- Email: [email protected]
Intra-arterial thrombolysis in basilar artery occlusion and recent haemorrhagic stroke due to arteriovenous malformation
642 Moscato et al.
times more likely to develop multicentric spread than those with nonhypothalamic tumours. The authors in this report did not comment on the possibility of an association between histologic subtype and biologic aggression. Cerebrospinal dissemination of juvenile pilocytic astrocytomas may be due to proximity of the tumour to the subarachnoid space or invasion of leptomeninges. Surgically induced dissemination is another possible mechanism of metastasis.6;11 A subgroup of pilocytic astrocytomas of the hypothalamic/chiasmatic region with a distinctive monomorphous pilomyxoid pattern and possibly more aggressive biological behaviour has been recently described.1–3 Like their classical juvenile pilocytic counterparts, pilomyxoid astrocytomas are composed of elongated, hair-like cells (or pilocytes), however, they show several distinctive features. These include a monomorphous loose microcystic growth pattern rather than the typical biphasic pattern of alternating loose and more compact zones; a prominent myxoid background; angiocentric formations; and the absence of eosinophilic granular bodies and Rosenthal fibres.1;3 Pilomyxoid astrocytoma occurs in the younger age group and tends to have more aggressive behaviour with earlier recurrences and may have a higher rate of CSF dissemination.1;3 It remains unclear whether pilomyxoid astrocytoma represents an aggressive variant of classical juvenile pilocytic astrocytoma, or an entirely distinct clinico-pathological entity. Larger series and new molecular techniques may answer this question in the future.
Intra-arterial thrombolysis in basilar artery occlusion and recent haemorrhagic stroke due to arteriovenous malformation G. Moscato1 MD, P. Maritato1 MD, S. Gallerini1 MD, C. Sonnoli1 MD, R. Padolecchia2 MD, G. Orlandi1 1 Department of Neuroscience – Clinic of Neurology and 2Neuroradiological Unit, Pisa, Italy
The authors thank Dr. R. Wilson for his expertise in contributing to the management of this patient. We thank Professor G. Fuller for his contribution in making the diagnosis.
Summary We report the case of a young patient suffering from a severe ischaemic stroke due to basilar artery occlusion occurring during selective digital subtraction angiography. This examination was performed in order to assess an arteriovenous malformation in posterior cerebral artery territory responsible for haemorrhagic stroke occurring 17 days before. Intra-arterial thrombolysis with urokinase was performed and basilar artery recanalization was obtained 8 h after stroke onset. Despite the severe neurological impairment, the prolonged symptoms of ischaemia and the high bleeding risk due to the recent cerebral haemorrhage in the same vascular territory involved in thrombolysis, the treatment determined a very favourable clinical outcome. ª 2004 Elsevier Ltd. All rights reserved.
REFERENCES
Journal of Clinical Neuroscience (2004) 11(6), 642–644 0967-5868/$ - see front matter ª 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2003.09.015
ACKNOWLEDGEMENTS
1. Burger PC, Cohen KJ, Rosenblum MK, Tihan T. Pathology of diencephalic astrocytomas. Pediatr Neurosurg 2000; 32(4): 214–219. 2. Tihan T, Burger PC. A variant of pilocytic astrocytoma: a possible distinct clinicopathological entity with a less favourable outcome. J Neuropathol Exp Neurol 1998; 57: 500 (Abstract). 3. Tihan T, Fisher PG, Kepner JL, Godfraind C, McComb RD, Goldthwaite PT, Burger PC. Paediatric astrocytomas with monomorphous pilomyxoid features and a less favorable outcome. J Neuropathol Exp Neurol 1999; 58: 1061–1068. 4. Hayostek CJ, Shaw EG, Scheithauer B, O'Fallon JR, Weiland TL, Schomberg PJ, Kelly PJ, Hu TC. Astrocytomas of the cerebellum. A comparative clinicopathologic study of pilocytic and diffuse astrocytomas. Cancer 1993; 72(3): 856–869. 5. Kocks W, Kalff R, Reinhardt V, Grote W, Hilke J. Spinal metastasis of pilocytic astrocytoma of the chiasma opticum. Child's Nerv Syst 1989; 5: 118–120. 6. Versari P, Talamonti G, D'Aliberti G, Fontana R, Colombo N, Casadei G. Leptomeningeal dissemination of juvenile pilocytic astrocytoma: case report. Surg Neurol 1994; 41(4): 318–321. 7. Obana WG, Cogen PH, Davis RL, Edwards MSB. Metastatic juvenile pilocytic astrocytoma. Case report. J Neurosurg 1991; 75: 972–975. 8. Mamelak AN, Prados MD, Obana WG, Cogen PH, Edwards MSB. Treatment options and prognosis for multicentric juvenile pilocytic astrocytoma. J Neurosurg 1994; 81: 24–30. 9. Morantz RA. Low grade astrocytomas. In: Kaye AH, Laws ER (eds) Brain tumours. second ed. Churchill Livingstone; 2001. p. 485–488. 10. Wallner KE, Gonzales MF, Edwards MSB, Wara WM, Sheline GE. Treatment results of juvenile pilocytic astrocytoma. J Neurosurg 1988; 69: 171–176. 11. Civitello LA, Packer RJ, Rorke LB, Siegel K, Sutton LN, Schut L. Leptomeningeal dissemination of low-grade gliomas in childhood. Neurology 1988; 38: 562–566. 12. Ho-Keung Ng, Leung CHS, Boet R, Poon WS. Spinal cord pilocytic astrocytoma with cranial meningeal metastases. J Clin Neurosci 2001; 8(40): 374–377. 13. Mclaughlin JE. Juvenile astrocytomas with subarachnoid spread. J Pathol 1976; 118: 101–107. 14. Senaratna S, Hanieh A, Manson J, Toogood I. Multiple cystic brain lesions in a patient with pilocytic astrocytoma. J Clin Neurosci 2001; 8(4): 363–366.
