Recent evidence suggests that borderline personality disorder (BPD) is related to reduced size of the parietal lobe. Dissociative symptoms occur in the majority of individuals with BPD. Structural magnetic resonance imaging (3D-MRI) was used to assess volumes of the superior (precuneus, postcentral gyrus) and inferior parietal cortices in 30 young women with BPD who had been exposed to severe childhood sexual and physical abuse and 25 healthy control subjects. Compared with control subjects, BPD subjects had significantly smaller right-sided precuneus (− 9%) volumes. The left postcentral gyrus of BPD subjects with the comorbid diagnosis of dissociative amnesia (DA) or dissociative identity disorder (DID) was significantly increased compared with controls (+ 13%) and compared with BPD subjects without these disorders (+ 11%). In BPD subjects, stronger depersonalization was significantly related to larger right precuneus size. Possibly, larger precuneus size in BPD is related to symptoms of depersonalization. Increased postcentral gyrus size in BPD may be related to the development of DA or DID in the presence of severe childhood abuse.
Borderline personality disorder (BPD) is defined as an intermediate level of personality organization that is considered to occupy a borderline area between neurosis and psychosis (Kernberg, 1967). Stress-related dissociative symptoms occur in about 75% of individuals with BPD (Skodol et al., 2002) and in about 40% of individuals with posttraumatic stress disorder (PTSD) (Bremner et al., 1992 and David et al., 1999). Use of the Structured Clinical Interview for DSM-IV Dissociative Disorders has shown that dissociative amnesia is the area most strongly affected in persons who had been exposed to traumatic stress ( Bremner et al., 1993). Childhood abuse, particularly chronic abuse beginning at early ages, was shown to be related to the development of high levels of dissociation, including dissociative amnesia (DA) and dissociative identity disorder (DID) ( Boon and Draijer, 1993, Lewis et al., 1997 and Chu et al., 1999).
Research so far has established size reduction and pronounced dysfunction of amygdala, hippocampus and prefrontal cortices in individuals with BPD (for review, see Zanarini, 2005). A recent study (Vermetten et al., 2006) demonstrated reduced amygdala and hippocampal size in subjects with DID and posttraumatic stress disorder (PTSD) who had been exposed to severe childhood abuse. Dissociative symptoms of survivors of childhood abuse with or without BPD have been repeatedly related to small hippocampal size (Bremner et al., 1997, Bremner et al., 2003 and Stein et al., 1997). Increased activity of the precuneus has been found in individuals with depersonalization disorder (Simeon et al., 2000) and in PTSD subjects with dissociative states (Lanius et al., 2002). BPD subjects were shown to have elevated pain thresholds that were correlated with dissociative symptoms (Ludäscher et al., 2007) and associated with reduced activity of the right-sided posterior parietal cortex (Schmahl et al., 2006).
Research on individuals with epilepsy of the temporal or parietal lobes has consistently demonstrated that abnormal EEG activity, seizures, and brain stimulation of the temporal or parietal cortices are associated with dissociative states (Halgren et al., 1978, Mesulam, 1981, Gloor et al., 1982, Salanova et al., 1995 and Blanke et al., 2002). Stimulation of the parietal cortex typically leads to somatosensory aura or disturbed bodily perceptions (Salanova et al., 1995 and Blanke et al., 2002). Lesion studies provide evidence that the superior parietal cortex is engaged in the generation and maintenance of an internal (sensorimotor) representation of the body (Sirigu et al., 1996, Berlucchi and Aglioti, 1997 and Wolpert et al., 1998).
In previous investigations, we found reduced size of the parietal lobe (Irle et al., 2005) and reduced glucose metabolism of the precuneus (Lange et al., 2005) in a sample of women with BPD who had been exposed to severe childhood abuse. Subjects presented with pronounced dissociative and psychotic symptoms. In the present investigation, the size of specific parietal cortices of BPD subjects (who were also included in earlier reports: Irle et al., 2005 and Lange et al., 2005) were compared with those of a healthy matched control group. To our knowledge, there is only one previous study on BPD that used an automated whole-brain investigation; it yielded negative results for all cerebral cortical areas (Rusch et al., 2003). The goals of our study were to investigate whether superior parietal cortices have abnormal size in BPD and whether superior parietal cortex size abnormalities are related to dissociative symptoms. Special emphasis was placed on the investigation of BPD subjects with the comorbid diagnosis of DA or DID. A further concern was to specify whether psychotic symptoms in BPD are related to size abnormalities of the inferior parietal cortex, as was previously suggested for subjects with schizophrenia (Frederikse et al., 2000 and Niznikiewicz et al., 2000).
