallidotomy revisited. Analysis of posteroventral pallidotomy.

Posteroventral pallidotomy (PVP) has been shown to alleviate motor symptoms in Parkinson's disease (PD), e.g., rigidity, secondary akinesia due to existence of muscle rigidity and slight tremor, but not the marked tremor. For the latter, additional lesion of the ventral intermediate nucleus of the thalamus is necessary. Akinesia was divided into three subtypes, and the influence of PVP on each type is described. Primary akinesia is not changed by either PVP or thalamotomy but responds well to L-dopa. Psychological symptoms, i.e., depressive mood, loss of initiation or abulia, and lowered emotional activity, which are generally termed as bradyphrenia, benefit well from PVP but less from thalamotomy. This effect is interpreted as due to the lesion extending into the ventral pallidum, where a small posterior part of the limbic-motor projections may possibly be involved. Such experience suggests that the third type of akinesia in PD, named the 'psychomotor or limbic-motor type' by the author, can be improved by the surgical procedure on the ventral globus pallidus. These observations offer an important chance to understand the psychological symptoms in PD as a result of dopamine deficiency of ventral tegmental area neurons projecting to the ventral striatum, which further influences the ventral pallidum.

Aged↗
PubMed1987

Management of tetanus.

Two cases of tetanus are presented, and the diagnosis, clinical features, and management of tetanus are reviewed. The first patient, an 86-year-old woman, had marked muscle rigidity but was able to breathe spontaneously. A dark eschar with purulent drainage was noted on her left foot, but Clostridium tetani was not isolated. She was placed in a semidark room and was treated with penicillin G; tetanus immune globulin (TIG) 5000 units i.m.; tetanus toxoid 0.5 mL i.m.; diazepam, chlorpromazine, and morphine for sedation, muscle relaxation, and analgesia; ranitidine for stress ulcer prophylaxis; heparin for prevention of deep-vein thrombosis; and peripheral-vein nutrition. Her condition improved gradually, and she was discharged to a rehabilitation institute after 32 days. The second patient, a 46-year-old woman, experienced progressive descending paralysis and required ventilatory support. She had a periodontal abscess, but cultures of the drainage were negative. She was placed in a semidark room and treated with erythromycin, TIG, tetanus toxoid, diazepam, pancuronium bromide, morphine, ranitidine, and heparin. Autonomic instability occurred during the second and third weeks, but cardiac output was maintained without treatment. The patient was extubated after five weeks, and was transferred out of the intensive-care in the following week. The diagnosis of tetanus is based primarily on characteristic findings of muscle rigidity and reflex spasms; cultures for C. tetani are of limited value. A history of trauma or injury is common. Pulmonary infections and cardiovascular instability are the most common complications. Therapy consists of ventilatory support; control of neuromuscular symptoms with benzodiazepines, narcotics, and neuromuscular blockers; antibiotic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1982

Malignant hyperthermia. Current concepts.

At least three myopathies have been associated with malignant hyperthemia (MH). The clinical manifestations of MH are variable and depend on the nature of the underlying myopathy and the anesthetic agents administered. Unless muscle relaxants are used, fever and muscle rigidity may be delayed at onset. Tachycardia and tachypnea are often the earliest manifestations and can occur immediately or several hours into a surgical procedure. Life-threatening cardiac arrhythmias may result from hyperkalemia and acidosis. A hyperthermic reaction developed in an 8-year-old boy with a family history of Duchenne's muscular dystrophy one hour after induction of anesthesia. Temperature elevation and muscle rigidity were minor components of the condition. Determination of arterial blood gas concentrations and the serum potassium level established the diagnosis and enabled the start of lifesaving therapy.

Anesthesia↗
PubMed2000

[Malignant neuroleptic syndrome. A review of epidemiology, risk factors, diagnosis, differential diagnosis and pathogenesis of MNS].

