324 Omahen and Findlay After recanalization of the SSS, however, it may re-occlude as in the present case. This is a rare case in which surgically recanalized SSS re-occluded during the postoperative course. One needs to know that re-occlusion of the SSS may occur possibly due to a change in the surrounding structure and hypercoagulopathy. Journal of Clinical Neuroscience (2004) 11(3), 324–328 0967-5865/$ - see front matter ª 2003 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2003.06.002 Keywords: intracranial aneurysm, basilar artery, giant aneurysm, fusiform aneurysm, parent vessel ligation, ischemic attack, transient, brainstem compression Received 29 March 2003 Accepted 6 June 2003 REFERENCES 1. Caudill CM, French LA. Increased intracranial pressure following compression of the superior sagittal sinus. Neurology 1953; 3: 231–233. 2. Du Plessis JJ. Depressed skull fracture involving the superior sagittal sinus as a cause of persistent raised intracranial pressure: a case report. J Trauma 1993; 34: 290–292. 3. Meltzer H, LoSasso B, Sobo E. Depressed occipital skull fracture with associated sagittal sinus occlusion. J Trauma 2000; 49: 981. 4. Uzan M, Ciplak N, Dashti SG, Bozkus H, Erdincler P, Akman C. Depressed skull fracture overlying the superior sagittal sinus as a cause of benign intracranial hypertension. J Neurosurg 1998; 88: 598–600. 5. Borgstrom S, Gelin LE, Zederfeldt B. The formation of vein thrombi following tissue injury, An experimental study in rabbits. Act Chirurg Scand (Suppl) 1959; 247: 3–36. 6. Gates PG, Barnett HJM. Venous Disease: Cortical Veins and Sinuses. Stroke. Churchill Livingstone, New York; 1986;2:731–743. 7. Kannuki S, Cervos-Navarro J, Matsumoto K. 38 autopsied cerebral sinus-vein thrombosis. Neurol Surg 1990; 42: 781–787. A giant fusiform basilar aneurysm treated by bilateral vertebral artery occlusion Correspondence to: J. Max Findlay, Clinical Professor, Division of Neurosurgery, Department of Surgery, University of Alberta, 2D1.02 WMHSC, 8440-112 Street, Edmonton, Alta., Canada T6G 2B7. Tel.: +1-780-407-3548; Fax: +1-780-407-8203; E-mail: mfindlay@cha.ab.ca INTRODUCTION It has been estimated that as many as 80% of patients with symptomatic and untreated giant aneurysms become severely disabled or die within 5 years of presentation.1 Presenting most commonly with either brainstem compression (including blockage of cerebrospinal fluid [CSF] flow and hydrocephalus) or ischemia,2 these aneurysms can also rupture.3 Elimination of these aneurysms is difficult because their fusiform morphology usually prevents maintenance or reconstruction of the parent vessel, leaving as the only option proximal parent arterial occlusion (sometimes referred to as “Hunterian ligation” in older literature).3 We present the case of a man who had become unable to walk, maintain a safe airway, or swallow due to severe brainstem compression by a large and growing vertebrobasilar fusiform aneurysm, who was treated successfully with bilateral vertebral artery occlusion. CASE PRESENTATION David A. Omahen BSC MD, J. Max Findlay MD PHD Division of Neurosurgery, Department of Surgery, University of Alberta, Edmonton, Canada T6G 2B7 Summary Objective and importance. Fusiform aneurysms of the vertebrobasilar arteries that progressively enlarge causing symptomatic brainstem compression are dangerous and their treatment is difficult. A patient with such an aneurysm treated successfully with staged, microsurgical occlusions of the proximal vertebral arteries is described, and the literature pertaining to this rare condition is briefly reviewed. Clinical presentation. A 48-year-old man with a fusiform basilar trunk aneurysm of uncertain etiology presented initially with transient ischemic attacks (TIAs) of the posterior circulation that ceased with anticoagulation. Four years later he presented again with progressive ataxia, dysphagia and dysphonia due to considerable enlargement of the aneurysm causing brainstem compression. Intervention. Staged microsurgical vertebral artery occlusions proximal to the aneurysm were performed. The second (left) vertebral artery was clipped only after the patient passed its temporary occlusion with an endovascular test balloon. The aneurysm subsequently thrombosed, the distal basilar artery kept patent by a single (left) posterior communicating artery. The patient’s clinical condition improved markedly over a number of months as