Original Article Transient Cerebral Arteriopathy: A Disorder Recognized by Serial Angiograms in Children With Stroke Stéphane Chabrier, MD; Georges Rodesch, MD; Pierre Lasjaunias, MD; Marc Tardieu, MD; Pierre Landrieu, MD; Guillaume Sébire, MD, PhD ABSTRACT Repeated clinical evaluation and cerebral arteriography during the evolution of ischemic strokes of idiopathic origin allowed us to characterize a transient cerebral arteriopathy. We retrospectively studied the clinical characteristics, course, and neuroimaging features of this disorder in nine children. Of 34 children with ischemic strokes seen consecutively between 1984 and 1995, 9 (26%) were diagnosed as having transient attack of the cerebral arterial wall, termed transient cerebral arteriopathy. All of these patients had previously been in good health. The mean age at the time of the first stroke was 6 years (range, 2 /12 years to 13 9 /12 years). All children presented with acute hemiplegia. A recurrence of the stroke 4 took place 3 months at the latest after the initial infarct in three children (mean clinical follow-up 2 /12 years). Cerebral 7 in imaging in all the patients showed small subcortical infarcts located basal ganglia or internal capsule. Arteriography revealed multifocal lesions of the arterial wall (focal stenosis or segmental narrowing), mostly located in the initial parts of basal arteries of the carotid system. Longitudinal arteriographic follow-up showed initial worsening of these arterial lesions (n 5) for a maximum duration of 7 months followed by complete regression (n 2), improvement (n 5), or stabilization of the lesions (n 2). Five patients had a complete clinical recovery. Further studies are necessary to confirm a presumed inflammatory cause of this arteriopathy. (J Child Neurol 1998; 13:27-32). = = = = Ischemic strokes in childhood arise from various mechanisms such as arteriopathy, thrombosis, or embolism, each related to different causes. A small proportion of patients have chronic arterial disorders leading to repeated strokes, such as moyamoya disease, vascular dysplasia, chronic vasculitis, angiopathy of sickle cell disease, or metabolic diseases. Causes of embolic or thrombotic strokes (mainly cardiopathy or hemostasis disorders) can be detected in most patients. In contrast, little is known about acute ischemic stroke unrelated to embolic or thrombotic disease, although it is a frequent form of stroke in childhood.2>3 Received July 9, 1996. Received revised Sept 25, 1996. Accepted for publication Oct 3, 1996. From the Service de Neurologie, Département de Pédiatrie (Drs Chabrier, Tardieu, Landrieu, and Sébire) and Service de Neuroradiologie Vasculaire Diagnostique et Interventionnelle (Drs Rodesch and Lasjaunias), Hôpital de Bicêtre, Le Kremlin-Bicêtre Cedex, France. Address correspondence to Dr Guillaume S6bire, Service de Neurologie, D6partement de Pediatrie, H6pital de Bic6tre, 78 rue du G6n6ral Leclerc, 94275, Le Kremlin-Bicetre Cedex, France. Repeated cerebral arteriograms during the evolution of acute ischemic strokes allowed us to characterize an acute cerebral arteriopathy with a transient evolution. We defmed the clinical characteristics, course, and neuroimaging features of this disorder. - . ~~---- - ---- - - - ----- ---- - - PATIENTS AND METHODS Thirty-four children with ischemic strokes (postbacterial meningitis and neonatal strokes excluded) were referred consecutively to our center between 1984 and 1995. Cerebral angiography was performed in 28 patients with no obvious etiology provided by prior medical history or cardiac echography. Arterial wall lesions (focal or regular segmental narrowing, tail-like occlusion) were detected in 24 children. Twelve of these 24 patients had specific arteriographic or histologic features, namely moyamoya disease, chronic vasculitis, human immunodeficiency virus (HIV) I-associated vasculopathy,l sickle cell disease, arterial dissection, and vascular dysplasia. The remaining 12 patients had an idiopathic arteriopathy. Our concern about the risk of progressive arteriopathy 27 Downloaded from jcn.sagepub.com at Monash University on June 4, 2015 28 prompted us to institute a longitudinal clinical and arteriographic follow-up available in nine patients. We focused our study on these nine patients. All patients had cerebral computed tomographic (CT) scan (n 9) or magnetic resonance imaging (MRI) (n = 5). Cerebral arteriography was performed by transfemoral selective catheterization of internal carotid arteries, external carotid arteries, and vertebral arteries. They were repeated from 2 months to 2 years after the initial stroke. Nine patients underwent 23 conventional arteriograms