 MEMORY SUPPRESSION
Experiment shows brain can banish unpleasant memories, a finding that could have implications for treating depression
Electrode implants boost brain-crippled patient
PARIS
Pioneering surgeons said they had implanted electrodes to stimulate the badly damaged brain of a man who had been lying in a virtually unconscious state for six years, enabling him to speak, eat, and recover some limb movement.
The 38-year-old patient had suffered a traumatic brain injury that had left him bed-ridden and under 24-hour nursing care, incapable of moving or communicating except with slight movements of the eye or finger.
Reporting in Nature, the US team used deep-brain stimulation, a technique in which electrodes deliver impulses to the central thalamus, the region that helps adjust brain activity to match cognitive demands. They used computer-generated maps, image-guided navigation and 3-D mapping of the brain to maneuver the electrodes in place with millimeter accuracy and connect them to programmable pacemaker batteries, implanted in the chest.
Sixteen months after the operation, the patient has enjoyed "remarkable and sustained" improvement, said lead author Ali Rezai of the Center for Neurologic Restoration at the Clevic Clinic Foundation, Ohio.
The patient now interacts with family and friends, using words and gestures, and responding swiftly to questions. In addition, he now chews and swallows his food, whereas previously he needed a feeding tube. He can also perform some complex movements, including those required for drinking from a cup or brushing hair, although long years of immobility and tendon damage crimp his ability to carry out those tasks, said Joseph Giacino, a neuropsychologist at JFK Johnson Rehabilitation Institute and the New Jersey Neuroscience Institute.
Patients in a so-called minimally conscious state (MCS) may seem comatose but their diagnosis is technically different from that of people in a coma or persistent vegetative state. People in MCS show occasional signs of awareness and may even attempt fleetingly to communicate using simple sounds or signals. Such activity points to the existence of a still-functioning brain network in which, in theory, the thalamus would play a key regulatory role.
"Our theory was that electrical impulses targeted to this area would help amplify the existing low level of activity that we thought was already there," said Giacino. "In other words, we assume that the signals that help drive speech and movement are still present in the brain-we're just 'bumping up' their efficiency and function to help get them working better."
Deep-brain stimulation is routinely used to relieve symptoms among people suffering from Parkinson's disease, and trials are under way in the United States for using it to treat epilepsy, obsessive-compulsive disorder, and depression.
But this is the first time that it has been used on a patient in MCS. A total of 12 such operations have been authorized by the US Food and Drug Administration in a pilot study.
If the success is replicated, the implants could sweep away conventional ways of perceiving and treating people in MCS, argued Joseph Fins, director of medical ethics at Weill Cornell. "It will force us to take a second look at each case and-for appropriate patients-move away from the therapeutic nihilism that has so plagued this population, most of whom are ignored, receiving what is euphemistically described as custodial care."
In a commentary carried by Nature, US neurologists Michael Shadlen and Roozbeh Kiani cautioned that such intervention could only help those patients who have an undamaged cerebral cortex, which is essential for thought and memory.
Study reveals anatomy of suppressed memories
CHICAGO
US researchers have identified the parts of the brain that are involved with suppressing unpleasant memories, a finding that could have implications for treating depression or posttraumatic-stress disorder (PTSD).
The concept of memory suppression has been a controversial one among psychologists for a century, but in this study neuroscientists used brain scans to show that volunteers who have been asked to banish disturbing memories show very specific patterns of brain activity. The scans showed that two specific regions of the prefrontal cortex-what neuroscientists call the seat of cognitive control-appear to work in tandem to modulate posterior brain regions like the visual cortex, the hippocampus, and amygdala. These areas are involved in tasks such as visual recall, memory encoding and retrieval, and emotional expression.
"These results indicate memory suppression does occur, and, at least in nonpsychiatric populations, is under the control of the prefrontal cortex," the investigators reported in Science.
For the purpose of the experiment, the 16 volunteers were given 40 pairs of photographs to study. In each case, an image of a neutral human face was paired with an emotionally disturbing image such as a car crash, a wounded soldier, an electric chair, or a violent crime scene. After memorizing each pair, the volunteers underwent magnetic resonance imaging (MRI) while being shown only the neutral face images and instructed to either actively recall the associated image or to actively suppress it.
