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EEG Studies

EEG studies have tended to find increased slowing of cortical electrical activity in children with ADHD, although there have been conflicting findings. Increased theta (4-7 Hz) activity in ADHD subjects compared with normal controls has been found in several studies, particularly in frontal regions (Clarke et al., 1998; Mann et al., 1992; Matsuura et al., 1993; Chabot & Serfontein, 1996). Increased delta (1-3 Hz) activity, especially in posterior regions, has also been observed (Clarke et al., 1998; Matousek et al., 1984). Mann et al. (1992) found that frontal theta power was increased in children with ADHD compared to normal controls during a resting condition and increased further during cognitive tasks. As theta activity decreases with age (Gasser et al., 1988), the findings for children with ADHD resembled those of younger children, suggesting a maturational delay in children with ADHD (Mann et al., 1992). Matsuura et al. (1993) also related their findings to brain immaturity in children diagnosed with ADHD. Chabot & Serontein (1996) also found increased theta in children with ADHD, which was greatest in frontal regions, but concluded that this represented a deviation from normal development rather than a maturational lag. Clarke et al. (1998) found increased theta power in children with ADHD in all regions including midline frontal. Frontal theta was greater for the ADHD-Combined type group than for the ADHD-Inattentive type group. The authors suggested this finding may be related to an association between frontal dysfunction and the overt behavioural problems exhibited by children with ADHD-Combined type (Clarke et al., 1998).

Reduced or slower alpha (8-12 Hz) activity has been found in children with ADHD (Callaway et al., 1983; Chabot & Serfontein, 1996; Clarke et al., 1998; Dykmanetal., 1982; Matsuura et al., 1993;Shetty, 1971), as has reduced or slower beta (13-21 Hz) activity (Callaway et al., 1983; Caresia et al., 1984; Chabot & Serfontein, 1996; Clarke et al., 1998; Dykman et al., 1982; Mann et al., 1992; Oades, 1987). Mann et al. (1992) found reduced beta activity in children with ADHD in posterior and temporal regions during cognitive tasks, and related this finding to maturational delays in brain systems involved in attention. Clarke et al. (1998) also found less beta activity in posterior regions in children with ADHD, and in addition found decreased alpha in all regions with the greatest difference in posterior regions. As fast frequency activity increases with age (Gasser et al., 1988), they suggested that their findings support the idea of a maturational lag in ADHD.

These findings of increased slow EEG activity (delta and theta) and decreased fast EEG activity (alpha and beta) suggest EEG slowing in children with ADHD and have been interpreted in terms of cortical underarousal and less active information processing (Ackerman et al., 1994; Chabot & Serfontein, 1996; Lubar, 1991; Mann etal., 1992; Oades, 1998; Tannock, 1998). This is supported by findings of increased deficits when the EEG is recorded during reading or drawing (Lubar, 1991; Mann et al., 1992). Some researchers have suggested that increased EEG slowing reflects delayed brain maturation in children with ADHD (Clarke et al., 1998; Matsuura et al., 1993; Ucles & Lorente, 1996; Tannock, 1998), while others disagree or suggest that development is deviant from normal rather than delayed (Callaway et al., 1983; Chabot & Serfontein, 1996).

This characteristic EEG slowing in children with ADHD has led to the use of Neurometrics or Quantitative EEG (QEEG) techniques, which have been claimed to be useful in diagnosing ADHD and in distinguishing between subtypes of the disorder. There are reports of these techniques being able to correctly classify between 75% and 95% of subjects as either normal or ADHD (Chabot et al., 1996; Chabot & Serfontein, 1996;Lubar, 1991; Mannetal., 1992; Monastra et al., 1999). Lubar (1991) suggests that the ratio of theta to beta is the best measure to distinguish those with ADHD from controls, although this is based on studies of children with attention deficit disorder without hyperactivity (Mann et al., 1992) and with learning disabilities (LD) with attention deficits (Lubar et al., 1985). Chabot et al. (1996) suggest that discriminant functions using combinations of QEEG features best discriminate children with ADHD from those with LD and from normal controls. However, Neurometrics is not generally viewed as a valid diagnostic tool for ADHD due to the lack of evidence supporting its clinical usefulness (Levy & Ward, 1995; Zametkin et al., 1998).

