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Thursday, August 30, 2007

Abstinent Alcoholics Can Have Reduced Brain Activation Without Apparent Structural Damage


presented by Md Moshiur Rahman sponsored by www.careerbd.net


Researchers know that heavy alcohol intake can lead to structural and functional changes in the brain, but have not been able to establish direct links between these changes and specific cognitive functions


New findings show that even when structural damage may not be apparent, brain activation can still be reduced. Researchers refer to this alcohol-induced damage as "latent lesions." A new examination of memory retrieval among recovering alcoholics has found lower activation than among nonalcoholics in key areas of the brain even in the absence of demonstrable brain structural damage.


"Even in the alcoholic brain without apparent structural brain changes, some cognitive impairment exists," said Motoichiro Kato, associate professor in the department of neuropsychiatry at Keio University in Japan. "We believed that the associated functional changes could be visualized by neuroimaging techniques." Kato is also corresponding author for the study.


"Impairment in different aspects of cognitive, sensory or motor function can arise from problems with impairment in neurochemical systems that enable information to be carried quickly and efficiently between brain regions," explained Edith V. Sullivan, professor in the department of psychiatry and behavioural sciences at Stanford University School of Medicine. "Such deficits in neurotransmission are not visible with conventional magnetic-resonance imaging methods. However, Doctor Kato used another method, functional magnetic resonance imaging (fMRI), which is sensitive to localized changes in brain-blood volume that occur when an individual engages in a cognitive or motor task. fMRI has been demonstrated to be useful in identifying compromised functional brain systems even in the absence of detectable brain lesions."


Study authors gave a modified "false recognition task," a word-matching exercise, to two groups: nine (8 men, 1 woman) alcoholic patients whose onset ages were less than 30 years of age and who were abstinent for an average of 40 months; and nine (7 men, 2 women) community-based "controls" matched on age and education. All participants were scanned with fMRI while performing the task.


Results showed that long-term memory retrieval induced by the task led to lower brain activity in the prefrontal lobes, anterior cingulate cortex, thalamus, and ventral striatum of the alcoholics than the controls.


"Even though both groups of participants performed similarly on the task, what distinguished them were their brain activation levels while engaged in the memory task," said Sullivan. "The attenuated activations were in brain regions that are known to contribute to goal-directed behaviour, error monitoring, drug-seeking behaviour, and declarative memory, that is, memory for new events."


"We call this phenomenon 'latent lesions' or 'subclinical pathology'," said Kato. "To date, brain damages induced by alcohol are known to cause structural changes such as brain atrophy and shrinkage. Conversely, latent lesions mean brain damages not seen in a structural brain examination. Latent lesions may occur without apparent cognitive impairments, so that people continue drinking alcohol without noticing damage to their brain."


"This functional brain imaging study focused on young to middle-aged adults with a relatively long drinking history and current abstinence period," added Sullivan. "Other studies of brain structure commonly find that this age group has less evidence for structural brain damage than older alcoholics. But this research group has shown that, in spite of the absence of visible brain lesions or other brain dysmorphology, these younger alcoholics showed differences from controls in brain responsivity to their test stimuli. In other words, alcoholics carry untold liability for brain damage, whether functional or structural."


Results are published in the September issue of Alcoholism: Clinical & Experimental Research.


Alcoholics Show Deficits In Their Ability To Perceive Dangerous Situations


Previous brain-imaging studies have suggested cognitive deficits in alcoholic patients. New findings indicate that alcoholic patients show emotional processing deficits as well. These deficits primarily affect processing for negative emotional expressions


Alcoholics tend to be deficient in both cognitive and emotional processes. Previously, most brain-imaging research focused on cognition rather than emotion. A new study uses functional magnetic imaging (fMRI) to examine emotional processing, finding that alcoholics have stunted abilities to perceive dangerous situations.


"We knew that alcoholics show a deficit in accurate recognition of facial emotions," said Jasmin B. Salloum, research scientist at the National Institute on Alcohol Abuse and Alcoholism and corresponding author for the study. "This can lead to insensitivity to, and overestimation and/or misattribution of, certain facial expressions."


"Relatives and friends of alcoholics often wonder why they continue to drink even though they intellectually know how detrimental this is for them," added Andreas Heinz, director and chair of the department of psychiatry at Charité -- University Medical Center Berlin. "Patients often relapse when entering previous drinking situations, that is, entering a bar or a shop in which you can buy alcoholic drinks. One reason may be that they fail to perceive dangerous situations. This study suggests that there is a neurobiological correlate of this often-reduced ability to perceive dangerous situations."


Study participants comprised 11 male subjects who met DSM-IV criteria for alcohol dependence, as well as 11 healthy male subjects or "controls." All participants were given a facial-emotion decoding task during which they were asked to determine the intensity level of a target emotion displayed via facial expressions of happy, sad, anger, disgust and fear. Researchers used fMRI to examine the subjects' brain-blood oxygenation level dependent (BOLD) responses (a BOLD signal will increase when that part of the brain is engaged in active processing of information).


Results showed that the greatest deficit among the alcohol-dependent individuals was in brain activation during decoding of negative emotional expressions, particularly in the affective division of the anterior cingulate cortex. The anterior cingulate is part of the prefrontal brain area.


"The cingulate is involved in many higher order executive functions such as focused attention, conflict resolution and decision making," said Salloum. "Alcoholic patients are known to be sensation seekers and are less likely to shy away from signals that suggest danger. Both sensation seeking and avoidance of danger are characteristic of subjects with axes II personality disorders, which many of our subjects had. The findings in this study may shed some light on some of the problematic and psychopathological behaviors that are manifest in this patient group. It remains to be determined if the dysfunction of the anterior cingulate precedes alcoholism or is a result of long term drinking."


There is, however, a silver lining, added Heinz. "Now we can begin to understand why patients have problems avoiding dangerous situations and, particularly, why they may not react to the concerns of their friends and relatives: the brain area that should help them appreciate these concerns is functioning at a reduced level. Furthermore, the authors also observed a normal or even increased brain response to happy faces. Our group recently made a similar observation, in that patients with strong brain responses to pleasant pictures have a reduced relapse risk. So, relatives and friends may want to support alcoholic patients with positive messages that strengthen their self-esteem while being particularly careful, and even repetitive, in pointing out the dangers of alcohol and alcohol-associated environments. Otherwise, the patients may miss the message."


Full results are published in the September issue of Alcoholism: Clinical & Experimental Research.




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