Cognitive and Behavioral Neurology最新文献

The last 2 decades have seen an explosion of neuroscience research on morality, with significant implications for brain disease. Many studies have proposed a neuromorality based on intuitive sentiments or emotions aimed at maintaining collaborative social groups. These moral emotions are normative, deontological, and action based, with a rapid evaluation of intentionality. The neuromoral circuitry interacts with the basic mechanisms of socioemotional cognition, including social perception, behavioral control, theory of mind, and social emotions such as empathy. Moral transgressions may result from primary disorders of moral intuitions, or they may be secondary moral impairments from disturbances in these other socioemotional cognitive mechanisms. The proposed neuromoral system for moral intuitions has its major hub in the ventromedial prefrontal cortex and engages other frontal regions as well as the anterior insulae, anterior temporal lobe structures, and right temporoparietal junction and adjacent posterior superior temporal sulcus. Brain diseases that affect these regions, such as behavioral variant frontotemporal dementia, may result in primary disturbances of moral behavior, including criminal behavior. Individuals with focal brain tumors and other lesions in the right temporal and medial frontal regions have committed moral violations. These transgressions can have social and legal consequences for the individuals and require increased awareness of neuromoral disturbances among such individuals with brain diseases.

Background: Decision-making is essential to human functioning, and resolving uncertainty is an essential part of decision-making. Impaired decision-making is present in many pathological conditions, and identifying markers of decision-making under uncertainty will provide a measure of clinical impact in future studies of therapeutic intervention for impaired decision-making.

Objective: To describe EEG event-related potentials (ERPs) correlating with decision-making under uncertain conditions when compared with certain conditions.

Method: We used a novel card-matching task based on the Wisconsin Card Sorting Test to describe the neural correlates of uncertainty, as measured by EEG, in a group of 27 neurotypical individuals. We evaluated 500-ms intervals in the 2 seconds after card presentation to identify ERPs that are associated with maximal uncertainty compared with maximal certainty.

Results: After correcting for multiple comparisons, we identified an ERP in the 500-1000-ms time frame (certain > uncertain, max amplitude 12.73 µV, latency 914 ms) in the left posterior inferior region of the scalp. We also found a P300-like ERP in the left frontal and parietal regions in the 0-500-ms time frame when the individuals received correct versus incorrect feedback (incorrect feedback > correct feedback, max amplitude 1.625 µV, latency 339 ms).

Conclusion: We identified an ERP in the 500-1000-ms time frame (certain > uncertain) that may reflect the resolution of uncertainty, as well as a P300-like ERP when feedback is presented (incorrect feedback > correct feedback). These findings can be used in future studies to improve decision-making and resolve uncertainty on the described markers.

A selective impairment for making hand postures that are required to use specific tools has rarely been reported in individuals with acquired brain injury, and such an impairment has not been documented at all in individuals with degenerative disorders. We describe an individual with posterior cortical atrophy and probable corticobasal syndrome who was unable to use tools because of an inability to make the proper hand posture required for each tool. This individual was, however, able to use the tools properly once her hand postures were corrected, and her ability to manipulate the tools (ie, timing, arm posture, and amplitude) was intact. Also, she had no difficulty with a test of her manipulation knowledge. Areas of hypoperfusion observed by single-photon emission computerized tomography included the anterior intraparietal sulcus in the left parietal lobe, which is an area that has been proposed to control hand postures. This selective impairment might be explained by the reasoning-based hypothesis for apraxia, which attributes hand posture errors in the absence of manipulation errors to dysfunction in one of the three independent pathways that subserve tool use, rather than the manipulation-based hypothesis for apraxia, which attributes hand posture errors to impaired manipulation knowledge. This is the first case with a degenerative disorder that revealed a selective impairment for making hand postures for tool use, which might be explained mainly by apraxia of hand postures along with visuospatial dysfunction (simultanagnosia) and/or sensory disturbance.

