388 Segal et al abling angina pectoris treated by in­ trathecal opiates. From the description, this treatment seemed to be successful and did not mask the development of a myocardial infarction. This article suggests that in selected patients with medically intractable an­ gina pectoris, continuous intrathecal administration of morphine may re­ duce cardiogenic pain. This is particu­ larly interesting given the growing Eu­ ropean experience that spinal cord stimulation in the mid- to upper tho­ racic area can also alleviate anginal symptoms. Kim J. Burchiel Portland, Oregon This is a unique use of opioid infu­ sion, which commands attention. Few patients are likely to be candidates, be­ cause incapacitating angina is a rarity. The technique is likely to be used in a very small number of patients who are well chosen by cardiologists. The possi- Acute Subdural Hematoma Caused by a Ruptured Giant Intracavernous Aneurysm: Case Report Department of Neurological Surgery (MRMcL, H-DJ), University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, and Department of Neurological Surgery (YK), University of Ulsan College of Medicine, Seoul, Korea A CASE OF a giant intracavernous carotid artery aneurysm that presented as an acute subdural hematoma is reported. The patient was initially treated unsuccessfully with endovascular aneurysmal embolization and subse­ quently underwent attempted microsurgical clipping with preservation of the parent artery. At operation, an angiogram showed occlusion of the parent vessel, and the aneurysm was trapped by occlusion of the internal carotid artery. The patient did well for 2 days postoperatively but then developed contralateral progressive hemiplegia and aphasia. Emergent sub­ sequent exploration and middle cerebral artery embolectomy were per­ formed, and the hemiplegia and aphasia resolved rapidly. At 2-year followup, the patient continues to do well. To our knowledge, this is the first reported case of a patient who survived an acute subdural hematoma caused by an intracavernous carotid artery aneurysm. (Neurosurgery 38:388-392 1996) Key words: Balloon embolization, Carotid artery, Cavernous sinus, Cerebral aneurysm, Subdural hematoma I (SDH). Two fatal SDHs caused by ruptured ICCAAns have previously been reported (2, 14). To our knowledge this is the first reported survival after an SDH caused by a ruptured ICCAAn. neurosurgery, Vol. 38. No. 2, February 1996 Donlin M. Long Baltimore, CASE REPO RT A 48-year-old woman with a histc: of hypertension presented to an emer­ gency room with a 5-day historyIf lift eyelid and facial swelling, progress! pulsatile ophthalmoplegia, and facial numbness. She initially was treated fora paranasal sinus infection. When a sue den severe headache developed, a cor puted tomographic (CT) scan of th* head was obtained that showed a let hemispheric acute SDH. The patient was then referred to our center. Despite a severe headache, she was alert and communicating appropriately. She de nied any history of head trauma and any previous symptoms of retro-orbital or facial pain or diplopia. She had le proptosis, conjunctival injection, am eyelid swelling. A neurological exami­ nation showed complete left ophthal­ moplegia, trigeminal hypesthesia am hypalgesia in the VI and V2 distribu tion, and left blindness. Magnetic resonance (MR) imagingre vealed a left hemispheric acute SD and a cavernous sinus mass (F/gs-1^ 2). Four-vessel cerebral arteriograp revealed this to be a giant aneurysm0 the left intracavernous internal caro artery (ICA) (Fig. 3, and B). BaltoJ test occlusion (BTO) of the le t caused no change in the neuro0^ status of the patient, and a xen0V hanced CT blood flow study^vvl| BTO did not show any signii* change in cerebral