Case Report
Early Relapsing Calcified Cerebral Embolism Alfonso Cerase, MD,* and Irene Grazzini, MD†
Calcified cerebral emboli are rarely reported, but may be recurrent and devastating. Misdiagnosis at interpretation of initial brain computed tomography (CT) scan may occur in up to 27% of cases. The purpose of this case report was to describe clinical, CT, and CT angiography findings in a 79-year-old woman undergoing early recurrent stroke from calcified cerebral embolism. Neuroradiology should not overlook calcified cerebral embolism, and this confirms the role of CT in the assessment of stroke. Key Words: Calcified embolism—embolic stroke—computed tomography—recurrent stroke. Ó 2015 by National Stroke Association
Calcified cerebral embolism (CCE) has been described by brain computed tomography (CT) for the first time in 19811 and occurs more commonly than previously assumed, accounting for nearly 3% of patients undergoing CT for stroke.2 Middle cerebral artery is the most common site (up to 83%), followed by anterior and posterior cerebral arteries, and internal carotid artery. CCEs have been generally reported to occur after invasive cardiac or carotid procedures or cardiac resuscitation,2-4 however more recently it has been suggested that up to 86% of the cases occur spontaneously.2 In up to 43% of cases, CCE is a cause of relapsing stroke.2,5 Despite the association
From the *Unit of Neuroimaging and Neurointervention, Department of Neurological and Sensorineural Sciences, ‘‘Santa Maria alle Scotte’’ General Hospital, Azienda Ospedaliera Universitaria Senese, Siena; and †Department of Medical, Surgical and Neuro Sciences, Diagnostic Imaging, University of Siena, Siena, Italy. Received November 21, 2014; revision received January 19, 2015; accepted January 30, 2015. Both the authors have no sponsorship, funding arrangements relating to their research, nor any possible conflicts of interest. Address correspondence to Alfonso Cerase, MD, Unit of Neuroimaging and Neurointervention, Department of Neurological and Sensorineural Sciences, ‘‘Santa Maria alle Scotte’’ General Hospital, Azienda Ospedaliera Universitaria Senese, Siena, Viale Mario Bracci 16, Siena 53100, Italy. E-mail: [email protected]; [email protected]. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2015.01.038
between CCE and left heart valvular/annular calcifications is still debated6-8, bilateral CCE suggests left heart valvular/annular calcifications and proximal aortic arch as a source, whereas recurrent ipsilateral events suggest calcified carotid disease. Thus, the identification of CCE seems to help localize embolism source and thereby treatment decision making. However, unfortunately up to 27% of CCE may be misdiagnosed at initial interpretation and up to 9% may be overlooked at preliminary interpretation by on-call radiology residents.2 A 79-year-old woman with hypertension, diabetes, and hypercholesterolemia presented with a wake-up onset of confusion and speech disorder. Neurologic examination revealed aphasia, left homonymous hemianopsia, and right facial droop (National Institutes of Health Stroke Scale [NIHSS] score 5 10). Brain CT (Fig 1, B) was consistent with left temporal ischemia; however, a calcified embolus was overlooked. Aortic arch and cervicocranial arteries CT angiography (CTA; Fig 1, C) revealed carotid bulbs and left vertebral artery origin calcified plaques, with less than 50% stenosis by North American Symptomatic Carotid Endarterectomy Trial criteria. Electrocardiography showed ventricular tachycardia (115 beats per minute) and diffuse altered ventricular repolarization. Echocardiography showed hypertrophic cardiomyopathy with normal aortic valve, dilated left atrium with septal aneurysm, mitral insufficiency, and no mitral valve calcifications. In the following days, the patient
Journal of Stroke and Cerebrovascular Diseases, Vol. 24, No. 5 (May), 2015: pp e125-e126
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Figure 1. Pre- and post-CCE CT studies. Serial nonconsecutive brain CT images obtained 32 months before stroke (A), for memory and cognitive impairment, are negative. At first diagnosis, similar serial nonconsecutive brain CT images (B) show a dense area (arrow) corresponding to calcified material in the pial surface of left temporal lobe, associated with a subtle area of ischemic infarction in the ipsilateral temporal opercular region. Source CT angiography axial images (C) show parietal calcifications of the aortic arch, proximal epiaortic arteries, and left carotid bifurcation ,50% stenosis. At disease recurrence (D), new calcific gyral areas (arrows) are evident in the left sylvian fissure, consistent with recurrent CCE in branches of the ipsilateral middle cerebral artery. Source CT angiography axial images (E) are unchanged. Follow-up brain CT (F) shows progressive reduction of the evidence of calcified emboli. Abbreviations: CCE, calcified cerebral embolism; CT, computed tomography.
