Neuroradiology
Neuroradiology 18, 273-275 (1979)
© by Springer-Verlag 1979
Transient Bilateral Occipital Lobe Ischemia: Microembolization Through a Trigeminal Artery R. M. Quencer 1 and J. Simon 2 ~Department of Radiology,Division of Neuroradiologyand 2Department of Neurology,Universityof Miami School of Medicine, Jackson Memorial Hospital, Miami, Florida, USA
Summary. Microembolization from an ulcerated carotid artery to both occipital lobes via a persistent trigeminal artery was observed in a patient presenting with episodic bilateral central scotomata. Symptomatic relief was obtained following carotid endarterectomy. This unique pathway which resulted in occipital lobe ischemia has not been previously reported. K e y words: Microembolization - Transient ischemic
attacks - Trigeminal artery - Vision loss
Introduction
Transient cerebral and ocular ischemia secondary to microembolization is a well-known phenomen; however, microembolization from ulcerated carotid arteries to the posterior circulation via persistent embryonic vessels has been reported in only four cases [1, 2]. In each case transient ischemia of the brain stem resulted (Table 1). We present a case of transient ischemia of both occipital lobes resulting from n~croembolization to the posterior cerebral arteries via a persistent trigeminal artery.
Case Report
A previously healthy 63-year-old male experienced in one year 15 episodes of transient bilateral central vision loss, each lasting for approximately 4 min. This was then followed by brief flashes of light which crossed his visual fields in a zig-zag pattern during which
there was bilateral dimming of his vision. There were no prodromal symptoms and the patient specifically denied headaches, nausea, vomiting, sensory disturbances, weakness, or other symptoms of cerebral or brain stem dysfunction. Physical, neurologic, and ophthalmologic examinations were normal. Computed tomography of the brain and electroencephalography were negative. Cerebral angiography via femoral catheterization demonstrated an ulcerated plaque along the posterolateral wall of the right internal carotid artery and a persistent trigeminal artery connecting the proximal cavernous portion of the right internal carotid artery to the basilar artery (Fig. 1). The left carotid, left vertebral, and aortic arch arteriograms were normal. An endarterectomy was performed to remove the ulcerated plaque from the right carotid, and seven days later he was discharged from the hospital without medication. With the exception of two brief episodes of transient vision loss which occurred shortly after his discharge, he has remained asymptomatic for the past 12 months.
Discussion
The primary clinical diagnostic consideration in this patient, who presented with recurrent bilateral central scotomata and scintillating fortifications, was occipital lobe ischemia due to either migraine or occlusive vascular disease. Migraine was felt to be less likely because it is primarily a disease of the second and third decade of life and the disturbance of vision, which begins in the central field and spreads toward the periphery, is usually unilateral[3]. The scotomata and the scintillating fortifications which m a y outline them last for approximately 20 min and they are restricted to one half of the visual field [4]. 0028-3940/79/0018/0273/$01.00
274
R.M. Quencer and J. Simon: Microembolization via Trigeminal Artery
Table 1. Reports of microemboli through persistent embryonic arteries Author
Clinical data
Waller et al. (2 cases)
Stern etal. (2 cases)
Quencer and Simon (1 case)
Ischemic area
Persistent embryonic artery
Postoperative follow-up
1. 54-year-old: bilateral 5th, left 7th nerve Brain stem paresis 2. 62-year-old: vertigo, left 5th nerve paresis, Brain stem loss of consciousness
Trigeminal
Asymptomatic (at 18 months) Asymptomatic (at 4 months)
3.68-year-old: dizziness, vertigo, visual blur- Brain stem ring, left leg numbess 4. 57-year-old: nausea, vomiting, dizziness, ~Brain stem dysequilibrium
Trigeminal
5. 63-year-old: bilateral central visual loss Occipital lobes with scintillating fortifications
Trigeminal
Trigeminal
Hypoglossal
Asymtomatic (at 11 months) Asymptomatic (at 14 months) Asymptomatic 12 months)
(at
Fig. 1 a and b. Right carotid arteriogram. Ulcerated ather0sclerotic plaque (closed straight arrow) of fight internal carotid artery is seen in both the lateral (a) and base (b) projections. A trigeminal artery (open arrow) connects the proximal cavernous internal carotid artery to the basilar artery, with filling of both posterior cerebral arteries (curved arrows). The base view, an adjunct to the routine AP and lateral views, helps exclude significant atherosclerotic disease along the course of the trigeminal artery
This is c o m m o n l y followed b y severe unilateral headaches. D u r i n g these attacks the patient m a y also experience nausea, vomiting, and prostration [5]. It is postulated that these migraine auras m a y result f r o m vascular insufficiency of the visual cortex[6]. O n the o t h e r hand, m i c r o e m b o l i z a t i o n to the occipital lobes is a condition which occurs in older patients and a l t h o u g h the episodes of visual disturb-
