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PubMed2001

[Current diagnosis and therapy of malignant hyperthermia].

Malignant hyperthermia is an autosomal dominant disorder which results in a severe reaction to anesthetic agents in approximately 0.0005 to 0.5% of patients exposed to general anesthesia. Malignant hyperthermia is characterized by severe muscle rigidity, myoglobunuria, high fever, tachycardia, and arrhythmia precipitated by depolarizing muscle relaxants (succinylcholine) and inhalational anesthetic agents (halothane). When MH occurs, the anesthetic agents must be discontinued immediately and dantrolene should be administered.

English Abstract↗

PubMed1992

Neuroleptic malignant syndrome.

NMS is a life-threatening, hyperpyrexic syndrome that follows the blockage of certain central dopaminergic receptor sites; it is commonly associated with the use of neuroleptic medications. Clinical signs usually include hyperthermia, altered mental status, muscle rigidity, and autonomic instability. Treatment is mainly supportive. Dopamine agonists and muscle relaxants are often used in therapy; however, their effectiveness has never been adequately determined in controlled studies.

Adult↗

PubMed1987

[Amplitude of the tension developed by glycerinated muscle fibers during rigidity depends on the nature of the structural reorganizations in F-actin induced by formation of the actomyosin complex].

Dependence between the amplitude of tension, developed by glycerinated muscle fibers during rigidity, and the character of structural changes in F-actin, induced by the formation of actomyosin complex, was studied by polarized microfluorimetry and tensiometry. It is shown that during rigidity the anisotropy of intrinsic tryptophan residues as well as of rhodamine phalloidin bound to F-actin, and amplitude of tension depend on pH (6-8) and ionic strength (mu = 0.07 M-0.14 M) of solution. Greater changes in polarized fluorescence and in amplitude of tension were registered during rigidity in solutions with low ionic strength (mu = 0.07 M) and pH 8. It suggested that the amplitude of muscle fibre tension depends on the relative quantity of actin monomers, being in the "switched on" state.

Actins↗

PubMed2002

The stiff-person syndrome. Case report.

The stiff-person syndrome is a rare and disabling disorder, characterized by muscle rigidity with superimposed painful spasms involving axial and limb musculature. The clinical symptoms are continuous contraction of agonist and antagonist muscles caused by involuntary motor-unit firing at rest and the spasms that are precipitated by tactile stimuli, passive strach, volitional movement of affected or unaffected muscles, startling noises and emotional stimuli. Both the rigidity and the spasms are relieved by sleep, general anaesthesia, myoneural blockade and peripheral nerve blockade. The cause of the stiff-person syndrome is unknown but an autoimmune pathogenesis is suspected because 1) the presence in the cerebrospinal fluid (CSF) of antibodies against glutamic acid decarboxylase (GAD), the rate-limiting enzyme for the synthesis of the inhibitory neurotrasmitter gamma-aminobutyric acid (GABA), 2) the association of the disease with other autoimmune disorders, 3) the presence of various autoantibodies and 4) a strong immunogenetic association. The stiff-person syndrome is clinically elusive but potentially treatable and should be considered in patients with unexplained stiffness and spasms. Drugs that enhance GABA neurotransmission, such as diazepam, vigabatrin and baclofen, provide modest relief of clinical symptoms. Immunomodulatory agents such as steroids, plasmapheresis and intravenous immunoglobulin, seem to offer substantial improvement.

Aged↗

PubMed2000

[Malignant hyperthermia susceptibility in 3 patients with malignant neuroleptic syndrome].

Hyperthermia, skeletal muscle rigidity, rhabdomyolysis, acidosis and multiple system insufficiency characterize malignant hyperthermia. Anaesthetic malignant hyperthermia follows halogenated volatile agents and/or depolarizing muscle relaxants utilization. Diagnosis is based on in vitro muscle contracture in response to halothane and/or caffeine exposure. Neuroleptic malignant syndrome affects patients taking neuroleptic drugs; clinical findings include hyperthermia, extrapyramidal rigidity, acidosis, neurovegetative instability and neurological signs. We report three neuroleptic malignant syndrome patients with positive muscle contracture tests which shows that muscle from neuroleptic malignant syndrome patients may in some instances show alterations similar to those of anaesthetic malignant hyperthermia.

Adult↗

PubMed2004

Stiff-person syndrome.

