350 Surg Neural 1988;30:350-8 Venous Angiomas: of Intracranial An Underestimated Hemorrhage Ghaus M. Malik, M.D., Jay K. Morgan, James I. Ausman, M.D., Roushdy and Neuroradiology, The Henry Ford Neurosurgical Malik GM, Morgan JK, Boulos RS, Ausman JI. Venous angiomas: an underestimated cause of intracranial hemorrhage. Surg Neural 1988;30:350-8. Cerebral venous angiomas are considered by many investigators as infrequent and incidental. Our experience, however, has been different. Since 1975, we have compiled a group of 21 patients with 23 venous angiomas. Nine patients (43%) presented with intracranial hemorrhage, and two in this group had recurrent hemorrhage. of the venous angioma was perSurgical extirpation formed in all nine cases. An additional resection of a frontal venous angioma was performed in a woman with intractable seizures and headache. We experienced limited morbidity and no mortality. Although venous angiomas may be uncommon clinically, they have a significant potential for hemorrhage, and particularly, rehemorrhage if left untreated. WORDS: Venous S. Boulos, M.D., and M.D., Ph.D. Departments of Neurosurgery Detroit, Michigan KEY Cause angioma; Hemorrhage; Seizures; Surgery Vascular malformations of the intracranial circulation classically have been divided into four groups; telangiectasias, cavernous angiomas, arteriovenous malformations, and venous angiomas {13,14,231. Venous angiomas refer to a subgroup of these congenital vascular lesions which upon angiographic and histologic examination are composed of venous structures only. Although Sarwar and McCormick 1271 have described these lesions as the most common vascular malformations discerned at autopsy, venous angiomas have been relatively uncommon from a clinical standpoint. The management of patients with venous angiomas thus remains a controversial topic. Many authors consider Address reprint reque& to: Ghaus M. Malik, M.D., Department of Neurosurgery, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, Michigan 48202. Received April 8, 1988; accepted May 24, 1988. 8 1988 by ElsevierScience PublishingCo., Inc. Institute, Henry Ford Hospital Division, these lesions as incidental findings with relatively little clinical significance [1,3,11,13,26,27,31], whereas other case reports have emphasized their tendency to hemorrhage [9,10,16-18,231. Since 1975, we have compiled a group of 2 1 patients with 23 venous angiomas documented by cerebral angiography or histologic characteristics or both. Nine of these patients presented with an associated intraparenchymal hemorrhage. Another patient presented with intractable seizures, and the remaining 11 patients had venous angiomas found as incidental findings. It is the purpose of this report to present our experience with these lesions and, in particular, those that have hemorrhaged. Materials and Methods Twenty-one patients with a total of 23 venous angiomas were seen at Henry Ford Hospital between January 1, 1975 and July 30, 1987. Each patient underwent computed tomography (CT) scanning without and with intravenous contrast medium on either an EMI 5005, GE 9800, or Picker International 1200. Selective threeor four-vessel cerebral angiography had also been perdocumenting the venous formed in each patient, angioma. Summary of Clinical Findings In this series, there were 7 male and 14 female patients (Table 1). The average age was 38 years with a range of 15-74 years. Eleven of the lesions were supratentorial with six presenting in the frontal lobe, three in the parietal lobe, one in the temporal lobe, and one in the occipital lobe. All of these lesions drained into a superficial cortical venous system, predominantly the superior sagittal sinus. Of the 12 infratentorial lesions, six drained from the cerebellar hemispheres, one from the superior vermis, two from the mesencephalon, and three from the pontine region. Two of these lesions, 0090-3019/88/$3.50 23/F 18/F 41/F 17/M 21/F 33/F 75/M 34/M 50/F 43/M 461~ 45/F 39/M 36/F 34/F 36/F 54/F 43/F 45/M 30/F 15/M 1 2 3 4 5 6 7 8 9 10 II I2 13 14 I5 16 17 18 19 20 21 Abbreviations: FrontaI HA, sex no. Left hemispheric HA, head HA, HA HA, by valsalva “awea. Headache, numbness. venrilatory intracerebral support apnea Sleep ICH, requiring (?) HA, headache; HA vomiting Ataua photophobia of cbromc right hemisensory left V2-V3 uld history Intenninent deficit bemiparesis 2 mo. Hr of progressive 6 yr. Hx of temp internuclear vertigo. mild lobe seizures bilateral deficit, seizures seizures VII CT left MCA right central injury TIA’s Ir. paresthesias vakaIva Dysphasia increased ophrhrlmoplegin dysarthrin. Ilt. hemikory Chronic dysnomia Chronic Severe aneurysm Closed Rt. hemispheric intermittent Diffuse photophobia HA increved P&y ITF presentation infarct - with frontll frontal frontal frontal parietal versian parietll lateral ventricle IVH. inrraventrudar medullary jU”Cfl0” Ponto