Effects of transcutaneous acupoint electrical stimulation combined with low-dose sufentanil pretreatment on the incidence and severity of etomidate-induced myoclonus: A randomized controlled trial.

BACKGROUND: Myoclonus is an undesirable phenomenon that occurs after induction of general anesthesia using etomidate. Opioids such as sufentanil are considered effective pretreatment drugs for myoclonus inhibition, although high doses are required. Transcutaneous acupoint electrical stimulation (TAES), a noninvasive technique involving electrical stimulation of the skin at the acupuncture points, exhibits analgesic effects, promotes anesthetic effects, decreases the dose of anesthetic drugs, and increases endogenous opioid peptide levels. In the present study, we investigated the effects of TAES combined with low-dose sufentanil pretreatment on the incidence and severity of etomidate-induced myoclonus in patients undergoing elective hysteroscopy. METHODS: In a double-blind manner, 172 patients (American Society of Anesthesiologists class I-II; age, 20-55 years) scheduled to undergo elective hysteroscopy were randomized into the following groups (n = 43 each): control (false TAES followed by saline injection after 30 min), TAES (TAES followed by saline injection after 30 minutes), sufentanil [false TAES followed by low-dose sufentanil (0.1 µg/kg) injection after 30 minutes], and sufentanil plus TAES (TAES followed by low-dose sufentanil injection after 30 minutes). In all groups, general anesthesia was induced by etomidate 0.3 mg/kg after sufentanil or saline injection. The incidence and severity of myoclonus were assessed for 2 minutes after etomidate administration. The visual analogue scale (VAS) scores for pain at 1 hour after surgery were recorded. The heart rate (HR), mean arterial pressure (MAP), and peripheral capillary oxygen saturation (SPO2) were recorded before premedication, after etomidate injection, after uterus expansion, and after recovery from anesthesia. RESULTS: The incidence of myoclonus was highest in the control group (88.3%), followed by TAES (74.4%), sufentanil (60.4%), and TAES plus sufentanil (48.8%) groups. Thus, the incidence was significantly higher in the control and TAES groups than in the sufentanil and TAES plus sufentanil groups. Grade 3 myoclonus occurred in 30.2%, 9.3%, 11.6%, and 9.3% patients in the control, TAES, sufentanil, and TAES plus sufentanil groups, respectively, with significant differences between the control group and the other 3 groups. Furthermore, the postoperative VAS scores for pain were significantly lower in the TAES, sufentanil, and TAES plus sufentanil groups compared with those in the control group. There were no significant differences in any other parameters among groups. CONCLUSION: Our results suggest that TAES combined with low-dose opioids such as sufentanil can decrease the incidence and severity of etomidate-induced myoclonus.

Assessment of the Anticonvulsant Potency of Ursolic Acid in Seizure Threshold Tests in Mice.

Ursolic acid (UA) is a plant derived compound which is also a component of the standard human diet. It possesses a wide range of pharmacological properties, i.e., antioxidant, anti-inflammatory, antimicrobial and antitumor, which have been used in folk medicine for centuries. Moreover, influence of UA on central nervous system-related processes, i.e., pain, anxiety and depression, was proved in experimental studies. UA also revealed anticonvulsant properties in animal models of epilepsy and seizures. The aim of the present study was to investigate the influence of UA on seizure thresholds in three acute seizure models in mice, i.e., the 6 Hz-induced psychomotor seizure threshold test, the maximal electroshock threshold (MEST) test and the timed intravenous pentylenetetrazole (iv PTZ) infusion test. We also examined its effect on the muscular strength (assessed in the grip strength test) and motor coordination (estimated in the chimney test) in mice. UA at doses of 50 and 100 mg/kg significantly increased the seizure thresholds in the 6 Hz and MEST tests. The studied compound did not influence the seizure thresholds in the iv PTZ test. Moreover, UA did not affect the motor coordination and muscular strength in mice. UA displays only a weak anticonvulsant potential which is dependent on the used seizure model.