While increased slow EEG activity is found in most studies, there have been some conflicting findings. Kuperman et al. (1996) found increased beta activity in children with ADHD compared with normal controls, and suggested that this finding indicated elevated mental activity and overarousal in children with ADHD, which might contribute to sustained attention difficulties. Their subjects were drawn from a community rather than a clinical sample, but met DSM-III-R criteria for ADHD according to teacher reports. Chabot and Serfontein (1996) found increased beta activity, especially in frontal regions, in a subgroup of their ADHD subjects (13%), suggesting hyperarousal of fronto-striatal systems in these children, in contrast to the hypoarousal found in the majority of ADHD subjects. Clarke et al. (1998) excluded four ADHD subjects from their analyses because they had much higher levels of beta activity (>3 SD above mean) than the rest of the group. They concluded that this subset of subjects in their study and in the study by Chabot and Serfontein (1996) suggested there may be a subtype of ADHD characterised by increased beta activity. Another issue which raises questions about the assumption that EEG slowing characterises ADHD is that EEG slowing has been found for other clinical populations, especially LD (Ackerman et al., 1994; Lubar et al., 1985).

Event Related Potential (ERP) Studies

P3 in ADHD In ERP studies of ADHD, the most commonly examined component is the P3 (also labelled P300 or P3b), which is a late positive wave with a latency of 300 to 800 ms (Klorman, 1991). The amplitude of the P3 is influenced by stimulus probability, relevancy or novelty (Johnson, 1988; Klorman, 1991; Levy & Ward, 1995; Pritchard, 1981), and the latency of the P3 is influenced by cognitive, perceptual or memory load (Ford et al., 1982; Klorman, 1991). Because of these effects on its amplitude and latency, the P3 component is thought to reflect allocation of attention and to mark the end of stimulus evaluation processes which precede response selection and execution (Klorman, 1991). It has also been related to updating of internal representations and to working memory (Tannock, 1998).

The majority of studies examining the P3 have found that the amplitude of this component is smaller in children with ADHD than in normal controls (Frank et al., 1994; Holcomb et al., 1985, 1986; Jonkman et al., 1997; Kemner et al., 1996; Klorman et al., 1979, 1983; Loiselle et al., 1980; Michael et al., 1981; Novak et al., 1995; Overtoom et al., 1998; Robaey et al., 1992; Satterfield etal., 1990,1994; Strandburg etal., 1996; VanLeeuwenetal., 1988; Verbaten et al., 1994; Winsberg et al., 1993). There are contradictory findings however, as some studies have reported no significant group differences in P3 amplitude (Frank et al., 1998; Satterfield et al., 1988; Taylor et al., 1993; Winsberg et al., 1997).

Smaller P3 amplitude in ADHD subjects has been found in both auditory and visual modalities and in response to both target and non-target stimuli and has been interpreted in different ways. It may reflect a general underarousal or underreactiv-ity to task relevant stimuli (Satterfield et al., 1990; Tannock, 1998), cognitive and information processing difficulties (Franketal., 1994; Klorman, 1991; Satterfield et al., 1994; Winsberg et al., 1993), or deficits in selective or sustained attention (Holcomb et al., 1985; Loiselle et al., 1980; Michael et al., 1981; Overtoom et al., 1998). The reduction in P3 amplitude in children with ADHD is generally associated with poorer performance on the task used to elicit the ERP, leading to the suggestion that it is likely to reflect deficient cognitive processing rather than a generalised neurophysiologic deficit (Klorman, 1991; Levy & Ward, 1995; Tannock, 1998).

The specific cognitive deficits associated with smaller P3 amplitude in children with ADHD are dependent on the tasks used to elicit the ERP. Visual continuous performance and oddball tasks fairly consistently elicit smaller P3 to target stimuli in children with ADHD than in normal controls and this result has been interpreted as reflecting attention deficits (Klorman et al., 1979; Michael et al., 1981; Overtoom et al., 1998) or inappropriate allocation of attentional resources (Holcomb et al., 1985). Auditory oddball or tone discrimination tasks have elicited smaller P3 amplitude to target tones in children with ADHD in some studies (Frank et al., 1994; Holcomb et al., 1986; Kemner et al., 1996), but not in others (Frank et al., 1998; Lazzaro et al., 1997; Winsberg et al., 1997). Kemner et al. (1996) found that reduced P3 to deviant auditory stimuli occurred irrespective of the task relevance of the stimulus and concluded that smaller P3 amplitude in ADHD is due to abnormal processing of deviant stimuli. Frank et al. (1994) suggested that the reduced P3 amplitude in their ADHD with LD group reflects cognitive and processing difficulties rather than an attention deficit.