Neuroleptic malignant syndrome (NMS) is a rare, potentially life-threatening disorder that results from the use of neuroleptics. NMS was first recognised as a complication of dopamine receptor antagonists characterized by extrapyramidal disturbances, hyperthermia, muscle rigidity, autonomic instability, mental status changes and elevated serum creatine kinase levels. Concepts of NMS have changed because medications other than classic neuroleptic drugs have been implicated as triggering agents. The incidence of NMS is about 0.2% with a mortality between 4-30%, which may be diminished by treatment. The neurochemical key features in all these conditions probably result from disruption of the dopamine system in the brain and the effects of neuroleptics on muscle. Recognition of NMS is the most important step in its management by discontinuation of the causative drugs and applying supportive care and therapeutic measures. Specific therapeutic measures include the application of dopamine receptor agonists, e.g. dantrolene and use of benzodiazepines. The differential diagnosis of NMS comprises an extensive list of disorders presenting with fever and with muscle rigidity. Neuroleptics may be reintroduced in the majority of patients by using an atypical neuroleptic drug such as clozapine.

Adolescent↗
PubMed1989

Malignant hyperthermia in an office surgery suite: a case report.

Malignant hyperthermia is a threat to the life of the surgical patient. It is a pharmacogenic disease that is brought on by contact with certain drugs and is manifest by a hypermetabolic crisis with tachycardia, ventricular ectopy, metabolic acidosis, and a rapid rise in body temperature. Muscle rigidity may or may not be present. Thanks to a reliable porcine animal model of malignant hyperthermia, dantrolene sodium has been found to be effective in the prevention and treatment of malignant hyperthermia. In this article a case report of malignant hyperthermia occurring in an office surgery suite is presented. The patient was 37 years old and underwent a routine septorhinoplasty under general anesthesia. The operation was complicated by ventricular ectopy, rapid rise in body temperature, and muscle rigidity at the end of the case. The malignant hyperthermia aborted spontaneously after 30 minutes; dantrolene was not given.

Adult↗
PubMed1992

[A case of neuroleptic malignant syndrome with acute renal failure].

Neuroleptic malignant syndrome is a potentially lethal side effect of neuroleptic drugs, characterized by fever, muscle rigidity, autonomic dysfunction, and altered consciousness. A 50-year-old female hospitalized three times in the past for psychiatric treatment was admitted to Umayabashi Hospital for treatment of a relapse of a schizophrenic psychosis. She had received 50 mg of chlorpromazine and one tablet of Vegetamin-A (chlorpromazine 25 mg, promethazine 12.5 mg, phenobarbital 40 mg). Approximately 24-36 hours later, the patient became febrile and lost consciousness, and eight days later, acute renal failure occurred with muscle rigidity. She was transported to Maebashi Red Cross Hospital to receive hemodialysis. On admission, the laboratory studies showed high levels of serum creatine phosphokinase, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, creatinine and blood urea nitrogen. She underwent hemodialysis for treatment of acute renal failure and recovered from it after 16 sessions of hemodialysis.

Acute Kidney Injury↗
PubMed2005

Downbeating nystagmus and muscle spasms in a patient with glutamic-acid decarboxylase antibodies.

PURPOSE: To report the ophthalmic findings and response to treatment in a patient with glutamic-acid decarboxylase antibodies. DESIGN: Case report. METHODS: A 55-year-old woman developed progressive, painful, low back muscle spasms, vertical diplopia, downbeating nystagmus, and asymmetric appendicular ataxia. RESULTS: Downbeating nystagmus was present in primary gaze with an alternating skew deviation in lateral gaze. Serum and cerebrospinal fluid GAD antibodies were detected. Treatment with diazepam led to resolution of spasticity, whereas repeated courses of intravenous immunoglobulin improved cerebellar function, including appendicular ataxia and downbeating nystagmus. CONCLUSIONS: Patients with GAD antibodies may have elements of both Stiff-person syndrome (muscle rigidity and spasms) and prominent cerebellar dysfunction. Treatment with diazepam rapidly improved Stiff-person symptoms, whereas IVIg was partially effective at the early stage of cerebellar dysfunction.

Autoantibodies↗
PubMed2001

[Two pediatric cases of malignant hyperthermia caused by sevoflurane].

