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Vertebrobasilar dolichoectasia causing a presentation resembling basilar-type migraine
Clinical Neurology and Neurosurgery 115 (2013) 784–786
Contents lists available at SciVerse ScienceDirect
Clinical Neurology and Neurosurgery journal homepage: www.elsevier.com/locate/clineuro
Case report
Vertebrobasilar dolichoectasia causing a presentation resembling basilar-type migraine Lin Huang a , Chuan-Yong Yu a , Bei-Na Wang b , Hui-Min Zhang a , Liang-Yong Li a , Yu Wang a,∗ a b
Department of Neurology, Epilepsy and Headache Group, The First Hospital of Anhui Medical University, Jixi Road 218, Hefei 230022, China Department of Neurology, 105th Hospital of PLA, Hefei 230011, China
a r t i c l e
i n f o
Article history: Received 15 March 2011 Received in revised form 7 May 2012 Accepted 5 July 2012 Available online 9 August 2012 Keywords: Basilar-type migraine Brainstem Vertebrobasilar dolichoectasia Antiepileptic drug
1. Introduction Vertebrobasilar dolichoectasia (VBD) is characterized by marked elongation, dilatation and tortuosity of the vertebral and the basilar arteries. It can cause many clinical presentations related to the following pathophysiologic mechanisms: acute brain ischemia; a progressive course related to compression of cranial nerves, the brain stem, or the third ventricle; and catastrophic outcome caused by vascular rupture [1]. But VBD has never been reported to be associated with a clinical manifestation analogous to basilar-type migraine. Here, we described a patient with clinical manifestations analogues to basilar-type migraine together with VBD detected by magnetic resonance imaging. The possible causal relationship between these two events was discussed. 2. Case report A 64-year-old man presented with a 5-year history of recurrent left-sided or global headaches accompanied with vertigo, phonophobia and photophobia, nausea, or vomiting. The headache usually attacked in a frequency ranged from one time every two months to three times every one week, and in a duration of several hours. A typical attack would begin with a vertigo lasting for less than 1 h, and the headache would occur while he was complaining of vertigo. The headache and the accompanying symptoms
∗ Corresponding author. Tel.: +86 551 2922665. E-mail address: [email protected] (Y. Wang). 0303-8467/$ – see front matter © 2012 Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.clineuro.2012.07.007
would be alleviated by sleep or analgesics but exacerbated by movement or similar physical activity. The headache was never preceded by visual symptoms of flickering or black spots in both visual fields. But in recent half year, this patient experienced several times of short duration (about 15 min) of vertigo followed by sudden loss of consciousness with duration of about 10 min. No jerk, urinary incontinence, or tongue bite were reported. When consciousness recovered, the patient would have a terrible headache with no confusional status and the headache could be aborted by ibuprofen. Before this event, he had neither personal nor family history of headaches. Neurological examination was unremarkable. No history of hypertension, cardiac disease or diabetes mellitus was reported and physical examinations were normal. Blood tests revealed that the blood cholesterol, triglyceride, glycemia and homocysteine were normal. A clinical diagnosis of basilar-type migraine was made, based on the clinical manifestations which fulfilled the International Headache Society (ICHD-II) criteria for basilar-type migraine. Brain magnetic resonance imaging (MRI) showed focal areas of hyperintensity in the periventricular white matter and in pons in T2-weighted magnetic resonance (MR) images, and no enhancement in postcontrast T1-weighted images; the ventricles and cerebral cisterns were normal in size and shape. Diffusion weighted imaging (DWI) did not reveal any fresh infarct (Fig. 1). Magnetic resonance angiography (MRA) of cranial vessels showed dolichoectasia of the left vertebral artery (VA) and the entire basilar artery (BA) till its bifurcation and severe stenosis of the right VA (Fig. 2). The maximum diameter of BA was 11.5 mm and the left VA 10.7 mm. These radiological findings are consistent with that of
L. Huang et al. / Clinical Neurology and Neurosurgery 115 (2013) 784–786
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Fig. 1. Identical axial sections of T2 weighted (A1, B1), flair (A2, B2) and diffusion weighted (A3, B3) magnetic resonance (MR) images of the brain. Mild hyperintensive signals can be identified in the periventricular white matter (arrowheads on A1) and in pons (arrowheads on B1) on T2 weighted images. Stronger hyperintensive signals can be identified in the periventricular white matter (arrowheads on A2) and in pons (arrowheads on B2) on flair images. No abnormal signal can be found on diffusion weighted imaging (DWI) (A3 and B3).
