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Parkinson's Disease (parkinson's + disease)
Kinds of Parkinson's Disease Terms modified by Parkinson's Disease Selected AbstractsQUETIAPINE-INDUCED DYSTONIA AND AGITATION IN PARKINSON'S DISEASE WITH DEMENTIA: A CASE REPORTJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 5 2009Julio Leey MD No abstract is available for this article. [source] BOTULINUM TOXIN TYPE A IN THE TREATMENT OF SIALORRHEA IN PARKINSON'S DISEASEJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 1 2009Ailton Melo MD No abstract is available for this article. [source] WALKING WHILE TALKING: A DOPAMINE-RESPONSIVE TASK IN EARLY PARKINSON'S DISEASEJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 4 2005Paul S. Kwon MD No abstract is available for this article. [source] GRAPE SEED PROANTHOCYANIDIN EXTRACT CHELATES IRON AND ATTENUATES THE TOXIC EFFECTS OF 6-HYDROXYDOPAMINE: IMPLICATIONS FOR PARKINSON'S DISEASEJOURNAL OF FOOD BIOCHEMISTRY, Issue 2 2010TZU-HUA WU ABSTRACT Proanthocyanidins are potent antioxidants associated with protection against diseases. We tested the reducing capacity, iron chelating activity, and anti-auto-oxidation ability of grape seed proanthocyanidin extract (GSPE). The mechanisms underlying GSPE attenuation of oxidative processes induced by 6-hydroxydopamine (6-OHDA), a neurotoxin used to induce Parkinson's disease, were investigated in cell-based systems. At high concentrations, GSPE (50 µg/µL) was a mild pro-oxidant in a Fenton-type reaction. GSPE (300 µg/mL) was as potent as 30 µM deferoxamine in its iron-chelating capacity, and as efficient as 5 mM ascorbic acid in delaying 6-OHDA auto-oxidation. In PC-12 cell cultures, 100 and 300 µg/mL GSPE significantly protected (P < 0.05) cells from 6-OHDA-induced (400 µM) toxicity. GSPE-induced cytoprotection is enhanced by a nitric oxide synthase inhibitor (NOSI), implying that the cytoprotective effect of GSPE does not require NOS activation. In conclusion, the iron-chelating activity of GSPE minimizes its pro-oxidant activity and delays 6-OHDA auto-oxidation to provide cytoprotection. PRACTICAL APPLICATIONS Parkinson's disease is a neurodegenerative disorder characterized by the degeneration of dopaminergic neurons. The recognized pharmacological strategies to prevent or treat Parkinson's disease include the minimization of oxidative stress, iron release and excitotoxicity resulting from excess nitric oxide formation. One of the best ways to delay or prevent the onset of the disease is to improve the biological antioxidant status by providing additional radical scavengers that are not pro-oxidants. The pro-oxidant activity, such as that of the antioxidant ascorbic acid, enhances radical cycling under certain conditions, and therefore may be detrimental. Grape seed proanthocyanidin extracts (GSPEs) are used as a dietary supplement in food products in several countries. Our current report provides evidence that GSPE has limited pro-oxidant activity, presumably because of its iron-chelating abilities, and protects cells from neurotoxic insults. GSPE may be effective as a dietary supplement for prophylactic use against the progressive neurodegeneration seen in Parkinson's disease. [source] OESTROGEN AND NIGROSTRIATAL DOPAMINERGIC NEURODEGENERATION: ANIMAL MODELS AND CLINICAL REPORTS OF PARKINSON'S DISEASECLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2007Bin Liu SUMMARY 1The exact nature of oestrogen (positive, negative or no effect) in the dopaminergic neurodegenerative disorder Parkinson's disease is controversial. 2In the present review, we summarize the data on oestrogen and nigrostriatal dopaminergic neurodegeneration in animal models and clinical reports of Parkinson's disease. 3Most animal studies support the ability of oestrogen to function as a neuroprotectant against neurotoxins that target the nigrostriatal dopaminergic system. 4Retrospective and prospective clinical studies generally support the findings from animal studies that oestrogen exerts a positive, or, at worst, no effect, in Parkinson's disease. 