the aneurysm mass atrophied. Conclusion. Giant vertebrobasilar aneurysms are rare but treacherous lesions, sometimes justifying aggressive management. Carefully selected patients with progressive and severe symptoms due to brainstem compression may tolerate proximal vertebral artery occlusions, provided there is adequate collateral flow to the basilar termination and all of its perforating branches. ª 2003 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2004) 11(3) A 48-year-old Caucasian male presented in 1998 after four discrete episodes of ataxia combined with left-sided weakness, each attack lasting minutes and resolving completely. The patient was a Fig. 1 Axial CT scan of the posterior fossa and base of the brain showing a fusiform and partly calcified aneurysmal dilatation of the basilar artery. ª 2003 Elsevier Ltd. All rights reserved. Treatment of a giant fusiform basilar aneurysm Fig. 2 Digital subtraction right vertebral angiogram showing an irregular fusiform aneurysm of the proximal to mid basilar artery. 325 Fig. 4 Saggital T1-weighted MRI scan showing severe brain stem distortion from a giant, ventrally placed basilar aneurysm. Fig. 3 CT angiogram demonstrating the relationship of the elongated and aneurysmal basilar artery to the skull base. reformed cigarette smoker and had recently begun treatment for hypertension, but his past health was otherwise unremarkable. There was no history of connective tissue disease or systemic vasculopathy. A computed tomographic (CT) scan suggested ectasia of the vertebrobasilar arteries (Fig. 1), and a large fusiform aneurysm of the basilar artery was confirmed by digital subtraction angiography and CT-angiography (Figs. 2 and 3). It was noted that the patient had a dominant left-sided posterior inferior cerebellar artery (PICA), supplying both the left and right inferior cerebellar hemispheres. The clinical diagnosis was transient brainstem ischemia resulting from intraaneurysmal thrombosis or thromboembolism, and the patient was treated with coumadin. The patient remained well for 4 years, but presented again in 2002 following several months of worsening balance and dysphagia. On examination the patient demonstrated severe truncal ª 2003 Elsevier Ltd. All rights reserved. Fig. 5 Axial T2-weighted MRI scan again showing severe brain stem distortion from a now giant fusiform aneurysm. The presence of laminated intraluminal thrombus is seen as layers of mixed signal intensity. ataxia, moderate dysarthria and impaired gag reflexes. Magnetic resonance imaging (MRI) (Figs. 4 and 5) showed considerable aneurysm enlargement, to over 3 cm in diameter. The aneurysm contained laminated thrombus and was causing severe brainstem compression and obstructive hydrocephalus (Fig. 6) Despite ventriculoperitoneal shunting, the patient’s condition deteriorated. Over several weeks he acquired aspiration pneumonia requiring mechanical ventilation and tracheostomy. A percutaneous enteral feeding tube was also necessary. An “Alcock Test” was performed to test for angiographic patency of the posterior communicating arteries. This test involves Journal of Clinical Neuroscience (2004) 11(3) 326 Omahen and Findlay Fig. 8 Left carotid angiogram showing filling of the terminal basilar artery in both posterior cerebral arteries via the left posterior communicating artery (arrow). Fig. 6 CT scan prior to insertion of ventriculoperitoneal shunt, showing lateral ventriculomegally. manual compression of each cervical carotid artery during contrast injection of a vertebral artery; if present and of sufficient size (i.e., >1 mm in diameter) the posterior communicating artery will be visualized during this maneuver supplying contrast to the supraclinoid carotid artery and its branches.1 The presence of a posterior communicating artery suggests the possibility that the basilar termination and its branches will be provided collateral Fig. 7 Left vertebral angiogram following left vertebral artery occlusion immediately distal to dominant left posterior inferior cerebellar artery supplying the inferior aspect of both cerebellar hemispheres (arrows). Journal of Clinical Neuroscience (2004) 11(3) blood flow from the carotid in the event of deliberate proximal basilar artery or bilateral vertebral artery occlusion. Our patient had a patent left posterior communicating artery, which opacified the left middle cerebral artery on temporary manual occlusion