BACKGROUND: Stiff-person syndrome (SPS) is a rare neurologic disorder with autoimmune features. It is characterized by progressive, severe muscle rigidity or stiffness most prominently affecting the spine and lower extremities. REVIEW SUMMARY: Superimposed muscle spasms result in simultaneous contraction of agonist and antagonist muscles which are detectable by electromyography (EMG) and relieved by administration of benzodiazepines. The exacerbation of SPS by emotional stressors often results in the referral of these patients for psychiatric assessment although this was more common before the discovery of an association with antibodies to glutamic acid decarboxylase (GAD antibodies). Formerly known as stiff-man syndrome, the female to male ratio is 2:1 and the principle paraneoplastic variant is associated with breast cancer. Although rare, this is a disease of middle age that severely curtails the functional capacity of those it strikes. It is frequently associated with diabetes and other autoimmune diseases. IVIg is recently demonstrated to be effective in the treatment of SPS; diazepam remains useful in managing the symptoms. CONCLUSIONS: This article summarizes the history of SPS, describes important clinical features, discusses management, touches upon areas of uncertainty, and postulates some avenues for research.

Diagnosis, Differential↗

PubMed1988

Vecuronium in the management of tetanus. Is it the muscle relaxant of choice?

Two cases of severe tetanus admitted to ITU with muscle rigidity and convulsions and needed mechanical ventilation had a continuous infusion of vecuronium as muscle relaxant. The cardiovascular changes of the two patients are described. It is concluded that vecuronium because of its minimal cardiovascular effects is the relaxant of choice in the management of severe tetanus.

Aged↗

PubMed1998

A rat model of spontaneous myopathy and malignant hyperthermia.

Malignant hyperthermia is a main cause of death during general anesthesia, particularly in children. However, research has been hampered by the lack of a convenient animal model, the only one available being a special strain of pig. In this study, we describe spontaneous myopathy and a fatal syndrome of generalized muscle rigidity triggered by halothane in an outbred strain of rat. Histological examination of skeletal muscle reveals severe abnormalities indicating chronic underlying myopathy. The association of histological abnormalities with an acute, fatal syndrome clinically resembling malignant hyperthermia provides a strong basis for a new and extremely useful animal model to study this fatal disorder.

Animals↗

PubMed2001

Malignant hyperthermia.

Malignant hyperthermia is an autosomal-dominant inherited disorder of the skeletal muscle cell characterized by a hypermetabolic response to all commonly used inhalational anaesthetics and depolarizing muscle relaxants. The clinical syndrome includes muscle rigidity, hypercapnia, tachycardia and myoglobinuria as result of increased carbon dioxide production, oxygen consumption and muscle membrane breakdown. In human beings and animals susceptible to malignant hyperthermia, it is generally accepted that an increase in the level of myoplasmic free calcium is the cause of the syndrome. Various hypotheses have been proposed to account for the increase of intracellular calcium levels, e.g. a defect in the calcium release channel of the sarcoplasmic reticulum (ryanodine receptor), an abnormality of the excitation-contraction coupling mechanisms, or alterations in second messenger systems of skeletal muscles. This review gives an overview of the main features of this disease and recent advances in research including pathophysiology, treatment, diagnosis and genetics as well as association with other disorders.

Anesthesia↗

PubMed2002

[Anesthesia in neuromuscular disorders. Part 2: specific disorders].

The neuromuscular disorders described are divided into four groups: motoneuron diseases, peripheral neuropathies, disturbances of neuromuscular transmission and myopathies. In motoneuron diseases problems mainly result from respiratory insufficiency and the predisposition for aspiration caused by progressive muscular weakness. Depolarising muscle relaxants may elicit myotonic reaction and massive hyperkalemia. In contrast to non-depolarising muscle relaxants there may be an extreme hypersensitivity. In peripheral neuropathies the cardiac function is often limited whereby dysautonomia may enhance cardiovascular instability. The negative inotropic effect of anaesthetic agents must be observed with care and patients with higher degree of AV blocks may need a cardiac pacemaker during general anaesthesia. The Charcot-Marie-Tooth-Syndrome is characterized with a high sensitivity to thiopental. Disturbances of neuromuscular transmission frequently cause respiratory problems The fluctuating weakness of bulbar and respiratory muscles may impair swallowing and can lead to recurrent aspirations. Due to the reduced number of acetylcholine receptors the sensitivity to non-depolarizing muscle relaxants is elevated and the response to succinylcholine is reduced. Drugs reducing neuromuscular transmission such as antibiotics and beta-blockers may enhance these symptoms and should be avoided. In progressive muscular dystrophies the anaesthetic risk is mainly dependent on cardiac and respiratory impairment. Administration of succinylcholine leads to the risk of hyperkalmic cardiac arrest. Patients with metabolic myopathies are also at risk due to the involvement of cardiac muscle but respiratory problems are less frequent. Muscle metabolism should be supported by administration of substrates depending on the underlying disorder. In membrane disorders muscle rigidity (myotonic reactions) or weakness may lead to respiratory insufficiency. In addition to the depolarising muscle relaxants also anticholinesterase drugs, hypothermia and dyskalaemia can evoke myotonic reactions.

