Recurrent Falls Associated with Lower Limb Deep Vein Thrombosis

주재정,안병준,권겸일 대한신경과학회 2017 Journal of Clinical Neurology Vol.13 No.1

우울증을 초기증상으로 발현한 가족성 크로이츠펠트-야콥병

주재정,양영순,강진호,이선화,하상원,한정호,조은경,김두응 대한치매학회 2012 Dementia and Neurocognitive Disorders Vol.11 No.2

Creutzfeldt-Jakob disease (CJD) is a degenerative neurological disorder that is incurable and invariably fatal. It is characterized by rapidly progressive dementia presenting with memory loss, personality changes and hallucinations. The symptoms of CJD are caused by progressive death of neurons in the central nervous system, which is associated with build-up of the abnormal prion proteins forming amyloids. In human, CJD can be acquired genetically through a mutation of the gene encoding for the prion protein (PRNP). This occurs in only 5-10% of all CJD cases. We report a 64-year old woman with CJD carrying a V180I mutation that features late onset, rapid progression, no periodic sharp wave complexes on electroencephalography, and cortical signal change and edema in bilateral frontotemporoparietal lobes and basal ganglia on MRI.

Improvement of Frontal Lobe Dysfunctions in Neuromyelitis Optica after Treatment: A Case Report

주재정,Sul-Ki Lee,황인하,Kyum-Il Kwon,Byoung June Ahn,양영순 대한치매학회 2016 Dementia and Neurocognitive Disorders Vol.15 No.1

BackgroundNeuromyelitis optica (NMO) is characterized by optic neuritis and longitudinally extensive transverse myelitis. Generally, the brain had been considered healthy in NMO patients, though recent studies have demonstrated that T2-weighted abnormalities may be observed in various brain regions. Logically, NMO brain lesions are localized at sites of high aquaporin-4 expression. Case ReportA 68-year-old right-handed man with dysuria, weakness in the bilateral upper and lower limbs, and decreased sensation of the lower extremities, was diagnosed with neuromyelitis optica. The patient was gradually speaking less, was showing reduced interest in hobbies, and had undergone changes in character and behavior. An examination was performed using the Seoul Neuropsychological Screening Battery (SNSB), which revealed that the profile of frontal lobe dysfunctions was prominent as compared with other cognitive domains. The patient was treated with prednisolone and azathioprine for about 1 year without recurrence, and showed prognostic improvement according to further SNSB testing. ConclusionsFurther studies are considered necessary in order to find the most effective medication regimen for improving cognitive functions in those accurately diagnosed with NMO, and to develop systematic treatment using even more diversified immune-related agents.

Posterior Cortical Atrophy with Acute Onset and Rapid Progressive Visual Symptoms: A Case Report

주재정,Sul-Ki Lee,황인하,Kyum-Il Kwon,안병준,양영순 대한치매학회 2015 Dementia and Neurocognitive Disorders Vol.14 No.2

Background Posterior cortical atrophy (PCA) is characterized by slowly progressive early onset dementia with cortical visual dysfunctionand disproportionate atrophy of the posterior cortex. Case Report A 55-year-old right-handed woman developed visuo-spatial impairments that progressed rapidly into cortical blindness overthe following 3 months. Neuro-psychological evaluation revealed Gerstmann syndrome and severe constructional impairments with all componentsof Balint syndrome. However, her memory, insight, and judgment were preserved. Her brain MRI was normal. However, 18F fluorodeoxyglucosepositron emission tomography revealed a marked hypometabolism in the bilateral parieto-occipital region. Conclusions Although rapid progression of visuo-spatial dysfunction without memory impairment occurred, we considered PCA as well.

기억장애가 유일한 임상양상으로 확인된 척수소뇌실조 2형 1예

주재정,한상우,하상원,한정호,김두응,양영순 대한치매학회 2014 Dementia and Neurocognitive Disorders Vol.13 No.1

Spinocerebellar ataxia (SCA) is one of a group of genetic disorders characterized by slowly progressive in-coordination of gait and often associated with poor coordination of hands, speech, and eye movements. There are more than 35 different types of spinocerebellar ataxias, each caused by a different genetic mutation. Spinocerebellar ataxia type 2 (SCA2) is a subtype of type I autosomal dominant cerebellar ataxia (ADCA type I) characterized by truncal ataxia, dysarthria, slowed saccades and less commonly ophthalmoparesis and chorea. The age at onset varies from 3 to 79 years (mean 33). Usually, the first symptom of the disease is the gait ataxia, followed by the cerebellar dysarthria. Of late, other clinical manifestations of SCA2 are the cognitive dysfunctions, which include frontal executive impairment, verbal short-term memory deficits as well as reduction of attention and concentration. We report a 56-year old woman identified as spinocerebellar ataxia type 2 (SCA2) with only clinical feature of memory impairment.

