Monday, 30 April 2012

Attention Deficit Disorder (ADD/ADHD) and Avoiding the Problem of Medicating a Developing Brain

Attention Deficit Disorder (ADD) appeared first in the 1980 Diagnostic and Statistical Manual of the American Psychological Association. Today ADD means different things to different professionals, depending upon their field, their level of experience and medical knowledge, and their cultural beliefs about how children should act.

Parents are often surprised to learn that there is no particular medical or neurological abnormality present in individuals diagnosed with attention deficit. Instead, the diagnosis depends upon subjective assessments by parents, teachers, or professionals with little or no understanding of the neuroscience of learning and behavior.

In fact, the National Institutes of Health (NIH) issued a consensus statement in 1999 warning that the causes and treatments of ADD are only speculative. In a very real sense, the diagnosis itself is only speculative.

In spite of this, individuals and even very young children who are given a diagnosis of ADD are typically given a prescription for an amphetamine, usually methylphenidate. This amphetamine is very similar to cocaine in terms of its effects on the brain (see Volkow et al, 1995); both drugs compete for the same binding sites on brain cells, both are taken up into the same areas of the brain, and both produce similar psychological effects. Perhaps the major differences are that methylphenidate remains in the brain much longer and the psychological expectations associated with the drug are much different.

Both methylphenidate and cocaine affect the brain by increasing levels of dopamine in the frontal lobes, an area responsible for motor planning, learning, problem solving, impulse control, memory, attention, language, analytical thinking and social behavior, and the striatum, an area responsible for processing and integrating sensory information.

Increased levels of dopamine make the brain feel powerful and happy and can produce addictive behaviors and responses. Elevated levels of dopamine also alter other neurochemicals and affect control muscle movements, sleep/wake cycles, hunger and satiety, arousal, heart rate, blood pressure, and stress responses.

If these altered levels of neurochemicals persist for too long (e.g. several weeks), the brain begins to try to bring the levels back to normal. If a neurochemical has been elevated for too long, the brain will begin to shut down some of the receptors for that neurochemical and will begin to kill off some of the transporters that move the neurochemical through the brain. We call this effect "downregulation."

After about three weeks it is possible to see these architectural changes with the electron microscope; after about four months the changes are significant. Four months on methlyphenidate, for example, will result in the loss of about 75% of the dopamine transporters and 20% of the dopamine receptors in the striatum (Vles et al, 2003). The striatum is an area of the brain critical for sensory processing, learning and memory.

Downregulation can have significant effects on the developing brain long after the drug has been withdrawn. Early exposure to methylphenidate, for example, has been linked to decreased interest in sex, food, emotional experiences, and novelty, and an increase in anxiety and stress levels in adolescence and adulthood (Bolanos, et al, 2003).

Of course, the brain can also "upregulate" by growing more transporters or receptors or making the remaining receptorsor more sensitive. However, upregulatio takes time.

It is dangerous to abruptly stop taking a medication after downregulation has occurred, so following a weaning schedule is recommended. The speed at which an individual is weaned from a drug like methylpheidate is based on the length of time they have been taking the medication and the dosage that they were receiving. A physician familiar with the neurological properties of the drug should be consulted before attempting to wean someone off such a drug.

Regardless of the problems associated with medications used to "treat" attention deficit, the question remains as to why a child is having problems paying attention. There are a host of metabolic, immunological, neurolgoical sensory and psychological causes of inattention including: metabolic disorders, allergies, toxins, sleep disorders, vitamin or fatty-acid deficiencies, thyroid disorders, diabetes, depression, boredom intolerance, high intelligence, high creativity, frontal lobe dysfunction, auditory or vestibular processing disorders, and learning disabilities.

Correctly identifying the underlying cause of inattention can help parents and medical professionals avoid the problems of exposing a developing brain to medications that alter neurochemicals, produce downregulation or create long-term side effects that may be far more serious than inattention.

The author, Michelle L. MacAlpine, Ph.D., is a cognitive developmental neuroscientist specializing in the assessment and treatment of sensory processing disorders, attention deficit, and developmental, academic and cognitive delays.

More information can be found at

Volkow ND, Ding YS, Fowler JS, Wang GJ, Logan J, Gatley JS, Dewey S, Ashby C, Liebermann J, Hitzemann R, et al. 1995 "Is methylphenidate like cocaine? Studies on their pharmacokinetics and distribution in the human brain." Arch Gen Psychiatry. 52(6):456-63.

Vles JS, Feron FJ, Hendriksen JG, Jolles J, van Kroonenburgh MJ, Weber WE. 2003 "Methylphenidate down-regulates the dopamine receptor and transporter system in children with attention deficit hyperkinetic disorder (ADHD)." Neuropediatrics. Apr;34(2):77-80.

BolaƱos CA, Barrot M, Berton O, Wallace-Black D, Nestler EJ. 2003."Methylphenidate treatment during pre- and periadolescence alters behavioral responses to emotional stimuli at adulthood." Biol Psychiatry. 54(12):1317-29

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