Alcohol-induced depersonalization

CASE REPORT Alcohol-Induced Depersonalization Eric B. Raimo, Richard A. Roemer, Mark Moster, and Yang Shan Background: A case of alcohol-induced depersonalization disorder is presented. The subject had experienced several depersonalization states following the consumption of alcohol rather than from a psychogenic etiology, and the episodes were transient, not chronic. Methods: Three quantitative EEG (QEEG) studies were performed on the subject, one during the index depersonalization episode and two subsequent studies when the subject was clinically asymptomatic. Results: Slow wave activity (relative theta power) was significantly increased when symptomatic. This slowing was still present over the occiput 3 days after the symptoms had remitted but was absent 17 days after symptoms had ameliorated. Conclusions: The time course of EEG slowing suggests a metabolic encephalopathy, a condition which likely contributes to the manifestations of depersonalization syndrome. Biol Psychiatry 1999;45:1523–1526 © 1999 Society of Biological Psychiatry Key Words: Quantitative EEG, substance-induced depersonalization disorder, alcohol

Introduction

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ymptoms of depersonalization (persistent or recurrent feeling of being detached from one’s mental processes or body that is accompanied by intact reality testing) may be seen in clinical settings as a reaction to ingestion or administration of a variety of substances including psychedelic drugs, marijuana, alcohol, and general anesthetics. Up to 41% of a substance abusing population may have had dissociative experiences (Dunn et al 1993). Durations of depersonalization episodes as long as 10 years and as short as a few hours have been described (Davison 1964; Good 1989; Noyes Jr, Kuperman, Olson 1987; Nuller 1982; Szymanski 1981). Shorter, more transient episodes often result from a reaction to a foreign substance, while longer episodes are more chronic in nature and often are idiopathic. DSM-IV criteria for

From the Temple University Health Sciences Center (EBR, RAR, MM, YS), Belmont Center for Comprehensive Treatment (EBR, RAR), and Albert Einstein Medical Center (MM, YS), Philadelphia, PA 19140. Address requests for reprints to: Richard A. Roemer, PhD, D.M.S., Temple University School of Medicine, Department of Psychiatry & Behavioral Science, 3401 N. Broad Street, Philadelphia, PA 19140. Received March 27, 1997; revised November 10, 1997; revised May 11, 1998; accepted May 11, 1998.

© 1999 Society of Biological Psychiatry

depersonalization disorder (300.6) requires that the symptoms not be due to direct physiologic effects of a substance such as drugs or alcohol. Thus, substance-induced depersonalization can not yield a DSM-IV diagnosis of depersonalization disorder. The DMS-III-R criteria for alcohol idiosyncratic intoxication (AII) included maladaptive behavioral changes, e.g., usually aggressive or assaultive behavior, occurring within minutes of ingesting an amount of alcohol insufficient to induce intoxication in most people in the absence of concomitant mental disorders and subsequent amnesia for the period of intoxication. The duration is brief, ceasing within a few hours. AII has been deleted in DSM-IV (Urschel and Woody 1996) because of the lack of clear empirical evidence to support its existence. Urschel and Woody (1996) extensively reviewed the literature on AII. They concluded only one of the articles could make the claim of a true minimal alcohol intake without concomitant organic or psychiatric factors associated with AII symptoms. We present a case which appears to meet the DSM-III-R criteria for AII. However, the symptoms were of depersonalization and not of an aggressive or assaultive nature. In addition, the duration of symptoms was about 2 weeks rather than ceasing within a few hours. The case is of interest as the subject is a highly credible observer who is high-functioning with no psychiatric or organic impairment in the absence of the symptoms described here. Quantitative electroencephalograms (QEEG) studies were performed. The first while the subject was experiencing depersonalization symptoms, and two after the symptoms had subsided.

Case Report The subject, AE, a 23-year-old male, had experienced ten depersonalization episodes during the previous 6 years during high school and college, nine of which occurred after consumption of the equivalent of 3 to 6 ounces of absolute alcohol, and one which occurred after an appendectomy. We have no evidence that AE’s observations and reports are not credible. He is consistently earning superior grades while attending an Ivy League college and has no evidence of psychiatric disorders according to clinical interview and SCID evaluations. According to AE, the symptoms of each episode have been virtually identical save for the duration of deperson0006-3223/99/$20.00 PII S0006-3223(98)00257-1

