- Email: [email protected]
Spontaneous recanalization of the internal carotid artery resulting in thromboembolic occlusion of the ipsilateral ophthalmic artery and visual loss
1244
Case Reports / Journal of Clinical Neuroscience 16 (2009) 1244–1246
Spontaneous recanalization of the internal carotid artery resulting in thromboembolic occlusion of the ipsilateral ophthalmic artery and visual loss M.J. Binning, G. Jackson, W.T. Couldwell * Department of Neurosurgery, University of Utah, 175 North Medical Drive East, Salt Lake City, Utah 84132, USA
a r t i c l e
i n f o
Article history: Received 17 October 2008 Accepted 29 November 2008
Keywords: Internal carotid artery Spontaneous recanalization Atherosclerotic disease
a b s t r a c t We report a 54-year-old man who suffered a stroke from a complete right internal carotid artery (ICA) occlusion. Two months later, he presented with right eye blindness. Imaging demonstrated 50% recanalization of his right ICA. He underwent a right carotid endarterectomy to prevent contralateral stroke from emboli through a patent anterior communicating artery. Recanalization of a completely occluded proximal ICA due to atherosclerotic disease has been reported but is rare, but such patients emphasize the importance of follow-up vascular studies. Ó 2009 Elsevier Ltd. All rights reserved.
1. Introduction Spontaneous recanalization of the proximal internal carotid artery (ICA) in the neck has been well described in cases of arterial dissection. It is much less common, however, in atherosclerotic disease of the proximal ICA. We report a 54-year-old man who suffered a stroke from complete right ICA occlusion but subsequently had recanalization of the ICA. 2. Case report A 54-year-old man presented with a massive right-sided ICA ischemic stroke (Fig. 1), requiring a decompressive hemicraniectomy. Vascular studies at that time revealed a complete right ICA stenosis at the bifurcation on a duplex ultrasound scan; on formal angiography the carotid did not fill beyond the cavernous portion (Fig. 2). Two months later, during rehabilitation for his infarction, he presented with a sudden loss of vision in the right eye. This was initially thought to be probably due to emboli from the right ICA through the ophthalmic artery. CT angiography (CTA) was repeated and revealed recanalization of the occluded right ICA, associated with only 50% right ICA stenosis (Fig. 3). The patient was admitted to hospital, treated with aspirin and commenced on a heparin drip. He underwent an uncomplicated carotid endarterectomy because of concerns of a contralateral embolic stroke through a competent anterior communicating artery. The patient tolerated the procedure well, but did not regain vision in the right eye and remains with a fixed deficit from his prior ICA stroke, which included dense left-sided hemiparesis (arm greater than leg). He was discharged again to the rehabilitation service.
Fig. 1. Axial CT scan taken prior to a decompressive hemicraniectomy showing a significant right hemispheric infarction.
3. Discussion Spontaneous recanalization of the ICA after complete occlusion from atherosclerosis is an infrequent but previously described phenomenon.1–10 Carotid stenosis of atherosclerotic origin has widely known and accepted cardiovascular risk factors, yet little is known about the natural course of carotid artery occlusion and possible recanalization. Our case suggests a regression from complete to 50% stenosis of the common carotid artery at the bifurcation, with a resultant embolic occlusion of the ipsilateral ophthalmic artery as the most likely cause for the blindness observed in this patient. * Corresponding author. Tel.: +1 801 581 6908; fax: +1 801 581 4138. E-mail address: [email protected] (W.T. Couldwell).
Fig. 2. Antero-posterior (left) and lateral (right) angiography taken at the time of the right internal carotid artery (ICA) stroke showing near-complete occlusion of the right ICA at the bifurcation of the common carotid artery (arrows), associated with no flow in the supraclinoid carotid.
