Etiology

There have been several studies using MRI’s which have demonstrated smaller size of the prefrontal cortex, caudate nucleus and cerebellar vermis in individuals who have symptoms of ADHD compared to normal control groups.  Jay Giedd, MD. Of the National Institute of Mental Health (NIMH), has used MRI to study ADHD and found that the right frontal lobe volume is nearly 10% smaller in children with ADHD compared to their own left frontal lobe and compared to both lobes in age-matched controls.  Dr. Giedd and his team found that one part of the cerebellum was also smaller in children with ADHD.  Interference with the frontal cortex-cerebellum loop may disrupt functioning in the right frontal lobe.

Tomas Paus, MD/PHD, has performed PET studies of attention functions and ADHD in Hungary and at the Montreal Neurological Institute.  Dr. Paus studied boys with and without ADHD at age 9.  During PET scanning, a visual task is presented repeatedly with an occasional and unexpected distracting visual intrusion.  Changes in blood flow on PET imaging varied between the control group and the ADHD group.    The ability to suppress visual distraction develops between ages 9 and 10 years and appears to be related to maturation of the frontal lobe.  This is consistent with findings by Dr. Giedd and the NIMH team.

Rubia, et al 24 used MRI to investigate functional brain activation during inhibitory control in hyperactive adolescents and a comparable control group.  Their findings suggest that ADHD is associated with a decrease of brain activity in frontal regions and the increase of brain activity in sub cortical regions indicating a dynamic imbalance in interconnections between right frontal cortex and basal ganglia, which may be the underlying cause for the disinhibitory pathology in ADHD.

Current thinking is that a chemical imbalance of norepinephrine and dopamine neurotransmitters, found primarily in the frontal lobe area, have been suggested to be associated with the lack of arousal in the brain of those with attention deficit hyperactivity disorder. These messengers arouse the brain, and provide an alert state of mind; thus, a deficiency of these neurochemicals produce a mode of somnolence. Varying amounts of neurotransmitters at the neuron’s receptor site results in ADHD symptoms being able to change at any moment.

There is now a growing awareness that ADHD severely disturbs sleep in both children and adults.  Just as ADHD does not go away with age, it also does not go away at night.  Eighty percent of people with ADHD report disturbed sleep almost every night of their lives.  In childhood it presents as initiation insomnia, sleepwalking and talking, enuresis, and falling asleep in class.  In adults, the most common problem is an initiation insomnia of an average of almost two hours almost every night that is poorly relieved by sedative/hypnotic medications.  The individual reports that his mind restlessly “jumps” from one worry or concern to another.  In the morning the person has difficulty waking up and being alert.  This is not sleep deprivation but rather is an intrusion of theta waves (transitional waves between the alpha/beta waves of alertness and the delta waves of sleep).  This theta intrusion can also occur in 40% of people with ADHD when unchallenged or bored.  Commonly this is mistaken for Narcolepsy.  The mean age of onset of the adult sleep disturbance pattern is 12.4 years of age.25

References:

24 Rubia K, Department of Child and Adolescent Psychiatry, Institute of Psychiatry, London, UK.

25 Dodson WW, Prevalence of Sleep Disorders in Adults with ADHD and the Effectiveness of Psychostimulant Therapy. Poster: Am Psych Assoc Convention, Washington, DC, May 28, 1999

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