Neuroradiology (1994) 36:430-431 Neuro-radiology 9 Springer-Verlag 1994 Striatocapsular infarction: MRI and MR angiography P. Croisille 1, F. Turjman 1, B. Croisile 2, P. Tournut 1, J. C. Laharotte 1, G. Aimard 2, M. Trillet 2, J. Duquesnel 1, J. C. Froment 1 1 Department of Neuroradiology, H6pital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon, France 2 Department of Neurology, H6pital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon, France Abstract. We present a case of left striatocapsular infarction manifest clinically as a transient right hemiparesis. M R I showed a left striatocapsular infarct. Striatocapsular infarction, unlike lacunar infarction, is often associated with occlusive disease of the carotid artery. In order to screen the carotid vessels, cervical M R angiography ( M R A ) was p e r f o r m e d during the same examination, demonstrating a left internal carotid artery occlusion, confirmed by contrast arteriography. M R A , a noninvasive modality, can be a useful adjunct to M R I , when diagnostic information concerning the cervical carotid artery is needed. Key words: Carotid arteries, M R studies - Carotid arteries, occlusion - Brain, ischaemia Striatocapsular infarcts, unlike lacunar infarcts, are an indication for imaging of the carotid arteries. We describe a case in which c o m b i n e d M R I and M R angiography provided all the relevant data. Case report A 44-year-old right-handed woman experienced sudden onset of aphasia and right brachiofacial weakness without hemisensory disturbance. Her blood pressure was normal and no cervical bruits were found. Laboratory blood analysis, electrocardiogram and echocardiography were normal. Her only risk factor was smoking (10 packets/year). CT 3 days later revealed a low density commashaped lesion involving the head of the left caudate nucleus, the anterior limb of the internal capsule and the putamen (Fig. 1). MRI was performed the next day on a 1.5 Tesla imaging system. T1weighted sagittal and T2-weighted axial images showed increased signal in the same location as that in CT (Fig. 2). The diagnosis of a large striatocapsular infarct in the territory of the lateral group of lenticulostriate arteries was made. Its haemorrhagic component was revealed only on MRI. Despite the normal appearance of the carotid siphon on MRI, cervical MR angiography (MRA) was performed during the same examination, using a sequential two-dimensional (2DFT) time-offlight technique. Projection MR images were created using a maximum-intensity-proj ection (MIP) algorithm. Complete occlusion of the left internal carotid artery (ICA) was found; the right carotid Correspondence to: ETurjman, D6partement de Radiologie, H6pital Neurologique et Neurochirurgical, 59 Boulevard Pinel, BP Lyon-Montchat, F-69394 Lyon Cedex, France artery and vertebrobasilar system were normal (Fig.3). Digital substraction angiography confirmed the left ICA occlusion (Fig. 4). The blood supply of the affected hemisphere was derived from cortical anastomoses via the posterior and anterior communicating arteries. The patient recovered ten days later and neurological examination was normal. Discussion Striatocapsular infarction has recently b e e n described [i] as a distinct f o r m of subcortical infarction. Distinct size, shape, position, pathogenesis and clinical features distinguish it f r o m lacunar infarction. Striatocapsular infarcts involve the territory of the medial and lateral lenticulostriate branches of the middle cerebral artery, sparing the overlying cortex [1, 2]. The clinical s y n d r o m e usually includes hemiparesis, affecting mainly the u p p e r limb, with aphasia, neglect or apraxia. CT and M R I d e m o n s t r a t e a lesion conforming to the area of supply of the lenticulostriate arteries. The lesion is triangular, lentiform, or typically comma-like, with its rostral portion in the h e a d of the caudate nucleus and anterior limb of the internal capsule, and its tail in the putamen. The m a x i m u m d i a m e t e r is usually a b o u t 3 cm, with a lower limit of 2 cm, chosen because this is the arbitrary cut-off size for lacunes [3, 4]. The lenticulostriate arteries are end-arteries, whereas the cortical branches of the middle cerebral artery ( M C A ) have transcortical and transdural anastomoses. Most of the lenticulostriate arteries arise f r o m the M1 segment of the M C A . Three main pathophysiological subgroups of striatocapsular infarction can be identified: 1. cardiac emboli to the origin of striatocapsular arteries; 2. severe extracranial carotid occlusive disease with pres u m e d embolism to the same site, or h a e m o d y n a m i c disturbances; 3. stenosis of the M1 segment of M C A occluding the origin of small vessels [5, 6]. In these circumstances, collateral flow f r o m the anterior cerebral artery m