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| 22. |
- Hariz, Marwan
(författare)
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Twenty-five years of deep brain stimulation : Celebrations and apprehensions
- 2012
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Ingår i: Movement Disorders. - : Wiley. - 0885-3185 .- 1531-8257. ; 27:7, s. 930-933
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- The year 2012 marks the 25th anniversary of the birth of modern deep brain stimulation (DBS), which was introduced by Benabid et al in 1987, initially to treat tremor with DBS of the ventral intermediate nucleus of the thalamus. The subsequent extension of DBS to the subthalamic nucleus (STN), demonstrating its efficacy on virtually all symptoms of advanced Parkinson's disease (PD), sparked an era of intense clinical and research activities, eventually transcending PD and movement disorders to encompass mood and mind. Investigations of the role of DBS in a variety of neurological, psychiatric, cognitive, and behavioral conditions is ongoing. Serendipitous discoveries and advances in functional imaging are providing new brain targets for an increasing number of pathologies. Toward the end of this quarter of a century of DBS, there have been some indications that the field may be at risk of gliding down a slippery slope, reminiscent of the excesses of the old-era DBS. Although there are many reasons this year to celebrate the achievements of 25 years of modern DBS, there are also reasons to fear the opening of a new Pandora's box.
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| 23. |
- Heckman, Michael G., et al.
(författare)
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Population-specific Frequencies for LRRK2 Susceptibility Variants in the Genetic Epidemiology of Parkinson's Disease (GEO-PD) Consortium
- 2013
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Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 28:12, s. 1740-1744
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundVariants within the leucine-rich repeat kinase 2 gene are recognized as the most frequent genetic cause of Parkinson's disease. Leucine-rich repeat kinase 2 variation related to disease susceptibility displays many features that reflect the nature of complex, late-onset sporadic disorders like Parkinson's disease. MethodsThe Genetic Epidemiology of Parkinson's Disease Consortium recently performed the largest genetic association study for variants in the leucine-rich repeat kinase 2 gene across 23 different sites in 15 countries. ResultsHerein, we detail the allele frequencies for the novel risk factors (p.A419V and p.M1646T) and the protective haplotype (p.N551K-R1398H-K1423K) nominated in the original publication. Simple population allele frequencies not only can provide insight into the clinical relevance of specific variants but also can help genetically define patient groups. ConclusionsEstablishing individual patient-based genomic susceptibility profiles that incorporate both risk factors and protective factors will determine future diagnostic and treatment strategies. (c) 2013 International Parkinson and Movement Disorder Society
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| 24. |
- Kalliolia, Eirini, et al.
(författare)
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Plasma Melatonin Is Reduced in Huntington's Disease
- 2014
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Ingår i: Movement Disorders. - : Wiley. - 0885-3185 .- 1531-8257. ; 29:12, s. 1511-1515
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Tidskriftsartikel (refereegranskat)abstract
- This study was undertaken to determine whether the production of melatonin, a hormone regulating sleep in relation to the light/dark cycle, is altered in Huntington's disease. We analyzed the circadian rhythm of melatonin in a 24-hour study of cohorts of control, premanifest, and stage II/III Huntington's disease subjects. The mean and acrophase melatonin concentrations were significantly reduced in stage II/III Huntington's disease subjects compared with controls. We also observed a nonsignificant trend toward reduced mean and acrophase melatonin in premanifest Huntington's disease subjects. Onset of melatonin rise was significantly more temporally spread in both premanifest and stage II/III Huntington's disease subjects compared with controls. A nonsignificant trend also was seen for reduced pulsatile secretion of melatonin. Melatonin concentrations are reduced in Huntington's disease. Altered melatonin patterns may provide an explanation for disrupted sleep and circadian behavior in Huntington's disease, and represent a biomarker for disease state. Melatonin therapy may help the sleep disorders seen in Huntington's disease. (c) 2014 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
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| 27. |
- Linder, Jan, 1957-, et al.