cerebella, Bilateral to the with cerebellum extension R&t I(rghr mesencephalon floor 4th ventricle _ MCA, TS vein internal of Gale” TS sss sss of Gale” sss sss cerebral Right Vein hemorrhage; 2 4.5 I 2 3.5 Left cerebellar 4 2 3.5 2 sss 2 sss of Galen TS Vein Vein sss TS TS mlddle cerebral artery; Med Juncoo” Lesmn at Ponto + +/ICH +/ICH +/ICH +/SAH +/SAH +/SAH +/ICM +/ICM +/IVH sss sss PInill Drainage 3 4 3 I 2 1.5 1.0 1.5 (cm) findings Angiographic Size Left frontal Left parietal Superior Left pnried Right (? multiple) Right Left cerebellum Right vermian frontnl Superior Right Right cerebellum Right 4th Ventricle extension Pontine Right into Location Left parietal (parenchymal); angioma “e”oU.5 from Hemorrhage hemorrhage 12179 and p&es vomiting heminnopsia nnd 6th Nerve Bitemporal atrophy nerve numbness. E/75 worsening nausea, HA; crvlial perioral CSF; 9178 fame of HA, Chronic multiple Diplopia, Optic recurrence left facial seizures (postpartum) HA, 2nd with rt. hemiparesis 9175; possible trimester and durmg signs Symptoms HA and Syncope age and C.ae Patient ’s Table 1. Venous Anniomas vein) vein) subarachnoid (no enhancement) (drammg + + vein) (no draining + + Partial SSS. superior exc,s,on excision hemorrhage. Parttal Partial and resection Evacuation lesion 4th of hemaroma excision excision excision resection hemorrhage. after of hemaroma resection ventricular Partial + PartraI Complete recurrent partial resection resectlo” Operation Evacuation Complete Complete + + + + + + + + + + contrast (d&kg SAH. - CT sagittal sinus, + + + + + _ + + + Ant. aneurysm TS. transverse sinus swallowing. movements tongue (Improving) tmpaired well well controlled setzures of sensory full hemiparesis, of I&O residual Difficulty controlled No deficit, No change seizures Moderate recovery with almost resolution deficit Postoperative HA Artery recovery aneurysm dysphasia functional Lt. MCA Transient Good SAH Asymptomatic with HA) of migraine Asymptomattc (? Assoc. Diagnosis Corn. intermittent from SAH intacr of Continued Asymptomatic Asymptomatic Asymptomatic NeuroIogralIy deficit resolution preop. Goad intact, we11 controlled Neurologically seizures status. result controlled to preop. seizures + Return Clinical Pathology 352 Surg Neural 1988;30:350-8 one from the mesencephalon and one from the superior vermis, drained into the vein of Galen. The rest of the infratentorial lesions drained into the transverse sinus. The average diameter of the radial array of medullary veins (caput of the medussa) was 2.4 cm with a range of l-4 cm. There was no correlation between this measurement and associated hemorrhage. Computed tomography scanning was helpful in localizing these venous angiomas in 80% of the patients. The most important findings were a nodular area of increased density (medussa) on the unenhanced studies and either a linear or curvilinear transcortical structure (draining vein) on enhanced studies. In our series, 11 patients presented with symptoms unassociated with their venous angiomas, although vague headaches were frequently described. One patient presented with intractable seizures and nine patients presented with a total of 11 episodes of hemorrhage secondary to venous angioma (Table 1). All hemorrhages were documented by non-contrastenhanced CT and intraoperative examination. Findings consistent with venous angiomas were documented by neuropathologic examination. In the group of patients with hemorrhage there were three males and six females. The age range was 18-50 years with an average of 33 years. The location of these symptomatic hemorrhages was as follows: two frontal, three parietal, three pontine, 1 mesencephalon. Two of these patients, one with a frontal venous angioma and one with a pontine lesion, had documented rehemorrhage. Ten patients, including the nine with hemorrhagic complications and one patient with intractable seizures, underwent surgical resection of their venous angiomas. Four of these patients had complete resection of their lesions whereas six had partial resections. Of the four patients with complete resections, three involved the frontal lobes (two right and one left) and one involved the left parietal lobe. Of the six patients with partial resection, two involved the parietal area (one each left and right side), one was localized to the mesencephalon, and three involved the pontine parenchyma. Only one patient in the latter group had significant postoperative morbidity with difficulty swallowing and impaired tongue movements. These deficits are both improving. Illustrative Case 1 Malik et al left carotid artery was performed and gave negative results. The patient had an uneventful delivery via cesarean section and had complete resolution of her neurological symptoms. Four-vessel angiography revealed the presence of a deep, left parietal venous angioma extending from the subependymal surface of the atrium of