Mioclonías asociadas al tratamiento con ciprofloxacino / Myoclonus associated with Ciprofloxacin therapy

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Positive effects of ceftriaxone on pentylenetetrazol-induced convulsion model in rats.

AIMS: Many drugs have been associated with seizures as a side effect. Although they are defined as safe for nervous system. The effect on proconvulsant activity of beta lactam antibiotics have been also reported. We aimed to investigate whether ceftriaxone has an anticonvulsant effect on PTZ-induced seizures in rats. MATERIALS AND METHODS: 36 male Sprague-Dawley rats, 18 of them for EEG recording and 18 of them are for behavioral studies, were randomly divided in two groups: group A for EEG recordings and group B for behavioral assesment. About 70 mg/kg PTZ was used for behavioral studies after Ceftriaxone administiration. About 35 mg/kg PTZ were used for EEG recording after ceftriaxone administiration. The electrodes were implanted on dura over the left frontal cortex and the reference electrode was implanted over the cerebellum for EEG recording. The Racine convulsion scale, first myoclonic jerk onset time, spike percentages, brain MDA and SOD levels were evaluated between the groups. RESULTS: First myoclonic jerk onset time was significantly shorter in saline group than both 200 and 400 mg/kg ceftriaxone groups (p < 0.05). Racine's convulsion scale was significantly lower in 200 and 400 mg/kg ceftriaxone groups than saline group (p < 0.01, p < 0.0001). Both of two ceftriaxone groups have lower spike percentages than the saline group (p < 0.05). Significantly lower MDA levels and higher SOD activity were determined in 200 mg/kg ceftriaxone group compared with the saline group (p < 0.05). CONCLUSION: Our study demonstrated that ceftriaxone has protective effects on PTZ-induced convulsions and on oxidative damage associated with PTZ.

[A woman in her forties with cancer, syncope and spasms]. / En kvinne i 40-årene med kreft, synkope og kramper.

A female in her forties with advanced incurable rectal cancer presented to our emergency department after loss of consciousness followed by brief myoclonic jerks in her legs. A cerebral MRI was normal. Her electrocardiogram showed a prolonged QTc interval of 596 milliseconds and hypokalemia was present. She had no family history of congenital long QT syndrome or of cardiovascular disease. She was not on any medication apart from having ingested 100 g caesium carbonate over the previous 11 days as an alternative cancer treatment. Caesium chloride is postulated to increase pH and thereby induce apoptosis in cancer cells. In treatment doses caesium competes with potassium for membrane transport proteins in the cardiac cell membrane and in the reabsorption tubuli of the kidneys. A result is hypokalemia shortly after depolarization during the cardiomyocytes' repolarisation phase or delayed post-depolarisation. Torsade de pointes ventricular arrhythmias, ventricular tachycardia, pump failure and death can follow. A few case reports of adverse effects from caesium ingestion have been published, as well as reports on how caesium is used in animal models to induce ventricular tachycardia, but the hazards of caesium ingestion and its long half-life are not well known in the medical care profession or among patients. As this patient's QTc interval normalised slowly to 413 milliseconds 60 days after stopping caesium ingestion, we consider caesium intoxication and convulsive syncope from a self-terminating ventricular tachycardia as the most probable aetiology. The main message from this case is that alternative medicine can have life-threatening side effects.

Myoclonus associated with continuous dobutamine infusion in a patient with end-stage renal disease.

PURPOSE: The occurrence of myoclonus associated with continuous i.v. infusion of dobutamine in a patient with end-stage renal disease (ESRD) is described. SUMMARY: A 65-year-old Caucasian man was admitted to the hospital on January 26, 2006, for worsening congestive heart failure (CHF). He had been receiving dobutamine 3 mug/kg/min by intermittent i.v. infusion over four hours once weekly as an outpatient. His medical history included ischemic cardiomyopathy, pacemaker placement, ESRD, carotid artery disease, and type 2 diabetes mellitus. Along with receiving multiple other drugs, the patient was started on a continuous i.v. infusion of dobutamine 3 mug/kg/min. On January 29, the patient began having myoclonic muscle spasms. Clonazepam was given as needed, and the patient was discharged on February 1 with myoclonus that soon subsided. On March 13 the patient was again admitted for worsening CHF and was started on continuous dobutamine infusion. He was discharged on March 15; myoclonic muscle spasms began that afternoon. Myoclonic movements were noted when the patient arrived at the outpatient infusion center to begin his intermittent dobutamine infusion, and he was sent to the emergency department, where he was treated with calcium gluconate, regular insulin, and lorazepam and was instructed to stop his potassium supplements; he then received his dobutamine infusion. The myoclonic symptoms continued until March 18, when they subsided. CONCLUSION: A patient with CHF and ESRD developed myoclonic muscle spasms after receiving dobutamine by continuous i.v. infusion.

