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This study examines declarative memory retrieval in ASD depending on the availability and access to stored conceptual knowledge. Fifteen autistic participants and a matched control group of 18 typically-developed (TD) volunteers completed a Remember-Know paradigm manipulated by encoding-type (categorical, perceptual) and item-typicality (high-typical, low-typical). The autistic group showed worse and slower recognition and less recollection but equivalent familiarity-based memories compared to TDs. Notably, low-typical items did not improve their memories as they did for TDs, likely due to difficulties in matching low-fit information to the stored schema. Results suggest that memory decline in ASD may derive from the episodic system and its dynamics with the semantic system. These findings may inform interventional strategies for enhancing learning abilities in ASD.

BACKGROUND. Although mania is characteristic of bipolar disorder, it can also occur following focal brain damage. Such cases may provide unique insight into brain regions responsible for mania symptoms and identify therapeutic targets. METHODS. Lesion locations associated with mania were identified using a systematic literature search (n = 41) and mapped onto a common brain atlas. The network of brain regions functionally connected to each lesion location was computed using normative human connectome data (resting-state functional MRI, n = 1000) and contrasted with those obtained from lesion locations not associated with mania (n = 79). Reproducibility was assessed using independent cohorts of mania lesions derived from clinical chart review (n = 15) and of control lesions (n = 490). Results were compared with brain stimulation sites previously reported to induce or relieve mania symptoms. RESULTS. Lesion locations associated with mania were heterogeneous and no single brain region was lesioned in all, or even most, cases. However, these lesion locations showed a unique pattern of functional connectivity to the right orbitofrontal cortex, right inferior temporal gyrus, and right frontal pole. This connectivity profile was reproducible across independent lesion cohorts and aligned with the effects of therapeutic brain stimulation on mania symptoms. CONCLUSION. Brain lesions associated with mania are characterized by a specific pattern of brain connectivity that lends insight into localization of mania symptoms and potential therapeutic targets. FUNDING. Fundacao para a Ciencia e Tecnologia (FCT), Harvard Medical School DuPont-Warren Fellowship, Portuguese national funds from FCT and Fundo Europeu de Desenvolvimento Regional, Child Neurology Foundation Shields Research, Sidney R. Baer, Jr. Foundation, Nancy Lurie Marks Foundation, Mather's Foundation, and the NIH., Introduction Patients presenting with psychiatric symptoms after focal brain damage challenge the boundaries between neurology and psychiatry (1, 2). Such cases are of interest as they can provide causal links [...]

Background: Obsessive-compulsive disorder (OCD) may develop following brain lesions, but lesion distribution and connectivity patterns are unknown., Methods: OCD-associated lesions, identified from systematic literature search, were traced on common brain space and compared to control lesions (N=608). Topography was analyzed using brain atlases, and lesion location networks computed using normative functional connectivity (N=1000). Lesional network maps (LNMs) were contrasted to data from primary OCD., Results: Among 129 case-descriptions of lesional OCD, traced lesions (n=40) were more specifically located in orbitofrontal cortex bilaterally and right temporal pole, and more connected to orbitofrontal cortex and ventral basal ganglia, bilaterally. LNMs overlapped with primary OCD functional peaks from Neurosynth, revealed abnormal functional connectivity in patients with primary OCD (n=54) compared to controls (n=61), and aligned with brain stimulation targets., Conclusions: Lesional OCD has specific patterns of brain lesion topography and functional connectivity, with LNMs associated to brain functional patterns in primary OCD.