- Email: [email protected]
Primary central nervous lymphoma presenting as bilateral cerebellopontine angle lesions: a rare case report
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 M.C. Sharma2 MD
MBBS,
A.K. Mahapatra1
MCH DNB,
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.
CNS Iymphoma presenting as bilateral cerebellopontine angle lesions
Correspondence to: A.K. Mahapatra MCh, DNB, Department of Neurosurgery, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi 110029, India; Fax: +91-11-6862663; E-mail: [email protected]
INTRODUCTION Primary central nervous system lymphoma is a rare disease and accounts for 1–2% of intracranial tumours.1–3 Patients undergoing organ transplantation, with acquired immunodeficiency syndrome (AIDS)3–7 and congenital immunodeficiencies2;3;8;9 are at increased risk of developing this condition. An increasing trend has also been reported among immunologically competent individuals.10 Cerebellopontine angle lymphomas are rare and only 14 cases (8 primary and 6 secondary) have been reported so far.11 To date, only one case of primary central nervous system lymphoma presenting as bilateral cerebellopontine angle lesions has been reported.12 The case presented is the second such case in the world literature.
Fig. 1 MRI (brain) axial T-1 image showing hypointense mass in both cerebellopontine angles.
329
CASE REPORT A 36 year old man presented with a 10 year history of headache followed by 4 years of right sided hearing impairment with tinnitus and then one month of left sided hearing impairment, tinnitus and unsteadiness of gait. General physical examination revealed no lymphadenopathy or organomegaly. Chest, cardiac, skull bone and per rectal examination did not reveal any abnormality. He was conscious and oriented. Visual acuity and fields were normal. Fundus examination showed bilateral papilloedema and extra ocular movements showed bilateral mild lateral rectus palsies along with jerk nystagmus. He had a grade II right lower motor neuron type VII nerve palsy and moderate sensorineural hearing loss on the right side. VII and VIII nerves were normal on the left side. Lower cranial nerves were normal on both sides. Motor and sensory examination was normal, but he had cerebellar signs on the left side. Routine hematological parameters were within normal limits and a serological test for HIV was negative. Ultrasound study of abdomen was also normal. MRI was performed which showed bilateral cerebellopontine angle masses and also small masses in right lateral ventricle and anterior third ventricle region. All these masses were isointense on T1 (Fig. 1) and hyperintense on T2 weighted imaging with homogenous enhancement on administration of contrast (Figs. 2A and B). There was obstructive hydrocephalus. The patient underwent a right sided ventriculoperitoneal shunt and 3 days later, a left sided retromastoid suboccipital craniectomy was performed. The cerebellopontine angle tumor was encountered after the cerebellum was retracted. The tumor was soft to firm, moderately vascular with a poor plane of cleavage between the tumor and brain parenchyma. Beyond this the tumor merged imperceptibly with the brain parenchyma. A partial decompression was performed and following the frozen section report resection was discontinued. All the cranial nerves (V, VI, VII, VIII, IX and X) could be easily dissected from the tumor and preserved. Following surgery, the patient received ventilatory support and was then gradually weaned off and extubated. He was continued on antibiotics and corticosteroids and discharged after 2 weeks. At discharge, he was afebrile, conscious and obeying commands. He was referred to the medical oncology unit, where a complete workup for lymphoma elsewhere in the body was performed and found to be negative. The patient received 5500 rad irradiation to
Fig. 2 (A) Gadolinium enhanced MRI axial image showing enhancing masses in both cerebellopontine angles. (B) Gadolinium enhanced MRI coronal image showing enhancing masses in both cerebellopontine angles and right lateral ventricle.
ª 2003 Elsevier Ltd. All rights reserved.
