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The potency and anesthetic state produced by nitrous oxide alone were investigated in order to clarify its contribution to the effect of other anesthetic agents. Seven volunteers anesthetized with 1.55 atm absolute N2O in a pressure chamber displayed muscle rigidity with jerking movements, labored and rapid breathing, sweating, and dilated pupils. At 1.1 atm absolute N2O, relaxation and quiescence occurred, sweating ceased, and pupil size decreased. Determination of MAC (using tetanic electrical impulses as the noxious stimulus) produced a mean value of 1.04 +/- 0.10 (SE) atm absolute. All subjects complained of nausea and vomiting after anesthesia.
In experiments on random-bred rats, the synthetic hexapeptide Tyr-Gly-Gly-Phe-Leu-Arg caused the intensification of the muscle tone in the latent period of formation of the generator of pathologically enhanced excitation and in the stage where the generator activity did not manifest under normal conditions (clinical recovery). The effect described was shown both clinically by extension of the hind leg and electromyographically by the appearance of asynchronous electrical activity in the muscles of the hind leg. Control suboccipital administration of the related hexapeptide not containing D-leucin, or physiological solution did not produce the effect described.
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A group of 43 pigs from eight litters of purebred Pietrains were identified as malignant hyperthermia susceptible by halothane testing, and their reaction time (measured in seconds from the onset of halothane administration of the onset of skeletal muscle rigidity) was recorded. One week later, these pigs were treated with 0.02, 0.2, 0.5, 1.0 or 2.0 mg/kg of droperidol 1 hour prior to a second halothane test. Pigs with a post-droperidol reaction time of greater than 100.4 seconds (mean + 2.021 SD of initial reaction time) were considered to be protected from malignant hyperthermia. Droperidol afforded some degree of protection at all doses tested. The effective dose50 was determined to be 0.055 with 95% confidence limits of 0.017 to 0.183 mg/kg.
The behaviour of 48 children ranging from weeks to eight years was observed and compared after four different anaesthesia methods. Either ethrane or halothane was used with or without induction with ketamine i.m. (5 mg/kg bodyweight). Restlessness, the depth of postanaesthetic sleep, shivering, muscle rigidity and vomiting were evaluated every 15 min. up to one hour postoperatively using a graduation from 1--4. Ketamine combined with halothane showed significantly less postoperative restlessness than all other methods. No statistically proven differences were seen in the other criteria, which were noticed more than once. The psychic effects as well as the practical clinical application of this method are discussed.
Experiments in rats showed that intrastriatal administration of kainic acid in a dose of 100 but not 20 ng per side resulted in the development of behavioral disorders reminding those of Parkinsonian syndrome: bradykinesia, increased muscle rigidity, ptosis. Intrastriatal administration of galanin in doses of 10 and 50 ng induced only a decrease of locomotor activity in the "open field". When co-administered with kainic acid (20 ng), galanin displayed a dose-dependent potentiation of behavioral Parkinsonian-like disturbances the severity of which increased depending on the dose used. It is concluded that galanin potentiates the kainic acid-induced development of the generator of pathologically enhanced excitation in the striatum underlying the mechanisms of Parkinsonian syndrome. Thus, the increased galaninergic striatal activity could participate in the mechanisms of the above-mentioned CNS disorders.
Mescalbean (Sophora secundiflora) toxicity is reported in a dog. Mescalbean toxicity causes intolerance to exercise, muscle rigidity and collapse upon exercise, with a rapid recovery upon resting in dogs. Mescalbean toxicity is a rare cause of the periodic weakness/syncope class of diseases in dogs in areas of the habitat of Sophora secundiflora.
Lethal catatonia is often regarded as clinically similar to, and perhaps indistinguishable from, neuroleptic malignant syndrome. However, the two syndromes reveal differences in the mode of onset, signs and symptoms, and outcome. Lethal catatonia often begins with extreme psychotic excitement, which, if persistent, can lead to fever, exhaustion, and death. Neuroleptic malignant syndrome begins with severe extrapyramidally induced muscle rigidity. Early clinical differentiation is important, because lethal catatonia often requires neuroleptic treatment, and neuroleptic malignant syndrome necessitates immediate cessation of neuroleptics.
We report a 65-year-old female who have suffered from progressive gait disturbance for 3 years, followed by disorientation and forgetfulness. Neurological examination revealed dementia, constructional disability, limb kinetic apraxia, supranuclear gaze palsy, especially on downward gaze, symmetrical muscle rigidity and bradykinesia. Involuntary movements were undetectable. Brain MRI showed significant brain atrophy in the left fronto-parietal lobe. The three-dimensional surface display with 131I-IMP demonstrated decreased cerebral blood flow in the left frontoparietal cortex. The diagnosis of this case is discussed with regard to either progressive supranuclear palsy or corticobasal degeneration or both.
