دانلود مقاله ISI انگلیسی شماره 38470
ترجمه فارسی عنوان مقاله

رابط بین اختلال شخصیت مرزی و اختلالات طیف دوقطبی

عنوان انگلیسی
The interface between borderline personality disorder and bipolar spectrum disorders
کد مقاله سال انتشار تعداد صفحات مقاله انگلیسی
38470 2007 10 صفحه PDF
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Comprehensive Psychiatry, Volume 48, Issue 2, March–April 2007, Pages 145–154

ترجمه کلمات کلیدی
- اختلال شخصیت مرزی - اختلالات طیف دوقطبی
کلمات کلیدی انگلیسی
borderline personality disorder ,bipolar spectrum disorders,
پیش نمایش مقاله
پیش نمایش مقاله  رابط بین اختلال شخصیت مرزی و اختلالات طیف دوقطبی

چکیده انگلیسی

Abstract Objective This review examines whether borderline personality disorder (BPD) should be considered part of the bipolar spectrum. Methods A literature review examined studies of co-occurrence, phenomenology, family prevalence, medication response, longitudinal course, and etiology. Results Borderline personality disorder and bipolar disorder co-occur, but their relationship is not consistent or specific. There are overlaps but important differences in phenomenology and in medication response. Family studies suggest clear distinctions, and it is unusual for BPD to evolve into bipolar disorder. Research is insufficient to establish whether these disorders have a common etiology. Conclusions Existing data fail to support the conclusion that BPD and bipolar disorders exist on a spectrum but allows for the possibility of partially overlapping etiologies.

مقدمه انگلیسی

. Introduction It has been persistently suggested that borderline personality disorder (BPD) could be an atypical form of mood disorder [1], [2] and [3]. Originally, because of frequent comorbidity [4] and [5], the focus was on whether BPD is a variant of major depression (MDD) [6] and [7]. However, a significant body of research has established important differences between BPD and MDD: in phenomenology, family prevalence, medication response, pathogenesis [8], [9], [10] and [11], and, most recently, in their influence on each other's course [12]. The suggestion that BPD might be an atypical form of mood disorder has now shifted from MDD to bipolar disorder [13] and [14]. The concept of a bipolar spectrum expands the diagnostic construct to include a wider range of syndromes [13], [14], [15], [16], [17], [18] and [19]. In addition to bipolar I and bipolar II, spectrum disorders would include bipolar III (antidepressant-induced hypomania), and bipolar IV (ultra–rapid-cycling bipolar disorder) [19]. These subtypes might also supercede cyclothymic disorder, which is heterogeneous in phenomenology, family history, biologic correlates, and treatment [20]. It is now being suggested that a bipolar spectrum exists, including many cases of unipolar depression, anxiety disorders, substance abuse, eating disorders, as well as many personality disorders, most notably BPD [14], [18], [21] and [22]. The purpose of the present article is to critically evaluate the relationship between BPD and bipolar I disorder, as well as the proposed bipolar spectrum, notably bipolar II. We will examine 4 hypotheses regarding this relationship: (1) BPD is an atypical form (ie, phenotypic variant) of bipolar disorder; (2) bipolar disorder is a phenotypic variant of BPD; (3) BPD and bipolar disorder are independent disorders; and (4) BPD and bipolar disorder have overlapping etiologies. To examine these hypotheses, we review findings concerning co-occurrence, phenomenology, family prevalence, medication response, longitudinal course, and etiology. Medline and PsycInfo searches using the combined search terms borderline personality disorder and bipolar disorder elicited 147 published articles since 1966; this review focuses on empirical studies and theoretical articles shedding light on the relationship between these disorders

نتیجه گیری انگلیسی

Conclusions This review takes place within a historical context in which the DSM system leads to extensive comorbidity for most psychiatric disorders. More specifically, both bipolar disorder [142] and [143] and BPD [5], [7] and [144] have been found to have high levels and overlapping types of comorbidity, (ie, anxiety and substance abuse disorders). Yet, in contrast with bipolar disorder, the documentation of such comorbidity in BPD has recurrently raised the question as to whether it should be redefined as a variant of one or another Axis I disorder. Our conclusions are summarized in Table 3. After reviewing the evidence concerning co-occurrence rates, phenomenological distinctions, pharmacologic responsivity, family prevalence, and longitudinal course, it seems safe to conclude that the current separation of BPD from bipolar I, that is, hypothesis 3, is supported. The association with bipolar II is more complicated. Although evidence from family prevalence, longitudinal course, and pharmacologic response is largely nonexistent, the evidence from co-occurrence, phenomenology, and etiology is inconclusive, preserving the possibility of shared phenotypes (hypothesis 4). More epidemiological, longitudinal, pharmacologic, family, and genetic research is needed to answer this question. Table 3. Summary of conclusions Co-occurrence Phenomenology Family prevalence Response to medication Longitudinal course Etiology Bipolar I Increased co-occurrence; most cases distinct Some overlap but periods of elevated mood in bipolar-I vs affective instability in BPD. Bipolar I not frequent in families with BPD Lithium and mood stabilizers effective in bipolar I, mainly anti-impulsive effects in BPD Neither disorder frequently evolves into the other; BPD has a better outcome Insufficient evidence Bipolar II Increased co-occurrence; several points of overlap Hypomanic episodes in bipolar II, vs affective instability in BPD Not studied Some overlap in response to mood stabilizers Infrequent as outcome of BPD Insufficient evidence Conclusion Tends to support hypothesis 3 Tends to support hypothesis 3; other hypotheses possible for bipolar II Tends to support hypothesis 3 for bipolar I Tends to support hypothesis 3; other hypotheses possible for bipolar II Tends to support hypothesis 3 No conclusion