Journal of Clinical Neuroscience (2004) 11(6)
Keywords: arteriovenous malformation, basilar artery, stroke, thrombolysis Received 9 May 2003 Accepted 27 September 2003 Correspondence to: Giovanni Orlandi MD, Department of Neuroscience, Clinic of Neurology, University of Pisa, via Roma 67, 56126 Pisa, Italy. Tel.: +39-50-993100; Fax: +39-50-554808; E-mail: [email protected]
INTRODUCTION Basilar artery (BA) occlusion accounts for about 5% of cerebrovascular ischaemic events and is usually associated with a poor prognosis, with mortality ranging from 83% to 91%.1;2 Although no clinical trial has been conducted to date, a beneficial effect of intra-arterial thrombolysis has been documented in small series of patients.3–8 An overall recanalization rate of 60% with a decrease of mortality to 31% and a moderate disability in survived cases has been observed after thrombolytic therapy despite the risk of haemorrhagic transformation.9 We report the case of a young patient suffering from a severe ischaemic stroke due to BA occlusion occurring a few days after haemorrhage from an arteriovenous malformation. Due to the dramatic clinical picture and despite the recent bleeding, it was nevertheless decided to treat the patient with intra-arterial thrombolysis. ª 2004 Elsevier Ltd. All rights reserved.
Intra-arterial thrombolysis and haemorrhagic stroke due to arteriovenous malformation 643
CASE REPORT A 41-year-old white female was admitted to the Neurological Clinic of the University of Pisa to perform a cerebral selective digital subtraction angiography (DSA) in order to evaluate an arteriovenous malformation in the left parahippocampal region. The lesion had been partially treated by endovascular embolization about two years before. The patient had suffered a haemorrhagic stroke from the residual lesion 17 days before and had developed supratentorial hydrocephalus treated with ventricular diversion with no following residual disability. At the end of the DSA, the patient became agitated and complained of headache and vertigo. Afterwards, the clinical picture dramatically worsened progressing to coma and respiratory failure that required mechanical ventilation. Neurological examination showed brainstem dysfunction, with left hemiplegia and strabismus. CT scan showed no acute lesion and transcranial Doppler sonography documented systolic spikes on the BA suggesting occlusion that was confirmed by selective DSA (Fig. 1A). A microcatheter was placed in the occlusion site and 500,000 units of urokinase were infused over 1 h. Intravenous heparin, bolus 5000 units followed by 1000 units over 1 h were administered during the procedure. A full BA and posterior cerebral arteries recanalization were obtained 8 h from symptom onset (Fig. 1B). During the following hours, the patient showed a progressive clinical improvement, regained consciousness and became able to ventilate spontaneously; left hemiplegia, anarthria and dysphagia were observed. Intravenous heparin 25,000 units (PTT values range from 60 to 80 s) was administered during the following days and BA persistent recanalization was assessed by serial transcranial Doppler sonography controls. Cranial magnetic resonance was subsequently performed with a 1.5 T system. Sagittal T1-weighted images were obtained with spin echo (SE) sequences repetition time (TR) 500 ms, echo time (TE) 15 ms, 1 acquisition. Axial proton density (PD) and T2weighted images were obtained with fast spin echo (FSE) repetition time (TR 5000 ms, TE 18-19 ms, 1 acquisition) and with fluid attenuated inversion recovery (FLAIR) (TR 14,500 ms, TE 130 ms, time inversion TI 2650 ms, 1 acquisition) sequences. Magnetic resonance images (MRI) showed intensity changes indicating ischaemic lesions in the pons, in the right middle cerebellar peduncle, and in the right cerebellar hemisphere (Fig. 2). During the following days, the neurological condition continued to improve gradually and the patient was discharged. A six month follow-up showed a further clinical improvement with a residual slight left hemiparesis (modified Rankin scale score ¼ 2).
