Progress in Neuro-Psychopharmacology and Biological Psychiatry
Midline brain structures in teenagers with first-presentation borderline personality disorder
Introduction
Functional and morphologic abnormalities in brain structures related to emotion and impulsivity, such as the amygdala and other limbic regions, have been described in borderline personality disorder (BPD) (reviewed by Lis et al., 2007). While not consistently replicated (Zanetti et al., 2007), reduced thickness of the corpus callosum in BPD patients (Rüsch et al., 2007) further implicates the role of impaired interhemispheric connectivity in the neurobiology of BPD. However, it remains unknown whether other midline brain abnormalities are present in BPD.
The adhesio interthalamica (AI), a midline structure connecting the medial surfaces of the thalami across the third ventricle, is variable in size among individuals and missing in about 20% of human brains (Kretschmann and Weinrich, 1992, Percheron, 2004). Although its functional significance is obscure, schizophrenia patients are more likely to have a smaller AI, possibly reflecting early developmental abnormalities in the midline brain structures (Shimizu et al., 2008, Takahashi et al., 2008a, Takahashi et al., 2008c). On the other hand, the size of a cavum septum pellucidum (CSP), a midline brain structure formed by the incomplete fusion of the septum pellucidi (Rakic and Yakovlev, 1968), has been reported to be normal in schizophrenia (Rajarethinam et al., 2008, Takahashi et al., 2007, Takahashi et al., 2008d). A higher prevalence of BPD in recent-onset schizophrenic patients (Hogg et al., 1990) and the fact that psychotic episodes are not uncommon in BPD patients (Miller et al., 1993) raise the possibility that BPD patients share, at least partly, a common neurobiological basis with psychotic disorders. A narrower third ventricle in borderline patients (Lucas et al., 1989) might reflect abnormalities in the midline brain structures, since the AI develops in concert with prominent features of the ventricular system (O'Rahilly and Muller, 1990). To our knowledge, however, no magnetic resonance imaging (MRI) studies have examined the AI and CSP in BPD patients.
This MRI study investigated the size of the AI and CSP as well as the third ventricular volume in teenage BPD patients and healthy controls. Based on previous findings in schizophrenia (Takahashi et al., 2008a), we predicted that the AI would be smaller in BPD patients compared to controls.
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Participants
Twenty teenage patients meeting Structured Clinical Interview for DSM-IV Axis II Disorders (SCID-II) (First et al., 1997) criteria for BPD and 20 healthy controls were included in this study (Table 1); the characteristics of this sample have been previously described (Chanen et al., 2008b). A personality disorder feature was scored positive if it was present for 2 years and did not occur exclusively in the context of an Axis I disorder. All participants were physically healthy, and none had a
Results
ANCOVA of the AI length revealed a significant main effect for diagnosis [F (1,34) = 11.45, p = 0.002] and a non-significant trend for gender [F (1,34) = 4.02, p = 0.053] and no interaction; the BPD patients had a shorter AI than controls (Table 1). There were no AI missing subjects in the current sample. The AI length did not differ between BPD patients with (N = 10) and without (N = 10) comorbid mood and/or anxiety disorder [F (1,16) = 0.16, p = 0.691], those with (N = 10) and without (N = 10) disruptive
Discussion
To our knowledge, this is the first MRI study to report the size of both AI and CSP in BPD patients. We demonstrated that the AI was shorter in BPD patients compared with healthy controls, but there was no group difference in the CSP length. These findings suggest that different biological processes are responsible for the development of these midline brain structures and there might be a specific role for the AI in the neurobiology of BPD.
The CSP is thought to be a normal anatomical variant,
Conclusion
This MRI study found that teenagers with first-presentation BPD having minimal exposure to treatment (including medication) exhibit shorter AI length but no differences in CSP length, compared with healthy controls. The present findings implicate a role for the AI and its related brain regions in the biological processes associated with BPD, but further study is clearly needed to replicate our preliminary results.
Acknowledgements
The authors thank the staff of the HYPE Clinic at ORYGEN Youth Health. Thanks are also due to Ms. Caroline Weinstein, A/Prof. Warrick Brewer and Ms. Deidre Smith for assistance with data collection. This study was supported in part by grants 98-0198 from the Victoria Health Promotion Foundation, Melbourne, Australia and grant 990748 from the National Health and Medical Research Council (NHMRC), Canberra, Australia. ORYGEN Research Centre is supported by an unrestricted grant from the Colonial
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