• Title/Summary/Keyword: Anterograde amnesia

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

  • Cho, Han-Jin;Sung, Yun-Hee;Lee, Seung-Hwan;Chung, Jun-Young;Kang, Jong-Man;Yi, Jae-Woo
    • Journal of Korean Neurosurgical Society
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    • v.53 no.3
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    • pp.139-144
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    • 2013
  • 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.

Retro- and Ante-grade Amnesia after Conscious Sedation using Midazolam (Midazolam을 이용한 의식하진정법을 시행한 환자에서 나타난 선행성 및 후행성 기억상실)

  • Kim, Yeong-Wook;Keum, Yoon-Seon;Mo, Dong-Yub;Lee, Jang-Yeol;Kim, Hyoun-Chull;Lee, Sang-Chul
    • Journal of The Korean Dental Society of Anesthesiology
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    • v.11 no.2
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    • pp.153-158
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    • 2011
  • Midazolam is known to produce sedation as well as amnesia. Many articles reported about anterograde amnesia, but it is rare that articles about retrograde amnesia. The 61-year-old female patient (64 kg, 154 cm, ASA physical status I) was administered 3.02 mg (0.047 mg/kg) of midazolam during 2 hours. The patient's Modified Observer's Assesment of Alertness/Sedation Scale was 4. The patient who had been consciously sedated with midazolam, exhibited profound amnesia, both anterograde and retrograde after implantation. The patient's memory restoration was begun after 6 hours.

INTRAMUSCULAR MIDAZOLAM SEDATON IN AUTISM PATIENT FOR CARIES TREATMENT : CASE REPORT (미다졸람 근주요법을 이용한 자폐증 환자의 우식치료 : 증례보고)

  • Bae, Youngeun;Noh, Taehwan;Kim, Bomi;Jeong, Taesung
    • The Journal of Korea Assosiation for Disability and Oral Health
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    • v.11 no.1
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    • pp.17-20
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    • 2015
  • Autism is a life-long neurodevelopmental disorder characterized by qualitative abnormalities in reciprocal social interactions and patterns of communication. Patients with autism are difficult to manage during dental treatment. Thus they need special consideration like physical restraint, conscious sedation or general anesthesia. A 5-year-old male dental patient with autism was reffered to dental treatment under conscious sedation using intramuscular midazolam that creats anterograde amnesia. Dental procedure using midazolm which cause anterograde amnesia can be effective treatment strategy in autism patient.

A Case of Anterograde Amnesia with Bilateral Hippocampus Involvement After Acute Glufosinate Ammonium Intoxication (급성 글루포시네이트 암모니움 중독 후 양측성 해마 병변과 전향적 기억상실증을 보인 증례 1례 보고)

  • Youn, Sung Won;Kim, Ho Kyun;Lee, Hui Joong
    • Investigative Magnetic Resonance Imaging
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    • v.18 no.4
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    • pp.352-356
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    • 2014
  • 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.

ANTEROGRADE AMNESIC EFFECT OF MIDAZOLAM (Midazolam 투여시 선행성 건망증 발현에 관한 연구)

  • Lee, Jung-Ha;Kim, Mi-Ra;Lee, Nan-Young;Lee, Sang-Ho
    • Journal of the korean academy of Pediatric Dentistry
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    • v.31 no.3
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    • pp.412-420
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    • 2004
  • The purpose of this study was to assess the anterograde amnesic effect of Midazolam administrated by intranasal and oral route. Fifteen healthy volunteers(ASA I) were administrated with placebo, oral Midazolam(15mg), intranasal Midazolam(0.25mg/kg) every 2 weeks. First picture cards were shown to volunteers before medication. At 15, 30, 45 minutes, other picture cards were shown to volunteers. BP, $SpO_2$ and sedation scores were measured. After 24 hours, the volunteers were questioned about their memory of pictures. To assess amnesic effect, recall and recognition test were performed using a series of picture cards designed for this purpose. The obtained results were as follows; 1. Compared to placebo, Midazolam group(oral and intranasal) experienced a significant anterograde amnesic effect(P<0.01) 2. There was no difference between oral and intranasal Midazolam(P>0.01). 3. Anterograde amnesic effect of oral and intranasal Midazolam group began at 15minutes. It became increasingly, oral Midazolam group experienced extremely amnesic effect at 45minutes, intranasal Midazolam group was at 30minutes. 4. After 30minutes of Midazolam administration, anterograde amnesia of oral Midazolam group is more effective than intranasal Midazolam group.

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A Case of anterograde amnesia with hippocampal lesions following glufosinate intoxication (Glufosinate ammonium 중독 후에 발생한 해마 손상에 의한 선행성 기억상실 1례)

  • Seol Seung-Hwan;Park Hyeon-Soo;Ahn Jung-Hwan;Park Hee-Young;Lee Phil-Hyu;Kim Gi-Woon
    • Journal of The Korean Society of Clinical Toxicology
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    • v.4 no.1
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    • pp.61-64
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    • 2006
  • Glufosinate ammonium (GLA), a phosphinic acid derivate of glutamate, is a broad-spectrum contact herbicide. It structurally resembles glutamate, a typical excitatory amino acid in the central nervous system. In korea, the ingestion of GLA for suicidal attempt or accidental event has increased. The neurological complication of GLA intoxication are characterized by loss of consciousness, convulsion, or memory impairment. But, the exact mechanism of GLA toxicity is yet unknown. This report is about a patient with GLA intoxication who showed anterograde amnesia with selective bilateral hip-pocampal lesions supported GLA intoxication with literature reviews supported.

