Parkinson Disease: Planet Earth

Oberpichler-Schwenk H. · No affiliation provided · Med Monatsschr Pharm. · Pubmed #19445267 No free full text.

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Galvin JE. · No affiliation provided · J Am Med Dir Assoc. · Pubmed #19426934 No free full text.

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Martín Fernández F, Martín González T. · No affiliation provided · Actas Esp Psiquiatr. · Pubmed #19401861 links to  free full text

Abstract: Introduction. Prevalence of psychiatric disorders in patients suffering from Parkinson's disease varies from 12 to 90%. The most common disorder in the natural evolution of Parkinson's disease is depression. However, episodes of psychosis and hypomania are related to treatment with L-dopa and dopaminergic agents. Other recognized, although less frequent, psychiatric disorders are hypersexuality and development of certain addictive behaviors, which is compulsive gambling and overdosing of anti-Parkinson agents. Clinical case. A case is presented of a male patient diagnosed with Parkinson's Disease at an early age who was treated with L-dopa and a combination of dopaminergic agents. During the course of his evolution he manifested symptoms of hypersexuality and pathological gambling which were unrelated to psychotic or mood changes. Conclusions. A number of hospital admissions were needed into order to detect a pattern of abusive consumption of L-dopa as the main factor behind his behavior changes. The possibility of overdosage of L-dopa and dopaminergic drugs should be considered when there is pathological gambling conduct and/or hypersexuality, without psychotic or accompanying affective symptoms, in a male who develops Parkinson's disease at an early age and who undergoes treatment with these drugs and manifests motor fluctuations and dyskinesias. Early detection of the presence of these alterations, included within those described as <<dopaminergic dysregulation syndrome>>, would allow for an early intervention on the cause behind them and would hence avoid the possible medical and social complications. Key words: Parkinson's disease. Antiparkinson agents. Sexual dysfunctions. Patological gambling. Actas Esp Psiquiatr 2009;37(2):118-122.

Clark LN. · No affiliation provided · Neurology. · Pubmed #19386995 No free full text.

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Vingerhoets FJ. · No affiliation provided · Neurology. · Pubmed #19349599 No free full text.

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Moro E. · No affiliation provided · Eur J Neurol. · Pubmed #19348620 No free full text.

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Linazasoro G, Sesar A, Valldeoriola F, Compta Y, Herrero M, Martínez Castrillo J, López Lozano J, Bergaretxe A, Vela L, Fernández J, Castro A, Kulisevski J, Lezcano E, Vaamonde J, López Del Val J, Chacón J, Vivancos F, Luquin R, Aguilar M, Burguera J, Salvador C, Menéndez Guisasola L, Catalán M, Mir P, Campos V, Grandas F, Mínguez A, Balaguer E, Yáñez R, Leiva C, García Ruiz P, Cubo E. · Unidad de Neurología y Neurocirugía Funcional. Clínica Quirón. San Sebastián. Centro de Investigación Parkinson. Policlínica Guipuzkoa. · Neurologia. · Pubmed #19322690 links to  free full text

Abstract: Introduction. Currently used antiparkinsonian drugs neither stop nor slow-down the progressive nature of the disease. The final phase of PD is characterized by the presence of symptoms and signs resistant to dopaminergic agents, such as depression, dementia, freezing and falls. Therefore, it is urgent to develop therapies able to positively modify this outcome. Despite neuroprotection is a research priority in PD, no effective strategies have been found so far. Method. A key informants study was conducted. A group of experts in PD fulfilled a questionnaire of 10 questions to explore the most important topics related to neuroprotection. Afterwards a consensus about the cur-rent situation of neuroprotection in PD was established and future directions of development were suggested. Results. Most of the answers emphasized the need of new concepts, the limitations of animal models and the difficulties in the difficulties in demonstrating a neuroprotective effects in humans owing to a lack of biomarkers. Some of the experts believe that we are already exerting a disease modifying effect. Conclusions. The concept of neuroprotection should be widened. Animal models should be improved. A reliable biomarker to start neuroprotective therapies long before the appearance of motor symptoms and to evaluate the neuroprotective effect of any therapy should be urgently developed. Key words: Parkinson's disease. Neuroprotection. Animal models. Biomarkers. Neurología 2009;24(2):113-124.

