1.Transient Global Amnesia Developed after Zolpidem Intake
Jean Hee KIM ; Yooha HWANG ; Byung Seok KIM ; Joong Seok KIM
Journal of the Korean Neurological Association 2018;36(3):226-230
We report two patients who complained of transient anterograde amnesia and repetitive questioning, that developed after taking zolpidem and lasted for several hours. The clinical manifestations of these patients fulfill the clinical criteria for transient global amnesia (TGA). The typical clinical manifestation of TGA following the consumption of zolpidem suggests a possible relationship associated with its drug mechanism.
Amnesia, Anterograde
;
Amnesia, Transient Global
;
Humans
2.Hippocampal Lesions of Diffusion Weighted Magnetic Resonance Image in Patients with Headache without Symptoms of Transient Global Amnesia.
Jeong Hoon PARK ; Chung Geun OH ; Sung Hun KIM ; Seung Hwan LEE ; Jae Won JANG
Dementia and Neurocognitive Disorders 2017;16(3):87-90
BACKGROUND: The dot-like hippocampal signal intensity in diffusion-weighted MR images is well-known as a characteristic imaging feature in transient global amnesia, a neurological syndrome in which sudden forward-and-backward memory loss occurs that is slowly recovered within 24 hours. We here report on patients with this dot-like hippocampal hyperintensity who did not present with anterograde amnesia except for headaches. CASE REPORT: Two women without a specific medical history presented with sudden-onset headaches on the same day. Neither had any trauma or infection history before the symptom or any sudden emotional or postural changes. Brain MRI showed tiny hippocampal high signal intensity on diffusion-weighted images (DWI). CONCLUSIONS: Dot-like hippocampal lesions seen on DWI may be present without memory impairment, and more studies are needed to determine whether there is any association with headache as in this case.
Amnesia, Anterograde
;
Amnesia, Transient Global*
;
Brain
;
Diffusion*
;
Female
;
Headache*
;
Hippocampus
;
Humans
;
Magnetic Resonance Imaging
;
Memory
;
Memory Disorders
3.Zolpidem Induced Sleep-related Eating and Complex Behaviors in a Patient with Obstructive Sleep Apnea and Restless Legs Syndrome.
Young Min PARK ; Hyun Woo SHIN
Clinical Psychopharmacology and Neuroscience 2016;14(3):299-301
Zolpidem-induced sleep-related complex behaviors (SRCB) with anterograde amnesia have been reported. We describe herein a case in which the development of zolpidem-induced sleep-related eating disorder (SRED) and SRCB was strongly suspected. A 71-year-old Korean male was admitted to the Department of Psychiatry due to his repetitive SRED and SRCB with anterograde amnesia, which he reported as having occurred since taking zolpidem. The patient also had restless legs syndrome (RLS) and obstructive sleep apnea (OSA). His baseline serum iron level was low at admission. Zolpidem discontinuation resulted in the immediate disappearance of his SRED, but did not affect his RLS symptoms. These symptoms rapidly improved after adding a single i.v. iron injection once daily, and so he was discharged to day-clinic treatment. These findings indicate that zolpidem can induce SRCB. Although the pathophysiology of zolpidem-induced SRED and other SRCB remains unclear, clinicians should carefully monitor for the potential induction of complex behaviors associated with zolpidem in patients with comorbid RLS or OSA.
Aged
;
Amnesia, Anterograde
;
Eating*
;
Humans
;
Iron
;
Male
;
Restless Legs Syndrome*
;
Sleep Apnea, Obstructive*
4.Human Herpes Virus 6 Encephalitis Following Bone Marrow Transplantation with Uncommon Magnetic Resonance Imaging Findings.
Jihye HWANG ; Ji Eun KIM ; Jee Hoon ROH ; Jae Hong LEE
Dementia and Neurocognitive Disorders 2016;15(3):88-91
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.
