Case Report
Literature Review and Case Report of Intravenous Thrombolysis in Acute Cerebral Infarction Attributed to Cervical Arterial Dissection Zhihui Yan, PhD, Tianxia Yu, MS, Ying Wang, MS, Min Wang, MS, and Hui Liang, MS
Acute cerebral infarction (ACI) caused by cervical arterial dissection (CAD) is a rare clinical disease. Therapeutic approaches include anticoagulant therapy, antiplatelet aggregation, and thrombolytic therapy. Currently, anticoagulant therapy or antiplatelet aggregation is the primary choice, whereas the thrombolytic therapy is still controversial. In this article, we report a patient with ACI caused by right CAD, which led to a compensatory increase in blood supply to the right middle cerebral artery through the anterior communicating artery. After treatment with intravenous thrombolysis, the clinical symptoms of the patient improved, and the National Institutes of Health Stroke Scale (NIHSS) score declined to 2 points from the initial 14 points. In addition, cranial computed tomography scans showed that there were no signs of intracranial or extracranial hemorrhage, but that the vessel occlusion was still uncured. After 17 days of antiplatelet aggregation treatment, a cranial magnetic resonance angiography scan showed complete recanalization of the right internal carotid artery. Furthermore, the NIHSS score was reduced to 1 point when the patient discharged, and for 3 months of follow-up. Key Words: Intravenous thrombolysis—acute cerebral infarction—cervical arterial dissection—clinical case. Ó 2015 by National Stroke Association
Cervical arterial dissection (CAD) is a common cause of ischemic stroke in young people although it is rare in the overall population. Management of ischemic stroke caused by CAD remains uncertain, and most studies have focused on the use of antiplatelet drugs or anticoagulation therapy. At present, it is internationally accepted that intravenous (IV) thrombolysis is the preferred treatment in acute cerebral infarction (ACI) within 4.5 hours.
From the Department of Neurology, Yantaishan Hospital, Yantai, Shandong, China. Received February 28, 2015; revision received May 21, 2015; accepted May 30, 2015. Address correspondence to Hui Liang, MS, Department of Neurology, Yantaishan Hospital, 91 Jiefang Road, Yantai, Shandong 264001, China. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2015.05.028
However, there are few clinical reports regarding the safety and outcome of thrombolysis treatment in CAD. In this article, the clinical data of a patient with ACI caused by CAD are retrospectively analyzed. Furthermore, some relevant literature in the field is reviewed.
Case Report The patient was a 56-year-old man, presenting with a headache with paroxysmal inflexibility of left limbs and alalia. The patient started to experience a headache 3.5 hours before being hospitalized, with persistent pain mainly in the right occipitoparietal region. This was accompanied by loss of movement in the left limbs. Moreover, the patient could not walk or hold anything with his left hand and could only express himself verbally although slurring. The symptoms lasted for about 10 minutes and then eased. After half an hour, the symptoms above broke out again. The patient had no history of
Journal of Stroke and Cerebrovascular Diseases, Vol. -, No. - (---), 2015: pp e1-e5
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e2
smoking, drinking, or trauma but had a 10-year history of high blood pressure with the highest blood pressure recorded at 185/105 mm Hg and had never received any formal treatment. The patient’s first blood pressure reading after hospitalization was 182/103 mm Hg and was accompanied by drowsiness, dysarthria, a shallow left nasolabial groove, reduced muscle tone, level 2 left limb muscle, left hemihypalgesia, and a positive reflex of left pathologica. There were no other obvious positive signs. An initial craniocerebral computed tomography (CT) scan (Fig 1) showed a low-density shadow of frontal and parietal on the right cerebral hemisphere. The leukocyte concentration in blood was 12.65 3 109 cells/L with a neutrophil and granulocyte content of 83.4%. Four blood coagulation tests were normal, as well as electrocardiogram readings. The initial National Institutes of Health Stroke Scale (NIHSS) score was 14 points, which conformed to the IV thrombolysis standard. By consent of the patient’s family, approximately 4 hours after attack, alteplase IV thrombolysis was carried out; 7 mg of IV injection was first implemented followed by the remaining 63 mg pumped over a 60-minute period. One hour later, the symptoms improved and the NIHSS score declined to 2 points. After that, a series of tests were carried out, including 0.15 PNA urinary kallidinogenase injection test, kallidinogenase, butylbenzene, and medications administered including edaravone, atorvastatin, and aspirin. A CT scan performed the next day (Fig 2) showed a flaky low-density shadow in the right-side frontal lobe with an obscure boundary and indistinct sulcus. Brain magnetic resonance imaging (MRI; Figs 3 and 4)
Figure 1. Cranial computed tomography scans before intravenous thrombolysis.