Smaller P3 amplitude has also been found using selective attention tasks, which simultaneously present visual and auditory oddball paradigms and require the subject to attend to one modality or the other, or require subjects to attend to tones presented to one ear or the other. These results have been interpreted as suggesting that children with ADHD have a deficit in the activation of P3 processes (Jonkman et al., 1997), a selective attention dysfunction (Loiselle et al., 1980), a deficit in preferential processing of attended stimuli (Satterfield et al., 1994), or insufficient locus coeruleus activity that is normally triggered by attended, task-relevant stimuli (Satterfield et al., 1990). Other visual tasks employed in ERP studies that have resulted in findings of smaller P3 amplitude in children with ADHD include categorization (Robaey et al., 1992), spatial orienting (Novak et al., 1995) and delayed-go tasks (Brandeis et al., 1998). Smaller P3 amplitude in children with ADHD has been found in a variety of different task conditions and modalities, however, the P3 to target stimuli consistently shows the greatest reduction in amplitude in children with ADHD compared to normal controls, in particular when task performance is also deficient (Brandeis etal., 1998; Klorman, 1991). This common finding is therefore likely to reflect deficits in cognitive processing of task-relevant stimuli in children with ADHD.

Many studies have used only a few electrodes to record the ERP and have discussed overall P3 amplitude reductions in terms of cognitive processes but not in terms of topography. The P3 to visual targets is generally found to have a maximum amplitude over parietal regions (Klorman, 1991; Satterfield et al., 1988). Differences in topography in children with ADHD may be as important as overall differences in amplitude. Some recent studies have used larger numbers of electrodes and have examined the topography of the P3 in children with ADHD. Using 17 electrodes and an auditory tone discrimination task, Johnstone & Barry (1996) found that P3 amplitudes to target stimuli were smaller in the posterior brain region but larger in the frontal region for children with ADHD compared with normal controls. They suggested that the ADHD group utilized an additional frontally distributed cognitive process when processing task-relevant stimuli, which might reflect an attentional compensation mechanism (Johnstone & Barry, 1996). The laterality of the P3 component may also differ in children with ADHD. Oades et al. (1996) used 19 electrodes and an auditory tone discrimination task and found a right-biased P3 asymmetry in normal controls that was absent in their ADHD group, suggesting a right hemisphere impairment in terms of stimulus processing in children with ADHD.

Other researchers have used ERP microstates and source localization techniques to examine the topography of the ERP in children with ADHD and controls (Brandeis et al., 1998; Van Leeuwen et al., 1998). Microstates are successive ERP segments with stable topographies that vary in duration and are related to different stages of information processing (Brandeis & Lehmann, 1986). The global field power (GFP), defined as "the spatial standard deviation over all voltages in a map" (Van Leeuwen et al., 1998, p. 100) can be calculated for each microstate and is similar to an amplitude measure. Van Leeuwen et al. (1998) recorded the ERP at 30 electrode sites while children performed the A-X version of the CPT. They found no significant group differences in the topography of ERP microstates, but found reduced GFP in a CNV/P3 microstate to cues (the A) in the ADHD group. The topography of this microstate was defined by a posterior positivity in both the ADHD and control groups. Source localization analysis using low resolution electromagnetic tomography (LORETA: Pascual-Marqui et al., 1994) identified posterior sources for this microstate that were less right biased in the ADHD group. The authors concluded that their results suggest impaired orienting to cues in children with ADHD, possibly involving the posterior attention system (Van Leeuwen et al., 1998). Using a delayed-go task, Brandeis et al. (1998) also found reduced GFP in late P3 type microstates in their ADHD group and related this finding to less efficient posterior orienting mechanisms. These results are consistent with findings of reduced parietal P3 amplitude in children with ADHD and suggest that possible deficits in parietal brain mechanisms in ADHD and their relationship to well established frontal deficits should not be overlooked (Brandeis et al., 1998; Van Leeuwen et al., 1998).

