Cerebrovascular disease and stroke

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1 Downloaded from ad.bmj.om on January 15, Published by group.bmj.om Cerebrovasular disease and stroke J Pappahan and F J Kirkham Arh Dis Child : originally published online June 30, 2008 doi: /ad Updated information and servies an be found at: Referenes Open Aess alerting servie These inlude: This artile ites 45 artiles, 29 of whih an be aessed free at: Artile ited in: This is an open-aess artile distributed under the terms of the Creative Commons Attribution Non-ommerial Liense, whih permits unrestrited use, distribution, and reprodution in any medium, provided the original work is properly ited. Reeive free alerts when new artiles ite this artile. Sign up in the box at the top right orner of the online artile. Topi Colletions Artiles on similar topis an be found in the following olletions Unloked (555 artiles) Notes To request permissions go to: To order reprints go to: To subsribe to BMJ go to:

2 Downloaded from ad.bmj.om on January 15, Published by group.bmj.om Cerebrovasular disease and stroke J Pappahan, 1 F J Kirkham 1,2 1 Departments of Paediatri Intensive Care and Paediatri Neurology, Child Health Diretorate, Southampton General Hospital, Southampton, UK; 2 Institute of Child Health, London, UK Correspondene to: Professor Fenella Kirkham, The Wolfson Centre, Meklenburgh Square, London WC1N 2AP, UK; F.Kirkham@ih.ul.a.uk Aepted 21 April 2008 Published Online First 30 June 2008 This paper is freely available online under the BMJ Journals unloked sheme, see ad.bmj.om/info/unloked.dtl ABSTRACT Stroke and erebrovasular disorders are important auses of morbidity and mortality in hildren; they are already amongst the top 10 auses of hildhood death and are probably inreasing in prevalene. Aute treatment of stroke syndromes in adults is now evidene based. However, paediatri stroke syndromes are far less ommon and the differential diagnosis is very wide, but the individual health resoure impliations are muh greater beause of the life-long treatment osts in survivors. Reognition and onsultation with a paediatri neurologist should be rapid so that hildren an benefit from regional servies with emergeny neurologial, neuroradiologial and neurosurgial intervention and paediatri intensive are. This review fouses on the epidemiology, presentation, differential diagnosis, generi/ speifi emergeny management and prognosis of aute stroke in hildren. Its aim is to eduate and guide management by general paediatriians and to emphasise the importane of loal guidelines for the initial investigation and treatment and appropriate transfer of these hildren. Stroke and erebrovasular disorders are important auses of morbidity and mortality in hildren; they are already amongst the top 10 auses of hildhood death and are probably inreasing in prevalene. Reent epidemiologial data suggest inidene rates of 2 5/ hildren/year for hildhood stroke (at least 300 a year in the United Kingdom), 1 with a peak in the first year of life. Boys are at higher risk than girls. The inidene may have inreased over the last 25 years as a onsequene of inreased reognition, less invasive vasular diagnosis (MR/ CT angiography) and therapeuti advanes allowing hildren with predisposing onditions (eg, ongenital heart disease, anaemias, malignany, meningitis) to survive. However, this trend may be offset by sreening and primary prevention strategies in those at risk (eg, with sikle ell disease, (SCD). 2 3 Neonatal stroke is more ommon, with an inidene of up to 63 per live births. 4 Health are utilisation is not adequately refleted by inidene figures but is more appropriately desribed by disease outome. As well as a 20% mortality and a high reurrene rate, at least half of the survivors of these events have permanent ognitive or motor disability Rapid reognition 5, investigation 6 7 and appropriate management 5 8 (boxes 1 and 2, figs 1 5) should improve these disappointing figures. Haemorrhagi stroke (figs 1A, 2) inludes intraerebral haemorrhage (ICH), the ommonest form in hildren under 10, and subarahnoid haemorrhage (SAH), whih is more ommon in teenagers. 9 Arteriovenous malformation (AVM), avernous angioma, aneurysm and venous sinus thrombosis (VST) 9 10 are likely vasular pathologies often distinguishable with MR. 10 Patients with brain tumours, bleeding diatheses, anaemia (inluding SCD 11 ), leukaemia and metaboli disease are also at risk. Compared with ishaemi stroke (fig 1B F), mortality is higher (8 40%) and reurrene is lower (in a population-based study, 13% for those with medial aetiologies, mainly autely, and a 5-year umulative reurrene rate of 13% for those with unoperated AVMs or tumours 9 ), although funtional outome may be better, although only a quarter of patients have no physial or ognitive impairment. 