Case Reports / Journal of Clinical Neuroscience 16 (2009) 1244–1246
1245
Fig. 3. (A) Axial, (B) sagittal, and (C) coronal CT angiography obtained when the patient presented with emboli to the right ophthalmic artery and blindness, showing recanalization of the right internal carotid artery (arrows), now with about 50% stenosis.
In general, the outcome of patients who experience a stroke from a complete occlusion of the ICA is poor; such strokes are associated with severe disability in 40% to 69% of patients and a 16% to 55% mortality rate.11,12 The incidence of stroke when an ICA stenosis reaches complete occlusion is up to 25%; patients who do not suffer infarction vary from having a transient ischemic attack to being completely asymptomatic,11 as a result of developing collateral circulation via the external carotid artery and the Circle of Willis after a slowly progressive course of ICA narrowing. The actual incidence of spontaneous recanalization of carotid arteries after complete occlusion is relatively high in an early postocclusive time period for intracranial portions.8 The incidence of extracranial carotid recanalization varies, however, from very rare to as high as 15.8% in one study.7,9 There is also no consensus on the time course for early versus late recanalization. The early period is most commonly described as within 6 hours to 2 weeks, with some reports of as little as 1 hour to 4 hours after the onset of symptoms.7 As observed in our patient, the 2 month time period clearly represents a later recanalization. The incidence of recanalization after cervical artery dissection is, in contrast, much higher, at up to 85% within 3 months.13,14 Neurologic outcome, however, does not relate to the rate of recanalization after cervical artery dissection.15 Acute occlusion after a gradual accumulation of plaque leading to progressively greater stenosis is most commonly thought to result from thrombus formation over a ruptured plaque and, to a lesser extent, interplaque hemorrhage leading to complete vessel occlusion.16,17 Multiple mechanisms for recanalization have also been suggested, including reversal of vasospasm, distal clot embolization, spontaneous clot lysis, or possibly resorption of the hematoma within a hemorrhagic plaque.7 After complete occlusion, the use of tissue plasminogen activator (TPA) within the first 3 hours of symptom onset does not lyse large clots very effectively. In a recent retrospective study, most patients did not have recanalization of their ICA occlusion after intravenous TPA therapy. However, recanalization of associated proximal middle cerebral artery clots was found in 45% of patients and was associated with a good neurologic outcome.18 Aside from the use of fibrinolytic agents, management is limited to treatment of risk factors and using antithrombotic and anticoagulant agents. However, these have not been proven effective in the lysis of existing clots. Our patient was placed on heparin and aspirin therapy after presumed embolization of his ophthalmic artery to reduce the risk of further strokes. The significance of the late spontaneous recanalization observed in this patient is twofold. As suggested by Subramaniam et al. it supports routine preoperative use of duplex ultrasound in patients scheduled to undergo carotid endarterectomy to prevent unnecessary surgery, in case of lesion resolution, or progression to complete
