PURPOSE: This study was conducted to develop a comprehensive cognitive rehabilitation program that can be easily applied to brain injured patients by family members or nurses in community or hospital settings. METHODS: A Systemic literature review design was used. Thirty-three related studies were reviewed. RESULT: Based on the results of the literature review, the training tasks for attention were designated to enhancing 4 hierarchical areas, i.e., focused, selective, alternating, and divided attention. On the other hand, the memory rehabilitation tasks mainly consisted of mnemonic skills, such as the association method which helps patients memorize given information by linking together common attributes, the visual imagery method, and self-instruction method. The problem solving rehabilitation program included a task of games or plays which stimulated the patients' curiosity and interest. The training tasks for problem solving were to encourage the process of deriving reasonable solutions for a problematic situation resembling real problems that the patients were faced with in their everyday life. CONCLUSION: It is expected that the cognitive rehabilitation program developed from this study could help patients having difficulty in their every day life, due to a reduced cognitive ability resulting from brain injury, to effectively adapt to every day life.
Problem Solving ; Memory ; Humans ; *Cognitive Therapy ; Cognition Disorders/etiology/*rehabilitation ; Brain Injuries/complications/nursing/*rehabilitation

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 evaluate the psychological state of children with epilepsy and analyze its influencing factors.

METHODSThe Mental Health Scale for Child and Adolescent was used to survey 113 children with epilepsy and 114 normal children to evaluate and compare their psychological state. Questionnaires were used to investigate the general status of all subjects and the disease condition and treatment of children with epilepsy. The possible influencing factors for the psychological state of children with epilepsy were analyzed.

RESULTSThe mental health status of children with epilepsy was poorer than that of normal children in cognition, thinking, emotion, will-behavior, and personality traits (P<0.05). Multivariate logistic regression analysis showed that family education, family relations, seizure frequency, seizure duration, EEG epileptiform discharges in the last six months, and number of types of antiepileptic drugs were correlated with the psychological state of children with epilepsy.

CONCLUSIONSThere is a wider range of psychological health problems in children with epilepsy than in normal children. Poor family living environment, poor seizure control, and use of many antiepileptic drugs are the risk factors affecting the psychological state of children with epilepsy. Improving family living environment, controlling seizures, and monotherapy help to improve the psychological state of children with epilepsy.

Adolescent ; Child ; Epilepsy ; drug therapy ; psychology ; Female ; Humans ; Logistic Models ; Male ; Memory Disorders ; etiology

OBJECTIVEIt is known that hypertension may be implicated the development of memory dysfunction. Our study tests the hypothesis that prevalence of memory dysfunction is closely linked with the level of SBP (systolic blood pressure) and DBP (diastolic blood pressure) in hypertension patients.

METHODSNon-stroke hypertension patients aged 18-75 years (n = 196, age 54 ± 10, 101 male) with diagnosed hypertension for more than one year were included. Memory function was measured by the Rivermead Behavioral Memory Test Second Edition (RBMTII, 2003). The general information was obtained through questionnaire.

RESULTSRBMTII total score, the ability of recall name, remember storing article, recall faces, delayed route memory and orientation score were significantly decreased in proportion with increasing blood pressure (P < 0.05: hypertension III vs. II and I). RBMTII total score, the ability of recall name, and recall faces were significantly lower in hypertension II group compared to hypertension I group (P < 0.05). The age, male gender, years of hypertension, level of SBP and BMI were risk factors of memory dysfunction while the years of education was protective factor of memory dysfunction. The morbidity of memory dysfunction in patients with hypertension was higher and more serious with increasing blood pressure level (χ(2) = 10.389, P < 0.01).

CONCLUSIONSOur results suggest that blood pressure is positively related to increased risk of memory dysfunction. The age, male gender, years of hypertension, level of SBP and BMI are risk factors of memory dysfunction while the years of education is protective factor of memory dysfunction.

Adult ; Blood Pressure ; Female ; Humans ; Hypertension ; physiopathology ; psychology ; Male ; Memory Disorders ; etiology ; Middle Aged ; Risk Factors

This study explored the possibility of using event-related potentials (ERP) for the measurement of picture-recognition memory and examined its correlation with the Chinese Wechsler Memory Scale-revised (WMS-RC) in patients with memory disorder caused by severe traumatic brain injury (sTBI). The subjects included 20 sTBI patients with memory disorder and 22 healthy individuals. Memory function was measured by using WMS-RC. Behavioral and ERP responses were recorded on-line during performance on a battery of picture recognition and the responses were analyzed off-line for recognition memory effects. Mean memory quotient (MQ) of patients with sTBI was significantly lower than that of the control group. Mean reaction time (RT) was significantly longer and the mean correctness rate (CR) of picture recognition was significantly lower in sTBI group than that of the controls. In controls, the main components of average ERP of picture recognition includes two positive-going waves, designated as P(170) and P(500), that appear 170 ms and 500 ms after stimulation when the subject could later successfully recall and recognize the pictures. P(500) amplitude of target stimulus was significantly higher than that of non-target stimulus. Compared to controls, P(500) responses of sTBI group were significantly delayed in latency (P<0.001) and lower in amplitude (P<0.001). P(500) latency showed significant negative correlation with MQ and the scores of "addition", "visual recognition", "picture recall", "visual reproduction" and "tactile memory" in WMS-RC. ERP of picture recognition provides a neurophysiological approach to directly assess memory impairment, and P(500) may serve as a helpful index for memory disorder caused by sTBI in forensic practice.
Brain Injuries/*complications ; Case-Control Studies ; Evoked Potentials/*physiology ; Memory Disorders/*etiology ; Memory Disorders/*physiopathology ; Pattern Recognition, Physiological/*physiology ; Wechsler Scales ; Young Adult

