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Khosravani, S.

Publications and source records attributed to Khosravani, S..

3 recordsLinked to original sources

The methodological foundations of lesion network mapping remain sound

Lesion network mapping (LNM) and related techniques have been used in over 200 studies, primarily to test whether anatomically distributed lesions that cause the same symptom fall within a common brain network. A recent article1 challenges the specificity and validity of this technique, suggesting that lesion network maps primarily reflect intrinsic properties of the normative connectome rather than lesion-symptom relationships. However, the data and procedures in van den Heuvel et al. do not reflect those used in most LNM studies. Further, the main conclusions were based on similarity between maps, but similarity does not imply the absence of meaningful differences. In contrast, LNM provides evidence for meaningful differences using specificity testing. Exemplary analyses of 1090 lesion locations from 34 prior LNM studies do not support van den Heuvels concerns and confirm the lesion-deficit specificity of LNM. While we encourage further methodological investigation, the analyses of van den Heuvel et al. do not invalidate prior LNM findings or future applications.

neuroscience↗

Focal brain stimulation sites that modify autonomic arousal map to a convergent brain circuit and potential therapeutic target

Causal modulation of autonomic outflow could yield new therapeutic targets for autonomic hyperactivation. We employed three natural experiments in which different brain regions were targeted using transcranial magnetic stimulation (TMS) (n=139 sites, n=14 individuals), deep brain stimulation (n=392 sites, n=58 individuals), or low-intensity focused ultrasound (n=46 sites, n=23 individuals) with subsequent autonomic measurements. Using a human connectome database (n=1000) as a wiring diagram, we identified a convergent brain circuit that, when focally modulated, transiently reduces autonomic arousal. This circuit significantly resembled previously reported causal circuits for posttraumatic stress disorder (PTSD) and anxiety. In independent datasets, TMS to the autonomic arousal circuit reduced laboratory startle in healthy volunteers (n=28), lesions to this circuit reduced exaggerated startle in PTSD (n=193), and TMS to this circuit reduced anxiety-related autonomic symptoms in patients with clinically significant anxiety (n=30). Thus, the convergent circuit may serve as a potential neuromodulation target for autonomic hyperactivation.

neuroscience↗

Lesion Network Localization of a Stable Personality Trait

ObjectiveTo identify a convergent neuroanatomical substrate for novelty seeking (NS), a stable personality trait, which could serve as a therapeutic target for transcranial magnetic stimulation (TMS). MethodsWe analyzed two independent datasets (total n=136) in which the Temperament and Character Inventory (TCI) was used to document alterations across 7 stable personality traits before and after brain lesions surgically induced by glioma resection. Using lesion network mapping, we examined whether alterations in NS were causally associated with lesions to specific brain networks. We assessed for strength of replication across datasets and specificity against other personality traits. ResultsLesion locations that are linked to NS map to a common brain with its largest cluster in the dorsal cingulate. This map was specific to NS relative to other personality traits and overlapped with prior published neuroimaging findings related to the term "novelty". Utilizing a pre-computed connectome, we also derived a map highlighting potential targets for non-invasive brain stimulation that may alter this stable personality trait. ConclusionsWe derived and cross-validated a brain network that is functionally connected to lesions that are causally responsible for the stable personality trait "novelty seeking". Lesions to this network were associated with changes in NS. This includes a superficial node within the dorsolateral prefrontal cortex that may serve as a promising TMS target to modulate or protect against abnormal NS.

neuroscience↗