Lack of efficacy and potential aggravation of myoclonus with lamotrigine in Unverricht-Lundborg disease.

PURPOSE: Unverricht-Lundborg disease (ULD) is a progressive myoclonus epilepsy with tonic-clonic seizures, action myoclonus, mild ataxia, without dementia. Persistence of invalidating action myoclonus is a major problem. Drugs like phenytoin can aggravate ULD. In this study, we retrospectively analyzed the effect of add-on lamotrigine (LTG) in the five patients under our care who received LTG. METHOD: Three men and two women, aged 20-50 years who had ULD confirmed by molecular biology, followed in two epilepsy centers, received add-on LTG at 50-300 mg/d. All of them had valproate. The other drugs used in cotherapy were high-dose piracetam, benzodiazepines phenobarbital, topiramate, and primidone. The assessment of LTG was based on detailed interview and clinical examination. Aggravation was diagnosed when myoclonic jerks (MJ) increased without irregular intake of medication, inappropriate lifestyle, encephalopathic or metabolic complications, or overdosage. RESULTS: In two patients, LTG exacerbated MJ in a dose-dependent manner. In one patient, a delayed, severe exacerbation of myoclonus occurred that only ceased after LTG withdrawal and introduction of levetiracetam. These three patients had minor forms of ULD. In two patients with moderate to severe forms of ULD, LTG had no effect. CONCLUSION: Although symptoms may fluctuate in ULD, it was possible to pinpoint lack of improvement (2/5), dose-related exacerbation of myoclonus (2/5), and putative late-onset aggravation (1/5) in five patients treated with adjunctive LTG. LTG does not appear to be a sensible treatment option in ULD.

Neurologic manifestations in welders with pallidal MRI T1 hyperintensity.

BACKGROUND: Neurologic symptoms have been attributed to manganese fumes generated during welding. Increased T1 MRI signal in the basal ganglia is a biologic marker of manganese accumulation. Recent studies have associated welding and parkinsonism, but generally without MRI corroboration. OBJECTIVE: To characterize the clinical and neuropsychological features of patients with MRI basal ganglia T1 hyperintensity, who were ultimately diagnosed with neurotoxicity from welding fumes. METHODS: The medical records of welders referred to the Department of Neurology with neurologic problems and basal ganglia T1 hyperintensity were reviewed. RESULTS: All eight patients were male career welders with increased T1 basal ganglia signal on MRI of the brain. Several different clinical syndromes were recognized: a parkinsonian syndrome (three patients), a syndrome of multifocal myoclonus and limited cognitive impairment (two patients), a mixed syndrome with vestibular-auditory dysfunction (two patients), and minor subjective cognitive impairment, anxiety, and sleep apnea (one patient). Neuropsychometric testing suggested subcortical or frontal involvement. Inadequate ventilation or lack of personal respiratory protection during welding was a common theme. CONCLUSIONS: Welding without proper protection was associated with syndromes of parkinsonism, multifocal myoclonus, mild cognitive impairment, and vestibular-auditory dysfunction. The MRI T1 hyperintensity in the basal ganglia suggests that these may have been caused by manganese neurotoxicity.

Propriospinal myoclonus after treatment with ciprofloxacin.

The clinical and electrophysiological features of a truncal myoclonus in a 55-year-old man are described. The electromyographic characteristics point toward propriospinal myoclonus. It is suggested that a myoclonic generator was released after use of ciprofloxacin, by antagonising the gamma-aminobutyric acid metabolism.

