OBJECTIVES: Empathy has been conceptualized as the ability of emotional resonance and perspective-taking. Emotional awareness has been proposed as the basis of empathy. In this study we examined the relationship between empathy and mood awareness and their neural correlates in resting-state activity in normal controls and patients with schizophrenia. METHODS: Empathy and mood awareness scale scores were compared between 29 patients with schizophrenia and 21 normal controls by voxel-based t-tests and voxel-based correlation analyses of resting-state 18F-FDG PET images. RESULTS: Empathy and mood labeling scale scores were significantly decreased in schizophrenic patients. Mood monitoring was positively correlated with empathy score in normal controls, but not in schizophrenic patients. In normal controls, empathy was positively correlated with resting-state activities in the intraparietal sulcus and mood monitoring was positively correlated with the temporal pole, frontopolar cortex, inferior temporal gyrus, entorhinal cortex and the subgenual prefrontal cortex resting activities. The orbitofrontal cortex resting activity was positively correlated with mood monitoring-related subgenual prefrontal cortex activity in the normal controls. Patients with schizophrenia showed decreased orbitofrontal resting activity and loss of its correlations with mood monitoring-related regional activities. CONCLUSION: This study showed that alteration in the resting-state activity in schizophrenia may reflect dysfunctional empathy and distorted characteristic of emotional awareness. However, the resting-state activity may not reflect the relationship between emotional awareness and empathy.
Brain* ; Empathy* ; Entorhinal Cortex ; Fluorodeoxyglucose F18 ; Humans ; Prefrontal Cortex ; Schizophrenia*

Entorhinal Cortex/physiology* ; Hippocampus/physiology* ; Neural Pathways/physiology*

Epileptic spike is an indicator of hyper-excitability and hyper-synchrony in the neural networks. The inhibitory effects of spikes on theta rhythms (4-8 Hz) might be helpful to understand the mechanism of epileptic damage on the cognitive functions. To quantitatively evaluate the inhibitory effects of spikes on theta rhythms, intracerebral electroencephalogram (EEG) recordings with both sporadic spikes (SSs) and spike-free transient period between adjacent spikes were selected in 4 patients in the status of rapid eyes movement (REM) sleep with temporal lobe epilepsy (TLE) under the pre-surgical monitoring. The electrodes of hippocampal CA3 and entorhinal cortex (EC) were employed, since CA3 and EC built up one of key loops to investigate cognition and epilepsy. These SSs occurred only in CA3, only in EC, or in both CA3 and EC synchronously. Theta power was respectively estimated around SSs and during the spike-free transient period by Gabor wavelet transform and Hilbert transform. The intermittent extent was then estimated to represent for the loss of theta rhythms during the spike-free transient period. The following findings were obtained: (1) The prominent rhythms were in theta frequency band; (2) The spikes could transiently reduce theta power, and the inhibitory effect was severer around SSs in both CA3 and EC synchronously than that around either SSs only in EC or SSs only in CA3; (3) During the spike-free transient period, theta rhythms were interrupted with the intermittent theta rhythms left and theta power level continued dropping, implying the inhibitory effect was sustained. Additionally, the intermittent extent of theta rhythms was converged to the inhibitory extent around SSs; (4) The average theta power level during the spike-free transient period might not be in line with the inhibitory extent of theta rhythms around SSs. It was concluded that the SSs had negative effects on theta rhythms transiently and directly, the inhibitory effects aroused by SSs sustained during the spike-free transient period and were directly related to the intermittent extent. It was indicated that the loss of theta rhythms might qualify exactly the sustained inhibitory effects on theta rhythms aroused by spikes in EEG. The work provided an argumentation about the relationship between the transient negative impact of interictal spike and the loss of theta rhythms during spike-free activity for the first time, offered an intuitive methodology to estimate the inhibitory effect of spikes by EEG, and might be helpful to the analysis of EEG rhythms based on local field potentials (LFPs) in deep brain.
CA3 Region, Hippocampal ; physiopathology ; Electroencephalography ; Entorhinal Cortex ; physiopathology ; Epilepsy, Temporal Lobe ; physiopathology ; Humans ; Male ; Theta Rhythm

