%0 Journal Article
%T Reversible Cerebral Lession and Irreversible Cerebral Necrosis After Cardiorespiratory Arrest: A Case Report - Reversible Cerebral Lession and Irreversible Cerebral Necrosis After Cardiorespiratory Arrest: A Case Report - Open Access Pub
%A Dao-Ming Tong
%A Xiao-Dong Chen
%A Ye-Ting Zhou
%J OAP | Home | Journal of Neurological Research And Therapy | Open Access Pub
%D 2018
%X DOI10.14302/issn.2470-5020.jnrt-15-701 The differences infunctional outcomes and pathological finding safter brain damage from cardiorespiratory arrest, are not widely appreciated. Computed tomographic (CT) scan and magnetic resonance imaging (MRI) may provide insights into the mechanisms and distributions of early brain injury. We report one patient with classic post-resuscitation encephalopathy (PRE) from severe hypoxia or ischemia, whose prognosis correlated well with CT and MRI findings. Case Report A 46-year-old woman was found in cardiorespiratory arrest after she had an out-of-hospital an suddenly drop atroke lasting about 27 min. She was successfully resuscitated and admitted to the intensive care unit.The etiopathogenesis of cardiac arrest was ventricular fibrillation for patient. On initial examination, her pupils were 2 mm in diameter and nonreactive to light, and there was unresponse to external stimulation, and the score on the Glasgow Coma Scale was 3(E1V1M1). On admition, initial head CT revealed no significant findings. On the three days after onset, a repeat noncontrast CT images showed a whole cerebral brain swelling, caudal transtentorial Herniation, and microhemorrhages in the intercerebral and subarachnoid (Figure 1A). Diffusion- weighted magnetic resonance imaging (DWI) performed on day 14, the patient showed extensive lesions of the bilateral middle, hippocampus and the gray matter of the frontal and temporal cortices (Figure 1 B). In addition, brain MRI T2-weighted imaging showed bilateral symmetric high signal intensity in the caudate, putamen, thalami, occipital, parietal cortices and subcortical white matter (Figure 1C). After 20 days, her neurological status was improved, the GCS scale was 8 (E4V1M3). she did not show any signs of conscious perception regarding the different types of stimulation, including pain. She had been in a vegetative state. On follow-up MRI 60 days later, Fluid-attenuation inversion recovery image (FLAIR) showed cortical, subcortical white matter, and periventricular white matter confluent hyperintense lesions in the bilateral temporal, parietal, and occipital regions, and enlarged ventricles (Figure 1D-F). After three months, she did not perform requested commands and displayed spastic palsy to a higher extent in the lower limbs. The GCS scale was 9 (E4V1M4), and she was declared a persistent vegetative state. Figure 1. A) Brain CT showed a whole cerebral brain swelling, caudal transtentorial Herniation, and microhemorrhages in the intercerebral and subarachnoid; B) DWI showed extensive lesions of the
%U https://www.openaccesspub.org/jnrt/article/217