Fig. 1 Frontal angiographic view of basilar artery occlusion (A) and full basilar artery and posterior cerebral arteries recanalization after thrombolysis with evidence of arteriovenous malformation partially embolized (B).
ª 2004 Elsevier Ltd. All rights reserved.
Fig. 2 Cranial MRI: axial T2-weighted images (A), axial FLAIR images (B) and sagittal T1-weighted images (C) showing intensity changes indicating ischaemic lesions in the pons.
DISCUSSION This case documents that intra-arterial thrombolysis may allow a favourable clinical outcome in patients with BA occlusion despite a recent haemorrhagic stroke in the same vascular territory involved in thrombolysis. Indeed, previous cerebral haemorrhage usually contraindicates thrombolysis and the bleeding of cerebral arteriovenous malformation has been reported after thrombolysis in myocardial infarction10 and in stroke.11 Moreover, long time of occlusion3;12;13 and high severity of clinical deficit14;15 have been related to increased risk of haemorrhagic transformation of the ischaemic lesion. However, the average rate of symptomatic haemorrhagic transformation after intra-arterial thrombolysis in the posterior circulation stroke is lower (6.5%) compared to the anterior circulation (8.3%) and this may be due to higher ischaemic tolerance, improved collaterals and increased density of white matter tracts in the brainstem.16 Good outcome is strongly associated with BA recanalization after intra-arterial thrombolytic therapy.17 Recanalization has been reported from 50%5 to 78%7 of cases and good recovery may also include patients who had had locked-in syndrome.7 Moreover, distal and short-term occlusions have higher recanalization rates than proximal ones5;8;15;17 and involve fewer number of brainstem Journal of Clinical Neuroscience (2004) 11(6)
644 Yu et al.
perforating arteries allowing a good collateral supply that may restrict infarct volume and reduce disability.9 Emboli in the middle and distal BA are easier to lyse than atherosclerosis-related thrombi that usually involve the proximal tract of the vessel and young patients show higher recanalization rates probably due to the increased incidence of embolic occlusions seen in this age group.14 Clot composition may represent a further factor in recanalization success.18 Indeed fresh thrombi, which are fibrin and plasminogen rich, are easier to lyse than aged atherothrombi which are more organized and have low fibrin and plasminogen contents and high amounts of platelets and cholesterol.19 Prolonged vertebrobasilar symptoms do not seem to preclude survival and recovery and many series have included patients up to 12 h from stroke onset.3;5;7;8 Moreover, stroke severity seems not to impair prognosis and recovery has been documented also in patients with coma or tetraparesis.4;5;7;9 In light of the devastating natural course of BA occlusion, the results of this case are encouraging and suggest that intra-arterial thrombolysis may be a useful emergency treatment even in patients with very severe neurological deficit, prolonged symptoms of ischaemia and high risk of cerebral bleeding.