Z. YAN ET AL.
Figure 2. Cranial computed tomography scans 15 hours after intravenous thrombolysis.
revealed ACI in the right-side temporal insula, occipital lobe, and basal ganglia regions. Furthermore, magnetic resonance angiography (MRA; Fig 5) showed that the middle cerebral artery (MCA) on the right side became slim, with a reduced number of branches. Moreover, the right internal carotid artery (ICA) was underdeveloped, and the initiation was broken (Fig 6). After approximately 2 days after arriving at the hospital, the patient started to develop further symptoms including profuse sweating, decreased flexibility in the left limbs, dysarthria, palsy of the left side of the eyes, with the right
Figure 3. Diffusion-weighted imaging of cranial MRI 20.5 hours after intravenous thrombolysis, which showed cerebral infarction. Abbreviation: MRI, magnetic resonance imaging.
IV THROMBOLYSIS IN ACI ATTRIBUTED TO CAD
Figure 4. Perfusion-weighted imaging (PWI) of cranial MRI 20.5 hours after intravenous thrombolysis, which showed hypoperfusion area. Abbreviation: MRI, magnetic resonance imaging.
pupil diminishing, right frontal adiapneustia, shallow left nasolabial groove, a left upper limb muscle strength level 0, left lower limb muscle strength level 2, NIHSS score 12 points, and blood pressure 150/80 mm Hg. After being treated with expansion and ascension of the blood pressure, the left limb muscle strength improved to level 4. A further brain CT scan the next day showed that the right temporal lobe cerebral infarction had spread (Fig 7). After treatment for dehydration and depression
Figure 5. Cranial magnetic resonance angiography showed that the intracranial segment of ICA was invisible and the right MCA was supplied blood through the left side via anterior communicating artery. Abbreviations: ICA, internal carotid artery; MCA, middle cerebral artery.
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Figure 6. MRA of neck showed the distal segment 2 cm away from the crotch of the right ICA was invisible. Abbreviations: ICA, internal carotid artery; MRA, magnetic resonance angiography.
of the intracranial pressure with treatment including glycerin and fructose, the condition of the patient became stable and the NIHSS score was 1 point. Seventeen days later, we performed an MRA scan of the head and neck, which revealed a vague middle view of the bilateral posterior cerebral artery, a stenosis of the first segment of the bilateral ICA, and a fair farend view of the right ICA (Fig 8). At this time, the patient could function independently and left hospital. The modified Rankin Scale (mRS) score was 1 point for 3 months of follow-up.
Figure 7. Cranial computed tomography scans showed infarction area after the aggravation.
Z. YAN ET AL.
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Figure 8. Recanalization of the right ICA after antiplatelet aggregation treatment. Abbreviation: ICA, internal carotid artery.
Results After treatment of IV thrombolysis, multiple cranial CT scans displayed no sign of hemorrhage of the patient with ACI attributed to CAD, which confirms the safety of IV thrombolysis. Nevertheless, the validity of this procedure is still uncertain for the uncured vessel occlusion after IV thrombolysis. However, antiplatelet aggregation treatment in the latter treatment period led to a complete recanalization of the right ICA, and when the patient discharged, the NIHSS score declined to 1 point from the initial 14 points (Fig 9). In addition, the mRS score was 1 point followed up for 3 months.
