Cognitive impairment

• To evaluate the effectiveness of non-pharmacological multifactorial interventions on cognitive impairment in geriatric patients
• Characteristics and Changes of Cingulate Gyrus Function and Perfusion in Patients With Anti-N-Methyl-D-Aspartate Receptor Encephalitis
• Baseline characteristics of the U.S. Study to Protect Brain Health Through Lifestyle Intervention to Reduce Risk (U.S. POINTER): Successful enrollment of a diverse clinical trial cohort at risk for cognitive decline
• Differences in electrode placements between consensual and nonconsensual electroconvulsive therapy: retrospective chart review study
• Evaluation of the Drug-Drug Interaction Potential of the GlyT1 Inhibitor Iclepertin (BI 425809): A Physiologically Based Pharmacokinetic (PBPK) Modeling Approach
• Targeting synaptic plasticity to bridge translational gaps in sepsis-associated encephalopathy
• Evaluating the antioxidant-mediated neuroprotection of hamamelitannin against H₂O₂-induced oxidative damage
• Aerobic exercise ameliorates atherosclerosis-induced cognitive impairment via hippocampal IL-33/NF-kappaB signaling modulation

Cognitive impairment refers to difficulties in one or more areas of cognitive functioning, such as memory impairment, attention, language, perception, or problem-solving.

Cognitive impairment and dementia are related concepts, but they refer to different conditions with distinct characteristics.

Cognitive Impairment:

Definition: Cognitive impairment is a broad term that encompasses a range of cognitive function deficits, including memory, attention, language, and problem-solving skills. Scope: Cognitive impairment can be a temporary or permanent condition, and it may result from various factors such as medication side effects, nutritional deficiencies, sleep disorders, or other medical conditions. Severity: Cognitive impairment can vary in severity, from mild to moderate to severe. Reversibility: In some cases, cognitive impairment is reversible if the underlying cause is identified and treated. Dementia:

Definition: Dementia is a syndrome characterized by a decline in cognitive function that is severe enough to interfere with a person's daily life and activities. Scope: Dementia is generally a progressive condition and is often caused by neurodegenerative diseases such as Alzheimer's disease, vascular dementia, Lewy body dementia, or frontotemporal dementia. Symptoms: Common symptoms of dementia include memory loss, impaired judgment, difficulty with problem-solving, and changes in mood and behavior. Irreversibility: Unlike some forms of cognitive impairment, dementia is usually irreversible and tends to worsen over time. In summary, cognitive impairment is a broader term that can encompass various degrees and causes of cognitive decline, while dementia is a specific syndrome characterized by a significant and usually irreversible decline in cognitive function. Dementia is one of the potential outcomes of cognitive impairment, but not all individuals with cognitive impairment develop dementia. If someone is experiencing cognitive difficulties, it is essential to consult with a healthcare professional for a comprehensive evaluation and appropriate diagnosis.

Functional cognitive disorders are a group of overlapping conditions in which cognitive symptoms are present, which are genuine, distressing, and often disabling, but experienced inconsistently and not related to systemic or brain disease

Cognitive fatigability

Cognitive decline is a deterioration in cognitive function.

Several studies claimed that surgery in eloquent areas is possible without causing severe cognitive decline. However, this conclusion was relatively ungrounded due to the lack of extensive neuropsychological testing in homogenous patient groups.

Liu et al. retrospectively enrolled 92 consecutive patients with a confirmed diagnosis of Cushing's disease. A voxel-based analysis was performed to investigate the association between cerebral (18)F-fluorodeoxyglucose uptake and serum cortisol level. Relatively impaired metabolism of specific brain regions correlated with serum cortisol level was found. Specifically, notable correlations were found in the hippocampus, amygdala, and cerebellum, regions considered to be involved in the regulation and central action of glucocorticoids. Moreover, some hormone-associated regions were found in the frontal and occipital cortex, possibly mediating the cognitive decline seen in Cushing's disease. The findings link patterns of perturbed brain metabolism relates to individual hormone level, thus presenting a substrate for cognitive disturbances seen in Cushing's disease patients, as well as in other conditions with abnormal cortisol levels ¹⁾.

In the mid-1970s, the psychiatrist Edward Hare published two accounts of Michael Faraday's memory symptoms. He suggested the diagnostic possibilities of an amnesic syndrome related to a transient ischemic attack in the vertebrobasilar cerebrovascular system. This article revisits the contemporary evidence of Faraday's letters and the notes of his physician, Peter Mere Latham, and considers subsequent responses to and shortcomings of Hare's analysis. In light of more recent conceptualizations of memory disorders, a new formulation for Faraday's memory symptoms is suggested: namely, that he manifested a functional cognitive disorder ²⁾.

Cognitive impairment classification.

As Normal pressure hydrocephalus (NPH) progresses, cognitive impairment may become more generalized and less responsive to treatment.

Phenobarbital: Cognitive impairment (may be subtle and may outlast administration of the drug by at least several months), thus avoid in peds; sedation; paradoxical hyperactivity (especially in peds); may cause hemorrhage in newborns if the mother is on phenobarbital.

Vascular cognitive impairment (VCI) represents the second most common cause of dementia after Alzheimer's disease, and pathological changes in cerebral vascular structure and function are pivotal causes of VCI. Cognitive impairment caused by arterial ischemia has been extensively studied the whole time; the influence of cerebral venous congestion on cognitive impairment draws doctors' attention in recent clinical practice, but the underlying neuropathophysiological alterations are not entirely understood. A study by Wei et al. elucidated the specific pathogenetic role of cerebral venous congestion in cognitive-behavioral deterioration and possible electrophysiological mechanisms. Using cerebral venous congestion rat models, they found these rats exhibited decreased long-term potentiation (LTP) in the hippocampal dentate gyrus and impaired spatial learning and memory. Based on untargeted metabolomics, N-acetyl-L-cysteine (NAC) deficiency was detected in cerebral venous congestion rats; supplementation with NAC appeared to ameliorate synaptic deficits, rescue impaired LTP, and mitigate cognitive impairment. In a cohort of cerebral venous congestion patients, NAC levels were decreased; NAC concentration was negatively correlated with subjective cognitive decline (SCD) score but positively correlated with mini-mental state examination (MMSE) score. These findings provide a new perspective on cognitive impairment and support further exploration of NAC as a therapeutic target for the prevention and treatment of VCI ³⁾

Cognitive impairment diagnosis.