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INTRODUCTION: Postural balance impairment can affect the quality of life of patients with Parkinson's disease. Previous studies have described connections of the vestibular system with postural functions, suggesting a potential participation of the basal ganglia in receiving vestibular stimuli. This systematic review aims to summarize the evidence on the effectiveness of vestibular rehabilitation on postural balance in patients with Parkinson's disease. METHODS: A systematic review was conducted using the electronic databases: PubMed, Embase, Scopus and PEDro. The study selection was independently conducted by two reviewers, and disagreements were evaluated by a third reviewer. The included studies had no restrictions on publication dates or languages and the last update occurred in July 2023. RESULTS: From the 485 studies found in the searches, only 3 studies were deemed eligible for the systematic review involving a total of 130 participants. The Berg Balance Scale was described as the tool for evaluation of postural balance in all studies. The meta-analysis showed statistically significant results in favor of vestibular rehabilitation (MD = 5.35; 95% CI = 2.39, 8.31; P < 0.001), regardless of the stage of Parkinson's disease. Although the effect size was suggested as a useful functional gain, the analysis was done with caution, as it only included 3 randomized controlled trials. The risk of bias using the RoB-2 was considered as being of "some concern" in all studies. Furthermore, the quality of the evidence based on the Grading of Recommendations Assessment Development and Evaluation system, produced by pooling the included studies was considered very low. CONCLUSION: Compared to other interventions, vestibular rehabilitation has potential to assist the postural balance of patients with Parkinson's disease. However, the very low quality of the evidence demonstrates uncertainty about the impact of this clinical practice. More robust studies are needed to confirm the benefits of this therapy in patients with Parkinson's disease. This study was prospectively registered in PROSPERO: CRD42020210185.

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BACKGROUND: Patients with Parkinson's disease (PD) often report chronic pain, which is one of the most complex non-motor symptoms. Therefore, this study aims to review the literature on the characteristics of pain in patients with PD. METHODS: A systematic literature review was conducted following MOOSE recommendations. Observational studies reporting pain in patients with PD were included. No time restrictions were applied, but studies in Portuguese, Spanish, and English were considered. The search was performed in PubMed®, LILACS, and SciELO databases. RESULTS: Twenty-six articles of observational studies were identified, reporting an average pain prevalence of 67.36%, emphasizing the significance of this symptom in the PD population. Pain was reported in various body regions, including lower limbs, upper limbs, lumbar spine, cervical spine, and other joints. Pain classification varied, encompassing musculoskeletal pain, PD-related pain, neuropathic pain, and dystonic pain, among others. DISCUSSION: Pain in patients with PD is a prevalent and multifactorial condition, significantly impacting patients' quality of life. CONCLUSION: Heterogeneity in data across included studies was observed, highlighting the need for additional research to elucidate the underlying mechanisms of pain in patients with PD and develop effective therapeutic strategies to address this symptom and improve the quality of life for individuals living with the disease.

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The usual adverse events of amantadine are dizziness, dry mouth, and peripheral edema. Postmarketing experience has revealed abnormal movements such as tremors, involuntary muscle contractions, and gait abnormalities. Herein, we report a case of an elderly male who presented with generalized twitching associated with amantadine. A 64-year-old male presenting with jerking movements within one day of onset was admitted. Sudden and involuntary distal lower and upper limb muscle twitching was observed. The subject presented subsequent brief movements when attempting to stand or hold arms antigravity. He was diagnosed with Parkinson's disease three years ago. Eight days before the presentation to the emergency department, he consulted with his primary care physician, who prescribed amantadine to improve his motor symptoms. On the seventh day, he developed brisk abnormal movements. Laboratory exams, neuroimaging, and electroencephalogram were unremarkable. Amantadine was discontinued. After three days, the patient reported that his jerking movements had fully recovered. To the authors' knowledge, 22 individuals with amantadine-associated myoclonus had already been reported in the literature. The pathophysiology of amantadine-induced myoclonus is probably related to serotoninergic pathways. Myoclonus secondary to amantadine was slightly more common in men. The population affected was elderly, with a mean and median age of 67.7 and 64 years.

