Carotid-cavernous sinus fistula presenting as a posterior fossa mass
Case report BRUCE BARTLOW, M.D., AND RICHARD D. PENN, M.D.
Department of Neurosurgery~, Rush Medical College, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois ~" The authors report a case in which trigeminal neuralgia and hearing loss developed 14 years after a severe head injury. Arteriography demonstrated a carotid-cavernous sinus fistula producing a large venous mass in the posterior fossa. KEY WORDS
9 carotid-cavernous sinus fistula
9 posterior fossa
suffered fractures of the left jaw and left frontal bone in an automobile accident. He had residual diplopia for 3 weeks; as this symptom resolved he noted a "swooshing" sound in the left ear which kept him awake at night and was synchronous with his pulse, but gradually disappeared 3 weeks later, and did not recur. For 12 years he had no related symptoms. Three years prior to admission, he experienced a sharp, burning pain beginning in front of the left ear and shooting to the left temporal area and the lateral canthus of the left eye, lasting only a few seconds. The pain recurred several times per week, frequently extending to the left periorbital region or jaw, and was triggered by chewing, smiling, talking, brushing his teeth, or shaving. There were no persistent dysesthesias or numbness. Diazepam seemed to diminish the frequency and severity of the pains for about a month, Case Report but then they recurred and continued to the This 38-year-old man was admitted on present time. Sixteen months prior to admisFebruary 18, 1974, for evaluation of episodic sion, he noticed progressive difficulty in hearleft facial pain. In 1962, the patient had ing voices in the left ear; he began to listen to
A
CAROTiD-cavernous fistula (CCF), like any arteriovenous communication, may produce symptoms by diversion of arterial flow, redirection and overfilling of venous drainage, or mass effect of hypertrophied arteriovenous channels. Perhaps due to the low resistance of the ophthalmic vein, the majority of cases since Travers ''~ original description of this entity in 1811 have presented pulsating exophthalmos with ipsilateral bruit. Wolff and Schmid 2~ have shown several alternative routes from the cavernous sinus to the internal jugular veins. These variations in venous flow have resulted in cases of bilateral is and contralateral 7,14 pulsating exophthalmos. We are reporting a CCF that produced the symptoms of a cerebellopontine angle mass, but spared the orbit.
J. Neurosurg. / Volume 42 / May, 1975
585
B. B a r t l o w a n d R. D. P e n n
FIG. 1. Computerized axial tomography scan (left), with diagrammatic representation (right) of structures visualized. Scale on left illustrates density of structures involved.
the telephone only with the right ear. There was no nausea, vertigo, disequilibrium, or generalized headache. Examination. The patient was apparently healthy, alert, cooperative, and comfortable; the heart rate was 90/min, and blood pressure 130/80 mm Hg without orthostatic change. The left temporal artery was prominent, but not firm or tender; the left carotid artery was bounding with larger amplitude and more rapid fall-off than the normal right carotid pulse. There was no neck vein distention or adenopathy. A systolic bruit at the base of the left common carotid artery, systolic and diastolic components at the level of the bifurcation of the carotid artery, and a loud continuous bruit at the angle of the jaw and over the left eye were evident. The bruit did not change on compression of the carotid artery, nor did the patient complain of any other symptoms during this maneuver. The rest of the peripheral vascular examination was normal; the heart, lungs, and abdomen were also normal. Neurological Findings. There was slight left facial drooping that cleared on command or mimetic facial movements, and the left palpebral fissure was slightly larger than the right. Exophthalmometry showed no difference between the eyes. Visual fields were intact on confrontation and subsequent perimetry, eye movements were full and conjugate, and there was no nystagmus. Pupils were equal and reactive; fundoscopic examination was normal, the retinal veins were not engorged, and the disc margins were 586
