ناهنجاری های انسفالوگرافی در اختلال شخصیتی سرحد

Epilepsy and non-localized brain dysfunction have been invoked, among others, as underlying factors in borderline personality disorder. We have recorded 58 electroencephalograms in 20 borderline patients, first after complete drug washout and then under carbamazepine or placebo double-blind treatment. Taking into account only definite abnormal tracings, we found a 40% incidence of abnormal diffuse slow activity. No patient disclosed focal or epileptiform EEG features. Carbamazepine did not appear to modify the electroencephalogram.

Borderline personality disorder (BPD) is a well-recognized syndrome (American Psychiatric Association, 1987). Its main clinical features include brief episodes of affective manifestations, brief psychotic episodes, emotional instability, impulsive and unpredictable behavior, frequent self-mutilations and altered interpersonal relations. BPD has been associated with several psychiatric and organic pathological conditions. Schizophrenia (Gunderson et al., 1975; Gunderson, 1979; Schulz et al., 1989), schizoaffective psychoses (Andrulonis et al., 1982), atypical psychoses (Mitsuda and Fukuda, 1974; Andrulonis et al., 1982) and affective disorders (Akiskal, 1981; Carroll et al., 1981; Pope et al., 1983; Akiskal et al., 1985; Schulz et al., 1989) have been connected with BPD. Although BPD is the most frequently diagnosed personality disorder (Gunderson and Zanarini, 1987), the physiopathological processes involved in this syndrome remain unclear. Noradrenergic and opiate systems (Van der Kolk, 1987), serotonin (Brown et al., 1982; Coccaro et al., 1989; Hollander et al., 1994) and dopamine (Bonnet and Redford, 1982; Lucas et al., 1987) systems dysfunction have been proposed as components of BPD. Epilepsy-related phenomena have also been invoked since some of the clinical features of BPD resemble the psychological characteristics sometimes observed in epileptic patients with complex partial seizures (CPS) (Cowdry et al., 1980; Fenwick, 1981; Cowdry and Pickar, 1985; Cornelius et al., 1986). Case reports have described CPS in patients previously misdiagnosed as BPD (Snyder and Pitts, 1984; Cowdry and Pickar, 1985; Messner, 1986; Schmid et al., 1989). Searching for neurophysiologic abnormalities in BPD, Snyder and Pitts (1984), Cowdry and Pickar (1985)and Tanahashi (1988)have found significant abnormalities in the electroencephalographic scalp records of BPD patients. Other studies did not disclose significant abnormalities (Cornelius et al., 1986; Archer et al., 1988; Ogiso et al., 1993). Moreover, positron emission tomography studies have indicated that there is no metabolic evidence for the existence of temporal lobe epilepsy in BPD (De la Fuente et al., 1992 and De la Fuente et al., 1994). It has been proposed that the EEG abnormalities in BPD illustrate not the presence of abnormal cortical foci but rather a non-EEG-localizable brain dysfunction (Van Reekum, 1993), as noted by the increased incidence of slow-wave activity and other non-specific EEG changes. From a pharmacological point of view, one study (Cowdry and Gardner, 1988) suggested that carbamazepine (CBZ), an effective treatment for CPS (Dreifuss, 1983), might improve BPD. The purpose of the present study was to explore the scalp EEG recordings of 20 unmedicated BPD patients and to examine the evolution of the recordings under CBZ treatment.