5Oestrogen was chosen as one of the 12 neuroprotective compounds to be attractive candidates for further clinical trials (Phase II or III) in 2003. [source] Sensitive Electrochemical Detection of Native and Aggregated ,-Synuclein Protein Involved in Parkinson's DiseaseELECTROANALYSIS, Issue 13-14 2004Michal Masa Abstract The aggregation of ,-synuclein, a 14,kDa protein, is involved in several human neurodegenerative disorders, including Parkinson's disease. We studied native and in vitro aggregated ,-synuclein by circular dichroism (CD), atomic force microscopy (AFM) and electrochemical methods. We used constant current chronopotentiometric stripping analysis (CPSA) to measure hydrogen evolution catalyzed by ,-synuclein (peak H) at hanging mercury drop electrodes (HMDE) and square-wave stripping voltammetry (SWSV) to monitor tyrosine oxidation at carbon paste electrodes (CPE). To decrease the volume of the analyte, most of the electrochemical measurements were performed by adsorptive transfer (medium exchange) from 3,6,,L drops of ,-synuclein samples. With both CPE and HMDE we observed changes in electrochemical responses of ,-synuclein corresponding to protein fibrillization detectable by CD, fluorescence and AFM. Aggregation-induced changes in peak H at HMDE were relatively large in strongly aggregated samples, suggesting that this electrochemical signal may find use in the analysis of early stages of ,-synuclein aggregation. This assumption was documented by marked changes in the peak H potential and height in samples withdrawn at the end of the lag and the beginning of the elongation phase. Native ,-synuclein can be detected down to subnanomolar concentrations by CPSA. [source] Low frequency of Parkin, Tyrosine Hydroxylase, and GTP Cyclohydrolase I gene mutations in a Danish population of early-onset Parkinson's DiseaseEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2006J. M. Hertz Autosomal recessive Parkinson's disease (PD) with early-onset may be caused by mutations in the parkin gene (PARK2). We have ascertained 87 Danish patients with an early-onset form of PD (age at onset ,40 years, or ,50 years if family history is positive) in a multicenter study in order to determine the frequency of PARK2 mutations. Analysis of the GTP cyclohydrolase I gene (GCH1) and the tyrosine hydroxylase gene (TH), mutated in dopa-responsive dystonia and juvenile PD, have also been included. Ten different PARK2 mutations were identified in 10 patients. Two of the patients (2.3%) were found to have homozygous or compound heterozygous mutations, and eight of the patients (9.2%) were found to be heterozygous. A mutation has been identified in 10.4% of the sporadic cases and in 15.0% of cases with a positive family history of PD. One patient was found to be heterozygous for both a PARK2 mutation and a missense mutation (A6T) in TH of unknown significance. It cannot be excluded that both mutations contribute to the phenotype. No other putative disease causing TH or GCH1 mutations were found. In conclusion, homozygous, or compound heterozygous PARK2 mutations, and mutations in GCH1 and TH, are rare even in a population of PD patients with early-onset of the disease. [source] Mapping the Progress of Alzheimer's and Parkinson's DiseaseEUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2003K. A. Jellinger No abstract is available for this article. [source] Parkinson's Disease: A Guide for Patient and Family, 5th editionEUROPEAN JOURNAL OF NEUROLOGY, Issue 2 2002K. A. Jellinger No abstract is available for this article. [source] A Molecular Biology Approach to Parkinson's DiseaseEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2001K A Jellinger No abstract is available for this article. [source] The Role of c-Jun N-Terminal Kinase (JNK) in Parkinson's DiseaseIUBMB LIFE, Issue 4-5 2003Jun Peng Abstract Given the critical role that the c-Jun N-terminal kinase (JNK) pathway plays in regulating many of the cellular processes which are affected in Parkinson's disease (PD), the possible importance of JNK in disease pathogenesis is being increasingly recognized. Here we review recent findings implicating the JNK signaling pathway in animal models of Parkinson's disease and discuss the relationship between this pathway and the prominent pathological processes observed in the disease state. We suggest that regulation of the JNK signaling pathway may be a central facet in potential treatments for the disease. IUBMB Life, 55: 267-271, 2003 [source] Ethnic Differences in Singapore's Dementia Prevalence: The Stroke, Parkinson's Disease, Epilepsy, and Dementia in Singapore StudyJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 11 2008Suresh Sahadevan MBBS OBJECTIVES: To study the prevalence of dementia in Singapore among Chinese, Malays, and Indians. DESIGN: A two-phase, cross-sectional study of randomly selected population from central Singapore with disproportionate race stratification. SETTING: Community-based study. Subjects screened to have