sharp. The Weber test lateralized to the right ear. Cold caloric testing performed in the right ear produced appropriate nystagmus, nausea, and vertigo; there was no response to the same stimulation in the left ear. Facial sensation was intact. Corneal reflexes were present and symmetrical. Peripheral motor, sensory, and reflex examinations were normal. Plantar reflexes were downgoing, the Romberg test was negative, and there were no pathological reflexes, tremor, or dysmetria. Mental functions were normal. Special Studies. Audiometry revealed moderate loss of pure tone perception in the 250 to 750 Hz range in the left ear only. The threshold for speech reception was 28 db in the left ear, 12 db in the right. Speech discrimination in the left ear was reduced to 22% of normal at the 25 db speech level, and 40% of normal at the 40 db level, as contrasted with 100% of normal in the right. Electronystagmometry revealed no abnormalities. Tympanography demonstrated normal mobility, pressures, and impedance bilaterally. Phonogram of the carotid bruit showed it to have a peak frequency of 100 Hz, with maximum intensities in the range of 50 to 200 Hz. Skull films showed enlargement of the carotid canal, sella turcica, and superior orbital fissure, and mild erosion of the left internal auditory meatus. Brain scan showed a nonspherical area of intense uptake in the left cerebellopontine angle and extending over the left cerebellar hemisphere. Nuclide angiography showed rapid filling of the lesion, but an early venous phase could not be identified. Computerized axial tomography (CT) demonstrated a well-circumscribed rounded density slightly above the cerebellopontine angle or in the tentorial incisura, with symmetrically enlarged lateral and third ventricles; the density of the lesion was compatible with a calcified meningioma or blood clot (Fig. 1). Percutaneous selective cerebral angiography was performed by the femoral route. The entire flow from the left internal carotid artery passed into the left cavernous sinus (Fig. 2). The cavernous sinus was drained partly by the superior ophthalmic vein and intercavernous and basilar communications to the contralateral side; however, the major drainage was by way of a massively enlarged superior petrosal sinus to the sigmoid sinus, and the lateral pontomesencephalic vein
J. Neurosurg. / Volume 42 / May, 1975
Carotid-cavernous fistula in posterior fossa
F~G. 2. Left internal carotid cerebral angiogram. Left.-Anteroposterior projection. The entire flow from the left internal carotid artery enters the left cavernous sinus, to drain into the dilated posterior venous system. Contralateral flow to the basilar venous sinuses is also seen. The left carotid artery provides no cerebral perfusion. Right." Lateral view visualizes the venous mass in the region of the cerebellopontine angle. Drainage is faintly seen from the cavernous system through the lateral pontomesencephalic vein to the basal vein of Rosenthal. A dilated ophthalmic vein also drains the cavernous sinus. through the basal vein of Rosenthal to the straight sinus. The petrosal system in the region of the cerebellopontine angle was aneurysmally dilated in the area of increased density seen on CT. The left posterior cerebral artery was perfused by the vertebralbasilar system, the left middle cerebral artery by the vertebral artery and the right internal carotid arteries via the posterior and anterior communicating arteries, respectively. The right internal carotid artery also provided circulation to both anterior cerebral arteries and the right middle cerebral arteries. Blood flowed through the CCF from both internal carotid arteries, the left vertebral artery, and the left external carotid via the ophthalmic artery. The posterior cerebral artery was displaced upward and medially by a mass lesion in the region of the left cerebellopontine angle created by the enormously enlarged superior petrosal vein draining the left cavernous sinus. Discussion
