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(CEP)
[1–4] [PREPRINTER stage]
Brief Report
Reversible cerebral vasoconstriction syndrome: Is it more than just cerebral vasoconstriction?
Cephalalgia 0(0) 1–4 ! International Headache Society 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0333102414547139 cep.sagepub.com
Seby John1, Rula A Hajj-Ali2, David Min3, Leonard H Calabrese2, Russell Cerejo4 and Ken Uchino1 Abstract Background: Systemic vascular alterations have not been described in reversible cerebral vasoconstriction syndrome (RCVS). We present a case series of RCVS patients having cardiac dysfunction during ictus, with a subset showing complete resolution of cardiomyopathy. Methods: Retrospective case-series: Cardiac left ventricular ejection fraction (LVEF) and wall motion abnormalities (WMA) visualized on transthoracic echocardiography (TTE), performed during RCVS ictus and follow-up was analyzed. Results: Of 68 patients, 18 (26%) had a TTE performed around ictus. Three of 18 (17%) patients demonstrated WMA on initial TTE. All three patients were female without previous coronary artery disease or heart failure, and were asymptomatic from the cardiac dysfunction. WMA resolved completely on follow-up in Patients 1 and 2. Global LV dysfunction persisted for at least 90 days in Patient 3. Conclusion: Although the exact pathophysiology of the cardiomyopathy is uncertain, it may be related to localized coronary vasoconstriction causing myocardial ischemia/infarction. Vasoconstriction may not be limited to the cerebral vasculature and may involve extracerebral organs. Cardiac ventricular abnormalities may be a part of the RCVS spectrum. Keywords Reversible cerebral vasoconstriction syndrome (RCVS), cardiomyopathy, transient, heart-brain connection, stressinduced cardiomyopathy Date received: 19 May 2014; revised: 17 July 2014; accepted: 19 July 2014
Introduction Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by thunderclap headache, with or without neurological deficits, with evidence of reversible cerebral vasoconstriction on cerebral angiography (1). The pathophysiology of RCVS is thought to be secondary to alteration of intracerebral vascular tone. Systemic vascular alterations have not been described. We present a case series of RCVS patients having cardiac dysfunction during ictus, with a subset showing complete resolution of cardiomyopathy. We hypothesized that vasoconstriction in RCVS may not be limited to the cerebral vasculature.
Methods A retrospective analysis of patients diagnosed with probable or definite RCVS at our institution from
1990 to 2013 was conducted. Medical records were reviewed for demographics, symptoms and cerebral angiography. We analyzed cardiac left ventricular ejection fraction (LVEF) and presence of wall motion abnormalities (WMA) visualized on transthoracic echocardiography (TTE), performed during the ictus of RCVS and at follow-up if available. A cardiologist
1
Cerebrovascular Center, Cleveland Clinic, OH, USA Center for Vasculitis Care and Research, Department of Rheumatic and Immunologic Diseases, Cleveland Clinic, OH, USA 3 Department of Cardiovascular Medicine, Cleveland Clinic, OH, USA 4 Department of Neurology, Cleveland Clinic, OH, USA 2
Corresponding author: Ken Uchino, Cerebrovascular Center, Cleveland Clinic, 9500 Euclid Ave., S80, Cleveland, OH 44195, USA. Email: [email protected]
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(CEP)
[1–4] [PREPRINTER stage]
2
Cephalalgia 0(0)
independently reviewed all abnormal TTEs and electrocardiograms (EKGs).
Results Sixty-eight patients were included in the study. A TTE performed around the ictal stage was available in 18 (26%) patients including 16 (89%) women with mean age of 43 ( 12 SD) years. TTE was performed for stroke etiology evaluation in 17/18 patients. One patient also had chest pain at ictus for which TTE was recommended. Three of 18 (17%) patients demonstrated echocardiographic WMA on initial screen (Table 1). They were all female, and two were postpartum. All three patients had no previous history of coronary artery disease (CAD) or congestive heart failure (CHF). Patients 1 and 3 were asymptomatic from the cardiac dysfunction during the ictal stage and lacked evidence of acute cardiac ischemia on serial electrocardiograms or elevation of cardiac enzymes. Patient 2 was also asymptomatic, but had mild isolated elevation of creatinine kinase with non-specific EKG changes, insufficient to categorize as myocardial infarction (MI). Cardiac dysfunction improved on repeat TTE in Patients 1 and 2, two and seven days after initial TTE, respectively. Most remarkable was the complete resolution of WMA and hypokinesis. Global left ventricular (LV) dysfunction persisted for at least 90 days in Patient 3. All patients had diffuse vasoconstriction on initial cerebrovascular imaging and its resolution in Patients 2 and 3 started five and 28 days after symptom
onset, respectively, with eventual complete normalization. Reversal of vasoconstriction was not documented in Patient 1 since she was doing well and declined further testing. Of the remaining 15 patients without echocardiographic abnormalities, none had a previous history of CHF or cardiac symptoms around the ictus. Only one of 15 patients had transient elevation of cardiac enzymes and inferolateral ST-depression on EKG consistent with Type 2 non-ST elevation MI.
