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PubMed2003

Neuroleptic malignant syndrome following cardiac surgery: successful treatment with dantrolene.

Neuroleptic malignant syndrome (NMS) is a rare idiosyncratic reaction to neuroleptic drugs, which is potentially fatal. It has been occasionally reported that NMS occurs subsequently after surgery. We report a case of a 53-year-old male patient who developed NMS following cardiac surgery due to the resumption of zotepine. The patient was attacked with hyperthermia, sweating, significant shivering, trembling of the fingers, disturbed consciousness and extreme muscle rigidity after the resumption of zotepine. Furthermore, laboratory measurements revealed increased levels of serum blood urea nitrogen, creatinine and creatine phosphokinase. In addition, elevation in white blood cell counts and myoglobinemia were also observed. After a diagnosis of NMS was established, administration of zotepine was stopped and treatments with administration of dantrolene and a large amount of fluid infusion intravenously were started. Following these treatments, the clinical symptoms subsided and the laboratory findings improved without need for hemodialysis. Dantrolene, which is able to effectively impede the abnormal flow of calcium from the sarcplasmic reticulum into the muscle cytoplasm, was beneficial to reduce the clinical symptoms of NMS. We hereby present a patient with NMS following cardiac surgery, and discuss its subsequent management.

Dantrolene↗

PubMed1982

Malignant hyperpyrexia and Duchenne muscular dystrophy: A case report.

We report a patient with Duchenne muscular dystrophy who developed malignant hyperpyrexia during general anaesthesia. During anaesthesia bradycardia was followed by ventricular fibrillation, on which ventricular flutter supervened and a body temperature rise of 0.6 degrees C for 15 minutes, myoglobinuria and elevation of CPK level were observed. The caffeine sensitivity test of biopsied muscle fibers revealed an increase in sensitivity, although there was no sign of muscle rigidity during or after anaesthesia. Diagnosis of Duchenne muscular dystrophy was first established after the development of malignant hyperpyrexia in the present case as well as in previously reported cases. Determination of serum CPK is very important before general anaesthesia.

Adenosine Triphosphatases↗

PubMed1981

Cyclobenzaprine: a possible mechanism of action for its muscle relaxant effect.

Intravenously administered cyclobenzaprine (CBZ) (Flexeril), a clinically used, centrally acting muscle relaxant, abolished muscle rigidity in the intercollicular decerebrate rat. In animals in which the locus coeruleus was lesioned bilaterally previously, CBZ failed to attenuate the electromyogram. In the ventral horn of the cord, which receives a dense noradrenergic innervation from the locus coeruleus, CBZ caused an increase in the metabolism of noradrenaline. In the zona intermedia of the thoracic cord, which is not innervated by the locus coeruleus, CBZ caused only minimal effects on noradrenaline metabolism. Cells in the locus coeruleus were activated by CBZ. The results indicate that in the intercollicular decerebrate rat, an intact, coerulospinal, noradrenergic projection is essential for the muscle relaxant effect of CBZ. Muscle relaxation apparently results from an activation of locus coeruleus neurones, leading to an increased release of noradrenaline in the ventral horn of the cord and the subsequent inhibitory action of noradrenaline on alpha motoneurones.

Amitriptyline↗

PubMed1986

Dantrolene. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic use in malignant hyperthermia, the neuroleptic malignant syndrome and an update of its use in muscle spasticity.

