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Ocular and Cerebral Ischemic Mechanisms in Disease of the Internal Carotid Artery

Published online by Cambridge University Press:  18 September 2015

R.T. Ross  and
Ian M. Morrow
R.T. Ross*
Affiliation:
Section of Neurology, Departments of Medicine and Radiology, University of Manitoba and the Health Sciences Centre, Winnipeg, Canada
Ian M. Morrow
Affiliation:
Section of Neurology, Departments of Medicine and Radiology, University of Manitoba and the Health Sciences Centre, Winnipeg, Canada
*
GF543-700 William Avenue, Winnipeg, Manitoba R3E 0Z3 Canada
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Abstract:

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Stenosis of the internal carotid artery reduces the flow velocity in the ophthalmic artery. Lowered velocity permits increased red cell aggregation and decreased red cell deformability which increases viscosity.

Contrary to the theory of remotely originating emboli, this is an alternate hypothesis regarding transient attacks of ocular and cerebral ischemia.

The ophthalmic artery circulation time was measured in two groups of patients. The circulation time was defined as the interval between the appearance of contrast media in the siphon of the internal carotid artery and in the ocular choroid. The measurement was made on 151 angiograms of 108 subjects. These vessels were normal. An additional 76 patients had 108 angiograms which showed various amounts of internal carotid artery stenosis. These 76 patients had transient ischemic attacks; retinal, cerebral, or both.

There is a significant difference in the ophthalmic artery circulation time in the two groups. The slowing in the ophthalmic artery is related to the degree of internal carotid artery narrowing.

The circulation time in a cerebral branch of the internal carotid was not measured. It is presumed that stenosis of the internal carotid artery would have the same effect on a cerebral artery as on the ophthalmic artery.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 11 , Issue 2 , May 1984 , pp. 262 - 268
Copyright
Copyright © Canadian Neurological Sciences Federation 1984

References

Clay, C.Vignaud, J. (1971) Vascularisation de l’orbite, Encyclopedie Medico-Chirurgicale, Editor Laffant, A., Paris, 21006: 1–17.Google Scholar
Dintenfass, L. (1966) A preliminary outline of the Blood High Viscosity Syndromes, Ann. Int. Med. 118: 427–435.CrossRefGoogle ScholarPubMed
Dintenfass, L. (1981) The clinical impact of the newer research in blood rheology: an overview. Angiology 32: 217–229.CrossRefGoogle ScholarPubMed
Drummond, MM.Lowe, GDO., Belch, JJF. et al. (1980) An assessment of red cell deformability using a simple filtration method. J. Clin. Path. 33: 373–376.CrossRefGoogle ScholarPubMed
Duncan, GW.Pessin, MS., Mohr, JP. et al. (1976) Transient cerebral ischemic attacks. Adv. Intern. Med. 21: 1–20.Google ScholarPubMed
Easton, JD.Hart, RG. (1983) Underestimated causes of stroke. Ann. Roy. Coll. Phy. & Surg. 16 (1): 37–43Google Scholar
Fisher, CM. (1959) Observations of the fundus oculi in transient monocular blindness. Neurology 9: 333–347.CrossRefGoogle ScholarPubMed
Green, JR.Arana, R. (1948) Cerebral angiography. Am. J. Roentg. 59: 617–650.Google ScholarPubMed
Handel, S.Stargadter, FL., Glickman, MG., Newton, TH. (1973) Frequency of the ocular choroid blush during arteriography. Neuroradiology 6: 50–55.CrossRefGoogle ScholarPubMed
Hayreh, SS.Dass, R. (1962) The ophthalmic artery I. Origin and intracranial and intra-canalicular course. Brit. J. Ophthal. 46: 65–98.Google Scholar
Hegner, D.Piatt, D., Heckers, H. et al. (1979) Age-dependent physiochemical and biochemical studies on human red cell membranes. Mech. of Age & Dev. 10: 117–130.CrossRefGoogle ScholarPubMed
Lee, AG.Birdsall, NJM., Metcalf, JC. (1973) Nmr. studies of biological membranes. Chem. Br. 9: 116.Google Scholar
Millikan, CH. (1965) The pathogenesis of transient focal cerebral ischemia. Circulation 32: 438–449.CrossRefGoogle ScholarPubMed
Moller, W-D.Wolschendorf, K. (1978) The dependence of cerebral blood flow on age. xsEur. Neurol. 17: 276–279.CrossRefGoogle ScholarPubMed
Moore, WS.Hall, AD. (1970) Importance of emboli from carotid bifurcation in pathogenesis of cerebral ischemic attacks. Arch. Surg. 101: 708–716.CrossRefGoogle ScholarPubMed
Pessin, MS.Duncan, GW., Mohr, JP., Pokskanzer, DC. etal. (1977) Clinical and angiographic features of carotid transient ischemic attacks. NEJM 296: 358–362.CrossRefGoogle ScholarPubMed
Raney, RB.Raney, AA. (1950) The contribution of cerebral angiography in diagnosis. Calif. Med. 72: 342–349.Google Scholar
Reid, HL.Dormandy, JA., Barnes, AJ. et al. (1976) Impaired red cell deformability in peripheral vascular disease. Lancet I: 666–668.CrossRefGoogle Scholar
Ross, RT. (1977) Transient monocular blindness. Can. J. Neuro. Sci. 4: 143–150.CrossRefGoogle ScholarPubMed
Singer, SJ.Nicolson, GL. (1972) The fluid mosaic model of the structure of cell membrane. Science 175: 720.CrossRefGoogle Scholar
Thomas, DJ.Marshall, J., Ross-Russell, RW. et al. (1977) The effect of hematocrit on cerebral blood flow in man. Lancet 2: 941.CrossRefGoogle ScholarPubMed
Thomas, DJ. (1982) Whole blood viscosity and cerebral blood flow. Stroke 13: 285–286.CrossRefGoogle ScholarPubMed
Tracy, GD.Lord, RSA., McGrath, MA. (1981) The Role of Viscosity in Peripheral Vascular Disease. From Blood Viscosity in Heart Disease and Cancer. Eds., Dintenfass, L. and Seaman, G.V.F. p. 82, Pergamon Press, New York.Google Scholar