Discussion With the development of improvements in imaging technology, an increasing number of cerebral infarctions caused by CAD are being identified. One of the typical clinical manifestations is a ‘‘triad’’ of symptoms,1 which includes head or neck pain, Horner syndrome, and ischemic stroke. Also, vessel examinations show some typical changes, such as digital subtraction angiography, MRA, or computed tomography angiography. Clinical diagnosis of cerebral infarctions caused by CAD is not difficult,2,3 and the vessel will get excellent recanalization in the latter period after anticoagulation or antiplatelet therapy.4 However, there are no clear clinical guidelines which recommend whether to treat with thrombolytic therapy in ACI caused by CAD. In the latest version of the American Stroke Guidelines,5 the exclusion criteria of thrombolysis excludes CAD, and as a result, many clinicians
Figure 9. Neck MRA showed a completely recanalization of right ICA after treatment. Abbreviations: ICA, internal carotid artery; MRA, magnetic resonance angiography.
may feel concerned about safety and whether thrombolytic therapy is beneficial. In 2009, Stefan et al6 compared 55 patients with ACI caused by CAD with 1007 patients with ACI caused by other factors in 9 stroke centers in Switzerland and found there was no significant difference in both intracranial hemorrhage and stroke recurrence rate, and therefore the safety of this approach was affirmed. Similarly, in 2011, Zinkstok et al7 performed a meta-analysis of 180 cases of ACI caused by CAD after thrombolysis treatment. In addition, in 2012, through a multicenter prospective controlled study (with a total of 625 patients, including 16 CAD patients treated with IV thrombolysis and 27 CAD patients without IV thrombolysis), Fuentes et al8 reached a similar conclusion that IV thrombolysis was safe in patients with ACI caused by CAD with no symptomatic intracranial or extracranial bleeding. In conclusion, ACI caused by CAD should not be excluded from IV thrombolysis criteria.9 We examined the cranial CT scans of the patient reported previously several times after IV thrombolysis and found no intracranial or extracranial symptomatic intracranial hemorrhage. However, at present, the validity of IV thrombolytic therapy in ACI caused by CAD remains uncertain. Delgado et al10 reported a patient with an occlusive ICA dissection and MCA embolus, with collateral circulation through the ophthalmic artery and communicating anterior artery. He underwent IV thrombolysis, with subsequent MCA recanalization and achieved a good outcome. Also, Lewis et al11 reported a case in which the treatment of IV thrombolysis followed by endovascular thrombectomy resulted in a positive clinical outcome in a patient with tandem ICA and MCA occlusion
IV THROMBOLYSIS IN ACI ATTRIBUTED TO CAD 7
following ICA dissection. However, Zinkstok et al suggested that the validity of the non-CAD and CAD groups was similar and that the stroke severity and prognosis were closely related. Furthermore, Fuentes et al8 found that the improvement in NIHSS score was not obvious 7 days after IV thrombolysis in the CAD group. In addition, compared with the patients who were not treated with IV thrombolysis, there was no obvious difference in the therapeutic effect in patients with IV thrombolysis after 3 months. Moreover, Stefan et al6 found that 36% of CAD patients treated with IV thrombolysis achieved a favorable effect (mRS # 1), which was lower than the non-CAD IV thrombolysis group (44%). The study revealed that 90% of patients with CAD had CAD occlusion after IV thrombolysis, suggesting that IV thrombolysis may promote endothelial hemorrhage and luminal occlusion, which could aggravate ischemic damage. Similarly, Folgoas,12 Vergouwen,13 and Faivre14 reached similar conclusions. In this case, the clinical manifestations were typical headache, Horner syndrome, and ischemic stroke, which are in line with the characteristics of the CAD ‘‘triad’’ of symptoms. We considered the etiology of cerebral infarction was CAD, and NIHSS assessment was 14 points before thrombolysis. Although the score dropped to 2 points after thrombolysis, the brain MRI showed no obvious vessel recanalization and the condition of the patient aggravated in the latter period because of low blood volume. So the validity of thrombolytic treatment in the early period of treatment only lies in the improvement of collateral circulation. In contrast, after the patient received continuous antiplatelet therapy in the latter period, the brain MRI displayed absolute recanalization, which indicated that early antiplatelet therapy specification may be a reasonable treatment for ACI caused by CAD.15 This article focuses on 1 clinical case, and it is therefore impossible to reach a firm conclusion, which needs a larger sample size for robust statistical analysis. Considering clinical practice, it is the first choice to treat the patient with anticoagulant or antiplatelet therapy if the case can be confirmed as ACI due to CAD. Even if it is challenging to determine whether the symptoms conform to CAD or not, considering its relative safety, IV thrombolysis is worthy of consideration.