Parkinson's disease is a progressive neurodegenerative condition of unknown cause and with no known cure. The diagnosis is based on clinical findings of rest tremor, muscle rigidity, bradykinesia, and gait instability. Over 40% of patients develop a dementia syndrome that is largely distinct from Alzheimer's disease. Depression is common, also occurring in more than 40% of patients with PD. Careful evaluation in necessary to help distinguish Parkinson's disease from secondary causes of parkinsonism. Carbidopa/levodopa, dopamine agonists, and monoamine oxidase type B inhibitors are the mainstays of treatment. Anticholinergics and other agents may also be useful. Pharmacologic treatment must be carefully titrated to control symptoms and to avoid side effects. In advanced disease, dose-related dyskinesias, end-of-dose wearing-off effect, and unpredictable sudden motor fluctuations become very disabling and difficult to manage.
The electrophysiological, neurological, and neuropathological correlates of the spinal cord ischemia induced by the aortic cross-clamping of cats were studied with the goal of developing the reliable evoked spinal cord potentials (ESCPs) for the monitoring of spinal cord ischemia. The five types of ESCPs were elicited as follows; descending ESCPs recorded from the L2 and L5 vertebral levels, vertex motor evoked potential from the L2 vertebral level, ascending ESCP from the T1 vertebral level, and segmental ESCP after sciatic nerve stimulation. The late negative waves of both descending ESCP from L5 and segmental ESCP were susceptible to ischemia. The descending ESCP from L5 was not influenced by peripheral nerve ischemia or reflected ischemia in the whole spinal cord. Therefore, the late negative wave of the descending ESCP from L5 served as the most reliable index for spinal cord ischemia. When aortic clamping was continued for > or = 30 min after the disappearance of the late negative wave of descending ESCP from L5, the amplitude recovery of this wave decreased to 25%, resulting in paraplegia. Histologically, the posterior horn of the gray matter in the lumbar enlargement was the most vulnerable to ischemia.
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Neuroleptic Malignant Syndrome (NMS) is a specific, potentially lethal disorder related to the usage of dopamine antagonists. The four clinical hallmarks associated with this syndrome are 1) hyperthermia, 2) muscle rigidity, 3) mental status changes, and 4) autonomic instability. NMS has been estimated to occur in 0.02% to 3.23% of patients receiving dopamine antagonist therapy. The wide range of incidence is probably related to the variability in diagnostic criteria, survey techniques, and patient populations. Although the incidence of NMS is rare, the inherent mortality for patients developing NMS is significant. Fortunately, the mortality has gone from 25% before 1984 to 11.6% thereafter. This is probably related to greater awareness of the syndrome by the physician with early diagnosis and treatment and also to the advent of newer therapeutic modalities. Current methods of treatment include withdrawal of the dopamine antagonist, control of the hyperpyrexia, administration of a dopamine agonist, and the administration of dantrolene. Electroconvulsive therapy has been advocated in patients unresponsive to the above therapies. The reinstitution of dopamine antagonist therapy after an episode of NMS is possible. Specific protocols are available and are currently under revision by researchers. The current data indicate that the risk of a recurrence of NMS is about 30% if the protocol is followed.
A 55-year-old woman presented with a one-year history of painful muscle cramps and progressive flexion contractures of the arms, pelvic girdles and knees. Laboratory evaluation was summarized as follows: low plasma cortisol and ACTH levels, delayed response of plasma cortisol to ACTH administration, no response of plasma ACTH level to insulin administration, and normal plasma LH, FSH, GH, TSH and PRL levels. She was diagnosed as isolated ACTH deficiency. EMG was silent in contractured muscles at rest. Biopsy of the biceps femoris muscle revealed a marked reduction in fiber size, type 2 fiber atrophy and type 1 fiber predominance. The nerve conduction velocities of the peripheral nerves were found to be decreased. The biopsied specimen of the sural nerve revealed a loss of large myelinated fibers and segmental demyelination. Both flexion contractures and nerve conduction velocities were gradually improved with the replacement of hydrocortisone.
Cases of black widow (Latrodectus indistinctus) and brown widow (L. geometricus) spider bites referred to the Tygerberg Pharmacology and Toxicology Consultation Centre from the summer of 1987/88 to the summer of 1991/92 were entered into this series. Of a total of 45 patients, 30 had been bitten by black and 15 by brown widow spiders. It was evident that black widow spider bites caused a more severe form of envenomation than brown widow bites, characterised by generalised muscle pain and cramps, abdominal muscle rigidity, profuse sweating, raised blood pressure and tachycardia. The symptoms and signs of brown widow bites were mild and tended to be restricted to the bite site and surrounding tissues. Conditions which should be considered in the differential diagnosis include cytotoxic spider bite, scorpion sting, snakebite, acute abdominal conditions, myocardial infarction, alcohol withdrawal and organophosphate poisoning. To prevent the development of complications, the administration of black widow spider antivenom is recommended in severe cases because untreated latrodectism could become protracted, without improvement, for several days.