To evaluate the effect of acute high-altitude exposure on sensory and short-term memory using interactive software, we transported 30 volunteers in a sport utility vehicle to a 4280 m plateau within 3 h. We measured their memory performance on the plain (initial arrival) and 3 h after arrival on the plateau using six measures. Memory performance was significantly poorer on the plateau by four of the six measures. Furthermore, memory performance was significantly poorer in the acute mountain sickness (AMS) group than in the non-AMS group by five of the six measures. These findings indicate that rapid ascent to 4280 m and remaining at this altitude for 3 h resulted in decreased sensory and short-term memory, particularly among participants who developed AMS.
Acute Disease ; Adult ; Altitude ; Altitude Sickness ; epidemiology ; etiology ; China ; epidemiology ; Humans ; Male ; Memory Disorders ; epidemiology ; etiology ; Memory, Short-Term ; Time Factors ; Young Adult

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

BACKGROUNDObstructive sleep apnea (OSA) can cause cognitive dysfunction and may be a reversible cause of cognitive loss in patients with Alzheimer's disease (AD). Chronic exposure to intermittent hypoxia (IH), such as encountered in OSA, is marked by neurodegenerative changes in rat brain. We investigated the change of thioredoxin (Trx), spatial learning and memory in rats exposed to chronic intermittent hypoxia (CIH).

METHODSForty healthy male Sprague-Dawley (SD) rats were randomly divided into four groups of ten each: a CIH+normal saline (CIH+NS group), a N-acetylcystein-treated CIH (CIH+NAC) group, a sham CIH group (sham CIH+NS), and a sham NAC-treated sham CIH (CIH+NAC) group. Spatial learning and memory in each group was assessed with the Morris water maze. Real-time PCR and Western blotting were used to examine mRNA and protein expression of Trx in the hippocampus tissue. The terminal deoxynucleotidyl transferase-mediated dUTP-nick end-labeling (TUNEL) method was used to detect the apoptotic cells of the hippocampus CA1 region.

RESULTSCIH-rats showed impaired spatial learning and memory in the Morris water maze, including longer mean latencies for the target platform, reduced numbers of passes over the previous target platform and a smaller percentage of time spent in the target quadrant. Trx mRNA and protein levels were significantly decreased in the CIH-hippocampus, meanwhile, an elevated apoptotic index revealed apoptosis of hippocampal neurons of rats exposed to CIH. The rats, which acted better in the Morris water maze, showed higher levels of the Trx mRNA and protein in the hippocampus; apoptotic index of the neurons in the hippocampus of each group was negatively correlated with the Trx mRNA and protein levels.

CONCLUSIONThe Trx deficit likely plays an important role in the impaired spatial learning and memory in the rats exposed to CIH and may work through the apoptosis of neurons in the hippocampus.

Animals ; Apoptosis ; Hippocampus ; pathology ; Hypoxia ; complications ; Learning Disorders ; etiology ; Male ; Maze Learning ; Memory Disorders ; etiology ; Rats ; Rats, Sprague-Dawley ; Sleep Apnea, Obstructive ; complications ; Thioredoxins ; physiology

The present study was designed to observe the influence of cerebral ischemia/reperfusion injury on learning and memory in hyperlipidemic rats and estimate the changes of activity of autonomic nervous system. Twenty-three male Wistar rats were randomly divided into three groups, named control group (C group, n=10), hyperlipidemia group (H group, n=6) and hyperlipidemia-ischemia group (HI group, n=7), respectively. The rats in H and HI group were fed a high-fat diet for 2 weeks and the rats in all groups were examined through Morris water maze (MWM) task. The rats in HI group underwent ischemia/reperfusion by 2-vessel occlusion (2-VO) method, and had electrocardiogram (ECG) recording simultaneously. The MWM task and ECG recording were taken again after 7 d of recuperation. The following results were obtained: (1) In the second place navigation performance and probe trial performance, the frequency of memory in quadrant of hidden-platform and memory score decreased significantly in HI group compared to that in C and H groups. (2) The heart rate in HI group decreased slowly after ischemia; the power at high frequency band (HF) reduced gradually, meanwhile the power at middle frequency band (MF) and the ratio of power at MF and HF decreased clearly compared to baseline value. (3) After 7 d of ischemia/reperfusion, the heart rate in HI group was significantly higher than that in H group (P<0.05). While there was no statistical change in the power at MF, the power at HF decreased and the ratio of MF/HF increased significantly (P<0.05). The data demonstrated that ischemia/reperfusion decreased the activity of autonomic nervous system, and the reduction of sympathetic nerve activity was much more than that of vagus nerve activity. The results suggest that the hippocampus neuron injury caused by ischemia induces cognitive disorder and imbalance of vago-sympathetic nerve activity accompanied by vagus nerve suppression.
Animals ; Autonomic Nervous System ; physiopathology ; Brain Ischemia ; etiology ; physiopathology ; Heart Rate ; physiology ; Hippocampus ; physiopathology ; Hyperlipidemias ; complications ; Learning Disorders ; etiology ; physiopathology ; Male ; Memory Disorders ; etiology ; physiopathology ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; pathology ; physiopathology

Mice ; Animals ; Alzheimer Disease/complications* ; Entorhinal Cortex/metabolism* ; Brain-Derived Neurotrophic Factor/metabolism* ; Memory Disorders/etiology* ; Thalamus/metabolism* ; Disease Models, Animal