without complication (4 children had two angiograms; 5 children with worsening in arterial lesions on the second examination had a third angiogram; patient 3 had his first angiogram by venous puncture). Angiographic abnormalities were coded according to their presence, number, anatomical location, and evolution by a single neuroradiologic staff member (G.R. or PL.). Only patients whose parents gave informed consent had arteriography. Language assessment was performed in the five patients presenting with speech disturbances. We used the &dquo;Examen pour 1’Evaluation du Langage,&dquo; Wechsler Preschool and Primary Test of Intelligence and Wechsler Intelligence Scale for Children-Revised = (WISC- R). 5--7 Virologic studies were performed for four of five patients (patients 1, 2, 5, and 9) who had clinically diagnosed varicella zoster virus before stroke: titer of viral antibodies (varicella zoster, cytomegalovirus, herpes type 1, measles) in serum (n 4) and cerebrospinal fluid (n 2) determined by enzyme-linked immunosorbent assay (ELISA) or complement-fixing, polymerase chain reaction to detect varicella zoster viral DNA in the cerebrospinal fluid (n 1).~ Two patients had antiphospholipid antibody titration in serum samples. Statistical analysis was performed using the Xz test. The date of the first stroke was designated as day 0. = = CT scan of patient 1, 2 days after the second stroke (2 months after initial stroke) shows a lacunar hypodensity of the left lenticular nucleus. Left carotid angiograms performed at 2 months (A), shows focal stenosis located at the origin of insular and temporal branches of the left middle cerebral artery. B, Angiogram at 4 monthss shows increased stenosis at the same locations and, C, disappearance of abnormal images at 17 months. Figure 1. = Case Reports Patient 1, a 2-year-11-month-old girl, presented with transient right hemiparesis 9 months after varicella zoster virus infection. Two months later, she had right hemiplegia. A CT scan (day 2 after the second stroke) showed a lacunar hypodensity of the left lenticular nucleus and internal capsule. The arteriogram revealed focal stenosis located at the origin of the insular and temporal branches of the left middle cerebral artery (Figure 1) and on a branch of the right pericallosal artery. She recovered in a few days. She received aspirin (5 mg/kg daily) for 17 months. An arteriogram performed at 4 months showed increased stenosis at the same locations. At 19 months, arteriography was normal and a 2-year follow-up did not detect any new stroke. Patient 2, a 2-year-9-month-old girl, was admitted for abrupt onset right hemiplegia and mutism 47 days after a chickenpox rash. A CT scan (day 3) showed a lacunar hypodensity in the left internal capsule. An arteriogram (day 9) showed focal and regu- disappearance of the sylvian lesion and a further improvement of the insular lesion. ’Iwo years later, language evaluation was normal. No other stroke occurred after a 26-month period. Patient 6, an 8-year-10-month-old girl, suddenly presented with right hemiplegia, right homonymous lateral hemianopsia, global aphasia with stereotyped utterance (&dquo;nin-nin&dquo;), and a mild alteration of consciousness. She had had a chickenpox rash 8 months earlier. A CT scan revealed multiple hypodensities in the left lenticular nucleus and internal capsule and in large areas of the left frontal and parietal cortex. An arteriogram (day 6) showed irregular segmental narrowing involving the left supraclinoid carotid artery, the proximal segments of the left middle cerebral artery, and the left insular branches (Figure 3). Stenosis and tail-like occlusion were detected on cortical vessels of left sylvian origin. The alteration of consciousness regressed in less than 48 hours; however, motor and language deficits persisted. She was treated with aspirin (5 mg/kg daily). Two months later, the vascular anomalies worsened, resembling a &dquo;string of beads&dquo; on proximal segments of the left cerebral arteries. A diagnosis of fibromuscular dysplasia was suspected. The renal arteriogram was normal. At 14 months, there was still a regular narrowing of the initial part of the left middle lar stenosis located on the initial part of the left middle cerebral cerebral artery, but the other arteries had recovered normal cal- artery and at the origin of the left insular branch (Figure 2). She iber. Clinical evaluation after 2 years (age, 10 years 9 months) recovered in a few days. She received aspirin (10 mg/kg daily) for showed an aphasia affecting language expression and comprehension (speech level of an 8-year-old child) and severe facio- 7 months. Two months