Video monitoring improves therapy of Parkinson's disease

] Scientists have long known that anti-Parkinson medications occasionally spark compulsions like pathological gambling. Research published Thursday found another treatment, a pacemaker-like brain implant, can trigger a completely different kind of impulsiveness. How different? The drugs leave a subset of patients unlikely to learn from bad experiences, like a losing poker hand. The brain implant doesn’t hinder learning. In contrast, those patients can make hasty decisions as the brain loses its automatic tendency to hesitate when faced with conflict, University of Arizona researchers reported online in the journal Science. In fact, the first patient they studied displayed an alarming example when he saw something across the room he wanted and tried to dash over without his wheelchair. Neuroscientist Michael Frank had to catch the man before he fell. “Deep brain stimulation," or DBS, involves placing electrodes into a small region called the subthalamic nucleus, an area important for controlling movement. But it also is where scientists believe the brain yells: “Stop, weigh your options!" Frank’s theory: When electrodes fire to disrupt excessive movement, they also may block that signal. “It makes a lot of sense," said Dr. Valerie Voon, a psychiatrist with the National Institutes of Health’s neurology center, after reviewing the research. The study doesn’t offer easy solutions. But it could affect how neurologists counsel Parkinson’s patients after DBS surgery. “Because they don’t have those brakes in place, you need to teach someone to slow down” when faced with certain decisions, Voon said. [url=http://news.yahoo.com/s/ap/20071025/ap_on_he_me/parkinson_s_impulsiveness:
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] A glitch in the way cells clear damaged proteins could be the trigger for the symptoms of Parkinson’s disease, researchers said in a finding that could lead to new treatments for the incurable condition. The U.S. team focused on a process called autophagy in which cells digest and recycle damaged molecules, including proteins, that develop as cells grow older. This system essentially renews cells to keep them functioning properly. This mechanism is also important for nerve cells in the brain where defective proteins can kill cells and cause the debilitating symptoms of Parkinson’s, such as tremors, said Ana Maria Cuervo, a cell biologist who led the study. “We have found in Parkinson’s there are problems in removing abnormal proteins," said Cuervo of the Albert Einstein College of Medicine of Yeshiva University. The finding could potentially lead to drugs to treat the symptoms but not cure the disease, which affects more than a million patients in the United States alone and is marked by the death of brain cells that produce dopamine. Dopamine is a neurotransmitter, or message-carrying chemical, associated with movement. Cuervo had previously shown how mutant forms of a protein called alpha-synuclein — found in a tiny percentage of Parkinson’s patients — blocked the breakdown of substances and prevented cells from clearing damaged proteins. In the study in The Journal of Clinical Investigation on Wednesday, the team showed how in the majority of patients dopamine modifies normal proteins to act like the mutated ones to trigger tremors and other symptoms. “What we have found is dopamine modifies alpha-synuclein that really resembles the mutation," Cuervo said. “That is why they have the same symptoms." [url=http://www.abcnews.go.com/Health/story?id=4076779&page=1:
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] Scientists at Sacre Coeur Hospital at the University of Montreal report in the journal Neurology that Parkinson can be predicted relatively accurately up to 12 years before the first muscle tremors appear. People diagnosed with an unusual sleep condition called REM sleep disorder, in which they physically act out their dreams by kicking, screaming and even harming themselves and others lying next to them, are 18% more likely to develop a neurodegenerative disease like dementia or Parkinson within five years of their diagnosis, and 52% more likely after 12 years. “We have been aware of the potential connection between REM sleep disorder and these diseases for some time, but this is the largest and longest study to estimate the true risk of getting Parkinson and other neurodegenerative diseases if someone has the sleep disorder," says Dr. Ron Postuma, the study’s author and a neurologist at Montreal General Hospital. The trial involved nearly 100 men and women with an average age of 65, all diagnosed with REM sleep disorder. During normal sleep, our muscles become paralyzed when we enter the REM, or dream state, which explains why inside our dreams, we occasionally feel as if we can’t move or are operating in slow motion. People with REM sleep disorder, however, never achieve this muscle relaxation, and researchers now believe that this could be the first signs of Parkinson. The latest thinking on the disease holds that the uncontrolled movements that are the hallmark of Parkinson are only the latest, and most advanced signs of the disease, the final stage of a 10 or 20 year gradual decline in nerve function. In fact, experts believe that the condition actually begins with a loss of smell, with degeneration of nerves in the olfactory tract, then proceeds to the gut and brain stem. At some point along this march, the nerve damage hits the pons, a region in the brain that regulates sleep. “So in Parkinson, there is a period, that we don’t know how long it lasts, in which the neurons are dying in the brain, just not in the motor areas," says Postuma. “And sleep is an area where this degeneration occurs, indicating that the process of Parkinson has started." Postuma stresses that REM sleep disorder is a rare condition not to be confused with the tossing and turning that most of us do every night. People with the condition have vivid movements nearly every night, and unlike those who sleep walk or sleep talk and remain confused for a bit after they awake, these patients are completely alert and oriented once they wake up. REM sleep disorder itself can be treated with medications, but those drugs still won’t slow the decline in nerve function that’s responsible for Parkinson. But identifying Parkinson at this earlier stage may help scientists to come up with newer ways of protecting the motor neurons from further damage. “We don’t have agents now to stop the degeneration of Parkinson," says Postuma. “But once we have those agents, as far as I’m concerned, every patient with REM sleep disorder should be taking it." [url:
http://www.time.com/time/health/article/0,8599,1868646,00.html?imw=Y[/url]