Attention-deficit/hyperactivity disorder in adults: an overview
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"Attention-deficit/hyperactivity dis..." refers result in this paper
...Although these findings were not fully replicated in a similar PET study of adolescents (Zametkin et al 1993), which used siblings of ADHD children as control subjects, they are consistent with brain single photon emission computed tomography (SPECT) imaging in ADHD adolescents (Amen et al 1993). Ernst et al (1998) used PET with F18-DOPA to compare 17 ADHD adults and 23 healthy control adults. They used the ratio of the isotope concentration of specific regions to that of nonspecific regions to index DOPA decarboxylase activity and dopamine storage processes. Of three composite regions (prefrontal cortex, striatum, and midbrain), only the prefrontal cortex showed significantly lower F18-DOPA ratios in ADHD adults compared with control adults. The medial and left prefrontal areas were the most altered. Anterior cingulate cortex (ACC), lying on the medial surface of the frontal lobe, has strong connections to dorsolateral prefrontal cortex. Bush et al (1999) used a Stroop task to compare ACC activation in ADHD and non-ADHD adults....
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...Although these findings were not fully replicated in a similar PET study of adolescents (Zametkin et al 1993), which used siblings of ADHD children as control subjects, they are consistent with brain single photon emission computed tomography (SPECT) imaging in ADHD adolescents (Amen et al 1993). Ernst et al (1998) used PET with F18-DOPA to compare 17 ADHD adults and 23 healthy control adults. They used the ratio of the isotope concentration of specific regions to that of nonspecific regions to index DOPA decarboxylase activity and dopamine storage processes. Of three composite regions (prefrontal cortex, striatum, and midbrain), only the prefrontal cortex showed significantly lower F18-DOPA ratios in ADHD adults compared with control adults. The medial and left prefrontal areas were the most altered. Anterior cingulate cortex (ACC), lying on the medial surface of the frontal lobe, has strong connections to dorsolateral prefrontal cortex. Bush et al (1999) used a Stroop task to compare ACC activation in ADHD and non-ADHD adults. In contrast to control subjects, the ADHD adults failed to activate the ACC. Notably, in the prior study by Zametkin et al (1990), cingulate cortex was one of only four (out of 60) regions evaluated that still showed regional hypoactivity after global normalization. Because the stimulant medications are the treatment of choice for ADHD, several studies of ADHD adults examined changes in brain metabolism due to stimulant administration. They have not, however, produced consistent results (Ernst et al 1994; Matochik et al 1994; Matochik et al 1993). One study has used SPECT to assess dopamine transporter (DAT) activity in ADHD and control adults (Dougherty et al 1999). This study found DAT to be elevated by 70% in the ADHD adults compared with control adults, which is consistent with molecular genetic studies implicating DAT in ADHD (Faraone and Biederman 1999). In summary, the available data suggest that ADHD adults show frontal dopaminergic hypoactivity. In contrast, studies of adolescents show weaker results. Ernst et al (1998) offered two explanations of the differences between the adolescent and adult data....
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...Although these findings were not fully replicated in a similar PET study of adolescents (Zametkin et al 1993), which used siblings of ADHD children as control subjects, they are consistent with brain single photon emission computed tomography (SPECT) imaging in ADHD adolescents (Amen et al 1993). Ernst et al (1998) used PET with F18-DOPA to compare 17 ADHD adults and 23 healthy control adults....
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...Although these findings were not fully replicated in a similar PET study of adolescents (Zametkin et al 1993), which used siblings of ADHD children as control subjects, they are consistent with brain single photon emission computed tomography (SPECT) imaging in ADHD adolescents (Amen et al 1993). Ernst et al (1998) used PET with F18-DOPA to compare 17 ADHD adults and 23 healthy control adults. They used the ratio of the isotope concentration of specific regions to that of nonspecific regions to index DOPA decarboxylase activity and dopamine storage processes. Of three composite regions (prefrontal cortex, striatum, and midbrain), only the prefrontal cortex showed significantly lower F18-DOPA ratios in ADHD adults compared with control adults. The medial and left prefrontal areas were the most altered. Anterior cingulate cortex (ACC), lying on the medial surface of the frontal lobe, has strong connections to dorsolateral prefrontal cortex. Bush et al (1999) used a Stroop task to compare ACC activation in ADHD and non-ADHD adults. In contrast to control subjects, the ADHD adults failed to activate the ACC. Notably, in the prior study by Zametkin et al (1990), cingulate cortex was one of only four (out of 60) regions evaluated that still showed regional hypoactivity after global normalization....
[...]
...Although these findings were not fully replicated in a similar PET study of adolescents (Zametkin et al 1993), which used siblings of ADHD children as control subjects, they are consistent with brain single photon emission computed tomography (SPECT) imaging in ADHD adolescents (Amen et al 1993). Ernst et al (1998) used PET with F18-DOPA to compare 17 ADHD adults and 23 healthy control adults. They used the ratio of the isotope concentration of specific regions to that of nonspecific regions to index DOPA decarboxylase activity and dopamine storage processes. Of three composite regions (prefrontal cortex, striatum, and midbrain), only the prefrontal cortex showed significantly lower F18-DOPA ratios in ADHD adults compared with control adults. The medial and left prefrontal areas were the most altered. Anterior cingulate cortex (ACC), lying on the medial surface of the frontal lobe, has strong connections to dorsolateral prefrontal cortex. Bush et al (1999) used a Stroop task to compare ACC activation in ADHD and non-ADHD adults. In contrast to control subjects, the ADHD adults failed to activate the ACC. Notably, in the prior study by Zametkin et al (1990), cingulate cortex was one of only four (out of 60) regions evaluated that still showed regional hypoactivity after global normalization. Because the stimulant medications are the treatment of choice for ADHD, several studies of ADHD adults examined changes in brain metabolism due to stimulant administration. They have not, however, produced consistent results (Ernst et al 1994; Matochik et al 1994; Matochik et al 1993). One study has used SPECT to assess dopamine transporter (DAT) activity in ADHD and control adults (Dougherty et al 1999). This study found DAT to be elevated by 70% in the ADHD adults compared with control adults, which is consistent with molecular genetic studies implicating DAT in ADHD (Faraone and Biederman 1999). In summary, the available data suggest that ADHD adults show frontal dopaminergic hypoactivity. In contrast, studies of adolescents show weaker results. Ernst et al (1998) offered two explanations of the differences between the adolescent and adult data. First, the adolescent samples studied may have been more heterogeneous than the adult samples. Whereas all of the adults had persistent ADHD, some of the adolescent cases might have remitted by adulthood. Thus, frontal dopaminergic hypoactivity may be associated with persistent ADHD only. Alternatively, Ernst et al (1998) speculated that, because of brain maturation, the locus of ADHD’s dopamine abnormality might shift from the midbrain in childhood to the prefrontal cortex in adults....
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