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 505 records · Page 28Linked to original sources
PubMed1996

Norepinephrine does not potentiate porcine malignant hyperthermia.

Malignant hyperthermia (MH) is a rare genetic trait characterized by potential life-threatening episodes of hypermetabolism, hyperthermia, and muscle rigidity when susceptible humans or animals are exposed to triggering drugs. The role of norepinephrine (NE) in triggering MH is controversial. The purpose of this study was to show that NE does not initiate nor speed the onset of MH in susceptible swine exposed to known triggering drugs. Three groups of MH susceptible (MHS) pigs were exposed to two times the minimum alveolar anesthetic concentrations (MAC) halothane (2%) for 60 min and monitored continuously until a PaCO2 of 70 mm Hg was obtained as an end point for fulminant MH. This dose of halothane is associated with significant hypotension which was addressed by three modalities: no treatment; NE infusion at 8 micrograms.kg-1.min-1; and intraaortic balloon pump (IABP) with 1:1 augmentation (7.0-mL balloon catheter). NE and epinephrine (Epi) plasma levels were determined at 15-min intervals and at trigger time. All animals developed signs of MH during the study. There was no difference in pHa, lactate, PaCO2, or temperature at control or trigger times between groups. Time to trigger was longer in the untreated group compared to both the NE and the IABP groups which were equal. The NE group had greater NE and Epi plasma levels at all times than either the untreated or IABP group and the levels increased at each sample time. The IABP group had increased NE levels at time of trigger compared to control time period, however, Epi levels did not increase. In the untreated group, individual animals had marked increases in NE levels, but extreme variability in response prevented achievement of a single mean change. This group showed no increase in plasma Epi levels throughout the study. There was no difference in NE levels between the untreated and IABP groups. Three animals in the untreated group died prior to trigger due to complications of hypotension. In conclusion, addition of exogenous NE in high doses did not enhance triggering of MH. The large dose NE infusion resulted in increased total catecholamines throughout the study in the NE group with no effect on time to MH trigger compared to animals where mean arterial pressure (MAP) was maintained by IABP. Animals in all three groups with times to trigger of less than 30 min had significantly higher MAPs at control, 15 min, and trigger time than those with times to trigger of greater than 30 min. We conclude that NE does not trigger MH and that severe reduction of MAP delays the the onset of MH in susceptible swine.

Animals↗
PubMed1998

Tracheal intubation in ambulatory surgery patients: using remifentanil and propofol without muscle relaxants.

UNLABELLED: Using alfentanil followed by an anesthetic induction dose of propofol provides adequate conditions for tracheal intubation without neuromuscular relaxants. Remifentanil, which has a clinical onset similar to that of alfentanil, has not been investigated for this indication. Accordingly, 80 ASA physical status I and II premedicated outpatients were randomly assigned to one of four groups (n = 20/group). Remifentanil 1, 2, 3, or 4 micrograms/kg (Groups I-IV, respectively) was infused intravenously over 90 s. Sixty seconds after beginning the remifentanil infusion, propofol 2 mg/kg was infused over 5 s. Ninety seconds after the administration of propofol, laryngoscopy and tracheal intubation were attempted and graded. Clinically acceptable intubating conditions (i.e., jaw relaxed, vocal cords open, and fewer than two coughs in response to intubation) were observed in 35%, 75%, 100%, and 95% of patients in Groups I-IV, respectively. Clinically acceptable intubating conditions were significantly (P < 0.05) less likely to occur in Group I compared with all other groups. Excellent intubating conditions (i.e., vocal cords open, no movement in response to intubation) were observed in 30%, 50%, 80%, 80% of patients in Groups I-IV, respectively. Overall conditions at intubation were significantly (P < 0.05) better in Groups III and IV compared with Groups I and II. The mean time to resumption of spontaneous ventilation after induction was < 5 min in all groups. No patient manifested clinically significant muscle rigidity. The mean arterial pressure decreased 16%, 20%, 28%, 26% immediately before tracheal intubation in Groups I-IV, respectively. No patient was treated for hypotension or bradycardia. In conclusion, healthy, premedicated patients with favorable airway anatomy can be reliably intubated with good or excellent conditions 90 s after the administration of remifentanil 3-4 micrograms/kg and propofol 2 mg/kg. IMPLICATIONS: Remifentanil 3 micrograms/kg and propofol 2 mg/kg co-administered intravenously may reliably provide adequate conditions for tracheal intubation in healthy patients without neuromuscular relaxants. This combination of drugs may allow the rapid return of spontaneous ventilation.