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BACKGROUND: Fluoroquinolones (FQNs) are related to several central nervous system side effects. This review aims to evaluate the clinical-epidemiological profile, pathophysiological mechanisms, and management of FQNs-associated movement disorders (MDs). METHODS: Two reviewers identified and assessed relevant reports in six databases without language restriction between 1988 and 2022. RESULTS: A total of 45 reports containing 51 cases who developed MDs secondary to FQNs were reported. The MDs included 25 myoclonus, 13 dyskinesias, 7 dystonias, 2 cerebellar syndromes, 1 ataxia, 1 tic, and 2 undefined cases. The FQNs reported were ciprofloxacin, ofloxacin, gatifloxacin, moxifloxacin, levofloxacin, gemifloxacin, and pefloxacin. The mean and median age were 64.54 (SD: 15.45) and 67 years (range: 25-87 years). The predominant sex was male (54.16%). The mean and median time of MD onset were 6.02 (SD: 10.87) and 3 days (range: 1-68 days). The mean and median recovery time after MD treatment was 5.71 (SD: 9.01) and 3 days (range: 1-56 days). A complete recovery was achieved within one week of drug withdrawal in 80.95% of the patients. Overall, 95.83% of the individuals fully recovered after management. CONCLUSIONS: Future cases need to describe the long-term follow-up of the individuals. Additionally, FQN-induced myoclonus should include electrodiagnostic studies.

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The pathophysiology of the restless legs syndrome (RLS) is related to dopaminergic dysfunction, reduced iron and variations in gene expression, such as the protein tyrosine phosphatase receptor type delta gene (PTPRD). Animal models could be key to achieving a mechanistic understanding of RLS and to facilitate efficient platforms for evaluating new therapeutics. Thus, the aim of this study was to evaluate the expression of PTPRD, of genes and proteins associated with RLS, the sleep patterns and the cardiovascular parameters in an animal model of RLS (spontaneously hypertensive rat [SHR]). Rats were divided into two groups: (i) Wistar-Kyoto and (ii) SHR. Cardiovascular parameters were assessed by tail plethysmography. Polysomnography was used to analyse the sleep pattern (24 h). For the PTPRD analyses, quantitative polymerase chain reaction (qPCR) and indirect enzyme-linked immunosorbent assay (ELISA) techniques were used. To evaluate the tyrosine hydroxylase enzyme, dopamine transporter (DAT) and type 2 dopaminergic receptor, qPCR and Western Blotting techniques were used. For the quantification of iron, ferritin and transferrin, the ELISA method was used. SHRs had higher blood pressure, alterations in sleep pattern, lower expression of protein content of PTPRD, lower expression of DAT, and lower serum concentrations of ferritin. These data suggest that the behavioural, physiological, and molecular changes observed in SHRs provide a useful animal model of RLS, reinforcing the importance of this strain as an animal model of this sleep disorder.

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Phenytoin (PHT) was first synthesized as a barbiturate derivative and was approved in 1953 by the Food and Drug Administration. This work aimed to review the pathophysiology, epidemiology, clinical presentation, and treatment of PHT-associated movement disorders (MDs). Studies were searched in relevant databases (ScienceDirect, Google Scholar, Excerpta Medica, Latin American and Caribbean Health Sciences Literature, Medline, and Scientific Electronic Library Online) and were selected by two reviewers irrespective of language between 1963 and 2021. Papers of PHT-induced ataxia alone or tremor were excluded. In total, 127 reports with 219 individuals who developed MDs associated with PHT were encountered. MDs found: 126 dyskinesias, 49 myoclonus, 19 dystonia, 14 parkinsonism, 6 tics, 3 stuttering, and 2 restless legs syndrome. The mean age was 35 years (standard deviation [SD]: 23.5) and the predominant sex was male (53.4%). The mean PHT dose when the MD took place was 370.4 mg (SD: 117.5). A serum PHT concentration was reported in 103 cases, ranging from 4 to 110 µg/mL (median: 27.7 µg/mL). No significant relationship was found between PHT dose and age or PHT level. The mean onset time of PHT-associated MD was 23.4 months (SD: 4.4). The mean recovery time after MD management was 3.7 weeks (SD: 1.1). Regarding management, the most common form was PHT withdrawal in 90.4%. 86.3% of the individuals recovered fully. PHT-induced MD was extensively reported in the literature. Only general terms were used in the majority of the reports. The mechanisms underlying the adverse events caused by PHT probably depend on the presence of predisposing factors.

