Posterior cingulate gyri metabolic alterations in HIV-positive patients with and without memory deficits / Alterações metabólicas no giro do cíngulo posterior em pacientes HIV-positivos com e sem déficit de memória

Abstract Objective: We aimed to evaluate whether human immunodeficiency virus (HIV)-positive patients with and without clinically significant memory deficits and healthy control participants differ on in vivo hydrogen-1 magnetic resonance spectroscopy (H-MRS) in the posterior cingulate gyri. Materials and Methods: In total, 21 HIV-positive patients with memory deficit (HIV+wMD) were compared with 15 HIV-positive patients without memory deficit (HIV+wOMD) and 22 sex-, age-, and education-matched control participants. Memory impairments were classified based on the participants' performance on the Rey Auditory Verbal Learning Test. Short echo time (30 ms), single-voxel H-MRS was performed using a 1.5-T magnetic resonance scanner. Results: The HIV+wMD and HIV+wOMD groups had higher choline/creatine ratio in the posterior cingulate gyri than the control group. There were no significant metabolite ratio differences between the HIV+wMD and HIV+wOMD groups. Conclusion: HIV-positive patients with and without memory deficits had significantly higher choline/creatine ratios than controls in the posterior cingulate gyri, which may reflect cerebral inflammation, altered cell membrane metabolism, microgliosis, and/or astrocytosis.

Resumo Objetivo: Nós avaliamos se os pacientes HIV-positivos com e sem déficits de memória clinicamente significativos e controles saudáveis diferem na espectroscopia de prótons do giro do cíngulo posterior, por ressonância magnética (RM) cerebral. Materiais e Métodos: Vinte e um pacientes HIV-positivos com déficit de memória foram comparados com 15 pacientes HIV-positivos sem déficit de memória e 22 controles, pareados por sexo, idade e escolaridade. As deficiências de memória foram classificadas por meio do desempenho no Teste de Aprendizagem Auditivo-Verbal de Rey. A espectroscopia de prótons foi realizada com tempo de eco curto (30 ms), por voxel único, no giro do cíngulo posterior, utilizando aparelho de RM de 1,5 T. Resultados: Os pacientes HIV-positivos com e sem déficit de memória apresentaram aumento da relação colina/creatina no giro do cíngulo posterior, comparados aos controles. Não houve diferenças significativas nas relações metabólicas no grupo HIV-positivo com déficit de memória, em relação ao grupo de pacientes HIV-positivo sem déficit. Conclusão: Pacientes HIV-positivos com e sem déficits de memória apresentaram relações colina/creatina significativamente aumentadas em relação aos controles, no giro do cíngulo posterior, o que pode refletir inflamação cerebral, alteração do metabolismo da membrana celular, microgliose e/ou astrocitose.

Cymbopogon citratus aqueous leaf extract attenuates neurobehavioral and biochemical changes induced by social defeat stress in mice / 中草药·英文版

Objective: Psychosocial stress has been implicated in the genesis of psychiatric disorders such as memory deficits, depression, anxiety and addiction. Aqueous leaf extract of Cymbopogon citratus (CYC) otherwise known as lemongrass tea has antidepressant, anxiolytic and anti-amnesic effects in rodents. This study was designed to evaluate if C. citratus could reverse the neurobehavioral and biochemical derangements induced by social defeat stress (SDS) in the resident/intruder paradigm. Methods: Intruder male mice were divided into five groups (n = 7): group 1 received saline (10 mL/kg, p.o.; non-stress control), group 2 also received saline (10 mL/kg, p.o.; SDS control) while groups 3–5 had C. citratus (50, 100 and 200 mg/kg, p.o.) daily for 14 d. The SDS was carried out 30 min after each treatment from day 7 to day 14 by exposing each intruder mouse in groups 2–5 to a 10 min confrontation in the home cage of an aggressive resident counterpart. The neurobehavioral features (spontaneous motor activity-SMA, anxiety, memory, social avoidance and depression were then evaluated. The concentrations of nitrite, malondialdehyde and glutathione as well as acetylcholinesterase activity in the brain tissues were also determined. Results: C. citratus (50, 100 and 200 mg/kg) attenuated hypolocomotion, heightened anxiety, depressive-like symptom, memory deficit and social avoidance induced by SDS. The altered levels of oxidative stress and acetyl-cholinesterase in SDS-mice were positively modulated by C. citratus. Conclusion: The results of this study suggest that C. citratus might mitigate psychosocial stress-induced neurologic diseases in susceptible individuals.