Adolescent↗
PubMed1999

Fentanyl does not increase brain injury after focal cerebral ischemia in rats.

UNLABELLED: Recent reports have indicated that large-dose opiate anesthesia can increase neuronal injury in rats subjected to forebrain ischemia. However, most episodes of cerebral ischemia in the operating room setting are focal in nature, and the influence of large-dose opioid administration on the tolerance of the brain to focal cerebral ischemia has not been studied. Accordingly, we undertook the present study to evaluate the effect of fentanyl administration on outcome after focal cerebral ischemia. Three groups of fasted Wistar-Kyoto rats (awake, fentanyl, and isoflurane groups; n = 20 per group) were anesthetized with isoflurane (2.5% end-tidal). Pericranial temperature was servocontrolled at 37.0 degrees C. After surgical preparation fentanyl 50 microg/kg was administered IV over 10 min in the fentanyl group. Thereafter, an infusion was established at a rate of 50 microg x kg(-1) x h(-1). The end-tidal concentration of isoflurane was then reduced to 1.1%, one minimum alveolar anesthetic concentration (1 MAC) in all groups. Occlusion of the middle cerebral artery was achieved by advancing a 0.25-mm filament into the anterior cerebral artery via the common carotid artery. In the fentanyl and awake groups, isoflurane administration was then discontinued. In the isoflurane group, isoflurane anesthesia was maintained at 1.0 MAC. After 90 min of focal ischemia, the filament was removed, and the animals were allowed to recover. Seven days later, the volume of cerebral infarction in the animals was determined by image analysis of hematoxylin and eosin-stained coronal brain sections. There was no difference in the infarct volume between the fentanyl and awake groups. The infarct volume was the least in the isoflurane group. The results confirm the ability of isoflurane to reduce brain injury caused by focal cerebral ischemia. Fentanyl neither increased nor decreased brain injury compared with the awake unanesthetized state. IMPLICATIONS: Fentanyl is commonly used in surgical procedures in which there is a substantial risk of focal cerebral ischemia. Fentanyl did not affect cerebral injury produced by focal ischemia in the rat. The data suggest that, in doses that produce respiratory depression and muscle rigidity, fentanyl does not reduce the tolerance of the brain to a focal ischemic insult.

Analgesics, Opioid↗
PubMed2000

Is there a learning curve associated with the use of remifentanil?

UNLABELLED: This study prospectively determined whether there was a learning curve with the use of remifentanil, as indicated by decreased hemodynamic variability, improved recovery profile, and decreased incidence of opioid-related adverse events with increasing experience. Patients undergoing diverse surgical procedures (outpatient [n = 1340] and inpatient [n = 560]) were enrolled by investigators (n = 190) who had no previous experience with remifentanil use. Each investigator enrolled 10 patients. A standardized protocol for administration of remifentanil was used. Data were analyzed to determine differences between the first three patients and the last three patients enrolled for each anesthesiologist in the study. There were no differences in hemodynamic variables between the first triad and the last triad in either outpatients or inpatients. Requirements for hypnotic drugs and the doses of remifentanil used were also similar between groups. Analgesic medications administered at the end of surgery and in the postanesthesia care unit (PACU) were similar between groups, except that the last triad in the outpatient group received smaller doses of fentanyl compared with the first triad. Times to response to verbal command, tracheal extubation, and operating room discharge did not differ between groups. However, patients in the last triad undergoing outpatient surgery had shorter times to eligibility for PACU discharge, but times to eligibility for discharge home did not differ. The overall incidence of all adverse events (i.e., hypotension, hypertension, muscle rigidity, respiratory depression, apnea, nausea, and vomiting) was less in the last triad as compared with the first triad. When analyzed separately, only the incidence of vomiting (in the outpatient group) was decreased in the last triad as compared with the first triad. This study suggests that there is a learning curve that aids reduction of minor adverse effects associated with the use of analgesic medications administered at the end of surgery in outpatients, which might have reduced the incidence of postoperative vomiting and the duration of PACU stay. IMPLICATIONS: This study demonstrated that anesthesiologists rapidly acquire the ability to use remifentanil with limited experience. However, there is a learning curve that aids reduction of minor adverse effects associated with the use of analgesic medications administered at the end of surgery in outpatients, which might have reduced the incidence of postoperative vomiting and the duration of postanesthesia care unit stay.