Reduced P3 amplitude has also been found in several other clinical populations including children with autism, learning disabilities and schizophrenia, so this effect does not seem to be specific to ADHD (Klorman, 1991; Levy & Ward, 1995; Oades, 1998). A recent study addressed the issue of the specificity of abnormal ERPs to ADHD using auditory and visual oddball tasks, and found that only the parietal P3 amplitude to deviant auditory stimuli was smaller in children with ADHD than in groups of autistic and dyslexic children (Kemner et al., 1998). In an earlier study, Kemner et al. (1994) found that visual P3 amplitude in autistic children did not differ from that of children with ADHD or dyslexia. Frank et al. (1994) found that auditory P3 amplitude was smaller in children with learning disabilities (LD) and in children with LD and ADHD than in normal controls. They suggested that smaller P3 amplitude in children with LD and/or ADHD is due to cognitive processing difficulties rather than an attention deficit. In a later study (Frank et al., 1998), they found significantly smaller auditory P3 amplitude than normal controls in a LD group and a LD + ADHD group, but not in a pure ADHD group. They again suggested that P3 abnormalities in children with learning and attentional problems reflect processing rather than attentional deficits.

Abnormalities in P3 latency in children with ADHD have also been reported. Some studies that examined P3 latency to visual stimuli found it to be longer in ADHD subjects than in normal controls (Holcomb et al., 1985; Strandburg et al., 1996; Sunohara et al., 1997; Taylor et al., 1993). This finding has been interpreted as suggesting that stimulus evaluation and attentional processes are slower and more difficult for children with ADHD (Holcomb et al., 1985; Klorman, 1991; Tannock, 1998; Taylor et al., 1993). Holcomb et al. (1985) also found that P3 latency in their ADHD group increased across blocks of their visual target detection task, suggesting a deterioration of these processes over time. In contrast, shorter P3 latencies in children with ADHD have been reported for a visual categorization task (Robaey et al., 1992) and an auditory selective attention task (Loiselle et al., 1980), while other studies have found no significant group differences in P3 latency (Holcomb et al., 1986; Lazzaro et al., 1997; Michael et al., 1981; Satterfield et al., 1988, 1994). Some of the discrepancies in findings for P3 latency may be due to the different tasks employed. Visual target detection tasks may produce longer P3 latencies in children with ADHD due to slowed evaluation processes (Holcomb et al., 1985; Strandburg et al., 1996; Sunohara et al., 1997; Taylor et al., 1993), while tasks requiring selective attention or categorization may produce shorter P3 latencies due to less efficient modulation of processing speed according to task demands (Loiselle et al., 1980; Robaey et al., 1992).

N1 and N2 in ADHD While the majority of studies find that P3 amplitude, especially to target stimuli, is smaller in children with ADHD, it is less clear whether this is preceded by abnormalities in earlier ERP components and thus earlier stages of information processing (Tannock, 1998). The other most commonly examined ERP components in studies of ADHD are earlier negative waves, the N1 and N2. The N1, occurring at a latency of around 100ms, is generally larger to attended than to non-attended stimuli and is thought to reflect an attentive division between concurrent stimulus channels (Loiselle et al., 1980). The N2 occurs at a latency of around 200 ms, is generally larger to novel than to frequent stimuli, and is thought to reflect automatic orienting to deviant stimuli (Robaey et al., 1992; Satterfield et al., 1988). N2 has also been related to stimulus comparison and categorization (Oades, 1998; Robaey et al., 1992), and to inhibition (Overtoom et al., 1998; Yong-Liang et al., 2000). The increased negativity to rare versus frequent stimuli is termed mismatch negativity (MMN), while the difference between attended and non-attended stimulus ERPs is termed processing negativity (PN). These early negative components of the ERP have predominantly been studied in ADHD using selective attention tasks.

The N1 to attended auditory targets in a selective attention task using simultaneously presented visual and auditory oddball paradigms was found to be significantly smaller in children with ADHD than in normal controls (Satterfield et al., 1994). The 6 year old ADHD subjects in this study also showed a smaller difference in N1 amplitude between attended and non-attended stimuli than controls. A similar finding has been obtained for older ADHD subjects (12 to 14 years old) using an auditory selective attention task (Loiselle et al., 1980; Zambelli et al., 1977). These results have been interpreted as reflecting a selective attention dysfunction in children with ADHD (Klorman, 1991; Loiselle et al., 1980). In an auditory oddball task that did not require selective attention, no group differences in N1 amplitude were found (Winsberg et al., 1997).

