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I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's
diseases as well and thought it would be nice to have a place where
updated news is in one place. That is why I began this blog.
I am not responsible for it's contents, I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish. This is for you to read and to always keep an open mind.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please No advertisers, and No Information about Herbal treatments. This is a free site for all.
Thank you.


Tuesday, August 9, 2011

What is Deep Brain Stimulation for Parkinson's Disease?

 


Deep brain stimulation (DBS) is a surgical procedure used to treat a variety of disabling neurological symptoms—most commonly the debilitating symptoms of Parkinson’s disease (PD), such as tremor, rigidity, stiffness, slowed movement, and walking problems.  The procedure is also used to treat essential tremor, a common neurological movement disorder.  At present, the procedure is used only for patients whose symptoms cannot be adequately controlled with medications.
DBS uses a surgically implanted, battery-operated medical device called a neurostimulator—similar to a heart pacemaker and approximately the size of a stopwatch—to deliver electrical stimulation to targeted areas in the brain that control movement, blocking the abnormal nerve signals that cause tremor and PD symptoms. 
Before the procedure, a neurosurgeon uses magnetic resonance imaging (MRI) or computed tomography (CT) scanning to identify and locate the exact target within the brain where electrical nerve signals generate the PD symptoms.  Some surgeons may use microelectrode recording—which involves a small wire that monitors the activity of nerve cells in the target area—to more specifically identify the precise brain target that will be stimulated.  Generally, these targets are the thalamus, subthalamic nucleus, and globus pallidus.
The DBS system consists of three components:  the lead, the extension, and the neurostimulator.  The lead (also called an electrode)—a thin, insulated wire—is inserted through a small opening in the skull and implanted in the brain.  The tip of the electrode is positioned within the targeted brain area.
The extension is an insulated wire that is passed under the skin of the head, neck, and shoulder, connectng the lead to the neurostimulator.  The neurostimulator (the "battery pack") is the third component and is usually implanted under the skin near the collarbone.  In some cases it may be implanted lower in the chest or under the skin over the abdomen.
Once the system is in place, electrical impulses are sent from the neurostimulator up along the extension wire and the lead and into the brain.  These impulses interfere with and block the electrical signals that cause PD symptoms.

Is there any treatment?


What is the prognosis?


What research is being done?


The NINDS supports research on DBS to determine its safety, reliability, and effectiveness as a treatment for PD.  Currently, NINDS-supported scientists are trying to determine the site(s) in the brain where DBS surgery will be most effective in reducing PD symptoms.  These researchers are also comparing DBS to other PD therapies to find out which is more effective.

Although most patients still need to take medication after undergoing DBS, many patients experience considerable reduction of their PD symptoms and are able to greatly reduce their medications.  The amount of reduction varies from patient to patient but can be considerably reduced in most patients.  The reduction in dose of medication leads to a significant improvement in side effects such as dyskinesias (involuntary movements caused by long-term use of levodopa).  In some cases, the stimulation itself can suppress dyskinesias without a reduction in medication.

Unlike previous surgeries for PD, DBS does not damage healthy brain tissue by destroying nerve cells.  Instead the procedure blocks electrical signals from targeted areas in the brain.  Thus, if newer, more promising treatments develop in the future, the DBS procedure can be reversed.  Also, stimulation from the neurostimulator is easily adjustable—without further surgery—if the patient’s condition changes.  Some people describe the stimulator adjustments as "programming."

9th August 2011; THE LONG TERM EFFECTS OF DBS ON PARKINSON'S DISEASE

Archives of Neurology [2011] Published online August 8 (A.Castrioto, A.M.Lozano, Yu-Yan Poon, A.E.Lang, M.Fallis, E.Moro
Researchers assessed the outcome of Deep Brain Stimulation of the subthalamic nucleus (STN-DBS) in people with Parkinson's Disease over a period of 10 years. Deep Brain Stimulation (DBS) involves the use of electrodes that are implanted into the brain and connected to a small electrical device called a pulse generator that can be externally programmed. DBS requires careful programming of the stimulator device in order to work correctly. DBS improved the Parkinson's Disease symptom score by 25% in comparison to no treatment, including resting and action tremor by over 85%, and bradykinesia by 23%. It did not stop deterioration in speech, walking, and postural instability, including falling and freezing. L-dopa dosages reduced to about 63% of what they were initially. Daily living activity also improved. Dyskinesia and motor fluctuation scores also remained significantly lower. Potential adverse events included : a trend to weight loss, visual hallucinations, impulse control disorders possibly related to dopamine agonists, progressive cognitive decline culminating in dementia,  device related infections.