REFERENCES 1. Br€ uckmann H, Ferbert A, del Zoppo GJ, Macken W, Zeumer H. Acute basilar thrombosis: angiologic-clinical comparison and therapeutic implications. Acta Radiol 1987; 369(Suppl): 38–42. 2. Katzan IL, Furlan A. Thrombolytic therapy. In: Fisher M, Bogousslavsky J (eds) Current Review of Cerebrovascular Disease. third edn. Butterworth– Heinemann, Boston 1999; 185–193. 3. Hacke W, Zeumer H, Ferbert A, Bruckmann H, del Zoppo GJ. Intra-arterial thrombolytic therapy improves outcome in patients with acute vertebrobasilar occlusive disease. Stroke 1988; 19: 1216–1222. 4. Orlandi G, Moscato G, Padolecchia R, Sartucci F. Early thrombolysis in stroke due to basilar artery occlusion. Neurol Sci 2001; 22: 399–402. 5. Cross DT, Moran CJ, Akins P, Angtualo EE, Diringer MN. Relationship between clot location and outcome after basilar artery thrombolysis. Am J Neuroradiol 1997; 18: 1221–1228. 6. Zeumer H, Freitag HJ, Grzyska U, Neunzig HP. Local intra-arterial fibrinolysis in acute vertebrobasilar occlusion. Neuroradiology 1989; 31: 336–340. 7. Wijdicks EF, Nichols DA, Thielen KR et al. Intra-arterial thrombolysis in acute basilar artery thromboembolism: the initial Mayo Clinic experience. Mayo Clin Proc 1997; 72: 1005–1013. 8. Sliwka U, Mull M, Stelzer A, Diehl R, Noth J. Long-term follow-up of patients after intra-arterial thrombolytic therapy of acute vertebrobasilar artery occlusion. Cerebrovasc Dis 2001; 12: 214–219. 9. Brandt T, von Kummer R, Muller-Kuppers M, Hacke W. Thrombolytic therapy of acute basilar artery occlusion, variables affecting recanalization and outcome. Stroke 1996; 27: 875–881. 10. Sloan MA, Price TR, Petito CK et al. Clinical features and pathogenesis of intracerebral hemorrhage after rt-PA and heparin therapy for acute myocardial infarction: the thrombolysis in myocardial infarction (TIMI) II pilot and randomized clinical trial combined experience. Neurology 1995; 45: 649–658. 11. Wolpert SM, Bruckmann H, Greenlee R, Wechsler L, Pessin MS, del Zoppo GJ. Neuroradiologic evaluation of patients with acute stroke treated with recombinant tissue plasminogen activator. Am J Neuroradiol 1993; 14: 3–13. 12. Levy DE, Brott TG, Haley EC et al. Factors related to intracranial hematoma formation in patients receiving tissue-type plasminogen activator for acute ischemic stroke. Stroke 1994; 25: 291–297. 13. Ueda T, Hatakeyama T, Kumon Y, Sakaki S, Vraoka T. Evaluation of risk of hemorrhagic transformation in local intra-arterial thrombolysis in acute ischemic stroke by initial SPECT. Stroke 1994; 25: 298–303. 14. Matsumoto K, Satoh K. Intra-arterial therapy in acute ischemic stroke. In: Yamaguchi T, Mori E, Minematsu K, et al. (eds) Thrombolytic Therapy in Acute Ischemic Stroke III. Springer, Tokyo 1995; 279–287. 15. Huemer M, Niederwieser V, Ladurner G. Thrombolytic treatment for acute occlusion of the basilar artery. J Neurol Neurosurg Psychiatry 1995; 58: 227–228.
Journal of Clinical Neuroscience (2004) 11(6)
16. Becker KJ, Purcell LL, Hacke W, Hanley DF. Vertebrobasilar Thrombosis: diagnosis, management, and the use of intra-arterial thrombolytics. Crit Care Med 1996; 24: 1729–1742. 17. Levy EI, Firlik AD, Wisniewski S et al. Factors affecting survival rates for acute vertebrobasilar artery occlusions treated with intra-arterial thrombolytic therapy: a meta-analytical approach. Neurosurgery 1999; 45: 539–545. 18. Chimowitz M, Pessin M, Furlan A et al. The effect of source of cerebral embolus on susceptibility to thrombolysis. Neurology 1994; 44(Suppl 2): 356. 19. Hacke W. Thrombolysis: stroke subtype and embolus type. In: del Zoppo GJ, Mori E, Hacke W (eds) Thrombolytic Therapy in Acute Ischemic Stroke II. Springer, Berlin 1993; 153–159.