later, an arteriogram showed the same image on the left sylvian artery and an improvement of the insular branch lesion. A third arteriogram, at 7 months, showed the brachial paralysis. There was no recurrence of stroke after 3 years 2 months. Downloaded from jcn.sagepub.com at Monash University on June 4, 2015 29 Figure 2. CT scan of patient 2, at day 3, shows a lacunar hypodensity in the left internal capsule. Left carotid arteriograms show (A), at 9 days, focal and regular stenosis located on the initial part of the left middle cerebral artery and segmental regular narrowing at the origin ofthe left insular branch, (B) at 2 months, the same image on the left sylvian artery and improvement of the insular branch lesion and, (C), at 7 months, the disappearance of the sylvian lesion and further improvement of the insular lesion (arrow). CT scan of patient 6 reveals a large hypodensity in the left lenticular nucleus and internal capsule. Left carotid arteriograms show (A) at 6 days, multiple focal stenosis of the left supraclinoid carotid artery (filled arrows) and proximal segments of the left middle cerebral artery (open arrows), (B), at 2 months, worsening of the sylvian lesions with a string of beads appearance (arrows) and disappearance of the abnormal image of the carotid artery and, (C), at 14 months, general improvement but persistent stenosis of the initial part of the left middle cerebral artery. Figure 3. ’ RESULTS Clinical Features The patients ranged in age from 29/~z years to 134/12 years (mean age, 6 years). In children from 2 to 9 years of age, the strokes due to a transient arteriopathy occurred with a significantly higher frequency than strokes of other origin (89% versus 36%, P < .01) (Figure 4). The sex ratio (male: female) was 0.5. Three children had a first stroke from 2 to 3 months before admission (patients 1, 3, and 5) with the same symptoms as the main stroke, but rapid resolution. Five children had diffuse vesicular eruption clinically diagnosed as varicella zoster virus infection prior to the initial stroke (patients 1, 2, 5, 6, and 9). The delay between the rash and their first stroke varied from 9 days to 9 months (mean interval, 4 months). Motor symptoms prevailed with hemiplegia in all cases, most often proportional. This was associated with speech disorders in five patients: dysarthria (patients 3 and 9), mutism (patient 2), global aphasia (patient 6), and impaired naming abilities and verbal paraphasia (patient 7). Two patients had homonymous lateral hemianopsia. There was a mild alteration of consciousness in three children (patients 6, 7, and 9) that regressed in a few hours. Patient 9 had one focal motor seizure at the onset. Seven children had total recovery or only a mild deficiency (dystonia affecting the left arm in patient 8, slight left hemiparesis in patient 9). Language evaluation performed at least 3 months after the stroke showed complete recovery in four of five patients (patients 2, 3, 7, and 9) with initial speech disturbances. Two patients had severe disabilities: faciobrachial hemiplegia (patients 6 and 7) and aphasia (patient 6). The mean clinical follow-up was 2’/~2 years (range, 7 months to 7 years). Figure 4. Distribution of 34 patients from the entire series of ischemic strokes we observed between 1984 and 1995, according to age at first stroke. Comparison of age distribution between children with transient cerebral arteriopathy (black bars) and children with other etiopathogenic mechanisms (gray bars) is shown. Downloaded from jcn.sagepub.com at Monash University on June 4, 2015 30 Figure 5. Location, type, and course of arterial lesions as visualized on serial arteriographies are shown. + denotes site of arterial lesions at onset; +* indicates two lesions on the same arterial segment; +° denotes segmental narrowing; and All indicates secondary involvement on arteriographic controls. Neuroradiologic Findings 4). Two patients had normal cerebral arteriograms at their Eight patients presented with infarction located in the territory of the lateral lenticulostriate arteries (anterior arm of the internal capsule, putamen, and head of caudate nucleus), last examination at 4 and 17 months. with a lacunar appearance in four children. Patient 8 had a stroke located in the deep territory of the posterior cerebral artery. Two patients had associated cortical stroke (left frontoparietal cortex in patient 6, birolandic in patient 9). The strokes involved only one basal artery territory in all except one patient (bifrontal lesions, patient 9). Arterial lesions were mostly unilateral (8 patients) and restricted to the supraclinoid carotid system in all children (Figure 