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January2004 Vol.41 Issue:      1 Table of Contents
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Neurophysiological study and intelligence of conduct disorder

Wageeh Abd El-Nasser Hassan, Ola Ahmed Shawky, Aly Mohamed Aly
Department of Neuropsychiatry, Assiut University

ABSTRACT

Many studies presented the relation between children and adolescent with behavioral disorders and EEG changes and auditory event related potential (P300). This research was designed to study neurophysiological changes and intelligence associated with conduct disorder. P300 and EEG were done for 45 students with conduct disorder (CD) from different secondary schools in Assiut City and 45 normal students as a control group from the same schools. While Wechsler Intelligence Scale (WIS) was done for 101 students with CD and 100 normal students as a control group. The results of this study revealed that P300 amplitude is significantly lower in students with CD than control group. The commonest paroxysmal activity in EEG was spike and slow complex (55.5%), followed by sharp activity (28.9%). The background activity was significantly lower in students with CD than control group. CD students had significantly lower total and  performance IQ than control group, while no significant difference as regard  verbal IQ. These changes may suggest the presence of subtle anterior brain dysfunction among CD.

(Egypt J. Neurol. Psychiat. Neurosurg., 2004, 41(1): 313-325).

 




INTRODUCTION

 

Conduct disorder is a complicated group of behavioral and emotional problems in youngster. Children and adolescents with this disorder have great difficulty following rules and behaving in a socially acceptable way, they are often viewed by other children, adults and other social agencies as “bad” or delinquent, rather than mentally ill1.

The etiologies of conduct disorder (CD), antisocial personality disorder (APD), and other externalizing disorders have frequently been interpreted in a neurodevelopmental context2,3.

P300 is a positive going electroencephalographic potential elicited by auditory, visual or somatosensory stimuli that are both rare and demanding attention (i.e., task-relevant). P300 has been viewed as an electroencephalographic component of the orienting response4. Accordingly, the P300 decrements found in high risk groups have been viewed as reflecting impairment of those cognitive processes that subserve orienting ,such as arousal, selective attention , short term memory , or motivation5.

P300 component has been shown to be sensitive to a wide range of psychiatric disorders6,1,7,8,9 whose neurological effects are recognized as subtle.

A recent localization study employing both functional magnetic resonance imaging and dipole modeling techniques suggested that P300 recorded from the scalp originate from neural generators in frontal (anterior cingulate) and parietotemporal (supramarginal gyrus) regions of the brain10.

The last area of the brain to mature is the frontal region, which regulates higher level cognitive operation, including foresight and impulse control11. Positron emission topography (PET) was used to demonstrate reduced regional glucose metabolism in the prefrontal cortex (i.e. orbitofrontal, anterior medial, superior frontal) but not in other brain regions, among violent criminals compared with age and sex-matched control subjects12.

Brain maturation can interact with other variables, such as alcohol dependence or personality and indirectly affect P300 amplitude13.

Bauer et al.14, concluded that the frontal and parietotemporal generators of P300 are differentially sensitive to the effect of CD at different stages of brain development. They reported that among teenagers younger than 16.5 years with CD, P300 amplitude decrement were only detected over the posterior region. However among affected teenagers greater than this median age, P300 amplitude was only detectable over the frontal region.

Adolescents with conduct problems would be less able to shift their response set when required by task instructions. It was predicted that preservative responding would be related to reduced P300 amplitude at frontal electrode sites15.

This age related shift in the topography of P300 amplitude difference, from posterior to anterior regions, follows the normal topography of brain development. Also, they reported that the results of a number of studies point to frontal brain dysfunction as a factor that correlate with the continuance of CD problems in adulthood. In the study conducted by Bauer et al.11, the subjects with CD failed to show a maturational changes in frontal P300 amplitude across the age range of 14-20 years. Costa et al.,8 reported that the frontal brain of individuals with a history of serious CD fails to undergo the normal pattern of maturation. In non-drug dependent subjects, an association between reduced P300 amplitude and antisocial behavior has been found in children with conduct problems and in adults with antisocial personality disorder (APD)14. The P300 amplitude reduction was significantly correlated with the number of childhood conduct disorder symptoms1.