cognitive impairment at phase 1 in their homes were evaluated clinically for dementia at phase 2 in nearby community centers. PARTICIPANTS: Fourteen thousand eight hundred seventeen subjects aged 50 and older (67% participation rate). MEASUREMENTS: The locally validated Abbreviated Mental Test was used to screen for cognitive impairment at phase 1. Dementia was diagnosed at phase 2 as per Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria. Possible Alzheimer's disease (AD) and possible vascular dementia (VD) were diagnosed along the National Institute of Neurological and Communicative Disorders,Alzheimer's Disease and Related Disorders Association and National Institute of Neurological Disorders and Stroke,Association Internationale pour la Recherche et l'Enseignement en Neuroscienes criteria, respectively. RESULTS: The overall age- and race-standardized dementia prevalence was 1.26% (95% confidence interval (CI)=1.10,1.45). Prevalence (in 5-year age bands) was 0.08% (50,54), 0.08% (55,59), 0.44% (60,64), 1.16% (65,69), 1.84% (70,74), 3.26% (75,79), 8.35% (80,84), and 16.42% (,85). From age 50 to 69, 65% of dementia cases were VD; at older ages, 60% were AD. Logistic regression (adjusted for age, sex, education) showed that Malays had twice the risk for AD as Chinese, and Indians had more than twice the risk for AD and VD than Chinese. CONCLUSION: Singapore's dementia prevalence, primarily influenced by its Chinese majority, is lower than seen in the West. The striking interethnic differences suggest a need for a dementia incidence study and further investigation of underlying genetic and cultural differences between the three ethnic groups in relation to dementia risk. [source] Effect of Psychiatric and Other Nonmotor Symptoms on Disability in Parkinson's DiseaseJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 5 2004Daniel Weintraub MD Objectives: To examine the effect of depression and other nonmotor symptoms on functional ability in Parkinson's disease (PD). Design: A cross-sectional study of a convenience sample of PD patients receiving specialty care. Setting: The Parkinson's Disease Research, Education and Clinical Center at the Philadelphia Veterans Affairs Medical Center. Participants: One hundred fourteen community-dwelling patients with idiopathic PD. Measurements: The Unified Parkinson's Disease Rating Scale (UPDRS); Hoehn and Yahr Stage; Mini-Mental State Examination; Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, depression module; probes for psychotic symptoms; Hamilton Depression Rating Scale; Geriatric Depression Scale,Short Form; Apathy Scale; and Epworth Sleepiness Scale. Disability was rated using the UPDRS activity of daily living (ADL) score and the Schwab and England ADL score. Multivariate analysis determined effect of depression and other nonmotor symptoms on disability. Results: The presence of psychosis, depressive disorder, increasing depression severity, age, duration of PD, cognitive impairment, apathy, sleepiness, motor impairment, and percentage of time with dyskinesias were related to greater disability in bivariate analyses. Entering these factors into two multiple regression analyses, only the increasing severity of depression and worsening cognition were associated with greater disability using the UPDRS ADL score, accounting for 37% of the variance in disability (P<.001). These two factors plus increasing severity of PD accounted for 54% of the variance in disability using the Schwab and England ADL score (P<.001). Conclusion: Results support and extend previous findings that psychiatric and other nonmotor symptoms contribute significantly to disability in PD. Screening for nonmotor symptoms in PD is necessary to more fully explain functional limitations. Further study is required to determine whether identifying and treating these symptoms will improve function and quality of life. [source] Proteomics of brain extracellular fluid (ECF) and cerebrospinal fluid (CSF),MASS SPECTROMETRY REVIEWS, Issue 1 2010Martin H. Maurer Abstract Mass spectrometry has become the gold standard for the identification of proteins in proteomics. In this review, I will discuss the available literature on proteomic experiments that analyze human cerebrospinal fluid (CSF) and brain extracellular fluid (ECF), mostly obtained by cerebral microdialysis. Both materials are of high diagnostic value in clinical neurology, for example, in cerebrovascular disorders like stroke, neurodegenerative diseases like Alzheimer's Disease, Parkinson's Disease, amyotrophic