12 Ishaemi stroke is ommonly arterial (AIS) (figs 1B D, 3), but erebral VST is probably underreognised (figs 1E, 4) and should be exluded, partiularly in superfiial ortial and deep posterior infarts. The underlying ause or trigger may be a diagnosti lue to the distintion between ATS, VST and stroke mimis 518 (figs 3 5). AIS and VST are assoiated with death in 6 16% and 3 8% of patients, respetively, higher in those with premorbid onditions (figs 3, 4) and in the ritially ill, 19 while 40 60% of both groups have signifiant disability Reurrene rates are age and diagnosis dependent: 3% in neonates, 13 6% (3% erebral) after VST in hildren 2 years of age with no evidene for reurrene after neonatal VST, 20 and 10% stroke with an additional 20 35% transient ishaemi events (TIAs) after AIS in hildhood RISK FACTORS There are similarities and differenes between the predisposing onditions and intermediate risk fators for haemorrhagi stroke (figs 1A, 2), AIS (figs 1B D, 3), VST (figs 1E, 4) and stroke mimis (figs 1F, 5). Certain hromosomal (Down syndrome) and single gene disorders (SCD, homoystinuria) predispose to all (figs 2 5). Approximately half the hildren presenting with AIS have a predisposing ause 14 (symptomati AIS) (fig 3), while the remainder were previously well (ryptogeni AIS); around 80% of both groups have abnormal arterial imaging. 14 Intermediate risk fators inlude infetions, hypertension, anaemia (inluding iron defiieny), hyperhomoysteinaemia 26 and dyslipidaemias inluding elevated lipoprotein(a). 27 Thrombophilias suh as protein C defiieny, antiardiolipin antibodies and the fator V Leiden and prothrombin mutations are more frequent in ishaemi stroke populations than in ontrols 27 but may be more ommonly assoiated with VST rather than AIS, although some appear to be independent risk fators for reurrent ryptogeni AIS. At least a third of ases of hildhood stroke our in the ontext of infetion, 14 and the importane of prior variella infetion as a risk fator for 890 Arh Dis Child 2008;93: doi: /ad

3 Downloaded from ad.bmj.om on January 15, Published by group.bmj.om Figure 1 Neuroimaging in hildren with stroke. Row 1: CT sans; row 2: T2-weighted MRI sans; row 3: vasular imaging (A D: magneti resonane angiography (MRA); E: MR venography (MRV); F: watershed infartion); row 4: additional imaging whih may be useful in diffiult ases (A D: onventional angiography; E: venous thrombosis on MRI; F: potentially reversible signal abnormality on diffusion weighted imaging). Column 1: haemorrhage; olumn 2: extraranial dissetion; olumn 3: transient erebral arteriopathy; olumn 4: moyamoya; olumn 5: venous sinus thrombosis; olumn 6: posterior irulation stroke and stroke mimis posterior leukoenephalopathy, overt watershed ishaemia, hemiplegi migraine. A: Haemorrhage; A1: spontaneous intraerebral haemorrhage with midline shift; A2: MRI showing haemorrhage from myoti aneurysm in a patient with subaute baterial endoarditis; A3: myoti aneurysm on MRA; A4: onventional arteriography showing arteriovenous malformation. B: Dissetion; B1: infart in a hild who had suffered a minor head injury 24 h before; B2: large erebral infart after head injury; B3: fat-saturated T1 MRI of the nek showing haemorrhage in the vessel wall; B4: onventional arteriography showing tapering rat s tail appearane harateristi of extraranial dissetion. C: Transient erebral arteriopathy; C1: infart in a hild with stuttering stroke onset; C2: infart in a hild with reent variella; C3: short segment of middle erebral artery stenosis (MRA from hild in C2); C4: onventional arteriography from hild in C1 showing longer segment of middle erebral artery stenosis (the infart had extended in size on the post-arteriography CT san). D: Moyamoya; D1: bilateral frontal infartion in a hild with livedo retiularis; D2: bilateral frontal infartion in a hild with sikle ell anaemia; D3: bilateral middle erebral artery stenosis with ollateral formation obvious on MRA; D4: onventional arteriography showing attenuation of major intraranial vessels and ollaterals. E: Venous sinus thrombosis; E1: bilateral thalami signal hange in severe iron defiieny anaemia; E2: oipital signal hange in nephroti syndrome; E3: sagittal sinus thrombosis in systemi lupus erythaematosus presenting with psyhiatri symptoms; E4: transverse sinus thrombosis on plain MRI in hild in E1. F: Posterior irulation stroke and stroke mimis; F1: erebellar infartion in a boy with vertebral dissetion; F2: bilateral oipital signal hange suggestive of posterior leukoenephalopathy; F3: bilateral watershed infartion after faial infetion in sikle ell anaemia (MRA and MRV were normal); F4: diffusion-weighted imaging shows potentially reversible pathology in a patient with hemiplegi migraine and normal T2-weighted MRI. Arh Dis Child 2008;93: doi: /ad