Background: Given the sparse nature of acute mania or psychosis in primary adrenal insufficiency (PAI), physicians may not be aware of the association of these two entities.

Objective: To conduct a systematic review of the literature for the purpose of identifying all studies reporting mania and/or psychosis in individuals with PAI.

Method: We conducted a systematic review according to PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines using the PubMed, Embase, and Web of Science databases from June 22, 1970 to June 22, 2021, for the purpose of identifying all studies reporting instances of mania or psychosis associated with PAI.

Results: We identified nine case reports featuring nine patients (M age = 43.3 years, male = 44.4%) over eight countries that fit our inclusion/exclusion criteria. Eight (89%) of the patients had experienced psychosis. Manic and/or psychotic symptom resolution was achieved in 100% of the cases, of which steroid replacement therapy was efficacious in seven (78%) cases and was sufficient in six (67%).

Conclusion: Acute mania and psychosis in the context of PAI is a very rare presentation of an already uncommon disease. Resolution of acute psychiatric change is reliably achieved with the correction of underlying adrenal insufficiency.

Background: Although subjective sensory hypersensitivity is prevalent after stroke, it is rarely recognized by health care providers, and its neural mechanisms are largely unknown.

Objective: To investigate the neuroanatomy of poststroke subjective sensory hypersensitivity as well as the sensory modalities in which subjective sensory hypersensitivity can occur by conducting both a systematic literature review and a multiple case study of patients with subjective sensory hypersensitivity.

Method: For the systematic review, we searched three databases (Web of Science, PubMed, and Scopus) for empirical articles discussing the neuroanatomy of poststroke subjective sensory hypersensitivity in humans. We assessed the methodological quality of the included studies using the case reports critical appraisal tool and summarized the results using a qualitative synthesis. For the multiple case study, we administered a patient-friendly sensory sensitivity questionnaire to three individuals with a subacute right-hemispheric stroke and a matched control group and delineated brain lesions on a clinical brain scan.

Results: Our systematic literature search resulted in four studies (describing eight stroke patients), all of which linked poststroke subjective sensory hypersensitivity to insular lesions. The results of our multiple case study indicated that all three stroke patients reported an atypically high sensitivity to different sensory modalities. These patients' lesions overlapped with the right anterior insula, the claustrum, and the Rolandic operculum.

Conclusion: Both our systematic literature review and our multiple case study provide preliminary evidence for a role of the insula in poststroke subjective sensory hypersensitivity and suggest that poststroke subjective sensory hypersensitivity can occur in different sensory modalities.

Background: Perseveration is one of the most debilitating symptoms of Huntington disease (HD).

Objective: To study perseveration and its relationship to comorbid behavioral symptoms, motor decline, functional decline, and subject self-report accuracy by analyzing cross-sectional data tracking individuals who have or are at risk for HD and healthy controls (HC).

Method: We studied 96 individuals from HD families and 35 HC who were either family controls or gene negative. We used χ 2 tests to compare patient demographic and survey outcomes data and to analyze the presence of obsessions and compulsions (OC), depression, and apathy relative to the presence of perseveration.

Results: Individuals with HD and perseveration had a higher presence of OC, depression, and apathy compared with individuals with HD of the same stages without perseveration (19%, 47.6%, and 47.6% vs 15%, 40%, and 25%, respectively). In addition, individuals in HD Stages 1-3 with higher motor scores (showing a later stage of disease) displayed a significantly higher rate of perseveration than the HC ( P = 0.0476; P = 0.0499, respectively). The presence of an informant resulted in a significantly higher rate of perseveration reporting for individuals in HD Stages 1 and 2 (41.2% and 53.8% with informant vs 23.5% and 11.1% without informant, respectively).

Conclusion: Perseveration was seen across all motor and functional stages for the individuals with HD, without significant differences between the different stages. Additionally, informants were beneficial to obtaining accurate patient reports of perseveration. These findings should prove useful for physician evaluation and treatment considerations.