Neuromagnetic separation of secondarily bilateral synchronized spike foci: report of three cases H.Y. Yu1 MD, N. Nakasato2 MD PHD, M. Iwasaki3 H. Shamoto2 MD PHD, K. Nagamatsu3 MD PHD, T. Yoshimoto3 MD PHD
MD PHD,
1 Neurology Department, Neurologic Institute, Taipei Veterans General Hospital, Taipei, Taiwan, 2Department of Neurosurgery, Kohnan Hospital, Sendai, Japan, 3Department of Neurosurgery, Tohoku University Graduate School of Medicine, Japan
Summary To demonstrate the high spatiotemporal resolution of magnetoencephalography (MEG), we report three cases with focal epilepsy that exhibited bilateral synchronized spikes on simultaneous scalp EEG and MEG recording. Constant time lags (19.4 3.0 ms and 20.0 5.5) between the leading and the following contralateral spikes were noted on MEG and the current dipole sources were localized in the bilateral homotopic regions symmetrically in Cases 1 and 3. In Case 2, MEG indicated leading spikes in the left frontal region, with a time lag of 42.3 8.4 ms to reach the contralateral frontal and bilateral temporal regions as well. Chronic subdural EEG recording in Cases 1 and 2 confirmed that the leading spike focus in MEG was close to the seizure onset zone in cortical EEG. Spatio-temporal analysis of MEG spikes may be useful to identify the primary epileptic region in patients with synchronized bilateral epileptiform discharges. ª 2004 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2004) 11(6), 644–648 0967-5868/$ - see front matter ª 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2003.07.012
Keywords: magnetoencephalography, epilepsy, secondary bilateral synchrony, electroencephalography Received 12 June 2003 Accepted 20 July 2003 Correspondence to: Nobukazu Nakasato MD PhD, Department of Neurosurgery, Kohnan Hospital, 4-20-1 Nagamachi-Minami, Taihaku-ku, Sendai 982-8523, Japan. Tel.: +81-22-248-2131; Fax: +81-22-746-9568; E-mail: [email protected]
INTRODUCTION Bilaterally synchronized spikes can be seen on scalp EEG in patients with generalized and focal epilepsy. Differentiation of the secondarily synchronized spikes from the primary synchrony is important for diagnosis.1;2 ª 2004 Elsevier Ltd. All rights reserved.
times more likely to develop multicentric spread than those with nonhypothalamic tumours. The authors in this report did not comment on the possibility of an association between histologic subtype and biologic aggression. Cerebrospinal dissemination of juvenile pilocytic astrocytomas may be due to proximity of the tumour to the subarachnoid space or invasion of leptomeninges. Surgically induced dissemination is another possible mechanism of metastasis.6;11 A subgroup of pilocytic astrocytomas of the hypothalamic/chiasmatic region with a distinctive monomorphous pilomyxoid pattern and possibly more aggressive biological behaviour has been recently described.1–3 Like their classical juvenile pilocytic counterparts, pilomyxoid astrocytomas are composed of elongated, hair-like cells (or pilocytes), however, they show several distinctive features. These include a monomorphous loose microcystic growth pattern rather than the typical biphasic pattern of alternating loose and more compact zones; a prominent myxoid background; angiocentric formations; and the absence of eosinophilic granular bodies and Rosenthal fibres.1;3 Pilomyxoid astrocytoma occurs in the younger age group and tends to have more aggressive behaviour with earlier recurrences and may have a higher rate of CSF dissemination.1;3 It remains unclear whether pilomyxoid astrocytoma represents an aggressive variant of classical juvenile pilocytic astrocytoma, or an entirely distinct clinico-pathological entity. Larger series and new molecular techniques may answer this question in the future.
Intra-arterial thrombolysis in basilar artery occlusion and recent haemorrhagic stroke due to arteriovenous malformation G. Moscato1 MD, P. Maritato1 MD, S. Gallerini1 MD, C. Sonnoli1 MD, R. Padolecchia2 MD, G. Orlandi1 1 Department of Neuroscience – Clinic of Neurology and 2Neuroradiological Unit, Pisa, Italy
The authors thank Dr. R. Wilson for his expertise in contributing to the management of this patient. We thank Professor G. Fuller for his contribution in making the diagnosis.
Summary We report the case of a young patient suffering from a severe ischaemic stroke due to basilar artery occlusion occurring during selective digital subtraction angiography. This examination was performed in order to assess an arteriovenous malformation in posterior cerebral artery territory responsible for haemorrhagic stroke occurring 17 days before. Intra-arterial thrombolysis with urokinase was performed and basilar artery recanalization was obtained 8 h after stroke onset. Despite the severe neurological impairment, the prolonged symptoms of ischaemia and the high bleeding risk due to the recent cerebral haemorrhage in the same vascular territory involved in thrombolysis, the treatment determined a very favourable clinical outcome. ª 2004 Elsevier Ltd. All rights reserved.