4 Downloaded from ad.bmj.om on January 15, Published by group.bmj.om ryptogeni AIS and haemorrhage has reently been reognised and is apparently seondary to diret infetion of the arterial wall, although seondary pathophysiologies, inluding transient protein C and S defiieny, may play a synergisti role. High leukoyte ount is a risk fator for first haemorrhagi stroke in SCD, 11 as well as being a risk fator for reurrent AIS. 23 Host immunity and the ytokine milieu are probably important fators affeting endothelial funtion and ellular adhesion. CHILDHOOD STROKE AND CEREBROVASCULAR DISEASE The very different nature of the vasular, oagulation and nervous systems in neonates, infants and hildren means that linial and radiologial presentations are different from adults. Cerebrovasular disease assoiated with haemorrhagi stroke AVMs (fig 1A4) are defined by the presene of high flow arteriovenous onnetions without an intervening apillary network (a onsequene of abnormal developmental vasular remodeling). 7 9 Cavernous angiomas probably result from venous hypertension and are multiple lesions (intra- or extraranial) in 13% of sporadi and 50% of familial ases. Aneurysms are relatively rare in hildren; 10 15% are posttraumati and a similar proportion are myoti (fig 1A2, 1A3). VST may also ause intraerebral and subarahnoid haemorrhage. For haemorrhagi strokes, underlying onditions whih may require ative exlusion inlude hereditary haemorrhagi telangietasia, polyysti kidney disease, Ehler-Danlos syndrome type IV, anaemia and hypertension as well as bleeding disorders (fig 2). Cerebrovasular disease typially assoiated with arterial ishaemi stroke (AIS) Extra/intraranial dissetion Arterial dissetion (fig 1B) ours as a onsequene of a tear in the intima of an artery leading to extravasation of blood from the lumen into the intermediate layers of the artery and ausing loal ompression, distal embolism or propagation of lot. Clinial signs may therefore falsely loalise the pathologial arterial territory. Dissetion most ommonly ours in the internal arotid and vertebral arteries and risk fators inlude trauma (apparently minor as well as nek or penetrating pharyngeal injuries, for example falling with a penil in the mouth) and infetion (eg, hroni tonsillitis) While most anterior dissetions are intraranial (60%), most posterior dissetions arise extraranially (60%). 34 Intraranial arteriopathy Transient erebral arteriopathy (TCA) (fig 1C3, 1C4) refers to intraranial arterial pathology leading to linial signs assoiated with radiologial abnormalities that often stabilise and sometimes reverse, although there is a risk of early reurrene TCA probably represents an inflammatory response to infetions suh as variella, Borrelia or tonsillitis MR typially shows small subortial infarts with multifoal arterial wall lesions. Moyamoya is the Japanese for puff of smoke and desribes a erebral arteriopathy with bilateral severe stenosis/olusion of the terminal internal arotid arteries (ICAs) assoiated with the development of basal ollateral vessels. 37 It may be primary or seondary to SCD, Down syndrome or ranial irradiation. Moyamoya is an independent risk fator for reurrent stroke Figure 2 Flow diagram for the diagnosis and management of haemorrhagi stroke. ABCD, airway, breathing, irulation, disability; AVM, arteriovenous malformation; BP, blood pressure; CT, omputed tomography; CTV, CT venography; ICH, intraerebral haemorrhage; ICP, intraranial pressure; IIH, idiopathi intraranial hypertension; LOC, level of onsiousness; LP, lumbar punture; MCV, mean ell volume; MRA, magneti resonane angiography; MRV, magneti resonane venography; PCV, paked ell volume; SAH, subarahnoid haemorrhage; US, ultrasound. 892 Arh Dis Child 2008;93: doi: /ad

5 Downloaded from ad.bmj.om on January 15, Published by group.bmj.om Figure 3 Flow diagram for the diagnosis and management of haemorrhagi stroke. ABCD, airway, breathing, irulation, disability; MCA, middle erebral artery; MRA, magneti resonane angiography; MRV, magneti resonane venography; PHACES, posterior fossa malformations, haemangiomas, arterial anomalies, ardia defets, eye abnormalities, and sternal or ventral defets; RPLS, reversible posterior leukoenephalopathy syndrome; SCD, sikle ell disease; VST, venous sinus thrombosis. and TIA, 23 whih are probably redued after extraranialintraranial revasularisation. Venous sinus thrombosis (VST) The erebral veins drain into superfiial or deep erebral venous sinuses. Sinus blood flow rates are ditated by mean arterial pressure (MAP) and thrombosis therefore ours more ommonly in hypotension. The pathogenesis of VST in neonates remains unertain but may relate to anatomial distortion during hildbirth as well as dehydration and infetion. In older hildren trauma, malignany or sepsis play a larger role (fig 4). Dehydration, iron defiieny and inherited prothromboti disorders are additional risk fators VST may lead to venous hypertension, foal erebral oedema, haemorrhagi infartion, hydroephalus and pseudotumour erebri Although these sinuses may reanalise spontaneously with onservative management (rehydration, antibiotis), aute antioagulation may be onsidered, 6 8 as two trials in adults showed redued mortality and morbidity and a ohort study in hildren showed redued reurrene. 