Journal of Neuro-Ophthalmology, June 1999, Volume 19, Issue 2

Hemianopsia Related to Dissection of the Internal Carotid Artery

Spontaneous dissection of the internal carotid artery is typically associated with cerebral vascular infarction along the anterior and middle cerebral distribution, whereas occipital infarction is usually related to posterior circulation abnormalities. Hemianopsia with occipital infarction related to carotid artery dissection has therefore rarely been reported. A 40-year-old woman in whom acute-onset hemianopsia developed, related to occipital infarction secondary to internal artery dissection, is described. This atypical association is explained by anatomic variations of the posterior part of the circle of Willis. Neuroimages showed occipital infarction related to internal carotid artery dissection associated with hypoplasia of the proximal portion of the cerebral posterior artery (P1). The anatomic correlation of this atypical association and a review of the literature are presented.

Journal of Neuro- Ophthalmology 19( 2): 136- 139, 1999. © 1999 Lippincott Williams & Wilkins, Inc., Philadelphia Hemianopsia Related to Dissection of the Internal Carotid Artery Florence Bourcier- Bareil, M. D., Caroline Hommet, M. D., Jean- Philippe Cottier, M. D., Sophie Arsene, M. D., and Christian Rossazza, M. D. Spontaneous dissection of the internal carotid artery is typically associated with cerebral vascular infarction along the anterior and middle cerebral distribution, whereas occipital infarction is usually related to posterior circulation abnormalities. Hemi­anopsia with occipital infarction related to carotid artery dis­section has therefore rarely been reported. A 40- year- old woman in whom acute- onset hemianopsia developed, related to occipital infarction secondary to internal artery dissection, is described. This atypical association is explained by anatomic variations of the posterior part of the circle of Willis. Neuroim-ages showed occipital infarction related to internal carotid ar­tery dissection associated with hypoplasia of the proximal por­tion of the cerebral posterior artery ( PI). The anatomic corre­lation of this atypical association and a review of the literature are presented. Key Words: Anatomy- Circle of Willis- Internal carotid ar­tery- Occipital infarction. Spontaneous dissection of the cervical portion of the internal carotid artery ( ICA) is recognized as a cause of strokes and is reported in 2% to 4% of cases in the literature ( 1). The clinical manifestations of ICA isch­emia are mainly represented by hemiplegia, aphasia, be­havioral abnormalities, decreased vision related to retinal or choroidal ischemic syndrome, and, unusually, hemi­anopsia. Such strokes usually involve the region of the middle cerebral artery ( MCA) and/ or the watershed re­gion between the MCA and the anterior cerebral artery ( ACA). Rarely is the region of the posterior cerebral artery ( PCA) affected alone. We report an unusual case of isolated homonymous hemianopsia due to dissection of the ICA with occipital infarction related to persistent fetal origin of the PCA. This fetal configuration of the PCA arising primarily from the ICA is well known and described in the anatomic dissections reports. However, to our knowledge, this is the first clinical case of ICA Manuscript received February 12, 1998; accepted January 13, 1999. From the Service d'Ophtalmologie, Hopital Bretonneau, CHRU Tours, France. Address correspondence and reprint requests to F. Bourcier- Bareil, M. D., Service d'Ophtalmologie, Hopital Bretonneau, CHRU Tours, 2, boulevard Tonnelle, 37044 Tours Cedex, France. dissection associated with persistent fetal configuration of the PCA, involving the PCA region alone. We have compared it with the other cases of carotid occlusive disease with occipital infarction and discuss the anatomic variations of the posterior part of the circle of Willis previously described in the literature. CASE REPORT A 40- year- old woman with no vascular history sud­denly and spontaneously experienced a visual loss in the left part of the visual field, preceded a few hours before by diffuse headaches without diffusion to the neck or the jaw, described as " like a vice" by the patient. There was no history of trauma, and her family's medical histories were unremarkable. The symptoms persisted unchanged from the onset, and 1 day later the patient attended the ophthalmology emergency department. On ophthalmo­logic examination, isolated left homonymous hemianop­sia was confirmed using a Goldmann kinetic visual field; visual acuity was 20/ 20 in both eyes. There was no cer­vical or cranial bruit, and cardiac auscultation revealed normal heart sounds. Results of neurologic examination and routine blood