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PubMed2006

[Neuroleptic malignant syndrome after 30 years treatment with clozapine: a rarely seen differential diagnosis on intensive care units].

The neuroleptic malignant syndrome (NMS) is a rare, but potentially lethal side effect of conventional and atypical antipsychotic drugs. We present a 62 years old male patient who was admitted to our institution because of sudden onset of mild hyperthermia, muscle rigidity, stupor, leucocytosis and massive rhabdomyolysis after 30 years uneventful treatment with clozapine. The medication with clozapine was suspended because of the suspicion of NMS. When the acute symptoms were abated, the treatment with clozapine was resumed again after 14 days. The very next day, the patient suffered again from raised body core temperature, leucocytosis, elevated serum creatine kinase and new catatonia. The therapy with clozapine was stopped definitively and benzodiazepines were administered assuming a relapse of an alleviated, probably reconvening NMS. Under the treatment with benzodiazepines the patient was free of symptoms even after 1 month. To our knowledge, the latency of 30 years between the beginning of the treatment with clozapine and the onset of NMS is the longest period in the literature. According to our case, the differential diagnosis of NMS is not always trivial and is therefore discussed.

Antipsychotic Agents↗
PubMed1991

The relationship between stiffness of the musculature and static flexibility: an alternative explanation for the occurrence of muscular injury.

The static flexibility of the gleno-humeral joint of fourteen experienced male weight lifters was determined. Further the subjects performed a series of quasistatic muscular actions of the deltoid/pectoralis musculature during which a brief perturbation was applied. The damped oscillations resulting from such a procedure provided data pertaining to the stiffness of each subject's musculature. A significant correlation (r = -0.544, p less than 0.05) between maximal stiffness and static flexibility was observed. This relationship is discussed with reference to the popular belief that flexibility is related to the incidence of muscular injury. It is proposed that the injury-reducing benefits associated with a high degree of flexibility can be effectively explained through the relationship between flexibility and stiffness.

Adult↗
PubMed1996

[Perioperative management of the patient with atypical Parkinson disease].

Recent neuropathological findings define that 10-20% of the Parkinson patients belong to the atypical Parkinson's syndrome due to multi-system disease marked by typical Parkinsonian symptoms such as rigor, tremor and akinesia and early onset of severe autonomic, cerebellar or pyramidal disorders. Symptoms like postural hypotension, dysphagia, hypersalivation, urinary bladder dysfunction, thermodysregulation, abnormalities in eye movement, early falls or dementia etc. are frequently seen in these patients. In these patients dopamin depletion in the nigrostriatal pathway is combined with degeneration of other cerebral structures like olivopontocerebellar and intermediolateral columns. Patients need high dosages of L-dopa and other antiparkinsonian drugs with poor prognosis in general. First, we report on an atypical Parkinson patient who developed acute dyspnoea and muscle rigidity after general anaesthesia; second, on another patient who took a long time to recover from general anaesthesia. Both responded to antiparkinsonian drugs, the first to orally applied L-dopa, the second to intravenous amantadine. Most probably the interruption of the treatment with high dosages of L-dopa (in these patients given in 2-4 hours intervals) had caused these complications. The special nature of the anaesthesiological management of atypical Parkinson patients is reviewed.

Amantadine↗
PubMedDate not supplied

Parkinson's disease primer.

Parkinson's disease (PD) is a progressive, neurodegenerative disorder characterized by the primary motor symptoms of bradykinesia, muscle rigidity, resting tremor, and postural instability. PD most often affects people older than 65, although it does occur at younger ages. The purpose of this article is to provide a brief overview of the pathophysiology of PD and a review of current literature, assessment and diagnostic techniques, therapeutic interventions, and management protocols. Treatment goals are twofold: short-term treatment to alleviate symptoms and reverse functional disability and long-term treatment to maintain effectiveness and limit pharmacologic complications.

Age Distribution↗
PubMed1997

Alprazolam dependence prevented by substituting with the beta-carboline abecarnil.