Journal of Clinical Neuroscience (2004) 11(3)
330 Jaiswal et al.
Fig. 3 (A,B) Photomicrograph (high and low power) of cerebellopontine angle lymphoma showing sheets of round cells with scant to moderate cytoplasm with vesicular nuclei surrounded with coarse chromatin.
the whole brain over 5 weeks and also combination chemotherapy. The patient was doing well at follow up 6 months later. Pathological specimen examination The tumour tissue was fixed in buffered formalin and routinely processed. Five micron thick sections were cut for the examination. Microscopic examination revealed sheets of round cells with scant to moderate amounts of cytoplasm (Figs. 3A and B). Nuclei were vesicular and surrounded with coarse chromatin and some of them had prominent nucleoli on staining. Immuno-histochemical staining for leucocytic common antigen and B cell markers (L26, CD20) was positive but negative for T cell markers, cytokeratin, epithelial membrane antigen and GFAP. A final diagnosis of non Hodgkin’s lymphoma, diffuse large cell type (high grade) was made. DISCUSSION There are a variety of uncommon tumours that may occur in the cerebellopontine angle, accounting for the 10% of lesions at this site. In a series of 1354 cerebellopontine angle tumors after excluding acoustic neuromas (91.3%), meningioma (3.1%), cholesteatoma (2.4%) and cranial nerve schwannomas (1.4%), there were 25 rare tumors. These rare tumors included arachnoid cysts, haemangioblastomas, hemangiomas, gliomas, metastatic tumors, dermoids, lipomas and a teratoma.13 In a series of 32 non acoustic cerebellopontine angle tumors haemangiosarcomas were also recorded.14 Primary central nervous system lymphomas are those which are confined to the craniospinal axis without systemic involvement. Historically this entity was referred to as reticulam cell sarcoma, microglioma or perivascular sarcoma, but it is now well established that the cell of origin is a malignant lymphocyte.15–18 Primary central nervous system lymphomas are rare tumors accounting for 0.7–0.9% of lymphomas at all sites and 0.3–1.5% of all intracranial tumors.19 These can occur in both immunocompetent and immunocompromised individuals.1 Recently an increasing trend has been reported in immounocompetent individuals. The median age for diagnosis of primary central nervous system lymphoma is 55 years for immunocompetent patients and 31 years for AIDS patients, however, they can occur in all age groups. The male to female ratio is 3:2.20 They usually occur in the basal ganglia, corpus callosum, thalami and periventricular region.1 Malignant lymphoma presenting as a cerebellopontine angle mass is extremely rare and only 14 cases have been reported Journal of Clinical Neuroscience (2004) 11(3)
to date.11 . Of these 14 cases (8 primary and 6 secondary), the median age was 60 years and the male to female ratio equal.11;12;21–30 Primary central nervous system lymphomas present with signs and symptoms dependent on the site of lesion. Most of the tumors are supratentorial, but the majority of the infratentorial tumors are located in the cerebellum.1;12 Usually patients have a single lesion.2 This is different from secondary lymphoma in which chronic leptomeningeal infiltration and multiple cranial nerve palsies are common.31 It is difficult to diagnose cerebellopontine angle lymphoma on the basis of CT or MRI scan. Valvantis et al.28 have reported CT criteria for their diagnosis but the exceptional rarity of these tumors makes it unlikely preoperative diagonsis. The treatment modalities include surgical decompression followed by adjuvant radiotherapy and chemotherapy. In a review of 400 cases, no significant prognostic factor was observed, though diffuse mixed lymphomas and lymphomas located below the tentorium have a poorer prognosis.2 A frozen section should always be obtained in all suspected cases and radical decompression should be discouraged. Once the diagnosis is established, chemotherapy combined with radiotherapy provides the best mode of management.20 Compared to a systemic lymphoma with intracranial spread, primary central nervous system lymphomas have a better prognosis.
REFERENCES 1. Henry JM, Heffner RR, Diiard SH, Earle KM, Davis RL. Primary malignant lymphomas of the central nervous system. Cancer 1974; 34: 1293–1302. 2. Helle TL, Britt RH, Colby RV. Primary lymphoma of the central nervous system clinicopathological study of experience at Stanford. J Neurosurg 1984; 60: 94–103. 3. Hochberg FH, Miller DC. Primary central nervous system lymphoma. J Neurosurg 1988; 69: 835–853. 4. Schneck SA, Penn I. Cerebral neoplasms associated with renal transplantation. Arch Neurol 1970; 22: 226–233. 5. Patchell RA. Primary central nervous system l lymphoma in the transplant patient. Neurol Clin 1988; 6: 297–303. 6. Snider WD, Simposon DM, Aronyk KE, Nielsen SlL. Primary lymphoma of the central nervous system associated immunodeficiency syndrome. N Engl J Med 1983; 308: 45. 7. Bernal V, Peterman T, Berkelman R, Jaffe H. AIDS-associated non-Hodgkin’s lymphoma. Lancet 1991; 337: 805–809. 8. Frizzera G, Rosai J, Dehner LP, Spector BD, Kersy JH. Lymphoreticular disorders in primary immunodeficiencies: new findings based on an up-to-date histologic classification of 35 cases. Cancer 1980; 46: 693–699. 9. Filipovich AH, Heinitz KJ, Robinson LL, Frizzera G. The immunodeficiency cancer registry: a research resource. Am J Pediatr Hematol Oncol 1987; 9: 183– 184.
