Functional imaging studies with emotional, stressful, and sensory challenges
BPD was suggested to be part of a spectrum of stress-associated disorders together with PTSD, depression and dissociative disorders (Bremner, 2002) and reactivity to stress and stressful reminders appear to underlie affective dysregulation characteristic of patients with BPD. One method to test this reactivity is to expose subjects to emotional challenges or to stressful memories. Challenge studies are using either standardized materials such as emotional slides, or personalized material such as autobiographical scripts, e.g., depicting traumatic experiences. Imaging studies in conjunction with sensory challenges, such as exposure to painful heat stimuli, can reveal insight into neural processing of sensory stimuli. Disturbed pain processing is a characteristic feature of BPD probably underlying self-injurious behavior in this population and neuroimaging techniques can be used to localize this disturbance neuroanatomically.
Using standardized emotional slides which are supposed to evoke emotional responses, FMRI investigations in healthy subjects found activation of the amygdala region, (Irwin et al., 1996; Morris et al., 1998), anterior cingulate cortex as well as ventromedial prefrontal cortex areas (Mayberg et al., 1999; Teasdale et al., 1999). PET studies revealed neural correlates of different emotional states, such as grief, shame, guilt, and anger, using scripts specific for each emotion (Dougherty et al., 1999; George et al., 1995; Shin et al., 2000). For example, during the imagination of situations associated with anger, alterations of prefrontal blood flow with increased activity in ACC were found (Dougherty et al., 1999; Kimbrell et al., 1999). Using standardized negative emotional material from the International Affective Picture System (IAPS) Herpertz et al. (2001) found increased activity in the amygdala of six patients with BPD without comorbid psychiatric disorders compared to controls. In a larger sample of 12 BPD patients with comorbid anxiety and depressive disorders, these findings could be replicated (Herpertz, personal communication).
Another method of emotional challenge consists of presenting standardized pictures of faces which express a specific emotion such as anger, fear, or sadness (Ekman, 1993). Donegan et al. (2003) used this paradigm to investigate BPD patients with and without PTSD and controls. They found different effects for the two BPD groups: For BPD patients with PTSD left-lateralized amygdala hyper-reactivity was found, whereas those BPD patients without PTSD showed bilateral amygdala hyper-reactivity. In the cingulate cortex, these investigators found deactivation in response to fearful faces for patients with BPD and comorbid PTSD but not for those BPD patients without PTSD. In frontal polar prefrontal cortex (BA 10), they found an opposite pattern of deactivation for BPD patients without but not for those with PTSD. These findings are consistent with findings of left-lateralized amygdala hyper-reactivity (Rauch et al., 2000) as well as decreased cingulate activation in PTSD, which will be discussed below.
With the aid of personalized autobiographical scripts, neuroimaging studies in PTSD following childhood abuse have also demonstrated abnormalities in prefrontal brain areas, with a failure of activation in anterior cingulate (Shin et al., 1999; Bremner et al., 1999). Using the method of script-driven symptom provocation in conjunction with fMRI, Lanius et al. (2001, 2003) found decreased function in medial pre-frontal cortex, anterior cingulate and thalamus in patients with PTSD. However, these studies did not assess axis II pathology in traumatized patients. We expanded the method of challenging autobiographical scripts to investigate processing of stressful memories in patients with BPD. With personalized scripts of childhood abuse situations, findings in BPD patients were similar to those described above for PTSD. Memories of abuse were associated with increases in blood flow in right dorsolateral prefrontal cortex as well as decreased blood flow in left dorsolateral prefrontal gyrus in women without BPD. There was also increased blood flow in right anterior cingulate and left orbitofrontal cortex in women without BPD. Women with BPD failed to activate anterior cingulate gyrus as well as orbitofrontal cortex. Also, no blood flow differences were seen in dorsolateral prefrontal gyrus in women with BPD (Schmahl et al., 2004). Since fear of abandonment is one of the characteristic features of BPD and situations of abandonment appear to be an important stressor in the development of BPD, we also tested the effects of memories of situations of abandonment, again with the aid of autobiographical scripts (Schmahl et al., 2003b). Memories of abandonment were associated with greater increases in blood flow in bilateral dorsolateral prefrontal cortex (middle frontal gyrus, areas 9 and 10) as well as right cuneus (area 19) in women with BPD than in women without BPD. Abandonment memories were associated with greater decreases in right anterior cingulate (areas 24 and 32) in women with BPD than in women without BPD. A larger decrease in blood flow in women with BPD was also seen in left temporal cortex and left visual association cortex.
In a recent study (Driessen et al., 2004), neural correlates of traumatic memory versus aversive but nontraumatic memory were investigated in BPD patients with (n = 6) and without PTSD (n = 6). Comparing the reaction to the two memory types, differential responses for BPD patients with and without PTSD were found: Those without current PTSD showed a widespread activation of the orbitofrontal cortex (OFC) in both hemispheres, whereas those with current PTSD demonstrated only minor activation of the right more than the left OFC. Instead, there was a major right-sided activation of the anterior temporal lobe, including para-hippocampal gyrus and amygdala. These results may indicate the existence of different neural networks in trauma-associated mental disorders. Taken together, a dysfunction of dorsolateral and medial prefrontal cortex may be associated with the recall of traumatic memories in women with BPD.
As mentioned above, alterations of pain perception and pain processing are a characteristic feature of BPD and may underlie self-injurious behavior in patients with the disorder. Neuroimaging studies revealed the neuroanatomical correlates of pain processing in the brain (Peyron et al., 2000). Two anatomically distinct pathways, distinguished according to their projections through thalamic nuclei, have been identified (Treede et al., 1999): a sensory-discriminative ‘lateral’ pathway projecting from the lateral thalamic nuclei to the primary and secondary somatosensory cortex, and an affective-motivational ‘medial’ pathway projecting from the medial thalamic nuclei to the insula and anterior cingulate cortex. Functional neuroimaging investigations of pain perception in healthy individuals using heat stimuli could demonstrate an involvement of lateral as well as medial pathways in pain processing of healthy human subjects (Bornhoevd et al., 2002; Davis, 2000). Dorsolateral prefrontal cortex appears to have an important pain control function (Lorenz et al., 2003). We used painful heat stimuli in combination with functional magnetic resonance imaging to examine neural processing of pain in BPD (Schmahl and Seifritz, 2003). Compared to normal subjects, BPD patients showed a specific pattern of cortical responses to pain, which was characterized by less activation in posterior parietal cortex and a stronger activation in dorsolateral prefrontal cortex. In addition, patients but not controls revealed a strong deactivation in the perigenual ACC. This pattern of neural activation may be related to disturbed evaluation of pain in patients with BPD.
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