Adult
;
Amnesia, Anterograde
;
Amnesia, Retrograde
;
Atrophy
;
Bone Marrow Transplantation*
;
Bone Marrow*
;
Brain
;
Cerebrospinal Fluid
;
DNA
;
DNA, Viral
;
Encephalitis*
;
Female
;
Fever
;
Ganciclovir
;
Herpesvirus 6, Human
;
Humans*
;
Limbic Encephalitis
;
Magnetic Resonance Imaging*
;
Precursor Cell Lymphoblastic Leukemia-Lymphoma
;
Siblings
;
Temporal Lobe
5.Hippocampal Hyperintensities on Diffusion-Weighted MRI without Transient Global Amnesia.
Moonyoung JEONG ; Jeong Hee KIM ; Jaehyun JIN ; Hye Jin LEE ; Yeonsil MOON ; Jin Woo CHOI ; Hahn Young KIM
Journal of the Korean Neurological Association 2016;34(5):360-362
Dot-like hippocampal hyperintensities on diffusion-weighted magnetic resonance imaging (MRI) have been reported as an interesting imaging finding of transient global amnesia (TGA). We report three patients with such dot-like hippocampal hyperintensities who did not present with anterograde amnesia. Episodes associated with the Valsalva maneuver such as nausea or vomiting might have produced the dot-like hippocampal hyperintensities in these patients. However, depending on the individual susceptibility to hippocampal lesions, clinical symptoms of TGA might not be present even when hippocampal lesions are present.
Amnesia, Anterograde
;
Amnesia, Transient Global*
;
Hippocampus
;
Humans
;
Magnetic Resonance Imaging*
;
Nausea
;
Valsalva Maneuver
;
Vomiting
6.Etifoxine for Pain Patients with Anxiety.
The Korean Journal of Pain 2015;28(1):4-10
Etifoxine (etafenoxine, Stresam(R)) is a non-benzodiazepine anxiolytic with an anticonvulsant effect. It was developed in the 1960s for anxiety disorders and is currently being studied for its ability to promote peripheral nerve healing and to treat chemotherapy-induced pain. In addition to being mediated by GABA(A)alpha2 receptors like benzodiazepines, etifoxine appears to produce anxiolytic effects directly by binding to beta2 or beta3 subunits of the GABA(A) receptor complex. It also modulates GABA(A) receptors indirectly via stimulation of neurosteroid production after etifoxine binds to the 18 kDa translocator protein (TSPO) of the outer mitochondrial membrane in the central and peripheral nervous systems, previously known as the peripheral benzodiazepine receptor (PBR). Therefore, the effects of etifoxine are not completely reversed by the benzodiazepine antagonist flumazenil. Etifoxine is used for various emotional and bodily reactions followed by anxiety. It is contraindicated in situations such as shock, severely impaired liver or kidney function, and severe respiratory failure. The average dosage is 150 mg per day for no more than 12 weeks. The most common adverse effect is drowsiness at the initial stage. It does not usually cause any withdrawal syndromes. In conclusion, etifoxine shows less adverse effects of anterograde amnesia, sedation, impaired psychomotor performance, and withdrawal syndromes than those of benzodiazepines. It potentiates GABA(A) receptor-function by a direct allosteric effect and by an indirect mechanism involving the activation of TSPO. It seems promising that non-benzodiazepine anxiolytics including etifoxine will replenish shortcomings of benzodiazepines and selective serotonin reuptake inhibitors according to animated studies related to TSPO.
Amnesia, Anterograde
;
Anti-Anxiety Agents
;
Anticonvulsants
;
Anxiety Disorders
;
Anxiety*
;
Benzodiazepines
;
Flumazenil
;
Humans
;
Kidney
;
Liver
;
Mitochondrial Membranes
;
Nerve Regeneration
;
Neuralgia
;
Neurotransmitter Agents
;
Peripheral Nerves
;
Peripheral Nervous System
;
Psychomotor Performance
;
Receptors, GABA-A
;
Respiratory Insufficiency
;
Serotonin Uptake Inhibitors
;
Shock
;
Sleep Stages
7.Paraneoplastic Limbic Encephalitis in a Male with Squamous Cell Carcinoma of the Lung.