studies were normal with no serologic evidence of coagulopathy. On further questioning, the patient reported no history of transient monocular blind­ness or hemispheric attacks. A brain computed tomo­graphic ( CT) scan ( Fig. 1) showed an isolated right tem-poro- occipital infarction in the right PCA region. Cervi­cal ultrasonography revealed abnormal flow with signs of dissection of the right ICA. Although the brain lesion seen on CT scan was con­sistent with findings in the neuro- ophthalmologic exami­nation, the lesion was not located in an area normally supplied by the ICA. Thus, a cerebral angiography was performed that showed narrowing and stenosis of the right ICA beginning at its origin, suggesting a possible dissection of the middle third of its cervical portion ( Fig. 2). The left ICA injection showed ( Fig. 3) an efficient anterior communicating artery ( ACoA) with revascular­ization of the right MCA, the right ACA, and the right posterior communicating artery ( PCoA). A vertebral an­giogram revealed ( Fig. 4) a hypoplasia of the proximal 136 OCCIPITAL INFARCTION AND CAROTID DISSECTION 137 FIG. i. Axi'afnoncorurasi cornpuieu'tomographic scan showing a large right temporo- occipital infarct ( arrow). portion of the right PC A ( PI). In this fetal pattern the diameter of the right PCoA was greater than the diameter of the right PI. Thus, the diagnosis of occipital infarction possibly related to ICA dissection, associated with per­sistent fetal configuration of the proximal portion of the right PCA ( PI), was determined, and a direct communi­cation was documented between the right ICA and right PCA. The patient had intravenous heparin therapy for 10 days, then oral anticoagulant for 6 months. At the follow-up assessment 2 months after the onset, there was no further evidence of disturbed flow in the right ICA, but left homonymous hemianopsia remained. DISCUSSION Hemianopsia due to occipital infarcts is usually related to PCA occlusion and results either from thromboembo­lic sources or from vertebrobasilar atheromata ( 2^ 1). Some autopsy studies ( 4,5) have described infarction in the PCA region resulting from ICA occlusion, but no clinical features were detailed. Moreover, it is well known in anatomic dissections ( 5- 11) that one or both PCAs may arise primarily from the ICA rather than the basilar artery, but the clinical consequences of these ana­tomic variations are poorly documented. Two clinical cases of occipital infarct associated with carotid occlusive disease are reported in the literature ( 12,13). However, in our case the patient had an occipital infarction related to ICA dissection with persistent fetal configuration of PI, involving exclusively the PCA re­gion without infarcts in the MCA or ACA. Thus, the first difference between our case and the others ( 12,13) con­cerned the mechanism of ICA occlusion. Our patient had an ICA dissection associated with an abnormal PI, with­out atheromata or cardiopathy. In the earlier cases, one had a subtotal occlusion in relation with extended athero­mata, and the other had an ICA dissection associated with pseudo- aneurysm and no intraluminal abnormality of the PCA. The second difference concerned the area affected by infarction related to ICA occlusion. In the two previous cases, the patients had abnormal lesions in both regions, depending on ICA and PCA vasculariza­tion ( frontal, parietal, occipital lobes), whereas our pa­tient had no lesion in the usual right ICA region but had an infarct only in the right PCA region, which was mainly vascularized by the right ICA. Since the first description of the circle of Willis, many vascular variations have been described, especially in the posterior part of the circle ( 6- 11). Thus, in series of anatomic dissections ( 6- 11) one of the most frequent variations is the abnormality of the configuration formed FIG. 2. Lateral view: Right brachiocephalic trunk angiogram shows gradually tapering occlusion starting 1 cm distal to the bulb, suggesting dissection of the right internal carotid artery ( ar­row). J Neuro- Ophthalmol, Vol. 19, No. 2, 1999 138 F. BOURCIER- BAREIL ET AL. by the PCoA and the precommunicating part of the PCA ( PI). The persistence of a fetal configuration in which there is a hypoplasic PI with a large homolateral PCoA is frequently observed. In such cases, the diameter of PI is smaller than the diameter of the PCoA and the ICA supplies the blood to the occipital lobes. In the adult configuration, PI has a larger diameter than the PCoA. This fetal pattern is reported in the literature, with per­centages ranging from 10% to 32%, whereas the con­figuration is seen in 58% to 84% of brain anatomic dis­sections in adults ( 6- 11,14). The existence of such ana­tomic features can be explained