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alization. The first six episodes each lasted 8 days. AE was able to accurately predict when each episode was going to resolve based on the pattern of the previous episodes, “If I had drank on Friday night and woke up Saturday morning in the funk, I was able to predict that I would wake up the following Sunday morning (8 days later) and the daze would be gone—literally an overnight change.” The seventh episode lasted 10 days instead of the expected 8 days. The eighth episode occurred subsequent to AE’s appendectomy and it lasted 20 days. Thirteen months later, after drinking alcohol, AE experienced another episode. This episode lasted 12 days. AE then reported feeling completely normal for a period of 16 days following the incident. Then, after drinking a glass of champagne at a wedding reception, AE experienced the index episode. AE reported symptoms of feeling detached, cloudy, and “in a daze.” He complained of difficulty tasting, smelling, and feeling things tactually—symptoms of sensory anesthesia. He reported not feeling full after eating and he had a marked craving for sweets. AE had difficulty interpreting proverbs, doing so concretely. He reported difficulty differentiating between whether he had thought of something or had actually spoken. He described looking at his image in the mirror, stepping aside and forgetting the image he saw. He presented as being depressed, but attributed the depression to his debilitated state that prevented competent activity. Study and work were impaired, as was concentration. He was hypersomnolent (14 to 18 hours per day) while experiencing the syndrome and reported constant exhaustion. He was disheveled and unshaven on examination and indifferent about his appearance. AE received a complete neurologic exam, which was normal save for the difficulty interpreting proverbs. His blood pressure was 140/80, slightly elevated for his age.

QEEG Analysis The quantitative electroencephalogram (QEEG) analyses were carried out on a Cadwell Spectrum 32 computer (Caldwell Laboratories, Kennewick, WA). Eyes-closed, resting EEGs were recorded from 19 monopolar electrodes (referred to linked earlobes) of the 10-20 system using a Cadwell Spectrum 32 data acquisition system. Amplifier bandpass was 0.5 to 70 Hz (3 Db points) without notch filtering. Data were digitized at 200 Hz with 12-bit resolution. Following the standardized Spectrum 32 recording protocol, 15 minutes of continuous EEG data were collected on optical disk for subsequent editing and analyses. EEG records were evaluated as falling within normal limits by an electroencephalographer blind to the status of the subject. Using computer-assisted artifact detection in conjunction with visual inspection, 24 artifactfree 2.5 sec epochs of EEG were selected for quantitative

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analyses. Quantitative analyses of the EEG used neurometric methods of John et al (1988) as implemented on the Cadwell Laboratories Spectrum 32. Raw data were digitally filtered yielding a 0.5 to 30 Hz band pass. Power spectral analysis was performed using Fast Fourier Transformation (FFT). For each of the 19 channels, absolute and relative (%) power was computed in the delta (1.5 to 3.5 Hz), theta (3.5 to 7.5 Hz), alpha (7.5 to 12.5 Hz), and beta (12.5 to 25 Hz) frequency bands. Also computed were asymmetry of power and coherence between homologous derivations of the two hemispheres in these four frequency bands. Quantitative EEG (QEEG) features of the power spectral analyses are subjected to log-transformation and age-regression. These analytical methods have been welldocumented (Alper et al 1990; John et al 1988; Roemer et al 1995). On the basis distribution statistics obtained from a group of 150 normal subjects, ages 17 to 90 years, Z values (standard scores) were computed for the index case for each of the QEEG features and for each of the three QEEG analyses. Three QEEGs were performed on AE. The first QEEG was recorded on the fifth day of the 12-day depersonalization episode. The second was recorded 3 days after the episode had resolved clinically. The third was recorded 2 weeks after the second QEEG. All clinical EEG records were read as within normal limits by a clinical electroencephalographer. However, the QEEG analyses yielded significant findings. Figure 1 shows relative QEEG power (Z transforms) for the three recording sessions. The first QEEG, recorded while AE was symptomatic, revealed significant increases of relative delta and theta power and decreases of relative beta power. Also observed, but not illustrated, were greater right than left hemisphere power asymmetries in delta, theta, and alpha bands. In addition, interhemispheric coherence was reduced both frontally and posteriorly in these three frequency bands. Bipolar delta, theta, and total low frequency power (sum of delta and theta) were elevated, while bipolar beta and alpha power were lower than normative values. There was less bipolar interhemispheric coherence in the delta and theta bands. Coherence is a measure of correlation of EEG activity between electrode sites (John et al 1988). Anterior (measured at FP1) and posterior (measured at O2) mean alpha frequencies were 6.6 Hz and 7.1 Hz, respectively. The second and third QEEGs demonstrated a gradual progression towards normal values. In the second QEEG, relative theta power continued to be greater than normal posteriorly and beta power continued to be lower than normal. The previously reduced interhemispheric delta and theta coherence measures were within normal limits, as were asymmetry measures. The significant increases in relative theta power continued over the posterior region,