the left ventricle (Figure 1B). This had not been actually recognized on the first, single-vessel angiogram. Surgery was advised but was declined by the patient. She had an uneventful second pregnancy but presented in December 1979 with recurrent severe headache and right hemianesthesia. A repeat CT scan at that time was negative but owing to the potential for recurrent hemorrhage, the patient underwent a parietal occipital craniotomy and complete surgical resection (Figure 1C) of her venous angioma, which was documented by angiography and histologic examination. Her postoperative course was complicated by delayed-onset focal-sensory seizures which are well controlled with anticonvulsants. Neuropsychological testing revealed a mild parietal deficit but the patient was able to continue with her preoperative life-style and remains employed in her previous capacity. Case 2 This 18-year-old woman presented to our neurosurgical service in July 1977, approximately 10 days post partum, with persistent headaches and left focal seizures involving the face and the arm. An EM1 CT scan revealed an increased density in the right frontal lobe consistent with hemorrhage, and also showed a nodular enhancement around the hemorrhage (Figures 2A and B). Cerebral angiography revealed a small star-shaped collection of minute veins converging in the right frontal lobe and draining by a large transcortical vein into the superior sagittal sinus. This was seen only in the venous phase, without capillary blush (Figure 3A). This patient underwent a right frontal craniotomy with complete excision of the venous angioma, as documented by postoperative cerebral angiography (Figure 38). Histopathologic examination confirmed venous angioma. Postoperatively, the patient has remained well, with neuropsychological testing revealing no cognitive deficit. Cases This 23-year-old woman presented in September 1975 with severe headache and syncope during the second trimester of pregnancy with a subsequent right hemiparesis. Her CT findings were consistent with a left parietal intracerebral hemorrhage with extension into the lateral ventricle (Figure 1A). An angiogram of the Case 3 This patient has been previously reported in the literature by Pak et al [ 191. This 41-year-old woman presented initially on September 22, 1978, with progressive brainstem dysfunction which was considered most likely secondary to a pontine neoplasm. Her initial CT scan revealed a high-density lesion in the tectum of the Venous Surg Neural 1988;30:350-8 Angiomas 353 Figure 1.(A) Computed tomography scan showing left intraventricufar demonstration of the venous hemorrhage (care 1). (B) Cerebralangiographic angioma. (Note the conglomeration of medullary veins. and the drainage via the vein of Trolard into the superior sagittal sinus (arrowhead).) (C) Postoperative angiogram of the left carotid artery shows complete remozjat of angioma. c pons with effacement of the fourth ventricle. A cerebral angiogram was negative for vascular malformation but revealed an avascular mass lesion in the upper pons. Other studies including a pneumoencephalogram were also indicative of a brainstem neoplasm. At subsequent surgical exploration she was found to have an intrapon- tine hematoma extending into the fourth ventricle associated with an abnormal collection of venous structures. The hematoma was evacuated but no resection of these vessels was attempted because of their vital location. The patient had a good postoperative course with only a mild decrease to pinprick in the V2 Surg Neural 1988;30:350-8 Malik et al Figure 2.(A) Computed tomography scan without contrast enhancement revealing an increased density (arrowhead) in the right frontal lobe consistent with hemorrhage (case 2). (B) Computed tomography scan with contrast medium showing nodular enhancement (arrowhead) around the area of hemorrhage. distribution bilaterally and a persistent partial bilateral internuclear ophthalmoplegia. Five weeks postoperatively, a repeat cerebral angiogram disclosed a pontine venous angioma. She was treated conservatively but 2 years later she presented with-worsening truncal ataxia, internuclear ophthalmoplegia, and bilateral fifth nerve Figure 3.