PARKINSON'S DISEASE NEWS

30th November 2010 - New book

YOU NEVER MISS THE DOPAMINE (UNTIL THE BRAIN RUNS DRY) (VOLUME 2)

Bill Schmalfeldt

Publisher's description : Bill Schmalfeldt continues his series of sarcastic and hilarious essays in the "You Never Miss the Dopamine" series. This time, along with his weird dreams, liberal political opinions, descriptions of his declining health and rants about literary agents, Bill deals with a real family emergency. He includes an open letter to Michael J. Fox, wondering why there is no nationwide push for Parkinson's disease awareness and writes about his impending PD dementia with a sense of humor that may, in fact, be part of the madness. Both hilarious and poignant, this book is a must have for anyone with PD, anyone who knows or loves someone with PD, and anyone who might get the diagnosis someday. In other words -- you!  Click here for more details. For more books concerning Parkinson's Disease go to Parkinson's Disease Books.

28th November 2010 - History

THE HISTORY OF L-DOPA

Journal of Neurology [2010] 257 (Supplement 2) : S249-252 (O.Hornykiewicz) Complete text

L-dopa has been used for thousands of years for Parkinson's Disease. An ancient civilisation in India used a tropical legume called Mucuna Pruriens, whose seeds are a natural source of therapeutic quantities of L-dopa. L-dopa was first isolated in 1910-1913 from seedlings of Vicia faba. In 1938, L-dopa decarboxylase was discovered, the enzyme that turns L-dopa into dopamine. In 1957, dopamine was shown to occur in the brain, and in 1959 it was found to be enriched in a specific part of the brain. In 1960, postmortem studies showed that a severe dopamine deficiency occurred in Parkinson's Disease, thereby providing a basis for dopamine replacement therapy using L-dopa. Accordingly, in 1961, the first successful clinical trial with L-dopa was carried out. In 1963 dopamine deficiency in the substantia nigra in people with Parkinson's Disease was found. In 1967 the chronic, high dose L-dopa regimen was introduced in the treatment of Parkinson's Disease. 

There are now more than a dozen formats of L-dopa. Sinemet consists of L-dopa and Carbidopa (which helps to prevent the metabolism of L-dopa before it reaches the brain). There is a controlled release version, Sinemet CR, that spreads out the effect of the L-dopa. Madopar consists of L-dopa and Benserazide (which helps to prevent the metabolism of L-dopa before it reaches the brain). There is also a controlled release version called Madopar CR.

Parcopa is an orally disintegrating tablet version of Sinemet. Duodopa is a combination of L-dopa and Carbidopa in the form of a gel. It is administered throughout the day using a portable pump directly into the small intestine through a surgically placed tube. AcuForm is being added to a combination of L-dopa and carbidopa. AcuForm helps to deliver a drug like Sinemet over a longer period of time. Dual layer L-dopa combines the immediate release and the controlled release versions of L-dopa.

Stalevo consists of L-dopa, Carbidopa and Entacopone, which inhibits the COMT enzyme, thereby prolonging the effects of L-dopa.  Melevodopa is the methyl ester of L-dopa. Mucuna pruriens and Fava beans are natural sources of L-dopa. In order to refer to this article on its own click here.

14th November 2010 - New book

NON-DOPAMINE LESIONS IN PARKINSON'S DISEASE

Glenda Halliday (Editor), Roger Barker (Editor), Dominic Rowe (Editor)

Publisher's description : This book aims to provide a comprehensive review of the non-dopamine lesions in Parkinson's disease by assessing current knowledge of their presence and pathophysiology, how they relate to different symptoms, and discuss how they may be potentially treated. The book addresses most of the known symptoms in patients with Parkinson's disease. In addition to the classic motor triad, motor speech, eye movements, olfactory dysfunction, autonomic dysfunction, pain and sensory abnormalities, sleep disturbances, depression and apathy, dopamine dysregulation syndromes, hallucinations, psychoses, cognitive impairment, and dementia are reviewed. Click here for more details.  For more books concerning Parkinson's Disease go to Parkinson's Disease Books. In order to refer to this article on its own click here.

