©1979 vOL. 10,N0.4
CLINICAL ELECTROENCEPHALOGRAPHY
Electroencephalographic Correlates of Compulsive Eating John H. Rau, Frederick A. Struve, and Richard S. Green
The concept that binge eating may be caused by some subcortical, possibly hypothalamic, dysfunction was first advanced by Stunkard.(1-3) In his studies, Stunkard suggested that the eating behavior of "night eaters" seemed consistent with dysregulation in the satiation center of the hypothalamus; in contrast, the eating behavior of "binge eaters" seemed consistent with some dysfunction in the appetitive hypothalamic center. In a series of studies on obesity, Schacter(4) noted a remarkable similarity between the behavior of obese persons and hyperphagic rats with ventromedial lesions in the hypothalamus. Such rats have been observed to binge eat excessively.(5) More recently, Green and Rau(6-9) (in two uncontrolled studies) and others (10,11) (in one controlled study) have found that some binge eaters of varying weights (also referred to as "compulsive eaters"), with abnormal electroencephalograms, stopped binging after treatment with phenytoin (Dilantin). Despite two other uncontrolled studies (12,13) reporting unsuccessful treatment with phenytoin of only eight binge eaters, there is considerable suggestive evidence that certain compulsive eaters suffer from some form of presently undetected subcortical dysregulation. Additional analyses by Rau and Green (9) indicated that improvement among phenytoin treated compulsive eaters could be predicted by the presence of soft neurological signs (i.e. headaches, rage attacks, paresthesias) in patients with a variety of paroxysmal EEG dysrhythmias some of which may have a presumed subcortical origin. Each of our prior reports(6-9) involved too limited a number of subjects for adequate analyses of the distribution of EEG findings in this clinical population. This present report is based upon 59 compulsive eating patients drawn from various samples.
Method Subjects: Fifty-nine patients consisting of 51 females (mean age 27.6, SD 8.7) and 8 males (mean age 30.9, SD 7.4) who were involved periodically over the past four years in an investigation of the treatment of compulsive eating with phenytoin constitute the subjects for the present study. Patients were referred from various sources. A few were therapy patients of one of the authors (J.H,R. or R.S.G.) for psychological difficulties unrelated to eating. Some were referred by professionals either from within or without the medical center. Others were self-referred, largely as a result of publicity describing our initial pilot study.(6) Thirty patients were treated in a structured pilot study.(8,9) Nineteen patients were not involved in a formal study but participated in all of the procedures detailed below. Published case reports of two of these patients have appeared. (7) Twenty-seven patients weighed within normal limits when interviewed. Thirteen patients were underweight and classified as "emaciated"; that is, they weighed less than 75% of expected normal weight for their height and sex. Nineteen patients were overweight and classified as "obese"; that is, they weighed more than 125% of their expected normal weight.
From Long Island Jewish-Hillside Medical Center, Department of Psychiatry, Hillside Division, P.O. Box 38, Glen Oaks, New York 11004. John H. Rau, Ph.D" is senior psychologist and coordinator of inpatient services; Frederick A. Struve, Ph.D., is senior research associate and director, ClinicalResearch Electroencephalographic Laboratory and research associate professor of psychiatry, SUNY, Stony Brook, N.Y.; Richard S. Green, M.D., associate director, Department of Psychiatry, Hillside Division. Request for reprints should be sent to Dr. Rau at the above address. This work was supported, in part, by Long Island JewishHillside Medical Center internal grant funds.