slowly improved, with residual dysphasia. She was treated with antiaggregants therapy. One-week followup brain CT did not show calcified emboli. The patient was discharged (NIHSS score, 3; modified Rankin Scale score, 1). Twenty days after brain CT control, she presented with a right-sided hemiparesis and aphasia (NIHSS score, 24). Brain CT (Fig 1, D) showed a new left CCE associated with ipsilateral frontal ischemia. CTA (Fig 1, E) was unchanged. One week later, brain CT showed lower density of CCE. Electrocardiography showed isolated supraventricular extrasystoles, some episodes of paroxysmal supraventricular tachycardia, and a focal right blocked branch bundle. Echocardiography was unchanged. Antiaggregant therapy was changed into oral anticoagulant therapy and amiodarone was added. A partial recovery occurred, with some residual weakness in both right upper and lower limbs, together with residual word-finding difficulties. Ten days later, brain CT (Fig 1, F) showed reduction of the calcified lesion. She was discharged 20 days later (NIHSS score, 11; modified Rankin Scale score, 5). When CCE is found, a careful evaluation of CTA of epiaortic and intracranial arteries including the aortic arch and cardiac ultrasound with a focus on left heart valves are mandatory. However, this case report confirms that CCE may be overlooked, affects clinical course, and carries a potential and substantial risk for early relapse, despite a spontaneous nature. In conclusion, CCE should
not be overlooked, and the potential for brain CT in the assessment of stroke remains intact.
References 1. Yock DH Jr. CT demonstration of cerebral emboli. J Comput Assist Tomogr 1981;5:190-196. 2. Walker BS, Shah LM, Osborn AG. Calcified cerebral emboli, a ‘‘do not miss’’ imaging diagnosis: 22 new cases and review of the literature. AJNR Am J Neuroradiol 2014; 35:1515-1519. 3. Doiron A, Blais C, Bonneau D. Spontaneous cerebral embolus from a calcified aortic valve. AJR Am J Roentgenol 1996;167:955-956. 4. Martınez-Fern andez E, Gil-Neciga E, Mir P, et al. Embolismo c alcico cerebral espont aneo. Rev Neurol 2002;34: 354-357. 5. Kavanagh EC, Fenton DM, Heran MKS, et al. Calcified cerebral emboli. AJNR Am J Neuroradiol 2006;27:1996-1999. 6. Rodriguez CJ, Bartz TM, Longstreth WT Jr, et al. Association of annular calcification and aortic valve sclerosis with brain findings on magnetic resonance imaging in community dwelling older adults: the cardiovascular health study. J Am Coll Cardiol 2011;57:2172-2180. 7. De Marco M, Gerdts E, Casalnuovo G, et al. Mitral annular calcification and incident ischemic stroke in treated hypertensive patients: the LIFE study. Am J Hypertens 2013; 26:567-573. 8. Mostowik M, Palka I, Gajos G, et al. Mitral and aortic annular calcifications and cerebrovascular ischemic episodes in patients with coronary artery disease. Pol Arch Med Wewn 2014;124:373-379.