Tamara SAURI ; Angel IZQUIERDO ; LLuis RAMIO-TORRENTA ; Angel SANCHEZ-MONTANEZ ; Joaquim BOSCH-BARRERA ; Rut PORTA
Journal of Clinical Neurology 2015;11(1):87-91
BACKGROUND: Paraneoplastic limbic encephalitis (PLE) is a rare syndrome characterized by memory impairment, symptoms of hypothalamic dysfunction, and seizures. It commonly precedes the diagnosis of cancer. Small-cell lung cancer is the neoplasm that is most frequently reported as the etiology underlying PLE. CASE REPORT: This report describes a male patient who presented with neurologic symptoms consistent with anterograde amnesia, apathy, and disorientation. MRI revealed diffuse hyperintensities located predominantly in the medial bitemporal lobes, basal ganglia, frontal lobes, and leptomeninges on fluid attenuated inversion recovery images, suggesting PLE. Study of the primary tumor revealed squamous cell carcinoma of the lung. The patient was treated with neoadjuvant chemotherapy followed by surgery and adjuvant chemoradiotherapy, which resulted in his neurologic symptoms gradually improving. CONCLUSIONS: PLE might be a rare debut of squamous cell carcinoma of the lung. Treatment of the primary tumor may improve the neurologic symptoms.
Amnesia, Anterograde
;
Apathy
;
Basal Ganglia
;
Carcinoma, Squamous Cell*
;
Chemoradiotherapy, Adjuvant
;
Diagnosis
;
Drug Therapy
;
Frontal Lobe
;
Humans
;
Limbic Encephalitis*
;
Lung Neoplasms
;
Lung*
;
Magnetic Resonance Imaging
;
Male
;
Memory
;
Neurologic Manifestations
;
Paraneoplastic Syndromes
;
Seizures
8.A Case of Anterograde Amnesia with Bilateral Hippocampus Involvement After Acute Glufosinate Ammonium Intoxication.
Sung Won YOUN ; Ho Kyun KIM ; Hui Joong LEE
Journal of the Korean Society of Magnetic Resonance in Medicine 2014;18(4):352-356
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.
Ammonium Compounds*
;
Amnesia, Anterograde*
;
Brain
;
Diagnosis, Differential
;
Eating
;
Herbicides
;
Hippocampus*
;
Humans
;
Magnetic Resonance Imaging
;
Middle Aged
;
Occipital Lobe
;
Parahippocampal Gyrus
;
Poisoning
9.Isoflurane Induces Transient Anterograde Amnesia through Suppression of Brain-Derived Neurotrophic Factor in Hippocampus.
Han Jin CHO ; Yun Hee SUNG ; Seung Hwan LEE ; Jun Young CHUNG ; Jong Man KANG ; Jae Woo YI
Journal of Korean Neurosurgical Society 2013;53(3):139-144
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.
Adult
;
Amnesia, Anterograde
;
Anesthesia
;
Anesthesia, General
;
Animals
;
Blotting, Western
;
Brain-Derived Neurotrophic Factor
;
Fluorescent Antibody Technique
;
Hippocampus
;
Humans
;
Inhalation
;
Ischemia
;
Isoflurane
;
Male
;
Memory, Short-Term
;
Migraine Disorders
;
Nitrous Oxide
;
Oxygen
;
Polymethyl Methacrylate
;
Protein-Tyrosine Kinases
;
Rats
;
Rats, Sprague-Dawley
10.A Case of Neuro-Behcet's Disease Presenting as Anterograde Amnesia.
Jung Hwa SEO ; Go Un YUN ; Min Jeong PARK ; Kyung Won PARK ; Jae Woo KIM
Journal of the Korean Neurological Association 2006;24(4):367-371
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.
Amnesia, Anterograde*
;
Basal Ganglia
;
Brain
;
Erythema Nodosum
;
Humans
;
Magnetic Resonance Imaging
;
Memory
;
Middle Aged
;
Neurologic Examination
;
Stomatitis, Aphthous
;
Temporal Lobe
;
Thalamus
;
Ulcer

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