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CLINICAL ELECTROENCEPHALOGRAPHY
Procedure: Every patient was interviewed by one or two of the authors (J.H.R. and/or R.S.G.) to assess explicitly the nature and frequency of binge eating. The earliest patients were interviewed in an open-ended clinical manner when the focus had been on obtaining data on the phenomenology of compulsive eating. Later patients were interviewed in a structured joint interview format involving, in addition, an assessment of soft neurological signs (e.g. headaches, paresthesias, etc.) historical and familial variables, current height and weight, weight control behaviors and other matters. (8,9) Following the interview all patients were referred for EEG study in an open (i.e. not blind) clinical fashion. For all patients electroencephalograms were secured both awake and asleep by technicians trained to interpretively evaluate the tracing in progress. When sleep was not spontaneous it was induced with Seconal (maximum 3 grains). Monopolar technique utilizing either linked ear, single ear, or contralateral ear references was employed. In addition to references, disc electrodes were placed symmetrically over the bilateral frontal, anterior temporal, mid temporal, posterior temporal, parietal (central), and occipital areas as well as ground. All EEGs were interpreted by one of the authors (F.A.S.) A previous study(14) involving independent co-interpretation of 1,087 clinical EEGs has indicated that interinterpreter reliability of EEG assessment at our laboratory attains a high level of statistical significance. An additional study(15) of the test-retest reliability of EEG findings for 477 patients over time has also yielded statistically significant results. Forty-seven patients received a pharmacological trial with phenytoin adequate to assess its impact on binge eating. The minimum requirement for such a trial was at least 300 mg. of phenytoin for at least 14 days. Experience with our subjects indicated that the frequency of binge eating was sufficient for improvement over baseline to be noted within this period. The mean initial dosage was 300 mg daily. Some successfully treated patients were able to be maintained for long periods of time on 200 mg per day. No patient received more than 600 mg daily. Eight patients chose not to take the medication. Four patients received an inadequate trial either because they dropped out of the study
or because drug reactions (e.g. skin rash, leukopenia) necessitated drug withdrawal. Improved patients were seen for follow-up by one of the authors (R.S.G.) on a monthly basis, and after six months, on an irregular basis. No improved patient was seen for less than eight weeks and some patients have been followed for four years. "Improvement" was defined operationally as occurring if a patient met two of the three following criteria: (1) Patient reported a complete cessation of binge eating over at least two weeks. Patient reported an 80% or more (2) reduction in frequency of binge eating (relative to pre-phenytoin base levels) for as long as patient was medicated. Occasionally a patient would experience a sudden episode of binge eating, sometimes when under psychological stress but more often not. These "breakthroughs" were treated by a temporary increase in medication dosage. (3) Patient reported the subjective feeling that binge eating episodes were now under control. Those patients who binged from time to time were considered to have met this criterion if they indicated that these episodes were "voluntary" and related to psychogenic factors in their lives. Patients who reported that they were able to discriminate between two different kinds of binge eating compulsive eating involving an uncontrollable compulsion to binge which had decreased by at least 80% or ceased - and choice eating over which they freely assumed responsibility - were also considered to have met this criterion. Patients who met one of these criteria were classified as "questionably improved" while patients who met none of the criteria were considered "unimproved". Results and Discussion In Table 1 the EEG findings for our sample of 59 compulsive eaters are presented. A salient feature of these data is the markedly high incidence (64.4%) of EEG abnormality in this population. This is dramatically higher than that found with normal control populations(16) tested with the same EEG
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CLINICAL ELECTROENCEPHALOGRAPHY
methodology and interpretive criteria as used in our laboratory. The incidence figures are also substantially elevated as contrasted with the incidence of EEG abnormality among routinely tested unselected psychiatric patients in general. In our material(17), spanning nine years, the unweighted average incidence of EEG abnormality among unselected psychiatric patients is 40.5%with a year to year range of from 25% to 54%. Other reported data(18-20) from psychiatric centers using routine screening EEG provide abnormal incidence figures ranging from 20% to 50%. In a recent study of 1,000 consecutive psychiatric patients(21), 39.6% of the sample had abnormal EEGs. The high incidence of EEG abnormality in our compulsive eating sample, exceeding reported incidence figures for normals and general psychiatric populations, suggests that a disordered
neurophysiological substrate may contribute - either in a direct etiological role or indirect contributory fashion - to the genesis of compulsive binge eating in at least some' individuals. Electroencephalographic surveys of seemingly functional disorders usually result in a heterogeneous mixture of EEG findingsoften with an excess of slow tracings, some asymmetries, and some paroxysmal findings. Our findings also indicate a heterogeneous grouping of EEG patterns. However inspection of Table 1 reveals that the majority of discrete EEG patterns recorded (i.e. 84.3%) represent paroxysmal dysrhythmias. Furthermore among the 38 compulsive eating subjects with abnornmal EEGs, fully 94.7% displayed paroxysmal features in their EEG tracing. Compulsive binge eating represents an episodically occurring symptom cluster
TABLE 1 EEG Findings Among Compulsive Eating Patients with Waking and Sleep Electroencephalograms
Overall EEG Category
N
%
Normal Abnormal
21 38 59
35.6% 64.4% 100.0%
Discrete EEG Patterns*
N
% of Total Patient Sample (N=59)
% of Abnormal EEGs (N=38)
14&6/sec. Positive Spikes Mitten Patterns Small Sharp Spikes Paroxysmal Slowing Focal Slow** Minimal Generalized Slow** Focal Spiking Diffuse Spiking Minimal Generalized Fast** Rare Fast 6/sec. Spike & Wave High Voltage Slow with Spiking
22
37.3% 8.5% 8.5% 5.1% 5.1% 5.1% 3.4% 3.4% 3.4% 3.4% 1.7% 1.7%
57.9% 13.2% 13.2% 7.9% 7.9% 7.9% 5.3% 5.3% 5.3% 5.3% 2.6% 2.6%
Total
5 5 3 3 3 2 2 2 2 1 1
*Twelve Patients had more than one EEG finding. **Denotes non-paroxysmal dysrhythmias. The majority (84.3%) of discrete EEG patterns recorded were paroxysmal dysrhythmias. Ot patients with abnormal EEGs, 94.7% (36/38) displayed a paroxysmal finding.