Carotid-cavernous fistulas usually result in unilateral pulsating exophthalmos, ipsilateral bruit, and oculomotor palsies, and optic nerve damage?,.12,~e 18 Trigeminal nerve involvement is less frequent, 4 and when it occurs J. Neurosurg. / Volume 42 / May, 1975
hypesthesia8,11 or nonspecific orbital pain 4,1~ is most often found. Tic pain is rare and is largely confined to the ophthalmic division? ~ Acoustic nerve damage is even rarer and has been attributed to t r a u m a ) ,x~ Our case was distinctly atypical; the patient was spared the characteristic orbital manifestations of a CCF and developed instead signs and symptoms of an expanding cerebellopontine mass. The predominance of posterior venous run-off readily accounts for the unusual course. Wolff and Schmid 2~described multiple routes of egress of blood from the cavernous sinus to the internal jugular vein. These include the superior ophthalmic vein to the facial veins, the pterygoid plexus via the inferior ophthalmic vein, the superior and inferior petrosal sinuses to the sigmoid sinus and the Sylvian vein through anastamoses to the transverse sinus. The lateral mesencephalic, pontine plexus, pontomesencephalic, and basal veins along with the straight sinus create an alternative route from the superior petrosal sinus to the transverse and sigmoid sinuses. The superior ophthalmic vein usually provides the major drainage of the CCF, hence the prevalence of the ophthalmic division of fifth nerve neuropathies and of pulsating exophthalmos and 587
B. Bartlow chemosis. Other authors have demonstrated posteriorly-directed flow from the CCF 1'2's'9 and attempted to find a relationship between the direction of flow and the site of carotid perforation. 1~ Our patient's trigeminal neuralgia spanning all three divisions of the fifth nerve, and the ipsilateral loss of both auditory and vestibular neural function were clearly due to the left cerebellopontine angle mass. Part of the mass was clotted blood as demonstrated by CT; this was probably thrombus within or around the expanded posterior sinuses. The fact that CT added information that could not be gained directly from arteriography suggests the value of the technique in the study of arteriovenous malformations, carotid cavernous fistulas, and large aneurysms to detect clots and delineate the size of lesions? 3 The hydrocephalus, well delineated by the CT scan, was another manifestation of the posterior fossa mass. Hydrocephalus was not reported in the series studied pathologically by Dandy. 2 Review of the literature has revealed no similar case. In the large series of vascular and neoplastic cerebellopontine angle tumors analyzed by Evans and Courville? no CCF's are mentioned. The posteriorly directed flow via the petrosal sinus must be quite rare, but the consequent dilatation of the sinus to create a tumor-like mass of venous channels at the cerebellopontine angle explains our patient's condition. Acknowledgment
The authors express sincere appreciation to Allison Chmielarski for her assistance in preparing this paper. References
1. Clemens F, Lodin H: Some viewpoints on the venous outflow pathways in cavernous sinus fistulas: angiographic study of five traumatic cases. Clin Radiol 19:196-200, 1968 2. Dandy WE, Follis RH Jr: On the pathology of carotid-cavernous aneurysms (pulsating exophthalmos). Am J Ophthalmol 24:365-385, 1941 3. Evans N, Courville CB: The nervus acusticus. 2. Pathological conditions involving the eighth nerve and the cerebellopontine angle. Laryngoscope 42:432-455, 1932 4. Hamby WB: Carotid-Cavernous Fistula. Springfield, Ill, Charles C Thomas, 1966 588
and R. D. Penn