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References 1. Guillon B, Maiga Y, Desal H. Cervical and intracranial artery dissections. Rev Prat 2013;63:939-940. 942-6. 2. Rahme RJ, Aoun SG, McClendon J Jr. Spontaneous cervical and cerebral arterial dissections: diagnosis and management. Neuroimaging Clin N Am 2013;23:661-671. 3. Medel R, Starke RM, Valle-Giler EP, et al. Diagnosis and treatment of arterial dissections. Curr Neurol Neurosci Rep 2014;14:419. 4. Nedeltchev K, Bickel S, Arnold M, et al. R2-recanalization of spontaneous carotid artery dissection. Stroke 2009; 40:499-504. 5. Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management of patients with acute ischemic stroke: a stroke association Guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013;44:870-947. 6. Stefan TE, Matthieu PR, Florian H, et al. Intravenous thrombolysis in stroke attributable to cervical artery dissection. Stroke 2009;40:3772-3776. 7. Zinkstok SM, Vergouwen MD, Engelter ST, et al. Safety and functional outcome of thrombolysis in dissectionrelated ischemic stroke: a meta-analysis of individual patient data. Stroke 2011;42:2515-2520. 8. Fuentes B, Masjuan J, de Leci~ nana MA, et al. Benefits of intravenous thrombolysis in acute ischemic stroke related to extra cranial internal carotid dissection. Dream or reality? Int J Stroke 2012;7:7-13. 9. Georgiadis D, Baumgartner RW. Thrombolysis in cervical artery dissection. Front Neurol Neurosci 2005;20:140-146. 10. Delgado MG, Garcıa R, Murias E. Is intravenous thrombolysis useful in carotid artery dissection with tandem occlusion? J Stroke Cerebrovasc Dis 2012;21:87-88. 11. Lewis JB, Merwick A, Laoide RO, et al. Therapeutic decision making in acute stroke due to carotid artery dissection: a potential role for percutaneous vascular intervention following intravenous thrombolysis. Case Rep Vasc Med 2013;12:1696. 12. Folgoas E, Toulgoat F, Sevin M, et al. Ischemic stroke related to pauci-symptomatic acute aortic dissection. Risks of intravenous thrombolysis. Rev Neurol (Paris) 2012;168:357-362. 13. Vergouwen MD. Intravenous thrombolysis in ischaemic stroke secondary to cervical artery dissection: safe but not effective? Eur J Neurol 2012;19:1155-1156. 14. Faivre A, Sagui E, Canini F, et al. Intravenous thrombolysis with rt-PA in stroke: experience of the French military hospital of Toulon from September 2003 to June 2009. Rev Neurol (Paris) 2010;166:909-920. 15. Sarikaya H, da Costa BR, Baumgartner RW, et al. Antiplatelets versus anticoagulants for the treatment of cervical artery dissection: Bayesian meta-analysis. PLoS One 2013;8:e7269.