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Figure 1. Significance probability topographic scalp maps for three recording sessions, mean Z values for relative QEEG power for each of the four frequency bands. These maps represent the mean normalized deviates of index subject based on a healthy control population reference group (not shown). The scaling of the maps yields a region of white where the individual’s Z values (21.64) are lower than expected at p , .05, and a region of black when the values (1.64) are greater than expected at p , .05. Anterior is at the top of each map, occipital regions at bottom. Left hemisphere is on left.

but anteriorly, relative theta power was within normal limits. Anterior and posterior mean alpha frequencies were 6.7 Hz and 7.2 Hz, respectively. By the third QEEG, interhemispheric coherence, relative theta and alpha power were within normal limits; relative delta power became lower than normal. This suggests a time course of recovery associated with the original QEEG deviations. At the third QEEG recording, anterior and posterior mean alpha frequencies had increased to 9.6 Hz and 8.7 Hz respectively.

Discussion A case of alcohol-induced depersonalization is reported. This case was precipitated by alcohol consumption, which

is exclusionary to diagnosis of depersonalization disorder. A provisional diagnosis could be DSM-III-R alcohol idiosyncratic intoxication, since the episode was precipitated by consuming a small amount of alcohol. However, the case is not of brief duration, is without amnesia during the period of intoxication, and presents with depersonalization rather than aggressive or assaultive behavior. The index case presented 16 days after a previous episode. QEEG evidence is presented indicating altered central nervous system activity in association with the depersonalization episode. It seems a diagnosis based on DSM-IV criteria is not available for this case. QEEG analyses revealed several interesting neurophysiologic features related to AE’s condition. AE exhibited significant increase in slow wave activity while experienc-

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ing the syndrome. In the first QEEG, slow wave (delta and theta) power measures were greater than normal and fast wave (beta) power was less than normal. A combination of increased bipolar relative delta power and low bipolar interhemispheric coherence is considered to characterize a metabolic encephalopathy (Spehlmann 1981). When considering any single EEG record, a mean alpha frequency less than or equal to 8 Hz is considered abnormal (Spehlmann 1981). The initial QEEG featured reduced anterior and posterior mean alpha frequencies (6.6 Hz and 7.1 Hz) and a generalized increase in monopolar relative theta power. Three days after AE’s clinical symptoms had subsided, there still was evidence of increased slow wave activity, though less pronounced. Anterior and posterior mean alpha frequencies remained virtually unchanged from the first QEEG values. Several of the other QEEG features tended to approach normal values after AE’s clinical symptoms had subsided. For example, monopolar relative theta power had normalized in the anterior region. Seventeen days after the symptoms had abated, the QEEG revealed no significant increases of slow wave activity. Anterior and posterior mean alpha frequencies had normalized. When comparing two EEG records of the same subject, a difference in mean alpha frequency of 2 Hz or more is considered abnormal (Spehlmann 1981). Mean anterior alpha frequency at the first recording was 6.6 Hz, by the third recording the mean alpha frequency was 9.6 Hz. Monopolar relative theta power normalized over the entire head, and most of the other variables approximated normal values. Relative delta power became lower than normal. Some individuals experience dissociative-like states following ingestion of benzodiazepines (Good 1989). This was not the case when AE was administered diazepam. On the other hand, sodium pentothal, the general anesthetic administered to AE, presumably initiated the episode that he experienced following appendectomy. Davison (1964) has also reported cases of depersonalization following both a “minor operation” and an “appendectomy.” Davison’s fourth case report describes a case rather analogous to AE’s. Davison’s Mr. B.C. experienced depersonalization after alcohol ingestion, as has AE. Mr. B.C.’s episodes lasted 1 to 2 weeks and began and ended abruptly, paralleling this case. The major difference between the two cases is that Mr. B.C. reported no depression during his episodes, while AE exhibits a rather obvious depressive component during his episodes. Davison’s EEG findings parallel our computer-assisted QEEG findings.

Alpha frequency was lower during AE’s episode than 17 days after the symptoms had abated.

Conclusion We presented a case of depersonalization disorder secondary to alcohol ingestion. Three QEEG studies performed on the subject revealed an abnormal amount of slow wave activity during the syndrome, and a progression towards normalization following the syndrome. This slowing suggests a metabolic encephalopathy, a condition which likely contributes to the manifestations of depersonalization syndrome. It may be appropriate to differentiate a substance-induced state of depersonalization from the chronic, idiopathic depersonalization disorder based on the duration of an episode and/or its precipitating factors. Research supported, in part, by NS01357 (MM), DA06728 (RAR), MH12507, MO1-RR00349 and SO7-RR05417.

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