Dantrolene sodium acts primarily by affecting calcium flux across the sarcoplasmic reticulum of skeletal muscle. Recently, dantrolene has been used very successfully in the treatment of several rare hypercatabolic syndromes which have previously been associated with high mortality rates. In malignant hyperthermia, where early diagnosis and treatment usually with intravenous dantrolene in association with other supportive measures (and often subsequent dantrolene therapy) is performed, recovery is seen in virtually 100% of patients. There is a rapid resolution of hyperthermia, dysrhythmias, muscle rigidity, tachycardia, hypercapnia, mottled or cyanotic skin, and metabolic acidosis, and a slower normalisation of myoglobinuria and elevated serum creatine phosphokinase levels. In patients with family history or previous episodes of malignant hyperthermia, prophylactic treatment with dantrolene prior to anaesthesia prevents the syndrome occurring in most cases. Where malignant hyperthermia has developed patients have been successfully treated with further dantrolene therapy. Dantrolene has also been used successfully in the treatment of a few cases of heat stroke and the neuroleptic malignant syndrome--both of which have many similarities to malignant hyperthermia. Dantrolene is well established in the treatment of patients with muscle spasticity where it generally improves at least some of the components of spasticity (i.e. hyper/hypotonia, clonus, muscle cramps and spasms, resistance to stretch and flexor reflexes, articular movement, neurological and motor functions and urinary control). However, in some patients, particularly those with multiple sclerosis, dantrolene may not be effective, and in many cases muscular strength may diminish. Long term dantrolene therapy has been associated with hepatic toxicity and may cause problems in patients treated for disorders of muscle spasticity. Thus, dantrolene offers a unique advance in the therapy available for the treatment of hypercatabolic disorders and is also useful in the treatment of muscle spasticity of various aetiology.

Animals↗

PubMed1999

Study of central motor functions using magnetic stimulation in Parkinson's disease.

The pathophysiological abnormalities, the contribution of activity of facilitatory and inhibitory systems to muscle rigidity and hypokinesia in Parkinson's disease are not clarified in details. Transcranial magnetic stimulation of the motor cortex may provide useful data on the functional state of motor output of the central motor structures and on the functional condition of the intracerebral motor network. The abnormalities of the central motor functions and the modifying effect of L-dopa treatment in Parkinson's disease are the objectives of our study. Patients with Parkinson's disease were examined before and after L-dopa treatment. Transcranial and cervical magnetic stimulation were performed and the latency and amplitude of the motor evoked potentials from the first dorsal interosseus muscle, the central motor conduction time and the duration of cortical inhibition were measured. The motor latency and the silent period in patients before treatment were significantly shorter than those of the age-matched healthy controls. After six months of L-dopa substitution both motor latencies and silent periods increased and approached the normal values. The observed changes are thought to be in relation to the mechanisms originating in the basal ganglia and acting through inhibitory thalamo-cortical connections at cortical level and through rubro- and reticulospinal pathways at the level of spinal inhibitory neurons. The transcranial magnetic stimulation is a suitable method to assess the efficiency of drugs in patients with Parkinson's disease.

Aged↗

PubMed1995

Rhabdomyolysis and hyperthermia after cocaine abuse: a variant of the neuroleptic malignant syndrome?

Rhabomyolysis with myoglobinuria has been added relatively recently to the neurologic complications associated with the increased use of cocaine and the introduction of its alkaloid form (crack). This retrospective study reports our experience with 14 patients who presented with rhabdomyolysis after cocaine use in a municipal hospital over a 3-year period. Seven patients used "crack", 2 intravenous and 3 nasal insufflation. All patients but one had hyperthermia, 11 altered mental status, 8 tachycardia, and 4 muscle rigidity. Nine developed renal failure; 3 of these patients died. Two other patients died of cardiorespiratory arrest. Cocaine-related rhabdomyolysis has a high mortality. The observed association with hyperthermia and other central neurologic features resembles the neuroleptic malignant syndrome. Since chronic cocaine use may alter the availability of dopamine either through transmitter depletion or decrease in the number of dopamine receptors, a common pathogenetic mechanism is possible. However, other mechanisms, which are not mutually exclusive but rather frequently overlapping, may play an important role. These include agitation, hyperthermia, adrenergic overstimulation leading to vasoconstriction and ischemia or calcium release from the sarcoplasmic reticulum resulting in increased entry into the muscle cell leading to cell death; in addition, cocaine has direct toxic effect on the muscles.

Adult↗

PubMed2005

A case report of malignant hyperthermia in a dental clinic operating room.