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CLINICAL ELECTROENCEPHALOGRAPHY
usually associated with substantially reduced voluntary or cognitive control and not infrequently with a frank uncontrollable eating attack. That the dominate forms of EEG dysrhythmia in this population are paroxysmal or "epileptiform" is conceptually sensible and would be expected from the episodic "attack-like" nature of the syndrome under study. One cannot ascertain with precision actual brain loci of EEG findings from potentials recorded at the scalp. However, of patients with abnormal EEGs, 71.1% display either the 14 & 6/sec. positive spike or the B-Mitten pattern and both of these EEG patterns involve strong presumptive evidence of subcortical origin. The positive spike pattern was originally suggested(22) as thalamic or hypothalamic in origin, and subsequent studies(23-27) have tended to support the view that this finding does originate in subcortical regions although the precise anatomical locus or loci are elusive. A more recent depth electrode study(28) provides rather clear evidence of a phase reversal of 14 & 6 spike activity occurring within the thalamus. In this report the 14 & 6 pattern along with the patient's numerous severe visceral and pain symptoms disappeared following radio frequency ablative lesion largely involvi ng the ventralis anterior nucleus of the thalamus. Sleep recording studies of cortical and subcortical brain tumor patients(29) provide
strong evidence that mitten patterns may involve a variety of midbrain lesions, the most frequent area being the thalamus. Years earlier Halasz and Nagy(30) suggested such a mitten location based upon the scalp distri bution and wave form morphology of this EEG signal. It is plausible that some unknown proportion of the other dysrhythmias found in our sample may involve some degree of subcortical dysregulation although supportive evidence documenting this is not available. The above discussion is important since disorders of subcortical appetitive regu latory centers may be involved in certain compulsive eating behaviors (especially those uncontrollable "attack" behaviors of an ego-dystonic nature). The existence of a preponderance of subcortical EEG dysrhythmias associated with this disorder reinforces the heuristic value of a subcortical neurophysiological etiological hypothesis for at least some of those patients. The most frequent finding in our compulsive eating population was the 14 & 6/sec. positive spike pattern. The literature on this pattern is voluminous and the controversy over the abnormality of this finding will not be dealt with here. However this finding is accepted as characteristic of the young patient while being extremely rare in the adult - especially the adult beyond age 30. Recent studies(31-33) have focused on the 14 & 6 pattern in adults where adult symptomatic
TABLE 2 Incidence of 14 & 6/sec. Positive Spikes in Compulsive Eaters, Un selected Psychiatric Inpatients and Normal Controls as Function of Age
Age 0-19 20-24 25-29 30-39 40-59
Compulsive Eating N 14&6 % 4 8 50.0% 14 35.7% 5 16 7 43.8% 15 26.7% 4 6 33.3% 2
Psychiatric Inpatients 1 N 14&6 % 1259 678 428 413
345 142 57 26
27.4% 20.9% 13.3% 6.3%
N 669 196 79 116 165
1. Data abstracted from Wegner & Struve. 1977 2. Data abstracted from Gibbs & Gibbs, 1964
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Controlsf 14&6 % 19.0% 127 17 8.7% 1 1.3% 1 0.9% 0 0.0%
©1979 VOL. 10,N0.4
CLINICAL ELECTROENCEPHALOGRAPHY
TABLE 3 Treatment (Phenytoin) Response as a Function of EEG Results for 47 Adequately Medicated Compulsive Eaters
TREATMENT RESPONSE GOOD
UNCERTAIN
POOR
6
1
10
21
7
2
Normal EEG
Abnormal EEG
X2
= 15.74,
d.f.
