Journal of Affective Elsevier
147
Disorders, 11 (1986) 147-149
JAD 00399
EEG Abnormalities in Bipolar Affective Disorder Brian L. Cook ‘, Sashi Shukla 2 and Anne L. Hoff 2 ’ VA Medical Center and the Department of Psych&y, and 2 Department
of Psychiaty,
University of Iowa College of Medicine, Iowa City, IA 52232, State University of New York at Stony Brook, Stony Brook, NY II 794 (U.S.A.) (Received 17 February, 1986) (Accepted 30 July, 1986)
Forty-six patients with bipolar illness were evaluated with scalp-recorded electroencephalograms. Familial pattern of psychopathology was evaluated between groups with clinically normal and abnormal EEG tracings. Those with abnormal EEGs were noted to have a significantly negative family history of affective disorder when compared to the EEG normal group. These results may support the concept of some patients with mania having an acquired illness which occurs independent from its genetic loading.
Key words: EEG abnormality
- Bipolar affective disorder - Familial pattern
Introduction Kadrmas and Winokur (1979) noted a negative relationship between abnormal EEG recordings and familial history of affective disorder in probands with bipolar illness. Similar findings had earlier been noted by Dalen (1965), and supported by Hays (1976). Methodologically, however, this series of papers had several limitations. First, proband selection was probably not random except in the Hays (1976) paper which used a consecutive series of admissions. Second, the effect of medication on the EEG results was scantily addressed. Finally, demographic characteristics of the EEG-positive and -negative groups were not reported, and thus it is impossible to know if the comparison groups were otherwise similar. Taylor Reprints: Dr. B.L. Cook, Psychiatry Center, Iowa City, IA 52240, U.S.A. 0165-0327/86/$03.50
Service, VA Medical
0 1986 Elsevier Science Publishers
and Abrams (1980) did not find different rates of abnormal EEGs between familial and non-familial manics when many of these methodological issues were carefully eliminated. Because of these discrepant findings, an independent sample of bipolar manics was again studied. Subjects and Methods All subjects were in-patients of a university psychiatric hospital who had clinical electroencephalograms recorded during their hospital stay. During the period of study, all admissions routinely received a scalp-recorded 16-channel EEG using the international ten-twenty system of electrode placement. EEGs were performed during the first week of hospitalization, and an attempt was made to do this after a minimum 48-h drug wash-out period. All subjects had by history received previous pharmacotherapy including lithi-
B.V. (Biomedical
Division)
148 urn and neuroleptics. A neurologist ‘blind’ to the study clinically classified the recordings as being normal or abnormal. A consecutive series of 23 patients with abnormal EEGs was found who met DSM-III (American Psychiatric Association 1980) criteria for bipolar affective disorder, manic between 1981 and 1985. Family history data regarding DSM-III psychiatric illness was collected during subsequent follow-up in a lithium clinic at the same hospital utilizing a semi-structured interview with at least one first-degree relative in addition to the patient. All family history data was collected blindly in relationship to EEG interpretation. The same information was similarly obtained from 23 controls with mania and normal EEGs. Controls were selected using the nearest age- and sexmatched admission to the same psychiatric unit within a period of 6 months from the index case admission. Categorical data was analyzed using chi-square without continuity correction. Student t-tests were used to compare continuous demographic data.
significant (P > 0.05). Groups were thus similar on these variables. EEG abnormalities were varied. Abnormalities included generalized slowing (n = 7), left temporal-parietal slowing (n = l), left occipital slowing (n = l), left temporal spike waves (n = 5) right temporal spike waves (n = 2) left occipital spike and slow waves (n = l), left temporal slow waves (n = 2), right parietal slow waves (n = l), bilateral frontal-temporal spike slow waves (n = 2) and lastly right central sharp waves (n = 1). Table 1 summarizes the family history and EEG data. Each category of familial psychopathology was compared with EEG result. The abnormal EEG group had significantly less family history of affective disorder. As the definition of familial psychopathology was broadened to include suicide and alcoholism, these findings were less striking. When psychiatric illness of all types was included in the comparison, findings were essentially non-significant. Discussion
Results The bipolar group with abnormal EEGs included 11 females and 12 males. Sex was matched exactly in the group with normal EEGs. The mean age of the EEG-positive group was 32.8 years (SD 10.29), while the EEG-negative group had a mean age of 32.43 years (SD 10.95) which was nonTABLE FAMILY
These data once again support the negative relationship between the presence of an abnormal EEG and family history of affective disorder. These findings support the concept of bipolar illness being potentially more heterogeneous in etiology than is conventionally thought. As pointed out by Taylor and Abrams (1980), however, sub-
1 HISTORY
AND EEG RESULT Normal EEG (n = 23)
x2
P
3 5 5
10 13 15
5.25 5.84 8.85
< 0.025 i 0.025 < 0.005
4
10
3.69
NS
6
13
4.39
< 0.05
6 6
15 11
7.10 2.33
< 0.01 NS
9
14
2.11
NS
11
18
4.57
< 0.05
Abnormal EEG (II = 23) Affective disorder in first-degree relative Affective disorder in first- or second-degree relative Affective disorder in any relative Affective disorder, alcoholism or suicide in first-degree relative Affective disorder, alcoholism or suicide in first- or second-degree relative Affective disorder, alcoholism or suicide in any relative Any psychiatric illness in first-degree relative Any psychiatric illness in first- or second-degree relative Any psychiatric illness in any relative
149 grouping probands by family history does not preclude genetic transmission in the family history-negative group. Likewise, a positive family history does not in itself necessarily imply in a specific case genetic transmission. Given the consistency of finding a lack of family history in EEG-abnormal manics across four centers and three decades of study, we feel that this accumulation of data supports the concept of certain cases of mania possibly having an acquired etiology independent from its genetic loading. One must note that our study is limited by its lack of a lengthy drug wash-out period, but we feel it unlikely that previous medications had serious impact on these findings. Both groups were exposed to similar medication types, and there was no evidence that either group was more likely to have been on medication at the time of the recorded EEG. The issue of acquired mania deserves further pursuit utilizing research strategies involving analysis of phenomenology, treatment response and
course of illness to help in forming meaningful subtypes of mania. Many potentially helpful pieces of historical information regarding risk factors for development of acquired mania (e.g. head trauma) are often obscure or temporally remote, and thus may be easily overlooked. Such information may have potential clinical ramifications if significant prognostic or treatment differences can be established. References American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, 3rd ed., America1 Psychiatric Association, Washington, DC, 1980. Dalen, P., Family history, the electroencephalogram, and perinatal factors in manic conditions, Acta Psychiatr. Stand., 41 (1965) 527-563. Hays, P., Etiological factors in manic-depressive psychoses, Arch. Gen. Psychiatry, 33 (1976) 1187-1188. Kadrmas, A. and Winokur, G., Manic depressive illness and EEG abnormalities, J. Clin. Psychiatry, 40 (1979) 35-36. Taylor, M.A. and Abrams, R., Familial and non-familial mania, J. Affect. Disord., 2 (1980) 111-118.