Early Relapsing Calcified Cerebral Embolism Alfonso Cerase, MD,* and Irene Grazzini, MD†
Calcified cerebral emboli are rarely reported, but may be recurrent and devastating. Misdiagnosis at interpretation of initial brain computed tomography (CT) scan may occur in up to 27% of cases. The purpose of this case report was to describe clinical, CT, and CT angiography findings in a 79-year-old woman undergoing early recurrent stroke from calcified cerebral embolism. Neuroradiology should not overlook calcified cerebral embolism, and this confirms the role of CT in the assessment of stroke. Key Words: Calcified embolism—embolic stroke—computed tomography—recurrent stroke. Ó 2015 by National Stroke Association
Calcified cerebral embolism (CCE) has been described by brain computed tomography (CT) for the first time in 19811 and occurs more commonly than previously assumed, accounting for nearly 3% of patients undergoing CT for stroke.2 Middle cerebral artery is the most common site (up to 83%), followed by anterior and posterior cerebral arteries, and internal carotid artery. CCEs have been generally reported to occur after invasive cardiac or carotid procedures or cardiac resuscitation,2-4 however more recently it has been suggested that up to 86% of the cases occur spontaneously.2 In up to 43% of cases, CCE is a cause of relapsing stroke.2,5 Despite the association
From the *Unit of Neuroimaging and Neurointervention, Department of Neurological and Sensorineural Sciences, ‘‘Santa Maria alle Scotte’’ General Hospital, Azienda Ospedaliera Universitaria Senese, Siena; and †Department of Medical, Surgical and Neuro Sciences, Diagnostic Imaging, University of Siena, Siena, Italy. Received November 21, 2014; revision received January 19, 2015; accepted January 30, 2015. Both the authors have no sponsorship, funding arrangements relating to their research, nor any possible conflicts of interest. Address correspondence to Alfonso Cerase, MD, Unit of Neuroimaging and Neurointervention, Department of Neurological and Sensorineural Sciences, ‘‘Santa Maria alle Scotte’’ General Hospital, Azienda Ospedaliera Universitaria Senese, Siena, Viale Mario Bracci 16, Siena 53100, Italy. E-mail: [email protected]; [email protected]. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2015.01.038
between CCE and left heart valvular/annular calcifications is still debated6-8, bilateral CCE suggests left heart valvular/annular calcifications and proximal aortic arch as a source, whereas recurrent ipsilateral events suggest calcified carotid disease. Thus, the identification of CCE seems to help localize embolism source and thereby treatment decision making. However, unfortunately up to 27% of CCE may be misdiagnosed at initial interpretation and up to 9% may be overlooked at preliminary interpretation by on-call radiology residents.2 A 79-year-old woman with hypertension, diabetes, and hypercholesterolemia presented with a wake-up onset of confusion and speech disorder. Neurologic examination revealed aphasia, left homonymous hemianopsia, and right facial droop (National Institutes of Health Stroke Scale [NIHSS] score 5 10). Brain CT (Fig 1, B) was consistent with left temporal ischemia; however, a calcified embolus was overlooked. Aortic arch and cervicocranial arteries CT angiography (CTA; Fig 1, C) revealed carotid bulbs and left vertebral artery origin calcified plaques, with less than 50% stenosis by North American Symptomatic Carotid Endarterectomy Trial criteria. Electrocardiography showed ventricular tachycardia (115 beats per minute) and diffuse altered ventricular repolarization. Echocardiography showed hypertrophic cardiomyopathy with normal aortic valve, dilated left atrium with septal aneurysm, mitral insufficiency, and no mitral valve calcifications. In the following days, the patient
Journal of Stroke and Cerebrovascular Diseases, Vol. 24, No. 5 (May), 2015: pp e125-e126
e125
A. CERASE AND I. GRAZZINI
e126
Figure 1. Pre- and post-CCE CT studies. Serial nonconsecutive brain CT images obtained 32 months before stroke (A), for memory and cognitive impairment, are negative. At first diagnosis, similar serial nonconsecutive brain CT images (B) show a dense area (arrow) corresponding to calcified material in the pial surface of left temporal lobe, associated with a subtle area of ischemic infarction in the ipsilateral temporal opercular region. Source CT angiography axial images (C) show parietal calcifications of the aortic arch, proximal epiaortic arteries, and left carotid bifurcation ,50% stenosis. At disease recurrence (D), new calcific gyral areas (arrows) are evident in the left sylvian fissure, consistent with recurrent CCE in branches of the ipsilateral middle cerebral artery. Source CT angiography axial images (E) are unchanged. Follow-up brain CT (F) shows progressive reduction of the evidence of calcified emboli. Abbreviations: CCE, calcified cerebral embolism; CT, computed tomography.