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Myxedema coma is an emergency that develops from non-diagnosed or severe hypothyroidism and requires early recognition and management. Cardiac manifestations are uncommon and pose a challenge in the recognition of myxedema coma. We present the case of a 76-year-old male with a history of thyroidectomy secondary to a follicular carcinoma, who presented with dyspnea, generalized edema, drowsiness, disorientation, memory loss, and episodic generalized tonic-clonic seizures. Antiepileptic and diuretic treatment for seizures and heart failure exacerbation did not improve the symptoms. Further blood analysis revealed a thyroid-stimulating hormone and free thyroxine of 163 mUL/L and 0.64 ng/dL, respectively. Treatment with intravenous hydrocortisone and levothyroxine led to progressive clinical improvement. Uncommon clinical manifestations such as cardiac and non-specific neurologic symptoms should be considered as manifestations of myxedema coma. A comatose mental status is not a universal manifestation, and milder symptoms should be considered. An adequate assessment, including diagnostic scores and prompt hormonal supplementation prevents fatal consequences.

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Introduction: Functional neurological disorders (FND) are conditions that cause to alterations in nervous system functions. They are disabling and impair the quality of life of patients but that are potentially reversible provided they have specific management. Functional seizures (FS) and functional movement disorder (FMD) are among the most common subtypes. Studies suggest a strong overlap between FS and FMD; however, there are still no cross-sectional studies that compare the management between these two conditions. Thus, our focus was to carry out a research that compares how these two subtypes of FND are being managed, in addition to assessing rates of understanding and acceptance of a diagnosis of FND. Methods: It is a cross-sectional study with data collected from medical records and interviews with two patients' groups (FS and FMD) treated from a FND clinic of the public health system of Brazil. Results: From 105 medical records of patients with FND analyzed, 60 participants were eligible and agreed to participate in this research, being FS (n = 31) and FMD (n = 29). Statistically significant differences (p < 0.05) were found in the use of antiseizure (FS > FMD), opioids (FMD > FS), multi-professional follow-up (FMD > FS) and rates of understanding and acceptance of an FND diagnosis (FMD > FS). Similarities were found in sociodemographic profiles, medical follow-up, psychiatric comorbidities and use of antidepressants, anxiolytics, antipsychotics and mood stabilizers between two conditions. Conclusion: More similarities than differences in management were found between FS and FMD. Similarities may be related to overlaps in sociodemographic and clinical characteristics between the two groups. Differences may be related to specific issues of each patient and condition. Regardless of the group, patients who perform psychotherapeutic follow-up have higher rates of understanding and acceptance of an FND diagnosis.

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Autoimmune encephalitis can be defined as central nervous system inflammation, secondary to multiple causes, where we can possibly identify the formation of auto-antibody against neurotransmitter receptors or neuronal surface proteins. Approximately 50% of patients are seropositive; the auto-antibody against N-methyl-D-aspartate receptor (NMDAR) are the most common. In the pediatric population, the clinical presentation is characterized by movement disorders and seizures, psychiatric manifestations are more commonly found in young adults. An early intervention is associated with a better prognosis in these patients. In contrast to the seropositive group, seronegative autoimmune encephalitis is linked with less movement alterations and is related with a worse cognitive outcome. Much remains to be discovered about possible etiologies, molecular processes, detection, and interaction of yet undescribed antibodies,as well as increasing our knowledge about clinical manifestations in early disease and new diagnostic techniques that could improve the diagnosis of autoimmune encephalitis. The main goal of this document is to review the updates of the molecular field about the antibody against GluK2 and its clinical presentation in pediatric population; COVID-19 as a possible cause of autoimmune encephalitis; recognize the importance of psychiatric manifestation in early disease, especially catatonia as a marker of severity; additionally consider new imaging diagnostic method such as positron emission tomography (PET), which has shown to be more sensible than MRI (goal standard).

