ADHD: Learning Disability or Learning Difference
Many people are said to suffer from learning disabilities such as dyslexia or, very commonly, attention-deficit hyperactivity disorder (ADHD). Characteristic symptoms displayed by individuals with ADHD are impulsivity, hyperactivity, and lack of inhibition. Some people consider these types of conditions to be learning differences rather than learning disabilities. This paper argues that ADHD, in particular, is only a disability because society has been created in a way that caters to those who possess brain and social behavior that is closer to the average or the accepted norm. To do this I will start with an overview of the neurobiology of ADHD followed by a discussion of how the neurobiological differences contribute to the social construction of the idea of it being a disability. ADHD is more of a difference than a disability because disabilities are only socially constructed based on conditions that deviate from the norm. Individuals with ADHD have brains that function in different ways and at different speeds and intensities. As a result, they receive and process input differently than the average person but that does not necessarily have to qualify them as disabled.
Many biological, genetic, and environmental factors may contribute to ADHD. While very much research remains to be done in determining the causes, there are some fairly established ideas about the genetic and biological role players in the condition. Environmental factors, however, have been harder to prove and identify. Studies performed using twins suggest that there is a highly genetic component, accounting for up to 80%, of ADHD, which implies that there is also an environmental component. (3) Research comparing individuals with and without ADHD indicate that brain activity is different in the two. (2) Glucose levels were used as a measure of brain activity and researchers found that there were lower levels of glucose found in parts of the brain controlling attention in affected individuals than in unaffected individuals. (2) The lower levels of brain activity in individuals with ADHD point to specific parts of the brain that may not function in the same way or at the same speed as those without ADHD.
The frontal lobes of the brain are responsible for helping an individual concentrate and focus on tasks as well as for short-term memory. (1) The prefrontal cortex is an inhibitory mechanism, controlling behavior and inhibiting hyperactivity. (1) When the prefrontal cortex exhibits lower levels of activity than usual, as was the case in the studies that took measurements of glucose levels, inhibition is lowered. (4) Other parts of the brain, the caudate nucleus and the globus pallidus, control the rate at which signals from the prefrontal cortex are received. (4) In children with ADHD these parts of the brain will often be smaller than average at an early age. (4) This may indicate a reduction in inhibition function in the brains of individuals with ADHD, which could explain the impulsivity that is associated with ADHD. The reticular activating system is also central to whether or not an individual has ADHD because it excites the neurons of the prefrontal cortex. (1) If it does not excite them enough then the symptoms associated with ADHD can result. (1)
“Abnormal” levels of the neurotransmitters, dopamine and norepinephrine, are believed to be the cause of “abnormal” functioning in the prefrontal cortex and the reticular activating system respectively. (1) The functioning of the reticular activating system is largely dependent on the norepinephrine levels present. (1) If levels are lower than average this system will not excite the neurons of the prefrontal cortex as much as if levels were normal. Dopamine, when found in abnormally low levels, can limit the functioning of the prefrontal cortex. (4) Stimulant medications are often given to patients with ADHD with the expectation that levels of norepinephrine and dopamine in the brain will increase and allow the affected individuals to regain “normal” levels of inhibition. (1) There may, however, be a problem with how ADHD is viewed as a disability instead of a difference.
ADHD is commonly thought of as a learning disability because affected individuals cannot thrive in a learning environment or social setting the way non-ADHD individuals can. This is only the case, however, because the established learning environment caters to the average person whose brain functions “normally” as society defines it. “Abnormal” behavior is another characteristic associated with ADHD that is considered socially unacceptable. As a result, many children with ADHD are taught not to exhibit these behaviors. This viewpoint may be specific to different cultures because culture generally defines what behaviors are socially acceptable.
People with ADHD deviate from societal standards because their brains function differently than the average person. Therefore, they are labeled by society as disabled. The brain of an individual with ADHD has less ability to filter out extra input than the average brain. Why is it that someone who receives more input than the average person is disabled? Why are they not gifted or simply different? Color-blindness is also thought of as a disability. Individuals who can see fewer colors are receiving less visual input than the average person. ADHD and color-blindness are both labeled disabilities even though one implies extra input and the other less input than usual. It may be due largely to the established norms of society that guide the idea of disabilities. Differences in brain function are only disabling because people who have them live in societies where those differences result in a deviation from the established norm.
(2) Attention Deficit Disorder Association. <http://www.add.org/articles/causeadd.html>.
(3) Faraone, Stephen V. and Joseph Biederman (1998): Neurobiology of attention-deficit hyperactivity disorder. Biol Psychiatry 44:951-958.
(4) University of Maryland Medical Center. <http://www.umm.edu/patiented/articles/what_causes_attention-deficit_hyperactivity_disorder_000030_3.htm>.