5. Hamby WB: Intracranial Aneurysms, ed 1. Springfield, I11, Charles C Thomas, 1952 6. Hayes G J: Carotid cavernous fistulas. Diagnosis and surgical management. Am Surg 24:839-943, 1958 7. Jefferson G: Intracranial aneurysms, the Balfour Lecture, University of Toronto, October 18, 1950, in Hamby WB: Carotid Cavernous Fistula. Springfield, Ill, Charles C Thomas, 1966, p 122 8. Legr6 J, Salamon G, Dufour M, et al: Voies de drainage veineux mises en 6vidence par la soustraction, au cours de trois cas de fistules carotico-caverneuses post-traumatiques. Confrontation anatomo-radiologique. Neurochirurgie 11:387-391, 1965 9. List CF, Hodges F J: Intracranial angiography. I. Diagnosis of vascular lesions. J Nenrosurg 3:25-45, 1946 10. Locke CE Jr: Intracranial arteriovenous aneurysm of pulsating exophthalmos. Ann Surg 80:1-24, 272-285, 1924 11. Madsen PH: Carotid-cavernous fistulae. A study of 18 cases. Acta Ophthalmol 48:731-750, 1970 12. Martin JD, Mabon RF: Pulsating exophthalmos. Review of all reported cases. JAMA 121:330-334, 1943 13. New PFJ, Scott WR, Schnur JA, et al: Computerized axial tomography with the EMI scanner. Radiology 110:109-123, 1974 14. Ramos M, Mount LA: Carotid cavernous fistula with signs on contralateral side. Case report. J Neurosurg 10:178-182, 1953 15. Sattler CH: Pulsierender Exophthalmus, in Graefe A, Saemisch T (eds): Handbuch der gesamten Augenheilkunde, ed 2, volume 9. Berlin, Springer-Verlag, 1920, pp 1-268 16. Stehbens WE: Pathology of the Cerebral Blood Vessels. St. Louis, CV Mosby, 1972 17. Stern WE, Brown WJ, Alksne JF: The surgical challenge of carotid-cavernous fistula: the critical role of intracranial circulatory dynamic. J Neurosurg 27:298-308, 1967 18. Toole JF, Patel AN: Cerebrovascular Disorders. New York, McGraw-Hill, 1967, pp 219-234 19. Travers B: A case of aneurism by anastomosis in the orbit, cured by ligature of the common carotid artery. Med Chit Trib 2:1-16, 1811 20. Wolff H, Schmid B: Das Arteriogramm des pulsierenden Exophthalmus. Zentralbl Neorochir 4:241-250, 310-319, 1939
Address reprint requests to: Richard Penn, M.D., Department of Neurosurgery, Rush Medical College, Rush-Presbyterian-St. Luke's Medical Center, 1753 West Congress Parkway, Chicago, Illinois 60612. J. Neurosurg. / Volume 42 / May, 1975
Case report BRUCE BARTLOW, M.D., AND RICHARD D. PENN, M.D.
Department of Neurosurgery~, Rush Medical College, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois ~" The authors report a case in which trigeminal neuralgia and hearing loss developed 14 years after a severe head injury. Arteriography demonstrated a carotid-cavernous sinus fistula producing a large venous mass in the posterior fossa. KEY WORDS
9 carotid-cavernous sinus fistula
9 posterior fossa
suffered fractures of the left jaw and left frontal bone in an automobile accident. He had residual diplopia for 3 weeks; as this symptom resolved he noted a "swooshing" sound in the left ear which kept him awake at night and was synchronous with his pulse, but gradually disappeared 3 weeks later, and did not recur. For 12 years he had no related symptoms. Three years prior to admission, he experienced a sharp, burning pain beginning in front of the left ear and shooting to the left temporal area and the lateral canthus of the left eye, lasting only a few seconds. The pain recurred several times per week, frequently extending to the left periorbital region or jaw, and was triggered by chewing, smiling, talking, brushing his teeth, or shaving. There were no persistent dysesthesias or numbness. Diazepam seemed to diminish the frequency and severity of the pains for about a month, Case Report but then they recurred and continued to the This 38-year-old man was admitted on present time. Sixteen months prior to admisFebruary 18, 1974, for evaluation of episodic sion, he noticed progressive difficulty in hearleft facial pain. In 1962, the patient had ing voices in the left ear; he began to listen to
A
CAROTiD-cavernous fistula (CCF), like any arteriovenous communication, may produce symptoms by diversion of arterial flow, redirection and overfilling of venous drainage, or mass effect of hypertrophied arteriovenous channels. Perhaps due to the low resistance of the ophthalmic vein, the majority of cases since Travers ''~ original description of this entity in 1811 have presented pulsating exophthalmos with ipsilateral bruit. Wolff and Schmid 2~ have shown several alternative routes from the cavernous sinus to the internal jugular veins. These variations in venous flow have resulted in cases of bilateral is and contralateral 7,14 pulsating exophthalmos. We are reporting a CCF that produced the symptoms of a cerebellopontine angle mass, but spared the orbit.