We experienced two cases of malignant hyperthermia (MH) triggered by sevoflurane. Case 1 was a six-year-old girl, 15.8 kg, undergoing strabismus repair. She had flat back, elevated diaphragm and high arched palate. Anesthesia was induced and maintained with sevoflurane and nitrous oxide in oxygen. Her trachea was intubated without the use of muscle relaxant. Thirty minutes after the induction of anesthesia, ETco2 was over 60 mmHg despite hyperventilation. Muscle rigidity of legs and the rise in temperature were noted. MH was diagnosed and dantrolene i.v. was administered. Her maximum esophageal temperature was 40.2 degrees C. ETco2 and temperature returned to baseline values after dantrolene administration. Creatine phosphokinase (CK) level was 252 U.l-1 preoperatively, and 1690 U.l-1 next day. Case 2 was a year-and-9-month-old boy undergoing accessory ear resection. Anesthesia was induced with sevoflurane and nitrous oxide in oxygen. His trachea was intubated with an aid of vecuronium. Forty minutes after administration of sevoflurane his temperature rose to 38.6 degrees C with heart rate 191 bpm and Spo2 93%, and muscle rigidity of legs. MH was diagnosed and dantrolene was administered. His highest temperature was 39.3 degrees C and was reduced promptly after dantrolene. Postoperatively he was noted to have downslanting palpebral fissures, micrognathia, low set ears, and a single crease of the fifth finger and diagnosed as King syndrome which is reported to have association with MH. Both patients had no history of anesthesia nor abnormal family history. Both of them were rescued with dantrolene and recovered without sequelae.

Anesthetics, Inhalation↗
PubMed1981

Porcine stress syndrome and postmortem muscle characteristics of two purebreds and three specific terminal crosses.

The incidence of Porcine Stress Syndrome (PSS), determined by halothane screening, and parameters of muscle quality and carcass leanness were studied in 108 pigs from a larger population of 658 pigs of Pietrain (P), Minnesota No. 1 (M), Hampshire (H) x (P x M), Yorkshire (Y) X (P X M) and P X (P X M) breeding. The larger population was also surveyed by the halothane screening procedure for incidence of PSS, and growth rate was measured. At 6 to 14 weeks of age, pigs were classified as PSS if they exhibited muscle rigidity within 5 min after the commencement of anesthetization with 3% halothane in oxygen. The incidences noted for the larger population were: H x (P x M) and Minnesota No. 1, 0%; Pietrain, 88%; Y x (P x M), 3%, and P x (P x M), 17%. Results demonstrated that the H x (P x M) group displayed excellent carcass meatiness combined with acceptable meat quality and freedom from PSS.

Animals↗
PubMed2006

Rigidity and spasms from autoimmune encephalomyelopathies: stiff-person syndrome.

Stiff-person syndrome (SPS) is a disorder characterized by progressive muscle rigidity with superimposed painful muscle spasms and gait impairment due to continuous motor activity. Evidence has accumulated in favor of SPS representing an autoimmune, predominantly encephalomyelopathic disorder resulting from B-cell-mediated clonal production of autoantibodies against presynaptic inhibitory epitopes on the enzyme glutamic acid decarboxylase (GAD) and the synaptic membrane protein amphiphysin. Recognition of the clinical spectrum of SPS is important, particularly the upper-limb, cervical, and cranial nerve involvement that occurs in paraneoplastic variants. The correlation between antibody levels and severity of disease offers evidence for a pathogenic role for the anti-GAD and anti-amphiphysin autoantibodies. The scarcity of neuropathological correlates stand in sharp contrast with the severity of the disability in affected individuals and suggests that functional impairment of inhibitory circuits without structural damage is sufficient to develop the full clinical spectrum of SPS. The rarity of this condition limits the feasibility of controlled clinical trials in the treatment of SPS, but the available evidence suggest that drugs that increase cortical and spinal inhibition such as benzodiazepines and drugs that provide immune modulation such as intravenous immunoglobulin, plasmapheresis, and prednisone are effective treatments.

Autoantibodies↗
PubMed2003

Fatal acute poisoning by bentazon.

