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

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

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

Sleep loss can severely impact on the integrity of cognitive functions. This review highlights the recent functional neuroimaging studies on the brain's response while performing cognitive tasks when deprived of sleep. Among sleep-deprived healthy volunteers, reduced attention, accompanied by lowered parieto-occipital activation, may underlie performance decrements seen in other "higher cognitive domains". Functional neuroimaging in this setting has increased our understanding of how the brain responds to, and compensates for, sleep loss. Functional neuroimaging may also provide a safe, reproducible and non-invasive means to evaluate the cognitive and neural impact of therapeutic interventions designed to treat sleep disorders and/ or to reduce the negative cognitive impact of sleep loss.
Attention ; Brain ; anatomy & histology ; pathology ; Cognition Disorders ; etiology ; pathology ; Continuous Positive Airway Pressure ; Emotions ; Humans ; Magnetic Resonance Imaging ; Sleep Apnea, Obstructive ; complications ; pathology ; therapy ; Sleep Deprivation ; complications ; pathology ; physiopathology ; Sleep Initiation and Maintenance Disorders ; complications ; physiopathology ; Task Performance and Analysis

BACKGROUNDRecent autopsy study showed a high incidence of cerebrovascular lesions in Alzheimer's disease (AD). To assess the impact of cerebrovascular pathology in AD, we used diffusion tensor imaging (DTI) to study AD patients with and without cerebrovascular lesions.

MATERIALS AND METHODSConventional and DTI scans were obtained from 10 patients with probable AD, 10 AD/V patients (probable AD with cerebrovascular lesions) and ten normal controls. Mean diffusivity (D) and fractional anisotropy (FA) values of some structures involved with AD pathology were measured.

RESULTSD value was higher in AD patients than in controls in hippocampus and the cingulate gyrus. In AD/V patients, increased D value was found in the same structures and also in the thalamus and basal ganglia compared to controls. There was a significant difference of D value between AD and AD/V patients. FA value reduced in the white matter of left inferior temporal gyrus and in the bilateral middle cingulate gyrus in patients with AD/V compared with controls. The MMSE (mini-mental state examination) score significantly correlated with FA value in the right hippocampus (r=0.639, P<0.019), in the right anterior cingulate gyrus (r=0.587, P<0.035) and in left parahippocampal gyrus (r=0.559, P<0.047).

CONCLUSIONCerebrovascular pathology had stronger impact on the D value than the AD pathology alone did. Elevated D value in thalamic and basal ganglia may contribute to cognitive decline in AD/V patients. Reduced FA values in AD/V patients may indicate that cerebrovascular pathology induced more severe white matter damage than the AD pathology alone did.

Aged ; Alzheimer Disease ; complications ; pathology ; Brain ; blood supply ; pathology ; Cerebral Cortex ; pathology ; Cerebrovascular Disorders ; complications ; pathology ; Cognition ; Corpus Callosum ; pathology ; Diffusion Magnetic Resonance Imaging ; Female ; Hippocampus ; pathology ; Humans ; Male ; Temporal Lobe ; pathology

Periodontal disease is a potential predictor of stroke and cognitive impairment. However, this association is unclear in adults aged 50 yr and above without a history of stroke or dementia. We evaluated the association between the number of teeth lost, indicating periodontal disease, and cognitive impairment in community-dwelling adults without any history of dementia or stroke. Dental examinations were performed on 438 adults older than 50 yr (315 females, mean age 63+/-7.8 yr; 123 males, mean age 61.5+/-8.5 yr) between January 2009 and December 2010. In the unadjusted analysis, odds ratios (OR) of cognitive impairment based on MMSE score were 2.46 (95% CI, 1.38-4.39) and 2.7 (95% CI, 1.57-4.64) for subjects who had lost 6-10 teeth and those who had lost more than 10 teeth, respectively, when compared with subjects who had lost 0-5 teeth. After adjusting for age, education level, hypertension, diabetes, hyperlipidemia, and smoking, the relationship remained significant (OR, 2.0; 95% CI, 1.08-3.69, P=0.027 for those with 6-10 teeth lost; OR, 2.26; 95% CI, 1.27-4.02, P=0.006 for those with more than 10 teeth lost). The number of teeth lost is correlated with cognitive impairment among community-dwelling adults aged 50 and above without any medical history of stroke or dementia.
Aged ; Aged, 80 and over ; Cognition Disorders/*diagnosis/etiology ; Cohort Studies ; Dementia/pathology ; Female ; Humans ; Male ; Middle Aged ; Odds Ratio ; Periodontal Diseases/complications ; Residence Characteristics ; Stroke/pathology ; *Tooth Loss

OBJECTIVETo investigate the correlation between the diffusion anisotropy of the white matter fibers and the cognitive function in patients with leukoaraiosis (LA).

