Biomedical subjects

E B Skriver

Publications and source records attributed to E B Skriver.

26 records · Page 2Linked to original sources

PubMed1981

Blood-brain barrier integrity in patients with cerebral infarction investigated by computed tomography and serum-CSF-albumin.

Measurements of CSF-albumin, and S/CSF-albumin in two groups of patients with small and large infarcts failed to show BBB damage to albumin in about one half of the patients. No significant difference was found between the two groups of patients in regard to the above-mentioned parameters. The localization of the infarcts (close to the CSF or deep in the brain) did not influence the S/CSF-albumin. No correlation was found between the S/CSF-albumin and the time interval between the onset of the stroke and the lumbar puncture within 96 h. Some suggestions are put forward to explain the discrepancies between the CT-scan and S/CSF-albumin in the assessment of BBB damage.

Albumins↗

PubMed1981

Patterns of regional cerebral blood flow in acute stroke.

In a consecutive group of 56 stroke patients the regional cerebral blood flow was measured within 84 hours after stroke. A 254 multidetector scintillation camera and the intracarotid Xenon-133 injection method was used to study rCBF. Typical rCBF-patterns are described and compared to the findings on CT-scan. According to these studies focal brain areas exposed to ischemia appeared in 3 different forms; 1) As an ischemic area surrounded by a hyperemic borderzone, seen in areas with arterial occlusion and infarction on CT-scan. 2) As a pronounced hyperemic area without associated ischemia located in areas of infarction (seen on CT-scan) without arterial occlusion. This form is presumably due to arterial recanalization and reperfusion in an established infarct. 3) As a pronounced focal hyperemia also without ischemia, located in normal CT-areas without arterial occlusion. This form is probably due to recanalization of an occluded artery shortly after occlusion without development of infarction.

Acute Disease↗

PubMedDate not supplied

Focal cerebral hyperemia in acute stroke. Incidence, pathophysiology and clinical significance.

In a consecutive study comprising 41 patients with completed stroke of less than 72 hours duration, cerebral angiography and measurements of the regional cerebral blood flow (rCBF) were performed within 24 hours after admission. The rCBF study was done using the 133-Xenon intracarotid injection method and a 254 multi-detector camera. CT scan was done 24 hours after the rCBF study. Focal cerebral hyperemia was found in 16 patients. The study revealed 3 different types of hyperemia: Border-zone hyperemia, surrounding ischemic areas, was seen in patients with occluded arteries on angiography, presumably resulting from accumulation of acid metabolites in the border-zone of acute infarcts. Postischemic hyperemia was seen in patients without occlusion, presumably due to recanalization of a prior occluded artery. Remote hyperemia was found distant from the infarcted area, presumably due to local tissue pressure on brain tissue. Cortical infarcts (10 patients) all had extensive hyperemic areas. Because the 254 detector camera has an excellent resolution in the cortical surface, our findings strongly suggest that all acute cerebral infarcts are, in fact, associated with hyperemic areas. The hyperemic areas are often extensive and vascular reactivity is commonly impaired. It is suggested that treatment aimed at reducing blood flow in hyperemic areas might improve prognosis.

Aged↗

PubMedDate not supplied

Blood flow and vascular reactivity in collaterally perfused brain tissue. Evidence of an ischemic penumbra in patients with acute stroke.

In a group of 48 patients with completed stroke, 8 patients had viable collaterally perfused brain tissue which was accessible for rCBF recordings with a two dimensional technique. All 8 had deep subcortical infarcts on CT-scan, and angiographic occlusion of the arteries normally supplying the infarcted territory. The brain tissue overlying the deep infarcts appeared normal on CT-scan and was supplied by collateral circulation. rCBF was measured in all within 72 hours after the stroke. The intra-carotid Xe-133 injection method and a 254 multidetector camera were used to study rCBF. Relatively ischemic low flow areas were a constant finding in the collaterally perfused tissue. In 6 of the patients, the collaterally perfused part of the brain had low flow values comparable to those of an "ischemic penumbra" (viable, but functionally depressed brain tissue due to inadequate perfusion). Autoregulation was impaired in all of the collaterally perfused areas while the CO2-response always was preserved. Steal phenomena were not seen. In the surrounding brain tissue, autoregulation was normal in 5 patients and impaired in 3 while the CO2-response seemed to be normal. The results confirm the experimental finding of an ischemic penumbra associated with acute cerebral infarcts and suggest that early restoration of the blood flow in acute stroke patients might improve recovery and prognosis in selected patients.

Acute Disease↗

PubMedDate not supplied

Cause of cerebral infarction in the carotid territory. Its relation to the size and the location of the infarct and to the underlying vascular lesion.

