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Showing entries tagged parkinsons disease.  Show all entries

December 5, 2011

What will they think of next?


Who knew? In the 1960's up until the 1970's ablative stereotactic surgery was used to treat neurologic disorders and neuropsychiatric illness. This treatment was largely abandoned after the 70's due to the development of highly effective drugs to treat these problems, for example, "Levodopa" to combat Parkinson's disorder. Today there seems to be a virtual renaissance of similar techniques used to help those suffering.

The technique being employed uses high-frequency electrical deep brain stimulation (DBS) on specific targets to negate some disorders. Compared to the traditional ablative stereotactic surgery, which consists of lesions and very invasive brain surgery (irreversible), DBS is much less invasive in some respects. By applying high-frequency electrical stimulation to specific brain structures a similar (but different) effect of a lesion is essentially observed. Ever since this technique's rise in popularity (starting in the 1990's) people have the option of a "less permanent". These electrical pulses are delivered by electrodes chronically implanted into a persons brain at specific regions. The exact mechanism of action for DBS still isn't fully understood and clear, but the affects and benefits to patients are both lasting and clear.

Some of the diseases mentioned in the article include Parkinson's, Tourettes syndrome, obsessive compulsive disorder and depression. Patients receiving DBS to treat Tourettes syndrome had a >70% decrease of vocal or motor tics with disappearance of sensory urges. 35-70% of patients receiving DBS to treat OCD were benefitted by a significant reduction in obsessive and compulsive thoughts.

In my opinion, and it seems to be the case with most neurosurgical operations, DBS is the latest and greatest treatment available. Anytime patients can avoid a permanent/irreversible effect such as a lesion the better. My reasoning behind is vast. For example if a patient is suffering from body dissociation disorder and doesn't identify with their right arm and right leg and wants to have these two limbs removed. This persons could amputate these limbs without fully understanding the long term consequences involved or even without any benefit mentally. Or perhaps, the doctor could try a different technique, such as lesioning a brain region located using fMRI thought to be triggering body dissociation disorder. There is a chance the lesion might not properly treat the disorder or not treat it at all. Also the lesion may impair the individual in a more negative way in the long run, and since lesions are practically irreversible, the person is worse off. If DBS was used (tmi could be used as a pre-emptive mapping tool) the patient could be treated for their disorder in a non permanent way and avoid negative, unforeseen, long term issues.

I'm not entirely sure how invasive DBS is but the article made it out to be much less invasive as previous surgeries. Which to me makes sense since over time medical practices should become more and more efficient. Something haunts me about the fact little is truly known and fully understood about DBS and TMI. Little red flags go up in my head every time that fact is mentioned. Whether or not it is effective and beneficial I would prefer to know exactly why it is effective and beneficial before doctors implanted electrodes in my brain to deliver pulses of high-frequency electricity. This honestly sounds like something out of a science fiction story but the real freaky part is it seems to actually work. The big question is: Would you ever have DBS performed on yourself? My answer is yes.

http://www.sciencedirect.com/science/article/pii/S089662730600729X
Posted by      Dylan R. at 5:42 PM MST
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December 3, 2011

Deep Brain Stimulation - A Different Approach


Let's talk about Parkinson's Disease (PD). PD is one of the most prevalent neurodegenerative disorders in the world for people over the age of fifty; as the population has aged and people have started living longer, PD diagnosis has increased significantly. Some of the symptoms include tremor (shaking), akinesia (inability to initiate movement), muscle rigidity, and later in the progression of the disease, slowed speech, blank staring, and dementia. So there are motor and cognitive problems associated with PD, but this post will deal with the reduction of the earlier-onset motor symptoms.

There are two main types of treatment for PD motor symptoms: drugs and deep brain stimulation (DBS). The drugs usually have a compound called L-Dopa, which is a precursor in the formation of the neurotransmitter dopamine, the lack of which has been implicated in inducing the motor symptoms of PD.

The other treatment, DBS, can only be used on some patients, namely those for whom the drugs have had little to no effect and who are also healthy enough to undergo surgery and stay alive for longer than a few years. What they do is create an open-loop (i.e. not a closed circuit) by surgically inserting an electrode into a specific region of the brain, which is connected to a pacemaker-type device called a pulse generator (IPG) that they insert below the neck. Doctors then set the IPG to a certain frequency, so the electrode will send out electrical signals into the brain every so often, and this has been shown to reduce the motor symptoms of PD.

The whole process takes up to a year, with the surgery and adjustments to the properties of the stimulation being continuously modulated until the motor symptoms are reduced and the side effects of the stimulation are not too severe. But, since PD is a progressive disease, the motor symptoms will continue getting worse and the DBS stimulation will continue to need adjustments more and more frequently as the disease progresses.