ances m a y include s c o t o m a t a and bright flashes of light, the s c o t o m a t a are, in contrast to migraines, v e r y brief in d u r a t i o n [4]. I n addition, these microembolic episodes are frequently bilateral because the vascular disease involves the vertebral a n d / o r basilar arteries, resulting in transient ischemia to b o t h occipital lobes. B e c a u s e of these clinical considerations and the patient's successful r e s p o n s e to carotid
R. M. Quencer and J. Simon: Microembolization via Trigeminal Artery
endarterectomy, we felt that microembolization to the striate cortex of the occipital lobe was the cause of his visual disturbance. Under normal conditions microembolization to an occipital lobe from an ulcerated carotid plaque could occur only through a posterior communicating artery and, in that case, strictly unilateral occipital ischemia would occur. Only with a persistent carotid to basilar artery anastomosis could microembolization from an atherosclerotic carotid artery result in transient ischemia of the visual cortex of both occipital lobes. Trigeminal arteries, the most common of the persistent embryonic vascular connections between the carotid and basilar arteries, have been associated with aneurysms of the trigeminal artery itself [7], aneurysms of the circle of Willis [8], trigeminal nerve compression [9], and angiomatous malformations at the base of the skull [10]. Our case, along with the four cases of persistent embryonic vessels associated with brain stem ischemia [1, 2], indicates that these vessels have a clinical significance apart from the congenital anomalies or local mass effects with which they are generally associated. They can serve as a conduit for microemboli, arising from vessels which normally supply the anterior circulation, to the vessels of the posterior circulation. Tile resultant clinical picture will be that of either posterior fossa ischemia or, as in the case presented here, occipital lobe ischemia. All of these five cases have been successfully treated with carotid endarterectomy (Table 1).
References 1. Wailer, F. T., Simons, R. L., Kerber, C., Liesel, I. O., Tanabe, C.T.: Trigeminal artery and microemboli to the brain stem. Report of two cases. J. Neurosurg. 46, 10~106 (1977)
275 2. Stem, J., Correll, J.W., Bryan, N.: Persistent hypoglossal artery and persistent trigeminal artery presenting with posterior fossa transient ischemic attacks. J. Neurosurg. 49, 614-619 (1978) 3. Walsh, F. B., Hoyt, W. F.: Vascular lesions and circulatory disorders of the nervous system: ocular signs. In: Clinical neuroophthalmology, pp. 1653-1689. Baltimore: Williams and Wilkins 1969 4. Hoyt, W.F.: Ocular signs and symptoms. In: Extracranial occlusive cerebrovascular disease, pp. 88-92 (eds. E. S. Wylie and W. K. Ehrenfeld). Philadelphia: W. B. Saunders 1970 5. Smith, J.L.: Migraine. In: Neuro-ophthalmology update, pp. 345-349 (ed. J. L. Smith). New York: Masson 1977 6. Bowen, S.F.: Cause of scotoma and headache of migraine. JAMA 214, 2065-2066 (1970) 7. George, A.E., Lin, J.P., Morantz, R.A.: Intracranial aneurysm on a peristent primative trigeminal artery. Case report. J. Neurosurg. 3S, 601-604 (1971) 8. Wolpert, S.M.: The trigeminal artery and associated aneurysms. Neurology 16, 610-614 (1966) 9. Kempe, L.C., Smith, D.R.: Trigeminal neuralgia, facial spasm, intermedius and glossopharyngeal neuralgia with persistent carotid-basilar anastomosis. J. Neurosurg. 31, 445-451 (1969) 10. Karasawa, J., Harauhiko, K., Furuse, S., Sakaki, T., Yoshida, Y., Ohnishi, H.: Bilateral persistent carotid-basilar anastomoses. Am. J. Roentgenol. 12"/, 1053-1056 (1976)
Received: 27 April 1979
Dr. R. M. Quencer Division of Neuroradiology Department of Radiology (R-130) University of Miami School of Medicine P. O. Box 16960 Miami, FL 33101 USA
Neuroradiology 18, 273-275 (1979)
© by Springer-Verlag 1979
Transient Bilateral Occipital Lobe Ischemia: Microembolization Through a Trigeminal Artery R. M. Quencer 1 and J. Simon 2 ~Department of Radiology,Division of Neuroradiologyand 2Department of Neurology,Universityof Miami School of Medicine, Jackson Memorial Hospital, Miami, Florida, USA
Summary. Microembolization from an ulcerated carotid artery to both occipital lobes via a persistent trigeminal artery was observed in a patient presenting with episodic bilateral central scotomata. Symptomatic relief was obtained following carotid endarterectomy. This unique pathway which resulted in occipital lobe ischemia has not been previously reported. K e y words: Microembolization - Transient ischemic
attacks - Trigeminal artery - Vision loss
Introduction
Transient cerebral and ocular ischemia secondary to microembolization is a well-known phenomen; however, microembolization from ulcerated carotid arteries to the posterior circulation via persistent embryonic vessels has been reported in only four cases [1, 2]. In each case transient ischemia of the brain stem resulted (Table 1). We present a case of transient ischemia of both occipital lobes resulting from n~croembolization to the posterior cerebral arteries via a persistent trigeminal artery.