Discussion We present three patients without previous CAD who developed cardiomyopathy, most likely during the ictus of RCVS. In two patients, the echocardiographic abnormalities were transient, and resolved completely much like the reversal of cerebral vasoconstriction. Although test-retest variability could account for changes in the LVEF, the resolution of WMA on comparison was striking. The improvement in cardiac function occurred within five and 12 days of symptom onset, closely paralleling cerebral vasoconstriction normalization. At last follow-up three months from symptom onset, global hypokinesis persisted in Patient 3. Although we hypothesize that onset of cardiomyopathy was concurrent with the ictus of RCVS, the cardiac disease could be unrelated to RCVS. Other potential differential diagnoses include peripartum cardiomyopathy or cardiomyopathy secondary to hypertensive disease in pregnancy as explained below.
Table 1. Clinical characteristics, echocardiographic and cerebrovascular imaging findings. Initial TTE/days post-symptom onset
Follow-up TTE/days post-symptom onset
Days post-symptom onset when cerebral vasoconstriction normalization started
Day 5 LVEF 55% No WMA/ hypokinesis
Repeat vessel imaging not performed
Pt. Age/sex Trigger
Symptoms
Initial brain imaging
1
25/F
Gravida 3, eclampsia
Thunderclap headache post-delivery day 1
ICH post-right temporal lobe Diffuse vasoconstriction
Day 3 LVEF 50% Inferior wall hypokinesis
2
57/F
Head trauma
Dizziness
Ischemic stroke Bi-parietal, left occipital and left front lobes Diffuse vasoconstriction
Day 5 Day 12 LVEF 60% LVEF 45% Hypokinesis in left No WMA/ hypokinesis anterior descending artery territory
3
36/F
Acute headache Ischemic stroke Gravida 4, uncomplicated post-delivery day 0, Right parietal and delivery acute-onset hemifront lobe paresis three Diffuse vasoconstriction weeks post-delivery
Day 5
Day 90 Day 28 Day 24 LVEF 40% LVEF 40% Global hypokinesis Global hypokinesis
F: female; ICH: intracerebral hemorrhage; TTE: transthoracic echocardiography; LVEF: left ventricular ejection fraction; WMA: wall motion abnormalities.
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(CEP)
[1–4] [PREPRINTER stage]
3
John et al. The heart-brain connection causing acute stressinduced LV dysfunction (2) has been described with Takotsubo cardiomyopathy (3), and after subarachnoid hemorrhage causing neurocardiogenic stunning (4). With Takutsubo, transient LV WMA occurs in the apical and/or midventricular segments, with extension beyond a single epicardial coronary artery distribution, along with electrocardiographic changes. This was not the pattern seen in our patients. Another possibility specific to pregnancy is peripartum cardiomyopathy (5) and cardiomyopathy related to hypertensive pregnancy disorders (6), the etiology of which remains incompletely understood. The former has a variable course, with some showing rapid clinical and echocardiographic recovery, while others have persistent long-term cardiac dysfunction. In stress-induced cardiomyopathy, coronary spasm and myocardial adrenergic stimulation related to catecholamine excess from autonomic storming is postulated as the mechanism (2). Although we are uncertain of the exact pathophysiology of the cardiomyopathy in our patients, it may be related to localized coronary vasoconstriction causing myocardial ischemia/infarction. Indeed RCVS may be related to stress-induced, peripartum and pre-eclampsia/eclampia-induced cardiomyopathy and could represent a spectrum of the same pathophysiologic process in different vascular beds. Extracranial vessel involvement in RCVS has been reported with occurrence of cervical artery dissection. The association between these two conditions was observed in 12% of patients with RCVS, and 7% of patients with cervical artery dissection in a
