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PubMed2003

Influence of CGS 21680, a selective adenosine A(2A) agonist, on the phencyclidine-induced sensorimotor gating deficit and motor behaviour in rats.

RATIONALE: Recently it has been suggested that adenosine A(2A) receptor agonists may be potential antipsychotic drugs. It is, however, not clear whether these compounds may exert their antipsychotic effect without producing extrapyramidal side-effects (e.g. catalepsy, muscle rigidity, ataxia). It is known that such side-effects may be due to overactivation of the GABAergic strio-pallidal pathway, which may be estimated as an increased expression of proenkephalin (PENK) mRNA in the striatum. OBJECTIVE: The aim of this study was to determine whether CGS 21680, a selective adenosine A(2A) receptor agonist, can reverse the disruption of prepulse inhibition (PPI) of the acoustic startle response induced by the non-competitive antagonist of NMDA receptors phencyclidine (PCP) without producing motor side-effects in rats. RESULTS: Systemic administration of PCP (5 mg/kg) produced profound reduction of the PPI, which was reversed by CGS 21680 (1 mg/kg). CGS 21680 (0.1 and 1 mg/kg) was without effect on catalepsy, muscle rigidity and rotarod performance in rats as well as on the PENK mRNA expression in the striatum estimated by in situ hybridization. Only after the highest dose used (5 mg/kg) were signs of catalepsy (measured using a 9-cm cork test), disturbed balance and a loss of hind limb control (measured in the rotarod test) seen. Moreover, increased muscle resistance during passive extension measured mechanomyographically after this dose of CGS 21680 was observed. CONCLUSIONS: The present results support the hypothesis that adenosine A(2A) receptor agonists may be potentially useful antipsychotic agents with the low incidence of extrapyramidal side-effects.

Adenosine↗
PubMed1977

[The stiff-man syndrome. A case report with regard to clinical, electromyographical and pharmacological signs (author's transl)].

Our electromyographical findings show no evidence for a spinal or neurogenic origin of muscle stiffness in stiff-man syndrome. It is assumed that the tonic muscle rigidity is induced by abnormal impulses from the brainstem. The measured latencies of electrically induced muscle spasm in the legs are in accordance with this hypothetic site of origin. Muscle stiffness and spasm are decreased by the GABA derivative Baclofen as well as by Clonacepam, which is preferable to Diazepam because of less intense sedation. Spasms are increased by Chlorimipramine which may by used as a provocative test in uncertain cases. These pharmacological influences suggest an imbalance between a gabaminergic inhibitory and a noradrenergic and/or serotoninergic excitatory neuronal system.

Aged↗
PubMed2002

Enhanced synchrony among primary motor cortex neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine primate model of Parkinson's disease.

Primary motor cortex (MI) neurons discharge vigorously during voluntary movement. A cardinal symptom of Parkinson's disease (PD) is poverty of movement (akinesia). Current models of PD thus hypothesize that increased inhibitory pallidal output reduces firing rates in frontal cortex, including MI, resulting in akinesia and muscle rigidity. We recorded the simultaneous spontaneous discharge of several neurons in the arm-related area of MI of two monkeys and in the globus pallidus (GP) of one of the two. Accelerometers were fastened to the forelimbs to detect movement, and surface electromyograms were recorded from the contralateral arm of one monkey. The recordings were conducted before and after systemic treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rendering the animals severely akinetic and rigid with little or no tremor. The mean spontaneous MI rates during periods of immobility (four to five spikes/sec) did not change after MPTP; however, in this parkinsonian state, MI neurons discharged in long bursts (sometimes >2 sec long). These bursts were synchronized across many cells but failed to elicit detectable movement, indicating that even robust synchronous MI discharge need not result in movement. These synchronized population bursts were absent from the GP and were on a larger timescale than oscillatory synchrony found in the GP of tremulous MPTP primates, suggesting that MI parkinsonian synchrony arises independently of basal ganglia dynamics. After MPTP, MI neurons responded more vigorously and with less specificity to passive limb movement. Abnormal MI firing patterns and synchronization, rather than reduced firing rates, may underlie PD akinesia and persistent muscle rigidity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2001

Different action on dopamine catabolic pathways of two endogenous 1,2,3,4-tetrahydroisoquinolines with similar antidopaminergic properties.

