Table 1

Structural and functional imaging findings in frontolimbic regions

Region	Findings
Hippocampus	Reduced volume (Driessen et al., 2000; Tebartz van Elst et al., 2003; Schmahl et al., 2003a) Decreased baseline metabolism left (Juengling et al., 2003)
Amygdala	Reduced volume (Driessen et al., 2000; Tebartz van Elst et al., 2003; Schmahl et al., 2003a) Gray matter volume loss left (Ruesch et al., 2003) Increased activity in response to affective pictures (Herpertz et al., 2001) and fearful faces (Donegan et al., 2003)
Anterior cingulate cortex	Reduced volume right (Tebartz van Elst et al., 2003) Decreased baseline metabolism (De la Fuente et al., 1997)/Increased baseline metabolism (Juengling et al., 2003) Blunted response to fenfluramine (Siever et al., 1999) Deactivation in response to m -cpp (New et al., 2002, 2003) Reduced α-[(11)C]methyl-L-tryptophan trapping (Leyton et al., 2001) Deactivation in response to fearful faces (Donegan et al., 2003) Failure of activation in response to trauma scripts (Schmahl et al., 2004), deactivation in response to abandonment scripts (Schmahl et al., 2003b) Decreased activity in response to pain stimuli (Schmahl and Seifritz, 2003)
Medial and orbital prefrontal cortex	Reduced volume left orbital (Tebartz van Elst et al., 2003) Decreased metabolism (Soloff et al., 2003) Blunted response to fenfluramine (Siever et al., 1999; Soloff et al., 2000) and m -cpp (New et al., 2002, 2003) Reduced alpha-[(11)C]methyl-L-tryptophan trapping (Leyton et al., 2001) Failure of activation in response to trauma scripts (Schmahl et al., 2004)
Dorsolateral prefrontal cortex	Reduced N -acteylaspartate concentration (Tebartz van Elst et al., 2001) Decreased baseline metabolism (De la Fuente et al., 1997)/Increased baseline metabolism (Juengling et al., 2003) Blunted response to fenfluramine right (Siever et al., 1999) Failure of activation in response to trauma scripts (Schmahl et al., 2004), increased blood flow in response to abandonment scripts (Schmahl et al., 2003b) Increased activity in response to pain stimuli left (Schmahl and Seifritz, 2003)

However, a number of open questions remain. Although deactivation of ACC in response to stress is found throughout most challenge studies, assessment of baseline metabolism with FDG-PET has not shown consistent results, with studies finding increased as well as decreased prefrontal metabolism. Different findings between FDG-PET studies may be due to subgroup differences as well as differences in gender distribution. Overall, gender effects seem to play a very important role in the neurobiology of BPD. This is particularly true for studies assessing serotonergic function. The studies by New et al. (2003) and Leyton et al. (2001) yielded large differences in serotonergic function in pre-frontal areas between male and female BPD patients. This may be related to the fact that aggressive behavior is directed in different directions by male and female patients with BPD, with women showing mainly self-injurious behavior and men demonstrating more outwardly directed aggression. Another important conclusion from the research reviewed here is that frontolimbic dysfunction found in BPD is not a finding specific to the disorder, but can also be found in a variety of different disorders, such as PTSD, depression, or patients with impulsive and aggressive behavior. Thus, rather than being characteristic of a certain disorder, dysfunction of frontolimbic areas appears to underlie psychopathological clusters such as stress-related or impulsive syndromes.

Neuroimaging will certainly remain one of the most important methods for the study of the neurobiological underpinnings of BPD. Thus, future studies should focus on several points found to be important in the literature reviewed: different stress-related disorders, such as PTSD and BPD, should be compared directly using the same paradigms, such as emotional or stressful challenges. Also, given the large overlap of the two disorders BPD and PTSD, subgroups of BPD patients with and without comorbid PTSD should be investigated. This clear separation of study groups may help to elucidate similarities as well as differences in the neurobiology of the two disorders. Another fruitful avenue of research is to take a look at gender effects in BPD. It seems to be crucial not to investigate mixed gender BPD groups since clinical as well as neurobiological differences between men and women with the disorder appear to be too large to investigate them together. However, only focussing on women with BPD would mean leaving out interesting findings. Thus, comparing male and female BPD patients is an interesting starting point for research which may help to clarify the role of gender in this disorder. PET studies using radioactively labelled tracers, e.g. opioid ligands, will become important to elucidate the contribution of different neurochemical systems to BPD symptomatology. Also, conditioning experiments in conjunction with functional imaging (Büchel and Dolan, 2000) may help to elucidate neural mechanisms underlying disturbed learning processes in BPD. Finally, an important question is whether the abnormalities found in imaging studies represent state or trait characteristics of the disorder. One possible way to answer this question is to investigate effects of therapeutic interventions by comparing patients before and after therapy.

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