5). The most common lesion was a focal and regular stenosis located in basal arteries immediately after a bifurcation. An occlusion of large vessels was observed in two patients with a taillike aspect of the initial segment of the middle cerebral artery (patient 5) or of the anterior cerebral artery (patient 6). In three children some arterial segments were narrowed by a succession of stenoses giving a &dquo;string of beads&dquo; appearance. Patient 9 had cortical arterial lesions without visible involvement of basal vessels although she had multiple bilateral lacunar infarcts of basal ganglia. Renal arteriography performed in one patient was normal (patient 6). The superficial and deep venous system was normal in all patients. On sequential arteriograms, the lesions worsened in five patients within 2 to 7 months (Figure 5). Long-term followup showed improvement of arterial lesions in all but two children with stable lesions at 7 and 14 months (patients 3 and Patient 4 had 22 lymphocytes/J....L in cerebrospinal fluid (1 week after the stroke). Patient 9 had an increase in Creactive protein (51 ng/mL) and sedimentation rate (36 mm/hr). Antibody titers in the serum, measured in four patients (patients 1, 2, 5, and 9), confirmed acute (presence of IgM, patient 9) and less recent (detection of IgG, lack of IgM, in patients 1 and 2) varicella zoster virus infection. Varicella zoster virus antibodies (patients 5 and 9) as well as varicella zoster virus DNA (patient 9) remained undetectable in cerebrospinal fluid. Other paraclinical investigations were normal. Other Paraclinical Investigations Treatment No reccurence of stroke was observed in our nine patients on antiplatelet treatment (aspirin from diagnosis to arteriographic evidence for regression or stabilization of the dis- ease). DISCUSSION These nine patients had a homogeneous clinical and arteriographic course characterized by: (1) Subcortical infarcts (basal ganglia or internal capsule) associated with lesion(s) of the cerebral arterial wall (focal or segmental narrowing, Downloaded from jcn.sagepub.com at Monash University on June 4, 2015 31 tail-like occlusion visualized on arteriography) mostly located in the initial parts of basal arteries of the carotid system and (2) clinical (lack of late recurrence of stroke more than 3 months after the initial event) and arteriographic follow-up demonstrating regression or arrest of the evolution of the arteriopathy. All these children displayed classic clinical features of infarcts involving basal ganglia and the internal capsule, such as proportional hemiplegia, motor aphasia or dysarthria, and lack of seizure.9-13 The subcortical location of infarcts, affecting mostly lateral lenticulostriate arterial territory was confirmed on CT scan and MRI. Surprisingly, owing to the small size and deep location of parenchymal defects, arterial lesions involve large vessels (supraclinoid portion and initial branches of carotid artery) or superficial branches of anterior and middle cerebral arteries. Several hypotheses could account for this apparent discrepancy. (1) The arteriopathy could be more extensive than suspected on the basis of the imaging results since angiography does not enable visualization of anomalies of small vessels, such as lenticulostriate arteries, which could be associated with the lesions of large vessels. On the other hand, lesions of basal arteries detected by arteriography could be located on the origins of lenticulostriate arteries.13 (2) Severe reduction of blood flow could be induced by defects of large basal arteries with a more pronounced effect on deep areas than on cortical areas of the brain. 14 One of the most striking features of this arteriopathy is the transient activity of the pathologic process. This is demonstrated both arteriographically, by repeated examinations showing regression or stabilization of arterial lesions after an initial worsening, and clinically, by a long-term follow-up that revealed a lack of late reccurence. Such transient arteriopathy could represent an important fraction of ischemic strokes in childhood since it accounted for at least 26% of strokes we observed at the same time. 15 Previous studies have highlighted the high frequency of subcortical infarcts in childhood.2,3,16-23 Those patients shared several features with ours: (1) arteriographic images show focal or multifocal arterial lesions mostly located on the initial segment of the middle cerebral artery or on the supraclinoid carotid artery, (2) long-term clinical follow-up shows a good prognosis and lack of late stroke recurrence, and (3) most of these strokes are idiopathic. Although a few patients had