In neurosurgical literature, findings such as deep brain stimulation (DBS) electrode positions are conventionally reported in relation to the anterior and posterior commissures of the individual patient (AC/PC coordinates). However, the neuroimaging literature including neuroanatomical atlases, activation patterns, and brain connectivity maps has converged on a different population-based standard (MNI coordinates). Ideally, one could relate these two literatures by directly transforming MRIs from neurosurgical patients into MNI space. However obtaining these patient MRIs can prove difficult or impossible, especially for older studies or those with hundreds of patients. Here, we introduce a methodology for mapping an AC/PC coordinate (such as a DBS electrode position) to MNI space without the need for MRI scans from the patients themselves. We validate our approach using a cohort of DBS patients in which MRIs are available, and test whether several variations on our approach provide added benefit. We then use our approach to convert previously reported DBS electrode coordinates from eight different neurological and psychiatric diseases into MNI space. Finally, we demonstrate the value of such a conversion using the DBS target for essential tremor as an example, relating the site of the active DBS contact to different MNI atlases as well as anatomical and functional connectomes in MNI space.

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The role of distinct limbic areas in emotion regulation has been largely inferred from neuroimaging studies. Recently, the opportunity for intracranial recordings from limbic areas has arisen in patients undergoing deep brain stimulation (DBS) for neuropsychiatric disorders including major depressive disorder (MDD) and obsessive compulsive disorder (OCD). Here we test the hypothesis that distinct temporal patterns of local field potential (LFP) activity in the human limbic system reflect disease state and symptom severity in MDD and OCD patients. To this end, we recorded LFPs via implanted DBS electrodes from the bed nucleus of stria terminalis (BNST area) in 12 patients (5 OCD, 7 MDD) and from the subgenual cingulate cortex in 7 MDD patients (CG25 area). We found a distinct pattern of oscillatory activity with significantly higher α-power in MDD compared with OCD in the BNST area (broad α-band 8-14 Hz; P<0.01) and a similar level of α-activity in the CG25 area as in the BNST area in MDD patients. The mean α-power correlated with severity of depressive symptoms as assessed by the Beck depression inventory in MDD (n=14, r=0.55, P=0.042) but not with severity of obsessive compulsive symptoms in OCD. Here we show larger α-band activity in MDD patients compared with OCD recorded from intracranial DBS targets. Our results suggest that α-activity in the limbic system may be a signature of symptom severity in MDD and may serve as a potential state biomarker for closed loop DBS in MDD.