Clinical Movement Disorders Research Articles

Neighborhood Social Determinants of Health in Patients Seen in Neurology Movement Disorders Clinics.

Chronic health conditions are influenced by social determinants of health (SDH) including neighborhood-linked markers of affluence. We explored whether neighborhood socioeconomic factors differ in people with different types of clinical movement disorders (MDs). We conducted a retrospective study of patients seen in MD clinics at our center in 2021. Patient data were linked to the US National Neighborhood Data Archive linked to US census tract data. We evaluated variations in neighborhood socioeconomic factors across 8 different categories of MDs. Compared with the neighborhoods of patients with Parkinson disease, neighborhoods of patients with cerebellar ataxias, functional movement disorders, and Huntington disease were characterized by higher proportions of people earning less than 15,000 US dollars/year, people receiving public assistance, and people with less than a high school diploma. Neighborhood-linked SDH vary among different MDs. These findings have implications for public health interventions aimed at improving the care of people affected by MDs.

Genetic Testing in Clinical Movement Disorders: A Case-Based Review.

Genetics are fundamental to understanding the pathophysiology of neurological disease, including movement disorders. Genetic testing in clinical practice has changed dramatically over the last few decades. While the likelihood of establishing an etiological diagnosis is greater now with increased access to testing and more advanced technologies, clinicians face challenges when deciding whether to test, then selecting the appropriate test, and ultimately interpreting and sharing the results with patients and families. In this review, we use a case-based approach to cover core aspects of genetic testing for the neurologist, namely, genetic testing in Parkinson's disease, interpretation of inconclusive genetic test reports, and genetic testing for repeat expansion disorders using Huntington disease as a prototype.

What can kinematic studies tell us about the mechanisms of dystonia?

Clinical movement disorders are classified by an algorithm implemented by a practising movement disorder specialist based on information extracted during the history and clinical examination of a patient. Most simply, dystonia, is a classifier which is reached when a predominant abnormality of posture is noted. In this chapter we summarize studies that have used a variety of techniques to probe beyond the clinical examination and study kinematic features experimentally. We also outline our experimental work in DYT1 dystonia, a group of patients that share a genetically homogenous etiology and can be considered a prototypical dystonic disorder. Our results build on previous studies, confirming that motor variability on a trial-by-trial basis is selectively increased and provide evidence that increases in variability are negatively related to forms of motor learning essential for healthy motor control. Potential neural correlates of increased motor variability are discussed and the implications such work has for the rehabilitation of patients with dystonia are also highlighted.

Inhibition of microglial activation and induction of neurotrophic factors by flavonoids: a potential therapeutic strategy against Parkinson's disease.

Parkinson’s disease(PD)is characterized by the progressive degeneration of dopaminergic(DA)neurons and a decrease in striatal dopamine,which is associated with clinical movement disorders including a tremor at rest,rigidity of the limbs,bradykinesia(slowness and paucity of voluntary movement)and postural instability(a tendency to fall even in the absence of

Clinical movement disorders - a new era.

We are proud to announce the launch of a new open access journal, entitled Journal of Clinical Movement Disorders (JCMD). The aim of the journal is to offer an open access forum for the publication of scientifically rigorous articles focusing on the natural history, etiology, evaluation and treatment of patients with a wide range of movement disorders [1]. We are interested in topics important to the practicing clinician, but especially in articles that explore the ways in which translational approaches are changing the evaluation and treatment of patients with movement disorders in the 21st century. We are particularly pleased to launch JCMD as a fully open access journal. At present, only one journal devoted to movement disorders (Tremor and Other Hyperkinetic Disorders) offers an open access format. We believe that the open access format offers numerous advantages to traditional publication strategies. Articles will be published as soon as they are accepted, markedly decreasing the time for evaluation and distribution. All articles are available online at no cost throughout the world, enabling the widest possible reach for the journal irrespective of a reader’s location or economic resources [2]. Authors will continue to hold copyright for their work, and articles will be archived in PubMed Central. The online format allows articles to be published without constraints on length of text. Further, the format is a perfect vehicle for publication of videos demonstrating salient features in articles, a critical feature of clinical movement disorders. JCMD will publish articles covering the full spectrum of movement disorders including hypokinetic disorders (Parkinson’s disease, atypical parkinsonian disorders such as multiple system atrophy, progressive supranuclear palsy, corticobasal syndrome, dementia with Lewy body disease, frontotemporal dementia, etc.), and usual and unusual hyperkinetic disorders (myoclonus, chorea, tics, tremor, dystonia, stereotypies, paroxysmal movement disorders, etc.). We are interested in both descriptive articles that illustrate phenotype, as well as hypothesis driven articles that explore the etiology, genetics, pharmacology, neuroimaging and treatment options for these patients. Submissions on both adult and pediatric disorders are welcome, and we are particularly interested in novel treatments such as deep brain stimulation. Special features that we plan to integrate into the journal include a clinical phenomenology section, a section devoted to current controversies, and reviews that summarize important findings in the field. All manuscripts submitted to JCMD will be independently reviewed by two experts in the field, by a member of the Editorial Board and by the Editor-in-Chief. We are interested in publishing articles of the highest quality and novelty, but will also consider research that may be of more general interest to readers due to novel clinical or examination features, clinical relevance or unusual phenotype, even if the findings are confirmatory. We believe that clinical movement disorders is unique as a subspecialty area in neurology, in that many are drawn to the field by the complexity and subtlety of the clinical examination, and the way in which 21st century technologies can help illuminate these findings. The Editorial Board of JCMD includes 43 members from 11 different countries [3]. We believe that the broad expertise and international reputations of the Editorial Board attests to their confidence that JCMD will succeed. We hope that you enjoy JCMD, and that you will consider it when deciding where to publish your work. Welcome!