stenosis.19 It also supports reimaging of patients after a complete occlusion of the ICA. Duplex ultrasound is both sensitive and specific at detecting >70% carotid stenosis.20 It is also the least invasive and most cost-effective screening test to allow monitoring of potential arterial recanalization. Patients with partial resolution of a complete occlusion will receive potential benefit from carotid endarterectomy, as shown in the North American Symptomatic Carotid Endarterectomy Trial21 and the European Carotid Surgery Trial.22 Acknowledgment We thank Kristin Kraus, M.Sc., for editorial assistance in preparing this paper. References 1. Calleja S, De la Vega V, Llaneza JM, et al. Spontaneous recanalization of acute internal carotid artery occlusion. Ann Vasc Surg 2004;18:490–2. 2. Camporese G, Verlato F, Salmistraro G, et al. Spontaneous recanalization of internal carotid artery occlusion evaluated with color flow imaging and contrast arteriography. Int Angiol 2003;22:64–71. 3. Klonaris C, Alexandrou A, Katsargyris A, et al. Late spontaneous recanalization of acute internal carotid artery occlusion. J Vasc Surg 2006;43:844–7. 4. Manganaro A, Ruggeri M, Ando G, et al. Endothelial functions in pathophysiology of thrombosis and fibrinolysis: late spontaneous recanalization of an occluded internal carotid artery—a case report. Angiology 2002;53:99–103. 5. Markwalder TM, Starrett RW, Mumenthaler M. Spontaneous bilateral recanalization in bilateral internal carotid artery occlusion. Stroke 1980;11:95–8. 6. Meves SH, Muhs A, Federlein J, et al. Recanalization of acute symptomatic occlusions of the internal carotid artery. J Neurol 2002;249:188–92. 7. Nguyen-Huynh MN, Lev MH, Rordorf G. Spontaneous recanalization of internal carotid artery occlusion. Stroke 2003;34:1032–4. 8. Sindermann F, Brugel R, Giedke H. Spontaneous recanalization of internal carotid artery occlusions. Neuroradiology 1974;7:53–6. 9. Szabo K, Kern R, Gass A, et al. Early spontaneous recanalization following acute carotid occlusion. J Neuroimaging 2008;18:148–53. 10. Yang FC, Lin JC, Chen CY, et al. Spontaneous early recanalization of an acute symptomatic critical stenosis of the extracranial internal carotid artery: a case report. Ann Vasc Surg 2008;22:469–72. 11. Cote R, Barnett HJ, Taylor DW. Internal carotid occlusion: a prospective study. Stroke 1983;14:898–902. 12. Meyer FB, Sundt Jr TM, Piepgras DG, et al. Emergency carotid endarterectomy for patients with acute carotid occlusion and profound neurological deficits. Ann Surg 1986;203:82–9. 13. Guillon B, Levy C, Bousser MG. Internal carotid artery dissection: an update. J Neurol Sci 1998;153:146–58. 14. Steinke W, Rautenberg W, Schwartz A, et al. Noninvasive monitoring of internal carotid artery dissection. Stroke 1994;25:998–1005. 15. Caso V, Paciaroni M, Corea F, et al. Recanalization of cervical artery dissection: influencing factors and role in neurological outcome. Cerebrovasc Dis 2004;17:93–7. 16. Davies MJ, Richardson PD, Woolf N, et al. Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. Br Heart J 1993;69:377–81. 17. Imparato AM, Riles TS, Gorstein F. The carotid bifurcation plaque: pathologic findings associated with cerebral ischemia. Stroke 1979;10:238–45.
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Case Reports / Journal of Clinical Neuroscience 16 (2009) 1246–1249
18. Christou I, Felberg RA, Demchuk AM, et al. Intravenous tissue plasminogen activator and flow improvement in acute ischemic stroke patients with internal carotid artery occlusion. J Neuroimaging 2002;12:119–23. 19. Subramaniam M, Barnett AJ, Robinson TM, et al. Spontaneous resolution of carotid stenosis—a case for routine preoperative duplex ultrasound. Eur J Vasc Endovasc Surg 2006;31:251–2. 20. Furst G, Saleh A, Wenserski F, et al. Reliability and validity of noninvasive imaging of internal carotid artery pseudo-occlusion. Stroke 1999;30: 1444–9.
21. Beneficial effect of carotid endarterectomy in symptomatic patients with highgrade carotid stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 1991;325:445–53. 22. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70–99%) or with mild (0–29%) carotid stenosis. European Carotid Surgery Trialists’ Collaborative Group. Lancet 1991;337:1235–43.
