2.Herpes zoster ophthalmicus and delayed contralateral hemiparesis.
Ki Bum SUNG ; Seung Hyun KIM ; Ju Han KIM ; Kyung Cheon CHUNG ; Myung Ho KIM
Journal of Korean Medical Science 1988;3(2):79-82
Central nervous system is often involved by herpes zoster but it is very rarely seen that contralateral hemiparesis or hemiplegia developed after herpes zoster ophthalmicus. We report a case of herpes zoster ophthalmicus followed by the delayed contralateral hemiparesis. A 33-year-old man developed acute cerebral infarction and resultant right hemiparesis 44 days after herpes zoster ophthalmicus in the left side. Brain CT disclosed hypodense area in the left basal ganglia. Cerebral angiography revealed segmental narrowing of M1 portion of the right middle cerebral artery.
Adult
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Cerebral Angiography
;
Cerebral Arteries/pathology
;
Cerebral Infarction/*etiology/radiography
;
Dominance, Cerebral
;
Hemiplegia/*etiology
;
Herpes Zoster Ophthalmicus/*complications
;
Humans
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Male
;
Tomography, X-Ray Computed
;
Vasculitis/etiology
3.Synchronous lung cancer in operation and brain infraction.
Meiling LI ; Hongqin HE ; Wenjin WANG ; Jianli WANG
Chinese Journal of Lung Cancer 2010;13(5):560-562
Adult
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Cerebral Infarction
;
etiology
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Humans
;
Intraoperative Complications
;
etiology
;
Lung Neoplasms
;
pathology
;
surgery
;
Male
4.Impact of obstructive sleep apnea-hypopnea syndrome on cerebral microbleeds in patients with cerebral infarction.
Jiewen XU ; Liying DENG ; Xueliang ZOU ; Hao LIU ; Ye YU ; Yongmin DING
Journal of Southern Medical University 2012;32(9):1362-1365
OBJECTIVETo investigate the impact of obstructive sleep apnea-hypopnea syndrome (OSAHS) on cerebral microbleeds (CMBs) in patients with cerebral infarction.
METHODSConsecutive patients with acute cerebral infarction who had cerebral microbleeds shown by susceptibility-weighted imaging (SWI) were enrolled to undergo polysomnography (PSG). The patients were divided into two groups, namely non-OSAHS group with apnea-hypopnea index (AHI) less than 5 and OSAHS group with greater AHI, and the clinical and radiological features of cerebral microbleeds were compared between them.
RESULTSForty-nine patients were enrolled in this study, including 27 (55.1%) with both cerebral infarction and OSAHS and 22 (44.9%) with cerebral infarction but not OSAHS. A comparison of the risk factors showed that hypertension, a smoking history, and a history of stroke were more prevalent in patients with OSAHS than in those without OSAHS (P<0.05). The incidences of subclinical stroke in OSAHS and non-OSAHS patients were 37.0% (10/27) and 9.0% (2/22) (P<0.05), respectively. Neurological imaging revealed a greater number of cerebral microbleeds in OSAHS group than in non-OSAHS group (P<0.05). In OSAHS patients, 77.8% of the microbleeds were distributed in cortical-subcortical areas, 55.6% in the basal ganglia area, and 25.9% in the infratentorial area, as compared to the percentages of 50.0%, 40.9% and 50.0% in non-OSAHS patients, respectively (P<0.05). In OSAHS patients, 40.7% also had leukoaraiosis, and 48.1% had two or more causes, as compared to the percentages of 13.6% and 18.2% in non-OSAHS patients, respectively (P<0.05).
CONCLUSIONSOSAHS can be a risk factor for cerebral microbleeds. Patients with both cerebral infarction and OSAHS tend to have greater and more extensive lesions of cerebral microbleeds, more complicated cause of the disease, and a grater likeliness of stroke recurrence.
Aged ; Cerebral Hemorrhage ; etiology ; pathology ; Cerebral Infarction ; pathology ; Female ; Humans ; Male ; Middle Aged ; Risk Factors ; Sleep Apnea, Obstructive ; complications ; pathology
5.Diagnosis of 10 patients with cortical laminar necrosis.
Zhiguo WU ; Renkai LIU ; Bo XIAO ; Guoliang LI ; Li FENG ; Yong ZHANG
Journal of Central South University(Medical Sciences) 2009;34(8):781-784
OBJECTIVE:
To analyze the feature of cortical laminar necrosis (CLN) and to decrease the incidence of misdiagnosis and improve the treatment of CLN.
