OBJECTIVETo investigate whether DTI abnormalities in patients with nondemented subcortical ischemic vascular disease (SIVD) are correlated to general cognitive function and executive function independent of conventional MRI parameters.

METHODSSixty-six SIVD patients including 30 with cognitive impairment without dementia (VCIND) and 36 with normal cognition (NCI) underwent DTI and cognitive assessment of the general cognitive function and executive function. Conventional MRI parameters and DTI parameters were measured within the white matter lesions (WMLs), normal-appearing white matter (NAWM) and normal-appearing gray matter (NAGM). The independent predictors of general cognitive function and executive function in SIVD patients was analyzed.

RESULTSNCI and VCIND patients showed significant differences in the periventricular WMLs, ADC valus in NAWM and WMLs of the centrum semiovale, and FA values in NAWM of the anterior periventricular. Except for ADC values of the caudate nucleus, ADC and FA values in the subcortical NAGM showed significant difference between the two groups. After controlling for age and education, PVLs and ADC values in the WMLs and NAWM of the centrum semiovale and putamen, and FA values in the anterior periventricular NAWM, WMLs and putamen showed significant correlations to MMSE; the number of lacunar infarcts, ADC values in posterior periventricular NAWM and caudate nucleus, and FA values in anterior periventricular NAWM and thalamus showed significant correlations to CDT. Multivariate analysis showed independent correlations of the ADC values in WMLs and NAWM of the centrum semiovale to MMSE, and demonstarted correlations of the ADC values of the caudate nucleus and number of lacunar infarcts to CDT.

CONCLUSIONIn nondemented SIVD subjects, the integrity of the white matter in the centrum semiovale strongly correlates to the general cognition, and the microstructural damage of the caudate nucleus head predicts executive function impairment independent of other MRI variables.

Brain Ischemia ; pathology ; physiopathology ; psychology ; Case-Control Studies ; Caudate Nucleus ; pathology ; Cerebral Cortex ; pathology ; Cognition ; physiology ; Cognition Disorders ; pathology ; physiopathology ; Diffusion Tensor Imaging ; Humans ; Magnetic Resonance Imaging

Psychophysiological and functional neuroimaging studies have frequently and consistently shown that emotional information can be processed outside of the conscious awareness. Non-conscious processing comprises automatic, uncontrolled, and fast processing that occurs without subjective awareness. However, how such non-conscious emotional processing occurs in patients with various psychiatric disorders requires further examination. In this article, we reviewed and discussed previous studies on the non-conscious emotional processing in patients diagnosed with anxiety disorder, schizophrenia, bipolar disorder, and depression, to further understand how non-conscious emotional processing varies across these psychiatric disorders. Although the symptom profile of each disorder does not often overlap with one another, these patients commonly show abnormal emotional processing based on the pathology of their mood and cognitive function. This indicates that the observed abnormalities of emotional processing in certain social interactions may derive from a biased mood or cognition process that precedes consciously controlled and voluntary processes. Since preconscious forms of emotional processing appear to have a major effect on behaviour and cognition in patients with these disorders, further investigation is required to understand these processes and their impact on patient pathology.
Anxiety Disorders ; Bias (Epidemiology) ; Bipolar Disorder ; Cognition ; Depression ; Functional Neuroimaging ; Humans ; Interpersonal Relations ; Pathology ; Psychopathology* ; Schizophrenia

The seeds of addiction are typically sown years prior to the onset of addictive substance use or engagement in addictive behaviors, due to the priming of the reward pathway (RewP) by alterations in the mechanism of stress-signaling from the hypothalamic-pituitary-adrenal axis (HPA) and related pathways. Excessive stress from a single-event and/or cumulative life experiences during childhood, such as those documented in the Adverse Childhood Experiences Study, is translated into neurobiological toxicity that alters the set-point of the HPA axis and limbic system homeostasis [suggested new term: regulation pathway (RegP)]. The resultant alteration of the RegP not only increases the risk for psychiatric and physical illness, but also that for early onset and chronic addictions by dysregulating the RewP. This paper reviews the interface of these symbiotic pathways that result in the phenotypic pathology of emotional dysregulation, cognitive impairment, and compulsive behaviors, as well as morbidity and shorter life expectancy when dysregulated by chronic stress.
Behavior, Addictive ; Cognition Disorders ; Compulsive Behavior ; Homeostasis ; Life Change Events ; Life Expectancy ; Limbic System ; Pathology ; Reward

OBJECTIVETo explore the correlation between cognition disorder and morphologic change of hippocampal neurons after traumatic brain injury (TBI).

METHODSWistar rat models with severe TBI were made by Marmarou's method. The histopathological change of the neurons in the hippocampus area were studied with hematoxylin-eosin (HE) staining and terminal deoxynucleotidyl transferase-mediated X-dUPT nick end labeling (TUNEL), respectively. The cognitive function was evaluated with the Morris water maze test.