A case of fatal suicidal bentazon poisoning is presented along with a description of the different analytical methods involved. A 56-year-old farmer was examined by the family doctor 1 h after voluntarily ingesting 500 mL of FIGHTER (bentazon, 480 g/L water). He presented a Glasgow score of 15, polypnea, diarrhea, and vomiting. During transport by ambulance to the hospital, he tossed, sweated, and suddenly presented breathing difficulty followed by heart failure. Tracheal intubation was impossible (H1.5) despite use of different diameter cannulas because of extreme general muscle rigidity. All attempts at resuscitation failed, and the patient died within 2 h postingestion. Blood and urine samples were taken just before death. General basic and neutral drug screening by high-performance liquid chromatography-diode-array detection and gas chromatography-nitrogen-phosphorus detection showed no strychnine or other drugs or toxics except for citalopram (< 0.1 mg/L) and bentazon, but this weak acidic molecule (pKa3.3) was badly extracted in alkaline conditions. Plasma and urine levels, measured after acidic extraction, protein precipitation, or simple dilution, were 1500 and 1000 mg/L, respectively. Bentazon (M.W. 240) was confirmed by its basic mass spectrum (ESI-, m/z 239, 197, 175, 132) or by that of methylated derivative (El+, m/z 254, 212, 175). An hydroxylated metabolite (ESI-, m/z 255, 213, 191, 148; El+, m/z 284, 242, 163) and the N1-glucuronide conjugate of bentazon (ESI-, m/z 415, 239) were also detected in urine. (Quantitation ions are underlined.) This first case of bentazon poisoning with available analytical data revealed the high toxicity of this compound after large dose ingestion with early and heavy symptoms such as muscle rigidity probably related to muscular toxicity. Comparison with another nonfatal case and with toxicological data on animals is discussed.

Benzothiadiazines↗
PubMedDate not supplied

[Excitability curve of alpha motor neurons of the foot dorsal flexor in chemically induced parkinsonian rigidity prior to and following ethylbenzatropine administration].

For evaluation of the state of excitability of motoneurons in the dorsal flexor of the foot in patients with drug-induced muscle rigidity curves of excitability of motoneurons in the anterior tibial muscle were plotted in 10 patients not receiving psychotropic agents (controls) and 10 patients treated with chlorpromazine. Two variants of experiment wase used: in the 1st variant stimulation of the peroneal nerve behind the fibular capitulum served as the conditioning and testing stimulus, in the 2nd variant stimulation of the tibial nerve in the popliteal fossa was the conditioning stimulus and stimulation of the peroneal nerve in the above way was the testing stimulus. The investigations were carried out before and 30-50 min after intramuscular injection of ethylbenzatropine 5 mg. In the 1st variant the curve of excitability of the motoneurons of the anterior tibial muscle showed the same configuration as the curve of excitability of motoneurons of the soleus muscle in the control group as well as in the treated group. Similarly as in the excitability curve of the soleus muscle five phases could be differentiated in it. Phase III of depression was, however, deeper and phase IV of returning excitability was more evident. In variant II in phase III depression was observed lasting only 40 msec., then in place of return of excitability its decrease was observed. These results were similar to these obtained in the case of conditioning stimulation of afferent fibres of the anterior tibialis muscle, and testing stimulation of the afferent fibres of the soleus muscle. After ethylbenzatropine injection no changes were found in variant I, on the other hand, in variant II a rise of excitability was present in phase III in the control group and in phases III and IV in treated patients. Ethylbenzatropine seemed, thus, to have no effect on the excitability of motoneurons in the dorsal flexor of the foot in the case of conditioning afferent stimulation of the dorsae flexor of the foot.

Chlorpromazine↗
PubMed1993

Fentanyl-induced rigidity and unconsciousness in human volunteers. Incidence, duration, and plasma concentrations.

BACKGROUND: Muscle rigidity frequently accompanies induction of anesthesia with opioids. The authors sought to determine whether unconsciousness and amnesia occur when humans develop rigidity and apnea after intravenous fentanyl (without other concomitant anesthetics). METHODS: The incidence and duration of rigidity and level of consciousness were evaluated and associated plasma concentrations of fentanyl were measured in 12 healthy adult male volunteers given only intravenous fentanyl. Fentanyl was infused at a rate of 150 micrograms/min until a total of 15 micrograms/kg had been administered. Arterial blood samples for fentanyl assay were drawn and responsiveness, heart rate (HR), and systolic and diastolic arterial blood pressures were determined at frequent intervals during and after infusion. If rigidity was accompanied by an Spo2 < 90%, positive pressure ventilation with 100% O2 with a mask was instituted until spontaneous ventilation resumed. RESULTS: The incidence of muscular rigidity was 50% (6/12). All subjects who developed rigidity were apneic, unresponsive, and had no recall of commands to breathe or of positive pressure ventilation. Subjects not developing rigidity remained awake and responsive. No subject developing rigidity required neuromuscular blockade to allow positive pressure ventilation and adequate oxygenation (Spo2 > 90%). When rigidity occurred, it started 3 +/- 0.9 (range 1-4) min after the peak plasma fentanyl concentration and lasted for 11.5 +/- 5.8 (range 7-23) min. Rigidity started at a plasma fentanyl concentration of 21.5 +/- 4.4 (range 16-28) ng/ml and ended at 6.9 +/- 1.5 (range 5.2-8.7) ng/ml. Baseline HR was less in the subjects who subsequently developed rigidity (56.7 +/- 7.8 vs. 67.2 +/- 7.8 P = 0.04). No differences in fentanyl plasma concentrations or predicted effect site concentrations for rigidity were detected between subjects who developed rigidity and those who did not. CONCLUSIONS: These findings support the hypothesis that unconsciousness occurs in the unstimulated subject during fentanyl-induced apnea and rigidity.