Fig. 2. Brain magnetic resonance angiography (MRA) images of axial (A1), coronal (A3) and axial view rotated (A2). The left vertebral artery (VA) and the basilar artery (BA) are elongated, dilated and distorted to the left and the right vertebral artery is extremely stenotic (indicated by arrows) (A1–A3). The junction of the vertebral artery and the basilar artery is marked with arrowheads (A1–A3). Postcontrast images of sagittal (B1), axial (B2) and coronal (B3) view. Dilated vertebral artery compresses the pons (indicated by arrowheads on A1).
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VBD [2]. With these magnetic resonance (MR) findings, the initial diagnosis was then revised to secondary headache attributed to cranial vascular disorder (ICHD-II), as the criteria for basilartype migraine requires the exclusion of other disorders. He was treated with sodium valproate (compound sodium valproate and valproic acid sustained release tablets) 1000 mg per day as prophylactic treatment and he had an excellent response to this treatment with no new attack in the subsequent eight months’ follow-up. 3. Discussion The manifestations of VBD may be asymptomatic or symptomatic depending on the degree of ectasia and elongation of the BA and VA. The manifestations include posterior circulation infarcts, compression of cranial nerves or brainstem [1]. Here, we, for the first time, report a case of VBD in conjunction with a clinical event which is analogous to basilar-type migraine though the direct association between these two events in one case remains unproven. Previous reports showed that brainstem pathological changes, e.g. pontine capillary telangiectasia [3] and calcifications in the pontine tegmental nuclei [4], were associated with ‘secondary basilar-type migraine’. The recurrent attacks of ‘basilar-type migraine’-like syndrome including the aura of unconsciousness and vertigo in our patient may be originated from the pathological changes of brainstem due to the VBD induced chronic compression or ischemia. This is supported by the finding of hyperintensive signal in pons on T2-weighted MR images, and also supported by the fact that the patient had no other cerebrovascular risk factors reported or detected. On the other hand, a diagnosis of posterior circulation transient ischemic attacks (TIA) should also be considered as the recurrent events including headache, vertigo and unconsciousness may be caused by an acute ischemia of posterior circulation. But the recurrent events in this case seemly are not attributed to an acute ischemia of posterior circulation as prophylactic treatment with antiepileptic drug sodium valproate but not with agents affecting vascular or circulation successfully prevented the recurrence of the
events. This is in consistence with literature report that antiepileptic drugs, topiramate and valproate have been shown effective in the prophylactic treatment of primary basilar-type migraine [5]. Based on these, we hypothesize that the ‘basilar-type migraine’-like syndrome in the current case may share a same underlying mechanism with primary basilar-type migraine, i.e. chronic dysfunction of brainstem. The hypothesis of chronic pathological changes of the brainstem may also explain why the ‘basilar-type migraine’like syndrome occurred at an old age in our patient while the VBD may exist there for many years, as it is a progressive course related to the compression or ischemia induced by the elongation, dilatation and tortuosity of the vertebral and the basilar arteries [1]. 4. Conclusion We described a patient with a clinical manifestation analogous to basilar-type migraine together with a VBD detected by MRA. This case report suggested the hypothesis that VBD may cause a ‘basilar-type migraine’-like syndrome via inducing chronic pathological changes of the brainstem. In addition, we suggest that brain MR imaging should be considered if a diagnosis of basilar-type migraine is made. References [1] Lou M, Caplan LR. Vertebrobasilar dilatative arteriopathy (dolichoectasia). Annals of the New York Academy of Sciences 2010;1184:121–33. [2] Ubogu EE, Zaidat OO. Vertebrobasilar dolichoectasia diagnosed by magnetic resonance angiography and risk of stroke and death: a cohort study. Journal of Neurology, Neurosurgery, and Psychiatry 2004;75:22–6. [3] Beukers RJ, Roos YB. Pontine capillary telangiectasia as visualized on MR imaging causing a clinical picture resembling basilar-type migraine: a case report. Journal of Neurology 2009;256:1775–7. [4] Mishra NK, Cereda C, Carota A. Lifetime basilar migraine: a pontine syndrome? Headache 2008;48:476–8. [5] Baier B, Winkenwerder E, Dieterich M. Vestibular migraine: effects of prophylactic therapy with various drugs. A retrospective study. Journal of Neurology 2009;256:436–42.