REFERENCES
Journal of Clinical Neuroscience (2004) 11(6), 642–644 0967-5868/$ - see front matter ª 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2003.09.015
ACKNOWLEDGEMENTS
1. Burger PC, Cohen KJ, Rosenblum MK, Tihan T. Pathology of diencephalic astrocytomas. Pediatr Neurosurg 2000; 32(4): 214–219. 2. Tihan T, Burger PC. A variant of pilocytic astrocytoma: a possible distinct clinicopathological entity with a less favourable outcome. J Neuropathol Exp Neurol 1998; 57: 500 (Abstract). 3. Tihan T, Fisher PG, Kepner JL, Godfraind C, McComb RD, Goldthwaite PT, Burger PC. Paediatric astrocytomas with monomorphous pilomyxoid features and a less favorable outcome. J Neuropathol Exp Neurol 1999; 58: 1061–1068. 4. Hayostek CJ, Shaw EG, Scheithauer B, O'Fallon JR, Weiland TL, Schomberg PJ, Kelly PJ, Hu TC. Astrocytomas of the cerebellum. A comparative clinicopathologic study of pilocytic and diffuse astrocytomas. Cancer 1993; 72(3): 856–869. 5. Kocks W, Kalff R, Reinhardt V, Grote W, Hilke J. Spinal metastasis of pilocytic astrocytoma of the chiasma opticum. Child's Nerv Syst 1989; 5: 118–120. 6. Versari P, Talamonti G, D'Aliberti G, Fontana R, Colombo N, Casadei G. Leptomeningeal dissemination of juvenile pilocytic astrocytoma: case report. Surg Neurol 1994; 41(4): 318–321. 7. Obana WG, Cogen PH, Davis RL, Edwards MSB. Metastatic juvenile pilocytic astrocytoma. Case report. J Neurosurg 1991; 75: 972–975. 8. Mamelak AN, Prados MD, Obana WG, Cogen PH, Edwards MSB. Treatment options and prognosis for multicentric juvenile pilocytic astrocytoma. J Neurosurg 1994; 81: 24–30. 9. Morantz RA. Low grade astrocytomas. In: Kaye AH, Laws ER (eds) Brain tumours. second ed. Churchill Livingstone; 2001. p. 485–488. 10. Wallner KE, Gonzales MF, Edwards MSB, Wara WM, Sheline GE. Treatment results of juvenile pilocytic astrocytoma. J Neurosurg 1988; 69: 171–176. 11. Civitello LA, Packer RJ, Rorke LB, Siegel K, Sutton LN, Schut L. Leptomeningeal dissemination of low-grade gliomas in childhood. Neurology 1988; 38: 562–566. 12. Ho-Keung Ng, Leung CHS, Boet R, Poon WS. Spinal cord pilocytic astrocytoma with cranial meningeal metastases. J Clin Neurosci 2001; 8(40): 374–377. 13. Mclaughlin JE. Juvenile astrocytomas with subarachnoid spread. J Pathol 1976; 118: 101–107. 14. Senaratna S, Hanieh A, Manson J, Toogood I. Multiple cystic brain lesions in a patient with pilocytic astrocytoma. J Clin Neurosci 2001; 8(4): 363–366.
Journal of Clinical Neuroscience (2004) 11(6)
Keywords: arteriovenous malformation, basilar artery, stroke, thrombolysis Received 9 May 2003 Accepted 27 September 2003 Correspondence to: Giovanni Orlandi MD, Department of Neuroscience, Clinic of Neurology, University of Pisa, via Roma 67, 56126 Pisa, Italy. Tel.: +39-50-993100; Fax: +39-50-554808; E-mail: [email protected]
INTRODUCTION Basilar artery (BA) occlusion accounts for about 5% of cerebrovascular ischaemic events and is usually associated with a poor prognosis, with mortality ranging from 83% to 91%.1;2 Although no clinical trial has been conducted to date, a beneficial effect of intra-arterial thrombolysis has been documented in small series of patients.3–8 An overall recanalization rate of 60% with a decrease of mortality to 31% and a moderate disability in survived cases has been observed after thrombolytic therapy despite the risk of haemorrhagic transformation.9 We report the case of a young patient suffering from a severe ischaemic stroke due to BA occlusion occurring a few days after haemorrhage from an arteriovenous malformation. Due to the dramatic clinical picture and despite the recent bleeding, it was nevertheless decided to treat the patient with intra-arterial thrombolysis. ª 2004 Elsevier Ltd. All rights reserved.