The effect of single and multiple 1-methyl-1,2,3,4-tetrahydroisoquinoline (1MeTIQ) and 1-benzyl-1,2,3,4-tetrahydroisoquinoline (1BnTIQ) administration on concentrations of dopamine and its metabolites: homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3MT) in three brain areas was studied HPLC with electrochemical detection in Wistar rats. The rate of dopamine catabolism in the striatum along the N-oxidative and O-methylation pathways was assessed by calculation of the ratio of appropriate metabolites to dopamine concentration. In addition, the spontaneous and apomorphine-stimulated locomotor activity, and muscle rigidity was studied after acute administration of 1MeTIQ and 1BnTIQ. We have found that 1MeTIQ did not change the level of dopamine and HVA in all investigated structures both after a single and chronic administration. However, the levels of intermediary dopamine metabolites, DOPAC and 3MT, were distinctly affected. The level of DOPAC was strongly depressed (by 60-70%) while the level of extraneuronal matabolite 3MT was significantly elevated (by 170-200%). In contrast to 1MeTIQ, 1BnTIQ depressed the level of dopamine (by approximately 60%) and increased the level of total metabolite, HVA, (by 40%) especially in the striatum, but the levels of DOPAC and 3MT remained unchanged. The paper has shown that 1MeTIQ and 1BnTIQ produced different effects on dopamine catabolism. Potential neuroprotective compound 1MeTIQ did not change the rate of total dopamine catabolism, it strongly inhibited the monoamine oxidase (MAO)-dependent catabolic pathway and significantly activated the catechol-O-methyltransferase (COMT)-dependent O-methylation. In contrast 1BnTIQ, a compound with potential neurotoxic activity, produced the significant increase of the rate of dopamine metabolism with strong activation of the oxidative MAO-dependent catabolic pathway. Interestingly, both compounds produced similar antidopaminergic functional effects: antagonism of apomorphine hyperactivity and induction of muscle rigidity. The results may explain the biochemical basis of the neuroprotective and of the neurotoxic properties endogenous brain tetrahydroisoquinoline derivatives.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Porcine malignant hyperthermia: false negatives in the halothane test.

Purebred Pietrain pigs presumed (on the basis of pedigree) to be homozygous for malignant hyperthermia (MH) susceptibility were subjected to a 3% halothane challenge test. A few (6%) pigs that should have been MH susceptible on the basis of parental genotype did not develop muscle rigidity in response to repeated halothane tests. Three of these animals were brought into the laboratory, and muscle biopsy specimens were obtained for in vitro analysis. Bundles of intact muscle cells dissected from biopsy specimens were electrically stimulated, and mechanical responses were monitored during exposure to halothane. In all instances, the muscle bundles from the halothane-negative (ie, not sensitive to halothane), but genetically susceptible, pigs gave in vitro responses that were similar of those of halothane-positive MH-susceptible pigs in that tetanic tension was depressed, tetanus relaxation was slowed, and small contractures were produced upon halothane exposure. Thus, the presence of a halothane-sensitive abnormality in the skeletal muscles, in and of itself, is not always sufficient for development of in vivo muscle rigidity during a brief halothane test. Furthermore, when the halothane testing of pigs is conducted by recommended techniques, false negatives still occur in a small percentage of the genetically MH-susceptible animals.

Animals↗
PubMed1996

[Controlled reperfusion of the extremities for preventing local and systemic damage after prolonged ischemia. An experimental study with the swine model].