blood flow. Treatment options discussed wi patient included observation, micros0 gical clipping of the aneurysm, endo^ Downloaded from https://academic.oup.com/neurosurgery/article-abstract/38/2/388/2888472 by University of Glasgow user on 28 October 2018 Mark R. McLaughlin, M.D., Hae-Dong Jho, M.D., Ph.D., Yang Kwon, M.D., Ph.D. ntracavernous carotid artery aneuIrysms (ICCAAns) occasionally rupture into the cavernous sinus (22, 24, 26), rarely rupture into the subarachnoid space (8, 16, 25), and almost never cause a subdural hematoma ““mcutiy For a rare patient, this may be a tui­ tion-saving device; however, them®) of using such an expensive technia, for a relatively short period of freedt from symptoms can still be debate Nevertheless, 1 think the technique h, merit and the report of its success is worth knowing. S ~ SDH from Intracavernous Aneurysm 389 stroke, and the transient ischemic at­ tacks resolved. A J Because the patient failed endovascu­ lar embolization (additional coil or bal­ loon embolization was thought to be too risky in the presence of intramural thrombi) and a large portion of the an­ eurysm remained patent, it appeared that the patient was still at risk for sub­ sequent hemorrhage and propagation of the SDH. Therefore, 2 days later, she underwent a left frontotemporal B craniotomy for clipping of the aneu­ rysm and evacuation of the SDH. Al­ FIGURE 1. Axial MR image showing though she tolerated BTO by both clin­ - acute left panhemispheric SD H and left ical and cerebral blood flow criteria, cavernous sinus mass. direct clipping was attempted in lieu of carotid sacrifice because of her young \ age and the known 4 to 5% incidence of \ late permanent deficits with occlusion, Ik even in patients tolerating BTO (13, 23). iB With temporary occlusion of the proxi­ i FIG U R E 3. A, left lateral ICA angio­ mal ICA in the neck and distal ICA at it gram demonstrating the ICCAAn. B, left the supraclinoid portion, the aneurys­ anteroposterior view ICA angiogram mal neck was successfully clipped, ap­ i demonstrating the ICCAAn. parently preserving the parent artery. a The total temporary occlusion time was a( A approximately 1 hour, during which d time no heparin was used. Despite clip­ li ping of the aneurysmal neck, intraoper­ P* ative arteriography showed complete k FIGURE 2. Coronal MR image demon­ occlusion of the ICA. Because the pa­ it strating the SDH originating from the tient had tolerated preoperative BTO, I ) ' J k dome of the cavernous sinus mass. the aneurysm was trapped with ligation * \ of the ICA in the neck and clipping of or. cular therapy (either intra-aneurysmal the ICA proximal to the ophthalmic ar­ aa embolization or carotid sacrifice), and ! tery. Another intraoperative arterio­ carotid ligation. Because the patient gram showed good collateral flow B & presented with a hemorrhage, observa­ from the opposite ICA. Somatosensory /a* tion was not an acceptable option. evoked potentials stayed stable through­ a Given that an open surgical approach out the procedure. The patient recov­ i would carry a relatively high risk of ered from anesthesia uneventfully and morbidity and mortality, endovascular did well for 2 days. ir. embolization was recommended as an On the 2nd postoperative day, the pa­ initial therapy. The patient opted for en­ tient developed progressive left hemi­ dovascular treatment, which was per­ spheric ischemic symptoms that began formed 2 days later, with detachable with mild right upper-extremity weak­ i coils (GDC; Target Therapeutics, San ness and dysphasia and progressed over Jose, CA). Twenty coils were placed in­ F IG U R E 4. A , left lateral ICA angio­ 2 hours to complete aphasia and right­ side the aneurysm and filled approxi­ gram