Bilateral Thalamic Glioma in a Young Woman: a Case Report

Bilateral thalamic gliomas (BTGs) are rare brain tumors. In general, the prognosis is poor because of the involvement of bilateral thalami and limitations of surgical excision. Consequently, patients with symptoms of personality changes and memory impairment must be differentiated from others. Magnetic resonance imaging (MRI) is essential for the diagnosis of BTGs and reveals a hypo-intense lesion on T1-weighted images and a hyper-intense lesion on T2 images. We report a case of a 17-year-old female patient suffering from progressive cognitive dysfunction and personality changes and subsequent rehabilitation treatment. Brain MRI showed an enlarged bilateral thalamus, with hyperintensity on T2-weighted images and iso-intensity on T1-weighted images. A biopsy was performed, and the pathology revealed a high-grade glioma. The patient was referred for radiotherapy and chemotherapy. She also underwent rehabilitation treatment for 5 weeks and showed improvement in standing balance, endurance, and speech fluency. The patient's Modified Barthel Index scores also improved. Cancer rehabilitation is important in brain tumor patients because they have a higher incidence of neurological sequelae than others. Rehabilitation of patients with a malignant brain tumor is also important for improving health-related quality of life by maintaining the general condition and preventing complications during and after cancer treatment.

Which Neural Tract Plays a Major Role in Memory Impairment After Multiple Cerebral Infarcts? A Case Report

Injury to the thalamocortical tract (one in the Papez circuit) that leads to memory impairment following brain injury is very rare. In this study, we present a case of partial injury to the thalamocortical tract that causes memory impairment after concurrent thalamic and hippocampal infarct. A 20-year-old male complained of memory impairment 1 month after partial injury to the thalamocortical tract. Using a probabilistic diffusing tensor tractography, it was found that the right thalamocortical tract was thinner than the left thalamocortical tract. However, all other neural tracts including the fornix, cingulum, and mammillothalamic tract were intact on both hemispheres. Therefore, the memory impairment in this patient was considered as being due to thalamic infarct based on the observation that the fornix from hippocampal infarct was intact. This case suggests that the assessment of lesions in the neural tracts of the Papez circuit might be useful for understanding the mechanism of memory impairment following cerebral infarction.

alpha-Asarone Ameliorates Memory Deficit in Lipopolysaccharide-Treated Mice via Suppression of Pro-Inflammatory Cytokines and Microglial Activation

alpha-Asarone exhibits a number of pharmacological actions including neuroprotective, anti-oxidative, anticonvulsive, and cognitive enhancing action. The present study investigated the effects of alpha-asarone on pro-inflammatory cytokines mRNA, microglial activation, and neuronal damage in the hippocampus and on learning and memory deficits in systemic lipopolysaccharide (LPS)-treated C57BL/6 mice. Varying doses of alpha-asarone was orally administered (7.5, 15, or 30 mg/kg) once a day for 3 days before the LPS (3 mg/kg) injection. alpha-Asarone significantly reduced TNF-alpha and IL-1beta mRNA at 4 and 24 hours after the LPS injection at dose of 30 mg/kg. At 24 hours after the LPS injection, the loss of CA1 neurons, the increase of TUNEL-labeled cells, and the up-regulation of BACE1 expression in the hippocampus were attenuated by 30 mg/kg of alpha-asarone treatment. alpha-Asarone significantly reduced Iba1 protein expression in the hippocampal tissue at a dose of 30 mg/kg. alpha-Asarone did not reduce the number of Iba1-expressing microglia on immunohistochemistry but the average cell size and percentage areas of Iba1-expressing microglia in the hippocampus were significantly decreased by 30 mg/kg of alpha-asarone treatment. In the Morris water maze test, alpha-asarone significantly prolonged the swimming time spent in the target and peri-target zones. alpha-Asarone also significantly increased the number of target heading and memory score in the Morris water maze. The results suggest that inhibition of pro-inflammatory cytokines and microglial activation in the hippocampus by alpha-asarone may be one of the mechanisms for the alpha-asarone-mediated ameliorating effect on memory deficits.

