Cognitive and Behavioral Neurology最新文献

Background: Postural instability is a common and debilitating symptom in Parkinson disease (PD) that impacts daily functioning and quality of life. Executive function, a domain of cognitive functioning, has been associated with postural control. Impairments in executive function, therefore, may lead to postural instability. Here, we hypothesize that cognitive flexibility may be particularly relevant to postural instability and use specifically selected cognitive assessments to evaluate cognitive flexibility and other key aspects of executive function.

Objective: To examine the relationship between postural instability and cognitive flexibility in PD.

Methods: We assessed 36 individuals, including 12 with PD and postural instability (PDPI+), 12 with PD without postural instability (PDPI-), and a control group of 12 age-matched individuals without PD. Cognitive assessments included the MoCA and the NIH Toolbox Cognition Battery. We also calculated a clinical balance score (CBS) during clinical evaluation. We used ANOVA, ANCOVA, Pearson correlation, and partial correlation analyses.

Discussion: The PDPI+ group exhibited significant cognitive deficits compared to the control group. We observed strong negative correlations between CBS and cognitive flexibility in all participants with PD, suggesting a robust connection between cognitive flexibility and postural control. These associations remained significant after controlling for age, disease duration, and levodopa-equivalent daily dose.

Conclusions: Our findings underscore the importance of the relationship between cognitive flexibility and postural control in individuals with PD. These results highlight the potential for targeted interventions to improve cognitive flexibility and, consequently, postural stability in individuals with PD.

Hate toward people groups is a significant cause of human suffering, yet we understand relatively little about its neurocognitive and neuroanatomical bases. While definitions of hate vary, most agree that it can be defined as an aversion to certain others that motivates attempts to expel them through methods ranging from physical violence to passive avoidance. The evolutionary roots of group hate are in the ingroup-outgroup distinction, in which the individual favors ingroup members over outgroup members. Earlier studies on the effects of hate speech and propaganda show that the dehumanization of outgroup members facilitates hate. Although several mechanisms have been proposed, evidence suggests that dehumanization leads to hate due to the perceived failure of outgroup members to meet a moral ideal of right and wrong. As such, hate can be understood as an innate moral sentiment that enhances themes of ingroup loyalty and purity by expelling the offending outgroup. It involves regions of the brain active in social cognition, emotion, empathy, and behavioral regulation, such as the medial prefrontal cortex, inferior frontal gyrus, anterior cingulate cortex, amygdala, insula, and temporoparietal junction. By examining these neurobiological aspects of hate and understanding them in the context of the social and cultural factors that foster hate, we can gain deeper insights into this harmful phenomenon and how best to combat it.

Movement and maintenance of posture involve many interacting factors that rely on a broad neural network. These factors include proprioception, body schema, and peripersonal and extrapersonal space, all of which may be affected in individuals with neurocognitive disorders. Frontal release signs are a common clinical finding in such individuals, resulting from the disruption of the related neural networks. In this case series, we discuss the potential clinical relevance of midline hand drift (MHD). MHD is a rarely documented physical exam finding in which one or both hands move toward the midline when the individual is seated upright with their eyes open, arms outstretched, and palms facing upwards. Upon examination, 24 individuals with a chief complaint of worsening memory were found to have MHD. All 24 individuals with MHD had at least mild cognitive impairment, and 22 were also diagnosed with a neurodegenerative disorder. The most common diagnoses among these individuals were Parkinson disease dementia, Lewy body dementia, and vascular dementia. Nine of the 24 patients demonstrated no frontal release signs upon examination. MHD may be a useful clinical finding that aids in the diagnosis of an underlying neurocognitive disorder. Assessing for MHD may be most beneficial for individuals who are in the earlier stages of neurocognitive decline. They may show mild impairment on the Mini-Mental State Examination or the Montreal Cognitive Assessment, but no other characteristic findings (eg, frontal release signs).