Abrupt termination of the treatment of humans with benzodiazepines (BDZs) leads to a rapid onset of discontinuation syndrome characterized by anxiety, muscle spasms, and occasionally convulsions. For this reason, it is recommended in clinical practice to reduce the dose of the BDZs gradually at the end of treatment. Nevertheless, many clinicians report signs of dependence even during gradual reduction of doses (tapering) of the BDZs in a large proportion of patients. Thus, there is considerable interest in discovering means of weaning patients away from BDZs without the risk of discontinuation syndrome. In the present study, mice withdrawn from chronic treatment with alprazolam showed anxiety, muscle rigidity, and seizures between days 1 and 28 after termination of the treatment. Replacement of alprazolam with the beta-carboline abecarnil for 7 days prevented the occurrence of the signs of dependence. In contrast, substitution of the beta-carboline antagonist ethyl-5-isopropoxy-4-methyl-beta-carboline-3-carboxylate (ZK93426) for alprazolam worsened the discontinuation syndrome. Replacement therapy with abecarnil after long-term treatment with the BDZs offers a novel method for rapid tapering.

Alprazolam↗
PubMed2006

Fyn is required for haloperidol-induced catalepsy in mice.

Fyn-mediated tyrosine phosphorylation of N-methyl-D-aspartate (NMDA) receptor subunits has been implicated in various brain functions, including ethanol tolerance, learning, and seizure susceptibility. In this study, we explored the role of Fyn in haloperidol-induced catalepsy, an animal model of the extrapyramidal side effects of antipsychotics. Haloperidol induced catalepsy and muscle rigidity in the control mice, but these responses were significantly reduced in Fyn-deficient mice. Expression of the striatal dopamine D(2) receptor, the main site of haloperidol action, did not differ between the two genotypes. Fyn activation and enhanced tyrosine phosphorylation of the NMDA receptor NR2B subunit, as measured by Western blotting, were induced after haloperidol injection of the control mice, but both responses were significantly reduced in Fyn-deficient mice. Dopamine D(2) receptor blockade was shown to increase both NR2B phosphorylation and the NMDA-induced calcium responses in control cultured striatal neurons but not in Fyn-deficient neurons. Based on these findings, we proposed a new molecular mechanism underlying haloperidol-induced catalepsy, in which the dopamine D(2) receptor antagonist induces striatal Fyn activation and the subsequent tyrosine phosphorylation of NR2B alters striatal neuronal activity, thereby inducing the behavioral changes that are manifested as a cataleptic response.

Animals↗
PubMed2003

Effector-specific visual information influences kinesthesis and reaction time performance in Parkinson's disease.

Twelve patients diagnosed with idiopathic Parkinson's disease and 11 age-matched control participants performed a continuous bimanual wrist flexion-extension tracking task while vision of their hands was manipulated. Participants were required to match the frequency and amplitude of movements of 1 limb that was driven at 0.6 Hz by a torque motor by actively moving the contralateral limb. In half the trials, the more affected limb (subdominant for controls) was driven, and in the other half, the less affected limb (dominant for controls) was driven. Vision of both hands, vision of the driven hand only, vision of the active hand only, or no vision of the hands was allowed. Simple and probe reaction times were assessed. Parkinson's disease patients performed the tracking task to a reasonable level of temporal and spatial accuracy as compared with control participants in terms of hand phasing and root mean square error. Patients demonstrated a marked posture deviation (toward flexion), which was exaggerated when the less affected limb was active. Amplitude deviations were smaller in both groups when the less affected (dominant) limb was active and when participants had vision of the driven hand. Overall, patients delivered slower responses in both simple and probe conditions. Reaction times of Parkinson's disease patients who were allowed vision of only the active hand were longer than were those of patients in all other visual conditions, whereas visual conditions did not affect the reaction times of control participants. The authors conclude that central demands increase when movement regulation must be based solely on kinesthetic information and when vision directs attention away from the most relevant source of kinesthetic information.