A smaller N2 amplitude to auditory targets in children with ADHD has been found in some studies (Satterfield & Braley, 1977; Satterfield & Schell, 1984; Satterfield et al., 1988, 1994; Winsberg et al., 1993). In addition, children with ADHD have been found to have a smaller difference in N2 amplitude between attended and non-attended stimuli (Satterfield et al., 1994) and between target and non-target stimuli (Satterfield et al., 1988). These findings of reduced N2 amplitude have been suggested to reflect deficiencies in children with ADHD in preferential processing of attended stimuli and in orienting to target or novel stimuli (Satterfield et al., 1988, 1994). In contrast, using visual categorization tasks Robaey et al. (1992) found that ADHD boys had a larger N2 amplitude than normal controls, as did Prichep et al. (1976) using an auditory guessing paradigm. Robaey et al. (1992) suggested that the parieto-occipital N2 was related to stimulus classification and was larger in ADHD subjects due to enhanced automatic processes. Prichep et al. (1976) related their finding of larger N2 amplitude to low arousal levels in children with ADHD, as N2 amplitude was reduced after administration of methylphenidate. In other studies, no differences in N2 amplitude were found between ADHD subjects and normal controls using an auditory oddball task (Winsberg et al., 1997), visual feature detection tasks (Holcomb et al., 1985; Taylor et al., 1993) or the continuous performance task (Overtoom et al., 1998). Overtoom et al. (1998) did find however, that N2 amplitude was smaller in a subgroup of children with ADHD and comorbid ODD. They suggested that the fronto-central N2 component to non-targets in the AX-CPT (A followed by not X) was related to inhibitory processes and that deficiencies in these processes or increased impulsivity may be restricted to the comorbid group. Yong-Liang et al. (2000) found that frontal N2 amplitude was larger for no-go stimuli in a go/no-go task and suggested that it reflected inhibition of responding. This N2 amplitude was smaller in ADHD subjects than in controls, but only when the no-go task was performed second, suggesting an inhibitory regulation problem in ADHD (Yong-Liang et al., 2000). A related finding is that of Johnstone & Barry (1996), who found that frontal N2 amplitude to non-targets in a tone discrimination task was smaller for children with ADHD compared to normal controls. Johnstone & Barry (1996) also found that N2 amplitude was larger in the posterior region in children with ADHD, perhaps consistent with the findings of Robaey et al. (1992).

Mismatch negativity (MMN), an enhancement of early negativity in the ERP to infrequent target stimuli compared to that to frequent standard stimuli, is thought to be related to automatic orienting to novel stimuli and to be a process which is not under voluntary control (Satterfield et al., 1988). MMN was found to be smaller in children with ADHD in a selective attention task (Satterfield et al., 1988), but was found to be normal using an auditory oddball task (Winsberg et al., 1997). Children with ADHD are often said to be less responsive to target stimuli, but this is more frequently linked with smaller P3 than with smaller MMN. Oades et al. (1996) found that MMN was left lateralized in children with ADHD but right lateralized in normal controls, which in conjunction with a similar finding for P3 laterality was interpreted as suggesting right hemisphere impairment in ADHD.

Processing negativity (PN) is an enhancement of early negativity in the ERP to attended compared to non-attended stimuli and is thought to reflect attentional processes that are under voluntary control (Satterfield et al., 1988). PN has been found to be smaller in children with ADHD in several studies using selective attention tasks (Jonkman et al., 1997; Satterfield et al., 1988, 1990, 1994). These findings have been interpreted as suggesting poor discrimination and poor preferential processing of attended stimuli and are consistent with deficits in selective attention (Klorman, 1991; Satterfield et al., 1988, 1994). Reduced PN in the frontal region in children with ADHD may also be consistent with findings of reduced frontal blood flow (Lou et al., 1984, 1989) and reduced frontal metabolism (Zametkin et al., 1990) in ADHD (Satterfield et al., 1988).