ª 2003 Elsevier Ltd. All rights reserved.
Possible participation of clip rotation
10. Eby NL, Gruyfferman S, Flannelly CM, Schold SC, Vogel FS, Byurger PC. Increasing incidence of primary brain lymphoma in the US. Cancer 1988; 62: 2461–2465. 11. Jaiswal AK, Tripathi M, Chandra PS, Sharma MC, Mahapatra AK. An unusual case of primary lymphoma of the skull base extending from cerebellopontine angle to cavernous sinus and orbit: A case report. J Neurosurg Sci 2000; 44: 145– 149. 12. Garth RJN, Coddington R, Brightwell AP. Primary cerebral lymphoma presenting with bilateral cerebellopontine angle lesions. J Laryngol Otol 1993; 107: 937–939. 13. Brackmann DE, Bartels LJ. Rare tumors of the cerebellopontine angle. Otolaryngol Head Neck Surg 1980; 88: 555–559. 14. Hitselberger WE, Gardener G. Other tumors of the cerebellopontine angle. Arch Otolaryngol 1968; 88: 164–166. 15. Habnbery JW, Dugger GS. Perithelial sarcoma of brian. A clinico pathological study of 13 cases. Arch Neurol Psych 1964; 74: 732. 16. Barnett LN, Schwartz E. Cerebral reticulam cell sacroma agfter multiple renal transplant. J Neurol Neurosurg Psychiat 1974: 37–966. 17. Benedeck L, Juba A. Uber das microgliom dtsch Z nervehnheilk 1941; 152: 159. 18. Schaumberg HH, Plank CR, Adam RD. The reticulam cell sacroma, microglioma group of brain tumors. Brain 1972; 95: 199. 19. Jellinger K, Skowik F, Sluga E. Primary intracranial lymphomas; a fine structural cytochemical and CSF immunological study. Clin Neurol Neurosurg 1979; 81: 173–184. 20. Howard AF, Jay SL. Primary central nervous system lymphoma. In: George OC, Lister TA, Jeffery LS (eds) The Lymphoma. W.B. Saunders, Philadelphia 1998: 483. 21. Nishimura T, Uchida Y, Fukuoka M, One Y, Kurisaka M, Mori K. Cerebelloponite angle lymphoma: a case report and review of literature. Surg Neurol 1998; 50: 480–485. 22. Karia SM, Nishizaki K, Aoji K, Akagi H. Primary malignant lymphoma in the cerebellopontine angle. J Laryngol Otol 1998; 11: 476–479. 23. Nschwitz A, Gerhardt HJ, Paris S, Villringer A. Lymphoma of the cerebellopontine angle as etiology of retrochochlear damage case report and review of the literature. HNO 1998; 46: 542–547. 24. Inatomi Y, Inoue T, Nagata S, Matsuno H, Itoh Y. Trigeminal neuralgia caused by the metastasis of malignant lymphoma to trigeminal nerve: a case report. No shinkei Geka 1998; 26: 401–405. 25. Angeli SI, Brackmann EE, Xenelis JE, Poletti BJ, Carberry JN, Hitselberger WE. Primary lymphoma of the internal auditory canal. Case report and review of the literature. Am Otol Rhinol Laryngol 1998; 107: 17–21. 26. Shuangshoti S. Solitary primary lymphoma of the cerebelloponitinc angle: case report. Neurosurgery 1995; 36: 595–598. 27. Nerciano J, Jimenex C, Figols J, Ferreres JC, Combarros O, Arjona R et al. Primary leptomeningeal lymphoma presenting as cerebellopontine angle lesion. Neuroradiology 1994; 36: 369–371. 28. Valvantis A., Imhof HG, Klaiber R, Dabir K. The diagnosis of solitary primary reticulum cell sarcoma of the posterior fossa with computed tomography. 1981;21: 217–313. 29. Ierokomos A, Goin DW. Primary CNS lymphoma in the cerebellopontine angle. Arch Otolaryngol 1985; 111: 50–52. 30. Yang PJ, Seeger JF, Carmody RF, Metha BA. Cerebellopontine angle lymphoma. Am J Neurorad 1987; 8: 368–369. 31. Mackintosh FR, Colby TV, Podolsky WJ, Burke JS, Hoppe RT, Rosenfelt FP, Rosenberg SA, Kaplan HS. Central nervous system involvement in non-Hodgkin’s lymphoma: an analysis of 105 cases. Cancer 1982; 49: 586–595.