RESULTSThe comprehensive neuronal degeneration and necrosis could be observed in CA2-3 regions of hippocampus at 3 days after injury. Apoptotic positive neurons in CA2-4 regions of hippocampus and dentate gyrus increased in the injured group at 24 hours following TBI. They peaked at 7 days and then declined. Significant impairment of spatial learning and memory was observed after injury in the rats.

CONCLUSIONSThe rats have obvious disorders in spatial learning and memory after severe TBI. Meanwhile, delayed neuronal necrosis and apoptosis can be observed in the neurons in the hippocampus area. It suggests that delay ed hippocampal cell death may contribute to the functional deficit.

Animals ; Apoptosis ; Brain Injuries ; complications ; pathology ; Cognition Disorders ; etiology ; pathology ; Hippocampus ; pathology ; In Situ Nick-End Labeling ; Male ; Memory Disorders ; etiology ; pathology ; Necrosis ; Rats ; Rats, Wistar

PURPOSE: This study was conducted to synthesis the results of research on relationships of cognitive impairment with multi-dimensional correlates of rheumatic disease through a systematic literature review and meta-analysis. METHODS: For the study purpose, 23 studies were selected through a systematic process of searching the literature. RESULTS: The study results showed that among general characteristics, age and education were the variables having a significant relationship with cognitive impairment. Among health risk factors, obesity appeared to have a significant positive relationship with cognitive impairment. For past history, diabetes and hypertension were shown to have a significant positive relationship with cognitive impairment. It was noted also that aPL, one of the physiological factor, had significant association with cognitive impairment. None of the medication related factors had a significant relationship with cognitive impairment. Results showed that among disease related factors, disease activity had the highest relationship with cognitive impairment. Depression, among psychological factors, was the only variable having a significant relationship with cognitive impairment. CONCLUSION: The findings indicate that the variables strongly impacting on cognitive impairment in rheumatic disease are depression and disease activity.
Anxiety ; Cognition ; Cognition Disorders/complications/*pathology ; Databases, Factual ; Depression/complications ; Humans ; Hypertension/complications ; Obesity/complications ; Rheumatic Diseases/complications/*pathology ; Risk Factors

This study aimed to explore the cognitive dysfunction of and hippocampal neuron damage to Wistar rats with STZ-induced diabetes at different morbidity time. All Wistar rats in the tests received intraperitoneal injections of streptozotocin (STZ; 60 mg/kg) to induce type 1 diabetes. The concentration of blood glucose and the body weight were investigated, the cognitive ability of rats was assessed using a standardized Y-maze, and the apoptotic neurons in the CA1 of the hippocampus were also examined by using the HE staining. While the sickening time was prolonged, the blood glucose concentration of the experimental rats increased continuously and the body weight decreased. On the 70th day after STZ administration, the neuronal loss in the hippocampal CA1 region increased and the working errors increased in rats with the diabetes. The results showed that Wistar rats could complicate with diabetic encephalopathy in 70 days after injection of STZ for inducing the diabetes.
Animals ; Blood Glucose ; Body Weight ; CA1 Region, Hippocampal ; cytology ; pathology ; Cognition ; Cognition Disorders ; physiopathology ; Diabetes Mellitus, Experimental ; physiopathology ; Diabetes Mellitus, Type 1 ; Neurons ; pathology ; Rats ; Rats, Wistar ; Streptozocin

OBJECTIVETo explore the diagnostic value of magnetic resonance (MR) diffusion tensor imaging (DTI) in detecting brain white matter (WM) damage of patients with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) and evaluating their cognitive dysfunction.

METHODSThirteen patients with DEACMP and thirteen age- and sex-matched volunteers underwent DTI using 1.5T MR scanner. FA and ADC values of 16 WM regions of interests (ROIs) were measured on DTI by two experienced radiologists independently with double blind methods, cognitive functions were evaluated by another experienced neurologist blinded to patient's medical history using the Montreal cognitive assessment (MoCA). ADC and FA values in DEACMP patients, and their correlations with cognitive dysfunction were analyzed.

RESULTSADC values of DEACMP patients increased significantly in all ROIs (P < 0.05) in comparison with the corresponding ROIs of healthy controls, whereas FA values were significantly decreased in all ROIs (P < 0.05) in comparison with that in controls except the bilateral optic radiations, anterior and posterior internal capsules. MoCA scores were positively correlated with FA values of bilateral lower frontal (r(L) = 0.736, P = 0.011; r(R) = 0.762, P = 0.003) lobe, temporal lobe (r(L) = 0.605, P = 0.016; r(R) = 0.559, P = 0.021) and total average WM (r(A) = 0.688, P = 0.001), however it inversely correlated with ADC values of bilateral lower frontal WM (r(L) = -0.674, P = 0.007; r(R) = -0.681, P = 0.019).