Case Report
A previously healthy 63-year-old male experienced in one year 15 episodes of transient bilateral central vision loss, each lasting for approximately 4 min. This was then followed by brief flashes of light which crossed his visual fields in a zig-zag pattern during which
there was bilateral dimming of his vision. There were no prodromal symptoms and the patient specifically denied headaches, nausea, vomiting, sensory disturbances, weakness, or other symptoms of cerebral or brain stem dysfunction. Physical, neurologic, and ophthalmologic examinations were normal. Computed tomography of the brain and electroencephalography were negative. Cerebral angiography via femoral catheterization demonstrated an ulcerated plaque along the posterolateral wall of the right internal carotid artery and a persistent trigeminal artery connecting the proximal cavernous portion of the right internal carotid artery to the basilar artery (Fig. 1). The left carotid, left vertebral, and aortic arch arteriograms were normal. An endarterectomy was performed to remove the ulcerated plaque from the right carotid, and seven days later he was discharged from the hospital without medication. With the exception of two brief episodes of transient vision loss which occurred shortly after his discharge, he has remained asymptomatic for the past 12 months.
Discussion
The primary clinical diagnostic consideration in this patient, who presented with recurrent bilateral central scotomata and scintillating fortifications, was occipital lobe ischemia due to either migraine or occlusive vascular disease. Migraine was felt to be less likely because it is primarily a disease of the second and third decade of life and the disturbance of vision, which begins in the central field and spreads toward the periphery, is usually unilateral[3]. The scotomata and the scintillating fortifications which m a y outline them last for approximately 20 min and they are restricted to one half of the visual field [4]. 0028-3940/79/0018/0273/$01.00
274
R.M. Quencer and J. Simon: Microembolization via Trigeminal Artery
Table 1. Reports of microemboli through persistent embryonic arteries Author
Clinical data
Waller et al. (2 cases)
Stern etal. (2 cases)
Quencer and Simon (1 case)
Ischemic area
Persistent embryonic artery
Postoperative follow-up
1. 54-year-old: bilateral 5th, left 7th nerve Brain stem paresis 2. 62-year-old: vertigo, left 5th nerve paresis, Brain stem loss of consciousness
Trigeminal
Asymptomatic (at 18 months) Asymptomatic (at 4 months)
3.68-year-old: dizziness, vertigo, visual blur- Brain stem ring, left leg numbess 4. 57-year-old: nausea, vomiting, dizziness, ~Brain stem dysequilibrium
Trigeminal
5. 63-year-old: bilateral central visual loss Occipital lobes with scintillating fortifications
Trigeminal
Trigeminal
Hypoglossal
Asymtomatic (at 11 months) Asymptomatic (at 14 months) Asymptomatic 12 months)
(at
Fig. 1 a and b. Right carotid arteriogram. Ulcerated ather0sclerotic plaque (closed straight arrow) of fight internal carotid artery is seen in both the lateral (a) and base (b) projections. A trigeminal artery (open arrow) connects the proximal cavernous internal carotid artery to the basilar artery, with filling of both posterior cerebral arteries (curved arrows). The base view, an adjunct to the routine AP and lateral views, helps exclude significant atherosclerotic disease along the course of the trigeminal artery
This is c o m m o n l y followed b y severe unilateral headaches. D u r i n g these attacks the patient m a y also experience nausea, vomiting, and prostration [5]. It is postulated that these migraine auras m a y result f r o m vascular insufficiency of the visual cortex[6]. O n the o t h e r hand, m i c r o e m b o l i z a t i o n to the occipital lobes is a condition which occurs in older patients and a l t h o u g h the episodes of visual disturb-