demonstrating the placement of sided hemiplegia. An emergent CT scan t mately one-third of the aneurysmal coils within the aneurysm. B, left showed no postoperative hemorrhage, k space, but embolization was then termi­ anteroposterior view ICA angiogram and the ischemic symptoms were attrib­ demonstrating coil placement within it nated because no more coils were availuted to a left middle cerebral artery theday, aneurysm. tt able (Fig. 4,A and B). The next thromboembolic occlusion, prompting if placement of intra-aneurysmal coils was an emergent subsequent exploration. sensory transient ischemic attacks, last­ again attempted, but the procedure was After an arteriotomy was made at the ing 10 to 20 minutes, in her right upper aborted when intramural thrombi were M2 portion and after removal of the extremity. Intravenous heparin was in­ found. On arrival at the intensive care thrombus with a Fogarty catheter, excelstituted to prevent thromboembolic unit, the patient developed multiple A \r Neurosurgery, Vol. 38, No. 2, February 1996 Downloaded from https://academic.oup.com/neurosurgery/article-abstract/38/2/388/2888472 by University of Glasgow user on 28 October 2018 t 390 McLaughlin et al. D IS C U S S IO N James Adams (1), in 1869, was the first to report a patient who presented with ophthalmoplegia and was found to have an ICCAAn. Three years later, Roberts Bartholow (3) described the symptom complex presumed to be caused by ICCAAns. His description, although inclusive of some rare find­ ings, is accurate in elucidating the pro­ gression of symptoms as ICCAAns en­ large (3). Recently, Linskey et al. (19) reported a relatively large series con­ firming the predominantly benign nat­ ural history of ICCAAns. ICCAAns represent 3 to 5% of all in­ tracranial aneurysms and —14% of those arising from the carotid artery (10, 1820, 29, 30). The true incidence may be obscured, because some smaller ICCAAns rupture and present as carotid cavernous fistulae (22, 24, 26). ICCAAns can be asymptomatic or may cause symptoms of mass effect or hem­ orrhage. Because these aneurysms are enveloped by the dural walls of the cav­ ernous sinus, many of them remain asymptomatic until the surrounding structures are compressed. The mass ef­ fect usually manifests as ophthalmople­ gia, trigeminal pain, Horner's syn­ drome, or diminished visual acuity; hemorrhages can present as carotid cav­ ernous fistulae, epistaxis, or subarach­ noid hemorrhage. There are two case reports of ICCAAns presenting as SDHs. The incidence of SDHs caused by rup­ tured aneurysms is between 0.5 and 7.9% (4, 6, 7, 9, 11, 12, 21, 27, 28, 31, 32). Clarke and Walton (7) provided a grad­ ing system for this occurrence, based on the size and significance of the SDH. Two proposed mechanisms of SDH for­ mation from aneurysmal rupture are through dural adhesions to the arach­ noid membrane of the aneurysmal dome and direct disruption of the arach­ noid from the pressure wave of blood into the subdural space (7, 17). SDHs associated with ruptured aneu­ rysms of carotid origin are well docu­ mented (4-6, 9, 11, 12, 15, 25, 27, 28, 32). The majority of reports describe aneu­ rysmal rupture from extracavernous portions of the ICA and are most com­ monly located at the origin of the pos­ terior communicating artery (6, 7, 11, 12, 17, 27, 28, 32). There are only two re­ ported cases of SDHs caused by wholly ICCAAns, both of which were lethal (2, 14). To our knowledge, this report is the first in the literature of a patient surviv­ ing an SDH caused by an ICCAAn. Nishioka et al. (25) reported a case of subarachnoid hemorrhage caused by a wholly ICCAAn and theorized that the subarachnoid blood was caused by blood coursing along the carotid artery through a