Adult↗
PubMed1982

The relationship between parkinsonian rigidity and hypokinesia in the orofacial system: a quantitative analysis.

Muscle rigidity was quantified in the labial muscles of parkinsonian and normal subjects by applying known forces and observing the resultant displacements to determine labial stiffness coefficients. In parallel, labial speech movements were observed from these same subjects to evaluate hypokinesia. Labial rigidity was consistently correlated with decrements in the range of lip movement. EMG from orbicularis oris and mentalis muscles indicated a causal relationship between rigidity and hypokinesia.

Aged↗
PubMedDate not supplied

[Freeman-Sheldon syndrome: generalized muscular rigidity after anesthetic induction].

We describe a case of generalized muscle rigidity in a 2-year-old patient with Freeman-Sheldon syndrome undergoing surgery for eventration of the diaphragm after anesthetic induction with halothane and succinylcholine. Anesthetic induction was by mask with oxygen, nitrous oxide and halothane, with succinylcholine as a muscle relaxant. Approximately 10 minutes after start of induction, muscular rigidity appeared and developed rapidly, becoming severe and compromising ventilation. Tracheal intubation was attempted without success, owing to stiffness of the masseter muscles. Sodium dantrolene 2.5 mg/kg was administered and relaxation was achieved immediately for both masseter and peripheral muscles, such that the patient recovered spontaneous breathing. We conclude that there is risk of association between Freeman-Sheldon syndrome and malignant hyperthermia.

Abnormalities, Multiple↗
PubMed1988

Wakefulness during the induction with high-dose fentanyl and oxygen anesthesia.

The purpose of this study was to investigate the state of wakefulness during the induction of anesthesia with high-dose fentanyl using the isolated forearm technique. Ten patients scheduled for elective cardiovascular surgery were premedicated with morphine (0.15 mg/kg) and scoploamine (0.3-0.4 mg) intramuscularly one hour before induction. The induction of anesthesia was performed by intravenous administration of 100 micro g/kg of fentanyl in 15 min or over. The pneumatic tourniquet applied on the left upper arm was inflated to 220-240 mmHg after 10 micro g/kg of fentanyl was given and then pancuronium was administered. Verbal commands were given to the patient after 25, 50, 75 and 100 micro g/kg of fentanyl was administered. Eight patients out of 10 responded to the verbal commands after administration of 25 micro g/kg of fentanyl. Six patients also responded after administration of 100 micro g/kg of fentanyl and diazepam 5 mg was given to prevent tachycardia and rigidity during endotracheal intubation. Muscle rigidity and tachycardia were noticed in three and four patients respectively. These complications disappeared by diazepam administration. It was noted that wakefulness frequently occurred during the induction by high-dose fentanyl and oxygen anesthesia. To prevent such wakefulness therefore, it is necessary to use anesthetic supplements which do not cause cardiovascular depression.

Journal Article↗
PubMed1988

Rapid death during cocaine abuse: a variant of the neuroleptic malignant syndrome?

A mechanism for rapid death in cocaine abusers is proposed based on the neuroleptic malignant syndrome (NMS). The mechanism involves decreased postsynaptic availability of dopamine either through direct receptor blockade, as postulated in classical NMS, or through relative dopamine depletion, as postulated in cocaine withdrawal. The hallmark symptoms of NMS include hyperpyrexia and muscular rigidity, but the cocaine associated syndrome is atypical in having minimal rigidity. This lack of muscle rigidity, however, appears to be consistent with NMS-like syndromes accompanying other conditions involving dopamine depletion rather than blockade. Treatment implications are that dopamine antagonists, which are usually prescribed for cocaine overdose, may be contraindicated and instead, dopamine agonists may reverse this rapidly fatal syndrome.

Body Temperature Regulation↗