J. Neurosurg. / Volume 42 / May, 1975
585
B. B a r t l o w a n d R. D. P e n n
FIG. 1. Computerized axial tomography scan (left), with diagrammatic representation (right) of structures visualized. Scale on left illustrates density of structures involved.
the telephone only with the right ear. There was no nausea, vertigo, disequilibrium, or generalized headache. Examination. The patient was apparently healthy, alert, cooperative, and comfortable; the heart rate was 90/min, and blood pressure 130/80 mm Hg without orthostatic change. The left temporal artery was prominent, but not firm or tender; the left carotid artery was bounding with larger amplitude and more rapid fall-off than the normal right carotid pulse. There was no neck vein distention or adenopathy. A systolic bruit at the base of the left common carotid artery, systolic and diastolic components at the level of the bifurcation of the carotid artery, and a loud continuous bruit at the angle of the jaw and over the left eye were evident. The bruit did not change on compression of the carotid artery, nor did the patient complain of any other symptoms during this maneuver. The rest of the peripheral vascular examination was normal; the heart, lungs, and abdomen were also normal. Neurological Findings. There was slight left facial drooping that cleared on command or mimetic facial movements, and the left palpebral fissure was slightly larger than the right. Exophthalmometry showed no difference between the eyes. Visual fields were intact on confrontation and subsequent perimetry, eye movements were full and conjugate, and there was no nystagmus. Pupils were equal and reactive; fundoscopic examination was normal, the retinal veins were not engorged, and the disc margins were 586
sharp. The Weber test lateralized to the right ear. Cold caloric testing performed in the right ear produced appropriate nystagmus, nausea, and vertigo; there was no response to the same stimulation in the left ear. Facial sensation was intact. Corneal reflexes were present and symmetrical. Peripheral motor, sensory, and reflex examinations were normal. Plantar reflexes were downgoing, the Romberg test was negative, and there were no pathological reflexes, tremor, or dysmetria. Mental functions were normal. Special Studies. Audiometry revealed moderate loss of pure tone perception in the 250 to 750 Hz range in the left ear only. The threshold for speech reception was 28 db in the left ear, 12 db in the right. Speech discrimination in the left ear was reduced to 22% of normal at the 25 db speech level, and 40% of normal at the 40 db level, as contrasted with 100% of normal in the right. Electronystagmometry revealed no abnormalities. Tympanography demonstrated normal mobility, pressures, and impedance bilaterally. Phonogram of the carotid bruit showed it to have a peak frequency of 100 Hz, with maximum intensities in the range of 50 to 200 Hz. Skull films showed enlargement of the carotid canal, sella turcica, and superior orbital fissure, and mild erosion of the left internal auditory meatus. Brain scan showed a nonspherical area of intense uptake in the left cerebellopontine angle and extending over the left cerebellar hemisphere. Nuclide angiography showed rapid filling of the lesion, but an early venous phase could not be identified. Computerized axial tomography (CT) demonstrated a well-circumscribed rounded density slightly above the cerebellopontine angle or in the tentorial incisura, with symmetrically enlarged lateral and third ventricles; the density of the lesion was compatible with a calcified meningioma or blood clot (Fig. 1). Percutaneous selective cerebral angiography was performed by the femoral route. The entire flow from the left internal carotid artery passed into the left cavernous sinus (Fig. 2). The cavernous sinus was drained partly by the superior ophthalmic vein and intercavernous and basilar communications to the contralateral side; however, the major drainage was by way of a massively enlarged superior petrosal sinus to the sigmoid sinus, and the lateral pontomesencephalic vein