lateral sclerosis (ALS), traumatic brain injury and cerebral infectious and inflammatory disease, such as multiple sclerosis. Moreover, there are standard procedures for sampling. In a number of studies in recent years, biomarkers have been proposed in CSF and ECF for improved diagnosis or to control therapy, based on proteomics and mass spectrometry. I will also discuss the needs for a transition of research-based experimental screening with mass spectrometry to fast and reliable diagnostic instrumentation for clinical use. © 2008 Wiley Periodicals, Inc., Mass Spec Rev 29:17,28, 2010 [source] A 3-D QSAR Study of Catechol- O -Methyltransferase Inhibitors Using CoMFA and CoMSIAMOLECULAR INFORMATICS, Issue 10 2008Chunzhi Ai Abstract Inhibitors of Catechol- O -Methyltransferase (COMT) play an important role in the treatment of Parkinson's Disease (PD). A new Three-Dimensional Quantitative Structure,Activity Relationship (3-D QSAR) analysis was performed on 36 previously reported COMT inhibitors employing Comparative Molecular Field Analysis (CoMFA) and Comparative Molecular Similarity Indices Analysis (CoMSIA) methodologies to correlate the molecular fields and percent inhibition values and three predictive models were derived. The CoMFA and CoMSIA models with steric and electrostatic field yielded cross-validated rs of 0.585 and 0.528, respectively whereas the conventional rs were 0.979 and 0.891, respectively. The CoMSIA model with hydrophobic field exhibited a r of 0.544 and a r of 0.930. The individual inspection of 3-D contours generated from these models helps in understanding the possible region for structural modification of molecules to improve the inhibitory bioactivity. These 3-D QSAR models are also useful for designing and predicting novel COMT inhibitors. [source] Abstracts of the Fourteenth International Congress of Parkinson's Disease and Movement DisordersMOVEMENT DISORDERS, Issue S2 2010Article first published online: 20 MAY 2010 First page of article [source] Program: Twenty Fourth Annual Symposium on Etiology, Pathogenesis, and Treatment of Parkinson's Disease and Other Movement DisordersMOVEMENT DISORDERS, Issue 6 2010Article first published online: 26 APR 2010 The symposium will consist of current issues in genetic and environmental contributions to Parkinson's disease and other movement disorders with peer-reviewed platform and poster presentations designed to communicate recent research advances, including new pharmacological and non-pharmacological treatment options, in the field of Parkinson's disease, Huntington's disease, ataxia, dystonia, myoclonus, Tourette's syndrome, tremor and other movement disorders thereby enhancing patient care. [source] Program: Twenty Third Annual Symposium on Etiology, Pathogenesis, and Treatment of Parkinson's Disease and Other Movement DisordersMOVEMENT DISORDERS, Issue 12 2009Article first published online: 11 SEP 200 The symposium will consist of two keynote speakers and peer-reviewed platform and poster presentations designed to communicate recent research advances, including new pharmacological and non-pharmacological treatment options, in the field of Parkinson's disease, Huntington disease, ataxia, dystonia, myoclonus, Tourette's syndrome, Essential Tremor and other movement disorders thereby enhancing patient care. Professionals in neurology and related disciplines as well as practitioners, psychologists, educators, and researchers are invited to attend. The gaps in clinical practice we wish to address are the unmet needs pertaining to the translational and clinical evaluation, along with the care and treatment of patients and families affected by Parkinson's disease and other movement disorders. At the conclusion of this session, participants should be able to: 1) Identify and describe by scholarly review, oral presentation and group discussion the current research into the diagnosis, prevention and treatment of Parkinson's disease (PD) and Essential Tremor (ET) which may be relevant to current treatment or which may lead to the development of further research protocols; 2) Distinguish and assess the important advances in research and clinical treatments relating to Parkinson's disease and Essential Tremor in terms of available treatment options or new methodologies for clinical research; 3) Explain new pharmacological and non-pharmacological treatment options available for Parkinson's disease and other movement disorders in connection with their clinical practice or with regard to further clinical research methods; 