Aged↗
PubMed2003

Early recognition of neuroleptic malignant syndrome during traumatic brain injury rehabilitation.

Neuroleptic malignant syndrome is a rare disorder that manifests with hyperthermia, muscle rigidity and autonomic instability. Presented is a case series of individuals with traumatic brain injury and agitation who, when treated with neuroleptics, developed neuroleptic malignant syndrome. Although the incidence of this syndrome is rare, it is associated with significant morbidity and mortality. The onset of symptoms inconsistent with the patient's current level of recovery should alert the clinician to consider other possible diagnosis and failure to distinguish the features of neuroleptic malignant syndrome from post-traumatic agitation will delay appropriate intervention for this potentially life-threatening disorder.

Adult↗
PubMed2006

Successful treatment of six patients with neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure.

Neuroleptic malignant syndrome is a rare but potentially lethal, rare reaction to neuroleptics which is characterized by altered levels of consciousness, extrapyramidal effects, autonomic instability, hyperthermia, and elevated serum creatine phosphokinase levels. The most serious complication of neuroleptic malignant syndrome is acute renal failure. We investigated six cases of neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure due to rhabdomyolysis and effect of hemodialysis or hemodiafiltration. The patients were five males and one female with a mean age of 43.5 yr. All of the patients, who developed acute renal failure induced from rhabdomyolysis, had previously received butyrophenone (haloperidol), phenothiazine, benzamide, iminomide, benzisoxazole, antidepressants, and hypnotics (benzodiazepine and barbiturate) for the treatment of schizophrenia. The clinical manifestations of neuroleptic malignant syndrome were characterized by altered consciousness, muscle rigidity and weakness, fever, and excessive perspiration. The peak laboratory data were blood urea nitrogen 102 +/- 26 (mean +/- SD) mg/dL, serum creatinine 9.1 +/- 2.1 mg/dL, serum creatine phosphokinase 229,720 +/- 289,940 IU/L, and all of them developed oliguric acute renal failure. Dantrolene sodium administration was given to five cases and hemodialysis or hemodiafiltration was performed in all of them. The serum creatinine level after hemodialysis or hemodiafiltration was 1.4 +/- 1.0 mg/dL. All patients were successfully cured of acute renal failure by hemodialysis or hemodiafiltration. As a result, myoglobulinemic acute renal failure associated with neuroleptic malignant syndrome was successfully treated by hemodialysis or hemodiafiltration.

Acute Kidney Injury↗
PubMed2001

Dextromethorphan and dexmedetomidine: new agents for the control of perioperative pain.

Most traditional opioids and non-steroidal anti-inflammatory drugs that are used to control perioperative pain have substantial side effects. The number of choices in clinical use was recently increased by two promising groups of drugs: N-methyl-D-aspartate receptor antagonists and central alpha2 agonists. One N-methyl-D-aspartate antagonist, dextromethorphan, blocks the generation of central pain sensation that arise from peripheral nociceptive stimuli by moderating the activity of N-methyl-D-aspartate. It pre-empts the sensation of acute pain at doses of 30-90 mg without serious side effects, while reducing the amount of analgesics required perioperatively by 50%. It is available in oral form and has a confirmed lack of effect on haemodynamics and respiration. Dexmedetomidine is a relatively new, highly selective central alpha2 agonist. Its sedative, pro-anaesthetic and pro-analgesic effects at 0.5-2 microg/kg given intravenously stem mainly from its ability to blunt the central sympathetic response by as yet unknown mechanism(s) of action. It also minimises opioid-induced muscle rigidity, lessens postoperative shivering, causes minimal respiratory depression, and has haemodynamic stabilising effects.

Adrenergic alpha-Agonists↗
PubMed1983

Extensibility of the myofilaments in vertebrate skeletal muscle as revealed by stretching rigor muscle fibers.