loose portion of the dense fibrous ring that fixes the artery wall at the roof of the cavernous sinus. No spe­ cific theories have been proposed for the cause of aneurysmal SDHs caused by ICCAAns, most likely because of the rarity of such an event. The cause of SDH from an ICCAAn could be the transdural rupture of an aneurysm that has exceeded not only the size of the cavernous sinus that invests it but also the tensile strength of the enveloping dura. Another possibility could be ero­ sion of the dural wall with subsequent rupture of the aneurysm into the sub­ dural space. The clinical history of our patient sug­ gested that she initially had rupture of an ICCAAn within the cavernous sinus and developed a carotid cavernous fis­ tula manifested by left eyelid and facial swelling, progressive ophthalmoplegia, Neurosurgery, Vol. 38, No. 2, February 1996 and facial numbness. Given the sudden * onset of headache 5 days later, it seerm likely that the aneurysm ruptured through the enveloping dura into the subdural space, causing the panhemi- I spheric acute SDH. MR imaging demon­ strates the SDH originating from the dome of the aneurysm and projects into the middle fossa. This finding is consistent with our theory that the an­ eurysmal pressure exceeded the tensile strength of the enveloping cavernous D d u ra. a a ACKN O W LED GM EN TS I We thank Helene Marion for editorial 01 assistance and Douglas Kondziolka, M.D., for helpful comments in the prep­ aration of this manuscript. ■r R eceiv ed , M arch 1, 1995. A ccep ted , Ju n e 5, 1995. R e p rin t re q u ests: Mark R. McLaughlin, M.D., D ep artm ent of Neurological Surgery, Suite B-400, Presbyterian University Hospi­ tal, U niversity of Pittsburgh Medical Center, 200 Lothrop Street, Pittsburgh, PA 152132582. Downloaded from https://academic.oup.com/neurosurgery/article-abstract/38/2/388/2888472 by University of Glasgow user on 28 October 2018 lent blood flow was visualized through the left middle cerebral artery and the brain became much more relaxed with good pulsations. Postoperatively, the patient's right-sided function improved dramatically, with only mildly impaired finger movement remaining from her previous hemiplegia. Her aphasia also improved significantly. A subsequent xenon-enhanced CT study showed good blood flow in the left middle cerebral artery distribution. Her residual dys­ phasia and impaired finger movements recovered almost completely after 6 weeks of physical therapy. At 2-year fol­ low-up, the patient had blindness but good extraocular movement of her left eye with minimal limitation in superior and inferior gaze, a dilated and fixed left pupil, subtle trigeminal hypalgesia and hypesthesia in the left VI and V2 distribution, and normal speech and motor function. ■1 q A *;■ REFEREN C ES :r 1. A d a m s J: A n e u r y s m of internal carotid in the n* c a v e r n o u s sinus cau sin g paralysis of the third, “1 d fourth, fifth, an d sixth nerves. Lancet 2:/68, > n 1869. 2. Barr H W K , B lack w o od W , Meadows SP: Intra­ •0'.: c a v e rn o u s ca ro tid an eu ry sm s: A clinical-patho­ vDO J, logical report. B rain 9 4 :6 0 7 -6 2 2 , 1971. 3. B arth o lo w R: A n e u ris m s of the arteries at the !<* I base of the brain: Their symptomatology, diag­ a nosis an d treatm en t. A m J Med Sci 64:373-386, Cl 1872. 4. Bassett RC, L e m m e n LJ: Subdural hematoma asso ciated with bleeding i n t r a c r a n i a l aneurysm. T' J N eurosurg 9 :4 4 3 - 4 5 0 , 1952. ^ 5. B oop W C Jr, C h o u SN, French LA: Ruptured ob in tracran ial a n e u r y s m complicated by subdural n h e m a to m a . J N eurosurg 18:834-836, 1961. M b 6. C a se re co rd s of the M assachusetts General Hos Into pital. N En g l J M ed 2 2 6 :6 1 3 -6 1 6 , 1942. N 7. C lark e E, W alto n JN: Subdural h e m a t o m a com cl plicating intracranial aneu rysm and angion^* B rain 7 6 :3 7 8 - 4 0 4 , 1953. 