4) Interpret the mechanisms (genetic, environmental, pathophysiology, neurobiology) linked to Parkinson's disease and other movement disorders when assessing Parkinson's disease or other movement disorder patients or when developing new research protocols; and 5) Employ diagnostic approaches and tools available for assessing Parkinson's disease and Essential Tremor when diagnosing new patients or when conducting clinical research. [source] Cognitive impairment in Parkinson's disease: Tools for diagnosis and assessment,,MOVEMENT DISORDERS, Issue 8 2009Jaime Kulisevsky MD Abstract Cognitive impairment (CI) and dementia are frequent and debilitating features associated with Parkinson's disease (PD). Formal neuropsychological examination is required to ascertain the degree and pattern of CI over the course of the disease. The use of different tools may explain heterogeneous data obtained from studies to date. Normative data for extensively used scales [Mattis Dementia Rating Scale (MDRS), Mini-Mental State Examination (MMSE)] is incomplete in PD populations. According to sample characteristics, statistical analyses, and methodological quality, 33 studies using scales not specific to PD (MDRS, MMSE, Cambridge Cognitive Assessment, FAB) or PD-specific scales (Mini-Mental Parkinson, Scales for Outcomes of Parkinson's disease,Cognition, Parkinson's Disease,Cognitive Rating Scale, and Parkinson Neuropsychometric Dementia Assessment) were eligible for the critical analysis of their appropriateness to assess cognition in PD. Of the four scales specifically designed for PD, the SCOPA-COG and the PD-CRS have undergone extensive and rigorous validation processes. While the SCOPA-COG mainly assesses "frontal-subcortical" cognitive defects, the PD-CRS also assesses "instrumental-cortical" functions, allowing better characterization of the different patterns of CI that may be present in PD from the earliest stages. The MMP and PANDA scales were designed as brief screening tests for CI and have not yet been subjected to extensive clinimetric evaluations. Further research on PD-specific tools seems mandatory to help establish accurate cut-off scores for the diagnosis of mild PDD, detect cognitive profiles more prone to the future development of dementia, and allow comparisons between different descriptive or interventional studies. © 2009 Movement Disorder Society [source] Abstracts of The Movement Disorder Society's Thirteenth International Congress of Parkinson's Disease and Movement DisordersMOVEMENT DISORDERS, Issue S1 2009Article first published online: 27 MAY 200 [source] Circadian rest-activity rhythm is altered in Parkinson's disease patients with hallucinationsMOVEMENT DISORDERS, Issue 8 2008Daisy L. Whitehead PhD Abstract The sleep-wake cycle in Parkinson's Disease (PD) is profoundly disrupted, but less is known about circadian rhythm in PD and its relationship to other important clinical features. This study compared rest-activity rhythms in healthy older adults and PD patients with and without hallucinations. Twenty-nine older adults and 50 PD patients (27 with hallucinations, 23 without) were assessed using wrist-worn actigraphy for 5 days. Disease-related and cognitive data were also collected. PD patients demonstrated reduced amplitude of activity (F = 12.719, P < 0.01) and increased intradaily variability (F = 22.005, P < 0.001), compared to healthy older adults, independently of age, and cognitive status. Hallucinators showed lower interdaily stability (F = 7.493, P < 0.01) significantly greater activity during "night-time" (F = 6.080, P < 0.05) and significantly reduced relative amplitude of activity (F = 5.804, P < 0.05) compared to nonhallucinators, independently of clinical factors including motor fluctuations. PD patients with hallucinations display altered rest-activity rhythm characterized by an unpredictable circadian pattern across days, likely arising from damage to brainstem and hypothalamic sleep centers. Treatment of sleep and rest-activity rhythm disturbance is an important target in Parkinson's Disease. © 2008 Movement Disorder Society. [source] Abstracts of The Movement Disorder Society's Twelfth International Congress of Parkinson's Disease and Movement DisordersMOVEMENT DISORDERS, Issue S1 2008Article first published online: 28 MAY 200 [source] Abstracts of The Movement Disorder Society's Eleventh International Congress of Parkinson's Disease and Movement DisordersMOVEMENT DISORDERS, Issue S16 2007Article first published online: 24 APR 200 [source] Current