serial arteriography during the course of the disease showing improvement of arterial wall lesions, specific clinical and paraclinical features of this transient cerebral arte- riopathy were not provided.’7,24,25 The arteriographic appearance observed in this study, characterized by focal or segmental stenosis and tail-like occlusions, does not support either an embolic or thrombotic process, but is consistent with abnormalities of the arterial wall. The acute and regressive course suggests an acute process such as angiitis, dissection, or vasospasm. Lack of anamnestic events, such as drug absorption and relative persistence of arterial lesions, makes the hypothesis of a vasospasm unlikely. Arteriographic findings in arterial dissections did not show multifocal lesions, as seen in most of our patients.26,27 Moreover, clinical findings in dissections are different, characterized by previous head or neck trauma followed by headache, frequent seizures, and worse prognosis (higher frequency of cortical lesions). Thus, an inflammatory process affecting the arterial wall, possibly triggered by infections, such as by varicella zoster virus, seems to be the most likely pathophysiologic hypothesis for this transient cerebral arteriopathy. The relationship between ischemic strokes in young patients and local (tonsillitis or cervical lymphadenopathy) or general inflammatory diseases (varicella zoster virus infection) has already been suspected in several studieS28-30 and anatomically confirmed in some reports.31,32 A causal relationship between herpes zoster ophthalmicus and hemiplegia due to necrotizing angiitis is well established in adulthood.33,34 In our series, five children had clinically diagnosed varicella zoster virus infection prior to stroke. Twenty-three children with strokes following infection by varicella zoster virus are reported in the literature.22,35-41 Those patients shared many features with ours: age at onset (mean, 4 years; range, 1 year to 76/~2 years), strokes delayed relative to the rash (mean, 2 months; range, 3 weeks to 9 months), infarcts (mostly lacunar) located in basal ganglia and the internal capsule, and arterial lesions (focal stenosis or segmental narrowing or occlusion) involving preferentially initial parts of the anterior and middle cerebral arteries. Seven patients had recurrent strokes from a few days to 6 months after the initial infarct. Most children had complete recovery or only a mild deficiency. Arteriographic follow-up was not done. In conclusion, that a patient with presumed transient cerebral arteriopathy should undergo an early arteriogram and another 1 year later could be debated in order to confirm the diagnosis, determine the prognosis by ruling out a progressive arteriopathy, and manage the treatment. Whether magnetic resonance angiography and transcranial Doppler ultrasonography have a role in the diagnosis and follow-up needs to be evaluated. Investigations looking for infectious agents suspected to be involved in angiitis (varicella zoster virus, cytomegalovirus, coxsackie infections, and cat-scratch must be performed (cultures of blood, ceredisease)16>42>43 brospinal fluid, and other potentially infected sites; polymerase chain reaction to detect recent or persistent infection; and repeated antibody titration in serum and cerebrospinal fluid). We suggest an antiplatelet treatment for at least 1 year (depending on the results of late arteriography) because of the risk of recurrence of stroke. Other studies will be essential to better define the course of this disorder and, if infectious and secondary inflammatory and thrombotic processes are confirmed, to test the efficiency of antiviral, anticoagulant, or anti-inflammatory drugs. Finally, some children with progressive arteriopathy have initial angiographic findings similar to those described here. That so many of these children recover, both clinically and radiographically, within such a short period of time, should discourage surgical treatment, at least until progression is certain. Frequent spontaneous improvement will also have Downloaded from jcn.sagepub.com at Monash University on June 4, 2015 32 to be considered when assessing the results of any treatment 21. protocol. 22. Acknowledgments We are very grateful to Elisabeth Dussaix, V6ronique Leroy-Malherbe, Luc Outin, and Nathalie Seibel for their important contributions. 23. 24. 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Chalhub EG, Devivo DC, Siegel BA, et al: Coxsackie A9 focal encephalitis associated with acute infantile hemiplegia and poren- cephaly. Neurology 1977;27:574-579. Downloaded from jcn.sagepub.com at Monash University on June 4, 2015