Skip to main content
Log in

Hemodynamic study of internal carotid artery stenosis and occlusion: value of combined isotopic measurements of regional cerebral blood flow and blood volume

Estudio hemodinamico de la estenosis y oclusion de la arteria carotida interna: valor de la combinación de la medida de flujo regionam cerebral y volumen sanguíneo mediante isótopos

  • Original Articles
  • Published:
Annals of Vascular Surgery

Abstract

The assessment of the intracranial hemodynamic consequences of obstructive lesions of the carotid artery by measuring resting rCBF is inadequate because cerebral blood flow may remain constant in spite of significant drops in the intraluminal pressure due to autoregulation. Moreover, flow may be permanently decreased following cerebral infarction, even if the arterial anatomical conditions have resumed their normal state because of the decreased metabolic demand of an infarcted area. Measurement of the regional cerebral blood volume (rCBV) helps with the hemodynamic assessment of these conditions, since there is a linear and inverse relationship between intraarterial pressure and intracranial blood volume. In 24 patients exhibiting various carotid and ischemic brain lesions we studied both rCBF and rCBV. The latter is a comparative measure between hemispheres obtained by single photon emission tomography after autotransfusion of 99m Technetium labeled erythrocytes. There was no correlation between rCBF and clinical status, CT scan or arterial lesions. There was no correlation between rCBV and clinical status or CT scan. There was, however, an interesting correlation between rCBV and the severity of the arterial lesion. The rCBV was symmetrical in all patients with normal or moderately stenotic carotid arteries before and after operation. In some patients with severe unilateral stenosis or occlusion, there was a significant relative increase of rCBV in the hemisphere downstream from the lesion, which disappeared after surgery (endarterectomy or extra-intracranial bypass). In some patients with severe and bilateral carotid lesions, we noted an asymmetry in rCBV that disappeared after a unilateral operation. Other patients with similar lesions develop asymmetry only after an operation that resulted in a relative increase in rCBV in the hemisphere supplied by the non-operated artery. In conclusion analysis of these results suggests that in this series of patients, rCBV modifications were the consequence of cerebral autoregulation distal to the arterial lesions and provided satisfactory assessment of hemodynamic improvement after surgical repair.

Resumen

Mediante la combinación de medidas de flujo sanguíneo cerebral y volumen sanguíneo cerebral con isótopos se han estudiado 24 enfermos (16 varones y 8 mujeres) clínicamente todos ellos menos uno, presentaban ataque isquémico cerebral en el territorio de la silviana, siendo 7 transitorios y 16 ictus no masivos. En todos se efectuó un CT-scan y Doppler así como también, angiografía. Los hallazgos radiológicos fueron divididos en 4 grados: S1 cuando el diámetro verdadero/diámetro teórico era mayor de 0.5; S2 cuando este valor estaba entre 0.2 y 0.5; S3 cuando era menor de 0.2 y S4 oclusión. En 14 enfermos se efectuó una endarterectomía carotídea, valorándose la permeabilidad postoperatoria mediante el Doppler. El flujo cerebral regional se midió con xenon 133 (método inhalatorio), siendo el parámetro obtenido el índice de descenso inicial (IDI). La medición del flujo regional relativo se efectuó con tomografía computarizada de emisión simple de fotones mediante la inyección de hematíes marcados con pertecnetato de Te99. En los casos de isquemia cerebral transitoria no se encuentran differencias ni asimetrías entre un hemisferio y otro cuando se mide el flujo regional cerebral. Si por el contrario hay una estenosis severa u oclusión unilateral siempre hay un valor del volumen cerebral regional mayor en el lado sano. Si esta lesión es bilateral hay un valor relativamente aumentado en el hemisferio sintomático. Las magnitudes de las asimetrías oscilaron entre el 16 y el 48%. Cuando se consideraron los casos de endarterectomía, no se vio ninguna modificación del flujo regional cerebral entre el pre y el postoperatorio. Considerando sólo el volumen sanguíneo cerebral se encuentra que en los 5 pacientes que había asimetría preoperatoria se normalizaron a la semana de la endarterectomía (siempre en casos de estenosis severas u oclusiones). En 7 a pesar de la lesión importante, no se pudo encontrar medidas asimétricas interhemisféricas y tampoco hubo cuando éstas se midieron en el postoperatorio. Los autores reconocen las limitaciones del método que son básicamente la inexactitud en la evaluación de las áreas profundas cerebrales; es un método semi-cuantitativo, ya que sólo valora datos en relación con el hemisferio contralateral y no se sabe exactamente lo que se mide (volumen arterial, arteriolar, capilar, venoso, etc.). Los parámetros estudiados en este trabajo pueden ser útiles para los estadíos I y II, suficientes en casos de lesiones unilaterales. Por el contrario, en caso de lesiones bilaterales se precisan de métodos cuantitativos para conocer más sobre la circulacíon cerebral. Con estos parámetros también se queden evaluar el beneficio obtenido por la reparación quirúrgica.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. YASARGIL M.G.—Microsurgery and applied to neurosurgery. Georg. Thieme Verlag. Academic Press 1969.