controversies: Levodopa in the treatment of Parkinson's diseaseMOVEMENT DISORDERS, Issue 5 2005Jagdish C. Sharma FRCP Companion letters have been published in Movement Disorders: Levodopa in the Treatment of Parkinson's Disease: Current Controversies, by Gerlach, Reichmann, and Riederer and Reply: Levodopa in the Treatment of Parkinson's Disease, by Olanow, Agid, and Mizuno. [source] The Unified Parkinson's Disease Rating Scale (UPDRS): Status and recommendationsMOVEMENT DISORDERS, Issue 7 2003Article first published online: 18 MAR 200 Abstract The Movement Disorder Society Task Force for Rating Scales for Parkinson's Disease prepared a critique of the Unified Parkinson's Disease Rating Scale (UPDRS). Strengths of the UPDRS include its wide utilization, its application across the clinical spectrum of PD, its nearly comprehensive coverage of motor symptoms, and its clinimetric properties, including reliability and validity. Weaknesses include several ambiguities in the written text, inadequate instructions for raters, some metric flaws, and the absence of screening questions on several important non-motor aspects of PD. The Task Force recommends that the MDS sponsor the development of a new version of the UPDRS and encourage efforts to establish its clinimetric properties, especially addressing the need to define a Minimal Clinically Relevant Difference and a Minimal Clinically Relevant Incremental Difference, as well as testing its correlation with the current UPDRS. If developed, the new scale should be culturally unbiased and be tested in different racial, gender, and age-groups. Future goals should include the definition of UPDRS scores with confidence intervals that correlate with clinically pertinent designations, "minimal," "mild," "moderate," and "severe" PD. Whereas the presence of non-motor components of PD can be identified with screening questions, a new version of the UPDRS should include an official appendix that includes other, more detailed, and optionally used scales to determine severity of these impairments. © 2003 Movement Disorder Society [source] Poster session 1: A. Basic science, genetics, neuropharmacology, Parkinson's DiseaseMOVEMENT DISORDERS, Issue S5 2002Article first published online: 21 OCT 200 [source] Poster session 2: Parkinson's DiseaseMOVEMENT DISORDERS, Issue S5 2002Article first published online: 21 OCT 200 [source] Poster session 3: Parkinson's DiseaseMOVEMENT DISORDERS, Issue S5 2002Article first published online: 21 OCT 200 [source] Deep brain stimulation for Parkinson's disease: Patient selection and evaluationMOVEMENT DISORDERS, Issue S3 2002Anthony E. Lang MD, FRCPC Abstract Critical to the successful application of deep brain stimulation for the treatment Parkinson's disease is the proper selection of patients who will reliably benefit from this procedure and the successful evaluation of the responses obtained. This review will discuss the various factors influencing patient selection and summarize the recommended approach to patient assessment by using the Core Assessment Program for Surgical Interventions and Transplantation in Parkinson's Disease (CAPSIT-PD). © 2002 Movement Disorder Society [source] Multiple-Cell Spike Density and Neural Noise Level Analysis by Semimicroelectrode Recording for Identification of the Subthalamic Nucleus During Surgery for Parkinson's DiseaseNEUROMODULATION, Issue 1 2008Toshikazu Kano MD ABSTRACT Objective.,, For targeting the subthalamic nucleus (STN), we attempted to quantify the changes in multiple cell activities by computing the neural noise level and multiple-cell spike density (MSD). Methods.,, We analyzed the neural noise level and MSD by stepwise recording at every 0.25-mm increment during the final tracking in 90 sides of 45 patients with Parkinson's disease. The MSD was analyzed with cut-off levels ranging from 1.2- to 2.0-fold the neural noise level in the internal capsule or zona incerta in each trajectory. Results.,, The dorsal boundary of the STN was identified from an increase in the neural noise ratio in all sides. The ventral boundary was identifiable, however, from a decrease in the neural noise ratio in only 70 sides (78%). In contrast, both the dorsal and ventral boundaries were clearly identified from an increase and a decrease in the MSD, respectively, in all of the 90 sides. Conclusion.,, MSD analysis by semimicroelectrode recording represents a useful, practical, and apparently reliable means for identifying the boundaries of the STN. [source] | |||||||||||||||||||||||||||||||