The method of directly using speed information and angle information to drive attractors model of grid cells to encode environment has poor anti-interference ability and is not bionic. In response to the problem, this paper proposes a grid field calculation model based on perceived speed and perceived angle. The model has the following characteristics. Firstly, visual stream is decoded to obtain visual speed, and speed cell is modeled and decoded to obtain body speed. Visual speed and body speed are integrated to obtain perceived speed information. Secondly, a one-dimensional circularly connected cell model with excitatory connection is used to simulate the firing mechanism of head direction cells, so that the robot obtains current perception angle information in a biomimetic manner. Finally, the two kinds of perceptual information of speed and angle are combined to realize the driving of grid cell attractors model. The proposed model was experimentally verified. The results showed that this model could realize periodic hexagonal firing field mode of grid cells and precise path integration function. The proposed algorithm may provide a foundation for the research on construction method of robot cognitive map based on hippocampal cognition mechanism.
Action Potentials ; Computer Simulation ; Computer Systems ; Entorhinal Cortex ; Grid Cells ; Hippocampus ; Models, Neurological

OBJECTIVE: The aim of this study was to explore the prognostic values of biomarkers of neurodegeneration as measured by magnetic resonance imaging (MRI) and amyloid burden as measured by amyloid positron emission tomography (PET) in predicting conversion to Alzheimer's disease (AD) in patients with mild cognitive impairment (MCI). METHODS: PubMed and EMBASE databases were searched for structural MRI or amyloid PET imaging studies published between January 2000 and July 2014 that reported conversion to AD in patients with MCI. Means and standard deviations or individual numbers of biomarkers with positive or negative status at baseline and corresponding numbers of patients who had progressed to AD at follow-up were retrieved from each study. The effect size of each biomarker was expressed as Hedges's g. RESULTS: Twenty-four MRI studies and 8 amyloid PET imaging studies were retrieved. 674 of the 1741 participants (39%) developed AD. The effect size for predicting conversion to AD was 0.770 [95% confidence interval (CI) 0.607–0.934] for across MRI and 1.316 (95% CI 0.920–1.412) for amyloid PET imaging (p<0.001). The effect size was 1.256 (95% CI 0.902–1.609) for entorhinal cortex volume from MRI. CONCLUSION: Our study suggests that volumetric MRI measurement may be useful for the early detection of AD.
Alzheimer Disease* ; Amyloid* ; Biomarkers ; Entorhinal Cortex ; Follow-Up Studies ; Humans ; Magnetic Resonance Imaging* ; Mild Cognitive Impairment* ; Positron-Emission Tomography

OBJECTIVETo elucidate the volume changes of cortical and subcortical reward circuitry in patients with type 2 diabetes mellitus.

METHODSHigh-resolution three-dimensional T1-weighted fast spoiled gradient recalled echo MRI images were obtained from 16 patients with type 2 diabetes mellitus and 16 normal controls, and 11 type 2 diabetic patients also received the same MRI scans after insulin therapy for 1 year. Volumetric analysis was performed and analysis of covariance and paired t test were applied.

RESULTSA decreased volume was found in the left insular lobe, left nucleus accumbens area, right hippocampus, putamen and amygdala in type 2 diabetic patients compared with normal controls (P<0.05). After insulin therapy for 1 year, an increased volume of bilateral cortical reward structures was observed (left, 33.65∓3.66 ml; right, 33.35∓4.25 ml) compared the baseline level (left, 31.45∓2.90 ml; right, 31.12∓2.97 ml) in diabetic patients (P<0.05). No significant volume change in the bilateral basal ganglia structures was found after insulin therapy for 1 year (P>0.05), and bilateral ventral diencephalon area showed an increased volume after the treatment (left, 3.26∓0.68 ml; right, 3.20∓0.78 ml) compared with the baseline (left, 2.96∓0.76 ml; right, 2.82∓0.90 ml)(P<0.05).