A healthy 5-year-old boy presented for arch bar placement under general anesthesia in an operating room in a dental school. The patient had previously undergone general anesthesia without complication, and no family history of anesthetic problems were reported. Halothane mask induction, intravenous catheter placement, and nasal intubation proceeded uneventfully without the aid of a muscle relaxant. Halfway through the procedure, signs and symptoms of malignant hyperthermia, including muscle rigidity, hypercarbia, tachypnea, and tachycardia were noted. Immediate treatment, including discontinuation of the triggering agent, dantrolene administration, and cooling measures were applied, and once stable, the child was transferred to Columbus Children's Hospital for further management. The patient experienced no postoperative complications. Further discussion regarding the pathophysiology and management of malignant hyperthermia is provided.

Anesthetics, Inhalation↗

PubMed2003

Malignant hyperthermia.

Malignant hyperthermia (MH) is an uncommon, life-threatening, acute pharmacogenetic disorder of the skeletal muscle cell. It manifests in susceptible individuals as a hypermetabolic response on exposure to halogenated volatile anaesthetics and depolarizing muscle relaxants. There may also be a relationship between susceptibility to MH, heat stroke and exercise-induced rhabdomyolysis. The pathophysiology of the crisis involves an uncontrolled release of cytoplasmic free calcium from the sarcoplasmic reticulum leading to activation of energy-producing biochemical pathways. Organ system failure and rhabdomyolysis may occur as a result of high fever, hyperkalaemia and acidosis. The ryanodine receptor, the calcium-release channel of the sarcoplasmic reticulum, is the primary locus for malignant hypothermia susceptibility. Multiple mutations in the gene for the ryanodine receptor protein are causative. Other genes may also be involved. A classical fulminant crisis presents with a rising end-tidal carbon dioxide, skeletal muscle rigidity, tachycardia, hyperthermia and acidosis. Mortality may be as high as 70% if the syndrome is not recognized and treated. Immediate discontinuation of triggering agents, oxygenation, and correction of acidosis and electrolyte abnormalities, cooling and dantrolene are essential for treatment of the syndrome. Thanks to clinical and research investigations, widespread education and the introduction of dantrolene sodium, the mortality from MH is less than 5%. This chapter provides an overview and an update of MH.

Anesthesia↗

PubMed2000

[Value of intrathecal baclofen in the treatment of severe tetanus in the tropical milieu].

Tetanus continues to be a cause of high mortality in developing countries, where resources for muscle relaxation and respiratory support are not readily available. Baclofen, a GABAB receptor agonist, directly restores physiologic inhibition of alpha motoneuron, that is blocked by tetanus toxin. Its use has been suggested at high dosage by intrathecal (i.t.) route, as part of the treatment of tetanus-induced contractures, and to limit the need for general anesthesia and for tracheal intubation in afflicted patients. This review reports personal experience and focuses on published data about i.t. baclofen for severe tetanus. Although statistical analysis are difficult to perform, i.t. baclofen appears to be effective in resolving muscle rigidity and in avoiding the need for deep sedation and for tracheal intubation, thus achieving lower mortality. Nevertheless, i.t. baclofen has a narrow therapeutic range, and a large interindividual pharmacodynamic variability. Thus, its use should be reserved for patients who would have been intubated without it. I.t. baclofen is a fairly simple and cost-effective modality, with significant advantages for management of severe tetanus, especially in tropical environment.

Adult↗

PubMed1995

Malignant hyperthermia suggestive hypermetabolic syndrome at emergence from anesthesia.

A 6-year old female child received succinylcholine (1 mg.kg-1) and isoflurane (concentrations of 1.5-2 percent) and developed at the end of surgery a hypermetabolic syndrome suggestive of malignant hyperthermia (MH) with masseter muscle spasm, muscle rigidity, tachypnea, systolic hypertension (140 mm Hg), tachycardia (205 beats.min-1), hypercarbia (end expiratory CO2 71 mmHg), and an increase in body temperature (39.2 degrees C). The child responded well to therapy which included cooling, hyperventilation with pure oxygen and dantrolene administration. However, blood creatine kinase and myoglobin elevations were moderate (respectively 375 IU.L-1 and 114 micrograms.L-1) and an in vitro halothane and caffeine contracture test was negative. Differential diagnostic proposals are discussed and compared to the clinical incident.