Contents lists available at SciVerse ScienceDirect
Clinical Neurology and Neurosurgery journal homepage: www.elsevier.com/locate/clineuro
Case report
Vertebrobasilar dolichoectasia causing a presentation resembling basilar-type migraine Lin Huang a , Chuan-Yong Yu a , Bei-Na Wang b , Hui-Min Zhang a , Liang-Yong Li a , Yu Wang a,∗ a b
Department of Neurology, Epilepsy and Headache Group, The First Hospital of Anhui Medical University, Jixi Road 218, Hefei 230022, China Department of Neurology, 105th Hospital of PLA, Hefei 230011, China
a r t i c l e
i n f o
Article history: Received 15 March 2011 Received in revised form 7 May 2012 Accepted 5 July 2012 Available online 9 August 2012 Keywords: Basilar-type migraine Brainstem Vertebrobasilar dolichoectasia Antiepileptic drug
1. Introduction Vertebrobasilar dolichoectasia (VBD) is characterized by marked elongation, dilatation and tortuosity of the vertebral and the basilar arteries. It can cause many clinical presentations related to the following pathophysiologic mechanisms: acute brain ischemia; a progressive course related to compression of cranial nerves, the brain stem, or the third ventricle; and catastrophic outcome caused by vascular rupture [1]. But VBD has never been reported to be associated with a clinical manifestation analogous to basilar-type migraine. Here, we described a patient with clinical manifestations analogues to basilar-type migraine together with VBD detected by magnetic resonance imaging. The possible causal relationship between these two events was discussed. 2. Case report A 64-year-old man presented with a 5-year history of recurrent left-sided or global headaches accompanied with vertigo, phonophobia and photophobia, nausea, or vomiting. The headache usually attacked in a frequency ranged from one time every two months to three times every one week, and in a duration of several hours. A typical attack would begin with a vertigo lasting for less than 1 h, and the headache would occur while he was complaining of vertigo. The headache and the accompanying symptoms
∗ Corresponding author. Tel.: +86 551 2922665. E-mail address: [email protected] (Y. Wang). 0303-8467/$ – see front matter © 2012 Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.clineuro.2012.07.007
would be alleviated by sleep or analgesics but exacerbated by movement or similar physical activity. The headache was never preceded by visual symptoms of flickering or black spots in both visual fields. But in recent half year, this patient experienced several times of short duration (about 15 min) of vertigo followed by sudden loss of consciousness with duration of about 10 min. No jerk, urinary incontinence, or tongue bite were reported. When consciousness recovered, the patient would have a terrible headache with no confusional status and the headache could be aborted by ibuprofen. Before this event, he had neither personal nor family history of headaches. Neurological examination was unremarkable. No history of hypertension, cardiac disease or diabetes mellitus was reported and physical examinations were normal. Blood tests revealed that the blood cholesterol, triglyceride, glycemia and homocysteine were normal. A clinical diagnosis of basilar-type migraine was made, based on the clinical manifestations which fulfilled the International Headache Society (ICHD-II) criteria for basilar-type migraine. Brain magnetic resonance imaging (MRI) showed focal areas of hyperintensity in the periventricular white matter and in pons in T2-weighted magnetic resonance (MR) images, and no enhancement in postcontrast T1-weighted images; the ventricles and cerebral cisterns were normal in size and shape. Diffusion weighted imaging (DWI) did not reveal any fresh infarct (Fig. 1). Magnetic resonance angiography (MRA) of cranial vessels showed dolichoectasia of the left vertebral artery (VA) and the entire basilar artery (BA) till its bifurcation and severe stenosis of the right VA (Fig. 2). The maximum diameter of BA was 11.5 mm and the left VA 10.7 mm. These radiological findings are consistent with that of
L. Huang et al. / Clinical Neurology and Neurosurgery 115 (2013) 784–786
785
Fig. 1. Identical axial sections of T2 weighted (A1, B1), flair (A2, B2) and diffusion weighted (A3, B3) magnetic resonance (MR) images of the brain. Mild hyperintensive signals can be identified in the periventricular white matter (arrowheads on A1) and in pons (arrowheads on B1) on T2 weighted images. Stronger hyperintensive signals can be identified in the periventricular white matter (arrowheads on A2) and in pons (arrowheads on B2) on flair images. No abnormal signal can be found on diffusion weighted imaging (DWI) (A3 and B3).