a y take over m u c h of the function of the superior division of the ipsilateral M C A w h i l e collateral flow f r o m the posterior circulation m a y supply the territory of the inferior division of the M C A and thus preserve cortical tissue. W h e r e a s striatocapsular infarcts are usually related to large-vessel disease, lacunar infarcts follow occlusion of 431 Fig.1. Contrast-enhanced CT shows a comma-shaped low density lesion, involving head of the left caudate nucleus, the anterior limb of the internal capsule and putamen l~g.2, a Tl-weighted sagittal and b T2-weighted axial MRI shows a high signal intensity lesion, indicating a slightly haemorrhagic striatocapsular infarct Fig. 3. MRA (2DFT) in a frontal and b oblique projections demonstrate a complete left internal carotid artery occlusion. The right carotid and vertebral arteries are normal Fig.4. Left common carotid angiogram confirms the complete occlusion single long penetrating arteries, e.g., lenticulostriate artery. They have b e e n ascribed to a disseminated lipohyalinosis of small vessels which m a y progressively occlude different arteries, leading to a lacunar state [3, 4]. It is therefore assumed that angiography is not indicated if the history or imaging investigations suggests lacunar infarction, as any disease of the carotid arteries is likely to be coincidental. Weiller et al. [5], and D o n n a n et al. [6] r e p o r t e d 29 and 27 cases respectively in which conventional cerebral angiography was p e r f o r m e d on patients with striatocapsular infarcts; they found severe carotid artery occlusive disease in 31 and 44 % of cases. Contrast arteriography remains the definitive investigation for carotid artery disease. However, the invasiveness of this technique and its risks, particularly in patients who are a s y m p t o m a t i c or with improving, are drawbacks that strongly call for the d e v e l o p m e n t and i m p l e m e n t a t i o n of alternative diagnostic methods. The accuracy of D o p p l e r sonography is suboptimal [7]. M R A is poised to replace D o p p l e r sonography for screening and staging of carotid artery lesions. This noninvasive modality allows d e m o n s t r a t i o n not only of the cervical vessels, but also of the intracranial arteries, with the advantage of imaging in n u m e r o u s projections. Previous studies have shown a good overall correlation with angiography [8, 9], and A n d e r s o n et al. [10] showed that critical stenoses and occlusions could be differentiated; good correlation in grading of carotid lesions was obtained. In our case, the combination of M R A and M R I showed both the ischaemic insult to the brain and its aetiology, a left I C A occlusion. The normal a p p e a r a n c e of the carotid siphon on M R I was consistent with revascularisation of the terminal carotid artery via anastomoses. Despite the ability of M R I to d e m o n s t r a t e vessel thrombosis, M R A is better for assessment of carotid at- tery occlusive disease. This is particularly true in patients with striatocapsular infarcts, since I C A stenosis is m o r e frequent than complete thrombosis (18 and 6 cases respectively in one series [6] ). Carotid artery occlusion is infrequent in young adults, although sporadic cases and small series have b e e n reported. Acknowledgements. We wish to thank Dr. T. E Massoud for reviewing the manuscript and M. Zemit for his help in its preparation. References 1. Bladin PF, Berkovic SF (1984) Striatocapsular infarction. Large infarcts in the lenticulostriate arterial territory. Neurology 34: 1423-1430 2. Levine RL, Lagreze HL, Dobkin JA, Turski PA (1988) Large subcortical hemispheric infarctions: presentation and prognosis. Arch Neuro145:1074-1077 3. Fisher CM (1982) Lacunar strokes and infarcts: a review. Neurology 32:871-876 4. Mohr JP (1983) Lacunes. Neurol Clin 1:201-221 5. Weiller C, Ringelstein EB, Reiche W, Thron A, Buell U (1990) The Iarge striatocapsular infarct: a clinical and pathophysiological entity. Arch Neuro147:1085-1091 6. Donnan GA, Bladin PF, Berkovic SF, Longeley WA, Saling M (1991) The stroke syndrome of striatocapsular infarction. Brain 114:51-70 7. Chikos PM, Fisher LD, Hirsch JH, Harley JD, Thiele BL, Strandness DE (1983) Observer variability in evaluating extracranial stenoses. Stroke 14:885-892 8. Masaryk TJ, Ross JS, Modic MTet al (1988) Carotid bifurcation MR imaging. Radiology 166:461-466 9. Kido DK, Barsotti JB, Rice LZ et al (1991) Evaluation of the carotid artery bifurcation: comparison of magnetic resonance angiography and digital substraction arch aortography. Neuroradiology 33:48-51 10. Anderson C, Saloner D, Lee R, Nagakar S (1990) Magnetic resonance and conventional angiography of the carotid bifurcation: comparison of stenosis assessment in 40 bifurcations. Proc. 9th Annual Meeting, SMRM, 2641