Caffeine↗

PubMed1994

Alteration of intracellular Ca2+ transients in COS-7 cells transfected with the cDNA encoding skeletal-muscle ryanodine receptor carrying a mutation associated with malignant hyperthermia.

Malignant hyperthermia (MH), an inherited neuromuscular disease triggered by halogenated inhalational anaesthetics and skeletal-muscle relaxants, appears to be due to an alteration of intracellular Ca2+ homoeostasis. MH occurs in 1 out of 20,000 anaesthetized adults and is characterized by hypermetabolism, skeletal-muscle rigidity and elevation in body temperature, which is frequently fatal [MacLennan and Phillips (1992) Science 256, 789-794]. The defect responsible for the disease may lie within the mechanism controlling the release of Ca2+ from sarcoplasmic reticulum via the ryanodine-receptor (RYR) Ca2+ channel; in fact a point mutation in the RYR has been associated with MH in some human families, as well as in the MH-susceptible pig. To date, however, no direct evidence has been obtained demonstrating that the point mutation is both necessary and sufficient to cause functional alterations in RYR-mediated Ca2+ release. In the present report we show that the presence of the Arg-to-Cys point mutation in the recombinant RYR expressed in COS-7 transfected cells causes abnormal cytosolic Ca2+ transients in response to 4-chloro-m-cresol, an agent capable of eliciting in vitro contracture of MH-susceptible muscles.

Amino Acid Sequence↗

PubMed1990

Fatty acids modulate calcium-induced calcium release from skeletal muscle heavy sarcoplasmic reticulum fractions: implications for malignant hyperthermia.

Based on studies in swine, the malignant hyperthermia syndrome has been postulated to result from an enhanced sensitivity (low threshold) of the Ca2(+)-induced Ca2(+)-release process. However, fatty acid production is elevated in homogenates of skeletal muscle from pigs and humans susceptible to malignant hyperthermia. In the present study, we demonstrate that the threshold of Ca2(+)-induced Ca2+ release is normal in susceptible humans and in susceptible swine depleted of triglycerides. Exogenously added unsaturated fatty acids decreased the threshold of Ca2(+)-induced Ca2+ release to a much greater extent in porcine and equine muscle than in human muscle. When triglyceride and free fatty acid values were reduced to about 40 and 60%, respectively, of control values, malignant hyperthermia-susceptible swine did not exhibit muscle rigidity when challenged in vivo with halothane and succinylcholine and the threshold of the Ca2(+)-induced Ca2(+)-release process in heavy sarcoplasmic reticulum fractions was normal. Despite the reduced triglyceride and fatty acid levels, these swine had a positive in vitro contracture test for malignant hyperthermia. A low Ca2(+)-induced Ca2(+)-release threshold is not essential for malignant hyperthermia susceptibility, but appears to be the result of excessive free fatty acids produced during organelle isolation.

Animals↗

PubMed1985

An autopsy case of malignant hyperthermia.

A report is made of a 44-year-old female who died of malignant hyperthermia during general anesthesia for an operation of left subtrochanteric femoral fracture. Symptoms began with increases in heart rate and blood pressure after the introduction of anesthesia with halothane and were accelerated by the administration of succinylcholine, followed by muscle rigidity and high temperature. The typical wine red urine was observed. The oral temperature of 42 degrees C was recorded within 1 h after succinylcholine. The rectal temperature was 30 degrees C 22 h after death. Severe pulmonary edema and tubular necrosis of the kidney were found by postmortem examination. No latent myopathy was observed. The creatine phosphokinase levels in plasma obtained after the onset of malignant hyperthermia and at the time of autopsy were abnormally high and were 5632 and 34,854 mU/ml, respectively. Plasma myoglobin levels were 130,000 and 2.8 X 10(6) ng/ml, respectively.

Adult↗

PubMed1999

Malignant hyperthermia and neuroleptic malignant syndrome in a patient during treatment for acute asthma.

