IUeuro-- Neuroradiology (1993) 35:196-198 radiology 9 Springer-Verlag 1993 Pure motor hemiparesis in a case of vertebrobasilar arterial ectasia L. Milandre 1, P. Martini 2, S. Perot 2, and C. Mercier ~ Departments of ~Neurology, 2 Neuroradiology and 3 Vascular Surgery, CHU Timone, Marseille, France Received: 2 March 1992 Summary. A case of pure m o t o r hemiparesis due to a pontine lacunar infarct is reported. Infarction was related to vertebrobasilar ectasia identified on CT, M R I and M R angiography. M R studies p r o v i d e accurate i n f o r m a t i o n on anatomical location, residual lumen, partial thrombosis, mass effect on brain s t e m a n d C S F p a t h w a y s and vascular complications. Key words: Intracranial a n e u r y s m - Basilar a r t e r y - Ectasia - M a g n e t i c r e s o n a n c e imaging - M a g n e t i c r e s o n a n c e angiography I n 1965, Fisher and C u r r y [1] defined pure m o t o r hemiplegia as paralysis of the face, a r m and leg on one side w i t h o u t any o t h e r neurological finding, except for dysarthria. Since the paralysis was usually incomplete, the t e r m p u r e m o t o r hemiparesis ( P M H ) was considered m o r e appropriate. P M H is c o m m o n l y caused by a small, d e e p cerebral infarct or lacune located s o m e w h e r e along the corticospinal pathway. H o w e v e r , several other causes of P M H have b e e n described, including h a e m o r r h a g e s , tumours, multiple sclerosis or infections [2]. We report a case of P M H due to vertebrobasilar ectasia ( V B E ) identified on m a gnetic r e s o n a n c e imaging ( M R I ) and M R a n g i o g r a p h y (MRA). Case report A 67-year-old right-handed hypertensive man was admitted because of a right hemiparesis. Over about 6 months, he had developed a progressive gait disorder caused by weakness and hypertonia of the right leg. His wife had also noticed unmotivated crying and laughing. On the day of admission, his clinical state had suddenly worsened with marked weakness of the right limbs without associated signs. Neurological examination showed a right hemiparesis, more marked in the leg, a slight central facial paresis, and moderate dysarthria without dysphagia. Tendon reflexes were very brisk on both sides but plantar responses were flexor. The right arm was flaccid while the leg was markedly spastic. Detailed examination of sensation, visual fields, ocular movements, coordination and cognitive functions was normal. CT showed several loci of calcification in the left cerebellopontine angle. Contrast-enhancement showed a round, hyperdense mass deforming the left side of the pons. Additional hyperdense areas were seen in the parasellar region. These findings were suggestive of ectasia of the basilar artery (BA) and both carotid siphons. MRI was performed at 2 T, with a multisection, spin-echo techniqne. Tl-weighted images were obtained in sagittai, coronal, and axial planes with repetition time (TR) 480 ms and echo time (TE) 13 ms. T2-weighted images were obtained in the axial plane with TR 2600 ms and TE 22 and 80 ms. The right vertebral artery (VA) appeared elongated and tortuous. The BA originated in the left cerebellopontine angle cistern and was markedly elongated, its bifurcation indenting the floor of the third ventricle (Fig. 1). Its inferior half was markedly enlarged, with the appearance of a fusiform aneurysm deforming the left side of the pons (Fig. 1). Evidence of a large patent portion within the aneurysmal lumen was given by signal void or isointensity on T1- and T2-weighted sections (Figs. 1, 2). However, the residual lumen appeared of heterogeneous intensity, suggestive of partial thrombosis. A lacunar infarct was identified in the left paramedian part of the pons (Fig. 2). Three-dimensional fime-of-flight MRA was performed on a 1.5 T superconducting magnet, with fast imaging using steady precession (FISP) sequences, TR 36 ms, TE 7 ms. A field of view of 22 cm was used. The MRA showed an elongated right VA, an ectatic BA, and dilated carotid siphons (Fig. 3). Other laboratory tests, Doppler ultrasonography of cervical arteries and abdominal aorta, chest radiography, ECG and two-dimensional echocardiography were normal. The patient's state progressively improved and he was discharged home receiving acetylsalicylic acid, and having physiotherapy. Six months later, he had a residual spastic weakness of the right leg. Discussion O u r patient p r e s e n t e d with a right P M H caused by a small pontine infarct in the territory of the p a r a m e d i a n perforating b r a n c h e s of an ectatic B A . Prior to his stroke, he had progressive w e a k n e s s of the right leg which could be attributed to the c o m p r e s s i o n of the left anterior part of the lower pons by the ectatic vessel. P M H is the most comm o n lacunar syndrome, accounting for a b o u t half of cases [2]. T h e f r e q u e n c y of lacunar infarction involving the basis pontis is u n d e r e s t i m a t e d by CT. M R I identifies lacunes m o r e accurately [3]. 