of the left common carotid artery and vertebral artery contrast injection. Due to the patient’s severe clinical deterioration, an attempt at staged bilateral vertebral artery occlusions was recommended in the hope that aneurysm thrombosis and gradual shrinkage would decompress the brainstem. A posterior fossa exposure revealed ectatic vertebral arteries, and the left vertebral artery was occluded with a clip just distal to the dominant PICA and proximal to the visualized fusiform aneurysm. Endovascular permanent balloon occlusion of this vertebral artery was not performed because it was not considered possible to maintain patency of the PICA with this technique. The patient tolerated the procedure without neurological change. Several days later an endovascular test balloon occlusion of the right vertebral artery was performed with the patient awake and under full heparinization. The patient remained neurologically unchanged over 15 min of right vertebral artery occlusion, at which time the test balloon was deflated and withdrawn. It therefore appeared that the patient would tolerate hemodynamic loss of both vertebral arteries proximal to the giant basilar aneurysm. The following day the patient was returned to the operating room where clip ligation of the right vertebral artery just distal to a large brainstem perforator (appreciated at the time of his first surgery) was performed. Postoperative angiography showed occlusion of the vertebral arteries proximal to the basilar aneurysm, continued filling of the dominant PICA (Fig. 7), and filling of the distal basilar artery and both posterior cerebral arteries via the left internal carotid artery and its posterior communicating artery branch (Fig. 8). Follow-up CT scanning has shown aneurysm thrombosis and shrinkage. Over 8 months of follow-up to the time of this writing the patient has had his tracheostomy discontinued, has resumed normal feeding, has returned home and is ambulatory. Clopidogrel, which had been commenced prior to vertebral artery occluª 2003 Elsevier Ltd. All rights reserved. Treatment of a giant fusiform basilar aneurysm sions, was changed to aspirin (325 mg twice daily) 3 months following his surgery. DISCUSSION Fusiform aneurysms comprise less than 1% of vertebrobasilar aneurysms in some series,4;5 however the majority of giant aneurysms in this location are fusiform in shape.3 In many cases no identifiable underlying cause such as atherosclerosis or connective tissue disease is found.6 Pathological studies show attenuation of the smooth muscle layer of the arterial wall, with fragmentation of the elastic lamina.7 A similar disruption of the internal elastic lamina occurs in atherosclerosis.8 Acute and chronic inflammatory changes and atheromatous degeneration in the walls of some aneurysms have been documented.9 Despite this, many dispute a connection between atherosclerosis and aneurysm formation in all cases.2;10 Some authors have postulated the existence of an arteriopathy sharing the characteristic defect in the elastic lamina, but etiologically distinct from atherosclerosis.11 Intrinsic congenital defects in the internal elastic membrane and absence of the tunica media may play a role, especially in the pediatric population.12 De novo formation of fusiform vertebrobasilar aneurysms has been described in three children.13 Conditions which weaken the vessel wall such as collagen vascular disease,3 fibromuscular dysplasia,14 or maltase deficiency15 may also contribute. Hypertension is commonly associated with these lesions,16 and arterial dissection is presumed to play a role in the pathogenesis of some.16 Radiological studies of the natural history of incidentally discovered fusiform vertebrobasilar aneurysms have shown that hemorrhage into the vessel wall is associated with enlargement.17 In general, the natural history of giant aneurysms is that of progressive morbidity and mortality.18 Yasui et al. describe four patients with incidentally discovered fusiform aneurysms followed for a mean of 3.5 years. Two of the aneurysms increased in size, both associated with MRI-demonstrated hemorrhage into the vessel wall. When ischemic symptoms are present, anticoagulation is commonly used.5;19 Some authors advocate antiplatelet agents for all patients with fusiform vertebrobasilar aneurysms, regardless of the presence of ischemic symptoms.20 Many surgical strategies have been attempted including