Clinical Significance Of Brain Function Assessment In Patients With Acute Stroke

Objective: To observe the changes of electroencephalogram(EEG), evoked potential(EP), transcranial doppler(TCD) and the serum neuron-specific enolase(NSE) in patients with acute stroke and evaluate their value in brain function assessment.Methods: Ninty-six patients with acute stroke, including 58 cases of cerebral infarction, 27 cases of cerebral hemorrhage and 11 cases of subarachnoid hemorrhage (SAH), were studied. They received the test of EEG,EP,TCD and CT within 4 days and 12 days after disease onset respectively. The serum NSE were determined with ELISA and the damage of clinical neurological function were valued with China Stroke Score(CSS),the Barthel index and Glasgow-Pittsburgh Coma Scale at the same time. The relationship between the changes of these items and the damage of clinical neurological function was analyzed in different groups. 25 healthy adults were taken as the control group.Results: (1) The level of serum NSE in the patients with acute stroke was significantly higher than those of the control (p<0.01). The level of serum NSE in patients with cerebral infarction or cerebral hemorrhage was correlated positively with the volumes of the lesion (p<0.01) and the scores of CSS(P<0.01), while correlated negatively with the scores of Glasgow-Pittsburgh Coma Scale in the first 4 days and not correlated with the position of the lesion.(2)The abnormality of EEG after stroke was correlated with conscious state, the position and volume of lesion and the severities of the patient's condition. The EEG in patients with SAH manifested by diffuse slow wave which became localized after 5 days of onset. While the EEG in patients with cerebral hemorrhage supratentorial manifested by local abnormality related with lesion and diffuse slow wave background. In patients with brainstem hemorrhage, there might be α coma rhythm in EEG. But the EEG in patients with cerebella hemorrhage were almost normal. The EEG in patients with cerebral infarction often show localized slow wave.(3)The mean Velocity(Vm) and Pulsitive Index(PI) determined by TCD were abnormal obviously in patients with stroke. PI increased significantly within 4 days after SAH (p<0.01) . Both Vm and PI increased significantly in 5-12 days after onset (p<0.01) . The Vm in injured and uninjured side both decreased significantly (p<0.01) and PI was remarkably higer than normal control(p<0.01) in 12days after cerebral hemorrhage. In patients with cerebral infarction, Vm decreased significantly (p<0.01)only in ipsilateral of lesion hemisphere within 4 days after onset,while in 5-12d after onset, Vm and PI increased significantly (p<0.01) in both hemispheres. The Vm in Middle Cerebral Artery (MCA), Anterior Cerebral Artery (ACA) and Posterior Cerebral Artery (PCA) were correlated negatively with the scores of CSS in 4d in cases of cerebral infarction and cerebral hemorrhage(p<0.01).(4)The peak latency of P100 of visual evoked potential (VEP) in all cases of stroke prolonged significantly after stroke and became shorter gradually follwing the improvement of the patient's condition. The rate of VEP abnormality in cerebral hemorrhage infratentorial was higher than that in cerebral hemorrhage supratentorial (p<0.01). Whereas that was significant higer in baso-vertebral infarction than internal carotid infarction. In cerebral hemorrhage, the peak latency of P100 was correlated positively with the level of serum NSE and the scores of CSS within 4 days of onset (r= 0.43, r=0.41, respectively, p<0.01).(5)Within 4 days after stroke, the peak latency of Ⅰ,Ⅲ,Ⅴand the inter-peak latency of Ⅰ-Ⅲ,Ⅲ-Ⅴ in brianstem auditory evoked potential(BAEP) , especially the peak latency of Ⅲ,Ⅴ, were longer than those of the normal control(p<0.01). The rate of abnormality in BAEP in 4days was higer than that in 5-8day and 9-12day in cerebral infarction group and cerebral hemorrhage group. The peak latency of Ⅴwas correlated positively with the volume of lesion in infratentorial cerebral hemorrhage and baso-vertebral infarction (p<0.01). The peak latency of Ⅴ w...