20 Those in whom the risks may be outweighed by the benefits of antioagulation during periods of risk, for example after relapse of nephroti syndrome, inlude hildren over the age of 2 or with the prothrombin mutation. 20 Other erebrovasular disease Vein of Galen malformation (VGAM) is an embryoni arteriovenous fistula oasionally presenting with atastrophi neonatal heart failure whih within entres with an experiened multidisiplinary team may be endovasularly palliated 38 ;itis usually inappropriate to manage any assoiated hydroephalus separately. Sturge Weber syndrome (SWS) is haraterised by a faial apillary haemangioma and venous angiomata of the leptomeninges/horoids assoiated with intratable epilepsy (whih may require hemispheretomy) 39 and episodi stroke-like episodes leading to progressive hemiplegia and learning disability (redued with prophylati aspirin 39 ). Arh Dis Child 2008;93: doi: /ad

6 Downloaded from ad.bmj.om on January 15, Published by group.bmj.om STROKE MIMICS 518 These are diagnoses of exlusion whih should only be made after disussion with a paediatri neurologist or intensivist. Hemiplegi migraine There may be a family history. EEG usually shows unilateral slow bakground ativity. Aute disseminated enephalomyelitis (ADEM) The demyelination is usually obvious on MRI. Intravenous methyl prednisolone probably redues the duration of the illness and perhaps improves long term outome. Reversible posterior leukoenephalopathy syndrome (RPLS) This is haraterised by seizures, disorders of onsiousness, visual abnormalities and headahes assoiated with posterior white matter abnormalities on CT/MRI and has been desribed after aute hest syndrome in SCD, 40 after hypertensive enephalopathy and during immunosuppression. The majority of patients make a full linial and radiologial reovery after areful treatment of their underlying ondition, although infartion in the parieto-oipital or watershed (fig 1F3) an our. 40 If RPLS is assoiated with hypertension, the blood pressure should be redued very slowly to avoid preipitous drops and infartion. Vertebrobasilar dissetion, whih may present with ataxia, visual disturbane or oma rather than hemiparesis (figs 1F1, 3) and whih is muh ommoner in boys, 34 and VST (figs 1E, 4) are part of the differential diagnosis and should be exluded on emergeny imaging as their treatment and prognosis are different. Metaboli stroke There are often linial lues to the aetiology of metaboli stroke, for example persistent vomiting, hypoglyaemia or diabetes. Organi aidaemias, urea yle disorders and mitohondrial disorders an ause stroke-like episodes with imaging abnormalities in an atypial vasular distribution. Homoystinuria and Fabry disease are usually assoiated with erebrovasular disease. CLINICAL PRESENTATION Although stroke in hildhood is relatively rare, its linial presentation is usually obvious to the paediatriian, who an investigate both obvious and subtle presentations and initiate emergeny medial management. Hemiplegia, headahe, seizure or altered levels of onsiousness may all herald a potentially reversible or lethal medial or surgial stroke emergeny. If a stroke syndrome is suspeted, initial resusitation in onjuntion with the loal anaestheti/intensive are team should be followed by onsultation with regional paediatri neurologial servies before further imaging, investigation or treatment are planned and instituted. Although stroke is traditionally defined as a neurologial defiit lasting for >24 h, many hildren with a TIA lasting (24 h have had a reent erebral infartion/ haemorrhage on imaging. In addition to the underlying Figure 4 Flow diagram for the diagnosis and management of venous sinus thrombosis. IIH, idiopathi intraranial hypertension. ABCD, airway, breathing, irulation, disability; CTV, omputed tomography venography; LOC, level of onsiousness; MRV, magneti resonane venography. 894 Arh Dis Child 2008;93: doi: /ad