The extensibility of the myofilaments in vertebrate skeletal muscle was studied by stretching glycerinated rabbit psoas muscle fibers in rigor state and examining the resulting extension of sarcomere structures under an electron microscope. Although stretches applied to rigor fibers produced a successive yielding of the weakest sarcomeres, the length of the remaining intact sarcomeres in many myofibrils was fairly uniform, being definitely longer than the sarcomeres in the control, nonstretched part of rigor fibers. The stretch-induced increase in sarcomere length was found to be taken up by the extension of the H zone and the I band, whereas the amount of overlap between the thick and thin filaments did not change appreciably with stretches of 10-20%. The thick filament extension in the H zone was localized in the bare regions, whereas the thin filament extension in the I band appeared to take place uniformly along the filament length. No marked increase in the Z-line width was observed even with stretches of 20-30%. These results clearly demonstrate the extensibility of the thick and thin filaments. The possible contribution of the myofilament compliance to the series elastic component (SEC) in vertebrate skeletal muscle fibers is discussed on the basis of the electron microscopic data and the force-extension curve of the SEC in rigor fibers.

Animals↗
PubMed1999

Clinical pharmacology of neuromuscular blocking agents.

The clinical pharmacology of neuromuscular blocking agents is described. During neuromuscular blockade, succinylcholine attaches to receptors in the motor end plate and depolarizes the neuromuscular junction, making the end plate refractory to acetylcholine. The nondepolarizing relaxants have a structure similar to that of succinylcholine and bind to the same receptors. Instead of depolarizing the junction, they block acetylcholine from binding to the receptor and cause channel blockade. As the concentration of nondepolarizing relaxant increases relative to acetylcholine, neuromuscular transmission is compromised. This relationship is used clinically to facilitate recovery from nondepolarizing agents. Succinylcholine is popular because its onset is faster than that of the nondepolarizing relaxants and metabolism by pseudocholinesterase clears it quickly. It is commonly given as an i.v. bolus to facilitate tracheal intubation. The onset of these agents varies widely and is dose dependent. Large doses are usually given to hasten the onset of paralysis; subsequent doses are adjusted according to response. The nondepolarizing agents interact with inhaled anesthetics, magnesium, and many antimicrobials. Drugs like neostigmine, edrophonium, and pyridostigmine antagonize neuromuscular blockade; an anticholinergic drug is typically administered to counteract the cardiovascular effects. The most serious adverse effects of succinylcholine are malignant hyperthermia syndrome, masseter muscle rigidity, and bradycardia. Some nondepolarizing relaxants (atracurium, mivacurium, and pancuronium) are associated with histamine release, occasionally causing serious hypotension and tachycardia. Neuromuscular blocking agents are essential to anesthesia. Older compounds produce greater toxicity than newer compounds, and several of these older compounds therefore are no longer in clinical use.

Drug Interactions↗
PubMed1981

Alfentanil-oxygen anaesthesia for coronary artery surgery.

The anaesthétic properties of alfentanil were evaluated in 15 patients undergoing coronary artery bypass grafting operations. Alfentanil was infused at a rate of 3.0mg min-1 until the patients (breathing pure oxygen) became unconscious. Additional alfentanil 2.5-5.0mg i.v. was given if systolic arterial pressure increased by 15% or more from control values. Alfentanil produced unconsciousness in 75 +/- 18s, but muscle rigidity occurred in 27% of patients. Cardiovascular dynamics were minimally altered during the induction of anaesthesia and throughout most of the operation, although 60% of patients became hypertensive during sternotomy and 73% during sternal spread. Recovery from anaesthesia was rapid with patients regaining consciousness after 1.4 +/- 0.6h and fulfilling out criteria for extubation of the trachea 4.1 +/- 1.2h after operation. No patient was aware of laryngoscopy, endotracheal intubation or any aspect of the operation.

Adult↗
PubMed1995

Dexmedetomidine does not modify the neuromuscular blocking action of vecuronium in the anaesthetized rat.