prospective series (7). It is difficult to elucidate whether RCVS or dissection starts first, and whether RCVS is triggered by cervical artery dissection. Extracerebral vascular abnormalities including cardiac dysfunction have not been described in RCVS. Field et al. described a case of RCVS associated with internal carotid artery dissection, and a tight, non-atherosclerotic narrowing of the right renal artery at its mid-to-distal segment (8). However, the authors suggest that a unifying diagnosis would be fibromuscular dysplasia affecting both the carotid and renal arteries, and cerebral vasoconstriction developed after the carotid dissection. This study has multiple limitations. Our cohort does not represent consecutive cases, and in the wide clinical spectrum of RCVS likely represents those with severe vasoconstriction with ischemic or hemorrhagic strokes. Echocardiograms were unavailable for many patients, either because of lack of medical records or because they were not performed around the ictus of RVCS. For the three patients with echocardiographic abnormalities, we do not have prior echocardiograms to compare, but the quick normalization of cardiac dysfunction suggests that it is likely related to the underlying vasoconstrictive pathophysiology of RCVS. In conclusion, vasoconstriction may not be limited to the cerebral vasculature in RCVS and may involve extracerebral organ systems. Cardiac ventricular function abnormalities may be a part of the spectrum of RCVS. Our study is hypothesis generating, and further prospective studies of RCVS should investigate this hypothesis.
Clinical implications . The pathophysiology of reversible cerebral vasoconstriction syndrome (RCVS) is thought to be secondary to alteration of intracerebral vascular tone. Systemic vascular alterations have not been described. . We describe a case series of RCVS patients who developed cardiac dysfunction during the RCVS ictus. Three of 18 (17%) patients developed left ventricular wall motion abnormalities (WMA) seen on transthoracic echocardiography performed during RCVS ictus. In two of these patients, there was complete resolution of WMA within two weeks. . Although the exact pathophysiology of the cardiomyopathy is uncertain, it may be related to localized coronary vasoconstriction causing myocardial ischemia/infarction. . Vasoconstriction may not be limited to the cerebral vasculature in RCVS and may involve extracerebral organs. Cardiac ventricular abnormalities may be a part of the RCVS spectrum. Author contributions Dr Seby John: Study concept and design, acquisition of data, analysis and interpretation, critical revision of the manuscript for important intellectual content.
Dr David Min: Study concept and design, acquisition of data, analysis and interpretation, critical revision of the manuscript for important intellectual content.
Dr Rula A. Hajj-Ali: Study concept and design, analysis and interpretation, critical revision of the manuscript for important intellectual content, study supervision.
Dr Leonard Calabrese: Study concept and design, analysis and interpretation, critical revision of the manuscript for important intellectual content.
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(CEP)
[1–4] [PREPRINTER stage]
4 Dr Russell Cerejo: Study concept and design, acquisition of data, analysis and interpretation, critical revision of the manuscript for important intellectual content. Dr Ken Uchino: Study concept and design, analysis and interpretation, critical revision of the manuscript for important intellectual content.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest None declared.
References 1. Ducros A. Reversible cerebral vasoconstriction syndrome. Lancet Neurol 2012; 11: 906–917. 2. Bybee KA and Prasad A. Stress-related cardiomyopathy syndromes. Circulation 2008; 118: 397–409. 3. Sharkey SW, Windenburg DC, Lesser JR, et al. Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy. J Am Coll Cardiol 2010; 55: 333–341.
Cephalalgia 0(0) 4. Banki N, Kopelnik A, Tung P, et al. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg 2006; 105: 15–20. 5. Pearson GD, Veille JC, Rahimtoola S, et al. Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review. JAMA 2000; 283: 1183–1188. 6. Cunningham FG, Pritchard JA, Hankins GD, et al. Peripartum heart failure: Idiopathic cardiomyopathy or compounding cardiovascular events? Obstet Gynecol 1986; 67: 157–168. 7. Mawet J, Boukobza M, Franc J, et al. Reversible cerebral vasoconstriction syndrome and cervical artery dissection in 20 patients. Neurology 2013; 81: 821–824. 8. Field DK, Kleinig TJ, Thompson PD, et al. Reversible cerebral vasoconstriction, internal carotid artery dissection and renal artery stenosis. Cephalalgia 2010; 30: 983–986.