Seventy-three patients with acute nonhemorrhagic stroke in the carotid territory were investigated for the cause of the stroke: middle cerebral artery (MCA) occlusion/stenosis or internal carotid artery (ICA) occlusion/stenosis; embolus from the heart and extra-cranial arteries or thrombosis. The study is prospective and consecutive comprising stroke patients below the age of 75 years, admitted in the acute state i.e. within 3 days after stroke onset. Excluded were patients with intracerebral hematoma, subarachnoid hemorrhage, vertebrobasilar stroke and patients in whom another severe disease was present. Cerebral angiography and CT-scan were performed in all patients within one and two days after admission. CT-scan was repeated 2 weeks and 6 months later. Forty percent had MCA occlusion, none had MCA stenosis, 12% had ICA occlusion, 14% had severe ICA stenosis (half of these were associated with MCA occlusion) and 41% were without significant MCA/ICA lesions. Twenty-seven percent had large infarcts with a diameter greater than 3 cm; 34% had medium-sized infarcts with a diameter between 3 and 1.5 cm; 21% had small infarcts with a diameter less than 1.5 cm; 18% had no identifiable infarct on CT-scan. MCA occlusion was responsible for 62% of the large or medium-sized infarcts. ICA occlusion or severe ICA stenosis were responsible for only 27% of the large or medium-sized infarcts. Only 11% of the patients with small or no infarct on CT-scan had significant MCA/ICA lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Tissue damage at computed tomography following resolution of intracerebral hematomas.

Tissue damage as sequelae after spontaneous intracerebral hemorrhage in eight consecutive patients was investigated with computed tomography performed 3 days, 2 weeks and 6 months after the stroke. The presence of contrast enhancement after 2 weeks, hypodense areas after 6 months, and atrophy of adjacent structures were considered to be markers of irreversible tissue damage. Except for a narrow zone in the periphery of the hematoma (ring blush) contrast enhancement was not observed, neither in the hematoma nor in areas where resolution had taken place. After 6 months the site of the hematomas was not identifiable in 3 patients, and 4 patients had small 'lacunar' hypodense lesions. Only one patient had a more extensive hypodense area 6 months after the hemorrhage. The most prominent sequelae after intracerebral hematoma were atrophy of adjacent structures (i.e. atrophy of basal ganglia, thalamus and ventricular enlargement) which were seen in all patients even though irreversible de loco damage in the hematoma area was sparse or absent.

Atrophy↗

PubMedDate not supplied

Nitric oxide synthase expression and enzymatic activity in human brain tumors.

Nitric oxide (NO) is synthesized by NO synthases (NOS), existing in 3 isoforms. NO influences a great variety of vital functions including vascular tone and neurotransmission. Under conditions of excessive formation, NO emerges as an important mediator of neurotoxicity in a variety of disorders of the central nervous system (CNS). Inhibitors of NOS are available that may modify the activity of all isoforms, which may be of clinical relevance. The expression of the 3 NOS isoforms nNOS, iNOS and eNOS and NOS enzymatic activity was examined in 40 patients with primary CNS tumors (gliomas WHO grades I - IV and meningeomas WHO grades I - III) and in 13 patients with metastases from adenocarcinomas or malignant melanomas. A polyclonal antibody directed against nNOS and monoclonal antibodies directed against iNOS and eNOS were used for immunohistochemical staining. NOS enzymatic activity, measured by labeled arginine to citrulline conversion, was assessed in tissue specimens obtained from the same tumors. NOS data were compared with clinical variables and the degree of edema as judged from MR scanning. nNOS expression was increased in tumor cells of glial neoplasms and most pronounced in high-grade tumors, WHO grades III and IV, and in the carcinoma and melanoma metastases. Low-grade gliomas, WHO grades I and II and meningeomas expressed no or only little nNOS. iNOS was only expressed in a few tumors. eNOS was expressed sporadically in the tumor cells while the expression was increased in vascular endothelial cells in both the tumor itself and the peritumoral area of glial neoplasms, and in metastases. eNOS expression was sporadic in endothelial cells of meningeomas. NOS enzymatic activities were heterogeneous among tumor types (0 - 13.8 pmol/min/mg of protein) without correlation to the NOS expression found by immunohistochemical techniques. Likewise, NOS activity and expression was not correlated to the clinical scores or brain edema. In conclusion, nNOS expression may be a putative useful indicator of brain tumor differentiation and malignancy. The enhanced expression of eNOS in vascular endothelial cells of glial neoplasms and metastases raises the possibility that NO production in tumor endothelial cells may contribute to tumor blood flow regulation and possibly brain edema.

Adenocarcinoma↗

PubMedDate not supplied

Repeated computed tomography in lacunar infarcts of the brain.

This prospective and consecutive study of 74 patients with completed stroke elucidates occurrence, localization and evolution of lacunar infarcts on repeated CT examinations. Twenty patients had large infarcts (diameter greater than 3 cm), 25 medium-sized infarcts (diameter greater than or equal to 1.5 cm - less than or equal to 3 cm), and 16 had lacunar infarcts (diameter less than 1.5 cm). In 13 patients no infarct was seen. The lacunar infarcts were characterized by delayed appearance on CT, low incidence of fog effect, and infrequent presence of contrast enhancement. In 9 of the 16 patients (56%) the lacunar infarct could be identified on the first CT, performed approximately 3 days after the stroke. In 2 patients the infarct was first revealed on the second (2 weeks post stroke) and in 5 on the third CT (6 months post stroke). The delayed appearance might be due to a partial volume effect. Early development of fog effect may also be considered. As contrast enhancement was observed in only 8 per cent of the patients with lacunar infarcts on CT, and in 70 per cent of the entire group of patients in our series with ischemic infarcts, contrast enhancement seemed to be a function of lesion size.

Aged↗