J. Neurosurg. / Volume 42 / May, 1975
Carotid-cavernous fistula in posterior fossa
F~G. 2. Left internal carotid cerebral angiogram. Left.-Anteroposterior projection. The entire flow from the left internal carotid artery enters the left cavernous sinus, to drain into the dilated posterior venous system. Contralateral flow to the basilar venous sinuses is also seen. The left carotid artery provides no cerebral perfusion. Right." Lateral view visualizes the venous mass in the region of the cerebellopontine angle. Drainage is faintly seen from the cavernous system through the lateral pontomesencephalic vein to the basal vein of Rosenthal. A dilated ophthalmic vein also drains the cavernous sinus. through the basal vein of Rosenthal to the straight sinus. The petrosal system in the region of the cerebellopontine angle was aneurysmally dilated in the area of increased density seen on CT. The left posterior cerebral artery was perfused by the vertebralbasilar system, the left middle cerebral artery by the vertebral artery and the right internal carotid arteries via the posterior and anterior communicating arteries, respectively. The right internal carotid artery also provided circulation to both anterior cerebral arteries and the right middle cerebral arteries. Blood flowed through the CCF from both internal carotid arteries, the left vertebral artery, and the left external carotid via the ophthalmic artery. The posterior cerebral artery was displaced upward and medially by a mass lesion in the region of the left cerebellopontine angle created by the enormously enlarged superior petrosal vein draining the left cavernous sinus. Discussion
Carotid-cavernous fistulas usually result in unilateral pulsating exophthalmos, ipsilateral bruit, and oculomotor palsies, and optic nerve damage?,.12,~e 18 Trigeminal nerve involvement is less frequent, 4 and when it occurs J. Neurosurg. / Volume 42 / May, 1975
hypesthesia8,11 or nonspecific orbital pain 4,1~ is most often found. Tic pain is rare and is largely confined to the ophthalmic division? ~ Acoustic nerve damage is even rarer and has been attributed to t r a u m a ) ,x~ Our case was distinctly atypical; the patient was spared the characteristic orbital manifestations of a CCF and developed instead signs and symptoms of an expanding cerebellopontine mass. The predominance of posterior venous run-off readily accounts for the unusual course. Wolff and Schmid 2~described multiple routes of egress of blood from the cavernous sinus to the internal jugular vein. These include the superior ophthalmic vein to the facial veins, the pterygoid plexus via the inferior ophthalmic vein, the superior and inferior petrosal sinuses to the sigmoid sinus and the Sylvian vein through anastamoses to the transverse sinus. The lateral mesencephalic, pontine plexus, pontomesencephalic, and basal veins along with the straight sinus create an alternative route from the superior petrosal sinus to the transverse and sigmoid sinuses. The superior ophthalmic vein usually provides the major drainage of the CCF, hence the prevalence of the ophthalmic division of fifth nerve neuropathies and of pulsating exophthalmos and 587