by the embryologic development of the brain ( 6,8,14,15). Thus, at Padget stage 2 ( 15) ( embryo of 31 days' gestation), the ICA provides all the cerebral blood supply, including that to the posterior areas, through the PCoA. At this time, the PCA is not developed and represents only a branch of the caudal division of the ICA. However, at Padget stage 3 ( 15) ( embryo of 33 days' gestation) the formation of the vertebral arteries corresponding to the development of the posterior part of the brain causes the PCoA's invo­lution and the full development of the PCA including PI. Moreover, according to Larroche ( 16) and Van Over-beeke et al., ( 6) the fast growth of the occipital lobes has an important effect on the determination of the posterior part of the circle of Willis. This rapid growth occurs after the 20th week after conception and requires an increase in the vascularization of the lobes with enlargement of the afferent arteries to satisfy the increased functional demands. Our case illustrates the anatomic relationship between the ICA and the PCA and explains the possibility of hemianopsia caused by ICA dissection. Our experience should alert clinicians to the important but unusual clini- FIG. 3. Front view: Left ICA angiogram shows anterograde filling of the right anterior cerebral artery ( ACA) through an efficient anterior communicating artery ( ACoA) and the right posterior communicating artery ( PCoA; arrow). FIG. 4. Worm's view: Right vertebral artery angiogram shows filling of the basilar trunk and the left cerebral posterior artery and poor filling of the right cerebral posterior artery through a hypo­plasic P1 ( arrow). cal association between the PCA and extracranial ICA occlusive disease when confronted with hemianopsia re­lated to isolated occipital infarction. REFERENCES 1. d'Anglejean Chatillon J, Ribeiro V, Mas JL, Bousser MG, Laplane D. Dissection del'artere carotide interne extracranienne: soixante-deux observations. Presse Med 1990; 19: 661- 7. 2. Marinkovic SV, Milisavljevic MM, Lolic- Draganic VL, Ko-vacevic MS. Distribution of the occipital branches of the posterior cerebral artery. Stroke 1987; 18: 728- 32. 3. Pessin MS, Lathi ES, Cohen MB, Kwan ES, Hedges T, Caplan LP. Clinical features and mechanism of occipital infarction. Ann Neu­rol 1987; 21: 290- 9. 4. Castaigne P, Lhermitte F, Gautier JC, Derouesne C, Der Agopian P, Popa C. Arterial occlusions in the vertebrobasilar system: a study of 44 patients with post- mortem data. Brain 1973; 96: 133- 54. 5. Battacharji SK, Hutchinson EC, McCall AJ. The circle of Willis. The incidence of developmental abnormalities in normal and in-farcted brains. Brain 1967; 90: 747- 58. 6. Van Overbeeke JJ, Hillen B, Tulleken CAF. A comparative study of the circle of Willis in fetal and adult life: the configuration of the posterior bifurcation of the posterior communicating artery. JAnat 1991; 176: 45- 54. 7. Khamlichi El A, Azouzi M, Bellakhdar F, Ouhcein A, Lahlaidi A. Configuration anatomique du polygone de Willis de l'adulte etudi6 par les techniques d'injection. Neurochirurgie 1985; 31: 287- 93. 8. Caruso G, Vincentelli F, Rabehanta P, Guidicelli G, Grisoli F. Anomalies of the PI segment of the posterior cerebral artery: early bifurcation or duplication, fenestration, common trunk with the superior cerebellar artery. Acta Neurochir 1991; 109: 66- 71. 9. Tulleken CAF, Luiten MLFB. The basilar artery bifurcation: mi­croscopical anatomy. Acta Neurochir 1987; 85: 50- 5. 10. Zeal AA, Rhoton AL. Microsurgical anatomy of the posterior ce­rebral artery. J Neurosurg 1978; 48: 534- 59. J Neuro- Ophthalmol, Vol. 19, No. 2, 1999 OCCIPITAL INFARCTION AND CAROTID DISSECTION 139 11. Riggs He, Rupp C. Variations in form of the circle of Willis. The relation of the variation to collateral circulation: an anatomic analysis. Arch Neurol 1963; 8: 24- 30. 12. Goldstein LB, Gray L, Hulette CM. Stroke due to ipsilateral ca­rotid artery dissection in a young adult. Stroke 1995; 26: 480- 3. 13. Oessin MS, Kwan ES, Scott M, Hedges TR. Occipital infarction with hemianopsia from carotid occlusive disease. Stroke 1989; 2: 409- 11. 14. Padget DH. The circle of Willis. Its embryology and anatomy. In: Dandy WP, eds. Intracranial arterial aneurysms. Ithaca NY: Corn-stock Publishing, 1947: 67- 90. 15. Lazorthes A, Gouaze A, Santini JJ, Lazorthes Y, Laffont J. Le modelage du polygone de Willis. Role des compressions des voies artfirielles d'apport dans les mouvements de la colonne cervicale et de l'extr6mite' cfiphalique. Neurochirurgie 1971; 17: 361- 77. 16. Larroche JC. The development of central nervous system during intrauterine life. In: Falkner F, eds. Human development. Part II. Philadelphia: W. B. Saunders, 1966: 257- 76. J Neuro- Ophthalmol, Vol. 19, No. 2, 1999