VOLUME 9, NO.11                                                                        NOVEMBER 18, 2004

 

NJ ADD/ADHD ADULT NEWSLETTER

ADD ADULT SELF HELP SUPPORT GROUP

FOR ADD/ADHD ADULTS

AND THEIR SIGNIFICANT OTHERS

 

MEETING: THE NEXT MEETING OF THE ADD ADULT SELF HELP SUPPORT GROUP WILL BE ON NOVEMBER 18, 2004 AT 7:30 PM AT MONMOUTH MEDICAL CENTER, COMMUNITY MEETING ROOM , LONG BRANCH, NJ.  GO TO THE RECEPTION DESK IN THE MAIN LOBBY AND GET DIRECTIONS.  LAST MONTH’S TOPIC WILL BE REPEATED: HOW TO DEAL WITH ANXIETY, STRESS AND TRAUMA TO HELP MANAGE ADD.

 

RESEARCH: In a research study by E. Nofzinger etal. Functional Neuroimaging Evidence for Hyperarousal in Insomnia, Am. J. Psychiatry, 2004, 161 )11): 2126-2129, it was reported that brain glucose metabolism (brain activity) was significantly different in the sleep of patients with insomnia.  The insomnia sufferers had greater global brain glucose metabolism during both sleep and wakefulness than normal sleepers.  With insomnia there was less of a decline in relative metabolism from waking to sleep states in the areas of the brain that promote wakefulness.  (The “insomnia brain” did not decrease activity in the arousal parts of the brain well. There was a problem with the transition from the waking to the sleeping brain.)  More importantly and less obvious was the finding that patients with insomnia had less relative brain activity in the prefrontal cortex while awake.

COMMENTS: Although the study did not knowingly include ADDers, it seems very relevant to us.  Insomnia appears to be a lifelong hallmark of ADD.  Other studies have demonstrated that the ADDer’s prefrontal cortex is more “sleepy” than the average person’s. Our brains are more like those of the insomniacs.  What appears to be a pattern here is that chronic insomnia is associated with a sleepy prefrontal cortex, the executive function part of the brain. We could be making up for sleep deprivation with micro sleep episodes during our daydreaming, when we seem to be dissociated, when we don’t hear conversations, or miss parts of conversations, when we fail to make transitions smoothly etc. Other studies have found that psychostimulant medications appear to awaken the prefrontal cortex, the reticular activating system, the striatum and other areas, giving the ADDer an awake brain during the day.  Unfortunately, since insomnia is associated with increased brain activity in general, the psychostimulants may increase insomnia for some ADDers.   Here is a comparison list of the areas of decline in brain activity from waking to non-REM sleep: Normals: bilateral frontal cortex; anterior and posterior cingulate; medial prefrontal; left occipitoparietal; right temporoparietal; and thalamus. Insomniacs: bilateral frontal; right occipitoparietal; a small area of left temporoparietal; but no significant changes (declines in activity) in the thalamus, anterior cingulate or medial prefrontal cortex.   These brain areas with no change, function to monitor the environment, prepare for arousal, and deal with the significance of information. Here is a list of the areas of the awake brain in insomniacs that show hypo metabolism (low brain activity) when compared with normals: frontal cortex bilaterally, left superior temporal, left parietal, left occipital cortices, thalamus, hypothalamus and brainstem reticular formation.  These areas are required for academic performance and left brain verbal activity.  It is no wonder why insomnia in ADDers and others impairs thinking, verbal performance, communication etc. 

            In summary, sleep is very important for daytime arousal.  Insomnia impairs parts of the brain involved in verbal learning, thinking, stopping, attention and arousal in general.

 

                                                                                    PEACE!!!     Bob

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