Anesthesia↗

PubMed2002

Resistance to rocuronium in a child with Schwartz-Jampel syndrome type 1 B.

In Schwartz-Jampel syndrome micrognathia and jaw muscle rigidity may result in difficult or impossible tracheal intubation. Since the dose-response relationship to muscle relaxants is unknown in this rare disease we assessed by mechanomyography the neuromuscular response to the rocuronium in a two-year-old child with Schwartz-Jampel syndrome (SJS) Type 1 B. Rocuronium's dose-response curve was markedly shifted (3.5-fold dose) to the right when compared to healthy children and intubation conditions were improved. This resistance to NDMR may result from a lower acetylcholine degradation rate suggested as being the consequence of mutation of the gene encoding perlecan (HSPG2) in SJS. Thus, considerably higher doses of NDMR than usual may be required for facilitation of tracheal intubation in patients with SJS. Since evidence for genetic heterogeneity of SJS exists we also recommend incremental doses of a rapidly acting NDMR with continuous monitoring of neuromuscular function so as to assess the optimum relaxant dose.

Androstanols↗

PubMed1999

The stiff-person syndrome: an autoimmune disorder affecting neurotransmission of gamma-aminobutyric acid.

The stiff-person syndrome, a rare and disabling disorder, is characterized by muscle rigidity and episodic spasms that involve axial and limb musculature. Continuous contraction of agonist and antagonist muscles caused by involuntary motor-unit firing at rest are the hallmark clinical and electrophysiologic signs of the disease. Except for global muscle stiffness, results of neurologic examination are usually normal. Results of conventional computed tomography and magnetic resonance imaging of the brain are also normal. The cause of the stiff-person syndrome is unknown; however, an autoimmune pathogenesis is suspected because of 1) the presence of antibodies against glutamic acid decarboxylase (GAD), the rate-limiting enzyme for the synthesis of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA); 2) the association of the disease with other autoimmune conditions; 3) the presence of various autoantibodies; and 4) a strong immunogenetic association. Anti-GAD antibodies, which are found in high titers in most patients, seem to be directed against conformational forms of GAD. New evidence suggests that these antibodies may be pathogenic because they interfere with the synthesis of GABA. In addition, a reduction in brain levels of GABA, which is prominent in the motor cortex, has been demonstrated with magnetic resonance spectroscopy in patients with the stiff-person syndrome. The stiff-person syndrome is clinically elusive but potentially treatable and should be considered in patients with unexplained stiffness and spasms. Drugs that enhance GABA neurotransmission, such as diazepam, vigabatrin, and baclofen, provide mild to modest relief of clinical symptoms. Immunomodulatory agents, such as steroids, plasmapheresis, and intravenous immunoglobulin, seem to offer substantial improvement. Results of an ongoing controlled trial will elucidate the role of these agents in the treatment of the disease.

Adjuvants, Immunologic↗

PubMed1984

Serotonin in the control of the sleep-like states in frogs.

It has been established that brain serotonin (5-HT) is involved in the control of behavioral phenomena in amphibians. The transition of frogs from active wakefulness to sleep-like states was accompanied by alteration of brain 5-HT metabolism, i.e., in sleep-like state with plastic muscle tone 5-hydroxyindoleacetic acid (5-HIAA) level was reduced and in sleep-like state with rigid muscle tone both brain 5-HIAA and 5-HT were decreased. An experimental decrease of brain 5-HT level by inhibition of its biosynthesis by p-chlorophenylalanine (200 mg/kg) induced the sleep-like state of catatonic type, i.e., the state which was characterized by lowered brain 5-HT.

Animals↗

PubMed1999

[Neuroleptic malignant syndrome after treatment with olanzapine].