ances m a y include s c o t o m a t a and bright flashes of light, the s c o t o m a t a are, in contrast to migraines, v e r y brief in d u r a t i o n [4]. I n addition, these microembolic episodes are frequently bilateral because the vascular disease involves the vertebral a n d / o r basilar arteries, resulting in transient ischemia to b o t h occipital lobes. B e c a u s e of these clinical considerations and the patient's successful r e s p o n s e to carotid
R. M. Quencer and J. Simon: Microembolization via Trigeminal Artery
endarterectomy, we felt that microembolization to the striate cortex of the occipital lobe was the cause of his visual disturbance. Under normal conditions microembolization to an occipital lobe from an ulcerated carotid plaque could occur only through a posterior communicating artery and, in that case, strictly unilateral occipital ischemia would occur. Only with a persistent carotid to basilar artery anastomosis could microembolization from an atherosclerotic carotid artery result in transient ischemia of the visual cortex of both occipital lobes. Trigeminal arteries, the most common of the persistent embryonic vascular connections between the carotid and basilar arteries, have been associated with aneurysms of the trigeminal artery itself [7], aneurysms of the circle of Willis [8], trigeminal nerve compression [9], and angiomatous malformations at the base of the skull [10]. Our case, along with the four cases of persistent embryonic vessels associated with brain stem ischemia [1, 2], indicates that these vessels have a clinical significance apart from the congenital anomalies or local mass effects with which they are generally associated. They can serve as a conduit for microemboli, arising from vessels which normally supply the anterior circulation, to the vessels of the posterior circulation. Tile resultant clinical picture will be that of either posterior fossa ischemia or, as in the case presented here, occipital lobe ischemia. All of these five cases have been successfully treated with carotid endarterectomy (Table 1).
References 1. Wailer, F. T., Simons, R. L., Kerber, C., Liesel, I. O., Tanabe, C.T.: Trigeminal artery and microemboli to the brain stem. Report of two cases. J. Neurosurg. 46, 10~106 (1977)
275 2. Stem, J., Correll, J.W., Bryan, N.: Persistent hypoglossal artery and persistent trigeminal artery presenting with posterior fossa transient ischemic attacks. J. Neurosurg. 49, 614-619 (1978) 3. Walsh, F. B., Hoyt, W. F.: Vascular lesions and circulatory disorders of the nervous system: ocular signs. In: Clinical neuroophthalmology, pp. 1653-1689. Baltimore: Williams and Wilkins 1969 4. Hoyt, W.F.: Ocular signs and symptoms. In: Extracranial occlusive cerebrovascular disease, pp. 88-92 (eds. E. S. Wylie and W. K. Ehrenfeld). Philadelphia: W. B. Saunders 1970 5. Smith, J.L.: Migraine. In: Neuro-ophthalmology update, pp. 345-349 (ed. J. L. Smith). New York: Masson 1977 6. Bowen, S.F.: Cause of scotoma and headache of migraine. JAMA 214, 2065-2066 (1970) 7. George, A.E., Lin, J.P., Morantz, R.A.: Intracranial aneurysm on a peristent primative trigeminal artery. Case report. J. Neurosurg. 3S, 601-604 (1971) 8. Wolpert, S.M.: The trigeminal artery and associated aneurysms. Neurology 16, 610-614 (1966) 9. Kempe, L.C., Smith, D.R.: Trigeminal neuralgia, facial spasm, intermedius and glossopharyngeal neuralgia with persistent carotid-basilar anastomosis. J. Neurosurg. 31, 445-451 (1969) 10. Karasawa, J., Harauhiko, K., Furuse, S., Sakaki, T., Yoshida, Y., Ohnishi, H.: Bilateral persistent carotid-basilar anastomoses. Am. J. Roentgenol. 12"/, 1053-1056 (1976)
Received: 27 April 1979
Dr. R. M. Quencer Division of Neuroradiology Department of Radiology (R-130) University of Miami School of Medicine P. O. Box 16960 Miami, FL 33101 USA