Literature Review and Case Report of Intravenous Thrombolysis in Acute Cerebral Infarction Attributed to Cervical Arterial Dissection Zhihui Yan, PhD, Tianxia Yu, MS, Ying Wang, MS, Min Wang, MS, and Hui Liang, MS
Acute cerebral infarction (ACI) caused by cervical arterial dissection (CAD) is a rare clinical disease. Therapeutic approaches include anticoagulant therapy, antiplatelet aggregation, and thrombolytic therapy. Currently, anticoagulant therapy or antiplatelet aggregation is the primary choice, whereas the thrombolytic therapy is still controversial. In this article, we report a patient with ACI caused by right CAD, which led to a compensatory increase in blood supply to the right middle cerebral artery through the anterior communicating artery. After treatment with intravenous thrombolysis, the clinical symptoms of the patient improved, and the National Institutes of Health Stroke Scale (NIHSS) score declined to 2 points from the initial 14 points. In addition, cranial computed tomography scans showed that there were no signs of intracranial or extracranial hemorrhage, but that the vessel occlusion was still uncured. After 17 days of antiplatelet aggregation treatment, a cranial magnetic resonance angiography scan showed complete recanalization of the right internal carotid artery. Furthermore, the NIHSS score was reduced to 1 point when the patient discharged, and for 3 months of follow-up. Key Words: Intravenous thrombolysis—acute cerebral infarction—cervical arterial dissection—clinical case. Ó 2015 by National Stroke Association
Cervical arterial dissection (CAD) is a common cause of ischemic stroke in young people although it is rare in the overall population. Management of ischemic stroke caused by CAD remains uncertain, and most studies have focused on the use of antiplatelet drugs or anticoagulation therapy. At present, it is internationally accepted that intravenous (IV) thrombolysis is the preferred treatment in acute cerebral infarction (ACI) within 4.5 hours.
From the Department of Neurology, Yantaishan Hospital, Yantai, Shandong, China. Received February 28, 2015; revision received May 21, 2015; accepted May 30, 2015. Address correspondence to Hui Liang, MS, Department of Neurology, Yantaishan Hospital, 91 Jiefang Road, Yantai, Shandong 264001, China. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2015.05.028
However, there are few clinical reports regarding the safety and outcome of thrombolysis treatment in CAD. In this article, the clinical data of a patient with ACI caused by CAD are retrospectively analyzed. Furthermore, some relevant literature in the field is reviewed.
Case Report The patient was a 56-year-old man, presenting with a headache with paroxysmal inflexibility of left limbs and alalia. The patient started to experience a headache 3.5 hours before being hospitalized, with persistent pain mainly in the right occipitoparietal region. This was accompanied by loss of movement in the left limbs. Moreover, the patient could not walk or hold anything with his left hand and could only express himself verbally although slurring. The symptoms lasted for about 10 minutes and then eased. After half an hour, the symptoms above broke out again. The patient had no history of
Journal of Stroke and Cerebrovascular Diseases, Vol. -, No. - (---), 2015: pp e1-e5
e1
e2
smoking, drinking, or trauma but had a 10-year history of high blood pressure with the highest blood pressure recorded at 185/105 mm Hg and had never received any formal treatment. The patient’s first blood pressure reading after hospitalization was 182/103 mm Hg and was accompanied by drowsiness, dysarthria, a shallow left nasolabial groove, reduced muscle tone, level 2 left limb muscle, left hemihypalgesia, and a positive reflex of left pathologica. There were no other obvious positive signs. An initial craniocerebral computed tomography (CT) scan (Fig 1) showed a low-density shadow of frontal and parietal on the right cerebral hemisphere. The leukocyte concentration in blood was 12.65 3 109 cells/L with a neutrophil and granulocyte content of 83.4%. Four blood coagulation tests were normal, as well as electrocardiogram readings. The initial National Institutes of Health Stroke Scale (NIHSS) score was 14 points, which conformed to the IV thrombolysis standard. By consent of the patient’s family, approximately 4 hours after attack, alteplase IV thrombolysis was carried out; 7 mg of IV injection was first implemented followed by the remaining 63 mg pumped over a 60-minute period. One hour later, the symptoms improved and the NIHSS score declined to 2 points. After that, a series of tests were carried out, including 0.15 PNA urinary kallidinogenase injection test, kallidinogenase, butylbenzene, and medications administered including edaravone, atorvastatin, and aspirin. A CT scan performed the next day (Fig 2) showed a flaky low-density shadow in the right-side frontal lobe with an obscure boundary and indistinct sulcus. Brain magnetic resonance imaging (MRI; Figs 3 and 4)
Figure 1. Cranial computed tomography scans before intravenous thrombolysis.