doi:10.1016/j.jocn.2008.11.018
Regression of intracranial meningioma following intratumoral hemorrhage João Paulo C. de Almeida, Rory J. Petteys, Daniel M. Sciubba *, Gary L. Gallia, Henry Brem Department of Neurosurgery, Johns Hopkins University, 600 North Wolfe Street, Meyer Building 8-161, Baltimore, Maryland 21287, USA
a r t i c l e
i n f o
Article history: Received 16 October 2008 Accepted 29 November 2008
Keywords: Brain tumor Hemorrhage Intracranial Resolution
a b s t r a c t An intratumoral hemorrhage within a meningioma occurs infrequently; in less than 3% of all lesions. When hemorrhage does occur, however, it is associated with a poor prognosis and significant mortality rates. We report a 66-year-old woman with a 10-year history of multiple intracranial meningiomas managed conservatively who underwent surgical resection of a spheno-orbital lesion for decompression of the right optic nerve. Postoperatively, an intratumoral hemorrhage developed in a contralateral lesion, which was managed conservatively. During follow up, the hemorrhaged lesion became significantly smaller. To our knowledge there are no published reports of spontaneous resolution of a meningioma after intratumoral hemorrhage without surgical management. We review the literature on hemorrhage in meningiomas and postulate some pathophysiologic mechanisms for the bleeding and subsequent tumor resolution seen in this patient. Ó 2009 Elsevier Ltd. All rights reserved.
1. Introduction Meningiomas are the most common non-glial intracranial tumor, with an incidence of 2.3 to 5.5 per 100,000 people,1,2 accounting for 30% of all primary adult brain tumor diagnoses in the United States of America.3 Hemorrhage secondary to meningioma is rare, occurring in 1.3% to 2.4% of those lesions.4,5 Tumoral bleeding is associated with worse prognoses and higher mortality rates – the overall mortality for bleeding meningiomas has been reported to be 21.1% and 9.5% in surgically treated patients.6 Treatment for such hemorrhages has included tumor resection, hematoma evacuation and non-operative medical management.6,7 To our knowledge there are no reports in the literature that show regression of an intracranial meningioma following intratumoral hemorrhage. In this report, we describe a patient with multiple intracranial meningiomas who developed an intratumoral hemorrhage in one of the lesions, and experienced subsequent resolution of the tumor. In addition, we review the literature on intratumoral hemorrhage of meningiomas and propose possible pathophysiologic mechanisms by which resolution may have occurred in this patient. 2. Case report 2.1. History and physical examination A 66-year-old woman with a history of dizziness presented to our center after being diagnosed with left parietal and right anterior temporal enhancing lesions on MRI consistent with bilateral meningiomas. At that time, the patient had neurological symptoms other
* Corresponding author. Tel.: +1 410 491 8330; fax: +1 410 502 5768. E-mail address: [email protected] (D.M. Sciubba).
than her dizziness, which was attributed to Ménière’s Disease, and her extra-axial lesions were followed with serial MRI studies and clinical evaluations. Over the following 10 years, the patient remained both clinically and radiographically stable. She eventually noticed decreased vision in her right eye. At that time, she denied headaches, seizures, motor weakness, and sensory abnormalities. On examination, she was alert and oriented to person, place and time. She was fluent without signs of aphasia. Examination of cranial nerves II through XII was notable for normal vision in the left eye, but detection of hand motion only in the right eye, with a right afferent pupillary defect, and a temporally pale right optic disc on fundoscopy; consistent with a compressive right optic neuropathy. Motor examination was unremarkable except for mild weakness in the distal right lower extremity secondary to sciatic pain. Sensation, reflexes, coordination and gait were also unremarkable. 2.2. Imaging MRI performed after the development of visual impairment showed right temporal (2.4 cm 2.8 cm 3.2 cm) (Fig. 1) and left parietal (1.7 cm 2.85 cm 2.27 cm) (Fig. 2) extra-axial enhancing lesions with hyperostosis of the right greater wing of the sphenoid bone (Fig. 1B). The presumptive diagnosis was bilateral intracranial meningioma. 2.3. Procedure The patient elected to undergo surgical resection of the right spheno-orbital tumor. A right-sided frontotemporal craniotomy was performed with excision of the right temporal lesion and decompression of the right optic nerve. Pathologic examination of the resected lesion was compatible with meningioma, World Health Organization grade I.