wrapping of the aneurysm wall with various materials to reinforce it, vertebral artery occlusion (both single and bilateral), basilar artery occlusion, aneurysm resection with basilar artery reconstruction and trapping of the aneurysm (occlusion of the parent vessel proximal and distal to the aneurysm).1;3;16 Another technique used is extracranial–intracranial bypass followed by delayed endovascular occlusion of the parent artery.21 Sullivan et al.22 described trapping a giant basilar aneurysm followed by partial basilar resection and a cervical internal carotid-distal basilar saphenous vein graft, during profound hypothermia and circulatory arrest. Endovascular balloon occlusion, either alone,23 or in combination with surgical clipping, stenting and aneurysm coiling24;25 have been tried. Placement of a porous stent across a fusiform aneurysm has also been successfully performed.25 Finally, vessel transposition has been used to treat lower cranial nerve palsies due to compression.16 Results using any of these procedures have been highly variable. The benchmark case-series of giant fusiform VB aneurysms is that of Drake and Peerless.3 Their series of 120 surgically treated aneurysms contained 32 patients with basilar artery aneurysms. Bilateral VA occlusion was performed on three patients; one patient had an excellent outcome and two died. Another 17 patients underwent basilar occlusion; 12 had excellent outcomes, three had good outcomes and two died. Twenty-five percent of patients treated in this manner suffer a major neurological deficit within ª 2003 Elsevier Ltd. All rights reserved. 327 the first 4 weeks.1 Anson et al. treated 13 basilar, six vertebral and one PICA fusiform aneurysm, with 65% of patients experiencing good outcomes. Proximal parent artery occlusion usually leads to obliterative thrombosis of the aneurysm,3 usually within 1 month.1 The closer the site of occlusion is to the aneurysm, the more likely complete thrombosis will occur.1 The risk of infarction increases with the length of basilar artery involved,3 and with aneurysms more distally located along the vertebrobasilar complex.1 Tolerance of proximal arterial occlusion depends on collateral flow to distal branches. The posterior communicating artery size is an important predictor of success of basilar occlusion,1;3;26 with a posterior communicating artery diameter greater than 1 mm significantly related to tolerance of basilar artery occlusion (p ¼ 0:004), and a favorable long-term clinical outcome.1 Other predictors of tolerance include normal baseline cerebral blood flow and tolerance of balloon occlusion.27 Perforating vessels from the basilar artery supplying the pons have traditionally been thought of as end-arteries.28 The fact that brainstem infarcts can be avoided when perforating vessels arising from the walls of aneurysms are thrombosed have led to the speculation that collateral vessels exist within the brainstem.1 It may be that fusiform basilar aneurysms which involve the entire circumference of the vessel and contain laminated thrombus have developed collateral flow, since the ostia of perforating vessels have already been obliterated with thrombus. In contrast, eccentrically positioned aneurysms with areas of native vessel wall still exposed to the lumen may pose greater risks for ischemic complications, since the perforating vessels are still patent and collateral flow has not been recruited. In the past, brainstem compression was treated by aneurysm trapping and resection of either the aneurysmal segment or thrombus contained within it.1 More recently it has been appreciated that reversal of compressive symptoms can result from proximal occlusion or trapping alone, due either to elimination of the pulsatile “water-hammer” effect of the aneurysm mass on adjacent neural structures or to a delayed and progressive shrinkage of the thrombosed aneurysm.1;24 Endovascular techniques have gained an important role in the management of intracranial aneurysms.27;32–34 Temporary test balloon occlusion can assess collateral flow beyond an aneurysm and predict the hemodynamic consequences of parent artery occlusion, although not the thromboembolic risks.1 Permanent occlusion using detachable balloons or detachable coils are useful, noninvasive methods of achieving parent artery occlusion, providing the balloon or coil mass (normally a number of millimeters in length) does not cover and