METHODS:
Ten patients with CLN in Xiangya Hospital of Central South were included in this study from June 2005 to May 2007. The clinical feature, laboratory examination, image manifestation, treatment, and turnover of patients were analysed.
RESULTS:
CLN might happen at any age. The obstacle of brain energy metabolism with sugar and/or oxygen in central nervous system and heredities or acquired blemish could result in CLN. CLN was characterized in histopathology and imaging.
CONCLUSION
Many etiological factors can lead to CLN. It has different clinical features and can be easily misdiagnosed as some other hemorrhagic diseases.
Adult
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Brain Diseases
;
diagnosis
;
etiology
;
pathology
;
Cerebral Cortex
;
pathology
;
Cerebral Infarction
;
complications
;
Female
;
Humans
;
Magnetic Resonance Imaging
;
Male
;
Middle Aged
;
Necrosis
;
diagnosis
;
etiology
;
pathology
6.Cerebral Infarction as a Complication of Nephrotic Syndrome: A Case Report with a Review of the Literature.
Yeo Wook YUN ; Sungjin CHUNG ; Sun Jin YOU ; Dong Kyu LEE ; Kyu Yong LEE ; Sang Woong HAN ; Heng Ok JEE ; Ho Jung KIM
Journal of Korean Medical Science 2004;19(2):315-319
Arterial thrombosis is relatively rare compared with venous thrombosis in nephrotic syndrome. However, the assessment of its pathogenesis and risk factors in individual patient with nephrotic syndrome is necessary to allow appropriate prophylactic management because it is a potentially serious problem. Hereby, with review of the literature, we report a case of a 53 yr-old man with cerebral infarction associated with nephrotic syndrome due to focal segmental glomerulosclerosis during the course of treatments with diuretics and steroid. It reveals that the hypercoagulable state in nephrotic syndrome can be associated with cerebral infarction in adults. Prophylactic anticoagulants can be considered to reduce the risk of serious cerebral infarction in nephrotic patients with risk factors such as severe hypoalbuminemia and on diuretics or steroid treatment, even in young patients regardless of types of underlying glomerular diseases.
Cerebral Infarction/epidemiology/*etiology/pathology
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Human
;
Male
;
Middle Aged
;
Nephrotic Syndrome/*complications/epidemiology
;
Risk Factors
7.Traumatic cerebral infarction: a histopathological study of 17 cases.
Yi-xuan SONG ; Qing-song YAO ; Jia-zhen ZHU
Chinese Journal of Pathology 2004;33(5):416-418
OBJECTIVETo assess the morphologic changes in traumatic cerebral infarction and to discuss its mechanism.
METHODSSpecimens from seventeen cases of cerebral infarction were selected from 81 patients with severe brain injury, and subject to routine gross and histological examinations.
RESULTS(1) The cerebral infarction in all cases was hemorrhagic in nature with a wedged or irregular shape upon gross inspection. The lesions were found in occipital gyrus (8 cases), occipital lobes (3 cases), basal nuclei (3 cases), cingulate gyrus (2 cases), and lateral occipitotemporal gyrus (1 case). Histologically, the lesions were located at the junction between the cortex and medulla, showing congestion, edema, hemorrhage, necrotic nerve tissue and blood vessels. In severe cases, the lesion extended into the entire cortex and subarachnoid spaces. (2) Swelling of the brain and cerebral hernia were found in all cases, 8 of which demonstrated that the posterior cerebral artery was compressed and stenotic within the space between the crus cerebri and uncus.
CONCLUSIONBrain tissue necrosis in traumatic cerebral infarction is the result of brain swelling and cerebral hernia formation, following congestion, bleeding and ischemia due to vasculature compression.
Adolescent ; Adult ; Brain ; pathology ; Brain Edema ; complications ; Cerebral Infarction ; etiology ; pathology ; Craniocerebral Trauma ; complications ; Encephalocele ; complications ; Female ; Humans ; Male
8.Diagnosis and prognosis of neonatal cerebral infarction.
Ze-zhong TANG ; Cong-le ZHOU ; Yi JIANG ; Xin-lin HOU
Chinese Journal of Pediatrics 2004;42(6):429-432
OBJECTIVETo analyze the relationship between clinical characteristics and prognosis of neonatal cerebral infarction and to draw attention to the disease to improve the long-term outcome through early diagnosis and intervention.
METHODSThe clinical characteristics of 6 confirmed cases were summarized. Perinatal conditions and other factors were analyzed for possible causes of the disease. The survived patients were followed-up for 6-8 months.