7 Downloaded from ad.bmj.om on January 15, Published by group.bmj.om Figure 5 Flow diagram for the management of stroke mimis. ABCD, airway, breathing, irulation, disability; BP, blood pressure; CTV, CT venography; DWI, diffusion weighted imaging; LOC, level of onsiousness; MRA, magneti resonane angiography; MRV, magneti resonane venography. diagnosis (figs 2 5), the time from onset of symptoms to presentation is very useful diagnostially, for example arteriopathy is more likely to present with a stuttering onset, 41 suggesting the need for imaging to exlude dissetion (fig 1), and thunderlap headahes may be indiative of a subarahnoid haemorrhage warranting lumbar punture even if neuroimaging is normal. Stroke mimis may be benign and require no treatment, but in some ases timely intervention prevents neurologial disability or death Emergeny MR provides information that an guide management in individual hildren (figs 2 5). Any finanial onsequenes of overinvestigation that this approah may produe will almost ertainly be overridden by the potential benefits in terms of redued healthare and soio-eonomi osts resulting from prompt and appropriate treatment. If immediate transfer is deemed neessary after disussion with the on-all neurosurgeon or paediatri neurologist, liaison with the regional paediatri intensive are unit (PICU) is advisable. Children may present in oma, status epileptius, or with signs of intraranial hypertension or imminent herniation mandating liaison with loal anaestheti teams/regional PICUs, and appropriate retrieval/transport of hildren to regional entres for further imaging/management. MANAGEMENT AND INVESTIGATION Diagnosis independent management No studies have speifially examined the effet of the loss of ardio-respiratory integrity on stroke outome in hildren. However, based on priniples whih would be applied to the are of any autely ill hild (ABCD, airway, breathing, irulation, disability) inluding the maintenane of adequate oxygenation (non-invasively estimated by pulse oximetry), ardia output, systemi and erebral perfusion pressure, and tight ontrol of blood gluose and body temperature should be the aim. Hypertension should not be treated unless intraranial pressure is monitored if there is a spae-oupying lesion, and should only ever be lowered slowly. Children whose level of onsiousness deteriorates should be ventilated and transferred to the nearest neurosurgial/picu in ase they require drainage of a haematoma, ventriulostomy for hydroephalus or ranietomy for intratable intraranial hypertension. Management may be guided by intraranial pressure monitoring, whih should be onsidered in hildren who remain sedated and in whom there is radiologial/linial suspiion of a spae-oupying lesion. Seizures in the aute phase should be managed aggressively in aordane with onventional algorithms and loal guidelines as they signifiantly inrease the erebral metaboli rate for oxygen and an thus unfavourably affet the substrate supply demand balane. Consideration should be given to ontinuous erebral funtion monitoring in paralysed hildren. Emergeny neuroimaging Haemorrhagi stroke or AIS with mass effet should be exluded by emergeny CT, whih might also show some evidene of foal ishaemi damage but often only from 24 h after presentation. If CT is not available immediately at the loal site, disussion with a tertiary entre is mandatory and urgent onsideration should be given to transfer of the hild, even if this an only be ahieved safely by intubation and ventilation. The regional PICU should be involved in this deision, as this is an emergeny. If immediately available, MR Arh Dis Child 2008;93: doi: /ad

8 Downloaded from ad.bmj.om on January 15, Published by group.bmj.om Box 1 Differential diagnosis in hildren presenting with aute foal neurologial defiit All stroke syndromes are potential neurosurgial emergenies and should be disussed with a onsultant paediatri neurologist on presentation. Further management and any transfer may involve liaison with the nearest available PICU. Aute ishaemi arterial stroke haemorrhage mass effet Aute venous stroke haemorrhage venous infartion mass effet Primary haemorrhagi stroke mass effet Non-aidental injury subdural haematoma strangulation with ompression of internal arotid artery Posterior leukoenephalopathy (hyper/hypotension or immunosuppression) Unilateral hemispheri erebral oedema, for example seondary to diabetes, hyperammonaemia (ornithine arbamoyl transferase defiieny) Hemiplegi migraine (but diagnosis of exlusion migrainous symptoms seen in erebrovasular disease) Post-ital (Todd s paresis) short duration so neuroimaging essential if persistent hildren with prolonged seizures may develop permanent hemiparesis with seizures (hemiseizure-hemiplegiaepilepsy) Aute disseminated enephalomyelitis Brain tumour Enephalitis, for example seondary to Herpes simplex (usually have seizures) Rasmussen s enephalitis Mitohondrial enephalopathy with stroke-like episodes Alternating hemiplegia with diffusion weighting has advantages over CT as haemorrhage an be diagnosed or exluded (fig 1A2), RPLS (fig 1F2), hemiplegi migraine (fig 1F4) and ADEM an be distinguished from ishaemi stroke and venous or arterial pathology an usually be identified and this may alter aute management, whih in turn may redue the extent of the eventual infart. VST may be aompanied by infartion (sometimes haemorrhagi), typially in a parietal, oipital (fig 1E2), frontal or thalami (fig 1E1) distribution 17 ; if the diagnosis is not obvious on plain CT or MR (fig 1E4), emergeny CT or MR venography (fig 1E3) should be onsidered for all strokes unless there is obvious arterial pathology, so that antioagulation an be onsidered (see below). For AIS, if MRA is not diagnosti, T1-weighted spin eho of the nek with fat saturation should be performed to exlude dissetion (fig 1B3) as, again, these patients should be onsidered for antioagulation. Although there is a 1% risk of stroke, highest with intraranial stenosis (fig 1C4), onventional angiography may be required for the diagnosis of small vessel vasulitis, ortial venous thrombosis and sometimes for the diagnosis of dissetion (fig 1B4), partiularly in the posterior irulation, 34 as well as for the pre-surgial anatomial definition of moyamoya (fig 1D4), AVM (fig 1A4) or aneurysm. Speifi measures Haemorrhagi stroke 7 The management strategy should ensure optimal intravasular volume, normothermia and normoglyaemia. A neurosurgial Box 2 Emergeny imaging for hildhood stroke Magneti resonane imaging (MRI) (inluding diffusion and perfusion), arteriography (MRA), venography (MRV) to exlude haemorrhage to define extent and territory of infart MRA to define vasular anatomy of irle of Willis and nek vessels T1-weighted spin eho of the nek with fat saturation sequene to exlude dissetion MRV to exlude venous sinus thrombosis diffusion imaging to differentiate aute from hroni infartion perfusion imaging to demonstrate areas of abnormal erebral blood flow, blood volume and mean transit time CT san to exlude haemorrhage if MRI not available autely; onsider CT venography Conventional angiography if: haemorrhage without oagulopathy and ause not obvious on MRA or MRV ishaemi stroke, MRA normal and fat-saturated T1-MRI of the nek does not demonstrate dissetion opinion is mandatory for the disussion of haematoma drainage and the management of ompliations, inluding hydroephalus, vasospasm, perihaematomal oedema and brain shift. Intraranial pressure monitoring and osmotherapy targeted at maintaining an adequate erebral perfusion pressure may be required. Fluid restrition is not advisable initially but may be initiated if there is evidene of inappropriate ADH release. Vasospasm may ompliate subarahnoid haemorrhage, is detetable by transranial Doppler (TCD) and treatable with alium hannel antagonists. Blood pressure ontrol is a ontroversial topi as perfusion pressure must be maintained while the risk of reurrent haemorrhage may mandate avoidane of hypertension before definitive vasular treatment. If there is an underlying AVM or aneurysm, the reurrene risk 9 means that a vasular team with onsiderable experiene should evaluate and deide between the management options (neurosurgery, neuroradiology or stereotati radiotherapy) one the patient has reovered from the aute phase. Ishaemi stroke Some hildren presenting with AIS/VST are andidates for aute interventions (figs 3 and 4) after neuroimaging and paediatri neurologial onsultation. 6 8 Transfusion for aute stroke in sikle ell disease The population with sikle ell disease provides an ideal model for proative stroke prevention as the majority of strokes are predited by TCD. Blood transfusion is a mainstay of stroke prevention 42 as well as aute stroke management. Transfusion should ommene within 2 4 h of presentation with neurologial defiit; emergeny exhange, rather than top-up, transfusion at the time of first stroke appears to be assoiated with a redued risk of reurrene. 43 The aim is to redue the HbS % to (30% with a haematorit of.30%. Pathology an inlude haemorrhage, 11 VST, 17 RPLS, 40 aute nerotising enephalitis and arterial dissetion as well as territorial infartion seondary to arterial stenosis and silent or overt injury, generally in the watershed regions (fig 1F3) and often assoiated with transient neurologial symptoms and signs rather than overt stroke. If available, emergeny MR may guide management. 896 Arh Dis Child 2008;93: doi: /ad

