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Motzkin 2015 Cortex Vmpfc Lesion BNST Blood Flow.Pdf cortex 64 (2015) 281e288 Available online at www.sciencedirect.com ScienceDirect Journal homepage: www.elsevier.com/locate/cortex Research report Ventromedial prefrontal cortex damage alters resting blood flow to the bed nucleus of stria terminalis Julian C. Motzkin a,b,c, Carissa L. Philippi a, Jonathan A. Oler a, * Ned H. Kalin a, Mustafa K. Baskaya d and Michael Koenigs a, a Department of Psychiatry, University of Wisconsin-Madison, Madison, WI, USA b Neuroscience Training Program, University of Wisconsin-Madison, Madison, WI, USA c Medical Scientist Training Program, University of Wisconsin-Madison, Madison, WI, USA d Department of Neurological Surgery, University of Wisconsin-Madison, Madison, WI, USA article info abstract Article history: The ventromedial prefrontal cortex (vmPFC) plays a key role in modulating emotional re- Received 3 July 2014 sponses, yet the precise neural mechanisms underlying this function remain unclear. Reviewed 5 October 2014 vmPFC interacts with a number of subcortical structures involved in affective processing, Revised 3 November 2014 including the amygdala, hypothalamus, periaqueductal gray, ventral striatum, and bed Accepted 17 November 2014 nucleus of stria terminalis (BNST). While a previous study of non-human primates shows Action editor Angela Sirigu that vmPFC lesions reduce BNST activity and anxious behavior, no such causal evidence Published online 13 December 2014 exists in humans. In this study, we used a novel application of magnetic resonance im- aging (MRI) in neurosurgical patients with focal, bilateral vmPFC damage to determine Keywords: whether vmPFC is indeed critical for modulating BNST function in humans. Relative to Prefrontal cortex neurologically healthy subjects, who exhibited robust rest-state functional connectivity Bed nucleus of stria terminalis between vmPFC and BNST, the vmPFC lesion patients had significantly lower resting-state Emotion perfusion of the right BNST. No such perfusion differences were observed for the amyg- Lesion dala, striatum, hypothalamus, or periaqueductal gray. This study thus provides unique Anxiety data on the relationship between vmPFC and BNST, suggesting that vmPFC serves to promote BNST activity in humans. This finding is relevant for neural circuitry models of mood and anxiety disorders. © 2014 Elsevier Ltd. All rights reserved. this brain area is thought to be a key neural substrate under- 1. Introduction lying the pathophysiology of mood and anxiety disorders (Critchley, Mathias, & Dolan, 2001; Drevets, Price, & Furey, The ventromedial prefrontal cortex (vmPFC) plays a critical 2008; Milad, Rauch, Pitman, & Quirk, 2006; Myers-Schulz & role in human social and affective processing. Dysfunction in * Corresponding author. Department of Psychiatry, University of Wisconsin-Madison, 6001 Research Park Blvd., Madison, WI, 53719, USA. E-mail address: [email protected] (M. Koenigs). http://dx.doi.org/10.1016/j.cortex.2014.11.013 0010-9452/© 2014 Elsevier Ltd. All rights reserved. 282 cortex 64 (2015) 281e288 Koenigs, 2012; Price, 1999). However, the precise mechanisms Wagner, et al., 2013; Somerville, Whalen, & Kelley, 2010; by which vmPFC dysfunction contributes to affective psy- Straube, Mentzel, & Miltner, 2007; Walker, Toufexis, & Davis, chopathology are not fully understood. A leading neural cir- 2003). Moreover, a previous neuroimaging study in non- cuit model proposes that vmPFC serves to regulate negative human primates found that bilateral orbitofrontal cortex affect via top-down inhibition of brain regions involved in (OFC) lesions (which included regions of vmPFC) were asso- processing negative emotiondparticularly the amygdala- ciated with reduced BNST metabolism and reduced anxious dand that pathologically elevated levels of negative affect in behavior in a human intruder paradigm (Fox et al., 2010; Kalin, mood and anxiety disorders result from deficient vmPFC- Shelton, & Davidson, 2007). In addition, across the lesioned mediated inhibition of amygdala activity (Milad et al., 2006; and non-lesioned monkeys, the level of BNST metabolism Quirk & Gehlert, 2003; Rauch, Shin, & Phelps, 2006). While positively correlated with the degree of anxious behavior. this model is consistent with a considerable body of These findings suggest that vmPFC/OFC may play a crucial anatomical, behavioral, and neurophysiological data from role in generating or maintaining negative affect by promoting rodent fear conditioning paradigms (Milad et al., 2006), studies BNST activity. To explore this hypothesis in humans, we of human lesion patients suggest a more complex role of employed a magnetic resonance imaging (MRI) measure of vmPFC in affective function. For instance, although vmPFC resting cerebral blood flow (CBF) in a sample of neurosurgical lesion patients exhibit increased amygdala activity in patients with circumscribed bilateral vmPFC lesions. We hy- response to aversive stimuli (Motzkin et al., 2015), vmPFC pothesized that, consistent with the results of the non-human damage has been shown to reduce the likelihood of developing primate study (Fox et al., 2010), humans with bilateral vmPFC PTSD and depression (Koenigs, Huey, Calamia, et al., 2008; damage would exhibit reduced BNST blood perfusion, which Koenigs, Huey, Raymont, et al., 2008). These findings suggest would in turn correlate with self-report measures of negative that vmPFC may coordinate multiple neural processes critical affect and anxiety. Furthermore, we used rest-state fMRI in for the expression of negative affect in humans. Beyond top- the healthy adult comparison group to assess functional down inhibition of amygdala, vmPFC may also modulate ac- connectivity between BNST and vmPFC. tivity in other regions, such as the bed nucleus of the stria terminalis (BNST). The BNST is a basal forebrain structure that is considered 2. Methods to be a component of the “extended amygdala” complex, in light of similarities in development, connectivity, and 2.1. Participants cytoarchitecture to the adjacent central nucleus of the amygdala (Heimer, Harlan, Alheid, Garcia, & de Olmos, 1997). The lesion group consisted of four adult neurosurgical pa- The BNST and vmPFC are strongly interconnected (Avery tients with extensive bilateral parenchymal damage, largely et al., 2014), and BNST activity has been linked to anxiety- confined to the vmPFCddefined as the medial one-third of the related behavior (Davis & Whalen, 2001; Kalin, Shelton, Fox, orbital surface and the ventral one-third of the medial surface Oakes, & Davidson, 2005; Mobbs et al., 2010; Somerville, of prefrontal cortex, bilaterally (Fig. 1). Each of the four Fig. 1 e Lesion overlap of vmPFC patients. Color indicates the number of overlapping lesions at each voxel. All vmPFC patients had damage to the medial one-third of the OFC and the ventral one-third of medial surface of prefrontal cortex, bilaterally. This area includes Brodmann areas 11, 12, 24, 25, 32, and the medial portion of 10 below the level of the genu of the corpus callosum, as well as subjacent white matter. cortex 64 (2015) 281e288 283 patients underwent surgical resection of a large anterior cra- thickness ¼ 3 mm, gap ¼ .5 mm, 38 interleaved axial oblique nial fossa meningioma via craniotomy. Initial clinical pre- slices). Field maps were acquired using two separate acquisi- ¼ ¼ ¼ a ¼ sentations included subtle or obvious personality changes tions (TR 600 msec, TE1 7 msec, TE2 10 msec, 60 , over several months preceding surgery. On post-surgical MRI, FOV ¼ 240 Â 240 mm2, matrix ¼ 256 Â 128, slice although vasogenic edema largely resolved, there were thickness ¼ 4 mm, 33 axial oblique slices). Rest-state func- persistent T2-weighted signal changes, consistent with gliosis, tional images were collected while subjects lay still and in the vmPFC bilaterally. All experimental procedures were awake, passively viewing a fixation cross for 5 min. Scans conducted more than three months after surgery, when the were acquired in the following order: pcASL, field map, rest, expected recovery was complete. At the time of testing, all task, T1, T2-FLAIR. The fMRI task data from this scan session patients had focal, stable MRI signal changes and resection are presented in separate manuscripts (Motzkin et al., 2014, cavities and were free of dementia and substance abuse. 2015). Nineteen healthy adults with no history of brain injury, neurological or psychiatric illness, or current use of psycho- 2.3. Lesion segmentation and image normalization active medication were recruited as a normal comparison (NC) group. Demographic and neuropsychological data for the Individual vmPFC lesions were visually identified and manu- vmPFC and NC groups are summarized in Table 1. ally segmented on the T1-weighted images. Lesion boundaries were drawn to include areas with gross tissue damage or 2.2. MRI data acquisition abnormal signal characteristics on T1 or T2 FLAIR images. T1- weighted images were skull-stripped, rigidly co-registered All structural and functional MRI data were acquired using a with a functional volume from each subject, then diffeo- 3.0 T GE Discovery MR750 scanner equipped with an 8-channel morphically aligned to the Montreal Neurological Institute radio-frequency head coil array (General Electric Medical (MNI) coordinate system using a Symmetric Normalization & Systems; Waukesha, WI). High-resolution T1-weighted (SyN) algorithm (Avants Gee, 2004) with constrained cost- anatomical images were acquired using an inversion-recovery function masking to prevent warping of tissue within
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