B. Bartlow chemosis. Other authors have demonstrated posteriorly-directed flow from the CCF 1'2's'9 and attempted to find a relationship between the direction of flow and the site of carotid perforation. 1~ Our patient's trigeminal neuralgia spanning all three divisions of the fifth nerve, and the ipsilateral loss of both auditory and vestibular neural function were clearly due to the left cerebellopontine angle mass. Part of the mass was clotted blood as demonstrated by CT; this was probably thrombus within or around the expanded posterior sinuses. The fact that CT added information that could not be gained directly from arteriography suggests the value of the technique in the study of arteriovenous malformations, carotid cavernous fistulas, and large aneurysms to detect clots and delineate the size of lesions? 3 The hydrocephalus, well delineated by the CT scan, was another manifestation of the posterior fossa mass. Hydrocephalus was not reported in the series studied pathologically by Dandy. 2 Review of the literature has revealed no similar case. In the large series of vascular and neoplastic cerebellopontine angle tumors analyzed by Evans and Courville? no CCF's are mentioned. The posteriorly directed flow via the petrosal sinus must be quite rare, but the consequent dilatation of the sinus to create a tumor-like mass of venous channels at the cerebellopontine angle explains our patient's condition. Acknowledgment
The authors express sincere appreciation to Allison Chmielarski for her assistance in preparing this paper. References
1. Clemens F, Lodin H: Some viewpoints on the venous outflow pathways in cavernous sinus fistulas: angiographic study of five traumatic cases. Clin Radiol 19:196-200, 1968 2. Dandy WE, Follis RH Jr: On the pathology of carotid-cavernous aneurysms (pulsating exophthalmos). Am J Ophthalmol 24:365-385, 1941 3. Evans N, Courville CB: The nervus acusticus. 2. Pathological conditions involving the eighth nerve and the cerebellopontine angle. Laryngoscope 42:432-455, 1932 4. Hamby WB: Carotid-Cavernous Fistula. Springfield, Ill, Charles C Thomas, 1966 588
and R. D. Penn
5. Hamby WB: Intracranial Aneurysms, ed 1. Springfield, I11, Charles C Thomas, 1952 6. Hayes G J: Carotid cavernous fistulas. Diagnosis and surgical management. Am Surg 24:839-943, 1958 7. Jefferson G: Intracranial aneurysms, the Balfour Lecture, University of Toronto, October 18, 1950, in Hamby WB: Carotid Cavernous Fistula. Springfield, Ill, Charles C Thomas, 1966, p 122 8. Legr6 J, Salamon G, Dufour M, et al: Voies de drainage veineux mises en 6vidence par la soustraction, au cours de trois cas de fistules carotico-caverneuses post-traumatiques. Confrontation anatomo-radiologique. Neurochirurgie 11:387-391, 1965 9. List CF, Hodges F J: Intracranial angiography. I. Diagnosis of vascular lesions. J Nenrosurg 3:25-45, 1946 10. Locke CE Jr: Intracranial arteriovenous aneurysm of pulsating exophthalmos. Ann Surg 80:1-24, 272-285, 1924 11. Madsen PH: Carotid-cavernous fistulae. A study of 18 cases. Acta Ophthalmol 48:731-750, 1970 12. Martin JD, Mabon RF: Pulsating exophthalmos. Review of all reported cases. JAMA 121:330-334, 1943 13. New PFJ, Scott WR, Schnur JA, et al: Computerized axial tomography with the EMI scanner. Radiology 110:109-123, 1974 14. Ramos M, Mount LA: Carotid cavernous fistula with signs on contralateral side. Case report. J Neurosurg 10:178-182, 1953 15. Sattler CH: Pulsierender Exophthalmus, in Graefe A, Saemisch T (eds): Handbuch der gesamten Augenheilkunde, ed 2, volume 9. Berlin, Springer-Verlag, 1920, pp 1-268 16. Stehbens WE: Pathology of the Cerebral Blood Vessels. St. Louis, CV Mosby, 1972 17. Stern WE, Brown WJ, Alksne JF: The surgical challenge of carotid-cavernous fistula: the critical role of intracranial circulatory dynamic. J Neurosurg 27:298-308, 1967 18. Toole JF, Patel AN: Cerebrovascular Disorders. New York, McGraw-Hill, 1967, pp 219-234 19. Travers B: A case of aneurism by anastomosis in the orbit, cured by ligature of the common carotid artery. Med Chit Trib 2:1-16, 1811 20. Wolff H, Schmid B: Das Arteriogramm des pulsierenden Exophthalmus. Zentralbl Neorochir 4:241-250, 310-319, 1939
Address reprint requests to: Richard Penn, M.D., Department of Neurosurgery, Rush Medical College, Rush-Presbyterian-St. Luke's Medical Center, 1753 West Congress Parkway, Chicago, Illinois 60612. J. Neurosurg. / Volume 42 / May, 1975