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cerebral aneurysms. As for the etiology of de novo cerebral saccular aneurysms, hemodynamic stress is considered to be the most important factor. The woman whose case we present here had developed a ruptured anterior communicating aneurysm at the age of 52, and the aneurysm with its anterior projection was completely clipped. Eight years later, she suffered intraventricular hemorrhage. Angiogram showed a newly formed anterior communicating artery aneurysm, which projected to the side opposite the clip. Surgical exploration found the head of the clip had rotated and become trapped between optic nerves. We speculated the rotation of the clip used for the aneurysm at the first operation was one of the possible mechanisms, which caused a change in the direction of hemodynamics to the anterior communicating artery, leading to the development of de novo aneurysm. Every neurosurgeon should pay attention to the clip position until dural closure has been completed. ª 2003 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2004) 11(3), 331–334 0967-5868/$ - see front matter ª 2003 Elsevier Ltd. All rights reserved. doi:10.1016/S0967-5868(03)00199-1
Keywords: de novo aneurysm, hemodynamic stress, clip rotation Received 12 September 2002 Accepted 21 April 2003 Correspondence to: Yasuhiko Hayashi, Department of Neurosurgery, Graduate School of Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan. Tel.: +81-76-265-2384; Fax: +81-76-234-4262; E-mail: [email protected]
INTRODUCTION Hemodynamic stress is very important in the formation of cerebral aneurysms.1–6 Although newly formed (de novo) aneurysms have rarely been found after successful treatment, recent reports indicated that the de novo cerebral aneurysms of patients with a prior subarachnoid hemorrhage (SAH) more frequently develop than what they used to be considered.1;3;4;7;8 In this case, the patient had suffered a ruptured anterior communicating artery aneurysm (A. com. an.). She later manifested another ruptured A. com. an. projecting in the direction opposite to the previously used clip. The head of the clip had rotated and become trapped between optic nerves. A change in the direction of the hemodynamic stress as a result of the rotation of the clip might be considered to constitute the etiology for the formation of this de novo aneurysm.
CASE REPORT
Possible participation of clip rotation in the formation of de novo aneurysm Yasuhiko Hayashi1 MD, Makoto Kimura1 MD, Ryozou Satake2 MD, Akira Kinoshita1 MD 1 2
Department of Neurosurgery, Komatsu Municipal Hospital, Komatsu, Japan, Department of Neurology, Komatsu Municipal Hospital, Komatsu, Japan
Summary During long term follow-up after successful treatment of ruptured intracranial aneurysms, a few patients develop newly formed (de novo) aneurysms, which account for 0.9–1.1% of all
ª 2003 Elsevier Ltd. All rights reserved.
A 52-year-old woman consulted another hospital for sudden onset of headache. Computed tomography (CT)1 scan performed at admission showed SAH, isodensity in suprachiasmatic cistern and high density area in anterior interhemispheric cistern (Fig. 1A). Angiographic examination led to a diagnosis of ruptured A. com. an. with anterior projection. Left anterior cerebral artery (ACA, A1) was bow-shaped upward (Fig. 1B). The patient underwent a left fronto-temporal craniotomy and neck clipping of the aneurysm. The operative record showed the aneurysm directed forward and a straight clip was inserted parallel to the anterior communicating artery with complete obliteration of the aneurysm. There were any other aneurysms around the A. com. an. The patient 1
Abbreviations used: CT, computed tomography; SAH, subarachnoid hemorrhage; A. com. an., anterior communicating artery aneurysm; LAO, left anterior oblique; CAG, carotid angiogram. Journal of Clinical Neuroscience (2004) 11(3)
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 M.C. Sharma2 MD
MBBS,
A.K. Mahapatra1
MCH DNB,
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.