(CEP)
[1–4] [PREPRINTER stage]
Brief Report
Reversible cerebral vasoconstriction syndrome: Is it more than just cerebral vasoconstriction?
Cephalalgia 0(0) 1–4 ! International Headache Society 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0333102414547139 cep.sagepub.com
Seby John1, Rula A Hajj-Ali2, David Min3, Leonard H Calabrese2, Russell Cerejo4 and Ken Uchino1 Abstract Background: Systemic vascular alterations have not been described in reversible cerebral vasoconstriction syndrome (RCVS). We present a case series of RCVS patients having cardiac dysfunction during ictus, with a subset showing complete resolution of cardiomyopathy. Methods: Retrospective case-series: Cardiac left ventricular ejection fraction (LVEF) and wall motion abnormalities (WMA) visualized on transthoracic echocardiography (TTE), performed during RCVS ictus and follow-up was analyzed. Results: Of 68 patients, 18 (26%) had a TTE performed around ictus. Three of 18 (17%) patients demonstrated WMA on initial TTE. All three patients were female without previous coronary artery disease or heart failure, and were asymptomatic from the cardiac dysfunction. WMA resolved completely on follow-up in Patients 1 and 2. Global LV dysfunction persisted for at least 90 days in Patient 3. Conclusion: Although the exact pathophysiology of the cardiomyopathy is uncertain, it may be related to localized coronary vasoconstriction causing myocardial ischemia/infarction. Vasoconstriction may not be limited to the cerebral vasculature and may involve extracerebral organs. Cardiac ventricular abnormalities may be a part of the RCVS spectrum. Keywords Reversible cerebral vasoconstriction syndrome (RCVS), cardiomyopathy, transient, heart-brain connection, stressinduced cardiomyopathy Date received: 19 May 2014; revised: 17 July 2014; accepted: 19 July 2014
Introduction Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by thunderclap headache, with or without neurological deficits, with evidence of reversible cerebral vasoconstriction on cerebral angiography (1). The pathophysiology of RCVS is thought to be secondary to alteration of intracerebral vascular tone. Systemic vascular alterations have not been described. We present a case series of RCVS patients having cardiac dysfunction during ictus, with a subset showing complete resolution of cardiomyopathy. We hypothesized that vasoconstriction in RCVS may not be limited to the cerebral vasculature.
Methods A retrospective analysis of patients diagnosed with probable or definite RCVS at our institution from
1990 to 2013 was conducted. Medical records were reviewed for demographics, symptoms and cerebral angiography. We analyzed cardiac left ventricular ejection fraction (LVEF) and presence of wall motion abnormalities (WMA) visualized on transthoracic echocardiography (TTE), performed during the ictus of RCVS and at follow-up if available. A cardiologist
1
Cerebrovascular Center, Cleveland Clinic, OH, USA Center for Vasculitis Care and Research, Department of Rheumatic and Immunologic Diseases, Cleveland Clinic, OH, USA 3 Department of Cardiovascular Medicine, Cleveland Clinic, OH, USA 4 Department of Neurology, Cleveland Clinic, OH, USA 2
Corresponding author: Ken Uchino, Cerebrovascular Center, Cleveland Clinic, 9500 Euclid Ave., S80, Cleveland, OH 44195, USA. Email: [email protected]
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(CEP)
[1–4] [PREPRINTER stage]
2
Cephalalgia 0(0)
independently reviewed all abnormal TTEs and electrocardiograms (EKGs).
Results Sixty-eight patients were included in the study. A TTE performed around the ictal stage was available in 18 (26%) patients including 16 (89%) women with mean age of 43 ( 12 SD) years. TTE was performed for stroke etiology evaluation in 17/18 patients. One patient also had chest pain at ictus for which TTE was recommended. Three of 18 (17%) patients demonstrated echocardiographic WMA on initial screen (Table 1). They were all female, and two were postpartum. All three patients had no previous history of coronary artery disease (CAD) or congestive heart failure (CHF). Patients 1 and 3 were asymptomatic from the cardiac dysfunction during the ictal stage and lacked evidence of acute cardiac ischemia on serial electrocardiograms or elevation of cardiac enzymes. Patient 2 was also asymptomatic, but had mild isolated elevation of creatinine kinase with non-specific EKG changes, insufficient to categorize as myocardial infarction (MI). Cardiac dysfunction improved on repeat TTE in Patients 1 and 2, two and seven days after initial TTE, respectively. Most remarkable was the complete resolution of WMA and hypokinesis. Global left ventricular (LV) dysfunction persisted for at least 90 days in Patient 3. All patients had diffuse vasoconstriction on initial cerebrovascular imaging and its resolution in Patients 2 and 3 started five and 28 days after symptom
onset, respectively, with eventual complete normalization. Reversal of vasoconstriction was not documented in Patient 1 since she was doing well and declined further testing. Of the remaining 15 patients without echocardiographic abnormalities, none had a previous history of CHF or cardiac symptoms around the ictus. Only one of 15 patients had transient elevation of cardiac enzymes and inferolateral ST-depression on EKG consistent with Type 2 non-ST elevation MI.