9 Downloaded from ad.bmj.om on January 15, Published by group.bmj.om Thrombolysis with tissue plasminogen ativator (tpa) Despite a little published experiene, 44 whih is almost ertainly biased in favour of positive outomes, there is no evidene to support the use of tpa in the aute management of hildhood stroke. 6 8 Although hildren may present,3 h after stroke, its rarity, the low sensitivity of CT for aute infartion and the wide differential in this age group means that very few hildren are diagnosed in the time window desribed in adult trials of aute intervention in stroke. Generally, thrombolysis is ontraindiated. Very oasionally, and only as part of a strit researh protool, thrombolysis, with intravenous tissue plasminogen ativator (tpa) within 3 h or intra-arterial tpa within 6 h, may be onsidered for middle erebral artery olusion, or for basilar olusion, within 12 h, perhaps with balloon angioplasty. Aute antioagulation or aspirin The use of anti-oagulation remains ontroversial. Children are probably at less risk of haemorrhage than adults and there is a ase for aute antioagulation in AIS. 8 Antioagulation with low moleular weight heparin followed by warfarin should ertainly be onsidered in hildren with onfirmed VST (for 3 6 months or until omplete reanalisation) or extraranial arterial dissetion assoiated with AIS (for 3 6 months or until evidene of vessel healing). 6 8 The use of antioagulation in patients with ardia embolism is ontroversial and management should involve onsultants in ardiology and neurology. The use of aspirin probably redues AIS reurrene ; aspirin at a dose of 5 mg/kg/ day should be onsidered autely after AIS, exept where there is evidene of haemorrhage, with subsequent long term prophylaxis, partiularly if there is persistent vasulopathy, at 3 5 mg/kg/day. 6 8 Management of intratable intraranial hypertension If intraranial hypertension persists or there is evidene of impending herniation despite maximal medial therapy, deompressive ranietomy should be onsidered for AIS, VST and stroke mimis. Patients with hydroephalus seondary to large erebellar infarts may need ventriulostomy or erebelletomy. Rehabilitation and follow-up Physio-, oupational and speeh therapists should be available for hildren soon after stroke as part of the multidisiplinary team. Long term rehabilitation should inlude ognitive, 46 as well as physial, domains. THE FUTURE As there is a wide range of differential diagnoses, whih may be diffiult to reognise, and the multidisiplinary expertise available in stroke units has been shown to improve outome in adults, 48 it is important that ommuniation between primary, seondary and tertiary servies failitates the hild s pathway through aute diagnosis and treatment as well as longer term rehabilitation and seondary prevention. Further multi-entre, multi-national studies of epidemiology and risk fators for primary and seondary stroke should be urgently undertaken through ollaborations suh as the International Paediatri Stroke Study. We must then use these observational data to enourage and adequately power randomised interventional studies to establish appropriate evidene based guidelines for the treatment of this potentially salvageable paediatri emergeny. Funding: FJK was funded by the Wellome Trust ( B/92/2), Ation Medial Researh and the British Heart Foundation and benefited from R&D funding reeived from the NHS exeutive. Competing interests: None. REFERENCES 1. Zahurane DB, Brown DL, Lisabeth LD, et al. Is it time for a large, ollaborative study of pediatri stroke? Stroke 2005;36: Telfer P, Coen P, Chakravorty S, et al. Clinial outomes in hildren with sikle ell disease living in England: a neonatal ohort in East London. Haematologia 2007;92: Mazumdar M, Heeney MM, Sox CM, et al. Preventing stroke among hildren with sikle ell anemia: an analysis of strategies that involve transranial Doppler testing and hroni transfusion. Pediatris 2007;120:e Laugesaar R, Kolk A, Tomberg T, et al. Autely and retrospetively diagnosed perinatal stroke: a population-based study. Stroke 2007;38: Braun KP, Kappelle LJ, Kirkham FJ, et al. Diagnosti pitfalls in paediatri ishaemi stroke. Dev Med Child Neurol 2006;48: Royal College of Physiians Paediatri Stroke Working Group. Stroke in hildhood: linial guidelines for diagnosis, management and rehabilitation. Available from (aessed 4 July 2008). 7. Roah ES, Golomb MR, Adams R, et al. Management of stroke in infants and hildren: a sientifi statement from a Speial Writing Group of the Amerian Heart Assoiation Stroke Counil and the Counil on Cardiovasular Disease in the Young. Stroke 2008;39: Monagle P, Chalmers E, Chan A, et al. Antithromboti therapy in neonates and hildren: Amerian College of Chest Physiians Evidene-Based Clinial Pratie Guidelines (8th Edition). Chest 2008;133(6 Suppl):887S-968S. 9. Fullerton HJ, Wu YW, Sidney S, et al. Reurrent hemorrhagi stroke in hildren: a population-based ohort study. Stroke 2007;38: Liu AC, Segaren N, Cox TS, et al. Is there a role for magneti resonane imaging in the evaluation of non-traumati intraparenhymal haemorrhage in hildren? Pediatr Radiol 2006;36: Strouse JJ, Hulbert ML, DeBaun MR, et al. Primary hemorrhagi stroke in