12th November 2010 - New research

DBS REDUCES PARKINSON'S DISEASE DRUG USE

Ideggyógyászati szemle [2010] 63 (9-10) : 314-319 (Fehér G, Balás I, Komoly S, Dóczi T, Janszky J, Aschermann Z, Balázs E, Nagy F, Kovács N.Pécsi) Complete abstract

Deep Brain Stimulation (DBS) has been shown to greatly reduce the need for Parkinson's Disease drugs. DBS involves the use of electrodes that are surgically implanted into the brain and connected to a small electrical device called a pulse generator that can be externally programmed. DBS is intended to enable the reduction and need for L-dopa and related drugs. For more information go to Deep brain stimulation. All patients assessed in this study reduced their Parkinson's Disease drug intake after Deep Brain Stimulation (DBS). Before the operation, the patients used an average of 12 tablets per day of three different Parkinson's Disease drugs. After the operation the patients averaged 7 tablets per day of 1-2 Parkinson's Disease drugs. The use of amantadine, MAO-B and COMT inhibitors were also significantly decreased. The dose of dopaminergic drugs was lowered from 1136 mg to 706 mg L-dopa or the equivalent. Their Parkinson's Disease symptom scores improved by nearly 50%. In order to refer to this article on its own click here.

9th November 2010 - New research

WEARABLE SENSORS FOR ASSESSING PARKINSON'S DISEASE

IEEE transactions on bio-medical engineering [2010] Oct 28 [Epub ahead of print] (S.Patel, T.Buckley, R.Rednic, D.McClure, L.Shih, D.Tarsy, M.Welsh, P.Bonato) Complete study

Mercury is a wearable wireless sensor being developed as a means of enabling home monitoring of the motion of people with Parkinson's Disease. Patients wear wireless nodes equipped with sensors for monitoring their movement and physiological conditions. Mercury consequently has the capability of analyzing sensor data in order to reliably estimate clinical scores capturing the severity of the patient's tremor, bradykinesia, and dyskinesia. The basic approach is to capture data from each limb segment using wearable sensors. The patient wears up to eight sensors each day and recharges the sensors at night. A laptop in the patient's home serves as a base station to collect and store sensor data. The data is then delivered via the Internet to the clinic where it is visualized and further processed by physicians. The signals are subject to extensive processing in order to tie the sensor data to clinical measures that evaluate the patient’s progression of the disease. In order to refer to this article on its own click here.

8th November 2010 - New book

TAKE CHARGE OF PARKINSON'S DISEASE

Anne Cutter Mikkelsen (Author), Carolyn Stinson (Contributor)

Publisher's description : Take Charge of Parkinson’s Disease is for the half million North Americans with Parkinson’s disease who are focused on living a healthy lifestyle that emphasizes nutrition and exercise as a way of maintaining optimal health. Anne Mikkelsen, a professional chef, includes recipes that combine the widest variety of anti-oxidant, nutrient-rich ingredients, as well as liberal doses of herbs and spices known to favorably impact the brain and potentially reduce the effects of the disease. Healthy lifestyle recommendations are interspersed with Mikkelsen's memoir of her journey with her husband as they discover how to live well with Parkinson’s disease. Click here for more details.  For more books concerning Parkinson's Disease go to Parkinson's Disease Books.

5th November 2010 - News release

SAFINAMIDE CLINICAL TRIALS FOR PARKINSON'S DISEASE

Merck Serono have extended their previous six month clinical trial of Safinamide for Parkinson's Disease to 24 months. Safinamide is believed to have both dopaminergic and non-dopaminergic actions, including the inhibition of monoamine oxidase B (MAO-B), activity-dependent sodium channel antagonism and inhibition of glutamate release. It is intended to be added on to the existing use of L-dopa or dopamine agonists. In their previous six month study of Safinamide, dosages of 50mg to 100mg improved Parkinson's Disease symptoms, and reduced "off" time when added on to the use of existing Parkinson's Disease treatments. However, the reduction in "off" time in comparison to the use of a placebo was minimal, and the side effects of the clinical studies were not disclosed. Higher dosages did not have any beneficial effect. For more information go to the News release.

After 24 months of testing Safinamide, the improvement in dyskinesia was not statistically significant. The increase in "on" time beyond that of a placebo was only 40 minutes for 50mg safinamide, and 50 minutes for 100mg safinamide. They claimed that the “long-term treatment results are encouraging because they confirm the safety profile of safinamide." but did not disclose any of the side effects of Safinamide. For more information go to the News release. In order to refer to this article on its own click here.