Child ; Child Behavior Disorders ; etiology ; Cognition Disorders ; physiopathology ; Humans ; Sleep Apnea Syndromes ; psychology

BACKGROUNDDepression related cognitive deficits are frequently considered as simple epiphenomena of the disorder. However, whether or not the depression might directly bring about cognitive deficits is still under investigation. This study was to investigate the distinct pattern of cognitive deficits in patients with depression by comparing the cognitive function before and after anti-depressive drug therapy.

METHODSSixty cases of patients, first-time diagnosed with depression, were assessed by 17-item Hamilton Rating Scale for Depression (HAMD17scale). The memory ability was tested by quantitatively clinical memory scale, while the attention ability by modified Ruff 2&7 Selective Attention Test. Forty-two healthy volunteers were recruited as controls. The depressive patients were treated with Venlafaxine (75 - 300 mg/d), Fluoxetine (20 - 40 mg/d), Paroxetine (20 - 40 mg/d), and Sertraline (50 - 150 mg/d). After 12 weeks treatment, patients were tested again by HAMD17scale, quantitatively clinical memory scale, and modified Ruff 2&7 selective attention test to assess the effect of anti-depressive drugs on cognitive deficits.

RESULTSThe memory quotient (MQ) was significantly lowered in depressive patients. The selection speed was also significantly decreased and the number of missing and error hits increased in the depression group as compared to control. However, there was no significant difference in clinical memory scale and Ruff 2&7 selective attention test between mild-to-moderate and severe depression group. Importantly, after anti-depressive drug therapy, the HAMD17 scale scores in depressive patients were significantly decreased, but the MQ, directional memory (DM), free recall (FR), associative learning (AL), and face recognition were comparable with those before the treatment. Furthermore, the selection speed and the number of missing and error hits were also not significantly different after anti-depressive drugs treatment.

CONCLUSIONSDepressive patients suffer from short-term memory deficits, and attention extent, stability and rearrangement deficiency. Even though anti-depressive drugs sufficiently relieve the cardinal presentation of depression, they could not successfully alleviate the accompanying cognitive deficits. This might indicate a distinct pattern of cognitive deficits in patients with depression.

Adolescent ; Adult ; Antidepressive Agents ; therapeutic use ; Cognition Disorders ; etiology ; physiopathology ; Depression ; complications ; drug therapy ; physiopathology ; Female ; Humans ; Male ; Memory ; drug effects ; physiology ; Middle Aged ; Neuropsychological Tests ; Young Adult

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

PURPOSE: Patients with chronic kidney disease frequently show cognitive dysfunction. The association of depression and cognitive function is not well known in maintenance dialysis patients. We evaluated cognitive impairment and depression, as well as their relationship in regards to methods of dialysis, maintenance hemodialysis (MHD) and chronic peritoneal dialysis (CPD). MATERIALS AND METHODS: Fifty-six maintenance dialysis patients were recruited and their clinical and laboratory data were collected. The Korean version of the mini-mental state exam (K-MMSE) was applied to screen the patient's cognitive function, while the Korean version of the Beck Depression Inventory (K-BDI) was used for depression screening. RESULTS: The average age of the participants was 54.2+/-10.2 years; 29 (51.8%) were female. The average dialysis vintage was 4.2+/-3.8 years. The CPD group showed significantly higher K-MMSE score (27.8+/-2.9 vs. 26.1+/-3.1, p=0.010) and lower K-BDI score (12.0+/-8.4 vs. 20.2+/-10.4, p=0.003) compared with the MHD group. The percentage of patients with depression symptoms was higher in the MHD group (51.7% vs. 18.5%). There was a negative correlation between cognitive function and prevalence of depressive symptoms. Depression and education level were shown to be independent predictors for cognitive impairment in multivariate analysis. CONCLUSION: Cognitive impairment was closely correlated with depression. It is important to detect cognitive impairment and depression early in maintenance dialysis patients with simple bedside screening tools.
Adult ; Cognition Disorders/etiology/*physiopathology ; Depression/etiology/*physiopathology ; Female ; Humans ; Kidney Failure, Chronic/physiopathology/psychology/therapy ; Male ; Middle Aged ; Renal Dialysis/*adverse effects/*psychology

OBJECTIVETo investigate the relation between the progressive effects of chronic intermittent hypoxia (CIH) on cognitive function and the change of cholinergic neuron.