Z. YAN ET AL.
Figure 2. Cranial computed tomography scans 15 hours after intravenous thrombolysis.
revealed ACI in the right-side temporal insula, occipital lobe, and basal ganglia regions. Furthermore, magnetic resonance angiography (MRA; Fig 5) showed that the middle cerebral artery (MCA) on the right side became slim, with a reduced number of branches. Moreover, the right internal carotid artery (ICA) was underdeveloped, and the initiation was broken (Fig 6). After approximately 2 days after arriving at the hospital, the patient started to develop further symptoms including profuse sweating, decreased flexibility in the left limbs, dysarthria, palsy of the left side of the eyes, with the right
Figure 3. Diffusion-weighted imaging of cranial MRI 20.5 hours after intravenous thrombolysis, which showed cerebral infarction. Abbreviation: MRI, magnetic resonance imaging.
IV THROMBOLYSIS IN ACI ATTRIBUTED TO CAD
Figure 4. Perfusion-weighted imaging (PWI) of cranial MRI 20.5 hours after intravenous thrombolysis, which showed hypoperfusion area. Abbreviation: MRI, magnetic resonance imaging.
pupil diminishing, right frontal adiapneustia, shallow left nasolabial groove, a left upper limb muscle strength level 0, left lower limb muscle strength level 2, NIHSS score 12 points, and blood pressure 150/80 mm Hg. After being treated with expansion and ascension of the blood pressure, the left limb muscle strength improved to level 4. A further brain CT scan the next day showed that the right temporal lobe cerebral infarction had spread (Fig 7). After treatment for dehydration and depression
Figure 5. Cranial magnetic resonance angiography showed that the intracranial segment of ICA was invisible and the right MCA was supplied blood through the left side via anterior communicating artery. Abbreviations: ICA, internal carotid artery; MCA, middle cerebral artery.
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Figure 6. MRA of neck showed the distal segment 2 cm away from the crotch of the right ICA was invisible. Abbreviations: ICA, internal carotid artery; MRA, magnetic resonance angiography.
of the intracranial pressure with treatment including glycerin and fructose, the condition of the patient became stable and the NIHSS score was 1 point. Seventeen days later, we performed an MRA scan of the head and neck, which revealed a vague middle view of the bilateral posterior cerebral artery, a stenosis of the first segment of the bilateral ICA, and a fair farend view of the right ICA (Fig 8). At this time, the patient could function independently and left hospital. The modified Rankin Scale (mRS) score was 1 point for 3 months of follow-up.
Figure 7. Cranial computed tomography scans showed infarction area after the aggravation.
Z. YAN ET AL.
e4
Figure 8. Recanalization of the right ICA after antiplatelet aggregation treatment. Abbreviation: ICA, internal carotid artery.
Results After treatment of IV thrombolysis, multiple cranial CT scans displayed no sign of hemorrhage of the patient with ACI attributed to CAD, which confirms the safety of IV thrombolysis. Nevertheless, the validity of this procedure is still uncertain for the uncured vessel occlusion after IV thrombolysis. However, antiplatelet aggregation treatment in the latter treatment period led to a complete recanalization of the right ICA, and when the patient discharged, the NIHSS score declined to 1 point from the initial 14 points (Fig 9). In addition, the mRS score was 1 point followed up for 3 months.