(A) LateraL view of angiogram of the right carotid artery (fje,enousphase): uenoas angioma with a star-shaped collection of minute veins converging in the right frontal lobe drained by a larger transcortical vein into the superior sagittal sinus. (B) Postoperathe cerebral angiogram (venous phase), showing complete excision of venous angioma. Surg Neural Venous Angiomas 355 1088;30:350-8 dysfunction. On CT scan she was found to have recurrent hemorrhage (Figure 4). At this time she was also noted to have idiopathic thrombocytopenia with a platelet level of 40,000. After a course of prednisone therapy her platelets returned to the normal level and she underwent a suboccipital craniectomy with partial resection of this pontine venous malformation. Postoperatively the patient had a moderate truncal ataxia and slight worsening of her bilateral facial sensory deficit along with a bilateral internuclear ophthalmoplegia. She was ambulatory upon discharge and during the next 6 months her truncal ataxia resolved and only a mild internuclear ophthalmoplegia remained. Approximately 2 years after this operation she returned to work and is leading a quite functional life-style. She has not experienced any further hemorrhagic complications. Case 4 This 15-year-old boy presented with severe headache, nausea, and vomiting. He had a lumbar puncture showing grossly bloody spinal fluid and a CT scan documenting subarachnoid hemorrhage with a right posterior inferior frontal intracerebral hemorrhage. An enhanced scan revealed no abnormal enhancement. The initial cerebral angiogram in June 1975, and repeat angiogram at 7 months were unremarkable. The patient was treated conservatively and was discharged without neurologic deficit. He did well until approximately 3 Figure 4. Computed tomography scan without contwt shows ezidence of subacute hemorrhage in the pony (care .3 ). enhancement years after his initial event at which time he again presented with severe headaches and had a spinal tap consistent with subarachnoid hemorrhage. Again, his CT findings were positive for a recurrent right posterior inferior frontal intracerebral hemorrhage. No draining vein was seen on enhanced scan. Cerebral angiography at this time revealed a faint stain with no abnormal arterial feeders or draining veins in the area of hemorrhage. The possibility of an intraaxial mass lesion was considered. The patient subsequently underwent a frontal craniotomy with an interhemispheric approach to this lesion. He was found to have a conglomeration of abnormal veins draining into the anterior septal vein. This was resected in its entirety along with evacuation of the associated intracerebral hematoma. The histopathologic diagnosis was venous angioma (Figure 5). The patient had no postoperative deficits and has had no recurrence of symptoms since his surgery in 1978. Discussion Venous angiomas were first recognized by Cushing and Baily [7] in 1928 as a discrete entity in the group of vascular malformations. According to McCormick et al [13,14,27], these malformations are composed entirely of veins which are devoid of large quantities of smooth muscle and elastic tissue. Intervening neuroglial tissue is present, distinguishing these entities from cavernous angiomas [6,13,14]. In 1967, Wolf et al {32] were considered to be the first to describe a pathologically proven venous angioma detected by cerebral angiography. Actually, this patient had multiple venous angiomas and presented with an intracerebral hemorrhage from a venous angioma in the left temporal lobe. Since then, there have been several reports that yielded the classic description of venous angiomas on angiogram. They are described as a local network of small medullary veins, resembling a caput medussa, which converge centrally into a single venous channel that courses transcortically to reach the superficial and sometimes the deep venous systems [12,20,21,28,30]. In 1977, Michels et al [ 1 S] reported six cases of venous angioma found by CT analysis and documented these lesions with cerebral angiography. In this and many subsequent articles on CT analysis, the appearance of the draining vein is that of a linear or curvilinear density that is seen best on enhanced scan [5,8,12,15,20]. Since this time there have been increasing numbers of venous angiomas found incidentally on CT and more recently on magnetic resonance imaging [2,4] (Figure 6). During the mid 1960s through the 1970s the consensus was that these lesions are the rarest form of vascular abnormalities and that they are usually asymptomatic [15,24,27,29,31]. In 1978, Sarwar and McCor- 356 Surg Neural 1988;30:350-8 mick [27] reported on a prospective analysis of 4069 consecutive autopsies in which they found 165 vascular anomalies; 63% of these were venous angiomas and thus these authors concluded that venous angiomas are the most common of the vascular malformations. This is contrary to our experience at Henry Ford Hospital where telangiectasias are the most common vascular malformation found at autopsy (Chason, JL, personal communication, 1987). Sarwar and McCormick 127) also concluded that the venous angiomas are usually asymptomatic and only rarely present with seizures or with signs and symptoms of subarachnoid or intracerebra1 hemorrhage. At that time only 14 cases of angiographically proven venous angiomas had been listed in the literature. Three of these had presented with subarachnoid hemorrhage and one with intracerebral hematoma. Since then the clinical significance of these vascular malformations has been quite