It may be surprising to learn that professionals still do not agree about the symptoms of Attention Deficit, there is actually no neuropsychological test that can accurately identify attention deficit, and individuals diagnosed as ADD usually have normal brains when examined with MRI and PET scans. Attention deficit is diagnosed based on subjective assessments of a child’s behavior.  The criteria used to make a diagnosis differ from country to country and from professional to professional.

        In America, the definition of attention deficit is frequently based on the American Psychiatric Association’s three criteria: inattention, impulsivity and distractibility. This professional group identifies three types of attention deficit:

• Combined Type (inattentive and hyperactivity)

•  Hyperactive-Impulsive

•  Inattentive

      Only one of these types, the Combined Type, meets the World Health Organization’s criteria for attention deficit disor­der; the other two types are not recognized in other parts of the world.  

        In fact, in 1998 the National Institutes of Health published a consensus statement that stated in spite of over 30 years of clinical research, an independent diagnostic test for Attention Deficit did not exist, the causes of ADD remained only speculative, and the rational for using amphetamines to treat ADD was based only on short-term studies (the long-term effects of these drugs remained unknown).

       The most common reason parents give for seeking a diagnosis of ADD or medications for attention problems is that a child is having difficulty in school. Strangely, out of 4,074 scientific papers that had been published by 1998 on the use of meth­ylphenidate (e.g. Ritalin) for Attention Deficit, only 8 of those papers investigated its effects on math or reading scores.  Although these papers reported equivocal results (some found a small improvement, others did not), the use of medications to “treat” ADD continued to increase.

      Researchers actually know very little about the long-term effects of methylphenidate on brain structure and function. Methylphenidate acts primarily by blocking dopamine transporters in the brain, which increases the available amount of dopamine and alters levels of two other neurotransmitters, norepinephrine and serotonin (for a technical description see Yamashita et al (2006). These neurochemicals are involved in sleep/wake patterns, attention, feeding, arousal, stress responses, and learning.

      Of great concern to many researchers is the fact that cocaine and methylphenidate are strikingly similar. They both compete for the same binding sites in the brain and their uptake and distribution are identical (for details, see Volkow et al (1995) and (2005). Cocaine addicts report that the effects of methylphenidate and cocaine are similar, producing a sense of elation and empowerment in the user.   

        Cocaine and methylphenidate both increase activation in vestibular and sensory processing areas of the brain (e.g. the cerebellum, occipital cortex and thalamus). Both drugs increase heart rate and blood pressure, although the effects of methylphenidate last much longer than cocaine. Recent human and animal studies suggest that cocaine and methylphenidate both have immediate and long-term side effects that are of great concern.

        Exposing the brain to methylphenidate increases the amount of dopamine in the brain, and the brain responds to this by reducing the sensitivity of its dopamine receptors or destroying them. This process, called down-regulation,” results in a loss of about 20% of the dopamine receptors and 75% of dopamine transporters after just three months of drug use (see Vles et al,”Neuropediatrics. 2003 Apr;34(2):77-80.)

      This decrease in dopamine transporters decreases activity in the frontal lobes, areas of the brain responsible for motor planning, problem solving, spontaneity, memory, attention, language, judgement, impulse control, and following the rules of social behavior. The frontal lobes, which are not fully developed until adulthood, allow an individual to plan, solve problems, remember goals, look at situations from different perspectives, understand jokes and think in abstract terms. Recent research has demonstrated that children who were considered ADD had an average 3 year delay in frontal lobe maturation.  It is unclear whether this is a symptom of ADD or a result of the use of medication.   (read the abstract here)

          Researchers have also found that repeated exposure to methylphenidate during early development can affect the adult brain long after the medication is removed. These changes include increased anxiety and stress, decreased sensitivity to natural rewards, and decreased interest in novelty (see Bolanos, Barrot, Berton, Wallace-Black and Nestler (2003).

WHAT CAUSES ATTENTION DEFICIT?

      Researchers have identified both biochemical and cognitive causes of attention deficit.  Biochemical causes include:

·       allergies

·       environmental toxins

·       viruses

·       low-protein/high-carbohydrate diets

·       fatty acid deficiencies

·       amino acid deficiencies

·       thyroid disorders

·       diabetes

·       low blood sugar

·       genetic errors of metabolism

Cognitive causes include:

·       depression

·       high IQ

·       boredom intolerance

·       sensory processing disorders (auditory or vestibular)

·       developmental delays

·       frontal lobe dysfunction. 

For more information about these causes and their treatments, read more below:

Vestibular Disorders              Auditory Disorders              Frontal Lobe          HOME

or read more in Sensory Processing Disorders.