= 2,
p
CLINICAL ELECTROENCEPHALOGRAPHY
Electroencephalographic Correlates of Compulsive Eating John H. Rau, Frederick A. Struve, and Richard S. Green
The concept that binge eating may be caused by some subcortical, possibly hypothalamic, dysfunction was first advanced by Stunkard.(1-3) In his studies, Stunkard suggested that the eating behavior of "night eaters" seemed consistent with dysregulation in the satiation center of the hypothalamus; in contrast, the eating behavior of "binge eaters" seemed consistent with some dysfunction in the appetitive hypothalamic center. In a series of studies on obesity, Schacter(4) noted a remarkable similarity between the behavior of obese persons and hyperphagic rats with ventromedial lesions in the hypothalamus. Such rats have been observed to binge eat excessively.(5) More recently, Green and Rau(6-9) (in two uncontrolled studies) and others (10,11) (in one controlled study) have found that some binge eaters of varying weights (also referred to as "compulsive eaters"), with abnormal electroencephalograms, stopped binging after treatment with phenytoin (Dilantin). Despite two other uncontrolled studies (12,13) reporting unsuccessful treatment with phenytoin of only eight binge eaters, there is considerable suggestive evidence that certain compulsive eaters suffer from some form of presently undetected subcortical dysregulation. Additional analyses by Rau and Green (9) indicated that improvement among phenytoin treated compulsive eaters could be predicted by the presence of soft neurological signs (i.e. headaches, rage attacks, paresthesias) in patients with a variety of paroxysmal EEG dysrhythmias some of which may have a presumed subcortical origin. Each of our prior reports(6-9) involved too limited a number of subjects for adequate analyses of the distribution of EEG findings in this clinical population. This present report is based upon 59 compulsive eating patients drawn from various samples.
Method Subjects: Fifty-nine patients consisting of 51 females (mean age 27.6, SD 8.7) and 8 males (mean age 30.9, SD 7.4) who were involved periodically over the past four years in an investigation of the treatment of compulsive eating with phenytoin constitute the subjects for the present study. Patients were referred from various sources. A few were therapy patients of one of the authors (J.H,R. or R.S.G.) for psychological difficulties unrelated to eating. Some were referred by professionals either from within or without the medical center. Others were self-referred, largely as a result of publicity describing our initial pilot study.(6) Thirty patients were treated in a structured pilot study.(8,9) Nineteen patients were not involved in a formal study but participated in all of the procedures detailed below. Published case reports of two of these patients have appeared. (7) Twenty-seven patients weighed within normal limits when interviewed. Thirteen patients were underweight and classified as "emaciated"; that is, they weighed less than 75% of expected normal weight for their height and sex. Nineteen patients were overweight and classified as "obese"; that is, they weighed more than 125% of their expected normal weight.
From Long Island Jewish-Hillside Medical Center, Department of Psychiatry, Hillside Division, P.O. Box 38, Glen Oaks, New York 11004. John H. Rau, Ph.D" is senior psychologist and coordinator of inpatient services; Frederick A. Struve, Ph.D., is senior research associate and director, ClinicalResearch Electroencephalographic Laboratory and research associate professor of psychiatry, SUNY, Stony Brook, N.Y.; Richard S. Green, M.D., associate director, Department of Psychiatry, Hillside Division. Request for reprints should be sent to Dr. Rau at the above address. This work was supported, in part, by Long Island JewishHillside Medical Center internal grant funds.