3,4,5-Tricaffeoylquinic acid가 파킨슨증후군유발독소 1-methyl-4-phenylpyridinium에 의한세포자멸사에 미치는 억제효과

주재정,강진호,한정호,김두응,이정수 대한신경과학회 2014 대한신경과학회지 Vol.32 No.2

Background: 1-Methyl-4-phenylpyridinium (MPP+) causes a neuronal cell injury that is similar to the findings observedin Parkinson’s disease. Caffeoylquinic acid derivatives have demonstrated anti-oxidant and anti-inflammatory effects. Nevertheless, the effect of 3,4,5-tricaffeoylquinic acid (3,4,5-triCQA) on the neuronal cell death due to exposure ofparkinsonian toxin MPP+remains unclear. Methods: Using differentiated PC12 cells, the preventive effect of 3,4,5-triCQA on the MPP+-induced cell death inrelation to apoptotic process was examined. Results: MPP+induced a decrease in Bid, Bcl-2 and survivin protein levels, increase in Bax levels, loss of the mitochondrialtransmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), cleavage of PARP-1, and an increasein the tumor suppressor p53 levels. 3,4,5-Tricaffeoylquinic acid attenuated the MPP+-induced changes in theapoptosis-related protein levels, formation of reactive oxygen species, depletion of GSH, nuclear damage and cell death. 3,4,5-Tricaffeoylquinic acid attenuated another parkinsonian neurotoxin rotenone-induced cell death. Conclusions: 3,4,5-Tricaffeoylquinic acid may attenuate the MPP+-induced apoptosis in PC12 cells by suppressing theactivation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect seems tobe ascribed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH. Background: 1-Methyl-4-phenylpyridinium (MPP) causes a neuronal cell injury that is similar to the findings observedin Parkinson’s disease. Caffeoylquinic acid derivatives have demonstrated anti-oxidant and anti-inflammatory effects. Nevertheless, the effect of 3,4,5-tricaffeoylquinic acid (3,4,5-triCQA) on the neuronal cell death due to exposure ofparkinsonian toxin MPP+remains unclear. Methods: Using differentiated PC12 cells, the preventive effect of 3,4,5-triCQA on the MPP+-induced cell death inrelation to apoptotic process was examined. Results: MPP+induced a decrease in Bid, Bcl-2 and survivin protein levels, increase in Bax levels, loss of the mitochondrialtransmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), cleavage of PARP-1, and an increasein the tumor suppressor p53 levels. 3,4,5-Tricaffeoylquinic acid attenuated the MPP+-induced changes in theapoptosis-related protein levels, formation of reactive oxygen species, depletion of GSH, nuclear damage and cell death. 3,4,5-Tricaffeoylquinic acid attenuated another parkinsonian neurotoxin rotenone-induced cell death. Conclusions: 3,4,5-Tricaffeoylquinic acid may attenuate the MPP+-induced apoptosis in PC12 cells by suppressing theactivation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect seems tobe ascribed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.

왼쪽 내경동맥 협착에 의해 액체감쇠역전회복영상에서 보인 뇌척수액 고신호강도

주재정,하상원,강진호,한상우,양영순,한정호,조은경,김두응 대한신경과학회 2014 대한신경과학회지 Vol.32 No.2

가벼운 기억력 장애를 주소로 내원한 비부수 종양성 자가면역 항체 음성 변연뇌염 1예

한상우,주재정,강진호,하상원,양영순 대한치매학회 2014 Dementia and Neurocognitive Disorders Vol.13 No.3

Encephalitis that primarily involves limbic system structures such as the hippocampus and parahippocampal gyrus has been described in early papers, most commonly characterized by a subacute progressive impairment of short-term memory, psychiatric features and seizures. While these findings might be caused by viral infections or systemic autoimmune disorders, many patients with limbic encephalitis have an immune-mediated etiology (paraneoplastic or not) characterized with serum or CSF antineuronal antibodies. This case reports about non-paraneoplastic autoantibody-negative limbic encephalitis in which there are no detection of antigens and no evidence of tumors.

전두측두엽 치매와 파킨슨증의 임상양상을 보이는 권투선수치매 1예

양영순,주재정,강진호,한상우,하상원,한정호,조은경,김두응 대한치매학회 2013 Dementia and Neurocognitive Disorders Vol.12 No.3

Dementia pugilistica (DP) or chronic traumatic encephalopathy (CTE) is a neurodegenerative disease or dementia that may affect amateur or professional boxers as well as athletes in other sports who suffer concussions. The condition is thought to affect around 15% to 20% of professional boxers and caused by repeated concussive or subconcussive blows. CTE was in the past referred to as dementia pugilistica, which reflected the prevailing notion that this condition was restricted to boxers. Recent research, however, has demonstrated neuropathological evidence of CTE in retired American football players, a professional wrestler, a professional hockey player and a soccer player, as well as in nonathletes. It is probable that many individuals are susceptible to CTE, including those who experience falls, motor vehicle accidents, assaults, epileptic seizures, or military combat, and that repeated mild closed head trauma of diverse origin is capable of instigating the neurodegenerative cascade leading to CTE. We report a 62-year old man suspicious of dementia pugilistica with clinical features of frontotemporal dementia and parkinsonism.

복강경수술 이후 발생한 근막통증후군

배희원,한정호,주재정 대한신경과학회 2022 대한신경과학회지 Vol.40 No.1