CNS Iymphoma presenting as bilateral cerebellopontine angle lesions
Correspondence to: A.K. Mahapatra MCh, DNB, Department of Neurosurgery, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi 110029, India; Fax: +91-11-6862663; E-mail: [email protected]
INTRODUCTION Primary central nervous system lymphoma is a rare disease and accounts for 1–2% of intracranial tumours.1–3 Patients undergoing organ transplantation, with acquired immunodeficiency syndrome (AIDS)3–7 and congenital immunodeficiencies2;3;8;9 are at increased risk of developing this condition. An increasing trend has also been reported among immunologically competent individuals.10 Cerebellopontine angle lymphomas are rare and only 14 cases (8 primary and 6 secondary) have been reported so far.11 To date, only one case of primary central nervous system lymphoma presenting as bilateral cerebellopontine angle lesions has been reported.12 The case presented is the second such case in the world literature.
Fig. 1 MRI (brain) axial T-1 image showing hypointense mass in both cerebellopontine angles.
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CASE REPORT A 36 year old man presented with a 10 year history of headache followed by 4 years of right sided hearing impairment with tinnitus and then one month of left sided hearing impairment, tinnitus and unsteadiness of gait. General physical examination revealed no lymphadenopathy or organomegaly. Chest, cardiac, skull bone and per rectal examination did not reveal any abnormality. He was conscious and oriented. Visual acuity and fields were normal. Fundus examination showed bilateral papilloedema and extra ocular movements showed bilateral mild lateral rectus palsies along with jerk nystagmus. He had a grade II right lower motor neuron type VII nerve palsy and moderate sensorineural hearing loss on the right side. VII and VIII nerves were normal on the left side. Lower cranial nerves were normal on both sides. Motor and sensory examination was normal, but he had cerebellar signs on the left side. Routine hematological parameters were within normal limits and a serological test for HIV was negative. Ultrasound study of abdomen was also normal. MRI was performed which showed bilateral cerebellopontine angle masses and also small masses in right lateral ventricle and anterior third ventricle region. All these masses were isointense on T1 (Fig. 1) and hyperintense on T2 weighted imaging with homogenous enhancement on administration of contrast (Figs. 2A and B). There was obstructive hydrocephalus. The patient underwent a right sided ventriculoperitoneal shunt and 3 days later, a left sided retromastoid suboccipital craniectomy was performed. The cerebellopontine angle tumor was encountered after the cerebellum was retracted. The tumor was soft to firm, moderately vascular with a poor plane of cleavage between the tumor and brain parenchyma. Beyond this the tumor merged imperceptibly with the brain parenchyma. A partial decompression was performed and following the frozen section report resection was discontinued. All the cranial nerves (V, VI, VII, VIII, IX and X) could be easily dissected from the tumor and preserved. Following surgery, the patient received ventilatory support and was then gradually weaned off and extubated. He was continued on antibiotics and corticosteroids and discharged after 2 weeks. At discharge, he was afebrile, conscious and obeying commands. He was referred to the medical oncology unit, where a complete workup for lymphoma elsewhere in the body was performed and found to be negative. The patient received 5500 rad irradiation to
Fig. 2 (A) Gadolinium enhanced MRI axial image showing enhancing masses in both cerebellopontine angles. (B) Gadolinium enhanced MRI coronal image showing enhancing masses in both cerebellopontine angles and right lateral ventricle.
ª 2003 Elsevier Ltd. All rights reserved.
