Beyond the Decade of the Brain

Beyond the Decade of the Brain PDF Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 356

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Beyond the Decade of the Brain

Beyond the Decade of the Brain PDF Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 356

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Beyond the Decade of the Brain: Dopamine agonists in early Parkinson's disease

Beyond the Decade of the Brain: Dopamine agonists in early Parkinson's disease PDF Author: Charles Warren Olanow
Publisher:
ISBN: 9781859390481
Category : Dopamine
Languages : en
Pages : 258

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Beyond the Decade of the Brain

Beyond the Decade of the Brain PDF Author: Charles Warren Olanow
Publisher:
ISBN:
Category :
Languages : en
Pages : 0

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Etiology of Parkinson's Disease

Etiology of Parkinson's Disease PDF Author: Jonas H. Ellenberg
Publisher: CRC Press
ISBN: 9780824788230
Category : Medical
Languages : en
Pages : 600

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Book Description
This comprehensive reference provides a detailed overview of current concepts regarding the cause of Parkinson's disease-emphasizing the issues involved in the design, implementation, and analysis of epidemiological studies of parkinsonism.

An Essay on the Shaking Palsy

An Essay on the Shaking Palsy PDF Author: James Parkinson
Publisher:
ISBN:
Category : Parkinson's disease
Languages : en
Pages : 86

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Advances in Research on Neurodegeneration

Advances in Research on Neurodegeneration PDF Author: Werner Poewe
Publisher: Springer Science & Business Media
ISBN: 3709163692
Category : Medical
Languages : en
Pages : 150

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Book Description
The book contains original articles and reviews presented at the 6th International Winter Conference on Neurodegeneration, held from November 20–23, 1997 in Kitzbühel/Austria. The aim of this conference was to present and discuss recent data on the interface between neuroimmunology and neurodegeneration, in particular susceptibility to autoimmune and neurodegenerative processes, neuroprotection and restorative treatment strategies. These issues were discussed in the light of recent developments in multiple sclerosis, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease and multisystem atrophy. The articles highlight topics, which are particularly interesting for the clinician and the neuroscientist. Some of the neuroprotective strategies have already been developed or are at present clinically investigated. The neuroprotective role of deep brain stimulation, antiglutamatergic therapy and apomorphine will be verified in clinical studies in the near future. This is also the case for future therapeutic approaches to restoration of the damaged nervous system, such as somatic gene therapy, implantation of genetically modified cell-lines and medically controlled and directed development of embryonic cells. The conference highlighted the role of the glia, which seems to play a key role, both in traditionally as neuroimmunological and neurodegenerative disorders classified diseases, as indicated above. The topics discussed in the book are significant for recent developments in clinical neurology and neuroscience, as shown in the current literature and at international congresses.

Levodopa pharmacokinetics -from stomach to brain

Levodopa pharmacokinetics -from stomach to brain PDF Author: Maria Nord
Publisher: Linköping University Electronic Press
ISBN: 9176855570
Category :
Languages : sv
Pages : 72

