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According to recent studies, damage to the brain amongst abusers of methylphenidate (Ritalin) is similar to the damage caused by alcohol and cocaine.
Methylphenidate abuse damages the nerve endings of human brain cells that contain dopamine, chemical messengers responsible for memory, mood, and muscle coordination. Two recent studies probed further into the lasting effects methamphetamine has on the brain.
Researchers used Position Emission Tomograph (PET) scans to measure levels of Dopamine receptors and to assess the rate of glucose metabolism.
Brain cell activity was measured by PET scans in 15 methylphenidate abusers and 20 non-drug users. Results showed methylphenidate abusers had lower levels of dopamine receptors and a lower rate of glucose metabolism in certain portions of the brain than non-drug users.
PET scanned the orbitofrontal cortex, which is the portion of the brain associated with compulsive behaviors. Disruption of the metabolism in this area may contribute to compulsive drug intake in addicted individuals.
The second study, published in the Journal of Neuroscience, reported that methylphenidate-damaged brain cells may recover after prolonged abstinence — but, cognitive function may not be sufficiently restored.
PET scans measured the levels of dopamine transporters in five methylphenidate abusers who were enrolled in a California drug-court monitoring rehabilitation program, who were able to stay drug free during the study. Researchers found those who used methylphenidate for less time and in smaller quantities recovered more brain cells than long-time, heavy users of the drug. Two weeks after PETstudies were completed the subjects were tested to evaluate gross motor skills, which are associated with dopamine transporters — walking fast in a straight line, quickly inserting pegs into small holes, and memory function.
A slight improvement was noted in some motor and sensory skills in conjunction with the second PETscan, but researchers noted the improvements were not significant.
SOURCE: National Institutes of Health News Release, www.nih.gov, December 1, 2001.
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