Journal of Clinical Neuroscience (2004) 11(3)
330 Jaiswal et al.
Fig. 3 (A,B) Photomicrograph (high and low power) of cerebellopontine angle lymphoma showing sheets of round cells with scant to moderate cytoplasm with vesicular nuclei surrounded with coarse chromatin.
the whole brain over 5 weeks and also combination chemotherapy. The patient was doing well at follow up 6 months later. Pathological specimen examination The tumour tissue was fixed in buffered formalin and routinely processed. Five micron thick sections were cut for the examination. Microscopic examination revealed sheets of round cells with scant to moderate amounts of cytoplasm (Figs. 3A and B). Nuclei were vesicular and surrounded with coarse chromatin and some of them had prominent nucleoli on staining. Immuno-histochemical staining for leucocytic common antigen and B cell markers (L26, CD20) was positive but negative for T cell markers, cytokeratin, epithelial membrane antigen and GFAP. A final diagnosis of non Hodgkin’s lymphoma, diffuse large cell type (high grade) was made. DISCUSSION There are a variety of uncommon tumours that may occur in the cerebellopontine angle, accounting for the 10% of lesions at this site. In a series of 1354 cerebellopontine angle tumors after excluding acoustic neuromas (91.3%), meningioma (3.1%), cholesteatoma (2.4%) and cranial nerve schwannomas (1.4%), there were 25 rare tumors. These rare tumors included arachnoid cysts, haemangioblastomas, hemangiomas, gliomas, metastatic tumors, dermoids, lipomas and a teratoma.13 In a series of 32 non acoustic cerebellopontine angle tumors haemangiosarcomas were also recorded.14 Primary central nervous system lymphomas are those which are confined to the craniospinal axis without systemic involvement. Historically this entity was referred to as reticulam cell sarcoma, microglioma or perivascular sarcoma, but it is now well established that the cell of origin is a malignant lymphocyte.15–18 Primary central nervous system lymphomas are rare tumors accounting for 0.7–0.9% of lymphomas at all sites and 0.3–1.5% of all intracranial tumors.19 These can occur in both immunocompetent and immunocompromised individuals.1 Recently an increasing trend has been reported in immounocompetent individuals. The median age for diagnosis of primary central nervous system lymphoma is 55 years for immunocompetent patients and 31 years for AIDS patients, however, they can occur in all age groups. The male to female ratio is 3:2.20 They usually occur in the basal ganglia, corpus callosum, thalami and periventricular region.1 Malignant lymphoma presenting as a cerebellopontine angle mass is extremely rare and only 14 cases have been reported Journal of Clinical Neuroscience (2004) 11(3)
to date.11 . Of these 14 cases (8 primary and 6 secondary), the median age was 60 years and the male to female ratio equal.11;12;21–30 Primary central nervous system lymphomas present with signs and symptoms dependent on the site of lesion. Most of the tumors are supratentorial, but the majority of the infratentorial tumors are located in the cerebellum.1;12 Usually patients have a single lesion.2 This is different from secondary lymphoma in which chronic leptomeningeal infiltration and multiple cranial nerve palsies are common.31 It is difficult to diagnose cerebellopontine angle lymphoma on the basis of CT or MRI scan. Valvantis et al.28 have reported CT criteria for their diagnosis but the exceptional rarity of these tumors makes it unlikely preoperative diagonsis. The treatment modalities include surgical decompression followed by adjuvant radiotherapy and chemotherapy. In a review of 400 cases, no significant prognostic factor was observed, though diffuse mixed lymphomas and lymphomas located below the tentorium have a poorer prognosis.2 A frozen section should always be obtained in all suspected cases and radical decompression should be discouraged. Once the diagnosis is established, chemotherapy combined with radiotherapy provides the best mode of management.20 Compared to a systemic lymphoma with intracranial spread, primary central nervous system lymphomas have a better prognosis.
REFERENCES 1. Henry JM, Heffner RR, Diiard SH, Earle KM, Davis RL. Primary malignant lymphomas of the central nervous system. Cancer 1974; 34: 1293–1302. 2. Helle TL, Britt RH, Colby RV. Primary lymphoma of the central nervous system clinicopathological study of experience at Stanford. J Neurosurg 1984; 60: 94–103. 3. Hochberg FH, Miller DC. Primary central nervous system lymphoma. J Neurosurg 1988; 69: 835–853. 4. Schneck SA, Penn I. Cerebral neoplasms associated with renal transplantation. Arch Neurol 1970; 22: 226–233. 5. Patchell RA. Primary central nervous system l lymphoma in the transplant patient. Neurol Clin 1988; 6: 297–303. 6. Snider WD, Simposon DM, Aronyk KE, Nielsen SlL. Primary lymphoma of the central nervous system associated immunodeficiency syndrome. N Engl J Med 1983; 308: 45. 7. Bernal V, Peterman T, Berkelman R, Jaffe H. AIDS-associated non-Hodgkin’s lymphoma. Lancet 1991; 337: 805–809. 8. Frizzera G, Rosai J, Dehner LP, Spector BD, Kersy JH. Lymphoreticular disorders in primary immunodeficiencies: new findings based on an up-to-date histologic classification of 35 cases. Cancer 1980; 46: 693–699. 9. Filipovich AH, Heinitz KJ, Robinson LL, Frizzera G. The immunodeficiency cancer registry: a research resource. Am J Pediatr Hematol Oncol 1987; 9: 183– 184.