Acute asthma is well known to provoke complications. We report the case of a patient who needed intubation and mechanical ventilation for acute asthma. Despite a treatment with corticosteroids, bronchodilators, neuromuscular blocking drugs and magnesium sulfate, the situation remained uncontrolled and as a last resort, halothane became necessary. The patient then developed an episode of malignant hyperthermia with fever at 40 degrees C and rhabdomyolysis. At this time, halothane could be stopped and all the symptoms disappeared without modifying the rest of the treatment. Eight days later, he presented with a neuroleptic malignant syndrome following an injection of droperidol. Temperature rose to 42 degrees C, associated with muscle rigidity, sweating, tachycardia and severe circulatory collapse. The use of dantrolene in association with a symptomatic treatment of the collapse led to a favourable outcome in. Unfortunately, in vitro contracture test could not be performed in this case. The links between malignant hyperthermia and neuroleptic malignant syndrome remain unclear. Although these two pathologies share the same physiopathology, symptomatology and treatment, they are clearly individualized. This case seems to be the first description of their occurrence in the same patient.

Acute Disease↗

PubMed1992

Atypical reactions to halothane in a subgroup of homozygous malignant hyperthermia(MH)-susceptible pigs: indication of a heterogenous genetic basis for the porcine syndrome.

Malignant hyperthermia (MH) is a pharmacogenetic disorder of skeletal muscle. In genetically susceptible pigs, MH can be induced by volatile, halogenated anaesthetics such as halothane. Within a series of pharmacological investigations, a fulminant MH could be induced in 59 of 66 homozygous halothane-susceptible pigs by a challenge with 3% halothane for 15 minutes. The typical MH was characterized by sudden appearance of tachycardia, muscle rigidity with typical extension of the hindlimbs, increase of body temperature, acidosis-caused by rapid increase of CO2 and lactate production-, hyperkalaemia and increased activity of creatine kinase (CK) and aspartate transaminase (AST). In seven homozygous MH-susceptible pigs, this typical MH could not be induced by halothane. These animals responded with sudden appearance of bradyarrhythmia and decrease of arterial pressure. In these MH-atypical pigs (MHA) neither the typical extension of hindlimbs nor a hyperthermia occurred. Compared to a group of 6 MH-susceptible pigs with typical reactions to halothane (MHS), the biochemical alterations were significantly retarded in MHA-pigs. These atypical reactions to halothane could be the effect of decreased cardiac output. Concerning the atypical reactions, we observed a familiar predisposition in MH-susceptible pigs. Although atypical reactions were not found in a group of homozygous halothane-nonsusceptible pigs (MHN), a possible explanation for atypical reactions could be a MH-independent halothane-susceptibility of the myocardium+ in MHA-pigs. On the other side the data may indicate that a primary defect in both the skeletal muscle and also the myocardium is involved in MH. The different reactions to halothane in MH-susceptible pigs could point to a genetic heterogeneity.

Animals↗

PubMed2002

Abrupt withdrawal from intrathecal baclofen: recognition and management of a potentially life-threatening syndrome.

OBJECTIVE: To suggest guidelines for the prevention, recognition, and management of a life-threatening syndrome (high fever, altered mental status, profound muscular rigidity that sometimes progressed to fatal rhabdomyolysis) in patients who experience the abrupt withdrawal of intrathecal baclofen (ITB) therapy. DESIGN: Retrospective literature and safety-file review. SETTING: Expert panel drawn from physiatry, neurology, and neurosurgery. PARTICIPANTS: Experienced users of ITB therapy in the pediatric and adult populations in the United States. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: We reviewed literature reports, MedWatch reports to the US Food and Drug Administration, and our own experiences. We critically analyzed patient management and drug therapy in the context of the pharmacology of baclofen and other antispastic agents. RESULTS: An abrupt reduction in gamma-aminobutyric acid(B) (GABA) agonist activity in the central nervous system can cause the ITB withdrawal syndrome, which is clinically and pathophysiologically distinct from autonomic dysreflexia, malignant hyperthermia, and neuroleptic-malignant syndrome. ITB withdrawal evolves over 1 to 3 days, but may become fulminant if not recognized and treated early. The syndrome can be interrupted by the restoration of ITB therapy. However, supportive measures and high-dose benzodiazepine infusion may be life saving in the interval before ITB therapy is resumed. Dantrolene infusion may relieve muscle rigidity but does not reverse the other manifestations of GABAergic agonist withdrawal. CONCLUSIONS: Most episodes of severe ITB withdrawal were preventable. Patients at risk can be identified and educated prospectively and given medication for emergency use. Treatment with GABAergic agonist drugs may prevent potentially fatal sequelae.