Dexmedetomidine is a new alpha 2 adrenergic agonist anaesthetic adjuvant. In animal studies, dexmedetomidine produced muscle flaccidity and prevented opioid-induced muscle rigidity, apparently via a central mechanism. The effect of dexmedetomidine on the neuromuscular junction or on non-depolarizing neuromuscular block during anaesthesia has not been reported. We have studied in the anaesthesized rat, the effects of dexmedetomidine on vecuronium-induced twitch depression. Wistar rats (n = 35) were anaesthetized and their lungs ventilated to maintain normocapnia. An infusion of vecuronium of 2.3 (SEM 0.1) micrograms kg-1 min-1 produced a stable twitch height (T1) depression of the tibial nerve of 53 (2)% of control in all groups. Rats were allocated randomly to receive either saline or dexmedetomidine 10, 30 or 100 micrograms kg-1 i.v. and T1 height was measured continuously for 60 min. Dexmedetomidine did not significantly affect T1 height during the first 30 min of infusion. At later times there were minor differences between groups. With cessation of the infusion of vecuronium, T1 height recovered rapidly to normal in all groups. These data suggest that the neuromuscular blocking properties of dexmedetomidine are unlikely to be produced by action at the neuromuscular junction.

Action Potentials↗
PubMed1980

Neurochemical alterations in Huntington's chorea: a study of post-mortem brain tissue.

Dopamine, noradrenaline, glutamic acid decarboxylase and choline acetyltransferase were measured in various regions of brain obtained at autopsy from a large series of cases of Huntington's chorea, dying with advanced forms of the disease. Neurochemical values in the choreic cases were compared with those from control and schizophrenic cases. In brain tissue from choreic patients, highly significant increases in dopamine concentrations were found in the corpus striatum, nucleus accumbens and pars compacta of the substantia nigra. This is consistent with the hypothesis that the nigrostriatal dopamine system is spared and may exert a relatively unopposed action on striatal function. Noradrenaline concentrations were raised in the caudate nucleus, lateral pallidum and pars reticulata of the substantia nigra, indicating preservation of central noradrenergic pathways. Glutamic acid decarboxylase activity was reduced in all brain regions examined but, taking ante-mortem factors into account, the depletion was confined to the striatum and lateral pallidum. This is consistent with the view that striatal GABA-containing interneurons degenerate. Significant losses of choline acetyltransferase activity were observed in the striatum, nucleus accumbens, septal nuclei and hippocampus. The development of muscle rigidity in choreic patients did not significantly affect the neurochemical values. The neurochemical alterations in Huntington's chorea could not be attributed to differences in ante-mortem or post-mortem factors between the choreic group and the control and schizophrenic groups.

Adolescent↗
PubMed1992

Traumatic seromuscular rupture of intestine.

A vehicular accident victim sustained multiple transverse split-thickness intestinal lacerations. This rare and distinctive seatbelt injury results from the impact of intestinal loops against the abdominal restraint, whereby the rigid muscle coat ruptures, while the integrity of inner layers is preserved.

Adult↗
PubMed1999

Acute hypernatremia and neuroleptic malignant syndrome in Parkinson disease.

Neuroleptic malignant syndrome is a clinical syndrome characterized by fever, muscle rigidity, and mutism. Some patients with neuroleptic syndrome may have elevated creatine phosphokinase values and abnormal liver aminotransferase values. Precipitating factors are important clues for prompt diagnosis. Typical precipitating factors include antipsychotic agents and major tranquilizers. In Parkinson disease, drug withdrawal, menstruation, and hyponatremia are precipitating factors. We report a case of neuroleptic malignant syndrome in a patient with Parkinson disease and hypernatremia. In addition, we hypothesized that sudden change of sodium concentrations in the central nervous system could trigger neuroleptic malignant syndrome in patients with Parkinson disease. According to our experience, neuroleptic malignant syndrome is a clinical diagnosis and prompt diagnosis avoids unnecessary, expensive work-ups.

Acute Disease↗