Monday, August 8, 2011

Nicotine Protects Against Parkinson’s?

Northwest Parkinson's Foundation:

Bills SignatureThe addictive component of cigarettes saves dopamine neurons from a Parkinson’s-like decline, providing a new avenue for potential treatment.Jef Akst
The Scientist - Nicotine protects the brain against the loss of dopamine neurons, a characteristic sign of Parkinson’s disease, according to a study published this week in The FASEB Journal.

By activating the alpha-7 nicotinic receptor, nicotine—which increases dopamine levels in the brain—appears to be able to rescue mouse dopaminergic neurons cultured under conditions that favor their loss. Genetically engineered mouse cells that lacked a specific nicotine receptor (the alpha-7 subtype), however, were unaffected by nicotine treatment.

The findings suggest that new Parkinson’s therapies may be developed to target nicotine receptors, FierceBiotech reports. “This study raises the hope for a possible neuroprotective treatment,” said co-author Patrick P. Michel of the Institut du Cerveau et de la Moelle Épinière, Hôpital de la Salpêtrière, in Paris, France, in a statement.

But this is not an endorsement for cigarettes, FASEB noted. “If you’re a smoker, don’t get too excited,” Gerald Weissmann, editor-in-chief of The FASEB Journal, said in a statement. “Even if smoking protects you from Parkinson’s, you might not live long enough to develop the disease because smoking greatly increases the risk for deadly cancers and cardiovascular diseases.”

Sleep Disorder is Risk Factor for Parkinson’s

From the Northwest Parkinson's Foundation: Rick Nauert PhD

Bills SignaturePsych Central - A new European study suggests individuals suffering from REM sleep behavior disorders have an increased risk of developing Parkinson’s disease (PD).

REM sleep behavior disorders are characterized by dream nightmares in which a person is attacked and pursued leading an individual to scream, cry, punch and kick while sleeping.

The current study is the third work on the topic within the last five years to be published by Lancet Neurology.

The first work showed in 2006 that 45 percent of patients who suffer this sleep disorder develop Parkinson’s disease and other neurodegenerative diseases caused by a lack of dopamine in the brain.

The second article discovered that neuroimaging tests that measure dopamine in the brain, such as the brain SPECT scan (single-photon emission computed tomography), are useful to identify patients with REM sleep disorders with increased risk of developing a neurodegenerative diseases such as Parkinson’s disease.

In the current study, researchers used SPECT to conclude that the levels of dopamine in the brain are quickly lowering over the years in patients with REM sleep behavior disorder.

SPECT is the first neuroimaging technique to detect the disease progression at an early stage. The study involved comparing for three years the evolution of brain SPECT in 20 patients with REM disorder and 20 healthy controls.

The neuroimaging technique measures the presence of dopamine in the substantia nigra, a part of the brain associated with learning and harmony of body movements. In Parkinson’s disease, a deficiency of dopamine in the substantia nigra causes tremor, stiffness and movement slowness in patients.

Results showed that after three years of monitoring the production of dopamine in the control group was reduced by 8 percent due to age, while the group of REM sleep disorder patients experienced a reduction of 20 percent.

Once the three-year follow-up ended, three of 20 patients in the REM sleep disorder group had developed Parkinson’s disease and their dopamine reduction was around 30 percent.

Researchers conclude that more efforts are needed to create neuroprotective drugs that prevent the progression from REM sleep behavior disorders to Parkinson’s disease.

Authors of the study suggest that, to be considered effective, a neuroprotective drug should significantly prevent the dopamine concentration from dropping in these patients.