Case Reports / Journal of Clinical Neuroscience 16 (2009) 1244–1246
Spontaneous recanalization of the internal carotid artery resulting in thromboembolic occlusion of the ipsilateral ophthalmic artery and visual loss M.J. Binning, G. Jackson, W.T. Couldwell * Department of Neurosurgery, University of Utah, 175 North Medical Drive East, Salt Lake City, Utah 84132, USA
a r t i c l e
i n f o
Article history: Received 17 October 2008 Accepted 29 November 2008
Keywords: Internal carotid artery Spontaneous recanalization Atherosclerotic disease
a b s t r a c t We report a 54-year-old man who suffered a stroke from a complete right internal carotid artery (ICA) occlusion. Two months later, he presented with right eye blindness. Imaging demonstrated 50% recanalization of his right ICA. He underwent a right carotid endarterectomy to prevent contralateral stroke from emboli through a patent anterior communicating artery. Recanalization of a completely occluded proximal ICA due to atherosclerotic disease has been reported but is rare, but such patients emphasize the importance of follow-up vascular studies. Ó 2009 Elsevier Ltd. All rights reserved.
1. Introduction Spontaneous recanalization of the proximal internal carotid artery (ICA) in the neck has been well described in cases of arterial dissection. It is much less common, however, in atherosclerotic disease of the proximal ICA. We report a 54-year-old man who suffered a stroke from complete right ICA occlusion but subsequently had recanalization of the ICA. 2. Case report A 54-year-old man presented with a massive right-sided ICA ischemic stroke (Fig. 1), requiring a decompressive hemicraniectomy. Vascular studies at that time revealed a complete right ICA stenosis at the bifurcation on a duplex ultrasound scan; on formal angiography the carotid did not fill beyond the cavernous portion (Fig. 2). Two months later, during rehabilitation for his infarction, he presented with a sudden loss of vision in the right eye. This was initially thought to be probably due to emboli from the right ICA through the ophthalmic artery. CT angiography (CTA) was repeated and revealed recanalization of the occluded right ICA, associated with only 50% right ICA stenosis (Fig. 3). The patient was admitted to hospital, treated with aspirin and commenced on a heparin drip. He underwent an uncomplicated carotid endarterectomy because of concerns of a contralateral embolic stroke through a competent anterior communicating artery. The patient tolerated the procedure well, but did not regain vision in the right eye and remains with a fixed deficit from his prior ICA stroke, which included dense left-sided hemiparesis (arm greater than leg). He was discharged again to the rehabilitation service.
Fig. 1. Axial CT scan taken prior to a decompressive hemicraniectomy showing a significant right hemispheric infarction.
3. Discussion Spontaneous recanalization of the ICA after complete occlusion from atherosclerosis is an infrequent but previously described phenomenon.1–10 Carotid stenosis of atherosclerotic origin has widely known and accepted cardiovascular risk factors, yet little is known about the natural course of carotid artery occlusion and possible recanalization. Our case suggests a regression from complete to 50% stenosis of the common carotid artery at the bifurcation, with a resultant embolic occlusion of the ipsilateral ophthalmic artery as the most likely cause for the blindness observed in this patient. * Corresponding author. Tel.: +1 801 581 6908; fax: +1 801 581 4138. E-mail address: [email protected] (W.T. Couldwell).
Fig. 2. Antero-posterior (left) and lateral (right) angiography taken at the time of the right internal carotid artery (ICA) stroke showing near-complete occlusion of the right ICA at the bifurcation of the common carotid artery (arrows), associated with no flow in the supraclinoid carotid.
Case Reports / Journal of Clinical Neuroscience 16 (2009) 1244–1246
1245
Fig. 3. (A) Axial, (B) sagittal, and (C) coronal CT angiography obtained when the patient presented with emboli to the right ophthalmic artery and blindness, showing recanalization of the right internal carotid artery (arrows), now with about 50% stenosis.