La encefalitis autoinmune se puede definir como el proceso inflamatorio del sistema nervioso central, secundario a múltiples causas donde se consigue identificar o no, la creación de auto-anticuerpos contra receptores de neurotransmisores o proteínas de la superficie neuronal. Aproximadamente un 50% de pacientes son seropositivos, el anticuerpo contra el receptor N-metil-D-aspartato (NMDAR) es encontrado con mayor frecuencia. La presentación clínica característica en la población pediátrica es la alteración del movimiento, seguido por episodios convulsivos; en edades más avanzadas, priman las manifestaciones psiquiátricas. Muestra buen pronóstico si se impone un pronto tratamiento. En la encefalitis autoinmune seronegativa, se observa una menor alteración de movimiento, la cual, contrario al grupo seropositivo, se asocia con peor pronóstico cognitivo. Falta mucho por conocer sobre las posibles etiologías, procesos moleculares, la interacción y detección de anticuerpos aún no descritos,al igual que es necesario incrementar nuestro conocimiento sobre las manifestaciones clínicas en etapa temprana de la enfermedad e investigar propuestas que podrían mejorar el diagnóstico de la encefalitis autoinmune. El objetivo de este documento es revisar las actualizaciones en el ámbito molecular sobre el nuevo anticuerpo descrito (GluK2) y su presentación clínica en la población pediátrica; COVID-19 como posible causa del desarrollo de encefalitis autoinmune; reconocer la importancia de las manifestaciones psiquiátricas en etapa temprana, en especial la catatonia como marcador de gravedad, de igual manera, considerar nuevas propuestas para el diagnóstico de encefalitis autoinmune como: tomografía por emisión de positrones (PET), que ha mostrado mayor sensibilidad al detectar anomalías cerebrales que la RMN (estudio de elección).

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In 1949, Cade described "sedative effects" after injecting guinea pigs intraperitoneally with lithium (LTM) carbonate. Based on his experiments, he began treating psychiatric patients with LTM. This literature review aims to evaluate the clinical epidemiological profile, pathological mechanisms, and management of LTM-associated movement disorder (MD). Relevant reports in six databases (Excerpta Medica, Google Scholar, Latin American and Caribbean Health Sciences Literature, Medline, Scientific Electronic Library Online, and ScienceDirect) were identified and assessed by two reviewers without language restriction from 1949 to 2021. A total of 250 reports containing 1100 individuals who developed MD associated with LTM were identified. The MDs encountered 148 parkinsonism (PKN), 114 dyskinesia (DKN), 97 myoclonus, 22 dystonia (DTN), 20 Creutzfeldt-Jakob-like syndrome, 11 akathisia, 10 restless legs syndrome (RLS) symptoms, 6 tics, 5 cerebellar syndromes, and 3 stuttering. In the subgroup of cases not clearly defined, there were 320 individuals with extrapyramidal symptoms, 135 with DTN, 37 with DKN, 24 with PKN, and 7 with RLS. Other 141 individuals were only described as presenting an abnormal involuntary movement without further explanation. The mean age was 53.06 years (standard deviation [SD]: 15.64) and the predominant sex was female, i.e., 56.20% (154/274). The mean LTM dose was 963.03 mg/day (SD: 392.03). The mean serum LTM level was 1.53 mEq/L (SD: 1.08). The median onset time was 3 months (1 day to 40 years). The mean recovery time was 0.94 months (SD: 0.87). 45.94% had a full recovery. LTM-induced MD was extensively reported in the literature. Only general terms were used in the majority of the reports. LTM polytherapy probably affected the identification of the MD cause.