Theories linking adult APD to altered brain development derive from the fact that the DSM-IV diagnosis of APD also requires evidence of childhood CD. Thus the presence of APD indicates that a dysfunctional behavior pattern was present during childhood and failed to resolve in adulthood16. A comparable neurodevelopmental theory for adolescent CD is based on the premise that some behavioral problems are present in all young children but normally abate over time17.

Electroencephalographic (EEG) changes in CD have been the field of several studies long period ago. Long period before the presence of the term CD and its diagnostic criteria, many studies presented the relation between children and adolescents with behavioral disorders, behavioral problems, psychopaths with aggressive behavior, delinquent children and EEG changes 18.

Whitman et al.,19 and Hoare20 in their studies on children with behavioral disturbances including antisocial behavior, found a temporal lobe focus to be associated with the disturbed behavior during the recording and may do so in such a way as to import a paroxysmal quality to the record . Tsuboi21 in his study on children with CD found that they usually show nonspecific EEG abnormalities, positive spikes are recognized as the most common type of EEG changes in this population.

Three principle neuropsychological deficits have been reported in relation to CD. These include differences in IQ, impaired executive control functions (ECF) e.g. planning or delay of actions, anticipation of outcome, inhibiting or changing responses, maintaining purposeful effect, self-monitoring of behaviors, and language deficits22. Dery et al.,23 reported that, although juvenile delinquents can present with a wide range of cognitive impairment, as evidenced by their performance on neuropsychological tests, the deficits reported in the literature involve primarily verbal abilities and, to a lesser extent, executive functions. They hypothesized that neuropsychological deficits may be a risk factor for CD. Moffitt, et al.,17 found that poor neuropsychological status is related to early onset of delinquency and predicts subsequent persistent antisocial behavior.

The presence of CD has been associated with lower IQ scores even after controlling socioeconomic and demographic factors. Performance IQ is noticeably higher than verbal .IQ22. Also they noted that impairment may influence the course of the disorder through factors such as academic under-achievement.

The relationships of ECF indices to behavioral problems also appear to be relatively independent of IQ and non-executive cognitive function such as memory24.

ECF are believed to be subserved by the prefrontal cortical regions, so Raine et al.,25 by using magnetic resonance imaging and autonomic indices, found volumetric reductions in pre-frontal cortical regions in the antisocial group only compared to other psychiatric and non psychiatric disorders . Also Pennington et al.,26 suggest that early frontal dysfunctions may have main effect on CD.  

 

SUBJECTS AND METHODS

 

One hundred and one students with CD were selected from secondary schools of Assiut City. They include both technical and general schools. The age of students ranged from 14-18 years.

Students with CD were diagnosed according to Adolescence Psychopathology Scale (APS)27 and confirmed by clinical interview and diagnostic criteria of DSM-IV28.

Clinically, students with CD were classified into childhood onset type and adolescent onset type and the degrees of severity into mild, moderate and severe (APA)28.

One hundred students, who were negatively screened in the same schools, were considered as control group. They were matched with the positive groups as regard the age, sex and level of education.

 

Used Instruments:

1.      Adolescent Psychopathology Scale (APS)27.

2.      Clinical interview and diagnostic criteria of DSM-IV28 to confirm the diagnosis of CD.

3.      Instruments used in the psychometric study and neuropsychological study: -

a.   WIS according to the age of the students either we applied the adulthood or childhood form29,30.

b.   Convential wakefulness EEGs were obtained using an 8 channels Nihon Kohden equipment model (4217) employing scalp electrodes placed according to the international 10-20 system with bipolar and referential montages. Hyperventilation was used as a provocative test.

c.   Event related potentials (ERPs) were elicited with an auditory discrimination task paradigm by presenting a series of binaural 1,000 Hz (standard) versus 2,00 Hz (target) tones at 70 dB with a 10-ms rise/fall and 40 ms plateau time. Tones were presented at a rate of 1.1/s, with target tones occurring randomly with 0.2 probability. Subjects were sitting with their eyes closed and were instructed to mentally count the number of the target, but not the frequent tones, and then asked to report the number of target tones counted at the end of each run. Evoked potentials were recorded from the scalp electrodes placed at F3 and F4 and were referred to linked ears. Filter setting were 0.5 and 7- Hz, analysis time 1 second sensitivity 30 uV and duration of stimulus 0.1 ms. To assess performance accuracy at the end of each session, the patient’s count was compared with actual number of target tones presented. Two or three trials were performed in order to demonstrate the consistency of the wave forms. Latencies and amplitudes of P200 and P300 were measured from stimulus artifact to the first and second major positive peaks with a range of 150 to 250 and 250 to 500 ms, respectively.