In general, the outcome of patients who experience a stroke from a complete occlusion of the ICA is poor; such strokes are associated with severe disability in 40% to 69% of patients and a 16% to 55% mortality rate.11,12 The incidence of stroke when an ICA stenosis reaches complete occlusion is up to 25%; patients who do not suffer infarction vary from having a transient ischemic attack to being completely asymptomatic,11 as a result of developing collateral circulation via the external carotid artery and the Circle of Willis after a slowly progressive course of ICA narrowing. The actual incidence of spontaneous recanalization of carotid arteries after complete occlusion is relatively high in an early postocclusive time period for intracranial portions.8 The incidence of extracranial carotid recanalization varies, however, from very rare to as high as 15.8% in one study.7,9 There is also no consensus on the time course for early versus late recanalization. The early period is most commonly described as within 6 hours to 2 weeks, with some reports of as little as 1 hour to 4 hours after the onset of symptoms.7 As observed in our patient, the 2 month time period clearly represents a later recanalization. The incidence of recanalization after cervical artery dissection is, in contrast, much higher, at up to 85% within 3 months.13,14 Neurologic outcome, however, does not relate to the rate of recanalization after cervical artery dissection.15 Acute occlusion after a gradual accumulation of plaque leading to progressively greater stenosis is most commonly thought to result from thrombus formation over a ruptured plaque and, to a lesser extent, interplaque hemorrhage leading to complete vessel occlusion.16,17 Multiple mechanisms for recanalization have also been suggested, including reversal of vasospasm, distal clot embolization, spontaneous clot lysis, or possibly resorption of the hematoma within a hemorrhagic plaque.7 After complete occlusion, the use of tissue plasminogen activator (TPA) within the first 3 hours of symptom onset does not lyse large clots very effectively. In a recent retrospective study, most patients did not have recanalization of their ICA occlusion after intravenous TPA therapy. However, recanalization of associated proximal middle cerebral artery clots was found in 45% of patients and was associated with a good neurologic outcome.18 Aside from the use of fibrinolytic agents, management is limited to treatment of risk factors and using antithrombotic and anticoagulant agents. However, these have not been proven effective in the lysis of existing clots. Our patient was placed on heparin and aspirin therapy after presumed embolization of his ophthalmic artery to reduce the risk of further strokes. The significance of the late spontaneous recanalization observed in this patient is twofold. As suggested by Subramaniam et al. it supports routine preoperative use of duplex ultrasound in patients scheduled to undergo carotid endarterectomy to prevent unnecessary surgery, in case of lesion resolution, or progression to complete
stenosis.19 It also supports reimaging of patients after a complete occlusion of the ICA. Duplex ultrasound is both sensitive and specific at detecting >70% carotid stenosis.20 It is also the least invasive and most cost-effective screening test to allow monitoring of potential arterial recanalization. Patients with partial resolution of a complete occlusion will receive potential benefit from carotid endarterectomy, as shown in the North American Symptomatic Carotid Endarterectomy Trial21 and the European Carotid Surgery Trial.22 Acknowledgment We thank Kristin Kraus, M.Sc., for editorial assistance in preparing this paper. References 1. Calleja S, De la Vega V, Llaneza JM, et al. Spontaneous recanalization of acute internal carotid artery occlusion. Ann Vasc Surg 2004;18:490–2. 