Myoclonic involuntary movement associated with chronic manganese poisoning.

We report a 17-year-old man showing myoclonic involuntary movement (IVM) associated with chronic manganese (Mn) poisoning. The patient, a welder, showed myoclonic IVM mainly in the right upper and lower extremities, elevated levels of Mn in the blood and hair and high-intensity signals in the globus pallidus on T1-weighted MR images. Chelation therapy resulted in improvement of the myoclonic IVM and MRI abnormalities. This is the first report of Mn poisoning characterized by myoclonic IVM without parkinsonism.

Myoclonic spasms following intrathecal diamorphine.

The use of intrathecal diamorphine via an implanted portal system is described for pain control in a patient suffering from vertebral metastatic disease. The complication of myoclonic spasms affecting the lower half of the body occurred after 14 days, when increasing the bolus dose to 40 mg. The spasms lasted for 3 hr and then gradually subsided. Diamorphine was subsequently restarted at a lower dose of 15 mg twice daily. On increasing the dose to 20 mg diamorphine 10 days later, severe distressing myoclonic spasms recurred 20 min postinjection. Myoclonus could only be controlled by instituting a local anesthetic intrathecal block. The patient was finally managed with 20 mg diamorphine per day by intrathecal infusion, and the pain was reasonably well controlled for the following 10 weeks without any recurrence of myoclonic spasms.

The effects of non-competitive NMDA receptor antagonists on rats exposed to hyperbaric pressure.

The high pressure neurological syndrome (HPNS) occurs when man or animals are exposed to hyperbaric pressure. Four non-competitive N-methyl-D-aspartate (NMDA) antagonists - MK-801, phencyclidine (PCP), SKF 10,047 and ketamine were tested in rats for effects on the HPNS. All drugs were injected i.p. prior to compression; ketamine was also infused i.v. Control rats received saline. Rats were exposed individually to increasing helium pressure (PO2 0.5 atmospheres absolute ATA). Three endpoints were used to assess HPNS: onset pressures for tremor, myoclonus and convulsions. Neither MK-801 (0.03 and 0.3 mg/kg) nor SKF 10,047 (50 mg/kg) had any effect on the onset pressures for tremor, myoclonus or convulsions, although the type of seizure was modified from the clonic/tonic seizure seen in controls to purely clonic. PCP (5 mg/kg) had no effect on the endpoints, but pressure enhanced the excitation and stereotypy seen at 1 ATA. Ketamine (100 mg/kg i.p.) did not affect tremor or myoclonus; ketamine infused i.v. at pressure only prevented tremor and myoclonus at 'anaesthetizing' concentrations. Our results show that these non-competitive NMDA antagonists had little effect on HPNS, in contrast to competitive NMDA antagonists, such as AP7, which are highly effective. Possible explanations for this lack of effect include (1) interactions with NMDA receptor channels are pressure dependent; (2) other actions of these antagonists override their effects on the NMDA receptor channel.

Encephalopathy in chronic renal failure responsive to deferoxamine therapy. Another manifestation of aluminum neurotoxicity.

We describe a patient undergoing chronic hemodialysis who developed a neurologic syndrome consisting of seizures, progressive myoclonus, and mild dementia and who responded to chelation therapy with deferoxamine mesylate. Neither her serum nor bone aluminum concentrations indicated aluminum toxicity. However, the presence of a positive deferoxamine-infusion test was suggestive of an elevated body burden of aluminum. Treatment with deferoxamine resulted in marked clinical improvement in her neurologic status within two months. The utility of using the deferoxamine-infusion test rather than serum aluminum levels in evaluating aluminum toxicity in chronic renal failure is suggested.

Serotonin models of myoclonus in the guinea pig and rat.