Our previous studies in isolated rat hindlimbs using crystalloid perfusion solutions have shown that control of the initial reperfusion reduces postischemic complications. However, no experimental study has been undertaken to evaluate the concept of controlled limb reperfusion experimentally in an in-vivo blood-perfused model and to assess the local as well as systemic effects of normal blood reperfusion and controlled limb reperfusion. Of twenty pigs undergoing preparation of the infrarenal aorta and iliac arteries, six were observed for 7.5 hours and served as controls. Fourteen other pigs underwent 6 hours of complete infrarenal occlusion. Thereafter, embolectomy was stimulated in 8 pigs by removing the aortic clamp and establishing normal blood reperfusion at systemic pressure. In 6 other pigs, control of the composition of the reperfusate and control of the conditions of reperfusion was done during the first 30 min, followed by normal blood reperfusion. Six hours of infrarenal aortic occlusion lead to a severe decrease in high energy phosphates and muscle temperature and a slight increase in creating kinase (CK) and potassium in the systemic circulation. Normal blood reperfusion resulted in severe reperfusion injury: massive edema developed (80.6% vs. 76.6%, p < 0.0009), the tissue showed a marked decrease in oxygen consumption (7.3 +/- 1.1 vs. 14.3 +/- 2.5 mL )2/100 g/min, p < 0.02), glucose consumption (0.19 +/- 0.06 vs. 0.51 +/- 0.03 mg/100 g/min, p < 0.06), tissue ATP (18.3 +/- 1.9 vs. 36.1 +/- 0.9 mumol/g protein, p < 0.000001), total adenine nucleotides (26.3 +/- 2.6 vs. 45.8 +/- 1.5 mumol/g protein, p < 0.00001), muscle pH (5.9 +/- 0.1 vs. 7.3 +/- 0.1, p < 0.000006) and total calcium in the femoral vein (2. +/- 0.1 vs. 2.7 +/- 0.1 mmol/L, p < 0.002). Furthermore, a massive increase was seen in CK concentration (12,743 +/- 2,562 vs. 513 +/- 80 U/L, p < 0.0003), potassium (7.9 +/- 0.3 vs. 4.4 +/- 0.2 mmol/L, p < 0.000001) and muscle rigidity (60 +/- 11 vs. 122 +/- 1 degree, p < 0.00008). In sharp contrast, initial treatment of the ischemic skeletal muscle by controlled limb reperfusion resulted in normal water content (77.6 +/- 0.4 vs. 76.8 +/- 0.3%), oxygen consumption (13.2 +/- 1.6 vs. 14.9 +/- 3.2 mL O2/100 g/min), glucose consumption (0.58 +/- 0.18 vs. 0.46 +/- 0.11 mg/100 g/min), flow (5.4 +/- 1.1 vs. 4.6 +/- 4.6 +/- 0.5 mL/100 g/min) and muscle rigidity (106 +/- 4 vs. 122 +/- 1 degree). Furthermore, controlled limb reperfusion resulted in higher total adenine nucleotides content (78% vs. 57% of control), less tissue acidosis (6.6 +/- 0.2 vs. 5.9 +/- 0.1, p < 0.002), severely reduced CK release (2,618 +/- 702 vs. 12,743 +/- 2.562, p < 0.02) and potassium release (5.1 +/- 0.3 vs. 7.9 +/- 0.3 mmol/L, p < 0.0002) as compared to normal blood reperfusion. In conclusion this study shows that 6 hours of acute infrarenal aortic occlusion will result in a severe reperfusion injury (postischemic syndrome) if normal blood at systemic pressure is given in the initial reperfusion phase. In contrast, initial treatment of the ischemic skeletal muscle by controlled limb reperfusion reduces the metabolic, functional and biochemical alterations.

Animals↗
PubMed2000

[An autopsy case of corticobasal degeneration without prominent cortical pathology--an imitator of progressive supranuclear palsy].

We describe an autopsy case of parkinsonism with bradykinesia, muscle rigidity, and dementia as major symptoms. The patient had developed bradykinesia at the age of 62, and then muscle rigidity, a parkinsonian posture, bradylalia, and dementia gradually appeared. Neurological examination revealed rigidity in the neck and limbs, with motion and speech being generally slow. He lacked involuntary movements including alien hand, tremor, chorea, and dystonia. Vertical gaze palsy, both upward and downward was noted, but other cranial nerves were intact. He was diagnosed as suffering from PSP clinically based on vertical gaze palsy, bradykinesia, instability on standing and gait, and dementia. Levodopa was only transiently effective. Within three years he became bed-ridden and in a state of akinetic mutism. At age 65 he died from pneumonia. Neuropathology revealed severe neuronal degeneration and gliosis in the substantia nigra. Because atrophy of the tegmentum of brainstem, dentate nuclei, inferior olivary nuclei was very mild and Alzheimer neurofibrillary tangles in the brainstem were relatively few, PSP was ruled out. Cortical neuronal degeneration was not apparent, but in the deep layer of cingulate gyrus, frontal lobe, and insula, there were several ballooned neurons. Gallyas-Braak silver staining showed no tuft-shaped astrocytes, specific for PSP, but it disclosed astrocytic plaques in the basal ganglia and the cerebral cortex. At present, astrocytic plaques are recognized as a hallmark of corticobasal degeneration (CBD), along with ballooned neurons in the cerebral cortex. The present case thus illustrates that CBD has a wide spectrum and may include cases in which degeneration of cerebral cortex is very mild.

Aged↗
PubMedDate not supplied

Idiopathic hypocalcemia in foals.