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CLINICAL ELECTROENCEPHALOGRAPHY
Procedure: Every patient was interviewed by one or two of the authors (J.H.R. and/or R.S.G.) to assess explicitly the nature and frequency of binge eating. The earliest patients were interviewed in an open-ended clinical manner when the focus had been on obtaining data on the phenomenology of compulsive eating. Later patients were interviewed in a structured joint interview format involving, in addition, an assessment of soft neurological signs (e.g. headaches, paresthesias, etc.) historical and familial variables, current height and weight, weight control behaviors and other matters. (8,9) Following the interview all patients were referred for EEG study in an open (i.e. not blind) clinical fashion. For all patients electroencephalograms were secured both awake and asleep by technicians trained to interpretively evaluate the tracing in progress. When sleep was not spontaneous it was induced with Seconal (maximum 3 grains). Monopolar technique utilizing either linked ear, single ear, or contralateral ear references was employed. In addition to references, disc electrodes were placed symmetrically over the bilateral frontal, anterior temporal, mid temporal, posterior temporal, parietal (central), and occipital areas as well as ground. All EEGs were interpreted by one of the authors (F.A.S.) A previous study(14) involving independent co-interpretation of 1,087 clinical EEGs has indicated that interinterpreter reliability of EEG assessment at our laboratory attains a high level of statistical significance. An additional study(15) of the test-retest reliability of EEG findings for 477 patients over time has also yielded statistically significant results. Forty-seven patients received a pharmacological trial with phenytoin adequate to assess its impact on binge eating. The minimum requirement for such a trial was at least 300 mg. of phenytoin for at least 14 days. Experience with our subjects indicated that the frequency of binge eating was sufficient for improvement over baseline to be noted within this period. The mean initial dosage was 300 mg daily. Some successfully treated patients were able to be maintained for long periods of time on 200 mg per day. No patient received more than 600 mg daily. Eight patients chose not to take the medication. Four patients received an inadequate trial either because they dropped out of the study
or because drug reactions (e.g. skin rash, leukopenia) necessitated drug withdrawal. Improved patients were seen for follow-up by one of the authors (R.S.G.) on a monthly basis, and after six months, on an irregular basis. No improved patient was seen for less than eight weeks and some patients have been followed for four years. "Improvement" was defined operationally as occurring if a patient met two of the three following criteria: (1) Patient reported a complete cessation of binge eating over at least two weeks. Patient reported an 80% or more (2) reduction in frequency of binge eating (relative to pre-phenytoin base levels) for as long as patient was medicated. Occasionally a patient would experience a sudden episode of binge eating, sometimes when under psychological stress but more often not. These "breakthroughs" were treated by a temporary increase in medication dosage. (3) Patient reported the subjective feeling that binge eating episodes were now under control. Those patients who binged from time to time were considered to have met this criterion if they indicated that these episodes were "voluntary" and related to psychogenic factors in their lives. Patients who reported that they were able to discriminate between two different kinds of binge eating compulsive eating involving an uncontrollable compulsion to binge which had decreased by at least 80% or ceased - and choice eating over which they freely assumed responsibility - were also considered to have met this criterion. Patients who met one of these criteria were classified as "questionably improved" while patients who met none of the criteria were considered "unimproved". Results and Discussion In Table 1 the EEG findings for our sample of 59 compulsive eaters are presented. A salient feature of these data is the markedly high incidence (64.4%) of EEG abnormality in this population. This is dramatically higher than that found with normal control populations(16) tested with the same EEG
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©1979 VOL. 10.N0.4
CLINICAL ELECTROENCEPHALOGRAPHY
methodology and interpretive criteria as used in our laboratory. The incidence figures are also substantially elevated as contrasted with the incidence of EEG abnormality among routinely tested unselected psychiatric patients in general. In our material(17), spanning nine years, the unweighted average incidence of EEG abnormality among unselected psychiatric patients is 40.5%with a year to year range of from 25% to 54%. Other reported data(18-20) from psychiatric centers using routine screening EEG provide abnormal incidence figures ranging from 20% to 50%. In a recent study of 1,000 consecutive psychiatric patients(21), 39.6% of the sample had abnormal EEGs. The high incidence of EEG abnormality in our compulsive eating sample, exceeding reported incidence figures for normals and general psychiatric populations, suggests that a disordered
neurophysiological substrate may contribute - either in a direct etiological role or indirect contributory fashion - to the genesis of compulsive binge eating in at least some' individuals. Electroencephalographic surveys of seemingly functional disorders usually result in a heterogeneous mixture of EEG findingsoften with an excess of slow tracings, some asymmetries, and some paroxysmal findings. Our findings also indicate a heterogeneous grouping of EEG patterns. However inspection of Table 1 reveals that the majority of discrete EEG patterns recorded (i.e. 84.3%) represent paroxysmal dysrhythmias. Furthermore among the 38 compulsive eating subjects with abnornmal EEGs, fully 94.7% displayed paroxysmal features in their EEG tracing. Compulsive binge eating represents an episodically occurring symptom cluster
TABLE 1 EEG Findings Among Compulsive Eating Patients with Waking and Sleep Electroencephalograms
Overall EEG Category
N
%
Normal Abnormal
21 38 59
35.6% 64.4% 100.0%
Discrete EEG Patterns*
N
% of Total Patient Sample (N=59)
% of Abnormal EEGs (N=38)
14&6/sec. Positive Spikes Mitten Patterns Small Sharp Spikes Paroxysmal Slowing Focal Slow** Minimal Generalized Slow** Focal Spiking Diffuse Spiking Minimal Generalized Fast** Rare Fast 6/sec. Spike & Wave High Voltage Slow with Spiking
22
37.3% 8.5% 8.5% 5.1% 5.1% 5.1% 3.4% 3.4% 3.4% 3.4% 1.7% 1.7%
57.9% 13.2% 13.2% 7.9% 7.9% 7.9% 5.3% 5.3% 5.3% 5.3% 2.6% 2.6%
Total
5 5 3 3 3 2 2 2 2 1 1
*Twelve Patients had more than one EEG finding. **Denotes non-paroxysmal dysrhythmias. The majority (84.3%) of discrete EEG patterns recorded were paroxysmal dysrhythmias. Ot patients with abnormal EEGs, 94.7% (36/38) displayed a paroxysmal finding.