Adult↗
PubMed1986

Epidural and intravenous sufentanil in the rat: analgesia, opiate receptor binding, and drug concentrations in plasma and brain.

Doses of sufentanil (i.e., 0.01, 0.04, 0.16, 0.63, 2.5, 10, and 40 micrograms/rat) were injected either into the lumbar epidural space or intravenously in rats weighing +/- 250 g, and in vivo pharmacologic activities (i.e., prolongation of latency to tail withdrawal in response to noxious heat, blockade of cornea and pinna reflexes, increase of skeletal muscle tone), ex vivo mu-opiate receptor binding (i.e., displacement of specific 3H-sufentanil binding in thalamus, striatum, hippocampus, cortex, mamillary body-medulla oblongata segment, medulla oblongata, and in cervical, thoracic, and lumbar spinal cord), and drug concentrations in plasma, brain, cortex, and cerebellum, were determined. An ED50 dose of intravenous sufentanil of 0.075 micrograms/rat produced analgesia. CNS-mediated in vivo side effects (i.e., blockade of pinna and cornea reflexes, muscle rigidity) were apparent at 6-28 times higher doses. Epidural sufentanil also produced analgesia at an ED50 dose of 0.08 micrograms/rat, but CNS-mediated side effects occurred only at 35 to 76 times higher doses. This greater in vivo selectivity of epidural sufentanil in producing analgesia was consistent with ex vivo binding data that showed that in most areas of brain, but not in spinal cord, more mu-opiate binding occurs with intravenous than with epidural sufentanil. The two routes nonetheless differed by no more than a factor of approximately two in producing detectable levels of sufentanil both in plasma and in brain tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗
PubMed1990

Safety of general anesthesia in patients previously tested negative for malignant hyperthermia susceptibility.

Anesthetic management and outcome were examined in patients with negative in vitro contracture tests for malignant hyperthermia (MH). Contracture testing was performed in a standardized fashion using 3% halothane alone and incremental doses of caffeine alone. Medical records were examined for 54 anesthetic exposures in 42 MH(-) patients who had received anesthesia since their MH testing. Sixteen patients received anesthesia with known MH triggering agents on 23 occasions, all without incident. In six MH(-) patients with previous masseter muscle rigidity, no adverse reactions occurred in response to volatile anesthetic agents. Succinylcholine was avoided in these patients. Eleven MH(-) patients were managed as if MH-susceptible, although it was known that these patients had tested MH(-). Two of these patients also receive prophylactic iv dantrolene. These results suggest that "triggering" anesthetic agents may be safely administered to patients who test MH(-) by in vitro contracture testing. However, until the anesthetic experience of larger numbers of MH(-) patients is known, these results should be interpreted cautiously.

Anesthesia, General↗
PubMed1987

Neuroleptic malignant syndrome responsive to carbidopa/levodopa: support for a dopaminergic pathogenesis.

A 31-year-old man with psychosis and neuroleptic-induced tardive dystonia developed neuroleptic malignant syndrome (NMS) while taking haloperidol. Muscle rigidity responded to dantrolene, but hyperthermia did not abate until therapy with carbidopa/levodopa was initiated, after which temperature varied in direct relationship to subsequent levodopa administration. This supports the role for central dopaminergic mechanisms in the pathogenesis of NMS.

Adult↗
PubMed1979

Tetanus: a review.

Tetanus is caused by the organism Clostridium tetani, which produces tetanospasmin, a neurotoxin responsible for the clinical manifestations of muscle rigidity and reflex spasms. The majority of cases follow an anaerobic wound infection associated with trauma. Incubation period is usually 3 days to 3 weeks. 75% of patients present with trismus. Reflex spasms are seen in 70% of patients and characterize the severity of the disease. Treatment involves removal of the offending organism, neutralization of free neurotoxin, controlling rigidity and reflex spasm, and minimizing complications. Diazepam may be used alone in mild cases. Severe cases require the addition of nondepolarizing neuromuscular blocking agents and mechanical ventilation. Respiratory complications occur early and require aggressive airway management. A serious, late complication is the syndrome of sympathetic nervous system overactivity that is treated with alpha and beta blockade. High mortality rates seen in the United States may be due to delays in diagnosis and lack of familiarity with treatment. The disease is preventable with adequate immunization.