controversial. In 1985, Handa and Moritake [lo] reviewed the literature on this subject and found an association of intracranial hemorrhage in approximately 17% of the reported patients. They concluded that surgical removal is advisable if this lesion is accessible. This view was supported by Rothfus et al [23] in 1984 for posterior fossa venous angiomas. They reviewed 20 patients with Malik et al Figure 5. Pathology specimen shows typical uen2o.w.rtrurtures with intewening brain parencbyma (case 4). Figure 6. Magnetic- resonance imaging (coronal plane) showing right cerebellar ver2ou.fangioma. Surg Neural Venous Angiomas reported hemorrhage from cerebellar venous angiomas documented by angiography or histology, or both, in addition to four of their own patients. They found that these cerebellar venous angiomas had a higher percentage of hemorrhagic complications than cerebral venous angiomas and thus suggested a possible propensity of cerebellar venous angiomas to bleed in comparison to supratentorial lesions. Furthermore, once a venous angioma has bled in the cerebellum, rebleeding may occur at any time. Opposing views have been presented by Saito and Kobayashi 1261 who concluded that venous angiomas have little clinical significance and that they are developmental abnormalities of the venous system during embryogenesis. In respect to the posterior fossa lesions, Senegor et al 1291 presented a cerebellar venous angioma which had hemorrhaged. This patient presented with signs of brainstem compression and subsequently underwent resection of the venous angioma. The patient had a disastrous postoperative course with venous infarction of the brainstem and subsequent death. These authors stressed that venous angiomas of the posterior fossa may represent anomalous venous drainage for this area and that they are not amenable to surgical resection. Biller et al [3] reiterated this viewpoint in 1985 when they presented a patient with subacute cerebellar hematoma secondary to a venous angioma who underwent evacuation of the hematoma with excision of the venous angioma. This patient also postoperatively developed brainstem and cerebellar venous infarcts and died 3 weeks later. In the last 12 years we have treated 2 1 patients with the finding of venous angioma on cerebral angiography. Nine of these patients presented with intraparenchymal hemorrhage, five with supratentorial and four with infratentorial. Eight of these patients presented with the typical CT findings and/or cerebral angiography consistent with venous angiomas. All of the patients presenting with hemorrhage underwent surgical resection with excellent results. Two of these patients presented initially in the peripartum period with cerebral hematomas. In our series there was marked female preponderance in patients who bled, representing six out of nine patients. Two of these had hemorrhage in association with pregnancy. This is in contrast to our experience with arteriovenous malformations in which there is practically even distribution between males and females. It is also interesting to note that in two instances, venous angiomas were not seen on the initial angiographic study. We postulate that the mass effect of the associated hematoma obscured the lesion. This is supported by the fact that after evacuation of the hema- 357 1988;30:350-8 toma, as in case 3, repeat cerebral angiograms clearly revealed the venous angioma. Our data suggest that venous angiomas may be uncommon lesions in clinical practice, but that they have a real potential for hemorrhage, and particularly for rehemorrhage. From this material it can also be suggested that pregnancy may make venous angiomas more likely to hemorrhage, as has been reported with arteriovenous malformations and aneurysms 122). From our experience with cerebral venous angiomas, we recommend that in patients with venous angiomas and associated hemorrhage, surgical extirpation of the lesion should be considered. Similarly, patients with a seizure focus that is well localized to the area of the venous angioma may benefit from surgical resection. The patient with an asymptomatic lesion should be treated conservatively; however, in the case of women of childbearing age, surgical excision should be considered if the lesion is accessible. The venous angiomas in the posterior fossa are possibly a different matter. From the reports of Senagor et al [29] and Biller et al 131, there is a strong suggestion that some of the venous angiomas of the cerebellar hemispheres may provide anomalous venous drainage. This may not be the case, as suggested by our experience, when the venous angioma involves the brainstem. Our results with partial resection of the angiomas involving and removal of hematomas brainstem lesions have been satisfactory to this time, similar to the experience of Sadeh et al 1251. 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