Discussion With the development of improvements in imaging technology, an increasing number of cerebral infarctions caused by CAD are being identified. One of the typical clinical manifestations is a ‘‘triad’’ of symptoms,1 which includes head or neck pain, Horner syndrome, and ischemic stroke. Also, vessel examinations show some typical changes, such as digital subtraction angiography, MRA, or computed tomography angiography. Clinical diagnosis of cerebral infarctions caused by CAD is not difficult,2,3 and the vessel will get excellent recanalization in the latter period after anticoagulation or antiplatelet therapy.4 However, there are no clear clinical guidelines which recommend whether to treat with thrombolytic therapy in ACI caused by CAD. In the latest version of the American Stroke Guidelines,5 the exclusion criteria of thrombolysis excludes CAD, and as a result, many clinicians
Figure 9. Neck MRA showed a completely recanalization of right ICA after treatment. Abbreviations: ICA, internal carotid artery; MRA, magnetic resonance angiography.
may feel concerned about safety and whether thrombolytic therapy is beneficial. In 2009, Stefan et al6 compared 55 patients with ACI caused by CAD with 1007 patients with ACI caused by other factors in 9 stroke centers in Switzerland and found there was no significant difference in both intracranial hemorrhage and stroke recurrence rate, and therefore the safety of this approach was affirmed. Similarly, in 2011, Zinkstok et al7 performed a meta-analysis of 180 cases of ACI caused by CAD after thrombolysis treatment. In addition, in 2012, through a multicenter prospective controlled study (with a total of 625 patients, including 16 CAD patients treated with IV thrombolysis and 27 CAD patients without IV thrombolysis), Fuentes et al8 reached a similar conclusion that IV thrombolysis was safe in patients with ACI caused by CAD with no symptomatic intracranial or extracranial bleeding. In conclusion, ACI caused by CAD should not be excluded from IV thrombolysis criteria.9 We examined the cranial CT scans of the patient reported previously several times after IV thrombolysis and found no intracranial or extracranial symptomatic intracranial hemorrhage. However, at present, the validity of IV thrombolytic therapy in ACI caused by CAD remains uncertain. Delgado et al10 reported a patient with an occlusive ICA dissection and MCA embolus, with collateral circulation through the ophthalmic artery and communicating anterior artery. He underwent IV thrombolysis, with subsequent MCA recanalization and achieved a good outcome. Also, Lewis et al11 reported a case in which the treatment of IV thrombolysis followed by endovascular thrombectomy resulted in a positive clinical outcome in a patient with tandem ICA and MCA occlusion
IV THROMBOLYSIS IN ACI ATTRIBUTED TO CAD 7
following ICA dissection. However, Zinkstok et al suggested that the validity of the non-CAD and CAD groups was similar and that the stroke severity and prognosis were closely related. Furthermore, Fuentes et al8 found that the improvement in NIHSS score was not obvious 7 days after IV thrombolysis in the CAD group. In addition, compared with the patients who were not treated with IV thrombolysis, there was no obvious difference in the therapeutic effect in patients with IV thrombolysis after 3 months. Moreover, Stefan et al6 found that 36% of CAD patients treated with IV thrombolysis achieved a favorable effect (mRS # 1), which was lower than the non-CAD IV thrombolysis group (44%). The study revealed that 90% of patients with CAD had CAD occlusion after IV thrombolysis, suggesting that IV thrombolysis may promote endothelial hemorrhage and luminal occlusion, which could aggravate ischemic damage. Similarly, Folgoas,12 Vergouwen,13 and Faivre14 reached similar conclusions. In this case, the clinical manifestations were typical headache, Horner syndrome, and ischemic stroke, which are in line with the characteristics of the CAD ‘‘triad’’ of symptoms. We considered the etiology of cerebral infarction was CAD, and NIHSS assessment was 14 points before thrombolysis. Although the score dropped to 2 points after thrombolysis, the brain MRI showed no obvious vessel recanalization and the condition of the patient aggravated in the latter period because of low blood volume. So the validity of thrombolytic treatment in the early period of treatment only lies in the improvement of collateral circulation. In contrast, after the patient received continuous antiplatelet therapy in the latter period, the brain MRI displayed absolute recanalization, which indicated that early antiplatelet therapy specification may be a reasonable treatment for ACI caused by CAD.15 This article focuses on 1 clinical case, and it is therefore impossible to reach a firm conclusion, which needs a larger sample size for robust statistical analysis. Considering clinical practice, it is the first choice to treat the patient with anticoagulant or antiplatelet therapy if the case can be confirmed as ACI due to CAD. Even if it is challenging to determine whether the symptoms conform to CAD or not, considering its relative safety, IV thrombolysis is worthy of consideration.