Discussion We present three patients without previous CAD who developed cardiomyopathy, most likely during the ictus of RCVS. In two patients, the echocardiographic abnormalities were transient, and resolved completely much like the reversal of cerebral vasoconstriction. Although test-retest variability could account for changes in the LVEF, the resolution of WMA on comparison was striking. The improvement in cardiac function occurred within five and 12 days of symptom onset, closely paralleling cerebral vasoconstriction normalization. At last follow-up three months from symptom onset, global hypokinesis persisted in Patient 3. Although we hypothesize that onset of cardiomyopathy was concurrent with the ictus of RCVS, the cardiac disease could be unrelated to RCVS. Other potential differential diagnoses include peripartum cardiomyopathy or cardiomyopathy secondary to hypertensive disease in pregnancy as explained below.
Table 1. Clinical characteristics, echocardiographic and cerebrovascular imaging findings. Initial TTE/days post-symptom onset
Follow-up TTE/days post-symptom onset
Days post-symptom onset when cerebral vasoconstriction normalization started
Day 5 LVEF 55% No WMA/ hypokinesis
Repeat vessel imaging not performed
Pt. Age/sex Trigger
Symptoms
Initial brain imaging
1
25/F
Gravida 3, eclampsia
Thunderclap headache post-delivery day 1
ICH post-right temporal lobe Diffuse vasoconstriction
Day 3 LVEF 50% Inferior wall hypokinesis
2
57/F
Head trauma
Dizziness
Ischemic stroke Bi-parietal, left occipital and left front lobes Diffuse vasoconstriction
Day 5 Day 12 LVEF 60% LVEF 45% Hypokinesis in left No WMA/ hypokinesis anterior descending artery territory
3
36/F
Acute headache Ischemic stroke Gravida 4, uncomplicated post-delivery day 0, Right parietal and delivery acute-onset hemifront lobe paresis three Diffuse vasoconstriction weeks post-delivery
Day 5
Day 90 Day 28 Day 24 LVEF 40% LVEF 40% Global hypokinesis Global hypokinesis
F: female; ICH: intracerebral hemorrhage; TTE: transthoracic echocardiography; LVEF: left ventricular ejection fraction; WMA: wall motion abnormalities.
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(CEP)
[1–4] [PREPRINTER stage]
3
John et al. The heart-brain connection causing acute stressinduced LV dysfunction (2) has been described with Takotsubo cardiomyopathy (3), and after subarachnoid hemorrhage causing neurocardiogenic stunning (4). With Takutsubo, transient LV WMA occurs in the apical and/or midventricular segments, with extension beyond a single epicardial coronary artery distribution, along with electrocardiographic changes. This was not the pattern seen in our patients. Another possibility specific to pregnancy is peripartum cardiomyopathy (5) and cardiomyopathy related to hypertensive pregnancy disorders (6), the etiology of which remains incompletely understood. The former has a variable course, with some showing rapid clinical and echocardiographic recovery, while others have persistent long-term cardiac dysfunction. In stress-induced cardiomyopathy, coronary spasm and myocardial adrenergic stimulation related to catecholamine excess from autonomic storming is postulated as the mechanism (2). Although we are uncertain of the exact pathophysiology of the cardiomyopathy in our patients, it may be related to localized coronary vasoconstriction causing myocardial ischemia/infarction. Indeed RCVS may be related to stress-induced, peripartum and pre-eclampsia/eclampia-induced cardiomyopathy and could represent a spectrum of the same pathophysiologic process in different vascular beds. Extracranial vessel involvement in RCVS has been reported with occurrence of cervical artery dissection. The association between these two conditions was observed in 12% of patients with RCVS, and 7% of patients with cervical artery dissection in a