Five thoroughbred foals (4 fillies and 1 colt), all in good to excellent body condition, ranging in age from 4 days to 5 weeks at the time of onset of signs, were presented to 2 Kentucky equine hospitals from 1992 through 1996. All 5 foals presented with tachycardia, hyperhidrosis, diarrhea or a recent history of diarrhea, and muscle rigidity or stiff gait. Four of the 5 foals presented for recumbency, seizure-like activity with opisthotonos, or pronounced extensor muscle rigidity. All 5 foals were hypocalcemic. All foals either died or had euthanasia performed. None responded to oral calcium supplementation. The cause of the hypocalcemia was unknown. Different idiopathic hypocalcemia syndromes may exist in foals.

Animals↗
PubMed1994

Jaw relaxation after a halothane/succinylcholine sequence in children.

BACKGROUND: Lack of complete jaw relaxation after a halothane-succinylcholine sequence has been described in the literature. To date, however, most existing studies are retrospective, and lack agreement on the magnitude and incidence of this phenomenon. This prospective study examined the incidence and degree of incomplete jaw relaxation in 500 children who were given intravenous succinylcholine during halothane anesthesia. METHODS: Five hundred consecutive unmedicated children received a minimum dose of 2 mg/kg intravenous succinylcholine after induction of anesthesia with halothane. The degree of jaw relaxation was assessed 45-60 s later by the same observer using a standardized clinical scale. The degree of relaxation was correlated with the type of surgical procedure, and the presence and intensity of fasciculations. RESULTS: Complete relaxation (mouth opened easily and fully) occurred in 95.4% of study patients. Incomplete relaxation (firm manual separation required to open the mouth fully) was seen in 4.4% of the patients. One child (0.2%) had masseter muscle rigidity (mouth could not be fully opened but intubation possible). There were no incidents of trismus (teeth clamped shut and intubation via direct visualization impossible). The incidence of incomplete relaxation and masseter muscle rigidity did not correlate with the presence or degree of fasciculations or the type of surgical procedure. There were no clinical signs of a hypermetabolic state or myoglobinuria in any patient. CONCLUSIONS: Incomplete jaw relaxation after a halothane-succinylcholine sequence is not uncommon in children, and is considered a normal response.

Anesthesia↗
PubMed1987

Epidural and subcutaneous morphine, meperidine (pethidine), fentanyl and sufentanil in the rat: analgesia and other in vivo pharmacologic effects.

The experiments examined the characteristics of analgesia produced by different doses of morphine, meperidine (pethidine), fentanyl, and sufentanil after epidural and subcutaneous injection in rats. The specificity of the analgesia was also determined; other in vivo pharmacologic activities (i.e., blockade of pinna and cornea reflexes and production of skeletal muscle rigidity) were monitored as pharmacologic indices of opiate drug activity in the brain. After subcutaneous injection, the opiates produced dose-dependent analgesia, blocked the pinna and cornea reflexes, and induced muscle rigidity. After epidural injection, all four compounds produced dose-dependent analgesia and had greater potency, earlier onset, shorter duration, and greater specificity of analgesic action than was the case after subcutaneous injection. Specificity is defined here as the ratio of the ED50 dose that blocked the pinna reflex to the ED50 dose that produced analgesia. The gains in potency and specificity, but not the gains in onset time and the losses in duration of analgesia, differed considerably among the compounds that were examined. The subcutaneous-to-epidural potency ratio related in a linear manner with the lipid-to-water partition coefficient. The gain in specificity also appeared to be related to lipid solubility. The microgram X kg-1 doses at which the opiates produced analgesia in rats correlate well with the potency of these compounds in producing analgesia after epidural injection in humans. The rat epidural preparation reflected the doses, onset, and specificity, but not the duration, of analgesia produced by epidural opiates in humans.

Analgesia↗
PubMed1998

Contribution of the glycine site of NMDA receptors in rostral and intermediate-caudal parts of the striatum to the regulation of muscle tone in rats.

The aim of the present study was to assess the contribution of the glycine site of NMDA receptors in the striatum to the regulation of muscle tone. Muscle tone was examined using a combined mechanoand electromyographic method, which measured simultaneously the muscle resistance (MMG) of the rat's hind foot to passive extension and flexion in the ankle joint and the electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was induced by haloperidol (2.5 mg/kg i.p.). 5,7-dichlorokynurenic acid (5,7-DCKA), a selective glycine site antagonist, injected in doses of 2.5 and 4.5 microg/0.5 microl bilaterally, into the rostral region of the striatum, decreased both the haloperidol-induced muscle rigidity (MMG) and the enhanced electromyographic activity (EMG). 5,7-DCKA injected bilaterally in a dose of 4.5 microg/0.5 microl into the intermediate-caudal region of the striatum of rats not pretreated with haloperidol had no effect on the muscle tone. The present results suggest that blockade of the glycine site of NMDA receptors in the rostral part of the striatum may be mainly responsible for the antiparkinsonian action of this drug.

