뇌부종의 병태생리

정진헌 대한신경집중치료학회 2016 대한신경집중치료학회지 Vol.9 No.2

Brain edema is defined as an increase in brain volume resulting from abnormal accumulation of fluid within the brain parenchyma. Brain edema is a potentially life-threatening complication of neurocritical illness as it raises the intracranial pressure and may progress to brain herniation and death. The management of brain edema and increased intracranial pressure is a significant challenge in neurocritical care. The purpose of this review is to describe the pathophysiology of diverse types of brain edema.

국소저온이 대뇌에 미치는 영향에 관한 실험적 연구

조순구,박상덕,이훈갑,주정화 대한신경외과학회 1983 Journal of Korean neurosurgical society Vol.12 No.2

A study of local hypothermia upon the brain was performed in cats. Extravascular local cooling of brain was designed for the experiment using a head exchanger with a cuff. The cuff was circulated by a cold liquid, saline, at a temperature of 0°±1.1℃ and rested on brain surface. The thermocouples were inserted and placed at different depths of each 0.5㎝ in the brain, and then temperatures were measured at each depth before and during cooling every 10 minutes. The mean precooling temperatures were 32.0℃ at brain surface and 37.7℃ at 1.5㎝ depth in brain. During cooling, temperature lowering was the most marked and evident at extent of 1.0㎝ thickness in the subcortical tissue. The lowest mean temperature at each depth throughout the cooling were 18.9℃ at surface, 20.0℃ at 0.5㎝ depth, 22.9℃ at 1.0㎝ depth and 32.8℃ at 1.5㎝ depth in the brain. Temperature lowering in the area of brain injured by contusion was more marked and evident in its degree than that in the normal brain, especially within 10 minutes of cooling. Another design of this experiment was an evaluation of the effect of local hypothermia on cerebral edema induced by impaction injury of the brain. Immediately after the intravenous administration of fluorescein, impaction injuries were made on the area of suprasylvian gyri, and then the left part of hemisphere received local hypothermia while the counter part of same brain was untreated. These injuried brains were removed as specimens at various time intervals after trauma and their coronal sections were examined macroscopically under the ultraviolet illumination. In cooled hemisphere, there were lesser extent of spread and brightness of fluorescein than those in the untreated. Local cerebral cooling in this experimental condition was safe and beneficial in the treatment of trauma-induced vasogenic edema.

Brain abnormalities in Sjogren syndrome with recurrent CNS manifestations: association with neuromyelitis optica

Min, JH,Kim, HJ,Kim, BJ,Lee, KW,Sunwoo, IN,Kim, SM,Kim, BJ,Kim, SH,Park, MS,Waters, P,Vincent, A,Sung, JJ,Lee, KH SAGE Publications 2009 Multiple sclerosis journal: clinical and laborator Vol.15 No.9

<P><B>Background and objectives</B></P><P>Optic neuritis or longitudinally extensive myelitis in Sjogren syndrome (SS) suggests a neuromyelitis optica spectrum disorder (NMOSD). However, brain abnormalities of SS remain to be elucidated for the association with neuromyelitis optica (NMO).</P><P><B>Methods</B></P><P>Twelve primary SS patients (all women, 42?±?13.2?years) who had recurrent central nervous system (CNS) manifestations with brain involvement were retrospectively identified. Brain MRI, and neurologic and serologic findings were analyzed with the measurement of anti-aquaporin-4 antibody (AQP4-Ab).</P><P><B>Results</B></P><P>All patients showed brain lesions characteristic of NMO as follows: 1) the involved sites adjacent to the third and fourth ventricles and in the posterior limb of the internal capsule, 2) unique configurations, such as the longitudinal course from the internal capsule to the midbrain, large cerebral or cerebellar lesions over 3?cm, and cavity-like formations. AQP4-Ab was positive in six of eight patients tested, and all the seropositive patients showed lesions with increased diffusion, suggestive of vasogenic edema. Four patients met the revised criteria of NMO, and nine had features of NMOSDs. Of the remaining three patients showing only brain involvement, one had AQP4-Ab.</P><P><B>Conclusions</B></P><P>This study demonstrates that SS patients with recurrent CNS involvement have brain abnormalities characteristic of NMO and AQP4-Ab in Korea. The presence of AQP4-Ab in one SS patient with only brain involvement may suggest that the coexistence of NMO should be explored in SS patients with recurrent CNS manifestations, even without optic neuritis or myelitis.</P>

뇌자기공명영상에서 비특이적인 혈관성 부종을 보인 하시모토뇌병증

김건우,조남주,김병건,권오현,박종무,강규식,이웅우,이정주 대한신경과학회 2015 대한신경과학회지 Vol.33 No.3

Hashimoto’s encephalopathy (HE) is a rare autoimmune disorder characterized by a nonspecific encephalopathy with high titers of serum anti-thyroid antibody in the absence of other defined causes. A 54-year-old woman was admitted due to recurrent seizures and confusion. Her serum anti-thyroid antibody level was elevated, and brain MRI showed multiple instances of vasogenic edema. Her symptoms disappeared after treatment with high-dose steroids and antiepileptic drugs. We propose that HE should be considered in the differential diagnosis of multiple vasogenic edema on brain imaging.

