Muscle tremors observed in white rhinoceroses immobilised with either etorphine–azaperone or etorphine–midazolam: An initial study

Etorphine–azaperone is the most commonly used drug combination for chemical immobilisation of free-ranging white rhinoceroses, but causes several profound physiological disturbances, including muscle tremors. The addition of benzodiazepine sedatives, such as midazolam, has been proposed to reduce the muscular rigidity and tremors in immobilised rhinoceroses. Twenty-three free-ranging, sub-adult white rhinoceros bulls were darted and captured using a combination of etorphine plus either azaperone or midazolam. Skeletal muscle tremors were visually evaluated and scored by an experienced veterinarian, and tremor scores and distance run were compared between groups using the Wilcoxon rank sum test. No statistical differences were observed in tremor scores (p = 0.435) or distance run (p = 0.711) between the two groups, and no correlation between these variables was detected (r = –0.628; p = 0.807). Etorphine–midazolam was as effective as etorphine–azaperone at immobilising rhinoceroses, with animals running similar distances. Although the addition of midazolam to the etorphine did not reduce tremor scores compared to azaperone, it might have other beneficial immobilising effects in rhinoceroses, and further investigation is necessary to elucidate possible methods of reducing muscle tremoring during chemical immobilisation of rhinoceroses.

Analysis of the relationship of the vertical extension of mouth opening with muscle rigidity and sociodemographic factors in Parkinson's disease

Introduction Changes caused by the rigidity of Parkinson’s Disease (PD) can affect the mandibular musculature. However, few studies have been published about its impact on the oral opening. Objective To analyze the relationship of the vertical extension of the oral opening with muscular rigidity and sociodemographic factors of the elderly with PD. Material and method This is a cross-sectional, quantitative study that collected data from a primary study conducted at the Hospital das Clínicas of the Federal University of Pernambuco in 2018. Data were collected from medical records and from the questionnaire, Research Diagnostic Criterion for Temporomandibular Disorders (RDC/TMD). The sample was composed of 81 parkinsonians and characterized using: sociodemographic variables and the presence or absence of muscular rigidity. The measures of vertical extension of the oral opening evaluated were: mouth opening without assistance and without pain (ABASD), and maximum mouth opening without assistance (AMBSA). The Pearson’s linear correlation and Spearman’s correlation tests were applied to investigate the relationship among the continuous variables. Analyses of association were conducted using simple logistic regression. The level of significance was set at p<0.05. Result Limitation of the oral opening was not related to age or sex. The greatest level of significance was between mouth opening without assistance and without pain and muscular rigidity (p=0.012), and years of schooling (p=0.038). Conclusion The limitation of mouth opening in people with PD was shown to be related to muscular rigidity and fewer years of schooling.

Chlorpromazine and Trifluperazine Induced Parkinsonism in a Patient with Insomnia

Drug Induced Parkinsonism (DIP) can be described as reversible development of Parkinsonian syndrome in patients treated with drugs which impair dopamine function. It includes symptoms such as tremor, muscular rigidity and bradykinesia. Gastrointestinal prokinetics, calcium channel blockers, modern atypical antipsychotics, and antiepileptic drugs may cause DIP. This report is about a 40-year-old female patient who developed a DIP after taking the antipsychotic medication combination (chlorpromazine and trifluperazine) for insomnia after being prescribed from a psychiatric clinic. After four weeks of initiation of treatment, she developed tremors, muscular rigidity and slowness in movements. The patient was admitted with the following complaints and then the drugs chlorpromazine and trifluperazine were stopped. The patient was then treated with tablet levodopa and carbidopa 110 mg, trihexiphenidyl 2 mg and tablet alprazolam 0.25 mg after which she gradually improved and was feeling better after a week. Atypical antipsychotics indicated for psychiatric disorders have high potential to cause extrapyramidal symptoms. Hence, for the treatment of insomnia newer drugs such as zolpidem and zaleplon can be used to minimise the chances of occurrence of DIP.

Rhabdomyolysis and autoimmune variant stiff-person syndrome

Stiff-person syndrome (SPS) is a rare neurologic disorder characterized by waxing and waning muscular rigidity, stiffness and spasms. Three subtypes have been described: paraneoplastic, autoimmune and idiopathic. Rhabdomyolysis has been described in the paraneoplastic variant, but to our knowledge no case has been reported involving the autoimmune variant. We report a case report of a 50-year-old man with history of SPS who presented with recurrent episodes of severe limb and back spasms. He was hospitalized on two separate occasions for uncontrollable spasms associated with renal failure and creatinine phosphokinase elevations of 55,000 and 22,000 U/L respectively. Laboratory tests were otherwise unremarkable. The acute renal failure resolved during both admissions with supportive management. Rhabdomyolysis has the potential to be fatal and early diagnosis is essential. It should be considered in patients who have SPS and are experiencing an exacerbation of their neurologic condition.

Stiff Person Syndrome

Stiff person syndrome is an important autoimmune mediated disorder to consider in patients with unexplained pain and muscular rigidity. We review the proposed diagnostic criteria, common clinical features, and important serologic and electrophysiological tests to aid in diagnosis as well as medical and rehabilitative therapeutic options. In addition, we discuss the identification and management of possible paraneoplastic presentations.

DYSPHAGIA AND SIALORRHEA:

ContextDysphagia and sialorrhea in patients with Parkinson's disease are both automatically accepted as dependent on this neurological disease.ObjectiveThe aim were to establish if these two complaints are a consequence or associated manifestations of Parkinson's disease.MethodTwo Parkinson's diseases groups from the same outpatients' population were studied. Patients in the first group, with dysphagia, were studied by videofluoroscopy. The second, with sialorrhea, were studied by the scintigraphic method,ResultsVideofluoroscopic examination of the oral, pharyngeal and esophageal phases of swallowing showed that 94% of Parkinson's diseases patients present, structural causes, not related to Parkinson's diseases, able to produce or intensify the observed disphagia. The scintigraphic examination of Parkinson's diseases patients with sialorrhea showed that there is no increase of serous saliva production. Nevertheless, showed a significantly higher velocity of saliva excretion in the Parkinson's diseases patients.ConclusionsDysphagia can be due to the muscular rigidity often present in the Parkinson's diseases patient, or more usually by non Parkinson's disease associated causes. In Parkinson's diseases patients, sialorrhea is produced by saliva retention. Nevertheless, sialorrhea can produce discomfort in swallowing, although without a formal complaint of dysphagia. In this case, subclinical dysphagia must be considered. Sialorrhea is indicative of dysphagia or at least of subclinical dysphagia. As final conclusion, Parkinson's diseases can be an isolated cause of dysphagia and/or sialorrhea, but frequently, a factor unrelated to Parkinson's diseases is the main cause of or at least aggravates the dysphagia.