prospective series (7). It is difficult to elucidate whether RCVS or dissection starts first, and whether RCVS is triggered by cervical artery dissection. Extracerebral vascular abnormalities including cardiac dysfunction have not been described in RCVS. Field et al. described a case of RCVS associated with internal carotid artery dissection, and a tight, non-atherosclerotic narrowing of the right renal artery at its mid-to-distal segment (8). However, the authors suggest that a unifying diagnosis would be fibromuscular dysplasia affecting both the carotid and renal arteries, and cerebral vasoconstriction developed after the carotid dissection. This study has multiple limitations. Our cohort does not represent consecutive cases, and in the wide clinical spectrum of RCVS likely represents those with severe vasoconstriction with ischemic or hemorrhagic strokes. Echocardiograms were unavailable for many patients, either because of lack of medical records or because they were not performed around the ictus of RVCS. For the three patients with echocardiographic abnormalities, we do not have prior echocardiograms to compare, but the quick normalization of cardiac dysfunction suggests that it is likely related to the underlying vasoconstrictive pathophysiology of RCVS. In conclusion, vasoconstriction may not be limited to the cerebral vasculature in RCVS and may involve extracerebral organ systems. Cardiac ventricular function abnormalities may be a part of the spectrum of RCVS. Our study is hypothesis generating, and further prospective studies of RCVS should investigate this hypothesis.
Clinical implications . The pathophysiology of reversible cerebral vasoconstriction syndrome (RCVS) is thought to be secondary to alteration of intracerebral vascular tone. Systemic vascular alterations have not been described. . We describe a case series of RCVS patients who developed cardiac dysfunction during the RCVS ictus. Three of 18 (17%) patients developed left ventricular wall motion abnormalities (WMA) seen on transthoracic echocardiography performed during RCVS ictus. In two of these patients, there was complete resolution of WMA within two weeks. . Although the exact pathophysiology of the cardiomyopathy is uncertain, it may be related to localized coronary vasoconstriction causing myocardial ischemia/infarction. . Vasoconstriction may not be limited to the cerebral vasculature in RCVS and may involve extracerebral organs. Cardiac ventricular abnormalities may be a part of the RCVS spectrum. Author contributions Dr Seby John: Study concept and design, acquisition of data, analysis and interpretation, critical revision of the manuscript for important intellectual content.
Dr David Min: Study concept and design, acquisition of data, analysis and interpretation, critical revision of the manuscript for important intellectual content.
Dr Rula A. Hajj-Ali: Study concept and design, analysis and interpretation, critical revision of the manuscript for important intellectual content, study supervision.
Dr Leonard Calabrese: Study concept and design, analysis and interpretation, critical revision of the manuscript for important intellectual content.
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(CEP)
[1–4] [PREPRINTER stage]
4 Dr Russell Cerejo: Study concept and design, acquisition of data, analysis and interpretation, critical revision of the manuscript for important intellectual content. Dr Ken Uchino: Study concept and design, analysis and interpretation, critical revision of the manuscript for important intellectual content.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest None declared.
References 1. Ducros A. Reversible cerebral vasoconstriction syndrome. Lancet Neurol 2012; 11: 906–917. 2. Bybee KA and Prasad A. Stress-related cardiomyopathy syndromes. Circulation 2008; 118: 397–409. 3. Sharkey SW, Windenburg DC, Lesser JR, et al. Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy. J Am Coll Cardiol 2010; 55: 333–341.
Cephalalgia 0(0) 4. Banki N, Kopelnik A, Tung P, et al. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg 2006; 105: 15–20. 5. Pearson GD, Veille JC, Rahimtoola S, et al. Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review. JAMA 2000; 283: 1183–1188. 6. Cunningham FG, Pritchard JA, Hankins GD, et al. Peripartum heart failure: Idiopathic cardiomyopathy or compounding cardiovascular events? Obstet Gynecol 1986; 67: 157–168. 7. Mawet J, Boukobza M, Franc J, et al. Reversible cerebral vasoconstriction syndrome and cervical artery dissection in 20 patients. Neurology 2013; 81: 821–824. 8. Field DK, Kleinig TJ, Thompson PD, et al. Reversible cerebral vasoconstriction, internal carotid artery dissection and renal artery stenosis. Cephalalgia 2010; 30: 983–986.