As the above discussion indicates, the results for N1, N2, MMN and PN vary from study to study. Methodological differences between studies make it difficult to directly compare these results. Some of the discrepancies between results for N1

and N2 may be due to differences in the tasks and modalities used to elicit the ERP (Klorman, 1991), to differences in the age groups studied and developmental effects (Levy & Ward, 1995; Oades, 1998; Satterfield et al., 1990), to heterogeneity of subject groups and comorbidity in ADHD subjects, or to differences in the electrode sites used to record the ERP. Posterior/anterior differences (Johnstone & Barry, 1996) and laterality differences (Oades et al., 1996) suggest that topography may be important for the early negative ERP peaks, as for the P3. Smaller negative ERP components in children with ADHD are most consistently found in the auditory rather than the visual modality (Tannock, 1998), and when selective attention tasks are used that include a set of stimuli to be ignored and place greater demand for selective attention (Klorman, 1991).

Latencies for the early negative ERP peaks are not often reported. Using visual feature detection tasks Sunohara et al. (1997) found that N2 latency was longer in children with ADHD than normal controls, while Taylor et al. (1993) found no group difference in N2 latency. The latency of the auditory N1 component was found to be shorter in children with ADHD than in controls in two studies (Oades et al., 1996; Satterfield et al., 1994). This finding may suggest that children with ADHD process perceptual information faster than their normal peers (Oades, 1998; Oades et al., 1996). In contrast, Loiselle et al. (1980) found no group difference for auditory N1 latency.

ERP Studies of the CPT in ADHD The continuous performance task (CPT) has been used in several studies to examine attentional processes and the associated visual ERP. Klorman et al. (1979) found reduced P3 amplitude at Cz in hyperactive children compared with normal controls when they performed the X version of the CPT. P3 amplitude to both targets and non-targets was reduced in the hyperactive group, and their task performance was significantly worse. These results were replicated in afollow-up study (Michael et al., 1981), which in addition found reduced P3 amplitude at both Cz and Pz and deficient task performance in hyperactive children during a B-X version of the CPT (similar to CPT-AX, using B as the cue rather than A). The P3 to both targets and non-targets was significantly smaller in the hyperactive group for the CPT-X, while only the P3 to targets was reduced for the CPT-BX. These findings of reduced P3 amplitude in hyperactive children during the CPT were concluded to reflect deficits in sustained attention (Klorman et al., 1979; Michael et al., 1981).

More recently, Overtoom et al. (1998) recorded the ERP at Fz, Cz, Pz and Oz while children with ADHD and normal controls performed the A-X version of the CPT. They suggested that the parietal P3 to targets (X preceded by A) could be used as a measure of attentional processes, while the fronto-central N2 to non-targets (not-X preceded by A) could be used as a measure of inhibitory processes. The ADHD group had a smaller parietal P3 amplitude to targets, indicating attention deficits. But there were no group differences in fronto-central N2 to non-targets, indicating a lack of expected inhibition deficits in the ADHD group. These results were consistent with task performance results, as the ADHD group performed significantly worse on an inattention score but not on an impulsivity score. The authors concluded that deficient processing in the ADHD group was related to attention rather than to response inhibition (Overtoom et al., 1998). Similar results for early negative and late positive ERP components were obtained by Strandberg et al. (1996) for two versions of the CPT. These authors concluded that their findings of reduced P3 amplitude and longer P3 latency reflect processing problems in children with ADHD that occur in later rather than early stages, as ERP components related to earlier stages of processing were normal.

In a recent ERP microstate study of the CPT-AX, Van Leeuwen et al. (1998) found reduced GFP in a CNV/P3 microstate (277-605 ms) to the cue (A) in children with ADHD, but not to the target (X). The authors concluded that impaired orienting to cues involving a posterior attention system, rather than impaired target processing involving frontal executive processes, was involved in ADHD children's deficient performance of the CPT-AX (Van Leeuwen et al., 1998).

Steady-State Visually Evoked Potential

In our research we have examined differences in the steady-state visually evoked potential (SSVEP) between children with ADHD and healthy controls. Using the technique known as steady-state probe topography (SSPT) enables examination of disturbances in the spatial distribution and the dynamics of brain electrical activity in children with ADHD. Seventeen boys with ADHD (mean age = 10 years 9 months, SD = 2 years) and seventeen healthy male controls (mean age = 11 years, SD = 1 year 7 months) performed computerised tasks while their brain electrical activity was recorded from 64 scalp electrodes. A 13 Hz sinusoidal flicker was presented simultaneously to evoke the SSVEP. The subject characteristics and methods used are described in more detail in Silberstein et al. (1998). Subjects performed a low demand visual vigilance task (the reference task) and the AX version of the continuous performance task (CPT-AX).