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The oriental-western literatural study of Amnesia (건망증(健忘症)에 대(對)한 동서의학적(東西醫學的) 고찰(考察))

  • Yoon, Sang-hak;Lee, Sang-ryong
    • Journal of Haehwa Medicine
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    • v.9 no.2
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    • pp.293-313
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    • 2001
  • The oriental-western Literatural study of Amnesia, the results were as follows. 1. esia is caused by qi-depression resulted from excessive thought and deficiency of the kidney resulted from congenital deficiency and deficiency of the heart, the disharmony between the heart and the kidney, phlegm, stagnant blood, loss of the blood etc. resulted from deficiency of the heart blood. 2. The treatment method of Amnesia is as follows, the highest frequence was growing blood-tranquilization-regulating spleen, in descending order removing phlegm-stagnant blood-relaxing the mind and invigorate the heart-spleen-kidney and much tonification qi-blood and growing nutrient qi-manifesting source qi and regulating the harmony between the heart and the kidney and maintaining patency for the flow of gi were the most treatment method. 3. The treatment medicine of Amnesia is as follows, the highest frequence was Kuei Bi Tang(歸脾湯) in decending order Jeng Ji Whan(定志丸), Su Seng Whan(壽星丸), Chun Whang Boo Sim Dan(天王補心丹), Ju Jak Whan(朱雀丸), Doo Dam Tang(導痰湯), Yin Sin Kuei Sa Dan(引神歸舍丹), Ga Gam Go Bon Dan(加減固本丸), Ryung Ji Go(寧志膏), Jang Won Dan(壯元丹), Tong Ol Tang(通鬱湯). 4. In oriental medicine functional physiology and pathology was significant in differential diagnosis and treatment and in western medicine it was explained organically and psychologically. 5. In western medicine As one of memory disorder Amnesia is divided into psychogenic amnesia and organic amnesia, and organic amnesia is divided into anterograde amnesia and retrograde amnesia and psychogenic amnesia is divided into localized amnesia, generalized amnesia selective amnesia.

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Clinical Report of two TGA cases (일과성 전기억상실증으로 진단된 환자 치험 2례)

  • Oh, Kyong-Min;Yang, Dong-Ho;Cho, Youn-Song;Kim, Bo-Kyong
    • Journal of Oriental Neuropsychiatry
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    • v.19 no.3
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    • pp.265-276
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    • 2008
  • Transient global amnesia(TGA) is a clinical syndrome characterized by sudden, temporary dysfunction of anterograde and recent retrograde memory without other neurologic deficits. Different hypotheses have been considered for its etiology, but it still remains obscure. Recently the diffusion-weighted magnetic resonance imaging(DWI), has been considered as the sensitive tool to detect small punctate hyperintense lesions in the hippocampus in transient global amnesia(TGA). We report two TGA cases, all of them answers to TGA clinical criteria, and one of them showed two dot like high signal intense foci in Rt. hippocampus on DWI.

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CARIES TREATMENT OF A MIDAZOLAM-PREMEDICATED PATIENT WITH DEVELOPMENTAL DISORDERS : A CASE REPORT (미다졸람 경구 전투약을 이용한 발달장애 환아의 전신마취하 우식치료 증례보고)

  • Kim, Hyo-Eun;Shin, Teo-Jeon;Kim, Young-Jae;Kim, Jung-Wook;Jang, Ki-Taeg;Lee, Sang-Hoon;Kim, Chong-Chul;Hyun, Hong-Keun
    • The Journal of Korea Assosiation for Disability and Oral Health
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    • v.9 no.1
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    • pp.46-50
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    • 2013
  • Developmental disorders are a group of psychiatric conditions originating in childhood that involve serious impairments in different areas. These disorders comprise language disorders, learning disorders, motor disorders and autism spectrum disorders. Midazolam is a short-acting drug in the benzodiazepine class developed by Hoffmann-La Roche in the 1970s. The drug is used for treatment of acute seizures, moderate to severe insomnia, and for inducing sedation and amnesia before medical procedures. It possesses profoundly potent anxiolytic, amnestic, hypnotic, anticonvulsant, skeletal muscle relaxant, and sedative properties. The anterograde amnesia property of midazolam is useful for premedication before surgery to inhibit unpleasant memories. This article presents a case report including caries treatment of a 8-year-old male patient with developmental disorders using oral midazolam premedication as an alternative method of behavior management prior to general anesthesia.

Etifoxine for Pain Patients with Anxiety

  • Choi, Yun Mi;Kim, Kyung Hoon
    • The Korean Journal of Pain
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    • v.28 no.1
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    • pp.4-10
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    • 2015
  • 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 $GABA_A{\alpha}2$ receptors like benzodiazepines, etifoxine appears to produce anxiolytic effects directly by binding to ${\beta}2$ or ${\beta}3$ 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.