CONCLUSIONDTI can quantitatively reveal WM microstructure damage of DEACMP patients, indicate the severity of cognitive dysfunctions, and provide important information for pathogenesis and pathological study for DEACMP.

Brain ; pathology ; Brain Diseases ; diagnosis ; etiology ; Carbon Monoxide Poisoning ; complications ; Cognition ; Cognition Disorders ; Diffusion Magnetic Resonance Imaging ; Diffusion Tensor Imaging ; Double-Blind Method ; Humans ; White Matter ; pathology

OBJECTIVETo review the main neuropsychiatric disorders and cognitive deficits in patients with Cushing's disease (CD) and the associated pathophysiological mechanisms underlying CD. These mechanistic details may provide recommendations for preventing or treating the cognitive impairments and mood disorders in patients with CD.

DATA SOURCESData were obtained from papers on psychiatric and cognitive complications in CD published in English within the last 20 years. To perform the PubMed literature search, the following keywords were input: cushing's disease, cognitive, hippocampal, or glucocorticoids.

STUDY SELECTIONStudies were selected if they contained data relevant to the topic addressed in the particular section. Because of the limited length of this article, we have frequently referenced recent reviews that contain a comprehensive amalgamation of literature rather than the actual source papers.

RESULTSPatients with active CD not only suffer from many characteristic clinical features, but also show some neuropsychiatric disorders and cognitive impairments. Among the psychiatric manifestations, the common ones are emotional instability, depressive disorder, anxious symptoms, impulsivity, and cognitive impairment. Irreversible effects of previous glucocorticoid (GC) excess on the central nervous system, such as hippocampal and the basal ganglia, is the most reasonable reason. Excess secretion of cortisol brings much structural and functional changes in hippocampal, such as changes in neurogenesis and morphology, signaling pathway, gene expression, and glutamate accumulation. Hippocampal volume loss can be found in most patients with CD, and decreased glucose utilization caused by GCs may lead to brain atrophy, neurogenesis impairment, inhibition of long-term potentiation, and decreased neurotrophic factors; these may also explain the mechanisms of GC-induced brain atrophy and hippocampal changes.

CONCLUSIONSBrain atrophy and hippocampal changes caused by excess secretion of cortisol are thought to play a significant pathophysiological role in the etiology of changes in cognitive function and psychiatric disturbances. The exact mechanisms by which GCs induce hippocampal volume loss are not very clear till now. So, further investigations into the mechanisms by which GCs affect the brain and the effective coping strategy are essential.

Brain-Derived Neurotrophic Factor ; genetics ; Cognition Disorders ; etiology ; Glucocorticoids ; physiology ; Hippocampus ; pathology ; physiology ; Humans ; Mental Disorders ; etiology ; Neurogenesis ; Pituitary ACTH Hypersecretion ; complications ; pathology ; physiopathology ; Quality of Life ; Signal Transduction

Dandy-Walker variant is a developmental malformation consisting of cerebellar hypoplasia and cystic dilatation of the fourth ventricle. Previous research has proposed a possible role for the cerebellum in cognition and in schizophrenia. In this paper we report a schizophrenia-like psychotic disorder in a 30 year-old woman with Dandy-Walker variant. The patient was treated with risperidone 6 mg/day, biperiden 4 mg/day and risperidone depot 50 mg injections fortnightly, and most of the symptoms were ameliorated within 2 months. The similar cognitive profile to populations with cerebellar pathology and rarity of the condition strongly suggests that there may be direct relationship between cerebellar pathology and appearence of psychotic symptoms.
Adult ; Biperiden ; Cerebellum ; Cognition ; Comorbidity* ; Dandy-Walker Syndrome* ; Dilatation ; Female ; Fourth Ventricle ; Humans ; Pathology ; Psychotic Disorders* ; Risperidone ; Schizophrenia

Vascular dementia is a very frequent form of dementia. Debates over classification and diagnostic criteria, and controversy over identifiable treatment targets will continue until distinct pathophysiological mechanism of vascular dementia is found. Clinical diagnostic criteria are sufficiently strong to be useful for clinical trials, but need further refinement. Cognitive changes in vascular dementia are more variable than other disorders, and are dependent on the vascular pathology. Accurate diagnosis of vascular dementia is known to need the presence of reliable cerebrovascular disease on brain imaging. Although it seems obvious that cerebrovascular disease causes pathological damage and impaired cognition, it is very difficult to find the accurate contribution of cerebrovascular pathology to cognitive decline. Most studies have shown a small but significant benefit of cholinesterase inhibitors on cognition, the significance of this effect has been slight and benefits on global functioning, activities of daily living, and behaviour have not been consistently reported. Management of vascular dementia should focus on identifying and managing vascular risk factors.
Activities of Daily Living ; Cerebrovascular Disorders ; Cholinesterase Inhibitors ; Classification ; Cognition ; Dementia ; Dementia, Vascular* ; Diagnosis ; Neuroimaging ; Pathology ; Risk Factors