Almeida QJ. · No affiliation provided · J Neurol Neurosurg Psychiatry. · Pubmed #19228668 No free full text.

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Antonini A, Isaias IU. · No affiliation provided · Nucl Med Commun. · Pubmed #19194209 No free full text.

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Sherlock M, Toogood AA, Steeds R. · No affiliation provided · Heart. · Pubmed #19174419 No free full text.

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Britton TC, Chaudhuri KR. · No affiliation provided · Neurology. · Pubmed #19164135 No free full text.

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Defebvre L. · No affiliation provided · Presse Med. · Pubmed #19162435 No free full text.

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Moreau C, Destée A. · No affiliation provided · J Neurol Neurosurg Psychiatry. · Pubmed #19151015 No free full text.

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Balaji S. · No affiliation provided · J Am Coll Cardiol. · Pubmed #19147046 No free full text.

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Lang AE, Mikulis D. · No affiliation provided · Neurology. · Pubmed #19129504 No free full text.

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Deuschl G. · No affiliation provided · JAMA. · Pubmed #19126817 No free full text.

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Compston A. · No affiliation provided · Brain. · Pubmed #19098304 No free full text.

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Okun MS, Fernandez HH. · No affiliation provided · Neurology. · Pubmed #19092111 No free full text.

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Sharma A, Eberwine J. · No affiliation provided · Expert Rev Neurother. · Pubmed #19086872 No free full text.

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Burke RE, Dauer WT, Vonsattel JP. · Department of Neurology, Columbia University Medical Center, New York, NY, USA. · Ann Neurol. · Pubmed #19067353 No free full text.

Abstract: Braak and colleagues have proposed that, within the central nervous system, Parkinson's disease (PD) begins as a synucleinopathy in nondopaminergic structures of the lower brainstem or in the olfactory bulb. The brainstem synucleinopathy is postulated to progress rostrally to affect the substantia nigra and cause parkinsonism at a later stage of the disease. In the context of a diagnosis of PD, made from current clinical criteria, the pattern of lower brainstem involvement accompanying mesencephalic synucleinopathy is often observed. However, outside of that context, the patterns of synucleinopathy that Braak described are often not observed, particularly in dementia with Lewy bodies and when synucleinopathy occurs in the absence of neurological manifestations. The concept that lower brainstem synucleinopathy represents "early PD" rests on the supposition that it has a substantial likelihood of progressing within the human lifetime to involve the mesencephalon, and thereby cause the substantia nigra pathology and clinical parkinsonism that have heretofore defined the disease. However, the predictive validity of this concept is doubtful, based on numerous observations made in populations of aged individuals who, despite the absence of neurological signs, have brain synucleinopathy ranging up to Braak stages 4 to 6 at postmortem. Furthermore, there is no relation between Braak stage and the clinical severity of PD. We conclude that the relation between patterns of abnormal synuclein immunostaining in the human brain and the disease entity now recognized as PD remains to be determined.

Boivie J. · No affiliation provided · Pain. · Pubmed #19062166 No free full text.

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Klein C, Lohmann K. · No affiliation provided · Neurology. · Pubmed #18987349 No free full text.

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Krüger R. · Laboratory of Functional Neurogenomics, Center of Neurology and Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany. · BMC Med. · Pubmed #18986509 links to  free full text

Abstract: Parkinson's disease is the most common neurodegenerative movement disorder and affects about 2% of the population over the age of 60 years. In 2004, mutations in the LRRK2 gene were first described and turned out to be the most frequent genetic cause of familial and sporadic Parkinson's disease and may account for up to 40% of patients in distinct populations. Based on these findings, Latourelle and colleagues show that the penetrance of the most common LRRK2 mutation is higher in patients with familial compared with sporadic Parkinson's disease and identified a substantial number of affected relatives of mutation carriers not presenting with a LRRK2 mutation themselves. This commentary discusses the role of genetic and/or environmental susceptibility factors modulating the expressivity of the disease trait, how these factors may contribute to the phenomenon of phenocopies in genetically defined Parkinson's disease pedigrees, and how the findings of Latourelle and colleagues, published this month in BMC Medicine, relate to current concepts of genetic counselling.

Bronner G. · No affiliation provided · Eur J Neurol. · Pubmed #18973611 No free full text.

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Lowenstein PR. · No affiliation provided · Mol Ther. · Pubmed #18956015 links to  free full text

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