8. D ay A L , R h oton A L Jr: Aneurysm s and arteno lA ii 9 || v e n o u s fistula of the intracavernous carotid ar tery and its b ran ch es, in Y oum ans JR (ec^ ^Ll rological Surgery. Philadelphia, W.B. Saun efS r-% it C o ., 1982, ed 2, vol 3, p p 1764-1785. 9. E g g e rs FM , T o m sick TA , Lukin RR> Cham A A: R eco gn itio n of subdural h e m a to m a - o n d a r y to ru p tu re d an e u ry sm bv compute m o g r a p h y . Com put R adiol 6:309—313, 198-- I SDH from Intracavernous Aneurysm SI 10. Fox Aj, Vinuela F, Pelz DM, Peerless SJ, F e r g u ­ 2 7 . R yan HP: R u p tu re of intracranial a n e u ry s m son GG, Drake CG, D ebrun G: U se of d e t a c h ­ c a u sin g a c u te su b d u ral h e m a to m a , in fratem p o ­ a b l e balloon for proxim al artery o cclu sio n in the ral h e m a to m a , an d d ecereb ration , with s u r v iv ­ '‘I treatment of unclippable cereb ral a n e u ry s m s . u J Neurosurg 66:40—4:6, 1987. ar 11 Golden J, Odom GL, W o o d h a ll B: S u b d u ral he­ I matoma following su b arach n o id h e m o rrh a g e . ro: Arch Neurol Psychiatry 6 9 :4 8 6 - 4 8 9 , 1953. 1 12. Handel SF, Perpetuo FO, H a n d e l C H : Su b d u ral id hematomas due to ru p tu re d t: rysms: Angiographic d iagn o sis an d potential cerebral al: C a s e report. N eurosurgery 5 :6 9 8 - 7 0 0 , 1979. 28 du ral h e m a to m a and uncal herniation d u e to ru p tu red intracranial a n e u ry sm . Neurosurgery 3 : 6 6 - 6 7 , 1978. 29 1969. 30 509, 1978. rotid an d vertebral fistulas and in tracav ern o u s K, Dormandy B, Bell J, C a h a n L, Bentson JR: Intravascular detachable balloon em b olizatio n a n e u ry s m s . N euroradiology 2 4 :1 3 - 2 5 , 1982. 31 of intracranial aneurysm s: Indications an d tech ­ S tran g RR, Tovi D, H u g o sso n R: Subdural he­ m a to m a s resulting from the ru p tu re of in tracra­ niques. Acta Radiol 3 6 9 :5 9 4 - 5 9 6 , 1986. nial arterial a n eu ry sm s. Acta C h ir Scand 121: 14. Hodes JE, Fletcher W A , G o o d m a n DF, H o y t ec Scialfa C , Vaghi A, Valsecchi F, Bernardi L, T o n o n C: N eu ro rad iological treatm en t of c a ­ 13. Higashida RT, H ieshim a GB, H alb ach V, G o to I Sahs A L , Perret GE, Locksley HB (eds): Intracra- nial Aneurysms and Subarachnoid Hemorrhage: A Cooperative Study. Philadelphia, J.B. Lippincott, aneu­ pitfall for CT. A JR Am J Roentgenol 1 3 0 :5 0 7 - Sachs E, Bernat JL: R ecovery from acu te su b ­ WF: Rupture of cav ern o u s carotid a rte ry a n e u ­ rysm causing subdural h e m a to m a and death: id. Case report. J Neurosurg 6 9 :6 1 7 - 6 1 9 , 1988. he 15. Jaeger R: Aneurysm of the intracranial carotid artery: Syndrome of frontal h e a d a c h e with o c ­ 3 4 5 - 3 5 0 , 1961. 32 W e ir B, M yles T, Kahn M, M arou n F, M alloy D, Benoit B, M cD e rm o tt M, C o c h ra n e D, M oh r G, F e rg u so n G, Durity F: M a n a g e m e n t of acu te su b d u ral h e m a to m a s from a n eu ry sm al rupture. Can J N eurol Sci 1 1 :3 7 1 -3 7 6 , 1984. ulomotor nerve paralysis. JA M A 1 4 2 :3 0 4 - 3 1 0 , 1950. La S a n e u ry s m s of the internal carotid arterv J in the c a v e r n o u s sinus. B rJ Surg 2 6 :2 6 7 -3 0 2 , 1938. 17. Kondziolka D, Bernstein M, ter B ru g g e K, Schutz H: Acute subdural h e m a to m a from r u p ­ tured posterior co m m u n ica tin g a rtery aneu­ rysm. Neurosurgery 2 2 :1 5 1 - 1 5 4 , 1988. 18. Krayenbuhl H: Klassifikation und klinische Symptomatologie der zerebralen A n e u ry s m e n . Ophthalmologica 1 6 7 :1 2 2 -1 6 4 , 1973. 