A case of neuroleptic malignant syndrome (NMS) in a 23 year old male patient is reported. The symptoms were hyperthermia, muscle rigidity, change in mental status, sinus tachycardia, creatinine phosphokinase elevation and myoglobinuria. The patient suffered from severe muscle pain and compromised respiratory function. Treatment was cessation of neuroleptic medication and institution of intensive medical care focusing on symptomatic treatment. One week after admission clinical status and laboratory findings were normalized and the patient was readmitted to a psychiatric hospital. The neuroleptic medication of the reported patient had been olanzapine during seven months at a dose of 25 mg daily. The day before onset of NMS the pharmacological treatment was supplemented by 100 mg of clozapine. The cause of onset of NMS in this case is discussed. Clozapine, an atypical neuroleptic, is known to have reduced potential to cause NMS and in such cases without extrapyramidal symptoms. Olanzapine, however, has not yet been reported to cause NMS. Alternatively the cause of onset of NMS in this patient could be explained by the combination treatment and possible synergistic effect of the two antipsychotic drugs. Further research in this field is needed.

Adult↗

PubMed2006

An autopsy case of intraoperative death due to pulmonary fat embolism--possibly caused by release of tourniquet after multiple muscle-release and tenotomy of the bilateral lower limbs.

We report a case of a juvenile male with muscle rigidity caused by cerebral palsy who experienced intraoperative sudden death due to pulmonary fat embolism after multiple muscle-release and tenotomy of the bilateral lower limbs. Data were obtained through review of the surgical and anesthesia records, as well as from autopsy and histopathological examination. All surgical procedures were performed within the same operation, beginning with the right lower limb and then proceeding with the left lower limb, with application of a pneumatic tourniquet to avoid intraoperative hemorrhage. Slight changes in the hemodynamics were noticed after release of the right tourniquet. Further, sudden onset of hypotension, severe bradycardia, and a marked decrease in percutaneously monitored oxygen saturation occurred just after release of the left tourniquet when the left limb was raised for casting. The patient died despite immediate and vigorous cardiopulmonary resuscitation. At autopsy performed 20 h after death, examination of the lungs revealed a pale surface, slight edema, and obvious fat droplets in the vessels at the cut surfaces. Histopathological examination with fat staining was notable for the presence of pulmonary fat embolism. These results suggest that restoration of venous return after removal of the tourniquet combined with massive fat embolism from dead spaces was the likely cause of death.

Adolescent↗

PubMed2002

Degeneration of skeletal muscle fibers in the rat administrated carbon tetrachloride: similar histological findings of the muscle in a 64-year-old patient of LC with muscle cramp.

It is well known that painful muscle cramps occur frequently in patients with advanced liver cirrhosis (LC). Although many studies discuss the pathophysiological causes of these muscle cramps in various conditions, the results are not clear as far as the cause associated to LC is concerned. In order to investigate the cause of muscle cramps in LC, we examined the histological findings of skeletal muscle fibers in LC rat model and in a patient with LC. LC (n=9) was induced in rats by chronic carbon tetrachloride administration. The histological findings of skeletal muscle tissues from the lower leg in LC rats and those of the upper arm in a patient with LC were compared. The degenerated muscle fibers and centronucleus in LC rats were similar to the opaque fibers frequently observed in myotonic dystrophy with severe muscle rigidity in patients with LC. In conclusion, results of this study suggest that one of the causes for muscle cramps in patients with LC is due to skeletal muscle fiber degeneration. Therefore, histological observation of skeletal muscle fibers should be considered in the treatment of painful muscle cramps.

Journal Article↗

PubMed2000

Effect of early fasciotomy on intramuscular pressure and electrical excitability of muscles in experimental compartment syndrome.

Experiments on rabbits with compartment syndrome of the leg showed that the main pathogenetic factors of muscle injury are postischemic contracture leading to extravascular microcirculatory disorders and tissue necrosis(early postcompression period) and progressive subfascial edema (18 h-4 days). Therapeutic effect of fasciotomy in the early period consists in restoration of bloodflow due to relaxation of contracted muscles and in the late period in decompression of edematous muscles and prevention of secondary ischemia. Fasciotomy through a small section does not lead to sufficient relaxation of rigid muscles and does not essentially increase the subfascial volume. Fasciotomy decreases subfascial pressure and muscle excitability threshold, however they remain considerably elevated during day 1. An electrodiagnostic test is proposed for early (before subfascial edema) detection of postischemic contracture.

Animals↗

PubMed1983

Malignant hyperthermia-like reactions in three anesthetized horses.

Problems encountered during halothane anesthesia in 3 horses included increasing rectal temperature, muscle rigidity or movement during anesthesia, irregular breathing patterns, and difficulty in stabilizing blood pressure. One horse had prolonged muscle fasciculations and failure to relax after administration of succinylcholine in addition to halothane. That horse developed severe, bilateral myositis of the triceps, lumbar, and gluteal muscles. Problems encountered were similar to those caused by the disease known as malignant hyperthermia.

Anesthesia, General↗