Myoclonus could not be induced in rats with either L-5-HTP alone or hypoxia. Following amine depletion or destruction of the serotonin neurons with 5,7-DHT, myoclonus appeared as part of a complex serotonergic behavioral syndrome induced by serotonin agonists. On the other hand, in the guinea pig, L-5-HTP induces a pure myoclonic syndrome in a dose-dependent fashion. Myoclonus also was induced by injection of serotonin into the dorsal pons of the guinea pig. This is additional evidence confirming the importance of the brainstem structures in the L-5-HTP guinea pig model of myoclonus. Deoxyglucose (DG) autoradiography in guinea pigs following systemic L-5-HTP administration demonstrated increased glucose metabolism within thalamic and third nerve nuclei, with decreased metabolism in the cortex, and the molecular layer of the hippocampus. Since serotonin is an inhibitory transmitter, we hypothesize that the decreases observed in cortex may be the result of direct serotonergic inhibition, whereas the increases observed in the thalamus probably represent indirect effects via polysynaptic pathways.

Interactions between relatively selective monoamine oxidase inhibitors and an inhibitor of 5-hydroxytryptamine re-uptake, clomipramine.

Features of interactions with combined antidepressants in man were evoked by clomipramine in rats pretreated with both the relatively selective monoamine oxidase (MAO) inhibitors clorgyline and deprenyl, but not when clomipramine was given to rats pretreated with deprenyl or clorgyline alone, i.e. inhibition of both MAO A and B was a likely prerequisite for clomipramine to elicit the syndrome (with the larger dose of clorgyline and deprenyl, MAO A and B inhibition exceeded 95%). The features evoked were myoclonic--forelimb flexor-extensor movements, wet dog shakes and head and body twitches; hyperthermia and ECG anomalies also developed, and locomotor activity was augmented. Myoclonic phenomena were prevented when the above pretreatment also included p-chlorophenyl-alanine, but were unaffected or even intensified when pretreatment instead included alpha-methyl-p-tyrosine; these phenomena were attenuated or abolished by pirenperone, a 5HT2 antagonist. Relevance of these findings to safer combinations of antidepressants is discussed.

Functional anatomy of L-5-hydroxytryptophan-induced myoclonus in the guinea pig.

Myoclonus was induced in guinea pigs in a dose-dependent manner by intraperitoneal injection of L-5-hydroxytryptophan (L-5-HTP). At a dosage of 400 mg per kilogram, all animals developed myoclonus. Autoradiographic analysis, using the [14C]-deoxyglucose method, showed increased glucose utilization in the ventral and ventral anterior thalamic nuclei and decreased glucose utilization in the cortex and molecular layer of the hippocampus. These changes were dose-dependent and occurred to a lesser extent in both myoclonic and non-myoclonic guinea pigs given an ED50 of L-5-HTP, demonstrating that the autoradiographic changes are not dependent on the presence of myoclonus. We believe that the thalamus is the final common pathway for the expression of myoclonus induced by L-5-HTP.

Myoclonus with electrocerebral silence in a patient receiving penicillin.

Multifocal myoclonus is a well-recognized complication of high doses of penicillin. In man, the site of origin of penicillin-induced myoclonus has not been clearly established, but there is evidence from animal studies that it may originate at a cortical, subcoritcal, or spinal level. We report a case of multifocal myoclonus occurring in a patient receiving large doses of penicillin. The myoclonus appeared when there was no clinical or EEG evidence of upper brain stem or cerebral function. The observations reported suggest that penicillin-induced myoclonus may occur in man and may originate at a caudal brain stem or spinal level.

Restless legs, anxiety and caffeinism.

This clinical study of 62 patients with restless legs syndrome and associated anxious-depressed and other clinical states seems to indicate that caffeine is the major etiological factor in the causation of the restless legs syndrome. Anxiety, while modifying the subjective experience of the dysphoric sensation of restless legs, is not a causative factor. Caffeine is responsible for the increased nervous system arousal as well as for the direct peripheral contractile effect on the striated muscle. This arousal is often reflected psychologically in anxiety and sometimes depressive manifestations, insomnia, heightened proprioceptive awareness and physiologically in the toxic sensory experience of restless legs associated with increased neuromuscular reactivity which may include myoclonus and myokomia.