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usually associated with substantially reduced voluntary or cognitive control and not infrequently with a frank uncontrollable eating attack. That the dominate forms of EEG dysrhythmia in this population are paroxysmal or "epileptiform" is conceptually sensible and would be expected from the episodic "attack-like" nature of the syndrome under study. One cannot ascertain with precision actual brain loci of EEG findings from potentials recorded at the scalp. However, of patients with abnormal EEGs, 71.1% display either the 14 & 6/sec. positive spike or the B-Mitten pattern and both of these EEG patterns involve strong presumptive evidence of subcortical origin. The positive spike pattern was originally suggested(22) as thalamic or hypothalamic in origin, and subsequent studies(23-27) have tended to support the view that this finding does originate in subcortical regions although the precise anatomical locus or loci are elusive. A more recent depth electrode study(28) provides rather clear evidence of a phase reversal of 14 & 6 spike activity occurring within the thalamus. In this report the 14 & 6 pattern along with the patient's numerous severe visceral and pain symptoms disappeared following radio frequency ablative lesion largely involvi ng the ventralis anterior nucleus of the thalamus. Sleep recording studies of cortical and subcortical brain tumor patients(29) provide
strong evidence that mitten patterns may involve a variety of midbrain lesions, the most frequent area being the thalamus. Years earlier Halasz and Nagy(30) suggested such a mitten location based upon the scalp distri bution and wave form morphology of this EEG signal. It is plausible that some unknown proportion of the other dysrhythmias found in our sample may involve some degree of subcortical dysregulation although supportive evidence documenting this is not available. The above discussion is important since disorders of subcortical appetitive regu latory centers may be involved in certain compulsive eating behaviors (especially those uncontrollable "attack" behaviors of an ego-dystonic nature). The existence of a preponderance of subcortical EEG dysrhythmias associated with this disorder reinforces the heuristic value of a subcortical neurophysiological etiological hypothesis for at least some of those patients. The most frequent finding in our compulsive eating population was the 14 & 6/sec. positive spike pattern. The literature on this pattern is voluminous and the controversy over the abnormality of this finding will not be dealt with here. However this finding is accepted as characteristic of the young patient while being extremely rare in the adult - especially the adult beyond age 30. Recent studies(31-33) have focused on the 14 & 6 pattern in adults where adult symptomatic
TABLE 2 Incidence of 14 & 6/sec. Positive Spikes in Compulsive Eaters, Un selected Psychiatric Inpatients and Normal Controls as Function of Age
Age 0-19 20-24 25-29 30-39 40-59
Compulsive Eating N 14&6 % 4 8 50.0% 14 35.7% 5 16 7 43.8% 15 26.7% 4 6 33.3% 2
Psychiatric Inpatients 1 N 14&6 % 1259 678 428 413
345 142 57 26
27.4% 20.9% 13.3% 6.3%
N 669 196 79 116 165
1. Data abstracted from Wegner & Struve. 1977 2. Data abstracted from Gibbs & Gibbs, 1964
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Controlsf 14&6 % 19.0% 127 17 8.7% 1 1.3% 1 0.9% 0 0.0%
©1979 VOL. 10,N0.4
CLINICAL ELECTROENCEPHALOGRAPHY
TABLE 3 Treatment (Phenytoin) Response as a Function of EEG Results for 47 Adequately Medicated Compulsive Eaters
TREATMENT RESPONSE GOOD
UNCERTAIN
POOR
6
1
10
21
7
2
Normal EEG
Abnormal EEG
X2
= 15.74,
d.f.
= 2,
p