RESULTSThe authors diagnosed 6 cases of neonatal cerebral infarction in one year, which accounted for 0.6% (6/969) of all the in-patients in the same time period. Among them 3 cases were confirmed as cerebrovascular malformations by magnetic resonance angiography (MRA), In 1 case the infarction was due to severe bilateral intraventricular hemorrhage, and in another case the disease was related to comprehensive factors such as prematurity, maternal pregnancy induced hypertension and respiratory failure secondary to bronchopulmonary dysplasia (BPD), and in 1 case the cause was undetermined. Four out of the 6 patients presented with varied forms of convulsions, which became the second leading cause for all the neonatal convulsive events (20%). None of the patients had localized neurological signs in the early course except for abnormal muscular tone of some extent. Cerebral ultrasound scanning in 5 out of 6 cases showed positive results. The diffusion-weighted magnetic resonance imaging (DW-MRI) was highly valuable for early confirmative diagnosis. Only one case was found normal within one year of follow-up and all the other 5 cases had unfavorable prognoses of varied severity.
CONCLUSIONNeonatal cerebral infarction is not a rare condition and should be considered as one of the important causes for neonatal convulsion. Imaging study is the main technique for diagnosis. The prognoses were poor for those cases for whom early diagnosis and treatment can not be made or those with widespread cerebral lesions.
Brain ; blood supply ; pathology ; Cerebral Hemorrhage ; complications ; Cerebral Infarction ; diagnosis ; etiology ; Follow-Up Studies ; Humans ; Infant, Newborn ; Magnetic Resonance Angiography ; Male ; Prognosis ; Seizures ; etiology
9.Temporary amaurosis with persistent visual field defect following acute blood loss.
Bong Byun KIM ; Kyung Hwan SHYN
Korean Journal of Ophthalmology 1995;9(1):47-50
Visual loss and field defects commonly occur after acute blood loss. We present a case of bilateral permanent visual field defect in a 30-year-old man after a massive hemorrhage caused by large vessel injury during a right nephrectomy. His postoperative visual acuity decreased significantly, and his visual field showed peripheral constriction and inferior altitudinal field defect in both eyes. A year and a half after the operation, visual acuity recovered to the preoperative level, but the field did not show improvement. We advance that this is a possible result of extensive injury to the occipital area, excluding the corresponding area of the macula.
Acute Disease
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Adult
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Blindness/*etiology
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Blood Loss, Surgical/*physiopathology
;
Cerebral Infarction/complications/*etiology
;
Humans
;
Male
;
Nephrectomy
;
Occipital Lobe/pathology
;
Vena Cava, Inferior/injuries
;
Vision Disorders/*etiology
;
*Visual Fields
10.Canine model of ischemic stroke with permanent middle cerebral artery occlusion: clinical features, magnetic resonance imaging, histopathology, and immunohistochemistry.
Joon Hyeok JEON ; Hae Won JUNG ; Hyo Mi JANG ; Jong Hyun MOON ; Ki Tae PARK ; Hee Chun LEE ; Ha Young LIM ; Jung Hyang SUR ; Byeong Teck KANG ; Jeongim HA ; Dong In JUNG
Journal of Veterinary Science 2015;16(1):75-85
The purpose of this study was to identify time-related changes in clinical, MRI, histopathologic, and immunohistochemical findings associated with ischemic stroke in dogs. Additionally, the association of cerebrospinal fluid (CSF) and tissue levels of interleukin (IL)-6 with clinical prognosis was assessed. Ischemic stroke was induced by permanent middle cerebral artery occlusion (MCAO) in nine healthy experimental dogs. The dogs were divided into three groups according to survival time and duration of the experimental period: group A (survived only 1 day), group B (1-week experimental period), and group C (2-week experimental period). Neurologic status was evaluated daily. Magnetic resonance imaging (MRI) was performed according to a predetermined schedule. Concentration of IL-6 in CSF was measured serially after ischemic stroke. Postmortem examination was performed for all experimental dogs. During histopathological examination, variable degrees of cavitation and necrosis due to neuronal cytopathic effects, such as pyknotic nuclei and cytoplasmic shrinkage, were observed on the affected side of the cerebral cortex in all dogs. Immunohistochemistry specific for IL-6 showed increased expression in the ischemic lesions. CSF IL-6 concentrations and ischemic lesion volumes 1 day after ischemic stroke were significantly higher in group A compared to groups B and C.
Animals
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Brain Ischemia/*etiology
;
Dogs
;
Female
;
*Immunohistochemistry
;
*Infarction, Middle Cerebral Artery
;
*Magnetic Resonance Imaging
;
Male
;
Stroke/*pathology