Humans↗
PubMedDate not supplied

Bilateral mesial temporal sclerosis and kernicterus.

Two children with mental retardation, choreoathetosis, dystonia, and muscle rigidity are reported. They had a history of severe hyperbilirubinemia after birth as a result of Rh isoimmunization. The history and clinical picture suggested the diagnosis of kernicterus. The magnetic resonance imaging examination showed a bilateral signal intensity increase in the globus pallidus on T2-weighted images. Additionally, our patients showed symmetric bilateral hyperintensity and volume loss in the hippocampus, which is known to be another characteristic area of bilirubin deposition in kernicterus.

Child↗
PubMed1991

Neuroleptic malignant syndrome: occurrence in a child after reconstructive surgery.

The occurrence of the rare but potentially fatal neuroleptic malignant syndrome must be considered by the surgeon treating a patient who develops hyperthermia, mental abnormalities, autonomic instability, and muscle rigidity after exposure to phenothiazines or other neuroleptic drugs. The dopamine agonist bromocriptine appears to be the treatment of choice in adults and seemed to be effective and well tolerated in our patient. Although the syndrome cannot be prevented, recognition is crucial, since effective general and specific therapy is available. Differentiating neuroleptic malignant syndrome from malignant hyperthermia allows early appropriate treatment with bromocriptine.

Child↗
PubMed1999

Neuroleptic malignant syndrome due to promethazine.

A 42-year-old man came to our emergency room hyperthermic (oral temperature, 42.4 degrees C), diaphoretic, and delirious. Other findings included labile blood pressure, sinus tachycardia (heart rate, 138/min), tachypnea (respiratory rate 34/min), muscle rigidity, and incontinence. Two days earlier, he had gone to a local clinic with complaints of abdominal pain, nausea, and vomiting. Promethazine was prescribed, and this was the patient's only medication on admission. Laboratory studies showed leukocytosis, hypernatremia, metabolic acidosis, elevated creatinine phosphokinase level, elevated transaminase levels, azotemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and myoglobulinuria. The clinical and laboratory findings were characteristic of the neuroleptic malignant syndrome, with promethazine as the offending agent.

Acidosis↗
PubMed2004

Human pharmacology of MDMA: pharmacokinetics, metabolism, and disposition.

MDMA (3,4-methylenedioxymethamphetamine, ecstasy) is a widely misused psychostimulant drug abused among large segments of the young population. Pharmacologically it displays effects related to amphetamine-type drugs and a set of distinctive effects (closeness to others, facilitation to interpersonal relationship, and empathy) that have been named by some authors "entactogen" properties. MDMA is a potent releaser and/or reuptake inhibitor of presynaptic serotonin (5-HT), dopamine (DA), and norepinephrine (NE). These actions result from the interaction of MDMA with the membrane transporters involved in neurotransmitter reuptake and vesicular storage systems. The most frequent effects after MDMA/ecstasy administration are euphoria, well-being, happiness, stimulation, increased energy, extroversion, feeling close to others, increased empathy, increased sociability, enhanced mood, mild perceptual disturbances, changed perception of colors and sounds, somatic symptoms related to its cardiovascular and autonomic effects (blood pressure and heart rate increase, mydriasis), and moderate derealization but not hallucinations. Acute toxic effects are related to its pharmacologic actions. The serotonin syndrome (increased muscle rigidity, hyperreflexia, and hyperthermia), among others, is characteristic of acute toxicity episodes. MDMA metabolism is rather complex and includes 2 main metabolic pathways: (1) O-demethylenation followed by catechol-O-methyltransferase (COMT)-catalyzed methylation and/or glucuronide/sulfate conjugation; and (2) N-dealkylation, deamination, and oxidation to the corresponding benzoic acid derivatives conjugated with glycine. The fact that the polymorphic enzyme CYP2D6 partially regulates the O-demethylenation pathway prompted some expectations that subjects displaying the poor metabolizer phenotype may be at higher risk of acute toxicity episodes. In this metabolic pathway a mechanism-based inhibition of the enzyme operates because the formation of an enzyme-metabolite complex that renders all subjects, independently of genotype, phenotypically poor metabolizers after the administration of 2 consecutive doses. Therefore, the impact of CYP2D6 pharmacogenetics on acute toxicity is limited. One of the interesting features of MDMA metabolism is its potential involvement in the development of mid- to long-term neurotoxic effects as a result of progressive neurodegeneration of the serotonergic neurotransmission system.

