ABSTRACT
A severe or prolonged drop in blood pressure caused by syncope can lead to border-zone infarction in the absence of coexisting large artery disease. Syncope due to defecation represent special cases of reflex syncope for which the mechanisms are poorly understood and probably multifactorial. We experienced a 56-year-old woman was recurrent loss of consciousness duration defecation. Brain MRI revealed multifocal high signals in T2WI and FLAIR image on both end-artery border zone, but brain MRA revealed normal finding. Thus, We report a rare case of an old woman patient with end-artery border zone infarction due to prolonged hypoperfusion that was caused by defecation syncope.
Subject(s)
Female , Humans , Middle Aged , Arteries , Blood Pressure , Brain , Defecation , Infarction , Magnetic Resonance Imaging , Reflex , Syncope , UnconsciousnessABSTRACT
No abstract available.
Subject(s)
Humans , Encephalitis , Neurologic Manifestations , Sweet SyndromeABSTRACT
Heterotopic brain tissue usually involves extracranial midline structures of the head and neck such as nose, nasopharynx, and oral cavity. Its occurrence in the non-midline structures, including middle ear, is rare. We described a 50-yr-old-man with heterotopic glial tissue in the middle ear and mastoid bone. The patient presented with progressive hearing loss for 8 yr. There was no history of congenital anomalies, trauma, or ear surgery. Computed tomography revealed a mass-like lesion with soft tissue density occupying the middle ear cavity and mastoid antrum. At the operation, a graywhite fibrotic mass was detected in the epitympanic area. Mesotympanum and ossicles were intact. The patient underwent left simple mastoidectomy with type I tympanoplasty. During operation, definite cranial bone defect or cerebrospinal fluid leakage was not found. Histologically, the lesion was composed of exclusively mature, disorganized glial tissue with fibrovascular elements in a rather loose fibrillary background. Glial tissue showed diffuse positive reaction for glial fibrillar acidic protein and S100 protein on immunohistochemical study.
Subject(s)
Humans , Male , Middle Aged , Audiometry , Brain/pathology , Brain Diseases/pathology , Choristoma/diagnosis , Ear, Middle/pathology , Immunohistochemistry , Mastoid/pathology , Neuroglia/pathology , Tomography, X-Ray ComputedABSTRACT
Hypertensive encephalpathy is defined as severe hypertension in association with headache, nausea and vomiting, visual disturbances, confusion, stupor and coma. The pathophysiological mechanism is incompletely understood and causing as a result of failure of the upper limit of cerebral vascular autoregulation. Magnetic resonance imaging shows a characteristics posterior leukoencephalopathy, predominantly affects the white matter of the parietal and occipital lobes. Hypertensive encephalopathy are potentially reversible with timely and appropriate treatment. We experienced a case of hypertensive encephalopathy after normal vaginal delivery and report this case with a brief review of the literatures.
Subject(s)
Coma , Headache , Hemorrhage , Homeostasis , Hypertension , Hypertensive Encephalopathy , Leukoencephalopathies , Magnetic Resonance Imaging , Nausea , Occipital Lobe , Postpartum Period , Rabeprazole , Stupor , VomitingABSTRACT
Bilateral vocal cord paralysis (VCP) is a rare, life-threatening complication of stroke. We described the clinical course and treatment of bilateral VCP by acute ischemic stroke. We confirmed 4 cases of VCP. Two cases had brain-stem lesions, one case showed bilateral cerebral lesions and the last one had brainstem and cerebral lesions. One of the 4 cases showed spontaneous improvement of unilateral vocal cord function after 2 months. Among the rest, one under-went laser cordotomy, one remained tracheostomized, one was lost. (J Korean Neurol Assoc 19(4):400~403, 2001)
Subject(s)
Brain Stem , Cerebral Infarction , Cordotomy , Hoarseness , Laryngeal Nerves , Stroke , Vocal Cord Paralysis , Vocal CordsABSTRACT
BACKGROUND: Seizures after cerebral infarction are uncommon and their mechanisms are not yet elucidated. The aim of this study is to review the clinical features of the patients with cerebral infarction who developed seizures. METHODS: We retrospectively studied 22 patients who developed seizures after cerebral infarction. We examined the clinical features( onset and type ), EEG and CT findings from patient's clinical recordings and CT. The lesion size shown on CT scan was measured. RESULTS: The patients comprised 11 men and 11 women with their ages ranging from 46 to 78 ( mean 63.5 ) years. After cerebral infarction, ten patients developed seizures within 2 weeks after the onset, five between 2 weeks and 6 months after the onset, one between 6 months and 1 year and six 1 year after the onset of stroke. CT scans were available in all patients. The location of the cerebral infarction was ; the cortical is 14, subcortical in 2, basal ganglia in 8 and one had multiple infarcts. The size of infarction on CT was measured and twelve patients of 22 seizures after cerebral infarction were smaller than 20 cm2. Focal seizures were the most common seizure type. Eight patients showed focal slowing on EEG. CONCLUSIONS: In this study, we found the seizures after cerebral infarction are selectively frequent the frontal and temporal cortices and less frequent when the basal ganglia was involved. The seizures were frequent when the cerebral infarction was smaller than 20 cm2 were. We need to follow up the patient with small sized cortical cerebral infarction with a special attention to the occurrence of seizures.