                EEG and ERP (P300) and (P200) were done for 45 students with CD and 45 normal students as a control group.

 

Statistical Analysis:

-           Data were registered and analyzed using the statistical package SPSS. P values < 0.05 were considered statistically significant. Descriptive statistics (e.g. mean and standard deviation, frequencies, percentages) were calculated, and analysis was performed using the student’s T-test, Chi- square X2, and correlation coefficient(r).

-           Analysis of variance test (ANOVA): is used for comparison between different means in the study of more than one independent variable (3 or more) on a certain dependent variable e.g. P300 in different degrees of severity.

 

RESULTS

 

The results of this study can be demonstrated in the following tables:

Table (1) shows that students with CD had P300 amplitude significantly lower than control group (P <0.05).

Table (2) shows significant (P<0.05) prolongation of P300 latency in severe cases of CD than mild and moderate cases. Also, the amplitude of P300 was significantly (P<0.05) lower in severe cases than in mild and moderate cases.

No significant difference was observed between both clinical types (childhood and adolescent onset types) and P300 amplitude and latency.

Table (3) shows that 39 (86.7%) out of 45 patients with CD had abnormal EEG record, which was significantly higher than control group (p<0.001). Background activity in students with CD was significantly lower (7.91±0.70) than control group (8.31±0.31) (p<0.001). The commonest paroxysmal changes in EEG were spike and slow complex (55.5%) (p<0.001), followed by sharp activity (28.9%) (p<0.01), and these paroxysmal activity were significantly higher in students with CD than in control group.

As regard the clinical types (not shown in table), paroxysmal slow activity in childhood type was significantly higher (p<0.05) than adolescent type, while there is no significant difference between both clinical types in other types of EEG changes.

Table (4a) shows that students with CD had significantly lower total IQ than control group (P<0.001), and significantly lower performance IQ than control (P<0.001), while no significant difference in verbal IQ.

Table (4b) shows a lower significant difference in positive cases in subtests of performance I.Q. e.g. block design (p<0.05), object assembly (p<0.01),and digit symbol (P<0.001).

Table (4c) shows that, although there is no significant difference in total VIQ between positive and control groups, there is a lower significant difference in positive group in its subtests e.g. comprehension  (p<0.05), and arithmetic (p<0.01).

Table (5) shows that mild, moderate and severe cases of CD students in technical schools had significantly lower total IQ than students with CD in general schools. Also students with CD in technical schools had significantly lower performance IQ than general schools. As regard to verbal IQ, mild and severe cases only in technical schools had significantly lower scores than general schools.                                                                                  

Table (6) shows that total IQ and its subscales in mild cases of childhood onset type in technical schools were significantly lower than general schools (P<0.001). Severe cases of childhood onset in technical schools had significantly lower verbal IQ only (P<0.001). In adolescent onset type, moderate and severe cases in technical schools had significantly lower total IQ and performance IQ. Also mild cases had significantly lower total IQ and verbal IQ (P<0.01).

Table (7) illustrates the differences between IQ and its subscales in different schools according to the clinical types and the degree of severity. There is a lower statistically significant difference towards the childhood onset type [total IQ (P< 0.001), and performance IQ (P< 0.01)], in technical schools, while in general schools there is lower statistically significant difference towards the adolescent onset type in mild degree [verbal IQ (P<0.05)] and in the sever degree [verbal IQ (P< 0.05)].


 

Table 1. Latency and amplitude of P200 and P300 in students with CD and control groups.

 

Item

Positive Group

(N=45)

Control Group

(N=45)

P-value

P200 Latency

206.31 ± 44.708

200.56 ± 36.080

NS

P200 Amplitude

13.420 ± 14.85

12.180 ± 2.963

NS

P300 Latency

363.98 ± 60.548

362.11 ± 68.835

NS

P300 Amplitude

13.950 ± 2.11

17.076 ± 6.952

<0.05

 

 

Table 2. Comparison between the different degrees of severity of CD, latency and amplitude of P200 and P300.