197 Fib.1. a Sagittal; b,e coronal; d,e axial Tl-weighted (480/13) MRI shows an extra-axial, mainly hypointense mass in the left cerebellopontine cistern (arrowhead in a). It has a central linear signal void, representing an elongated and tortuous right vertebral artery (VA) and fusiform ectasia of the inferior half of the basilar artery (BA), the tip of which indents the floor of the third ventricle (in c). The ectatic vessel deforms the left anterior basis pontis.There is a lacunar infarct in the left basis pontis (arrowhead) Fig.2. T2-weighted (2600/22-80) axial MRI shows the heterogenous aneurysmal lumen with a lateral signal void (arrowhead) and medial hyperintensity (arrow). The left paramedian lacunar infarct is better seen. Fig.3. Three-dimensional MR angiogram (36/7, 40 ~flip angle, FISE multiple-volume acquisition) shows elongation of the right VA, an ectatic BA (star) and dilation of both carotid siphons V B E is a rare cause o f stroke. Yu et al. [4] f o u n d a ectasia of the vertebrobasilar system in 17, 11 of which were symptomatic, in 10,000 consecutive vertebral angiograms. Despite the fact that C T has simplified the recognition of V B E [5], the small n u m b e r of patients in recent series [6-8] confirms the rarity of s y m p t o m a t i c cases. S y m p t o m s can result f r o m compression (of cranial nerves, brain stein or C S F pathway), f r o m stroke (ischaemia rather than rupture) or both, as in our case. T h e ectatic arterial wall shows pathological changes consisting of extensive defects in the internal elastic lamina and severe reticular fibre deficiency in the m e d i a [9]. W h e t h e r these changes result f r o m 198 atherosclerosis [7] or f r o m an underlying structural arterial defect [9] remains controversial. W h a t e v e r the pathogenesis, severe atherosclerosis and intraluminal thrombus usually coexist with these morphological features. Pessin et al. [10] studied the mechanisms of infarction in patients with VBE. Thrombosis of the ectatic vessel usually causes a massive, fatal brain-stem infarct. Arterial embolism m a y account for infarction in the territory of the terminal or circumferential branches. A p a r a m e d i a n pontine infarct, as in our case, can be due to obstruction of a perforating arteriole at its origin by a t h e r o m a or intraluminal thrombus. Distortion of the perforating vessels, due to an elongated, tortuous BA, could also contribute to ischaemia. Most patients with V B E are hypertensive: arteriolar lipohyalinosis m a y therefore also play a causative role in lacunar infarcts. Two previous cases of P M H were reported in association with V B E [6, 8] indicating that infarction in the perforating artery territories m a y co-exist with large vessel obstruction [2]. M R I can be used for showing V B E and its consequences [11-15]. It shows the deformation of the pons, perianeurysmal oedema, and mass effect on the CSF pathways. Elongation and tortuosity of the vertebrobasilar arterial system can be easily d e m o n s t r a t e d on T l - w e i g h t e d coronal sections. The parent vessel, the patent portion of the aneurysmal lumen, and the arteries arising from the ectatic segment usually show signal void on T1- and T2weighted MRI, indicating rapid or turbulent flow. Signal void is replaced by high signal intensity when flow is slow in the ectatic vessel [12]. M R I often demonstrates the continuity of one or b o t h V A with the dilated BA. However, distinguishing V B E f r o m a giant saccular aneurysm or an arteriovenous malformation can be difficult [13]. T h e structural characteristics of the dolichoectatic artery can be delinated on CT or MRI. CT is superior to M R I for detecting mural calcification. Peripheral calcification appears as a rim of high attenuation on unenhanced CT, hypointense on MRI, but the latter can be missed or mistaken for haemosiderin [13]. Partial thrombosis appears as an area of n o n - e n h a n c e m e n t on contrastenhanced CT. M R I characteristics of intraluminal thrombus are complex and variable [12]. M R A provides additional informations on intracranial vascular lesions [16, 17]. However, slow flow lesions such as a partially t h r o m b o s e d giant aneurysm or vascular ectasia m a y be poorly visualized due to lack of flowrelated e n h a n c e m e n t [16]. In our case, a large patent lumen, with rapid or turbulent flow, explained good visualization of the VBE. Since V B E is not surgically treatable, cerebral angiography should be restricted to patients in w h o m the nature of the vascular lesion remains doubtful after CT and M R studies, especially when it resembles a giant saccular anenrysm or an arteriovenous malformation. References 1. Fisher CM, Curry HB (1965) Pure motor hemiplegia of vascular origin. Arch Neuro113:30-44 2. Orgogozo JM, Bogousslavsky J (1989) Lacunar syndromes. 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