Adrenergic Uptake Inhibitors↗
PubMed2006

Electroencephalographic responses to intraoperative subthalamic stimulation.

This study reports the effects of intraoperative stimulation of the subthalamic nucleus on brain electrical activity in advanced Parkinson's patients. To our knowledge, this is the first study about electroencephalographic responses in the very early phase of deep brain stimulation, during the implantation of the electrodes. We found an increase of gamma band bilaterally over the sensorimotor cortex in the range 45-55 Hz, which was associated with clinical improvement as assessed by means of muscle rigidity decrease. These results indicate that the electroencephalographic gamma responses to deep brain stimulation are present at the very beginning of the treatment process, and may help better understand the short and long-tem effects of deep brain stimulation.

Aged↗
PubMed1988

Positioning and handling: important considerations in the care of the severely head-injured patient.

Control of abnormal posturing is a challenge in the care of severely head-injured adults and must be a component of care in both critical care and acute rehabilitation stages of recovery. Severe head injury is indicated by a Glasgow Coma Scale rating of eight or less for at least six hours post-injury. Long-term disabilities are common among survivors, mostly men under 40 years of age. This paper examines the pathophysiology of abnormal posturing and positioning and handling techniques to prevent and/or control abnormal motor activity. The effect of positioning on intracranial pressure is also discussed.

Brain Damage, Chronic↗
PubMed1993

Neuroleptic malignant syndrome: a dangerous complication of neuroleptic therapy.

Neuroleptic malignant syndrome is a potentially fatal syndrome that can occur in patients taking neuroleptics or other psychotropic drugs. It is characterized by muscle rigidity, hyperthermia, altered mentation, autonomic dysfunction, increased CPK and leukocytosis. A primary factor in NMS may be a decrease in functioning of dopaminergic neurons. Treatment usually consists of discontinuation of the neuroleptic drug, drug therapy with bromocriptine and dantrolene and supportive measures. The key to successful medical and nursing management is aggressive supportive care with a focus on preventing complications. With the frequency of administration of neuroleptic drugs, neuroscience nurses should be aware of this potentially lethal complication of neuroleptic therapy.

Adult↗
PubMed1996

Pallidotomy: a surgical intervention for control of Parkinson's disease.

Parkinson's disease, a chronic incurable disorder, has a significant impact on quality of life. Parkinson's disease results from chronic degeneration of cells in the basal ganglia that produce dopamine. It typically affects elderly individuals producing muscle rigidity and akinesia. Traditionally, Parkinson's disease has been controlled by medications. However, for some patients, medications may no longer be effective, or may produce drug-related complications. For this group of patients, pallidotomy is gaining support as an intervention to control the debilitating symptoms of Parkinson's disease, thus enabling a person to perform everyday tasks. Although the procedure was developed in the 1950s, contemporary technology has allowed a resurgence of the intervention. With the focus on relief of two of the major symptoms of Parkinson's disease, the pallidotomy procedure is gaining support as a surgical intervention for this disease. Therefore, it is important for the health care team to have an understanding of the disease process, surgical intervention and postoperative care to enhance quality outcomes for this patient population.

Globus Pallidus↗
PubMed1977

Treatment of progressive systemic sclerosis (scleroderma, PSS) with a new drug influencing connective tissue.

Cyclofenil is a new diphenyl ethylene derivative related to stilboestrol without oestrogenicity but with marked effects on connective tissue metabolism. The drug has been tested, in a daily dose of 200mg X3, in six patients with progressive systemic sclerosis (PSS) to analyze the expected beneficial effects on the PSS symptoms. The typical skin hardness, joint and muscle rigidity, and reduced breathing capacity were improved to varying dgrees. The only side-effect was a slight transient liver enzyme elevation in 1 out of 6 patients. A slight increase was found in urinary calcium and hydroxyproline excretion. In several cases serum calcium, cholesterol, triglyceride and in some cases the serum uric acid levels were decreased. The ANF titres diminished to varying degrees in 4 out of 6 patients. These results indicate that further detailed clinical and laboratory studies on the therapeutic potential of cyclofenil in PSS and other diseases affecting connective tissue seen to be justified.

Administration, Oral↗