Animals↗
PubMed2002

The role of striatal metabotropic glutamate receptors in Parkinson's disease.

The primary cause of Parkinson's disease is a loss of dopamine in the corpus striatum. It has been postulated that this effect leads to disinhibition of the striopallidal pathway and secondarily, to a functional shift towards glutamatergic stimulation. The aim of the present study was to find out whether inhibition of glutamatergic transmission at a level of metabotropic glutamate receptors (mGluRs) in the striatum may alleviate parkinsonian-like symptoms in rats. The non-competitive antagonist of receptor subtype 5 (mGluR5), MPEP (1.0-10 mg/kg ip), or the agonist of group II mGluRs, LY354,740 (5-10 mg/kg ip), reduced haloperidol-induced muscle rigidity and catalepsy. Intrastriatal injections of the mGluR1 antagonist, (RS) AIDA (7.5-15 microg/0.5 microl), but not of the agonist of group II mGluRs, 2R,4R-APDC (7.5-15 microg/0.5 microl), inhibited the muscle rigidity induced by haloperidol. In order to search for an influence of mGluRs on the striopallidal pathway, the effect of MPEP or of the agonist of group II mGluRs, DCG-IV, on the proenkephalin (PENK) mRNA expression in the dorso-lateral striatum was examined by an in situ hybridization. Repeated MPEP (6 x 10 mg/kg ip) administration did not influence PENK expression in naïve rats, but diminished that increased by haloperidol. In contrast, repeated DCG-IV (3 x 1 nmol/4 microl icv) injections enhanced both the control and the haloperidol-increased levels of PENK expression. The obtained results suggest that blockade of group I mGluRs, or stimulation of group II mGluRs may be important to ameliorate parkinsonian symptoms. Striatal mGluRs may contribute to at least some of these effects.

Animals↗
PubMed1996

Evidence for mu1-opioid receptor involvement in fentanyl-mediated respiratory depression.

Several fentanyl analogs (Bagley et al., 1989, J. Med. Chem. 32, 663) were compared to fentanyl and morphine for their effects on respiratory depression as determined by arterial blood gas (pH, pCO2 and pO2) measurements. Fentanyl (0.1 mg/kg), morphine (10 mg/kg), #16 (1-phenethyl-4-[N-(pyridin-2-yl)-N-(methoxymethylcarbonyl)amino] piperidine, 1 mg/kg), #17 (1-phenethyl-4-[N-(pyridin-2-yl) -N-(2-furoyl)amino]piperidine, 0.5 mg/kg) and #29 (1-phenethyl-4-[N- (pyrimidin-2-yl)-N-(methoxy-methylcarbonyl) amino]piperidine, 10 mg/kg) produced significant respiratory depression in rats. Pretreatment with the mu1-opioid receptor selective antagonist, naloxonazine (10 mg/kg), blocked the respiratory effect of fentanyl and its analogs, but not that of morphine. The results suggest that the mu1-opioid receptor plays an important role in the respiratory effects of fentanyl and its analogs. Hence, the mechanism of fentanyl-induced respiratory depression appears to be distinct from that produced by morphine. The most likely explanation for this difference is the possible contribution of muscle rigidity and catalepsy to the observed changes in blood gas parameters caused by the fentanyl analogs, while the respiratory depression of morphine, measured by these same parameters, appears to be independent of its effect on muscle rigidity.

Animals↗
PubMed1990

[Etiology of the rigidity of axial muscles of the trunk in Moersh-Woltman syndrome].

A woman patient suffering from the rigid man syndrome (RMS) is described. Analyzing the clinical characteristics of the case, the anatomophysiological features of segmental innervation and suprasegmental control of the activity of axial muscles of the body, the authors suggest that the phenomenon of axial muscle rigidity is caused by the hyperreactivity of vestibular and reticular neurons stimulating via vestibulo- and reticulospinal fibers the motoneurons of the medial plates of the anterior cornua of the spinal cord (the segmental representation of axial muscles). The pathogenetic similarity of myotonic disorders in axial muscles in patients with the RMS and reflex manifestations of vertebral osteochondrosis is under discussion.