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Possible participation of clip rotation
10. Eby NL, Gruyfferman S, Flannelly CM, Schold SC, Vogel FS, Byurger PC. Increasing incidence of primary brain lymphoma in the US. Cancer 1988; 62: 2461–2465. 11. Jaiswal AK, Tripathi M, Chandra PS, Sharma MC, Mahapatra AK. An unusual case of primary lymphoma of the skull base extending from cerebellopontine angle to cavernous sinus and orbit: A case report. J Neurosurg Sci 2000; 44: 145– 149. 12. Garth RJN, Coddington R, Brightwell AP. Primary cerebral lymphoma presenting with bilateral cerebellopontine angle lesions. J Laryngol Otol 1993; 107: 937–939. 13. Brackmann DE, Bartels LJ. Rare tumors of the cerebellopontine angle. Otolaryngol Head Neck Surg 1980; 88: 555–559. 14. Hitselberger WE, Gardener G. Other tumors of the cerebellopontine angle. Arch Otolaryngol 1968; 88: 164–166. 15. Habnbery JW, Dugger GS. Perithelial sarcoma of brian. A clinico pathological study of 13 cases. Arch Neurol Psych 1964; 74: 732. 16. Barnett LN, Schwartz E. Cerebral reticulam cell sacroma agfter multiple renal transplant. J Neurol Neurosurg Psychiat 1974: 37–966. 17. Benedeck L, Juba A. Uber das microgliom dtsch Z nervehnheilk 1941; 152: 159. 18. Schaumberg HH, Plank CR, Adam RD. The reticulam cell sacroma, microglioma group of brain tumors. Brain 1972; 95: 199. 19. Jellinger K, Skowik F, Sluga E. Primary intracranial lymphomas; a fine structural cytochemical and CSF immunological study. Clin Neurol Neurosurg 1979; 81: 173–184. 20. Howard AF, Jay SL. Primary central nervous system lymphoma. In: George OC, Lister TA, Jeffery LS (eds) The Lymphoma. W.B. Saunders, Philadelphia 1998: 483. 21. Nishimura T, Uchida Y, Fukuoka M, One Y, Kurisaka M, Mori K. Cerebelloponite angle lymphoma: a case report and review of literature. Surg Neurol 1998; 50: 480–485. 22. Karia SM, Nishizaki K, Aoji K, Akagi H. Primary malignant lymphoma in the cerebellopontine angle. J Laryngol Otol 1998; 11: 476–479. 23. Nschwitz A, Gerhardt HJ, Paris S, Villringer A. Lymphoma of the cerebellopontine angle as etiology of retrochochlear damage case report and review of the literature. HNO 1998; 46: 542–547. 24. Inatomi Y, Inoue T, Nagata S, Matsuno H, Itoh Y. Trigeminal neuralgia caused by the metastasis of malignant lymphoma to trigeminal nerve: a case report. No shinkei Geka 1998; 26: 401–405. 25. Angeli SI, Brackmann EE, Xenelis JE, Poletti BJ, Carberry JN, Hitselberger WE. Primary lymphoma of the internal auditory canal. Case report and review of the literature. Am Otol Rhinol Laryngol 1998; 107: 17–21. 26. Shuangshoti S. Solitary primary lymphoma of the cerebelloponitinc angle: case report. Neurosurgery 1995; 36: 595–598. 27. Nerciano J, Jimenex C, Figols J, Ferreres JC, Combarros O, Arjona R et al. Primary leptomeningeal lymphoma presenting as cerebellopontine angle lesion. Neuroradiology 1994; 36: 369–371. 28. Valvantis A., Imhof HG, Klaiber R, Dabir K. The diagnosis of solitary primary reticulum cell sarcoma of the posterior fossa with computed tomography. 1981;21: 217–313. 29. Ierokomos A, Goin DW. Primary CNS lymphoma in the cerebellopontine angle. Arch Otolaryngol 1985; 111: 50–52. 30. Yang PJ, Seeger JF, Carmody RF, Metha BA. Cerebellopontine angle lymphoma. Am J Neurorad 1987; 8: 368–369. 31. Mackintosh FR, Colby TV, Podolsky WJ, Burke JS, Hoppe RT, Rosenfelt FP, Rosenberg SA, Kaplan HS. Central nervous system involvement in non-Hodgkin’s lymphoma: an analysis of 105 cases. Cancer 1982; 49: 586–595.