 

Item

Mild

(N=17)

Moderate

(N=20)

Severe

(N=8)

P-value

P200 Latency

196.82±48.847

208.65±45.618

220.63±31.514

NS

P200 Amplitude

11.094±1.892

16.145±22.173

11.550±2.464

NS

P300 Latency

338.00± 37.17

351.76 ± 41.97

380.88 ± 77.25

< 0.05

P300 Amplitude

13.371±4.914

13.870±6.117

10.100±3.40

< 0.05

 

Table 3. EEG changes in students with CD and control groups.

 

Item

Positive group

(N = 45)

Control group

(N = 45)

P-value

Normal EEG record

No

%

 

6

13.3 %

 

40

88.8 %

 

< 0.001

Abnormal EEG record

No

%

 

39

86.7 %

 

5

12.2 %

 

< 0.001

Background (Hz/ second) Mean ± SD

7.91 ± 0.7

8.31± 0.31

< 0.001

Paroxysmal activity

Sharp

No

%

 

13

28.9 %

 

3

6.7

 

< 0.01

Slow

No

%

 

2

4.4 %

 

0

0 %

 

NS

Spike and slow complex

No

%

 

25

55.5 %

 

6

13.7 %

 

< 0.001

Table 4a. Total IQ and its subscales in students with CD and control groups.

 

Item

Positive Group

(N=101)

Control Group

(N=100)

P-value
Total IQ

97.782 ± 9.338

103.01 ± 11.426

<0.001

Performance IQ

87.673 ± 13.903

95.222 ± 14.016

<0.001

Verbal IQ

103.85 ± 14.259

105.66 ± 14.757

NS

 

Table 4b. comparison between the positive and the control groups as regard to subtests of performance IQ.

 

Item

Positive Group

(N=101)

Control Group

(N=100)

P-value

Picture completion

10.099 ± 1.780

10.131 ± 1.941

NS

Picture arrangement

7.534 ± 3.288

8.111 ± 3.129

NS

Block design

7.019 ± 1.816

7.596 ± 1.683

<0.05*

Object assembly

7.752 ± 3.793

9.444 ± 3.780

<0.01**

Digit symbol

8.881 ± 3.965

11.101 ± 4.843

<0.001***

 

 

Table 4c. Comparison between the positive and the control groups as regard to subtests of verbal IQ.

 

Item

Positive Group

(N=101)

Control Group

(N=100)

P-value

Information

11.168 ± 3.271

10.838 ± 3.570

NS

Comprehension

14.101 ± 3.502

15.182 ± 3.342

<0.05*

Arithmetic

7.405 ± 2.683

8.424 ± 2.040

<0.01**

Similarities

11.505 ± 2.915

12.202 ± 2.773

NS

Vocabulary

8.861 ± 3.243

9.262 ± 3.170

NS

Digit span

8.940 ± 2.092

9.212 ± 2.858

NS

 

 

Table 5. IQ and its subscales in different groups of CD in students in technical schools and general schools.

 

Item

Technical schools

General schools

P-value

Total IQ

Mild

95.34± 9.677

103.67 ±8.516

<0.001

Moderate

97.48 ±7.632

104.60 ±13.557

<0.05

Severe

94.556 ±4.156

102.50 ±10.149

<0.001

Verbal IQ

Mild

101.30 ±12.920

112.73 ±13.128

<0.001

Moderate

103.36 ±14.846

111.60 ±24.946

NS

Severe

98.33 ±9.975

103.75 ±9.844

<0.05

Performance IQ

Mild

84.88 ±17.644

90.80 ±8.108

<0.05

Moderate

87.88 ±10.883

93.20± 9.731

<0.05

Severe

88.11 ± 8.313

96.75± 14.080

<0.01

Table 6. IQ and its subscales in different clinical types, school types, and different degrees of severity CD.