Adult↗
PubMed2006

Neuroleptic malignant syndrome: a review and report of six cases.

The typical symptoms and signs of neuroleptic malignant syndrome (NMS) consist of fever muscle rigidity (stiffness, myoclonus, rod-like), alterations of consciousness (confusion, agitation, aggression, or catatonia), autonomic nervous system disturbances (i.e., hypertension, tachycardia, tachypnea, profuse sweating, and urine incontinence), abnormal blood tests such as low serum electrolytes, elevated serum creatinine phosphokinase (CPK) level, and leukocytosis. Muscle rigidity is often associated with myonecrosis, myoglobinuria, and elevated serum CPK. The mortality among NMS cases is in the 10 to 70% range depending on the severity of the symptoms and time of therapeutic approach. Mandatory therapy should include removal of causative agents, correction of body fluid and electrolytes, administration of benzodiazepine, clonazepam and bromocriptine (dopamine agonist), proved life-saving medications. The authors reported herein six cases with unusual clinical features of NMS. Four of them had been on antipsychotic for a year before becoming anorexic, dehydrated, agitated, and violent with paranoid delusion. One instance with underlying delirium tremens developed NMS after receiving haloperidol (30 mg IV) in addition to diazepam (200 mg IV) within 24 hours. Another patient was found to suffer from severe NMS after receiving bupropion (Dopamine inhibitor antidepressant) 300 mg/day. All patients displayed cardinal signs and symptoms of NMS in addition to dehydration and pallor. They were treated in the psychiatric ward and recovered rapidly from NMS after receiving clonazepam and bromocriptine and removal of the offending agents.

Adolescent↗
PubMed1999

The role of striatal adenosine A2A receptors in regulation of the muscle tone in rats.

The aim of the present study was to assess contribution of striatal adenosine A2A receptors to regulation of the muscle tone in rats. The muscle tone was examined by a combined mechano- and electromyographic method, which measured simultaneously muscle resistance (MMG) of a rats hind foot to passive extension and flexion in the ankle joint and the electromyographic activity (EMG) of the antagonistic muscles: gastrocnemius and tibialis anterior. CGS 21680 (1 and 2 microg/0.5 microl), injected bilaterally into the rostral part of the striatum, dose-dependently increased both MMG and the EMG. The present results show that stimulation of striatal adenosine A2A receptors by CGS 21680 evokes parkinsonian-like muscle rigidity which may be due to activation of the GABAergic strio-pallidal pathway.

Adenosine↗
PubMed1995

Prevalence of unsuspected myopathy in infants presenting for clubfoot surgery.

The objective of this study was an evaluation of the prevalence of myopathies in paediatric patients scheduled for orthopaedic surgery (clubfoot) performed under regional anaesthesia. Seventeen infants scheduled for lower limb orthopaedic surgery were studied to verify coexisting neuromuscular disorders with electromyography and muscle biopsy during surgery. All surgical procedures were performed under caudal block or spinal anaesthesia, associated with light general anaesthesia. No major cardiorespiratory, neurological or malignant hyperthermic complications (muscle rigidity, arrhythmias, hyperpyrexia) were observed. Combined neurological, electromyographic and biopsy studies showed a high rate of myopathic changes (70%). Performance of clubfoot surgery under light general anaesthesia with regional techniques was free from any problems. The high rate of myopathic changes (70%) observed in the muscle biopsies suggests that precautions should be taken with paediatric patients for clubfoot surgery and a regional anaesthesia technique with adequate monitoring may be helpful to prevent possible malignant hyperthermia related problems.

Anesthesia, Conduction↗
PubMed2001

Neuroleptic malignant syndrome induced by droperidol.

A case of droperidol-induced neuroleptic malignant syndrome during anaesthesia is presented. An 86-year-old man underwent spinal anaesthesia for open reduction and internal fixation of a trochanteric hip fracture. He received droperidol 5 mg intravenously for sedation towards the end of surgery. He subsequently became very drowsy and experienced marked muscle rigidity and autonomic instability. He became febrile postoperatively. The clinical syndrome resolved after 12 hours. When using droperidol in anaesthesia or intensive care--especially when large doses are given--the development of neuroleptic malignant syndrome should be suspected if the patient becomes febrile and has muscle rigidity and autonomic instability.

Aged↗