  2. BARNETT H.J.M.—Delayed cerebral ischemia episodes distal to occlusion of major cerebral arteries.Neurology, 1978,28, 769–774.

    PubMed  CAS  Google Scholar 

  3. BARNETT H.J.M., PEERLESS S.J., KAUFMANN J.C.—Stump of internal carotid artery: a source for further cerebral embolic ischemia.Stroke, 1978,9, 448–456.

    PubMed  CAS  Google Scholar 

  4. BARNETT H.J.M.—Is there a place for cerebral revascularization?Clin Neurosurg, 1979,26, 314–320.

    PubMed  CAS  Google Scholar 

  5. FINKELSTEIN S., KEILMAN G.M., CUNEO R., BARINGER J.R. —Delayed stroke following carotid occlusion.Neurology, 1980,30, 84–88.

    Google Scholar 

  6. FISCHER C.M.—Occlusion of the internal carotid artery.Arch. Neurol Psych, 1961,65, 346–377.

    Google Scholar 

  7. HEROS R.C., SEKHAR L.N.—Diagnostic and therapeutic alternative in patients with symptomatic «carotid occlusion» referred for extracranial bypass surgery.J Neurosurg, 1981,54, 790–796.

    PubMed  CAS  Google Scholar 

  8. HASLEY J.H. Jr, NAKAI K., WARIYAR B.—Sensitivity of rCBF to focal lesions.Stroke, 1981,12, 631–635.

    Google Scholar 

  9. MEYER J., SHINOHARA Y., KANDA T. et al.—Abnormal hemispheric blood flow and metabolism despite normal angiogram in patients with stroke.Stroke, 1970,12, 219–223.

    Google Scholar 

  10. BULLOCK R., MENDELOW A.D., PATTERSON J. et al.—Inhalational rCBF measurement as an indicator of carotid artery disease in man.In: GREENHALGH R.M., CLIFFORD ROSE F.—Progress in Stroke Research 2. London, Pitman Press Pub., 1983, 305–313.

    Google Scholar 

  11. NORRVING B., NILSON B., RISBERG J.—rCBF in patients with carotid occlusion. Resting and hypercapnic flow related to collateral pattern.Stroke, 1982,13, 155–162.

    PubMed  CAS  Google Scholar 

  12. LASSEN N.A.—133Xenon tomography of cerebral blood flow in cerebrovascular disease.In: GREENHALGH R.M., CLIFFORD ROSE F.—Progress in Stroke Research 2. London, Pitman Press Publ., 1983, 197–204.

    Google Scholar 

  13. GIBBS J.M., WISE R.J.S., LEGG M.J.—Progress in emission tomography studies in acute stroke and in patients with carotid occlusion: pathophysiology of cerebral ischemia and diminished perfusion reserve.In: GREENHALGH R.M., CLIFFORD ROSE F.—Progress in Stroke Research 2. London, Pitman, 1983, 214–226.

    Google Scholar 

  14. POWERS W., MARTIN W., HERSCOVITCH P.—The value of regional cerebral blood volume measurements in the diagnosis of cerebral ischemia.J Cereb Blood Flow Metab, 1983,3 suppl. 1, s598-s599.