slowly improved, with residual dysphasia. She was treated with antiaggregants therapy. One-week followup brain CT did not show calcified emboli. The patient was discharged (NIHSS score, 3; modified Rankin Scale score, 1). Twenty days after brain CT control, she presented with a right-sided hemiparesis and aphasia (NIHSS score, 24). Brain CT (Fig 1, D) showed a new left CCE associated with ipsilateral frontal ischemia. CTA (Fig 1, E) was unchanged. One week later, brain CT showed lower density of CCE. Electrocardiography showed isolated supraventricular extrasystoles, some episodes of paroxysmal supraventricular tachycardia, and a focal right blocked branch bundle. Echocardiography was unchanged. Antiaggregant therapy was changed into oral anticoagulant therapy and amiodarone was added. A partial recovery occurred, with some residual weakness in both right upper and lower limbs, together with residual word-finding difficulties. Ten days later, brain CT (Fig 1, F) showed reduction of the calcified lesion. She was discharged 20 days later (NIHSS score, 11; modified Rankin Scale score, 5). When CCE is found, a careful evaluation of CTA of epiaortic and intracranial arteries including the aortic arch and cardiac ultrasound with a focus on left heart valves are mandatory. However, this case report confirms that CCE may be overlooked, affects clinical course, and carries a potential and substantial risk for early relapse, despite a spontaneous nature. In conclusion, CCE should
not be overlooked, and the potential for brain CT in the assessment of stroke remains intact.
References 1. Yock DH Jr. CT demonstration of cerebral emboli. J Comput Assist Tomogr 1981;5:190-196. 2. Walker BS, Shah LM, Osborn AG. Calcified cerebral emboli, a ‘‘do not miss’’ imaging diagnosis: 22 new cases and review of the literature. AJNR Am J Neuroradiol 2014; 35:1515-1519. 3. Doiron A, Blais C, Bonneau D. Spontaneous cerebral embolus from a calcified aortic valve. AJR Am J Roentgenol 1996;167:955-956. 4. Martınez-Fern andez E, Gil-Neciga E, Mir P, et al. Embolismo c alcico cerebral espont aneo. Rev Neurol 2002;34: 354-357. 5. Kavanagh EC, Fenton DM, Heran MKS, et al. Calcified cerebral emboli. AJNR Am J Neuroradiol 2006;27:1996-1999. 6. Rodriguez CJ, Bartz TM, Longstreth WT Jr, et al. Association of annular calcification and aortic valve sclerosis with brain findings on magnetic resonance imaging in community dwelling older adults: the cardiovascular health study. J Am Coll Cardiol 2011;57:2172-2180. 7. De Marco M, Gerdts E, Casalnuovo G, et al. Mitral annular calcification and incident ischemic stroke in treated hypertensive patients: the LIFE study. Am J Hypertens 2013; 26:567-573. 8. Mostowik M, Palka I, Gajos G, et al. Mitral and aortic annular calcifications and cerebrovascular ischemic episodes in patients with coronary artery disease. Pol Arch Med Wewn 2014;124:373-379.