  

Item

Childhood onset

Adolescent  onset

Technical

Schools

General

Schools

P-value

Technical

Schools

General

Schools

P-value

Mild

Total IQ

86.33±10.985

105.00±5.656

<0.001***

96.81± 8.761

103.46±9.033

<0.01**

Verbal IQ

95.83±17.668

120.650±6.364

<0.001***

102.19±12.067

111.54±13.642

<0.01**

Performance IQ

76.66±11.501

87.00±2.828

<0.001***

86.21±18.213

91.385±8.559

NS

Moderate

Total IQ

98.87±8.061

-

-

96.82±7.584

104.60±13.557

<0.05*

Verbal IQ

103.50±18.237

-

-

103.29±13.605

111.60±24.946

NS

Performance IQ

90.375± 11.439

-

-

86.70±10.763

93.20±9.731

<0.05*

Severe

Total IQ

94.60±5.412

100.50±10.607

NS

94.50±2.645

104.50±13.435

<0.01**

Verbal IQ

96.40±11.610

108.50± 0.717

<0.001***

100.75±8.460

99.00±14.142

NS

Performance IQ

89.20±10.616

89.00±15.556

NS

86.75±5.439

104.50±10.607

<0.001***

 

Table 7. Comparison between different school types, clinical types and severity as regard to IQ and its subscales.

 

Item

Technical schools

General schools

Child. onset

Adolescent onset

P-value

Child. onset

Adolescent onset

P-value

Mild

Total IQ

86.33 ± 10.985

96.81 ± 8.761

< 0.001***

105.00 ± 5.656

103.46 ± 9.033

NS

Verbal IQ

95.83 ± 17.668

102.19 ± 12.067

NS

120.650 ± 6.364

111.54 ± 13.642

< 0.05*

Performance IQ

76.66 ± 11.501

86.21 ± 18.213

<0.01**

87.00 ±  2.828

91.385 ±  8.559

NS

Moderate

Total IQ

98.87 ±8.061

96.82 ± 7.584

NS

-

104.60 ± 13.557

-

Verbal IQ

103.50 ± 18.237

103.29 ± 13.605

NS

-

111.60 ±  24.946

-

Performance IQ

90.375 ± 11.439

86.70 ± 10.763

NS

-

93.20 ± 9.731

-

Severe

Total IQ

94.60 ± 5.412

94.50 ± 2.645

NS

100.50 ± 10.607

104.50 ± 13.435

NS

Verbal IQ

96.40 ± 11.610

100.75 ±  8.460

NS

108.50 ± 0.717

99.00 ± 14.142

<0.01**

Performance IQ

89.20 ± 10.616

86.75 ± 5.439

NS

89.00 ± 15.556

104.50 ± 10.607

NS

 

 

 


DISCUSSION

 

In this study we found a significant lower difference in the P300 amplitude in students with CD, (table 1). This is in agreement with many other studies like31,32,33,11,14; who reported reduced P300 amplitude in children with CD. Moreover, they conclude that P300 decrements previously attributed to familial alcohol/ substance dependence might be the results of a coincident increase in the prevalence of CD. Rothenberger et al.,34 found that there is P300 decrement among the adolescents with ADHD + CD than those with ADHD only as well as ADHD + Tic disorder.

Lance et al.35, reported that among subjects older than 16.5 years with CD, small P300 amplitudes were detected over the frontal scalp, also, they reported that there is a significant negative correlation between frontal P300 amplitude and APD symptoms expressed during childhood (i.e., conduct disorders). Bauer1 reported that the P300 amplitude reduction was significantly correlated with the number of childhood conduct disorder symptoms. Adults with conduct problems (i.e., APD) who were 18-30 years of age failed to show a maturational change in frontal P300 amplitude36.

Lance et al.37, reported that boys with CD especially those with a history of violations failed to exhibit the normal maturational increase in P300 amplitude. Kim et al.15, reported that the conduct group showed a significantly lower hit rate on the Wisconsin Card Sorting Test (WCST) than the control group. In addition, the conduct group showed reduced P300 amplitude at Fz and Cz and prolonged P300 latency at Fz , and there was a significant correlation between P300 amplitude and stroop test performance. These results indicate that adolescents with conduct problems have impairment of executive function and inhibition, and that these impairments are associated with frontal dysfunction.