METHODSForty adult male Sprague-Dawley rats were randomly averagely divided into four groups: control group, CIH 1 week group, CIH 3 week group and CIH 5 week group. The cognitive function was assessed by the Morris Water Maze. The necrosis neurons in prefrontal cortex and hippocampus were observed and counted. The cholin acetyltransferase (ChAT) immunostained cells in prefrontal cortex and hippocampus were identified and quantitated.

RESULTSThe spatial learning and memory impairments progressed from 1 to 5 5 weeks in rats. Compared with the control group, the cognitive impairments in CIH5w group were significant (P < 0.05). The degeneration or necrosis neurons in prefrontal cortex and hippocampus were significantly increased in CIH rats, and worsen gradually along with the hypoxia. The ChAT immunostained cells in prefrontal cortex and hippocampus were gradually reduced. The ChAT immunostained cells of prefrontal cortex and hippocampus in CIH3w group and CIH5w group were less than that in control group (P < 0.05).

CONCLUSIONChronic intermittent hypoxia induced slowly progressive spatial learning and memory impairments in rats, which maybe associated with the damage of neurons and the reduction of ChAT in prefrontal cortex and hippocampus.

Animals ; Cholinergic Fibers ; pathology ; physiology ; Cholinergic Neurons ; pathology ; physiology ; Cognition ; physiology ; Hippocampus ; cytology ; physiopathology ; Hypoxia ; physiopathology ; Male ; Maze Learning ; physiology ; Memory Disorders ; etiology ; physiopathology ; Prefrontal Cortex ; cytology ; physiopathology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the sleep structure in patients with vascular cognitive impairment-no dementia (VCI-ND) and its differences from that of normal individuals.

METHODSThe whole night sleep record of 20 patients with VCI-ND were monitored by 32-head video-taped polysomnographic system, and the results were compared with the data of 20 normal subjects.

RESULTSCompared with normal subjects, patients with VCI-ND showed significantly reduced total sleep duration, increased waking times, increased stage 1 sleep, decreased stage 2 sleep, decreased stage 3 sleep, decreased rapid eye movement stage (REM) and reduced sleep efficiency.

CONCLUSIONIncreased light sleep as well as decreased slow-wave stage 3-4 sleep and decreased REM stage may be a specific electroneurophysiologic marker for VCI-ND, but large-sampled multi-centered randomized controlled trial is necessary to test the validity of these features as specific markers for screening and early diagnostic purposes.

Aged ; Case-Control Studies ; Cognition Disorders ; diagnosis ; etiology ; physiopathology ; Dementia, Vascular ; diagnosis ; Female ; Humans ; Male ; Middle Aged ; Polysomnography ; Sleep ; physiology ; Sleep Stages ; Sleep Wake Disorders ; etiology ; Stroke ; complications