Anti-Anxiety Agents↗

PubMed2003

Cyproheptadine for intrathecal baclofen withdrawal.

OBJECTIVE: To evaluate the efficacy of cyproheptadine in the management of acute intrathecal baclofen (ITB) withdrawal. DESIGN: Descriptive case series. SETTING: University hospital with a comprehensive in- and outpatient rehabilitation center. PARTICIPANTS: Four patients (3 with spinal cord injury, 1 with cerebral palsy) with implanted ITB infusion pumps for treatment of severe spasticity, who had ITB withdrawal syndrome because of interruption of ITB infusion. INTERVENTIONS: Patients were treated with 4 to 8mg of cyproheptadine by mouth every 6 to 8 hours, 5 to 10mg of diazepam by mouth every 6 to 12 hours, 10 to 20mg of baclofen by mouth every 6 hours, and ITB boluses in some cases. MAIN OUTCOME MEASURES: Clinical signs and symptoms of ITB withdrawal of varying severity were assessed by vital signs (temperature, heart rate), physical examination (reflexes, tone, clonus), and patient report of symptoms (itching, nausea, headache, malaise). RESULTS: The patients in our series improved significantly when the serotonin antagonist cyproheptadine was added to their regimens. Fever dropped at least 1.5 degrees C, and heart rate dropped from rates of 120 to 140 to less than 100bpm. Reflexes, tone, and myoclonus also decreased. Patients reported dramatic reduction in itching after cyproheptadine. These changes were associated temporally with cyproheptadine dosing. DISCUSSION: Acute ITB withdrawal syndrome occurs frequently in cases of malfunctioning intrathecal infusion pumps or catheters. The syndrome commonly presents with pruritus and increased muscle tone. It can progress rapidly to high fever, altered mental status, seizures, profound muscle rigidity, rhabdomyolysis, brain injury, and death. Current therapy with oral baclofen and benzodiazepines is useful but has variable success, particularly in severe cases. We note that ITB withdrawal is similar to serotonergic syndromes, such as in overdoses of selective serotonin reuptake inhibitors or the popular drug of abuse 3,4-methylenedioxymethamphetamine (Ecstasy). We postulate that ITB withdrawal may be a form of serotonergic syndrome that occurs from loss of gamma-aminobutyric acid B receptor-mediated presynaptic inhibition of serotonin. CONCLUSION: Cyproheptadine may be a useful adjunct to baclofen and benzodiazepines in the management of acute ITB withdrawal syndrome.

Acute Disease↗

PubMed1993

Free radicals and calcium homeostasis: relevance to malignant hyperthermia?

The regulation of intracellular free calcium ions (Ca2+) in skeletal muscle at rest and during contraction depends on mechanisms such as Na(+)-Ca2+ exchangers, Ca(2+)-ATPases, and the voltage-sensitive ryanodine receptor. The susceptibility of these regulatory mechanisms to free-radical-mediated damage may be increased because of their location within the lipid membranes of sarcolemma, sarcoplasmic reticulum, and mitochondrion with resultant uncontrolled increases in myoplasmic Ca2+ concentration and cell death. The potentially fatal pharmacogenetic disorder, malignant hyperthermia (MH), is characterised by muscle rigidity, arrhythmias, lactic acidosis, and a rapid rise in body temperature. The sequence of events responsible for the MH syndrome remains uncertain, but it has been variously ascribed to faults in many of the Ca2+ regulatory mechanisms. In swine the condition is associated with a specific mutation in the ryanodine receptor, whereas in humans the syndrome is genetically heterogenous. Free-radical-mediated peroxidation of membrane lipids and proteins also results in the rapid efflux of Ca2+ from organelles, and the detection of products of free radical reactions in tissue from MH-susceptible individuals using electron spin resonance spectroscopy provides evidence for the involvement of free radicals in the MH syndrome.

Animals↗