As regard to EEG records, we found a significant higher percentage of abnormal EEG records in students with CD than in control group. In agreement with our results, Jaspere et al.,38 concluded that 59% of 71 children with behavioral disorder yielded abnormal EEG activity. Henry39 found EEG alteration in the behaviorally disorder children in the form of paroxysmal slow activity more pronounced anteriorly.

Lomborso et al.40, recorded positive spike discharge in EEG of delinquent children. Sayed et al.41, in their studies on criminals recorded excessive EEG abnormalities. Williams42, added that in the habitually aggressive criminal, the EEG abnormalities exist in about two thirds of this population.

Harris43 reported an incidence of 50% to 60% of abnormal EEGs in children with behavioral disorder compared to 10 % to 15% in normal children.

Fenwick44 agreed with this results and added that there is a two to three folds increase in the incidence of EEG abnormality in children with CD, without gross neurological or mental handicap in comparison to normal children. The most common abnormality was spike activity.

Tsuboi21 recorded that positive spikes were recognized as the most common type of EEG changes in his study (49% to 56%), while slow activity was present in 9% of the records.

Bauer et al.45, revealed abnormalities in resting EEG record. Lahey et al.,46 reported that boys who had at least one registered criminal offense had greater amount of slow frequency activity. Bauer47 in a study to predict relapse of alcohol and drug abuse via quantitative EEG, revealed that the EEG difference between relapse-prone and abstinence-prone groups was related to the interaction of two premorbid factors as childhood CD and paternal alcoholism. Also Bauer48 in his study about the antisocial personality disorder and cocaine dependence, concluded that the number of conduct problems reported prior to age 15 was a better predictor of EEG changes than either the severity of cocaine dependence, alcohol, anxious or depressed mood.

In disagreement with our results, Phillip et al.49, who reported that 91% of his studied group with CD and behavior disorder had normal EEG records, while 9% had abnormal records in the form of slow background or paroxysmal discharges. Such EEG abnormalities indicate a disturbance of cerebral function of unknown nature in non epileptic or mentally retarded subjects which may be one of the factors contributing to the behavioral disorders detected in these children.

We found that there is a significant lower difference in students with CD than the control group as regard to the total IQ, this result is in agreement with the results of other studies as Moffitt50 who reported that the principle neuropsychological deficits (including IQ) have been reported in relation to CD. Also, these results are supported by the study of22,23,17, all of them conclude that the adolescents with CD have a significantly lower IQ than the control group, moreover, lower IQ may be a risk factor for CD.

Moffitt et al.51, reported that there was no significant differences between the two delinquent subgroups (those officially delinquent and those delinquent with no police records), but both these groups gained significantly lower mean IQs than non delinquent groups. Even when IQs are in the normal range, lower IQs scores are linked to stealing, lying and other symptoms of CD. Moreover, White et al.,52 reported the protective effects of high IQ in the prevention of delinquency in those at high risk of CD. He found that delinquents had significantly lower IQ than non delinquents and the very high IQ may help boys even those at high risk to stay free of delinquency altogether.

Regarding the relation between school type and IQ in the positive group, we found a significant lower difference towards the technical schools. This can be explained by that, general schools require a higher marks for acceptance which may reflect a higher level of IQ.

                As regard to comparison between both school types and clinical types, we found a lower significant difference in childhood onset type in technical school than in general school in mild degree (total IQ, PIQ and  VIQ) and in sever degree (VIQ), while in adolescent onset type, we found a lower significant difference in technical schools than the general schools in mild degree (total IQ and VIQ), moderate degree (total IQ and PIQ) and sever degree (total IQ and PIQ).

In this study, we found that the positive group is significantly lower than the control group, in the PIQ and some of its subtests (block design, object assembly and digit symbol). This can be explained by the following, executive control functions (ECF) as reported by Moffitt50 which simulates the subtests of PIQ are affected in CD. Also Felton and Enrico22 noticed impairment of these actions in children and adolescents with CD. Speltz, et al53 found that school age children and adolescents with CD typically exhibit deficits in executive control functions. So, we can conclude that CD has a significantly lower PIQ than the control group.

Although there is no significant difference in VIQ between the positive and the control groups, there is a lower significant difference in the positive group in its subtests (comprehension and arithmetic). Our results are supported by many studies like Dery et al.,23 who reported that juvenile delinquents can present with a wide range of cognitive impairments, primarily verbal abilities. Speltz et al.,53 reported that deficits in VIQ typically present in children with conduct problems. Pineda et al.,54 reported that VIQ and some of its subscales present statistically significant differences between CD and controls.