CONCLUSIONType 2 diabetic patients have a decreased volume of the cortical and subcortical reward circuitry, and insulin therapy can reverse such changes and improve the damage of reward circuitry.

Aged ; Cerebral Cortex ; pathology ; Diabetes Mellitus, Type 2 ; drug therapy ; pathology ; Entorhinal Cortex ; pathology ; Female ; Humans ; Insulin ; therapeutic use ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Nucleus Accumbens ; pathology

To investigate neuronal injury developed in an experimental model of temporal lobe epilepsy, the expression of c-FOS, c-JUN and HSP72 on the amygdala, hippocampus and temporal neocortex was studied. Epileptic seizure was induced in rats by microinjection of kainic acid(1microgrm/microl) dissolved in phosphate buffer(0.1 M, pH 7.4) into the left amygdala. Selective and delayed neuronal injuries appeared in the CA3 region of the hippocampus after 14 days and were characterized by swelling of cytoplasm and neurites, nuclear pyknosis and loss of neurons. Early induction of c-FOS and c-JUN was noted on the injection-side amygdala at 1-12h, and delayed expression developed at 7 days after the injection. HSP72 expression appeared continuously 3 hrs after the injection. Delayed induction of c-FOS, c-JUN and continuous expression of HSP72 were observed in the hippocampus and entorhinal cortex. In the hippocampus, c-FOS expression was relatively strong in the neurons of CA3 and dentate gyrus at 7~14 days after the injection. Similar findings were also noted in the neurons of the entorhinal cortex. Induction of HSP72 occurred slightly later than on that of c-FOS and c-JUN in the amygdala, with the prominent induction being noted in the neurons of amygdala, CA2, CA3, CA4 and dentate gyrus at 3 to 21 days after the injection. These results suggested that the delayed expressions of c-FOS and c-JUN in the hippocampus correlated well with impending clinical epileptic seizure.
Amygdala ; Animals ; Cytoplasm ; Dentate Gyrus ; Entorhinal Cortex ; Epilepsy ; Epilepsy, Temporal Lobe* ; Hippocampus ; Hydrogen-Ion Concentration ; Kainic Acid ; Microinjections ; Models, Theoretical ; Neocortex ; Neurites ; Neurons ; Rats* ; Temporal Lobe*

BACKGROUND: Retrograde amnesia (RA) refers to the failure to recall events that occurred before a brain injury. RA is known to be associated with brain lesions involving the hippocampus, entorhinal cortex and the frontal lobe. Anterior thalamic lesion often causes anterograde amnesia but rarely causes RA. The aim of the present study is in two parts . First, we discuss the neuroanatomical perspectives of RA based on our case with severe RA after a right anterior thalamic infarction. Second, we introduce a test for RA termed the "Korean Public Events Recall Test (K-PERT)", which was developed based on famous Korean public events from 1966 to 1997. METHODS: A 62-year-old woman with transient RA after a left anterior thalamic infarction 4 years ago presented severe and persistent RA following a right anterior thalamic infarction. We followed up the patient with neuropsychological tests. We also performed the K-PERT on the patient as well as on 14 women of the same age and education. RESULTS: Neuropsychological tests showed severe impairment in autobiographical memory with frontal lobe dysfunction. On K-PERT, the normal controls scored 13.7 +/- 3.7 in recall and 21.2 +/- 3.1 in recognition out of a maximum score of 30, whereas the patient obtained only 3/30 and 4/30, respectively. CONCLUSIONS: In our case, RA might have resulted from damage to the pathway that retrieves old memories, which are stored in the frontal lobe. Thus, anterior thalamus might be viewed as the gate of memory engram. Further studies are needed to elaborate the usefulness of K-PERT as an objective tool for investigating remote memory.
Amnesia, Anterograde ; Amnesia, Retrograde* ; Brain ; Brain Injuries ; Education ; Entorhinal Cortex ; Female ; Frontal Lobe ; Hippocampus ; Humans ; Infarction* ; Memory ; Memory, Episodic ; Memory, Long-Term ; Middle Aged ; Neuropsychological Tests ; Thalamus

