ویژگی تجزیه و تحلیل EEG کمی در بزرگسالان مبتلا به اختلال نقص توجه

Attention deficit hyperactivity disorder (ADHD) in children and adolescents is characterised by excessive restlessness and an extremely poor concentration span, resulting in impulsive and disruptive behaviour. Clinical observation of ADHD in adults suggests that the early hyperactivity is diminished in terms of its impact on social and academic function, while impulsive-type behaviours remain unchanged. EEG studies in children and adolescents with ADHD have reported significantly more low-frequency power (predominantly theta) and less high-frequency power (predominantly beta) than in normal subjects. In normal children and adolescents, a decrease in theta power and an increase in beta power are found with increasing age, leading some researchers to interpret the EEG anomalies in ADHD as evidence of developmental delay. Studies of adults with ADHD compared with normal adult control subjects have found a reduction in the difference between the two groups, suggesting that the reduced beta activity apparent in ADHD children and adolescents changes with age. Adults with ADHD thus appear to have elevated low-frequency power as their predominant EEG difference from normal control subjects. The present study examined whether this EEG profile was specific to adult ADHD patients. Quantitative EEGs were recorded at rest in an eyes-open condition and used to compare 50 adult patients diagnosed with ADHD with 50 non-ADHD subjects (who presented for ADHD assessment but failed to meet the diagnostic criteria) and 50 control subjects. The ADHD group differed from both the non-ADHD and the control groups on the basis of elevated theta activity. The ADHD and control groups did not differ in beta activity, but relative theta was reduced and relative beta power was elevated in the non-ADHD group compared with both the ADHD and control groups. These results suggest that quantitative EEG may be used to differentiate ADHD adults from both normal adults and adults who display some of the symptoms of ADHD, but fail to meet the diagnostic criteria of ADHD.

Attention deficit hyperactivity disorder (ADHD) is recognised as a common childhood disorder, although the nomenclature and diagnostic criteria have frequently been redefined since the beginning of this century. Only in recent years has the American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders mentioned the existence of the disorder in adults. The current DSM-IV (American Psychiatric Association, 1994) does not provide a specific list of symptoms found in adults, and therefore diagnosis is dependent on the skills and knowledge of the diagnostician. According to Wender (1998), as many as 60–70% of children with ADHD continue to present with some of the symptoms of the disorder in adulthood. Studies of ADHD in adulthood have revealed some interesting findings. Adults with ADHD tend to respond as well as children to stimulant medication, and the effect is just as dramatic. The disorder may be genetically transmitted and biologically mediated. ADHD may be linked to conduct and learning disorders in children, and psychiatric disorders in adults, including alcohol and drug abuse. Finally, it has been suggested that the disorder may occur as a result of a dysfunction in neurotransmitter activity (Wender, 1998). Early retrospective studies examining ADHD identified a range of symptoms thought to constitute an adult form of the disorder. Menkes et al. (1967) carried out a study in which 14 patients initially assessed with problems of hyperactivity and learning difficulties were traced and assessed 25 years later. This early study provided some evidence that a proportion of adults with problems of hyperactivity and learning difficulties as children continued to manifest a variety of difficulties related to the hyperactive syndrome. Borland and Heckman (1976) and Feldman et al. (1979) reported that the majority of adults previously diagnosed with hyperactive child syndrome were in stable employment and self-supporting, although half of the subjects continued to display symptoms. Both of these studies reported that adults with ADHD had significantly lower self-esteem and a higher level of antisocial behaviour than the control group. Feldman et al. (1979) reported that, compared to their control group, a higher proportion of adults with ADHD had used marijuana. Drug use was not reported in the Borland and Heckman (1976) study. Other researchers (e.g. Shelly and Riester, 1972 and Wood et al., 1976) identified a deviant adult population and, following comprehensive assessments, made a retrospective diagnosis based on the childhood history of these patients. Their findings confirmed that some of the symptoms of the hyperactive child syndrome had continued into adulthood. Weiss and Hechtman (1986) identified symptoms such as organisational problems and concentration difficulties as characteristic of adults with ADHD. Furthermore, adults with the disorder are often regarded as being rude and impolite, and they typically underachieve in academic and vocational areas. According to Barkley (1990), adults with ADHD tend to be of lower socio-economic status and frequently change jobs, move residence and have more part-time employment. Furthermore, employers rate adults with ADHD as less able to work without supervision, complete assignments and meet the demands of the job. In a prospective follow-up study by Weiss and Hechtman (1986), social skills and interaction problems in adults with ADHD were identified, and this was especially apparent in the area of heterosexual interactions and assertive behaviour. Almost 