Moffitt et al.,17 concluded that poorer neuropsychological status in related to early onset delinquency and predicts subsequent persistent antisocial behaviors, which support our significant differences between both clinical types in technical schools, while in general schools, the adolescent onset type is lower than the childhood onset type, and this can be explained by the very small number of childhood onset cases in the general schools.

All these results support the differences we found previously between both school types as regard to IQ. So the significant differences between school types and IQ is also reflected on the clinical types and severity of CD by the same differences.

From the above results, we can conclude that, cases with CD are associated with changes in the psychometric and neurophysiological studies which may reflect the pathological process in the brain that complicate CD as a disease generated by many pathological processes which open the question of more detailed investigations to clarify that illness, and recommend, that neurophysiological study (EEG and P300) and measurements of intelligence should be an integral part of evaluation of cases of CD.

 

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الملخص العربى

 

دراسة فسيولوجيا الأعصاب والذكاء فى حالات اضطراب السلوك

 

يعتبر الاضطراب السلوكى من أكثر الاضطرابات التى تصيب الأطفال والراشدين ويشمل هذا الاضطراب مجموعة من الأعراض المضادة للمجتمع والسلوك العنيف والتى تظهر بوضوح فى مرحلة الطفولة وقد تستمر الى مرحلة المراهقة وهذه الأعراض تشمل الكذب، السرقة، الهروب من المدرسة، تخريب ممتلكات الآخرين، الاعتداء على الآخرين، الهروب من البيت والاعتداءات الجنسية. ويسبب هذا الاضطراب السلوكى خللا فى وظائف الفرد المعرفية و علاقته بالآخرين مما يؤدى الى تأخره دراسيا وهناك عديد من الدراسات أظهرت العلاقة بين اضطراب السلوك عند الأطفال والمراهقين والتغيرات التى تظهر فى الجهد المستثار العقلى المتأخر  (ب300 )، رسام المخ الكهربائى ومنسوب الذكاء. وقد كان الهدف من هذا البحث هو دراسة فسيولوجيا الأعصاب والذكاء لحالات اضطراب السلوك عند الطلاب. وقد شملت هذه الدراسة مائة وواحد طالب وطالبة من المصابين بالاضطراب السلوكى من المدارس الثانوية الفنية و المدارس الثانوية العامة داخل مدينة أسيوط. وقد تم تطبيق مقياس وكسلر لمعدل الذكاء(للأطفال و الراشدين) لهذه المجموعة والمجموعة الضابطة وهى تتكون من مائة طالب وطالبة من نفس المدارس السابقة. أما الجهد المستثار العقلى المتأخر(ب300) ورسام المخ الكهربائى فقد تم تطبيقهم على خمسة وأربعين طالب وطالبة من المصابين بالاضطراب السلوكى وعلى نفس العدد للمجموعة الضابطة. وقد أظهرت نتائج الدراسة أن ارتفاع الموجة (ب300) أقل فى المجموعة المرضية عنها فى المجموعة الضابطة وكان ذو دلالة إحصائية وكانت فترة كمون الموجة (ب300) أطول فى المجموعة المرضية عنها فى المجموعة الضابطة أما بالنسبة لرسام المخ الكهربائى فقد وجدت تغيرات فى 86.7% من المجموعة المرضية أما بالنسبة للتغيرات فى المسح العام لنشاط المخ فقد وجد أنه أقل وأبطأ وذو دلالة إحصائية فى المجموعة المرضية مقارنة بالمجموعة الضابطة . بالنسبة لمنسوب الذكاء فقد وجدت فروقا ذات دلالة إحصائية فى المجموعة المرضية بالنسبة للقيمة الكلية لمنسوب الذكاء ومنسوب الذكاء العملى وقد كانت هذه العوامل أقل فى المجموعة المرضية مقارنة بالمجموعة الضابطة ومن نتائج هذه الدراسة نستنتج أن هناك احتمال وجود تغيرات فى الفص الأمامى من المخ عند المجموعة المرضية مصاحبة لهذه الحالات. 

 



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