Intra-arterial thrombolysis and haemorrhagic stroke due to arteriovenous malformation 643
CASE REPORT A 41-year-old white female was admitted to the Neurological Clinic of the University of Pisa to perform a cerebral selective digital subtraction angiography (DSA) in order to evaluate an arteriovenous malformation in the left parahippocampal region. The lesion had been partially treated by endovascular embolization about two years before. The patient had suffered a haemorrhagic stroke from the residual lesion 17 days before and had developed supratentorial hydrocephalus treated with ventricular diversion with no following residual disability. At the end of the DSA, the patient became agitated and complained of headache and vertigo. Afterwards, the clinical picture dramatically worsened progressing to coma and respiratory failure that required mechanical ventilation. Neurological examination showed brainstem dysfunction, with left hemiplegia and strabismus. CT scan showed no acute lesion and transcranial Doppler sonography documented systolic spikes on the BA suggesting occlusion that was confirmed by selective DSA (Fig. 1A). A microcatheter was placed in the occlusion site and 500,000 units of urokinase were infused over 1 h. Intravenous heparin, bolus 5000 units followed by 1000 units over 1 h were administered during the procedure. A full BA and posterior cerebral arteries recanalization were obtained 8 h from symptom onset (Fig. 1B). During the following hours, the patient showed a progressive clinical improvement, regained consciousness and became able to ventilate spontaneously; left hemiplegia, anarthria and dysphagia were observed. Intravenous heparin 25,000 units (PTT values range from 60 to 80 s) was administered during the following days and BA persistent recanalization was assessed by serial transcranial Doppler sonography controls. Cranial magnetic resonance was subsequently performed with a 1.5 T system. Sagittal T1-weighted images were obtained with spin echo (SE) sequences repetition time (TR) 500 ms, echo time (TE) 15 ms, 1 acquisition. Axial proton density (PD) and T2weighted images were obtained with fast spin echo (FSE) repetition time (TR 5000 ms, TE 18-19 ms, 1 acquisition) and with fluid attenuated inversion recovery (FLAIR) (TR 14,500 ms, TE 130 ms, time inversion TI 2650 ms, 1 acquisition) sequences. Magnetic resonance images (MRI) showed intensity changes indicating ischaemic lesions in the pons, in the right middle cerebellar peduncle, and in the right cerebellar hemisphere (Fig. 2). During the following days, the neurological condition continued to improve gradually and the patient was discharged. A six month follow-up showed a further clinical improvement with a residual slight left hemiparesis (modified Rankin scale score ¼ 2).
Fig. 1 Frontal angiographic view of basilar artery occlusion (A) and full basilar artery and posterior cerebral arteries recanalization after thrombolysis with evidence of arteriovenous malformation partially embolized (B).
ª 2004 Elsevier Ltd. All rights reserved.
Fig. 2 Cranial MRI: axial T2-weighted images (A), axial FLAIR images (B) and sagittal T1-weighted images (C) showing intensity changes indicating ischaemic lesions in the pons.
DISCUSSION This case documents that intra-arterial thrombolysis may allow a favourable clinical outcome in patients with BA occlusion despite a recent haemorrhagic stroke in the same vascular territory involved in thrombolysis. Indeed, previous cerebral haemorrhage usually contraindicates thrombolysis and the bleeding of cerebral arteriovenous malformation has been reported after thrombolysis in myocardial infarction10 and in stroke.11 Moreover, long time of occlusion3;12;13 and high severity of clinical deficit14;15 have been related to increased risk of haemorrhagic transformation of the ischaemic lesion. However, the average rate of symptomatic haemorrhagic transformation after intra-arterial thrombolysis in the posterior circulation stroke is lower (6.5%) compared to the anterior circulation (8.3%) and this may be due to higher ischaemic tolerance, improved collaterals and increased density of white matter tracts in the brainstem.16 Good outcome is strongly associated with BA recanalization after intra-arterial thrombolytic therapy.17 Recanalization has been reported from 50%5 to 78%7 of cases and good recovery may also include patients who had had locked-in syndrome.7 Moreover, distal and short-term occlusions have higher recanalization rates than proximal ones5;8;15;17 and involve fewer number of brainstem Journal of Clinical Neuroscience (2004) 11(6)