    Google Scholar 

  15. GIBBS J.M., LEENDERS K.L., WISE R.J.S., JONES T.—Evaluation of cerebral perfusion reserve in patients with carotid artery occlusion.Lancet, 1984,1, 182–186.

    Article  PubMed  CAS  Google Scholar 

  16. REIVICH M., OBRIST W., SLATER R., GOLDBERG H.—A comparison of the133Xenon intracarotid injection and inhalation techniques for measuring regional cerebral blood flow.In: MURRAY, HARPER et al.—Blood flow and metabolism in the brain. London. Chrurchill Livingstone, 1975, 83–86.

    Google Scholar 

  17. PENN R.D., WALSER R., ACKERMAN L.—Cerebral blood volume in man. Computer analysis of a computerized brain scan.JAMA, 1975,234, 1154–1155.

    Article  PubMed  CAS  Google Scholar 

  18. BUDINGER T.F., GULLBERG G.T.—Transverse reconstruction of gamma ray emitting radionuclides in patients.In: TER-POGOSSIAN M.M., PHELPS M.E., BROWNELL G.L.—Reconstruction tomography in diagnostic radiology and nuclear medicine. Baltimore, University Park Press, 1977, 315–342.

    Google Scholar 

  19. FREEDMAN G.S.—Tomography with gamma camera theory.J Nucl Med. 1970,11, 602–604.

    PubMed  CAS  Google Scholar 

  20. JASZCZAK R.J., MURPHY P.H., HUARD D., BURDINE J.A.— Radionuclide emission computed tomography of the head with99mTe and a scintillation camera.J Nucl Med, 1977,18, 373–380.

    PubMed  CAS  Google Scholar 

  21. KUHL D.E., REIVICH M., ALAVI A. et al.—Local cerebral blood volume determined by three dimensional reconstruction of radionuclide scan data.Circ Res, 1975,36, 610–619.

    PubMed  CAS  Google Scholar 

  22. CHANG L.T.—A method for attenuation correction in radionuclide computed tomography.IEEE Trans Nucl Sci, 1978, NS 25, 638–643.

    Google Scholar 

  23. MOORE S.C.—Attenuation compensation.In: ELL P.J. HOLMAN B.L. —Computerized emission tomography. Oxford University Press, 1982, 338–360.

  24. CELSIS P., GODMAN T., HENRIKSEN L., LASSEN N.A.—A method for calculating regional cerebral blood flow with tomography of inert gas concentrations.Comput Assist Tomogr, 1981,5, 641.

    Article  CAS  Google Scholar 

  25. LASSEN N.A., HENRIKSEN L., PAULSON O.B.—Regional cerebral blood flow in stroke by133Xenon inhalation using emission tomography.Stroke, 1981,12, 284–288.

    PubMed  CAS  Google Scholar 

  26. FOG M.—The relationship between the blood pressure and the tonic regulation of the pial arteries.J Neurol Psychiat, 1938,1, 187–197.

    Google Scholar 

  27. FORBES S.—The cerebral circulation: I. Observation and measurement of pial vessels.Arch Neurol Psychiat, 1928,19, 751–761.

    Google Scholar 

  28. CRAIGEN M.L., JENNETT S., WALLACE W.—Response of pial veins to changing blood pressure and systemic hypoxia. Proc. of 1st Int. Symposium on cerebral veins. Graz, Austria, 1982 (abstr.), 66.

  29. GRUBB R.L., PHELPS M.E., RAICHLE M.E., TER-POGOSSIAN M. —The effects of arterial blood pressure on the regional blood volume by X-ray fluorescence.Stroke, 1973,4, 390–399.

    PubMed  Google Scholar 

  30. PURVES M.J.—The physiology of the cerebral circulation. Cambridge University Press, 1972, 156–172.

  31. ASTRUP J., SIESJO B.K., SYMON L.—Thresholds in cerebral ischemia.Stroke, 1981,12, 723–725.

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

About this article

Cite this article

Derlon, JM., Bouvard, G., Lechevalier, B. et al. Hemodynamic study of internal carotid artery stenosis and occlusion: value of combined isotopic measurements of regional cerebral blood flow and blood volume. Annals of Vascular Surgery 1, 86–97 (1986). https://doi.org/10.1007/BF02732461

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF02732461

Key-words

Navigation