alpha-Asarone Ameliorates Memory Deficit in Lipopolysaccharide-Treated Mice via Suppression of Pro-Inflammatory Cytokines and Microglial Activation

alpha-Asarone exhibits a number of pharmacological actions including neuroprotective, anti-oxidative, anticonvulsive, and cognitive enhancing action. The present study investigated the effects of alpha-asarone on pro-inflammatory cytokines mRNA, microglial activation, and neuronal damage in the hippocampus and on learning and memory deficits in systemic lipopolysaccharide (LPS)-treated C57BL/6 mice. Varying doses of alpha-asarone was orally administered (7.5, 15, or 30 mg/kg) once a day for 3 days before the LPS (3 mg/kg) injection. alpha-Asarone significantly reduced TNF-alpha and IL-1beta mRNA at 4 and 24 hours after the LPS injection at dose of 30 mg/kg. At 24 hours after the LPS injection, the loss of CA1 neurons, the increase of TUNEL-labeled cells, and the up-regulation of BACE1 expression in the hippocampus were attenuated by 30 mg/kg of alpha-asarone treatment. alpha-Asarone significantly reduced Iba1 protein expression in the hippocampal tissue at a dose of 30 mg/kg. alpha-Asarone did not reduce the number of Iba1-expressing microglia on immunohistochemistry but the average cell size and percentage areas of Iba1-expressing microglia in the hippocampus were significantly decreased by 30 mg/kg of alpha-asarone treatment. In the Morris water maze test, alpha-asarone significantly prolonged the swimming time spent in the target and peri-target zones. alpha-Asarone also significantly increased the number of target heading and memory score in the Morris water maze. The results suggest that inhibition of pro-inflammatory cytokines and microglial activation in the hippocampus by alpha-asarone may be one of the mechanisms for the alpha-asarone-mediated ameliorating effect on memory deficits.

Remifentanil alleviates transient cerebral ischemia-induced memory impairment through suppression of apoptotic neuronal cell death in gerbils / 대한마취과학회지

BACKGROUND: During neurosurgical procedures, patients are often exposed to hypoxic and ischemic brain damage. Cerebral ischemia leads to neuronal cell death and eventually causes neurological impairments. Remifentanil is a new ultra-short acting phenylpiperidine opioid analgesic. In this study, we evaluated remifentanil to determine if it exerts an anti-apoptotic effect in the hippocampal dentate gyrus following transient global ischemia in gerbils. METHODS: Step-down avoidance task, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and immunohistochemical staining for caspase-3 were performed. RESULTS: The numbers of TUNEL-positive cells and caspase-3-positive cells in the dentate gyrus were increased by ransient global ischemia. Latency in the step-down avoidance task was increased by transient global ischemia. Results revealed that apoptotic cell death in the dentate gyrus was increased significantly following transient global ischemia, resulting in memory impairment. However, treatment with remifentanil suppressed ischemia-induced apoptosis in the dentate gyrus, thereby alleviating the memory impairment that was induced by ischemic cerebral injury. CONCLUSIONS: These results indicate that remifentanil may exert a neuroprotective effect on ischemic brain damage during surgery.

A Case of Epilepsy Exhibiting a Severe, Dose-Dependent, Memory Deficit after Zonisamide Administration / 대한간질학회지

Zonisamide (ZNS) has been proven as a safe, effective, and well-tolerated antiepileptic drug. We report an epilepsy patient who had a severe, dose-dependent, memory deficit after ZNS administration. A 65-year-old man visited our epilepsy clinic due to the occurrence of nocturnal convulsions. Despite the absence of seizures, he developed a severe impairment of verbal and visual memory functions after the increment of ZNS dosage from 200 mg/day to 300 mg/day. We substituted 1,000 mg/day valproic acid for ZNS. His cognitive performances were returned to original levels.