(författare)
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Incidence of Parkinson's disease and parkinsonism in northern Sweden : a population-based study
- 2010
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Ingår i: Movement Disorders. - : Wiley. - 0885-3185 .- 1531-8257. ; 25:3, s. 341-348
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Tidskriftsartikel (refereegranskat)abstract
- The differential diagnosis of parkinsonian disorders is difficult, especially early in the course of the diseases. The clinical subtypes of Parkinson's disease (PD) have not so far been described in newly diagnosed patients. We present a prospective incidence cohort study of patients with idiopathic parkinsonian syndromes in the Umeå region in northern Sweden identified over a 4-year period. The clinical diagnoses were re-evaluated at follow-up visits at 12 months. We found 138 patients with parkinsonism: 112 PD, 12 multiple system atrophy with predominant parkinsonism (MSA-P), six progressive supranuclear palsy (PSP) and eight unclassifiable patients. The crude incidences for all age ranges per 100,000 were: PD 19.7 (95% confidence interval 16.1-23.3); MSA-P 2.1 (1.1-3.7); PSP 1.1 (0.4-2.4); idiopathic parkinsonism 24.3 (20.2-28.4). Age-standardized to the average Swedish population 2004-2007: PD 22.5 (18.3-26.7); MSA-P 2.4 (1.2-4.2); PSP 1.2 (0.4-2.6); idiopathic parkinsonism 27.5 (22.9-32.1). The crude annual incidence rate for PD, with exclusion of patients with normal dopamine receptor uptake (FP-CIT-SPECT), was 18.8 per 100,000 (95% confidence interval 15.2-22.4), age-adjusted to the average Swedish population 2004 to 2007: 21.5 (17.4-25.6). The incidence rates did not differ significantly between men and women. The cumulative incidence of PD up to 89 years of age was for men 3.4%, for women 2.6%, and for both sexes combined 2.9%. The annual incidence rates found for PD, idiopathic parkinsonism, MSA-P and PSP are among the highest reported.
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| 30. |
- Martinez-Fernandez, Raul, et al.
(författare)
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Deep Brain Stimulation for Gilles de la Tourette Syndrome : A Case Series Targeting Subregions of the Globus Pallidus Internus
- 2011
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Ingår i: Movement Disorders. - New York, N.Y. : Raven Press. - 0885-3185 .- 1531-8257. ; 26:10, s. 1922-1930
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Tidskriftsartikel (refereegranskat)abstract
- Deep brain stimulation remains an experimental treatment for patients with Gilles de la Tourette syndrome. Currently, a major controversial issue is the choice of brain target that leads to optimal patient outcomes within a presumed network of basal ganglia and cortical pathways involved in tic pathogenesis. This report describes our experience with patients with severe refractory Gilles de la Tourette syndrome treated with globus pallidus internus deep brain stimulation. Five patients were selected for surgery, 2 targeting the posteroventral globus pallidus internus and 2 targeting the anteromedial region. The remaining patient was first targeted on the posterolateral region, but after 18 months the electrodes were relocated in the anteromedial area. Tics were clinically assessed in all patients pre- and postoperatively using the Modified Rush Video protocol and the Yale Global Tic Severity Scale. Obsessive-compulsive behaviors were quantified with the Yale Brown Obsessive Compulsive Scale. The Gilles de la Tourette Syndrome Quality of Life Scale was also completed. All patients experienced improvements in tic severity but to variable extents. More convincing improvements were seen in patients with electrodes sited in the anteromedial region of the globus pallidus internus than in those with posterolateral implants. Mean reduction in the Modified Rush Video Rating scale for each group was 54% and 37%, respectively. Our open-label limited experience supports the use of the anteromedial globus pallidus internus as a promising target for future planned randomized double-blind trials of deep brain stimulation for patients with Gilles de la Tourette syndrome.
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