Paroxysmal Kinesigenic Dyskinesia and Cervical Disc Prolapse With Cord Compression: More Than a Coincidence?

Paroxysmal Kinesigenic Dyskinesia and Cervical Disc Prolapse With Cord Compression: More Than a Coincidence?

Paroxysmal Kinesigenic Dyskinesia and Cervical Disc Prolapse With Cord Compression: More Than a Coincidence?

Paroxysmal Kinesigenic Dyskinesia and Cervical Disc Prolapse With Cord Compression: More Than a Coincidence?

Movement disorders fellowship training program at Columbia University Medical Center in 2001–2002

Data regarding the clinical experience of movement disorders subspecialty training are currently not available. In order to provide information to help design a well-rounded clinical experience, we reviewed the number and types of patients seen by all clinical movement disorders fellows over the course of 1 year at Columbia University Medical Center (CUMC). We conducted a retrospective analysis of all patients seen by four full-time clinical fellows and one part-time fellow during the 2001-2002 academic year, using billing records to tabulate all clinic visits and patient charts to certify diagnosis. One thousand six hundred sixty-two patients (1,132 new and 530 follow-ups) were seen by five fellows. Each full-time fellow evaluated and treated a mean of 263 new patients, 116 follow-up patients, and 15 in-patient consultations. The part-time clinical fellow evaluated and treated 81 new patients and 65 follow-up patients. Approximately half of the new patients had idiopathic Parkinson's disease. Full-time fellows saw equivalent numbers of patients but they evaluated few patients with uncommon movement disorders. Weekly video rounds allowed all fellows to see many more patients, aiding the recognition of movement phenomenology and enhancing understanding of diagnoses and treatment strategies. Thus, CUMC fellows evaluate a large number of patients with a wide range of diagnoses within a 1-year period. Video rounds allow greater exposure to uncommon diagnoses. Similar data from other movement disorder training programs are needed to help create guidelines for formal accreditation and to improve clinical training in this subspecialty.

Sex Differences and Effects of Estrogen on Dopamine and DOPAC Release from the Striatum of Male and Female CD-1 Mice

In the present study, we directly compare striatal dopamine metabolism in gonadectomized male and female CD-1 mice treated with 2 days of estrogen or oil vehicle. Basal and potassium-stimulated dopamine and 3,4-dibydroxyphenylacetic acid (DOPAC) release from in vitro superfused striatum as well as pre- and postsuperfusion tissue dopamine contents were measured. Both basal and potassium-stimulated dopamine release were significantly higher and DOPAC release was significantly lower in males than in females. However, striatal tissue dopamine content was lower in males than in females. Estrogen-treated female mice showed increased basal and potassium-stimulated dopamine release compared to oil-treated females without affecting tissue dopamine content. Estrogen did not affect striatal dopamine concentrations or release in males. These results demonstrate clear sex differences in striatal dopamine turnover and concentrations under conditions of equal hormonal status. The results also indicate that estrogen can exert substantial effects on striatal dopamine metabolism by acting specifically in females to increase neuronal dopamine synthesis and release without depleting dopamine content. These results have important implications for the observed sex differences in clinical movement disorders such as Parkinson's disease.

Distribution of catecholamine uptake sites in human brain as determined by quantitative [3H] mazindol autoradiography

Because of the importance of the catecholamine system in Parkinson's disease and its relevance to a variety of clinical movement disorders, catecholamine uptake sites were mapped in the human brain using [3H] mazindol autoradiography. Displacement studies with known dopamine (DA) and noradrenaline (NA) uptake blockers showed that binding in the striatum was to dopamine uptake sites; binding in the locus coeruleus was to noradrenergic uptake sites. By using the selective noradrenergic uptake blocker desmethylimipramine (DMI), a comprehensive map of both DA and NA uptake sites was generated. In general, catecholamine uptake sites were better seen in terminals than in cells of origin or axonal projections. In some areas, such as the locus coeruleus, punctate binding could be seen over individual pigmented cells. A variegated pattern of binding was seen in caudate nucleus and putamen and some correspondence of patches of low binding with striosomes was observed in the caudate. The highest levels of binding to DA uptake sites was observed in the striatum, where regional differences in binding occurred. The most dense binding was seen in the ventral striatum, and a rostral-to-caudal decrement in binding levels in caudate nucleus and putamen was evident. Binding was more intense in the putamen compared to the caudate and within the caudate lower values were seen laterally. The highest levels of binding to noradrenergic uptake sites were in the locus coeruleus and dorsal raphé, although these sites may be on terminals from other projections. Whereas uptake sites were more often evident in known catecholamine pathways, [3H] mazindol binding was seen in some areas where catecholamine neurons or terminals had not been identified previously. These maps of the catecholamine uptake system add further information concerning the nature of the distribution of catecholamines in human brain and provide an important baseline for the study of disease and ageing processes.