The issue with this is that no one really knows why DBS works, so all of the adjustments are guesses (systematic guesses, but guesses nonetheless) and patients need to keep coming into the hospital, which costs a lot of money, time, and frustration when their symptoms are not relieved. This is where research in the "closed-loop," or real-time adaptive, DBS comes in. This potential form of DBS also involves a chip that is used to record when natural electrical signaling occurs in the brain region the DBS electrode is in. The recording then sets the properties of the DBS stimulation on the IPG and sets a timer for when the electrode will deliver that stimulation, producing a feedback loop, and decreasing the need for the constant hospital visits.

One study found that given some specific criteria for the wait-time and the number of stimulations, some PD symptoms were reduced (namely akinesia) to a greater extent than with open-loop DBS. However, the study also found many problems with using closed-loop rather than open-loop DBS to alleviate motor symptoms, but these problems have to do with what actually causes the motor problems associated with PD. As such, the study concludes that with more research on the efficacy of closed-loop DBS and on the details of the cause of PD motor symptoms, closed-loop DBS could be used as a potential treatment for PD that will produce not only a more significant reduction of motor problems, but will also enhance the long-term efficacy of using DBS as PD progresses.

Rosin, B., Slovik, M., Mitelman, R., Rivlin-Etzion, M., Haber, S. N., Israel, Z., . . . Bergman, H. (2011). Closed-loop deep brain stimulation is superior in ameliorating Parkinsonism. Neuron, 72(2), 370-384. doi:10.1016/j.neuron.2011.08.023 Retrieved from http://www.cell.com/neuron/abstract/S0896-6273%2811%2900776-8
Posted by      Anna G. at 11:58 AM MST

October 24, 2011

Restoration of Bovine Sanity and a Cure for Neurodegeneration


Mad cow disease. This deadly, presently incurable, brain-eating disease has been the cause of many a steak-lover's trepidation. After all, who wants his brain looking like swiss cheese? It is caused by the consumption or spontaneous generation and accumulation of PrPSc - the misfolded form of cellular prion protein (PrP) - and is responsible for several forms of "swiss cheese brain" besides bovine spongiform encephalopathy (affectionately known as mad cow disease), including the sheep-transmitted scrapie and the human form known as Creutzfeldt-Jakob syndrome, among others. Unfortunately for its victims, PrPSc is much more stable than the properly folded form of the protein and is thus resistant to normal methods of protein digestion (i.e. with protease) and is only known to be degradable via incineration of the infected victim. Clearly, this is an undesirable outcome for the individual who has been unfortunate enough to come into contact with such a protein.

As the misfolded PrPSc aggregates, it forms amyloid fibrils, essentially converting the normally folded PrP to the dark side and eventually causing neuronal cell death and ultimately the death of the organism. However, a recent study of methods to stabilize mouse PrPSc species, published in the Journal of Neuroscience, has shown that prion activity can be reduced by trapping partially digested PrP(27-30) with thienyl pyrimidine compounds.

The process of PrP conversion to the abnormally β-sheet-rich PrPSc form is autocatalytic, that is, it happens spontaneously and independently of other types of molecules. In their study, the researchers discovered that the formation of amyloid fibrils may actually be the "result of a protective process to sequester more dangerous soluble oligomers". As a result, rather than attempting to break the prions apart into smaller, supposedly more easily digested pieces, they decided to attempt to isolate them to avoid increasing the infectivity. Using mouse neuroblastoma cell cultures, they performed various drug assays and blotting techniques, including incubation of fibrils with thienyl pyrimidine compound. When all was said and done, they only observed a minimal decrease in the rate of infectivity, but it was a decrease, nonetheless. They concluded that the binding of thienyl pyrimidine-based drugs diverted dimers and trimers of misfolded protein from their pathological aggregation pathway, trapping them thermodynamically in an energy valley where they could no longer fold into their mortality-causing fibril-forming shape.

Though the study was largely inconclusive, it is clear that meaningful advances were made in discovering that the treatment of prion diseases is not as hopeless as we have believed up to this point. Indeed, the thought of finding a cure seems a daunting task, as the mad cow protein only seems to become more stable under most reaction conditions. However, this study has shown that sometime in the not-so-distant future, the mechanism of misfolding will likely be discovered, a cure for a once incurable disease developed, and we will no longer have to fear prions as much as we have in the past. Also, not only does this research have significant implications for those of us who enjoy a good steak or lamb chop, it may also have far-reaching influence on the treatment of other "prionopathies", including Alzheimer's, Parkinson's and Huntington's Diseases. Since these are diseases which affect a significant fraction of the aging population, research in this vein is critical for the progress of gerontological studies as well.

http://www.jneurosci.org/content/31/42/14882.full
Posted by      Clarinda H. at 12:03 AM MDT




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