Leslie J. Cloud

Gastrointestinal Features of Parkinson’s Disease

Gastrointestinal (GI) symptoms are among the most common nonmotor manifestations of Parkinson’s disease (PD), and they have many important ramifications for patients. The purpose of this review is to raise awareness of the full spectrum of GI symptoms in PD which include weight loss, sialorrhea, dysphagia, nausea, constipation, and defecatory dysfunction. We will discuss their practical significance, and outline a clear approach to their evaluation and management. A brief discussion about the impacts of commonly used medical and surgical PD therapies on GI symptom manifestation is also included.

Treatment strategies for dystonia

Importance of the field: Dystonia is a neurological syndrome characterized by involuntary twisting movements and unnatural postures. It has many different manifestations and causes, and many different treatment options are available. These options include physical and occupational therapy, oral medications, intramuscular injection of botulinum toxins, and neurosurgical interventions. Areas covered in this review: In this review, we first summarize the treatment options available, then we provide suggestions from our own experience for how these can be applied in different types of dystonia. In preparing this review article, an extensive literature search was undertaken using PubMed. Only selected references from 1970 to 2008 are cited. What the reader will gain: This review is intended to provide the clinician with a practical guide to the treatment of dystonia. Take home message: Treatment of dystonia begins with proper diagnosis and classification, followed by an appropriate search for underlying etiology, and an assessment of the functional impairment associated with the dystonia. The therapeutic approach, which is usually limited to symptomatic therapy, must then be tailored to the individual needs of the patient.

Tardive Syndromes are Rarely Reversible after Discontinuing Dopamine Receptor Blocking Agents: Experience from a University-based Movement Disorder Clinic

Background Several studies have examined reversibility of tardive syndromes (TS), primarily in psychotic patients who are maintained on dopamine receptor blocking drugs. The results have varied widely. However, few have assessed remission rates after discontinuing the offending agents. This study evaluated reversibility of TS in patients who permanently withdrew the causative agent(s). We also examined for any possible clinical predictors of reversibility. Methods A retrospective cohort of 108 TS patients was studied. Most of the patients were not psychotic; most patients were being treated either for a mood disorder with atypical antipsychotics or for a gastrointestinal disturbance with metoclopramide. Patients were stratified on the basis of reversibility, and statistical tests were used for subgroup comparisons of relevant clinical variables. Logistic regression was undertaken to identify clinical variables predictive of reversibility. Results Only 13% of the cohort experienced reversibility of the TS, 2% without medical intervention. When stratified by reversibility, there were no significant differences in any study variables between subgroups. None of the study variables predicted reversibility in the logistic regression. Discussion Our study demonstrated a low remission rate for TS in a cohort of psychiatric and non-psychiatric patients seen in a movement disorder clinic after the offending agents were completely withdrawn. Such a finding has significant prognostic implications. It is possible that limitations of the retrospective design may have resulted in an underestimation. There is a clear need for prospective, multicenter, clinical trials in populations that can be safely withdrawn from dopamine receptor blocking agents so that true remission rates can be measured.

An Integrated Review of Psychological Stress in Parkinson’s Disease: Biological Mechanisms and Symptom and Health Outcomes

Parkinsons disease (PD) is characterized by complex symptoms and medication-induced motor complications that fluctuate in onset, severity, responsiveness to treatment, and disability. The unpredictable and debilitating nature of PD and the inability to halt or slow disease progression may result in psychological stress. Psychological stress may exacerbate biological mechanisms believed to contribute to neuronal loss in PD and lead to poorer symptom and health outcomes. The purpose of this integrated review is to summarize and appraise animal and human research studies focused on biological mechanisms, symptom, and health outcomes of psychological stress in PD. A search of the electronic databases PubMed/Medline and CINAHL from 1980 to the present using the key words Parkinsons disease and stress, psychological stress, mental stress, and chronic stress resulted in 11 articles that met inclusion criteria. The results revealed significant associations between psychological stress and increased motor symptom severity and loss of dopamine-producing neurons in animal models of PD and between psychological stress and increased symptom severity and poorer health outcomes in human subjects with PD. Further research is needed to fully elucidate the underlying biological mechanisms responsible for these relationships, for the ultimate purpose of designing targeted interventions that may modify the disease trajectory.

Chapter 40 - Other spinocerebellar ataxias

The spinocerebellar ataxias (SCAs) are a clinically and genetically heterogeneous group of dominantly inherited degenerative disorders characterized primarily by progressive ataxia. SCA numbers are applied sequentially as new forms are delineated: currently SCA1 through to SCA30 (Finsterer, 2009). The numbering is imperfect: 9 and 24 are “vacant”, SCA24 having been reassigned as spinocerebellar ataxia with saccadic intrusions or SCASI (HUGO: http://www.genenames.org/); the Japanese dominant ataxia associated with a PLEKHG4 mutation, its locus within the SCA4 critical region on chromosome 16q22, has not been assigned its own SCA number; SCA16 has recently been shown to be identical to SCA15 (Gardner, 2008); and SCA22 and SCA29 have not been excluded as representing allelic variants of SCA19 and SCA15, respectively. The causative gene has been discovered for SCA types 1–3, 5–8, 10–15, 17, and 27. In the remainder (SCA types 4, 18–23, 25, 26, 28, 29, 30, and the 16q22-linked spinocerebellar ataxia), assignment has been on the basis of a genetic locus having been established by linkage analysis. This chapter summarizes those SCAs that are not dealt with in the rest of this volume; in almost all of these, the phenotypic experience is limited to a small number of families. As the causative mutations get identified and additional families are examined, one may expect variations on the clinical features identified so far.

Biobehavioral Framework of Symptom and Health Outcomes of Uncertainty and Psychological Stress in Parkinson Disease.

Parkinson disease (PD) is a debilitating, progressive neurodegenerative disorder characterized by complex motor and nonmotor symptoms that fluctuate in onset, severity, level of disability, and responsiveness to treatment. The unpredictable nature of PD and the inability to halt or slow disease progression may result in uncertainty and psychological stress. Uncertainty and psychological stress have important implications for symptom and health outcomes in PD. Uncertainty and psychological stress have been shown to worsen symptoms, functional capacity, and quality of life in chronic illnesses; however, the causal mechanisms have yet to be elucidated. We propose a biobehavioral framework for examining uncertainty and psychological stress in PD. The framework considers factors that may contribute to uncertainty and neuroendocrine-immune mechanisms of uncertainty and psychological stress that may influence symptom and health outcomes in PD, for the ultimate purpose of improving symptom and disease progression, functional capacity, and quality of life.