occlude important branch vessels. Detachable coils are less useful within partially thrombosed aneurysms because of their tendency to sink within intra-aneurysmal clot over time, allowing recanalization.29–31 In the management of the patient described in this report, microsurgical clip occlusion was selected rather than endovascular vertebral artery occlusion in order to accurately preserve the dominant left PICA and a maximum number of perforating vessels arising from the distal vertebral arteries. CONCLUSION A patient with a giant fusiform basilar aneurysm causing hydrocephalus and progressive brainstem compression was treated by staged bilateral microsurgical vertebral artery occlusions leading to aneurysm thrombosis. This was possible because of the presence of a posterior communicating artery adequate to supply the basilar termination, as well as intra-aneurysmal clot that had already occluded perforating branches arising from the aneurysm wall. Journal of Clinical Neuroscience (2004) 11(3) 328 Jaiswal et al. ACKNOWLEDGEMENTS This case was presented at the 2002 joint meeting of the Australian Association of Neurologists and the Canadian Congress of Neuroscience. The authors thank Ms. Laurie Arneson for her assistance in the preparation of this manuscript. REFERENCES 1. Steinberg GK, Drake CG, Peerless SJ. Deliberate basilar or vertebral artery occlusion in the treatment of intracranial aneurysms. Immediate results and longterm outcome in 201 patients. J Neurosurg 1993; 79: 161–173. 2. Findlay JM, Hao C, Emery D. Non-atherosclerotic fusiform cerebral aneurysms. Can J Neurol Sci 2002; 29: 41–48. 3. Drake CG, Peerless SJ. Giant fusiform intracranial aneurysms: review of 120 patients treated surgically from 1965 to 1992. J Neurosurg 1997; 87: 141–162. 4. Pia HW. Classification of vertebrobasilar aneurysms. Acta Neurochir (Wien) 1979; 47: 3–30. 5. Yu YL, Moseley IF, Pullicino P, McDonald WI. The clinical picture of ectasia of the intracerebral arteries. J Neurol Neurosurg Psychiatry 1982; 45: 29–36. 6. Campdelacreu J, Munoz E, Blanco Y, Obach V, Chamorro A. Antithrombotic treatment of fusiform aneurysms of the basilar artery. Neurologia 2002; 17: 58–61. 7. De Caro R, Parenti A, Munari PF. Megalodolichobasilaris: the effect of atherosclerosis on a previously weakened arterial wall? Clin Neuropathol 1996; 15: 187–191. 8. Nakayama Y, Tanaka A, Kumate S, Tomonaga M, Takebayashi S. Giant fusiform aneurysm of the basilar artery: consideration of its pathogenesis. Surg Neurol 1999; 51: 140–145. 9. Shokunbi MT, Vinters HV, Kaufmann JC. Fusiform intracranial aneurysms. Clinicopathologic features. Surg Neurol 1988; 29: 263–270. 10. Sacks JG, Lindenburg R. Dolicho-ectatic intracranial arteries: symptomatology and pathogenesis of arterial elongation and distention. Johns Hopkins Med J 1969; 125: 95–106. 11. Steel JG, Thomas HA, Strollo PJ. Fusiform basilar aneurysm as a cause of embolic stroke. Stroke 1982; 13: 712–716. 12. van Donselaar CA, Stefanko SZ, van der Kwast TH, Arts WF, Koudstaal PJ. Basilar artery giant fusiform aneurysms caused by congenital defect of the internal elastic lamina and media. Clin Neuropathol 1988; 7: 68–72. 13. Johnston SC, Halbach VV, Smith WS, Gress DR. Rapid development of giant fusiform cerebral aneurysms in angiographically normal vessels. Neurology 1998; 50: 1163–1166. 14. Hirsch CS, Roessmann U. Arterial dysplasia with ruptured basilar artery aneurysm: report of a case. Hum Pathol 1975; 6: 749–758. 15. Matsuoka Y, Senda Y, Hirayama M, Matsui T, Takahashi A. Late-onset acid maltase deficiency associated with intracranial aneurysm. J Neurol 1988; 235: 371–373. 16. Anson JA, Lawton MT, Spetzler RF. Characteristics and surgical treatment of dolichoectatic and fusiform aneurysms. J Neurosurg 1996; 84: 185–193. 17. Yasui T, Komiyama M, Iwai Y, Yamanaka K, Nishikawa M, Morikawa T. Evolution of incidentally-discovered fusiform aneurysms of the vertebrobasilar arterial system: neuroimaging features suggesting progressive aneurysm growth. Neurol Med Chir (Tokyo) 2001; 41: 523–527, discussion 528. 18. Barrow DL, Alleyne C. Natural history of giant intracranial aneurysms and indications for intervention. Clin Neurosurg 1995; 42: 214–244. 19. Echiverri HC, Rubino FA, Gupta SR, Gujrati M. Fusiform aneurysm of the vertebrobasilar arterial system. Stroke 1989; 20: 1741–1747. 20. Nishizaki T, Tamaki N, Takeda N, Shirakuni T, Kondoh T, Matsumoto S. Dolichoectatic basilar artery: a review of 23 cases. Stroke 1986; 17: 1277–1281. 