OBJECTIVES: Hippocampal formation and entorhinal cortex play a part in learning and memory. This study sought to investigate the change of cell-death controlling factors in the hippocampal formation and entorhinal cortex of aged rats. METHODS: Ten aged rats and ten controls were studied. We performed immunocytochemical method using antibodies against NOS, VIP, c-fos , bcl-2, bax and p53 and in situ hybridization. RESULTS: 1) The number of nNOS-immunoreactive(IR) neurons in the entorhinal cortex was significantly decreased in the aged rats(>30%). Morphologically, the number of dendritic branches seemed to be decreased and the length of dendrites showed a tendency to by shortened in the aged group. A major loss of nNOS mRNA positive neurons was observed in the hippocampal formation of the aged rats(>30%). 2) VIP-IR neurons were predominantly bipolar cell. VIP-IR cells were mildly decreased in the hippocampus and subiculum(<15%), and moderately decreased in the dentate gyrus and entorhinal cortex of the aged rats(15-30%). The number and length of dendritic branches also appeared to have decreased and shortened in the aged group. 3) c-Fos immunoreactivity at cellular level was restricted only to the nucleus. c-Fos-IR nuclei were moderately decreased in the hippocampus(15-30%), and severely decreased in dentate gyrus, subiculum and entorhinal cortex of the aged rats(>30%). 4) Bcl-2 mRNA positive neurons were moderately decreased in the hippocampus, subiculum and entorhinal cortex(15-30%), and severely decreased in dentate gyrus of the aged rats(>30%). 5) Bax-IR neurons were similarly distributed between the control and the aged rats, but bax-IR neurons of the aged group, as compared to the control group, were weakly immunostained. 6) P53-IR neurons were only observed in hippocampal CA1 region of the aged rats. CONCLUSION: These results indicate the involvement of neuronal system containing NOS, VIP, c-fos, bcl-2 and p53 in the brain aging process, and provide the morphological evidence for the changes in immunoreactivity of cell-death controlling factors in the hippocampal formation and entorhinal cortex of aged rats.
Aging ; Animals ; Antibodies ; Brain ; CA1 Region, Hippocampal ; Dendrites ; Dentate Gyrus ; Entorhinal Cortex* ; Hippocampus* ; Immunohistochemistry ; In Situ Hybridization ; Learning ; Memory ; Neurons ; Rats* ; RNA, Messenger

Feature outcome of hippocampus and extra-hippocampal cortices was evaluated in melatonin treated lithium-pilocarpine epileptic rats during early and chronic phases of temporal lobe epilepsy (TLE). After status epilepticus (SE) induction, 5 and 20 mg/kg melatonin were administered for 14 days or 60 days. All animals were killed 60 days post SE induction and the histological features of the rosrto-caudal axis of the dorsal hippocampus, piriform and entorhinal cortices were evaluated utilizing Nissl, Timm, and synapsin I immunoflorescent staining. Melatonin (20 mg/kg) effect on CA1 and CA3 neurons showed a region-specific pattern along the rostro-caudal axis of the dorsal hippocampus. The number of counted granular cells by melatonin (20 mg/kg) treatment increased along the rostro-caudal axis of the dorsal hippocampus in comparison to the untreated epileptic group. The density of Timm granules in the inner molecular layer of the dentate gyrus decreased significantly in all melatonin treated groups in comparison to the untreated epileptic animals. The increased density of synapsin I immunoreactivity in the outer molecular layer of the dentate gyrus of untreated epileptic rats showed a profound decrease following melatonin treatment. There was no neuronal protection in the piriform and entorhinal cortices whatever the melatonin treatment. Long-term melatonin administration as a co-adjuvant probably could reduce the post-lesion histological consequences of TLE in a region-specific pattern along the rostro-caudal axis of the dorsal hippocampus.
Animals ; Axis, Cervical Vertebra* ; Axons* ; Dentate Gyrus ; Entorhinal Cortex ; Epilepsy, Temporal Lobe* ; Hippocampus* ; Melatonin* ; Neurons* ; Rats ; Status Epilepticus ; Synapsins ; Temporal Lobe*