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강규식 대한뇌졸중학회 2006 Journal of stroke Vol.8 No.1
We report a patient with acute right corona radiata infarction and left caudate hemorrhage, which developed simultaneously. The patient was a 55-year-old man with a history of hypertension and diabetes. He was admitted to the hospital due to dysarthria and weakness in his left limbs. Besides of acute lesions, there were old lacunar infarcts and muliple microbleeds on brain imaging. The small vessel diseases caused by chronic hypertension might have predisposed him to both cerebral infarction and cerebral hemorrhage simultaneously.
강규식,김병건 대한신경과학회 2019 대한신경과학회지 Vol.37 No.2
Intracranial hypotension usually arises in the context of known or suspected leak of cerebrospinal fluid (CSF). This leakage leads to a fall in intracranial CSF pressure and CSF volume. The most common clinical manifestation of intracranial hypotension is orthostatic headache. Post-dural puncture headache and CSF fistula headache are classified along with headache attributed to spontaneous intracranial hypotension as headache attributed to low CSF pressure by the International Classification of Headache Disorders. Headache attributed to low CSF pressure is usually but not always orthostatic. The orthostatic features at its onset can become less prominent over time. Other manifestations of intracranial hypotension are nausea, spine pain, neck stiffness, photophobia, hearing abnormalities, tinnitus, dizziness, gait unsteadiness, cognitive and mental status changes, movement disorders and upper extremity radicular symptoms. There are two presumed pathophysiologic mechanisms behind the development of various manifestations of intracranial hypotension. Firstly, CSF loss leads to downward shift of the brain causing traction on the anchoring and supporting structures of the brain. Secondly, CSF loss results in compensatory meningeal venodilation. Headaches presenting acutely after an intervention or trauma that is known to cause CSF leakage are easy to diagnose. However, a high degree of suspicion is required to make the diagnosis of spontaneous intracranial hypotension and understanding various neurological symptoms of intracranial hypotension may help clinicians.
액체-액체층을 보이는 결핵성 뇌농양의 확산강조영상과 수소자기공명분광분석
강규식,하재혁,이수호,이광우 대한신경과학회 2007 대한신경과학회지 Vol.25 No.2
We encountered a patient with tuberculous brain abscesses, which is very rare. Diffusion-weighted imaging showed high signal in the lower part of the large abscess cavity and low signal in the upper part of the cavity. Proton MRS showed resonances representing lactate. Combined studies with diffusion-weighted imaging and MRS are useful in the differential diagnosis of tuberculous abscess from other structures that feature ring-enhanced lesions.
강규식,박종무,윤병우 대한신경과학회 2006 대한신경과학회지 Vol.24 No.6
Idiopathic thrombocytopenic purpura (ITP) is an immunologic disorder that destroys platelets and megakaryocytes. Hemorrhagic complications are common in patients with ITP. However, thrombotic complications such as coronary artery disease and cerebral infarctions are infrequent. We report a patient with ITP who developed a cerebral infarction despite thrombocytopenia after long-term danazol therapy and was negative for the antiphospholipid antibody.
일시적 국소 뇌허혈을 일으킨 수컷 쥐의 뇌에서는 프로락틴이 새로운 세포 생성을 촉진하지 못할 가능성이 있다: 예비 연구
강규식,이순태,권형민,김민정,김영주,이경미,박종무,주건,김만호,윤병우 대한신경과학회 2006 대한신경과학회지 Vol.24 No.2
Background: Production of neuronal progenitors is usually stimulated in the forebrain subventricular zone of mice after the intracerebroventricular infusion of prolactin. As a preliminary study, we infused prolactin to the male rat brain to test the hypothesis that prolactin promotes new cell proliferation in the brain and functional recovery after focal ischemia. Methods: Male rats were subjected to intraluminal middle cerebral artery occlusion. Prolactin was administered to the surface of the brain for 5 or 14 days starting 24 or 48 hours after stroke onset at doses of 6.4 µg per day. We administered the same volume of saline to the other ischemic rats used as a control group. Some rats were killed 6 or 17 days after stroke for analysis of infarct volume and newly generated cells within the subventricular zone and the striatum. The other rats were tested for neurological recovery 24 days after stroke. Results: There was no significant difference of infarct volume among the experiment groups. Treatment with prolactin did not increase the numbers of bromodeoxyuridine-immunoreactive cells in the subventricular zone and the striatum. Treatment with prolactin did not enhance neurological recovery in all tests performed. Conclusions: In this preliminary study, prolactin did not enhance new cell generation in the male rat brain nor reduce the neurological deficits after ischemic stroke.