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Objective To investigate the screening significance of transcranial Doppler (TCD) for patients with patent foramen ovale ( PFO) induced cerebral embolism and to improve the treatment aiming at the causes.Methods Thirty-six patients of less than 60 years old with unknown-cause cerebral embolism and transient ischemic attack were enrolled.Besides conventional examination,the 24 h Holter,transthoracic echocariiography,carotid artery Doppler ultrasonography (CAU),routine TCD,TCD foaming test,transesophageal echocardiography (TEE),CT angiography (CTA) of head and neck,ultrasonography of vein in bilateral lower limbs were examined in all patients.Results All the patients showed no atrial fibrillation.No structural heart disease and intracardiac occupying lesion were shown in transthoracic echocardiography.No carotid stenosis was shown in carotid artery Doppler ultrasonography.Routine TCD showed no intracranial artery stenosis.No thrombus was found in ultrasonography of deep veins in bilateral lower limbs.CTA of head and neck showed everything was normal.Fourteen patients were observed with right-to-left shunt in heart by TCD foaming test,including 10 cases with microbubble signals(MBS) in 10 s,and 4 cases with MBS after Valsalva maneuver.Among 14 patients,12 patients were proved PFO by TEE.Conclusions PFO is one of the causes of cardiogenic cerebral embolism.TCD is accurate and reliable for the screening of PFO.
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0.02 kgf was considered as signifieant.All patients were studied within the first week of presentation with stroke, and underwent every day follow-up within the first month.Results Nine htmdred and fourteen patients were recruited into the study during 1-year period. WECSFP without lesion in brain stem was present in 4.4% of patients within the first week of stroke presentation.The patients with WECSFP had less JFS than the patients without WECSFP(P
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Objective To search the relative factors of cerebral damage, rebleeding, delayed cerebral ischaemia(DCI) and hydrocephalus after subarachnoid haemorrhage (SAH) by CT scans and clinical findings in acute phase. Methods To analyse the relationship between cerebral damage after SAH and clinical findings: CT scans resulte, age, sex, blood pressure, hyponatraemia, therapeutic methods. Results Cerebral damage were related to the pattern of distritution of SAH on brain CT and hyponatraemia. The high attack rate of rebleeding and DCI is related to presence of blood in the surface of brain, collection of blood in the ventricle, saccula aneurysms or cerebral arteriovenous malformation (AVM) (P＜0.01). Conclusions To forecast of cerebral damage after SAH by study of CT scans showing and clinical findings have clincal significance. According to these findings, we may take some therapeutics to prevent the cerebral damage after SAH.
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AIM: To observe the activity and distribution of astrocytes and glial fibrillary acid protein(GFAP) after middle cerebral artery occlusion (MCAO). METHODS: The rat MCAO model was made by two-kidney, tow clip renovascular hypertensive rat stroke prone(RHRSP). Rats were killed and brain samples were collected at the end of 1,3,6 and 9 weeks after MCAO, respectively. The ultrastructure of astrocytes was determined at broder of infarct (A area); distant of infarct (B area) and opposite of hemisphere (C area) by electron microscope. The number and optical density of GFAP-positive cells were also observed. RESULTS: The astrocyte proliferation distributed in the whole brain after MCAO. The highest numbers of GFAP-positive cells were observed at A area, then B area. The lowest numbers of GFAP positive cells were found in C area. The time course of GFAP-positive cell change was that the highest number was observed at 1 week after MCAO, then decreased by time from 3, 6 weeks to 9 weeks. The optical density of GFAP-positive cells showed the same patterns. CONCLUSION: The correlation between astrocyte proliferation and tissue damage after MCAO can be estimated by GFAP expression. The astrocyte proliferation plays an important role in healing process after MCAO.