The Seoul Neuropsychological Screening Battery (SNSB) is one of the standardized neuropsychological test batteries widely used in Korea. However, it may be a bit too lengthy for patients with decreased attention span; and it does not provide the score of global cognitive function (GCF), which is useful for monitoring patients longitudinally. We sought to validate a dementia version of SNSB (SNSB-D) that was shorter than the original SNSB and contained only scorable tests with a GCF score of 300. We administered SNSB-D to patients with mild cognitive impairment (MCI) (n=43) and Alzheimer's disease (AD) (n=93), and normal controls (NC) (n=77). MCI and AD groups had GCF scores significantly different from NC group, and GCF scores were able to distinguish patients with Clinical Dementia Rating of 0.5 and 1. Test-retest reliability was high, with a correlation coefficient of 0.918 for AD, 0.999 for MCI, and 0.960 for NC. The GCF score significantly correlated with the Mini-Mental State Examination (MMSE). Through ROC-curve analysis, GCF scores were found to yield more accurate diagnoses than the MMSE. The SNSB-D is a valid, reliable tool for assessing the overall cognitive function, and can be used to monitor cognitive changes in patients with dementia.
Alzheimer Disease/diagnosis/physiopathology ; Cognition Disorders/*diagnosis/etiology/physiopathology ; Dementia/complications/*diagnosis/physiopathology ; Humans ; Korea ; *Neuropsychological Tests/standards ; ROC Curve ; Reproducibility of Results ; Severity of Illness Index

Schizophrenia is a brain disease with differing symptomatic presentations, outcomes, and complex genetic mechanisms. A selection of recent work integrating clinical observations, human brain imaging and genetics will be reviewed. While the mechanics of brain dysfunction in schizophrenia remains to be well understood, the emerging evidence suggests that a number of interacting genetic mechanisms in dopaminergic and glutamatergic systems affect fundamental disease-related cognitive brain processes and may do so early in disease neurodevelopment. The availability of new imaging and genetic technologies, and institutional support for research in the translational neurosciences, extends the hope that increased understanding of these brain processes could yield meaningful clinical applications.
Cognition Disorders ; etiology ; genetics ; Dopamine ; genetics ; Glutamic Acid ; genetics ; Humans ; Magnetic Resonance Imaging ; Neurosciences ; Schizophrenia ; genetics ; physiopathology

The largely consistent columnar circuitry observed throughout the cortex may serve to continuously predict bottom-up activation based on invariant memories. This "memory-prediction" function is essential to efficient and accurate perception. Many of the defined cognitive deficits associated with schizophrenia suggest a breakdown of memory-prediction function. As deficits in memory-prediction function are proposed to lie more proximal to the biological causes of schizophrenia than deficits in standard cognitive constructs, tests that more directly probe memory-prediction function may be especially sensitive predictors of conversion in individuals at high-risk for schizophrenia. In this article, we review the conceptual basis for this hypothesis, and outline how it may be tested with specific cognitive paradigms. The accurate identification of cognitive processes that precede the onset of psychosis will not only be useful for clinicians to predict which young people are at greatest risk for schizophrenia, but will also help determine the neurobiology of psychosis onset, thus leading to new and effective treatments for preventing schizophrenia and other psychoses.
Cognition Disorders ; Humans ; Memory ; Neuropsychological Tests ; Predictive Value of Tests ; Risk Assessment ; Schizophrenia ; etiology ; physiopathology ; Schizophrenic Psychology

OBJECTIVETo investigate the clinical features and genetic diagnostic method of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).

METHODSA systematic study on the clinical manifestations, neuroimaging characteristics, therapeutic measures and molecular genetics was performed. An investigation on the onset and hereditary pattern of the family was also done.

RESULTSThe main clinical features including poor memory and history of stroke were found. And no risk factors of hypertension and arteriosclerosis were found. A positive family history was confirmed. Neuroimaging examination showed multiinfarct lesions and leukoencephalopathy. All these features are in conformity with those of CADASIL. A mutation in the third and fourth exon of the NOTCH3 gene was identified in the 10 cases of 4 generations. The clinical or subclinical onset in the 10 cases was consistent with classical autosomal dominant inheritance.

CONCLUSIONThe clinical and molecular genetic features of the family accord with CADASIL.

Adult ; CADASIL ; genetics ; pathology ; physiopathology ; Cognition Disorders ; etiology ; DNA Mutational Analysis ; Female ; Genetic Testing ; Humans ; Infarction ; etiology ; Male ; Middle Aged ; Mutation ; Neuromuscular Diseases ; etiology ; Receptors, Notch ; genetics ; Stroke ; etiology