The results indicated that the volunteers were able to "exert some control over their emotional memories," said lead author Brendan Depue, a doctoral student in neuroscience at the University of Colorado at Boulder. "By essentially shutting down specific portions of the brain, they were able to stop the retrieval process of particular memories," Depue said.
The authors of the paper said they hope that their work will promote further research into better therapies and possibly even drug for people suffering from conditions such as PTSD, phobias, and obsessive-compulsive syndrome. The symptoms of these disorders include flashbacks to disturbing events, and intrusive or obsessive thoughts.
"The first step is to understand how memory suppression works in healthy individuals, and what neural mechanisms are at work," said Depue. "Then you need to look at those same mechanisms in a clinical population and figure out why they aren't functioning properly."
New treatment could save legs from amputation
SYDNEY
Australian researchers have developed a world-first treatment that could save hundreds of thousands of smokers and diabetics from undergoing leg amputations. The procedure involves pumping blood at high pressure into limbs dying of vascular disease to stimulate the growth of new blood vessels, the researchers said, and has saved the leg of the first patient to be treated.
"This is a significant advance for the 340,000 patients in the Western world who lose a leg to surgical amputation every year due to peripheral vascular disease," said inventor and vascular surgeon Rodney Lane.
The clinical trial had been carried out on a 52-year-old Australian man, Malcolm Brown, who had been told by three surgeons that he needed a major lower-limb amputation, said Lane of Sydney's Royal North Shore Hospital.
The father of two had developed a clot in an artery near his knee, which severely restricted the blood supply to his lower leg. "Malcolm's foot lost sensation and became cold and white. Gangrenous ulcers formed on his feet and toes as the flesh started to die," said Lane.
Brown agreed to participate in the trial of the new procedure and had a device implanted in the femoral artery in the thigh, which was connected to a blood pump outside the body. His own blood was then pumped through the leg at high pressure, resulting in a 250-percent increase in the blood flow to the foot and stimulating new blood-vessel growth.
"After 50 hours on the pump over a five-day period, Malcolm's foot became warm and pink with marked improved sensation and notable healing of the ulcers on his feet and toes," Lane said. "Malcolm's leg was saved by stimulating the growth of his own blood vessels which ultimately restored the blood flow to his leg."
A year later Brown still has his leg and is walking. "We wanted to make sure that it stayed a success and what we saw immediately turned out to be a permanent cure," said Greg Roger, the chief executive officer of the company that makes the implanted device.
Roger, associate professor of bioengineering at Sydney University, said that further clinical trials would be completed by the end of the year to make the procedure available for general use.
Researchers eye Alzheimer's-glaucoma link
CHICAGO
British research has shown for the first time that a protein involved in Alzheimer's disease also plays an important role in glaucoma, the major cause of irreversible blindness worldwide. Using a novel optical technology, investigators at University College London (UCL) showed that beta-amyloid, which causes the so-called "plaque" lesions in the brains of Alzheimer's patients, also leads to nerve cell death in the retina, the innermost layer of the eye.
"We've seen for the first time that there is a clear link between what causes Alzheimer's disease and one of the most basic mechanisms behind glaucoma," said Francesca Cordeiro, a glaucoma specialist at UCL.
It was once thought that increased intraocular pressure (IOP) was the main cause of optic-nerve damage, but IOP is now seen only as a risk factor because even people with normal eye pressure can develop the condition. In experiments on rats, Cordeiro and her colleagues showed that the dying retinal cells had an accumulation of beta-amyloid. When they added the protein to retinal cells in test tubes, it induced cell death.
They also showed that drugs that work to prevent the buildup of beta-amyloid in Alzheimer's patients' brains can delay the onset of glaucoma in animal models. One such drug, bapineuzumab, is already being tested in clinical trials in the United States and Ireland. However, the investigators found that it was even more effective when combined with two other novel Alzheimer's treatments.
"We are trying a new approach that has never been tried before, not even to treat Alzheimer's disease," said Cordeiro. "Our success in treating glaucoma in the lab by combining different Alzheimer treatments represents a brand-new treatment strategy. Since we have shown that drugs for Alzheimer's disease can tackle glaucoma, then potentially we could use damaged retina to screen for Alzheimer drugs that target amyloid-beta buildup."
The study appears in the Proceedings of the National Academy of Sciences.
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