We found that, compared to the mean amplitude during the reference task, control subjects demonstrated SSVEP amplitude reductions during the A-X interval. Transient amplitude reductions occurred in frontal regions, while right parietal and occipital amplitude reductions were sustained throughout the 3.5 second A-X interval. Reductions in SSVEP amplitude during cognitive tasks have previously been associated with increased task related cortical activation (Farrow et al., 1996; Silberstein et al., 1990, 1995). In contrast to the control group results, ADHD subjects demonstrated much smaller frontal amplitude reductions and increased parieto-occipital amplitude, suggesting they failed to increase regional cortical activation according to task demands. Group differences in SSVEP amplitude were prominent in the right parietal region where sustained increased activation was

Figure 1. SSVEP amplitude during the CPT-AX target interval for ADHD and control groups at electrode 57 (right parietal). The dashed horizontal line represents the mean normalized amplitude for the reference task and is set to zero for both groups. CPT-AX related amplitude changes are therefore expressed as differences from the mean reference task amplitude. The vertical lines indicate the times of onset and offset of the cue A and onset of the target X.

Figure 1. SSVEP amplitude during the CPT-AX target interval for ADHD and control groups at electrode 57 (right parietal). The dashed horizontal line represents the mean normalized amplitude for the reference task and is set to zero for both groups. CPT-AX related amplitude changes are therefore expressed as differences from the mean reference task amplitude. The vertical lines indicate the times of onset and offset of the cue A and onset of the target X.

seen in the control group. Figure 1 illustrates the amplitude differences at electrode 57, a right parietal site. In this region the control group show a large amplitude reduction, which follows the appearance of the A and is sustained until after the appearance of the X. In the ADHD group there is a relative amplitude reduction at the disappearance of the A, but the amplitude is increased compared with the reference level throughout the A-X interval.

Control subjects also demonstrated significant SSVEP latency reductions in the right prefrontal region at the appearance and disappearance of the A and the appearance of the X. Reductions in SSVEP latency are interpreted as reflecting increased efficiency of coupling between neural networks and faster information processing (Silberstein et al., 1996; 1998). Right prefrontal latency reductions were much smaller and occurred later in the ADHD group, who predominantly demonstrated latency increases or slower processing at frontal and temporal sites throughout the A-X interval. Figure 2 illustrates the SSVEP latency at electrode 4, a right prefrontal site. In controls, the disappearance of the A coincides with a large reduction in SSVEP latency and smaller latency reductions occur at the appearances of the A and the X. However, in the ADHD group only very small latency reductions compared with the reference level are evident at the disappearance of the A and the appearance of the X.

Figure 2. SSVEP latency during the CPT-AX target interval for ADHD and control groups at electrode 4 (right prefrontal). The dashed horizontal line represents the mean latency for the reference task and is set to zero ms for both groups. CPT-AX related latency changes are therefore expressed as differences from the mean reference task latency. The vertical lines indicate the times of onset and offset of the cue A and onset of the target X.

Figure 2. SSVEP latency during the CPT-AX target interval for ADHD and control groups at electrode 4 (right prefrontal). The dashed horizontal line represents the mean latency for the reference task and is set to zero ms for both groups. CPT-AX related latency changes are therefore expressed as differences from the mean reference task latency. The vertical lines indicate the times of onset and offset of the cue A and onset of the target X.

The largest group differences occurred at the disappearance of the A (figure 3a). At this time, there is extensive activation in the controls, predominant in the parieto-occipital region. In contrast, in ADHD subjects increased activation is restricted to the prefrontal region and there is reduced activation in the parieto-occipital region. The disappearance of the A also coincides with large latency reductions in the controls at frontal and temporal sites, moreso in the right hemisphere. While in the ADHD group a latency increase is predominant in these regions. As the Hotelling's T maps show, the SSVEP differences in the control group at the disappearance of the A are highly significant for this single comparison in most regions.

In another study we examined changes in the SSVEP following methylphenidate administration in 60 boys with ADHD (mean age = 10 years 1 month, SD = 1 year 10 months), who were recently diagnosed according to DSM-IV criteria and had never previously been treated with stimulants. We compared SSVEP amplitude and latency during the A-X interval before methylphenidate with the SSVEP 90 minutes after administration of a 0.3 mg/kg dose of methylphenidate. We found regional increases in activation and reductions in latency that partly coincided with regions most active in the control group in

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