644 Yu et al.
perforating arteries allowing a good collateral supply that may restrict infarct volume and reduce disability.9 Emboli in the middle and distal BA are easier to lyse than atherosclerosis-related thrombi that usually involve the proximal tract of the vessel and young patients show higher recanalization rates probably due to the increased incidence of embolic occlusions seen in this age group.14 Clot composition may represent a further factor in recanalization success.18 Indeed fresh thrombi, which are fibrin and plasminogen rich, are easier to lyse than aged atherothrombi which are more organized and have low fibrin and plasminogen contents and high amounts of platelets and cholesterol.19 Prolonged vertebrobasilar symptoms do not seem to preclude survival and recovery and many series have included patients up to 12 h from stroke onset.3;5;7;8 Moreover, stroke severity seems not to impair prognosis and recovery has been documented also in patients with coma or tetraparesis.4;5;7;9 In light of the devastating natural course of BA occlusion, the results of this case are encouraging and suggest that intra-arterial thrombolysis may be a useful emergency treatment even in patients with very severe neurological deficit, prolonged symptoms of ischaemia and high risk of cerebral bleeding.
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16. Becker KJ, Purcell LL, Hacke W, Hanley DF. Vertebrobasilar Thrombosis: diagnosis, management, and the use of intra-arterial thrombolytics. Crit Care Med 1996; 24: 1729–1742. 17. Levy EI, Firlik AD, Wisniewski S et al. Factors affecting survival rates for acute vertebrobasilar artery occlusions treated with intra-arterial thrombolytic therapy: a meta-analytical approach. Neurosurgery 1999; 45: 539–545. 18. Chimowitz M, Pessin M, Furlan A et al. The effect of source of cerebral embolus on susceptibility to thrombolysis. Neurology 1994; 44(Suppl 2): 356. 19. Hacke W. Thrombolysis: stroke subtype and embolus type. In: del Zoppo GJ, Mori E, Hacke W (eds) Thrombolytic Therapy in Acute Ischemic Stroke II. Springer, Berlin 1993; 153–159.
Neuromagnetic separation of secondarily bilateral synchronized spike foci: report of three cases H.Y. Yu1 MD, N. Nakasato2 MD PHD, M. Iwasaki3 H. Shamoto2 MD PHD, K. Nagamatsu3 MD PHD, T. Yoshimoto3 MD PHD
MD PHD,
1 Neurology Department, Neurologic Institute, Taipei Veterans General Hospital, Taipei, Taiwan, 2Department of Neurosurgery, Kohnan Hospital, Sendai, Japan, 3Department of Neurosurgery, Tohoku University Graduate School of Medicine, Japan
Summary To demonstrate the high spatiotemporal resolution of magnetoencephalography (MEG), we report three cases with focal epilepsy that exhibited bilateral synchronized spikes on simultaneous scalp EEG and MEG recording. Constant time lags (19.4 3.0 ms and 20.0 5.5) between the leading and the following contralateral spikes were noted on MEG and the current dipole sources were localized in the bilateral homotopic regions symmetrically in Cases 1 and 3. In Case 2, MEG indicated leading spikes in the left frontal region, with a time lag of 42.3 8.4 ms to reach the contralateral frontal and bilateral temporal regions as well. Chronic subdural EEG recording in Cases 1 and 2 confirmed that the leading spike focus in MEG was close to the seizure onset zone in cortical EEG. Spatio-temporal analysis of MEG spikes may be useful to identify the primary epileptic region in patients with synchronized bilateral epileptiform discharges. ª 2004 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2004) 11(6), 644–648 0967-5868/$ - see front matter ª 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2003.07.012
Keywords: magnetoencephalography, epilepsy, secondary bilateral synchrony, electroencephalography Received 12 June 2003 Accepted 20 July 2003 Correspondence to: Nobukazu Nakasato MD PhD, Department of Neurosurgery, Kohnan Hospital, 4-20-1 Nagamachi-Minami, Taihaku-ku, Sendai 982-8523, Japan. Tel.: +81-22-248-2131; Fax: +81-22-746-9568; E-mail: [email protected]
INTRODUCTION Bilaterally synchronized spikes can be seen on scalp EEG in patients with generalized and focal epilepsy. Differentiation of the secondarily synchronized spikes from the primary synchrony is important for diagnosis.1;2 ª 2004 Elsevier Ltd. All rights reserved.