10% of adults with ADHD had attempted suicide, with 5% dying as a result of suicide or accidental injury. Early peer relationship difficulties often result in interpersonal problems in adulthood; 75% have interpersonal problems, greater heterosocial-skill problems and difficulties with assertiveness (Weiss and Hechtman, 1986 and Barkley, 1990). Biederman et al. (1995) also demonstrated that ADHD was a significant risk factor for substance abuse. Barkley et al. (1993) reported that teenagers and young adults with ADHD had less sound driving habits and were more likely to receive traffic citations, particularly for speeding. Psychophysiological measures, such as electroencephalography (EEG), event-related potentials (ERPs), galvanic skin response and heart rate, have been employed in investigations of brain function in young and adolescent patients with ADHD in an attempt to clarify the aetiology of this disorder, as well as other childhood behaviour problems. Many of the findings failed to distinguish ADHD and control groups; however, where differences between the groups were demonstrated, they were consistently in the direction of low or diminished arousal in those with ADHD (Barkley, 1997). ERP studies (e.g. Johnstone and Barry, 1996 and Johnstone et al., 2001) have reported smaller amplitudes in ERP components of ADHD subjects, suggesting dysfunction in the pre-frontal regions of the brain. Several studies (e.g. Sieg et al., 1995) comparing cerebral blood flow in ADHD and normal children have consistently reported decreased blood flow to the pre-frontal regions. Many studies using quantitative electroencephalographic (qEEG) analysis on children with ADHD have reported an increase in low-frequency power (predominantly theta) compared with the age-matched control group (Satterfield et al., 1972, Satterfield et al., 1984, Satterfield and Cantwell, 1974, Montagu, 1975, Lubar, 1991, Mann et al., 1992, Matsuura et al., 1993, Clarke et al., 1998, Clarke et al., 2001a and Clarke et al., 2001b). Callaway et al. (1983) found that hyperactive children had significantly less beta power than a control group, and that there were no significant differences in theta activity. They also reported a significant decrease in alpha activity. This study suggested that the lower beta power was the best discriminator of all the EEG variables measured. This finding was also consistent with that of Dykman et al. (1982), who used principal component analysis of the EEG spectra at P3, P4, T1 and T2 sites and found that hyperactive children had lower values on a factor that primarily loaded in the beta band. The WHO study of Matsuura et al. (1993) also found that children with ADHD had significantly lower beta power than either a deviant behaviour group or the control group. A recent study by the authors (Bresnahan et al., 1999) extended the above electrophysiological findings in children by reporting that, in adolescents and adults diagnosed with ADHD, the elevated low-frequency power (delta and theta) apparent in a child ADHD group remained. Furthermore, beta activity, which has been reported to be significantly reduced in children (Mann et al., 1992, Clarke et al., 1998, Clarke et al., 2001a and Clarke et al., 2001b), was generally reduced, but the effect diminished from children to adolescents to adults. That is, the difference in beta power between the ADHD and control groups reduced with age. It was suggested that this reduction in the beta power difference between the ADHD and control groups corresponded with the reduction in the level of hyperactivity reported in adults in the clinical setting, while the maintenance of elevated low-frequency power corresponded to their continued high levels of impulsivity. The ADHD group maintained a higher theta/beta ratio compared with the control group, which decreased with age. There was also a decrease in total power with age in both the ADHD and control groups. More recently, research has focused on the biological and genetic causal factors in ADHD. Researchers in the field of genetics (e.g. Cook et al., 1995) have implicated the dopamine transporter gene in ADHD. Faraone et al. (1999) reported an association between the dopamine D4 (DRD4) gene and ADHD. That is, the diagnosis of ADHD among family members was predicted by the number of seven-repeat alleles. The role of the catecholamine neurotransmitters, dopamine and norepinephrine, has been implicated in the neuropharmacology of attention. The commonly used amphetamine, d-amphetamine, acts by releasing dopamine from presynaptic dopamine terminals, and l-amphetamine releases norepinephrine, as well as dopamine, by a similar mechanism. The symptoms of hyperactivity and impulsivity in ADHD are also thought to be mediated by dopamine, but different pathways are involved (Stahl, 2000). It appears reasonable to believe that these biological differences underlie both the symptomatology and EEG profiles of ADHD. In this study we examined quantified, resting EEG from 50 adults diagnosed with ADHD, 50 non-ADHD subjects (who presented with some of the symptoms of ADHD, but failed to meet the diagnostic criteria) and 50 control subjects. Our aim was to replicate our previous findings on adults with ADHD compared with the control group, and to identify whether electrophysiological measures could differentiate adults diagnosed with ADHD and those presenting with some of the features of the disorder. In terms of the overlap of some symptoms between the ADHD and non-ADHD groups, we proposed that the electrophysiological measures might reflect some of the symptom differences between subjects diagnosed with ADHD and the non-ADHD group.