19. Linskey ME, Sekhar LN , H irsch W L , Y o n a s H, Horton JA: A neu rysm s of the in tra c a v e rn o u s oti carotid artery: Natural history and indications tt for treatment. Neurosurgery 2 6 :9 3 3 - 9 3 8 , 1990. nc 20. Locksley HB: Natural history of su b a ra ch n o id hemorrhage, intracranial a n e u ry sm s , and a r te ­ 5t lid riovenous malformation. J N eurosurg 2 5 : 2 1 9 239, 1966. I.' 21. Logue V: Chronic subdural effusions, in Feiling A (ed): Modern Trends in Neurology. L o n d o n , Butterworth and Co., 1951, pp 3 6 3 - 3 9 0 . 6i 22. Lombardi G, Passerini A, M igliavacca F: Intracavernous aneurysm s of the internal carotid a r ­ Iw tery. A JR Am J Roentgenol 8 9 :3 6 1 - 3 7 1 , 1963. 31 23. Mathis JM, Barr JD, H orton JA: T h erap eu tic I occlusion of major vessels, test occlusion and techniques. Neurosurg C lin N Am 5 :3 9 3 - 4 0 1 , 1994. I! -4 Meadows SP: Intracavernous aneurysm s of the 4 internal carotid artery, their clinical features 4 and natural history. Arch O p hthalm ol 6 2 : 5 6 6 !tO 574, 1959. J* 25‘ Nlshioka T Kondo A, A o y a m a I, N in K, T akahashi J. Subarachnoid s (6 1! h e m o rrh a g e possibly caused by a saccular carotid a rte ry a n e u ry s m V 'thin the cavernous sinus: C a se report. J Neu- The patient recently presented to us, 40 months after surgery, for severe headaches associated with malignant hypertension. A neurological examina­ tion revealed no new abnormalities since her last follow-up, and a lumbar puncture and a computed tomographic scan did not reveal any infection or hemorrhage. An old left middle cerebral artery infarct was identified by com­ puted tomography, despite the absence of any ischemic symptoms since her last follow-up. Repeat angiography showed an occluded left internal carotid artery with obliteration of the aneurysm. There was collateralization of the left middle cerebral artery territories via the left posterior communicating artery and the leptomeninges. After the adjustment of the patient's antihypertensive regimen and better control of her blood pressure, her headaches resolved and she was dis­ charged home. Presumably, she devel­ oped adequate vascular collateralization after embolectomy of her middle cere­ bral artery in 1992 to obviate any overt deficits from the infarct, demonstrated by computed tomography, which she sustained during her interim follow-up. rosurg 73:301-304, 1990. Obrador S, Gom ez-Bueno J, Silvela J: Sponta neUs carotid-cavernous fistula p ro d u ce d by rup- at* t»] I AD D EN D UM ured aneurysm of the m e n in g o h y p o p h y se a l ■anch of the internal carotid artery: C a se re- PUrt J Neurosurg 4 0 :5 3 9 -5 4 3 , 1974. CO M M EN TS True intracavernous aneurysms rarely rupture into the subarachnoid or Neurosurgery, Vol. 38, No. 2, February 1996 subdural space, presumably because an aneurysm in this location typically projects hemodynamically beneath the brain toward the superior orbital fissure and its own arterial wall is further sup­ ported by the venous walls of the cav­ ernous sinus and the overlying dural membranes. When extension beyond the sinus does occur, it is usually because the aneurysm has gradually eroded the overlying dura, such that a "teat" projects through the dura into the subarachnoid space. One site where this occurs is at the posterior bend, just as the artery ascends from the foramen lacerum and angles forward as the horizontal segment. The hemodynam­ ics at this site project the aneurysm's pul­ satile forces upwards toward the dura si­ nus roof superiorly, rather than anteriorly beneath the anterior clinoid process. A second (and much more common) site is the anterior vertical segment, a segment whose terminus is clearly extracavemous and is also called the clinoidal segment. This case does not represent either of those two lesions but represents