Right fornix column infarction: a case report / 中华神经科杂志

Isolated fornix infarction is very rare in cerebral infarction. A case of right column fornix infarction with acute anterograde amnesia as the only manifestation who was diagnosed in the Fifth Affiliated Hospital of Sun Yat-Sen University in March 2020 was presented. The clinical symptoms were the inability to recall recent events, repeated speech. Head magnetic resonance suggested right fornix column infarction and diffusion tensor imaging showed reduction of right fornix fiber bundles. The symptoms improved significantly after conventional treatment of cerebral infarction and improving intelligence treatment.

Human Herpes Virus 6 Encephalitis Following Bone Marrow Transplantation with Uncommon Magnetic Resonance Imaging Findings

BACKGROUND: Human Herpes Virus 6 (HHV6) is commonly associated with encephalitis following bone marrow transplantation. However, hippocampal atrophy and global hypometabolism are rare findings in HHV6 encephalitis. CASE REPORT: A 41-year-old right-handed woman with acute lymphoblastic leukemia presented with fever and mental changes 2 weeks after receiving a sibling bone marrow transplant. The patient's cerebrospinal fluid (CSF) was positive for HHV-6 deoxyribonucleic acid (DNA), but was negative for other viral DNA. Brain magnetic resonance imaging revealed atrophic changes in bilateral medial temporal lobes. Following 4 weeks of ganciclovir therapy, a CSF exam was negative for HHV-6 DNA and the patient's neurological symptoms partially improved. However, she was disoriented and had severe retrograde and anterograde amnesia. 18F-fluorodeoxyglucose-positron emission tomography indicated global hypometabolism in the medial temporal lobes and the fronto-parietal cortices. CONCLUSIONS: This is a rare and unusual case of hippocampal atrophy in the acute stage of HHV6 encephalitis. Our imaging findings may reflect the chronic indolent course of HHV6 encephalitis.

A Case of Anterograde Amnesia with Bilateral Hippocampus Involvement After Acute Glufosinate Ammonium Intoxication

A 51-year-old man developed anterograde amnesia following the ingestion of glufosinate ammonium. Brain MRI revealed hyperintense lesions involving the bilateral hippocampus and parahippocampal gyrus, and the right occipital lobe. The mechanism underlying acute glufosinate ammonium intoxication and the differential diagnosis of hippocampal lesions are discussed.

Isoflurane Induces Transient Anterograde Amnesia through Suppression of Brain-Derived Neurotrophic Factor in Hippocampus

OBJECTIVE: Transient anterograde amnesia is occasionally observed in a number of conditions, including migraine, focal ischemia, venous flow abnormalities, and after general anesthesia. The inhalation anesthetic, isoflurane, is known to induce transient anterograde amnesia. We examined the involvement of brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) in the underlying mechanisms of the isoflurane-induced transient anterograde amnesia. METHODS: Adult male Sprague-Dawley rats were divided into three groups : the control group, the 10 minutes after recovery from isoflurane anesthesia group, and the 2 hours after recovery from isoflurane anesthesia group (n=8 in each group). The rats in the isoflurane-exposed groups were anesthetized with 1.2% isoflurane in 75% nitrous oxide and 25% oxygen for 2 hours in a Plexiglas anesthetizing chamber. Short-term memory was determined using the step-down avoidance task. BDNF and TrkB expressions in the hippocampus were evaluated by immunofluorescence staining and western blot analysis. RESULTS: Latency in the step-down avoidance task was decreased 10 minutes after recovery from isoflurane anesthesia, whereas it recovered to the control level 2 hours after isoflurane anesthesia. The expressions of BDNF and TrkB in the hippocampus were decreased immediately after isoflurane anesthesia but were increased 2 hours after isoflurane anesthesia. CONCLUSION: In this study, isoflurane anesthesia induced transient anterograde amnesia, and the expressions of BDNF and TrkB in the hippocampus might be involved in the underlying mechanisms of this transient anterograde amnesia.

A Case of Neuro-Behcet's Disease Presenting as Anterograde Amnesia

Anterograde amnesia in Behcet's disease is a rare occurrence. A 50-year-old man presented with anterograde amnesia. He had been suffering multiple oral aphthous ulcers and genital ulcers with erythema nodosum. A neurological examination revealed prominent anterograde memory disturbance. Brain MRI revealed high signal intensity lesions involving the anterior thalamus, posterior part of the basal ganglia and the mesial temporal lobe. We report a rare case of Behcet's disease manifesting severe anterograde amnesia resulting from thalamic and mesial temporal lesions.

Changes of Regional Cerebral Blood Flow in Left Anterior Thalamic Infarction: Analysis of 99mTc-Ethyl Cysteinate Dimer (ECD) SPECT by using Statistical Parametric Mapping

BACKGROUND: The thalamus has multiple connections with areas of the cerebral cortex involved in arousal and cognition. Thalamic damage has been reported to be associated with variable neuropsychological dysfunctions and dementia. This study investigates the changes of regional cerebral blood flow (rCBF) by using SPM analysis of 99mTc-ECD SPECT and examining the neuropsychological abnormalities of 4 patients with anterior thalamic infarctions. METHODS: Four patients with left anterior thalamic infarctions and eleven normal controls were evaluated. K-MMSE and the Seoul Neuropsychological Screening Battery were performed within 2 days after stroke. The normalized SPECT data of 4 patients were compared to those of 11 controls for the detection of areas with decreased rCBF by SPM analysis. RESULTS: All 4 patients showed anterograde amnesia in their verbal memory, which was not improved by recognition. Dysexecutive features were occasionally present, such as decreased word fluency and impaired Stroop test results. SPM analysis revealed decreased rCBF in the left supramarginal gyrus, the superior temporal gyrus, the middle and inferior frontal gyrus, the medial dorsal and anterior nucleus of the left thalamus. CONCLUSIONS: The changes of rCBF in patients with left anterior thalamic infarctions may be due to the remote suppression on metabolism by the interruption of the cortico-subcortial circuit, which connects the anterior thalamic nucleus and various cortical areas. The executive dysfunction and dysnomia may be caused by the left dorsolateral frontal dysfunction of the thalamocortical circuit. Anterograde amnesia with storage deficit may be caused by the disruption of mamillothalamic tract.

Effects of propofol on anterograde and retrograde amnesia in the old mice / 中华麻醉学杂志

Objective To investigate the effects of propofol on learning and amnesia in the old miceMethods The normal Kunming mice were trained in a one-trial, step-through, light-dark passive avoidance paradigm Propofol (50 or 100 mg/kg) was administered intraperitoneally 15 min before training ,and propofol (100 or 200 mg/kg) separately 30 min and 6 h in the immediate post-training period The latency of escaping into a darkened chamber and the wrong number of entering darkened chamber were recorded Animals were tested for recall at 24th h post-training time The activity of acetyltransferase was determined with radiommunoassay in the brain 3h after administrationResults All control animals were liable to learn the task as judged by their increased latencies to enter the darkened chamber at 24th h post-training time After administration with propofol 50 mg/kg or 100 mg/kg, the latencies were reduced (246 and 208,repectively), compared with control (P