Fig. 2. Brain magnetic resonance angiography (MRA) images of axial (A1), coronal (A3) and axial view rotated (A2). The left vertebral artery (VA) and the basilar artery (BA) are elongated, dilated and distorted to the left and the right vertebral artery is extremely stenotic (indicated by arrows) (A1–A3). The junction of the vertebral artery and the basilar artery is marked with arrowheads (A1–A3). Postcontrast images of sagittal (B1), axial (B2) and coronal (B3) view. Dilated vertebral artery compresses the pons (indicated by arrowheads on A1).
786
L. Huang et al. / Clinical Neurology and Neurosurgery 115 (2013) 784–786
VBD [2]. With these magnetic resonance (MR) findings, the initial diagnosis was then revised to secondary headache attributed to cranial vascular disorder (ICHD-II), as the criteria for basilartype migraine requires the exclusion of other disorders. He was treated with sodium valproate (compound sodium valproate and valproic acid sustained release tablets) 1000 mg per day as prophylactic treatment and he had an excellent response to this treatment with no new attack in the subsequent eight months’ follow-up. 3. Discussion The manifestations of VBD may be asymptomatic or symptomatic depending on the degree of ectasia and elongation of the BA and VA. The manifestations include posterior circulation infarcts, compression of cranial nerves or brainstem [1]. Here, we, for the first time, report a case of VBD in conjunction with a clinical event which is analogous to basilar-type migraine though the direct association between these two events in one case remains unproven. Previous reports showed that brainstem pathological changes, e.g. pontine capillary telangiectasia [3] and calcifications in the pontine tegmental nuclei [4], were associated with ‘secondary basilar-type migraine’. The recurrent attacks of ‘basilar-type migraine’-like syndrome including the aura of unconsciousness and vertigo in our patient may be originated from the pathological changes of brainstem due to the VBD induced chronic compression or ischemia. This is supported by the finding of hyperintensive signal in pons on T2-weighted MR images, and also supported by the fact that the patient had no other cerebrovascular risk factors reported or detected. On the other hand, a diagnosis of posterior circulation transient ischemic attacks (TIA) should also be considered as the recurrent events including headache, vertigo and unconsciousness may be caused by an acute ischemia of posterior circulation. But the recurrent events in this case seemly are not attributed to an acute ischemia of posterior circulation as prophylactic treatment with antiepileptic drug sodium valproate but not with agents affecting vascular or circulation successfully prevented the recurrence of the
events. This is in consistence with literature report that antiepileptic drugs, topiramate and valproate have been shown effective in the prophylactic treatment of primary basilar-type migraine [5]. Based on these, we hypothesize that the ‘basilar-type migraine’-like syndrome in the current case may share a same underlying mechanism with primary basilar-type migraine, i.e. chronic dysfunction of brainstem. The hypothesis of chronic pathological changes of the brainstem may also explain why the ‘basilar-type migraine’like syndrome occurred at an old age in our patient while the VBD may exist there for many years, as it is a progressive course related to the compression or ischemia induced by the elongation, dilatation and tortuosity of the vertebral and the basilar arteries [1]. 4. Conclusion We described a patient with a clinical manifestation analogous to basilar-type migraine together with a VBD detected by MRA. This case report suggested the hypothesis that VBD may cause a ‘basilar-type migraine’-like syndrome via inducing chronic pathological changes of the brainstem. In addition, we suggest that brain MR imaging should be considered if a diagnosis of basilar-type migraine is made. References [1] Lou M, Caplan LR. Vertebrobasilar dilatative arteriopathy (dolichoectasia). Annals of the New York Academy of Sciences 2010;1184:121–33. [2] Ubogu EE, Zaidat OO. Vertebrobasilar dolichoectasia diagnosed by magnetic resonance angiography and risk of stroke and death: a cohort study. Journal of Neurology, Neurosurgery, and Psychiatry 2004;75:22–6. [3] Beukers RJ, Roos YB. Pontine capillary telangiectasia as visualized on MR imaging causing a clinical picture resembling basilar-type migraine: a case report. Journal of Neurology 2009;256:1775–7. [4] Mishra NK, Cereda C, Carota A. Lifetime basilar migraine: a pontine syndrome? Headache 2008;48:476–8. [5] Baier B, Winkenwerder E, Dieterich M. Vestibular migraine: effects of prophylactic therapy with various drugs. A retrospective study. Journal of Neurology 2009;256:436–42.