Vascular reactivity to Althesin in cerebral lesions.
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Biomedical subjects
Publications and source records attributed to P Constant.
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The effects of Etomidate on cerebral blood flow (C.B.F.) and cerebral oxygen consumption (C.02 C.) were studied in 13 patients in a neuroradiology department. Induction of anaesthesia was ensured using a standard dose of 15 mg of Etomidate, followed by a constant rate infusion (2.8 mg/kg/hour). Seven subjects were considered to be normal whilst six were suffering from tumour pathology. Under the influence of Etomidate, C.B.F. in the normal subjects decreased by 34 p. 100 and C.02 C. by 46.7 p. 100. The relationship between C.B.F. and arterial PC01 was studied under the influence of Etomidate: cerebral vasoactivity to C02 was maintained. A special study was made of focal changes in flow in patients with tumour pathology. Under the influence of Etomidate, there were zones of adaptation of flow, indicative of vasoparalysis situated opposite the tumour.
The effect of a barbiturate, Sodium thiopental (Nesdonal), on the cerebral circulation in 13 patients with a cerebral ischemic attack is studied. Its action is compared to the action of other intravenous anesthetics (Alfatésine - Etomidate - diazanalgésie) used in neuro-anesthésia. The study is on a total of thirty patients. The regional cerebral blood flow (RCBF) is measured by the intra-carotid injection of Xe133. The anesthetics studied acted like vasoconstrictive agents on the healthy brain. They diminish the RCBF. At the leel of ischemic lesions the response is abolished, even inversed : the flow remains unchanged, even increases. It is the inverse steal syndrome. This action, comparable to the action of hypocapnia, has both a diagnostic and a prognostic value.
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Tomometric tests were carried out in 54 patients with a clinical picture of stabilized or regressive aphasia, some time after the initial episode. The correlation between clinical and topographic findings were satisfactory in 90 p. 100 of the cases. The frequency of lesions extending into several lobes (70 cases) and of multiple lesions is stressed. There is a significant relationship between the severity of the clinical findings during tomometric testing and the volume or multiplicity of the lesions. The progression of the disease after 6 months, as studied in 31 patients, was also related to the volume of the lesion, but was not influenced by the presence of diffuse atrophy, except where the disease was deteriorating. The value of tomometry in the study of aphasia involves 3 factors: precise clinical and lesional correlation, and the effect of the volume of the lesion on its initial severity and progression. In the future, tomometry should enable a correlative symptomatic study of aphasic disorders to be made.
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Fifty cases of tumors of the base of the skull, facial skeleton and nasopharynx were studied by CT. The tumoral densities were measured and compared to the pterygoid muscle density which was used as reference. Results showed no relationship between tumoral density and histology, and intravenous contrast medium injection was not useful. CT, however, does offer many advantages in the diagnosis of nasopharynx tumors, (5 cases) and in the determination of the extension of facial skeleton tumors.
One hundred fifty-eight patients with cerebral ischemia, and divided into four clinical groups were studied with CT. The results were correlated with those of angiography, scintigraphy and regional cerebral blood flow measurement. CT evolution was closely correlated with clinical and anatomical evolution. Changes in cerebral parenchyma density, in relation to the ischemic lesion, are the result of two phenomena: first, edema showing a fairly stable peak of intensity in the 2nd week and disappearing totally before the 20th day; and second, necrosis, variable in extent from patient to patient at the onset with subsequent evolution towards cavitation and thus a density similar to that of cerebro-spinal fluid.
Sixty-eight cases of metastases affecting 34 patients were studied by computerized tomography (CT) before and after the injection of an iodinated contrast medium. CT data provided a diagnosis in most cases. After injection of the contrast medium, a ring aspect was found in half the cases. This morphological feature is a sign of blood-brain barrier impairment crossed by the contrast medium. The low density area inside the ring is not caused by central necrosis, nor is it caused by too little contrast medium. The increase in density is a sign of extra-vascular loss of iodinated molecules in the peritumoral cerebral tissue. Performance of CT should be improved using specific tracers of the tumoral cells.
The effects of large doses of morphinomimetics on the cerebral circulation were studied in 12 normal subjects (fentanyl 16 microgram/kg in 6 patients and fentathienyl 1.9 microgram/kg in 6 others). Mean hemispheric flow (corrected to a pCO2 of 40) changed from 50.8 +/- 4.4 ml/100 g/min in the conscious state to 50.3 +/- 25.1 under the influence of fentanyl, and flow in the grey matter from 78.8 +/- 10 to 84.3 +/- 65 ml/100 g/min. Mean flow changed from 49 +/- 3.1 ml/100 g/min in the conscious state to 55.5 +/- 10 under the influence of fentathienyl, flow in the grey matter increasing from 75 +/- 9 to 81.8 +/- 14.4. Whilst there was no variation in mean flow rates under the influence of morphinomimetics, individual behaviour was very variable, in particular in the case of fentanyl, the changes produced by fentathienyl being much more homogeneous. There was no obvious modification in the distribution of regional flow by these morphinomimetics. Individual variations in flow correlated perfectly with individual variations in cerebral oxygen consumption. Vascular reactivity to CO2 was increased b morphinomimetics. In one subject, fentanyl produced a very marked increase in cerebral blood flow (+ 104 p. 100) for which no explanation could be found.
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Two hundred epileptics presenting with partial epileptic attacks were subjected to investigation by Acta-Scanner. Results were normal in 100 cases. Also found were 20 tumours (13 of them astrocytomas), 7 epileptogenic softenings, 41 cerebral atrophies, 8 of which were porencephalies, 5 calcifications (3 isolated, 2 multiple, connected with Bourneville's disease), 5 post-operative lesions and 22 dubious conditions. Various correlations between the results of scanning, the clinical findings and the E.E.G. are considered. The value of scanning in screening for tumours developing under the cloak of isolated epilepsy is emphasized and attention is drawn to certain difficulties of interpretation.
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Seventy patients with clinical evidence of cerebral vascular accidents were studied by tomodensitometry. Forty-eight had clinical signs of acute ischaemia and, by means of 64 investigations, it was possible to follow the development of focal softening. Diagnostic difficulties encountered in the course of the first fortnight of development are described. Twenty-two patients exhibited clinical symptoms of meningeal or cerebro-meningeal haemorrhage. Eighteen haematomas were diagnosed and their development studied in 34 investigations.