Vasogenic Edema in Experimental Cerebral Fat Embolism

Park Byung-Rae,Koo Bong-Oh The Korean Society for Biomedical Laboratory Scien 2005 Journal of biomedical laboratory sciences Vol.11 No.1

To evaluate the magnetic resonance imaging and electron microscopic findings of the hyperacute stage of cerebral fat embolism in cats and the time needed for the development of vasogenic edema. Magnetic resonance imaging was performed at 30 minutes (group 1, n=9) and at 30 minutes and 1, 2, 4, and 6 hours after embolization with triolein (group 2, n= 10). As a control for group 2, the same acquisition was obtained after embolization with polyvinyl alcohol particles (group 3, n=5). Electron microscopic examination was done in all cats. In group 1, the lesions were iso- or slightly hyperintense on T2-weighted (T2W) and diffusion-weighted (DWIs) images, hypointense on the apparent diffusion coefficient (ADC) map image, and markedly enhanced on the gadolinium-enhanced T1-weighted images (Gd-T1WIs). In group 2 at 30 minutes, the lesions were similar to those in group 1. Thereafter, the lesions became more hyperintense on T2WIs and DWIs and more hypoinfense on the ADC map image. In group 3, the lesions showed mild hyperintensity on T2WIs at 6 hours but hypointensity on the ADC map image from 30 minutes, with a tendency toward a greater decrease over time. Electron microscopic findings revealed discontinuity of the capillary endothelial wall, perivascular and interstitial edema, and swelling of glial and neuronal cells in groups 1 and 2. The lesions were hyperintense on T2WIs and DWIs, hypointense on the ADC map image, and enhanced on Gd-T1WIs. On electron microscopy, the lesions showed cytotoxic and vasogenic edema with disruption of the blood-brain barrier.

Vasogenic Edema in Experimental Cerebral Fat Embolism

Park, Byung-Rae,Koo, Bong-Oh 대한의생명과학회 2005 Biomedical Science Letters Vol.11 No.1

To evaluate the magnetic resonance imaging and electron microscopic findings of the hyperacute stage of cerebral fat embolism in cats and the time needed for the development of vasogenic edema. Magnetic resonance imaging was performed at 30 minutes (group 1, n=9) and at 30 minutes and 1, 2, 4, and 6 hours after embolization with triolein (group 2, n=10). As a control for group 2, the same acquisition was obtained after embolization with polyvinyl alcohol particles (group 3, n=5). Electron microscopic examination was done in all cats. In group 1, the lesions were iso- or slightly hyperintense on T2-weighted (T2W) and diffusion-weighted (DWIs) images, hypointense on the apparent diffusion coefficient (ADC) map image, and markedly enhanced on the gadolinium-enhanced TI-weighted images (Gd-T1Wls). In group 2 at 30 minutes, the lesions were similar to those in group 1. Thereafter, the lesions became more hyperintense on T2WIs and DWIs and more hypoinfense on the ADC map image. In group 3, the lesions showed mild hyperintensity on T2WIs at 6 hours but hypointensity on the ADC map image from 30 minutes, with a tendency toward a greater decrease over time. Electron microscopic findings revealed discontinuity of the capillary endothelial wall, perivascular and interstitial edema, and swelling of glial and neuronal cells in groups 1 and 2. The lesions were hyperintense on T2WIs and DWIs, hypointense on the ADC map image, and enhanced on Gd-T1WIs. On electron microscopy, the lesions showed cytotoxic and vasogenic edema with disruption of the blood-brain barrier.

Blood-Brain Barrier Experiments with Clinical Magnetic Resonance Imaging and an Immunohistochemical Study

Park, Jun-Woo,Kim, Hak-Jin,Song, Geun-Sung,Han, Hyung-Soo The Korean Neurosurgical Society 2010 Journal of Korean neurosurgical society Vol.47 No.3

Objective : The purpose of study was to evaluate the feasibility of brain magnetic resonance (MR) images of the rat obtained using a 1.5T MR machine in several blood-brain barrier (BBB) experiments. Methods : Male Sprague-Dawley rats were used. MR images were obtained using a clinical 1.5T MR machine. A microcatheter was introduced via the femoral artery to the carotid artery. Normal saline (group 1, n = 4), clotted autologous blood (group 2, n = 4), triolein emulsion (group 3, n = 4), and oleic acid emulsion (group 4, n = 4) were infused into the carotid artery through a microcatheter. Conventional and diffusion-weighted images, the apparent coefficient map, perfusion-weighted images, and contrast-enhanced MR images were obtained. Brain tissue was obtained and triphenyltetrazolium chloride (TTC) staining was performed in group 2. Fluorescein isothiocyanate (FITC)-labeled dextran images and endothelial barrier antigen (EBA) studies were performed in group 4. Results : The MR images in group 1 were of good quality. The MR images in group 2 revealed typical findings of acute cerebral infarction. Perfusion defects were noted on the perfusion-weighted images. The MR images in group 3 showed vasogenic edema and contrast enhancement, representing vascular damage. The rats in group 4 had vasogenic edema on the MR images and leakage of dextran on the FITC-labeled dextran image, representing increased vascular permeability. The immune reaction was decreased on the EBA study. Conclusion : Clinical 1.5T MR images using a rat depicted many informative results in the present study. These results can be used in further researches of the BBB using combined clinical MR machines and immunohistochemical examinations.