METHODSThirty-one LA patients were enrolled in this study, including 13 with grade LA-1 (mild), 12 with grade LA-2 (moderate) and 6 with grade LA-3 (severe) condition. The control group consisted of 18 subjects who were free of obvious clinical symptoms or had only mild dizziness and headache but with negative history for neural system diseases and in the absence of cognitive dysfunction, brain trauma, positive signs in neurological examinations, or abnormities in MRI examination. The Mini-mental State Examination (MMSE) was applied to evaluate the patients' cognitive function. The LA patients underwent examination with diffusion tensor MR imaging (DTI), and the FA and MD values in the normal-appearing white matter (NAWM) were measured.

RESULTSThe cognitive function of the LA patients tended to decline with the decrease of the MMSE scores, and their scores for time orientation, place orientation and calculation were significantly lower than those of the control group (P<0.05). No significant difference was found in memory, language and comprehensive abilities between the LA and control groups. In LA-1, LA-2 and total LA cases, the FA value in the NAWM was positively, and the MD value inversely, correlated to the cognitive function with correlation coefficients ranging from 0.5 to 0.8 (P<0.05).

CONCLUSIONThe DTI parameters of NAWM region are correlated to the cognitive function of LA patients. DTI is far more sensitive than MRI in evaluating cognitive dysfunction in LA patients.

Aged ; Aged, 80 and over ; Anisotropy ; Case-Control Studies ; Cognition Disorders ; diagnosis ; etiology ; Diffusion Magnetic Resonance Imaging ; methods ; Female ; Humans ; Leukoaraiosis ; complications ; pathology ; Male ; Middle Aged ; Neuropsychological Tests

Brain ; diagnostic imaging ; pathology ; Cerebral Palsy ; diagnosis ; pathology ; Cognition Disorders ; diagnosis ; pathology ; Early Diagnosis ; Humans ; Infant, Newborn ; Infant, Premature ; Infant, Premature, Diseases ; diagnosis ; pathology ; Language Disorders ; diagnosis ; pathology ; Leukomalacia, Periventricular ; complications ; diagnosis ; pathology ; Magnetic Resonance Imaging ; methods ; Prognosis ; Radiography ; Severity of Illness Index

This article reviews the clinical and experimental researches on cognitive impairment related to diabetes in the recent decade. Most clinical studies indicate that the cognitive impairment in patients with type 1 diabetes mellitus is related to recurrent hypoglycemia closely. There is little research about whether or not hyperglycemia is related to cognitive impairment in patients with type 1 diabetes mellitus. Most studies indicate that the cognitive impairment in type 2 diabetes involves multiple factors through multiple mechanisms, including blood glucose, blood lipid, blood pressure, level of insulin, medication, chronic complication, etc. But, there has been no large-scale, multi-center, randomized controlled clinical trial in China recently. And what is more, some problems exist in this field of research, such as the lack of golden criterion of cognitive function measurement, different population of studied objects, and incomprehensive handling of confounding factors. Experimental studies found that hippocampal long-term potentiation (LTP) was impaired, which were manifested by impairment of spatial memory and decreased expression of LTP, but it's relation to hyperglycemia, the duration of diabetes, learning and memory has always been differently reported by different researches. Thus, there are a lot of unknown things to be explored and studied in order to clarify its mechanism. TCM has abundant clinical experience in treating cerebral disease with medicine that enforces the kidney and promotes wit. However, there has been no research on treating diabetic cognitive impairment, which requires work to be done actively and TCM to be put into full play, in order to improve the treatment of diabetes and enhance living quality of patients.
Animals ; Cognition Disorders ; etiology ; pathology ; physiopathology ; Diabetes Mellitus, Experimental ; pathology ; physiopathology ; psychology ; Diabetes Mellitus, Type 1 ; pathology ; physiopathology ; psychology ; Diabetes Mellitus, Type 2 ; pathology ; physiopathology ; psychology ; Drugs, Chinese Herbal ; therapeutic use ; Hippocampus ; pathology ; physiopathology ; Humans ; Hyperglycemia ; complications ; Hypoglycemia ; complications ; Long-Term Potentiation ; Neuronal Plasticity