e5
References 1. Guillon B, Maiga Y, Desal H. Cervical and intracranial artery dissections. Rev Prat 2013;63:939-940. 942-6. 2. Rahme RJ, Aoun SG, McClendon J Jr. Spontaneous cervical and cerebral arterial dissections: diagnosis and management. Neuroimaging Clin N Am 2013;23:661-671. 3. Medel R, Starke RM, Valle-Giler EP, et al. Diagnosis and treatment of arterial dissections. Curr Neurol Neurosci Rep 2014;14:419. 4. Nedeltchev K, Bickel S, Arnold M, et al. R2-recanalization of spontaneous carotid artery dissection. Stroke 2009; 40:499-504. 5. Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management of patients with acute ischemic stroke: a stroke association Guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013;44:870-947. 6. Stefan TE, Matthieu PR, Florian H, et al. Intravenous thrombolysis in stroke attributable to cervical artery dissection. Stroke 2009;40:3772-3776. 7. Zinkstok SM, Vergouwen MD, Engelter ST, et al. Safety and functional outcome of thrombolysis in dissectionrelated ischemic stroke: a meta-analysis of individual patient data. Stroke 2011;42:2515-2520. 8. Fuentes B, Masjuan J, de Leci~ nana MA, et al. Benefits of intravenous thrombolysis in acute ischemic stroke related to extra cranial internal carotid dissection. Dream or reality? Int J Stroke 2012;7:7-13. 9. Georgiadis D, Baumgartner RW. Thrombolysis in cervical artery dissection. Front Neurol Neurosci 2005;20:140-146. 10. Delgado MG, Garcıa R, Murias E. Is intravenous thrombolysis useful in carotid artery dissection with tandem occlusion? J Stroke Cerebrovasc Dis 2012;21:87-88. 11. Lewis JB, Merwick A, Laoide RO, et al. Therapeutic decision making in acute stroke due to carotid artery dissection: a potential role for percutaneous vascular intervention following intravenous thrombolysis. Case Rep Vasc Med 2013;12:1696. 12. Folgoas E, Toulgoat F, Sevin M, et al. Ischemic stroke related to pauci-symptomatic acute aortic dissection. Risks of intravenous thrombolysis. Rev Neurol (Paris) 2012;168:357-362. 13. Vergouwen MD. Intravenous thrombolysis in ischaemic stroke secondary to cervical artery dissection: safe but not effective? Eur J Neurol 2012;19:1155-1156. 14. Faivre A, Sagui E, Canini F, et al. Intravenous thrombolysis with rt-PA in stroke: experience of the French military hospital of Toulon from September 2003 to June 2009. Rev Neurol (Paris) 2010;166:909-920. 15. Sarikaya H, da Costa BR, Baumgartner RW, et al. Antiplatelets versus anticoagulants for the treatment of cervical artery dissection: Bayesian meta-analysis. PLoS One 2013;8:e7269.