2. Camporese G, Verlato F, Salmistraro G, et al. Spontaneous recanalization of internal carotid artery occlusion evaluated with color flow imaging and contrast arteriography. Int Angiol 2003;22:64–71. 3. Klonaris C, Alexandrou A, Katsargyris A, et al. Late spontaneous recanalization of acute internal carotid artery occlusion. J Vasc Surg 2006;43:844–7. 4. Manganaro A, Ruggeri M, Ando G, et al. Endothelial functions in pathophysiology of thrombosis and fibrinolysis: late spontaneous recanalization of an occluded internal carotid artery—a case report. Angiology 2002;53:99–103. 5. Markwalder TM, Starrett RW, Mumenthaler M. Spontaneous bilateral recanalization in bilateral internal carotid artery occlusion. Stroke 1980;11:95–8. 6. Meves SH, Muhs A, Federlein J, et al. Recanalization of acute symptomatic occlusions of the internal carotid artery. J Neurol 2002;249:188–92. 7. Nguyen-Huynh MN, Lev MH, Rordorf G. Spontaneous recanalization of internal carotid artery occlusion. Stroke 2003;34:1032–4. 8. Sindermann F, Brugel R, Giedke H. Spontaneous recanalization of internal carotid artery occlusions. Neuroradiology 1974;7:53–6. 9. Szabo K, Kern R, Gass A, et al. Early spontaneous recanalization following acute carotid occlusion. J Neuroimaging 2008;18:148–53. 10. Yang FC, Lin JC, Chen CY, et al. Spontaneous early recanalization of an acute symptomatic critical stenosis of the extracranial internal carotid artery: a case report. Ann Vasc Surg 2008;22:469–72. 11. Cote R, Barnett HJ, Taylor DW. Internal carotid occlusion: a prospective study. Stroke 1983;14:898–902. 12. Meyer FB, Sundt Jr TM, Piepgras DG, et al. Emergency carotid endarterectomy for patients with acute carotid occlusion and profound neurological deficits. Ann Surg 1986;203:82–9. 13. Guillon B, Levy C, Bousser MG. Internal carotid artery dissection: an update. J Neurol Sci 1998;153:146–58. 14. Steinke W, Rautenberg W, Schwartz A, et al. Noninvasive monitoring of internal carotid artery dissection. Stroke 1994;25:998–1005. 15. Caso V, Paciaroni M, Corea F, et al. Recanalization of cervical artery dissection: influencing factors and role in neurological outcome. Cerebrovasc Dis 2004;17:93–7. 16. Davies MJ, Richardson PD, Woolf N, et al. Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. Br Heart J 1993;69:377–81. 17. Imparato AM, Riles TS, Gorstein F. The carotid bifurcation plaque: pathologic findings associated with cerebral ischemia. Stroke 1979;10:238–45.
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Case Reports / Journal of Clinical Neuroscience 16 (2009) 1246–1249
18. Christou I, Felberg RA, Demchuk AM, et al. Intravenous tissue plasminogen activator and flow improvement in acute ischemic stroke patients with internal carotid artery occlusion. J Neuroimaging 2002;12:119–23. 19. Subramaniam M, Barnett AJ, Robinson TM, et al. Spontaneous resolution of carotid stenosis—a case for routine preoperative duplex ultrasound. Eur J Vasc Endovasc Surg 2006;31:251–2. 20. Furst G, Saleh A, Wenserski F, et al. Reliability and validity of noninvasive imaging of internal carotid artery pseudo-occlusion. Stroke 1999;30: 1444–9.
21. Beneficial effect of carotid endarterectomy in symptomatic patients with highgrade carotid stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 1991;325:445–53. 22. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70–99%) or with mild (0–29%) carotid stenosis. European Carotid Surgery Trialists’ Collaborative Group. Lancet 1991;337:1235–43.