a true horizontal segment giant intracavernous aneurysm, making it a truly rare entity. Presumably, as the authors suggest, rupture of this aneurysm produced a high-flow carotid cavernous fistula, which then extended via parasellar ve­ nous channels laterally into the sub­ dural space. This extension can proba­ bly be appreciated on Figure 2 of the article, where a small lateral "teat" of the aneurysm can be seen in direct con­ tinuity with the acute subdural hema­ toma (SDH). This case also demonstrates that there are risks of interventional neuroradiology, particularly in large-volume aneu­ rysms that are incompletely treated. Presumably, the placement of coils in this lesion led to intra-aneurysmal thrombosis that, because the aneurysm had a wide neck, allowed the clots easy access to the distal circulation. The au­ thors have done an excellent job with their acute recognition and intervention for the embolus, and they present a strong case for aggressive early inter­ vention for acute stroke in which the middle cerebral artery is occluded. Clearly, this case represents one in which the restoration of flow in that Downloaded from https://academic.oup.com/neurosurgery/article-abstract/38/2/388/2888472 by University of Glasgow user on 28 October 2018 16. Jefferson G: On saccular 391 392 McLaughlin et al vessel done in a timely fashion reversed an otherwise catastrophic situation. Arthur L. Day Gainesville, Florida Familial Colloid Cyst of the Third Ventricle: Case Report and Review of Associated Conditions Paul T. Akins, M.D., Ph.D., Richard Roberts, M.D., William S. Coxe, M.D., Bruce A. Kaufman, M.D. Departments of Neurology and Neurological Surgery, Washington University School of Medicine, St. Louis, Missouri THE CASES OF a father and his son who were diagnosed with pathologically confirmed colloid cysts of the third ventricle are presented. The familial occurrence of this tumor is rare and suggests that genetic factors may play a role in its formation. Consistent with the concept that the cyst originates as a developmental abnormality, it is associated with a variety of congenital defects. The conditions that are associated with these tumors are discussed. (Neurosurgery 38:392-395, 1996) Key words: Brain neoplasm, Colloid cyst, Third ventricle olloid cysts of the third ventricle are rare tumors presenting primarily in adults with hydrocephalus and headC ache. They arise in the anterior portion of the third ventricle and obstruct the foramina of Monro. Their tissue deriva­ Neurosurgery, Vol. 38, No. 2, February 1996 less than that for direct surgical treatnv of these aneurysms. The probable cause of the SDH w, the rupture of the aneurysm and tlv the extension of the hematoma in t! subdural space along the convexity aiv the tentorium, which rarely occurs r intracavernous aneurysms. To the best of our knowledge, this is the only n ported case of a patient surviving such, condition. This case report details the nuances of controversial treatment is­ sues for intracavernous aneurysm andis a valuable addition to the literature. John M. Tew, Jr, Jeffrey J. Larson Cincinnati, Ohio 1. L arso n J], T e w JM, T om sick TA, van Loveren HR: T re a tm e n t of a n eu ry sm s of the internal caro tid a rte ry by intravascular balloon occlu­ sion: L o n g -te r m follow -up of 58 patients. Neu­ r o s u r g e r y 3 6 :2 3 - 3 0 , 1995. tion is debated, but their congenital na­ ture is generally accepted (6, 16-18,23 Possible sources for these tumors in­ clude the paraphysis (27), choroid plexus (26), ependyma (6), primitive neuroectoderm (16), and primitive endodermal tissue (17, 18), but ultrastructural and immunohistochemica evidence argues against a simple cho­ roid plexus or ependymal origin (6,1