21. Hacein-Bey L, Connolly Jr ES, Duong H, Vang MC, Lazar RM, Marshall RS, Young WL, Solomon RA, Pile-Spellman J. Treatment of inoperable carotid aneurysms with endovascular carotid occlusion after extracranial–intracranial bypass surgery. Neurosurgery 1997; 41: 1225–1231, discussion 1231–1234. 22. Sullivan BJ, Sekhar LN, Duong DH, Mergner G, Alyano D. Profound hypothermia and circulatory arrest with skull base approaches for treatment of complex posterior circulation aneurysms. Acta Neurochir (Wien) 1999; 141: 1–11, discussion 11–12. 23. Aymard A, Hodes JE, Rufenacht D, Merland JJ. Endovascular treatment of a giant fusiform aneurysm of the entire basilar artery. AJNR Am J Neuroradiol 1992; 13: 1143–1146. 24. Kato N, Ezura M, Takahashi A, Yoshimoto T. Intra-aneurysmal embolization and parent artery trapping to treat a giant partial thrombosed vertebral artery aneurysm after surgical proximal clipping. No Shinkei Geka 2000; 28: 817–822. Journal of Clinical Neuroscience (2004) 11(3) 25. Higashida RT, Smith W, Gress D, Urwin R, Dowd CF, Balousek PA, Halbach VV. Intravascular stent and endovascular coil placement for a ruptured fusiform aneurysm of the basilar artery. Case report and review of the literature. J Neurosurg 1997; 87: 944–949. 26. Pelz DM, Vinuela F, Fox AJ, Drake CG. Vertebrobasilar occlusion therapy of giant aneurysms. Significance of angiographic morphology of the posterior communicating arteries. J Neurosurg 1984; 60: 560–565. 27. Hodes JE, Aymard A, Gobin YP, Rufenacht D, Bien S, Reizine D, Gaston A, Merland JJ. Endovascular occlusion of intracranial vessels for curative treatment of unclippable aneurysms: report of 16 cases. J Neurosurg 1991; 75: 694–701. 28. Parent A. Carpenter’s Human Neuroanatomy. Williams & Wilkins, Philadelphia 1996. 29. Gruber A, Killer M, Bavinzski G, Richling B. Clinical and angiographic results of endosaccular coiling treatment of giant and very large intracranial aneurysms: a 7-year, single-center experience. Neurosurgery 1999; 45: 793–803, discussion 803–804. 30. Malisch TW, Guglielmi G, Vinuela F, Duckwiler G, Gobin YP, Martin NA, Frazee JG. Intracranial aneurysms treated with the Guglielmi detachable coil: midterm clinical results in a consecutive series of 100 patients. J Neurosurg 1997; 87: 176–183. 31. Vinuela F, Duckwiler G, Mawad M. Guglielmi detachable coil embolization of acute intracranial aneurysm: perioperative anatomical and clinical outcome in 403 patients. J Neurosurg 1997; 86: 475–482. 32. Hoh BL, Putman CM, Budzik RF, Carter BS, Ogilvy CS. Combined surgical and endovascular techniques of flow alteration to treat fusiform and complex wide-necked intracranial aneurysms that are unsuitable for clipping or coil embolization. J Neurosurg 2001; 95: 24–35. 33. Gobin YP, Vinuela F, Gurian JH, Guglielmi G, Duckwiler GR, Massoud TF, Martin NA. Treatment of large and giant fusiform intracranial aneurysms with Guglielmi detachable coils. J Neurosurg 1996; 84: 55–62. 34. Boardman P, Byrne JV. Giant fusiform basilar artery aneurysm: endovascular treatment by flow reversal in the basilar artery. Br J Radiol 1998; 71: 332–335. Primary central nervous lymphoma presenting as bilateral cerebellopontine angle lesions: a rare case report Awadhesh K. Jaiswal1 MBBS, A.K. Mahapatra1 MCH DNB, M.C. Sharma2 MD 1 Department of Neurosurgery, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi 110029, India, 2Department of Neuropathology, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi 110029, India Summary The authors describe a rare case of primary central nervous system (CNS) lymphoma presenting as bilateral cerebellopontine angle lesions. Imaging showed bilateral cerebellopontine angle lesions and also a small mass in right lateral ventricle and anterior third ventricle region. The right cerebellopontine angle mass was surgically excised and radio- and chemotherapy given for the remaining lesions. This is the second case reported in the world literature. The case is discussed and the literature is reviewed. ª 2003 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2004) 11(3), 328–331 0967-5868/$ - see front matter ª 2003 Elsevier Ltd. All rights reserved. doi:10.1016/S0967-5868(03)00110-3 Keywords: cerebellopontine angle, lymphoma, brain neoplasm, cerebellar lymphoma Received 5 February 2003 Accepted 1 April 2003 ª 2003 Elsevier Ltd. All rights reserved.