doi:10.1016/j.jocn.2008.11.018
Regression of intracranial meningioma following intratumoral hemorrhage João Paulo C. de Almeida, Rory J. Petteys, Daniel M. Sciubba *, Gary L. Gallia, Henry Brem Department of Neurosurgery, Johns Hopkins University, 600 North Wolfe Street, Meyer Building 8-161, Baltimore, Maryland 21287, USA
a r t i c l e
i n f o
Article history: Received 16 October 2008 Accepted 29 November 2008
Keywords: Brain tumor Hemorrhage Intracranial Resolution
a b s t r a c t An intratumoral hemorrhage within a meningioma occurs infrequently; in less than 3% of all lesions. When hemorrhage does occur, however, it is associated with a poor prognosis and significant mortality rates. We report a 66-year-old woman with a 10-year history of multiple intracranial meningiomas managed conservatively who underwent surgical resection of a spheno-orbital lesion for decompression of the right optic nerve. Postoperatively, an intratumoral hemorrhage developed in a contralateral lesion, which was managed conservatively. During follow up, the hemorrhaged lesion became significantly smaller. To our knowledge there are no published reports of spontaneous resolution of a meningioma after intratumoral hemorrhage without surgical management. We review the literature on hemorrhage in meningiomas and postulate some pathophysiologic mechanisms for the bleeding and subsequent tumor resolution seen in this patient. Ó 2009 Elsevier Ltd. All rights reserved.
1. Introduction Meningiomas are the most common non-glial intracranial tumor, with an incidence of 2.3 to 5.5 per 100,000 people,1,2 accounting for 30% of all primary adult brain tumor diagnoses in the United States of America.3 Hemorrhage secondary to meningioma is rare, occurring in 1.3% to 2.4% of those lesions.4,5 Tumoral bleeding is associated with worse prognoses and higher mortality rates – the overall mortality for bleeding meningiomas has been reported to be 21.1% and 9.5% in surgically treated patients.6 Treatment for such hemorrhages has included tumor resection, hematoma evacuation and non-operative medical management.6,7 To our knowledge there are no reports in the literature that show regression of an intracranial meningioma following intratumoral hemorrhage. In this report, we describe a patient with multiple intracranial meningiomas who developed an intratumoral hemorrhage in one of the lesions, and experienced subsequent resolution of the tumor. In addition, we review the literature on intratumoral hemorrhage of meningiomas and propose possible pathophysiologic mechanisms by which resolution may have occurred in this patient. 2. Case report 2.1. History and physical examination A 66-year-old woman with a history of dizziness presented to our center after being diagnosed with left parietal and right anterior temporal enhancing lesions on MRI consistent with bilateral meningiomas. At that time, the patient had neurological symptoms other
* Corresponding author. Tel.: +1 410 491 8330; fax: +1 410 502 5768. E-mail address: [email protected] (D.M. Sciubba).
than her dizziness, which was attributed to Ménière’s Disease, and her extra-axial lesions were followed with serial MRI studies and clinical evaluations. Over the following 10 years, the patient remained both clinically and radiographically stable. She eventually noticed decreased vision in her right eye. At that time, she denied headaches, seizures, motor weakness, and sensory abnormalities. On examination, she was alert and oriented to person, place and time. She was fluent without signs of aphasia. Examination of cranial nerves II through XII was notable for normal vision in the left eye, but detection of hand motion only in the right eye, with a right afferent pupillary defect, and a temporally pale right optic disc on fundoscopy; consistent with a compressive right optic neuropathy. Motor examination was unremarkable except for mild weakness in the distal right lower extremity secondary to sciatic pain. Sensation, reflexes, coordination and gait were also unremarkable. 2.2. Imaging MRI performed after the development of visual impairment showed right temporal (2.4 cm 2.8 cm 3.2 cm) (Fig. 1) and left parietal (1.7 cm 2.85 cm 2.27 cm) (Fig. 2) extra-axial enhancing lesions with hyperostosis of the right greater wing of the sphenoid bone (Fig. 1B). The presumptive diagnosis was bilateral intracranial meningioma. 2.3. Procedure The patient elected to undergo surgical resection of the right spheno-orbital tumor. A right-sided frontotemporal craniotomy was performed with excision of the right temporal lesion and decompression of the right optic nerve. Pathologic examination of the resected lesion was compatible with meningioma, World Health Organization grade I.