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Parkinson’s disease (PD) is one of the most common neurodegenerative disorders and it is caused by a loss of dopamine (DA) producing neurons in the basal ganglia in the brain. The PD patient suffers from motor symptoms such as tremor, bradykinesia and rigidity and treatment with levodopa (LD), the precursor of DA, has positive effects on these symptoms. Several factors affect the availability of orally given LD. Gastric emptying (GE) is one factor and it has been shown to be delayed in PD patients resulting in impaired levodopa uptake. Different enzymes metabolize LD on its way from the gut to the brain resulting in less LD available in the brain and more side effects from the metabolites. By adding dopa decarboxylase inhibitors (carbidopa or benserazide) or COMT-inhibitors (e.g. entacapone) the bioavailability of LD increases significantly and more LD can pass the blood-brain-barrier and be converted to DA in the brain. It has been considered of importance to avoid high levodopa peaks in the brain because this seems to induce changes in postsynaptic dopaminergic neurons causing disabling motor complications in PD patients. More continuously given LD, e.g. duodenal or intravenous (IV) infusions, has been shown to improve these motor complications. Deep brain stimulation of the subthalamic nucleus (STN DBS) has also been proven to improve motor complications and to make it possible to reduce the LD dosage in PD patients. In this doctoral thesis the main purpose is to study the pharmacokinetics of LD in patients with PD and motor complications; in blood and subcutaneous tissue and study the effect of GE and PD stage on LD uptake and the effect of continuously given LD (CDS) on LD uptake and GE; in blood and cerebrospinal fluid (CSF) when adding the peripheral enzyme inhibitors entacapone and carbidopa to LD infusion IV; in brain during STN DBSand during oral or IV LD treatment. To conclude, LD uptake is more favorable in PD patients with less severe disease and GE is delayed in PD patients. No obvious relation between LD uptake and GE or between GE and PD stage is seen and CDS decreases the LD levels. Entacapone increases the maximal concentration of LD in blood and CSF. This is more evident with additional carbidopa and important to consider in avoiding high LD peaks in brain during PD treatment. LD in brain increases during both oral and IV LD treatment and the DA levels follows LD well indicating that PD patients still have capacity to metabolize LD to DA despite probable pronounced nigral degeneration. STN DBS seems to increase putaminal DA levels and together with IV LD treatment also increases LD in brain possibly explaining why it is possible to decrease LD medication after STN DBS surgery. Parkinsons sjukdom (PS) är en av de vanligaste s.k. neurodegenerativasjukdomarna och orsakas av förlust av dopamin(DA)producerande nervceller i hjärnan. Detta orsakar motoriska symptom såsom skakningar, stelhet och förlångsammade rörelser. Levodopa (LD) är ett ämne, som kan omvandlas till DA i hjärnan och ge symptomlindring och det är oftast förstahandsval vid behandling av patienter med PS. Flera faktorer påverkar tillgängligheten av LD, bl.a. den hastighet som magsäcken tömmer sig med och denna verkar förlångsammad hos personer med PS vilket ger sämre tillgänglighet av LD i blodet och därmed i hjärnan. LD bryts även ner i hög grad av olika enzym ute i kroppen vilket leder till mindre mängd LD som hamnar i hjärnan och till fler nedbrytningsprodukter som orsakar biverkningar. Tillägg av enzymhämmare leder till ökad mängd LD som kan nå hjärnan och omvandlas till DA. Det anses viktigt att undvika höga toppar av LD i hjärnan då dessa verkar bidra till utvecklandet av besvärliga motoriska komplikationer hos patienter med PS. Om LD ges mer kontinuerligt, exempelvis som en kontinuerlig infusion in i tarmen eller i blodet, så minskar dessa motoriska komplikationer. Inopererande av stimulatorer i vissa delar av hjärnan (DBS) har också visat sig minska dessa motoriska komplikationer och även resultera i att man kan minska LD-dosen. Huvudsyftet med den här avhandlingen är att studera LD hos patienter med PS; i blod och fettvävnad då LD ges i tablettform och se om det finns något samband med LD-upptag och hastigheten på magsäckstömningen (MT) och om kontinuerligt given LD påverkar LD-upptaget eller MT; i blod och i ryggmärgsvätska då enzymhämmarna entakapon och karbidopa tillsätts LD; i hjärna vid behandling med DBS och då LD ges både som tablett och som infusion i blodet. Sammanfattningsvis kan vi se att LD-upptaget är mer gynnsamt hos patienter med PS i tidigare skede av sjukdomens komplikationsfas. MT är förlångsammad hos patienter med PS och det är inget tydligt samband mellan LD-upptag och MT eller mellan MT och sjukdomsgrad. Kontinuerligt given LD minskar LDnivåerna. Enzymhämmaren entakapon ökar den maximala koncentrationen av LD i blod och ryggmärgsvätska och effekten är mer tydlig vid tillägg av karbidopa vilket är viktigt att ta i beaktande vid behandling av PS för att undvika höga toppar av LD i hjärnan. LD ökar i hjärnan då man behandlar med LD i tablettform och som infusion i blodet och DA-nivåerna i hjärnan följer LD väl vilket visar på att patienter med PS fortfarande kan omvandla LD till DA trots trolig uttalad brist av de DA-producerande nervcellerna i hjärnan. DBS verkar öka DA i vissa områden i hjärnan och tillsammans med LD-infusion i blodet verkar det även öka LD i hjärnan och det kan förklara varför man kan sänka LDdosen efter DBS-operation.

Scientific Basis for the Treatment of Parkinson's Disease

Scientific Basis for the Treatment of Parkinson's Disease PDF Author: Nestor Galvez-Jimenez
Publisher: CRC Press
ISBN: 020333776X
Category : Medical
Languages : en
Pages : 493

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Book Description
Completely updated including coverage of the Parkin gene, this second edition unveils advances in the genetics of Parkinson's Disease (PD). The author reviews the role of alpha synuclein in the genesis of PD and covers tau protein and related diseases, MPTP and drug induced PD, oxidative stress, mitochondrial dysfunction, and apoptosis. He explores pharmacological approaches to the treatment of PD such as the use of COMT inhibitors and dopamine agonist and advances in technology such as devices that provide additional treatment options including deep brain stimulation and transplantation. The book concludes with new chapters covering the differential diagnosis of PD and related disorders.

Principles of Treatment in Parkinson's Disease

Principles of Treatment in Parkinson's Disease PDF Author: Anthony Henry Vernon Schapira
Publisher: Elsevier Health Sciences
ISBN: 0750654287
Category : Medical
Languages : en
Pages : 384

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Book Description
This succinct volume offers an up-to-date review and comparison of the treatment options available for Parkinson's disease, and provides evidence-based recommendations on appropriate treatments for specific cases. Offers expert guidance on the best treatment options from authorities in the field. Delivers expert guidance on drug therapies, physical therapies, and surgical interventions. Discusses conditions such as depression ? hallucinations ? cognition ? and sleep disorders. Explores neuroprotection in Parkinson's disease. Provides insights into future therapies.

Neuropsychopharmacology

Neuropsychopharmacology PDF Author: W.W. Fleischhacker
Publisher: Springer Science & Business Media
ISBN: 3709160200
Category : Medical
Languages : en
Pages : 120

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