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cerebral aneurysms. As for the etiology of de novo cerebral saccular aneurysms, hemodynamic stress is considered to be the most important factor. The woman whose case we present here had developed a ruptured anterior communicating aneurysm at the age of 52, and the aneurysm with its anterior projection was completely clipped. Eight years later, she suffered intraventricular hemorrhage. Angiogram showed a newly formed anterior communicating artery aneurysm, which projected to the side opposite the clip. Surgical exploration found the head of the clip had rotated and become trapped between optic nerves. We speculated the rotation of the clip used for the aneurysm at the first operation was one of the possible mechanisms, which caused a change in the direction of hemodynamics to the anterior communicating artery, leading to the development of de novo aneurysm. Every neurosurgeon should pay attention to the clip position until dural closure has been completed. ª 2003 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2004) 11(3), 331–334 0967-5868/$ - see front matter ª 2003 Elsevier Ltd. All rights reserved. doi:10.1016/S0967-5868(03)00199-1
Keywords: de novo aneurysm, hemodynamic stress, clip rotation Received 12 September 2002 Accepted 21 April 2003 Correspondence to: Yasuhiko Hayashi, Department of Neurosurgery, Graduate School of Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan. Tel.: +81-76-265-2384; Fax: +81-76-234-4262; E-mail: [email protected]
INTRODUCTION Hemodynamic stress is very important in the formation of cerebral aneurysms.1–6 Although newly formed (de novo) aneurysms have rarely been found after successful treatment, recent reports indicated that the de novo cerebral aneurysms of patients with a prior subarachnoid hemorrhage (SAH) more frequently develop than what they used to be considered.1;3;4;7;8 In this case, the patient had suffered a ruptured anterior communicating artery aneurysm (A. com. an.). She later manifested another ruptured A. com. an. projecting in the direction opposite to the previously used clip. The head of the clip had rotated and become trapped between optic nerves. A change in the direction of the hemodynamic stress as a result of the rotation of the clip might be considered to constitute the etiology for the formation of this de novo aneurysm.
CASE REPORT
Possible participation of clip rotation in the formation of de novo aneurysm Yasuhiko Hayashi1 MD, Makoto Kimura1 MD, Ryozou Satake2 MD, Akira Kinoshita1 MD 1 2
Department of Neurosurgery, Komatsu Municipal Hospital, Komatsu, Japan, Department of Neurology, Komatsu Municipal Hospital, Komatsu, Japan
Summary During long term follow-up after successful treatment of ruptured intracranial aneurysms, a few patients develop newly formed (de novo) aneurysms, which account for 0.9–1.1% of all
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A 52-year-old woman consulted another hospital for sudden onset of headache. Computed tomography (CT)1 scan performed at admission showed SAH, isodensity in suprachiasmatic cistern and high density area in anterior interhemispheric cistern (Fig. 1A). Angiographic examination led to a diagnosis of ruptured A. com. an. with anterior projection. Left anterior cerebral artery (ACA, A1) was bow-shaped upward (Fig. 1B). The patient underwent a left fronto-temporal craniotomy and neck clipping of the aneurysm. The operative record showed the aneurysm directed forward and a straight clip was inserted parallel to the anterior communicating artery with complete obliteration of the aneurysm. There were any other aneurysms around the A. com. an. The patient 1
Abbreviations used: CT, computed tomography; SAH, subarachnoid hemorrhage; A. com. an., anterior communicating artery aneurysm; LAO, left anterior oblique; CAG, carotid angiogram. Journal of Clinical Neuroscience (2004) 11(3)