Summary

Given the complexity of interactions between neurotransmitters and their pharmacological effects, it seems unlikely that a simple deficiency or excess of any one neurotransmitter can account for the symptoms associated with ADHD or their improvement under drug treatment (Malone et al., 1994; Pliszka et al., 1996). Evidence suggests that dysfunctions of both noradrenergic and dopamin-ergic systems are involved, and several different theories have been suggested. One hypothesis is that noradrenergic deficits may be related to the cognitive and attentional problems associated with ADHD, while dopaminergic deficits may be related to hyperactivity (Mason, 1984). Another suggests that the central nora-drenaline system may be dysregulated in ADHD, leading to inefficient priming of the posterior attention system to external stimuli, while effective mental processing is affected by deficient dopaminergic function in the executive anterior attention system (Pliszka et al., 1996). Malone et al. (1994) suggest that excessive noradrenergic activity in the locus coeruleus and deficient dopaminergic activity in frontal-mesolimbic pathways results in the symptoms of ADHD, as stimulants have a dampening effect on the locus coeruleus and facilitate the release of dopamine from the striatum. However, as stimulants produce a similar behavioural response in individuals with and without ADHD, they may simply provide compensatory effects rather than targeting a specific neurochemical deficit (Solanto, 1998).

While the precise nature of the neurochemical deficits in ADHD remains unclear, there is growing evidence from several fields of biological research to suggest that dysfunction of frontal—basal ganglia dopamine pathways plays an important role (Castellanos, 1997; Swanson et al., 1998b). Mutations of dopamine receptor genes within this system that innervates fronto-striatal circuits may reduce dopamine activity and alter the normal development of dopamine systems (Swanson et al., 1998b,c) and may increase susceptibility for ADHD (Tannock, 1998). Children with ADHD may lack reciprocal inhibitory interactions between mesocortical and striatal dopamine neurons due to a deficit or delay in cortical development, resulting in reduced motor inhibition and goal-directed activity and increased environmentally dependant and inappropriate instinctual activity (Levy, 1991).

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Understanding And Treating ADHD

Understanding And Treating ADHD

Attention Deficit Disorder or ADD is a very complicated, and time and again misinterpreted, disorder. Its beginning is physiological, but it can have a multitude of consequences that come alongside with it. That apart, what is the differentiation between ADHD and ADD ADHD is the abbreviated form of Attention Deficit Hyperactive Disorder, its major indications being noticeable hyperactivity and impulsivity.

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