hildren with sikle ell disease is assoiated with reent transfusion and use of ortiosteroids. Pediatris 2006;118: Blom I, De Shryver EL, Kappelle LJ, et al. Prognosis of haemorrhagi stroke in hildhood: a long-term follow-up study. Dev Med Child Neurol 2003;45: Kurnik K, Kosh A, Strater R, et al. Reurrent thromboembolism in infants and hildren suffering from symptomati neonatal arterial stroke: a prospetive follow-up study. Stroke 2003;34: Ganesan V, Prengler M, MShane MA, et al. Investigation of risk fators in hildren with arterial ishemi stroke. Ann Neurol 2003;53: DeVeber G, Andrew M, Adams C, et al. Cerebral sinovenous thrombosis in hildren. N Engl J Med 2001;345: Heller C, Heineke A, Junker R, et al. Cerebral venous thrombosis in hildren: a multifatorial origin. Cirulation 2003;108: Sébire G, Tabarki B, Saunders DE, et al. Venous sinus thrombosis in hildren. Brain 2005;128: Shellhaas RA, Smith SE, O Tool E, et al. Mimis of hildhood stroke: harateristis of a prospetive ohort. Pediatris 2006;118: Jordan LC, van Beek JG, Gottesman RF, et al. Ishemi stroke in hildren with ritial illness: a poor prognosti sign. Pediatr Neurol 2007;36: Kenet G, Kirkham F, Niederstadt T, et al. Risk fators for reurrent venous thromboembolism in the European ollaborative paediatri database on erebral venous thrombosis: a multientre ohort study. Lanet Neurol 2007;6: Ganesan V, Hogan A, Shak N, et al. Outome after ishaemi stroke in hildhood. Dev Med Child Neurol 2000;42: Sträter R, Beker S, von Ekardstein A, et al. Prospetive assessment of risk fators for reurrent stroke during hildhood a 5-year follow-up study. Lanet 2002;360: Ganesan V, Prengler M, Wade A, et al. Reurrene after hildhood ishemi stroke. Cirulation 2006;114: Fullerton HJ, Wu YW, Sidney S, et al. Risk of reurrent hildhood arterial ishemi stroke in a population-based ohort: the importane of erebrovasular imaging. Pediatris 2007;119: Maguire JL, deveber G, Parkin PC. Assoiation between iron-defiieny anemia and stroke in young hildren. Pediatris 2007;120: Van Beynum IM, Smeitink JA, den Heijer M, et al. Hyperhomoysteinemia: a risk for ishemi stroke in hildren. Cirulation 1999;99: Nowak-Göttl U, Sträter R, Heineke A, et al. Lipoprotein (a) and geneti polymorphisms of lotting fator V, prothrombin and methylenetetrahydrofolate redutase are risk fators of ishaemi stroke in hildhood. Blood 1999;94: Sébire G, Meyer L, Chabrier S. Variella as a risk fator for erebral infartion in hildhood: a ase-ontrol study. Ann Neurol 1999;45: Askalan R, Laughlin S, Mayank S, et al. Chikenpox and stroke in hildhood: a study of frequeny and ausation. Stroke 2001;32: Miravet E, Danhaivijitr N, Basu H, et al. Clinial and radiologial features of hildhood erebral infartion following variella zoster virus infetion. Dev Med Child Neurol 2007;49: Danhaivijitr N, Miravet E, Saunders DE, et al. Post-variella intraranial haemorrhage in a hild. Dev Med Child Neurol 2006;48: Arh Dis Child 2008;93: doi: /ad

10 Downloaded from ad.bmj.om on January 15, Published by group.bmj.om 32. Fullerton HJ, Johnston SC, Smith WS. Arterial dissetion and stroke in hildren. Neurology 2001;57: Rafay MF, Armstrong D, Deveber G, et al. Cranioervial arterial dissetion in hildren: linial and radiographi presentation and outome. J Child Neurol 2006;21: Ganesan V, Chong WK, Cox TC, et al. Posterior irulation stroke in hildhood. Risk fators and reurrene. Neurology 2002;59: Chabrier S, Rodesh G, Lasjaunias P, et al. Transient erebral arteriopathy: a disorder reognized by serial angiograms in hildren with stroke. J Child Neurol 1998;13: Danhaivijitr N, Cox TC, Saunders DE, et al. Evolution of erebral arteriopathies in hildhood arterial ishemi stroke. Ann Neurol 2006;59: Fung LW, Thompson D, Ganesan V. Revasularisation surgery for paediatri moyamoya: a review of the literature. Childs Nerv Syst 2005;21: Fullerton HJ, Aminoff AR, Ferriero DM, et al. Neurodevelopmental outome after endovasular treatment of vein of Galen malformations. Neurology 2003;61: Maria BL, Neufeld JA, Rosainz LC, et al. Central nervous system struture and funtion in Sturge-Weber syndrome: evidene of neurologi and radiologi progression. J Child Neurol 1998;13: Henderson JN, Noetzel MJ, MKinstry RC, et al. Reversible posterior leukoenephalopathy syndrome and silent erebral infarts are assoiated with severe aute hest syndrome in hildren with sikle ell disease. Blood 2003;101: Braun KP, Rafay MF, Uiterwaal CS, et al. Mode of onset predits etiologial diagnosis of arterial ishemi stroke in hildren. Stroke 2007;38: Adams RJ, Brambilla D, Optimizing Primary Stroke Prevention in Sikle Cell Anemia (STOP 2) Trial Investigators. Disontinuing prophylati transfusions used to prevent stroke in sikle ell disease. N Engl J Med 2005;353: Hulbert ML, Sothorn DJ, Panepinto JA, et al. Exhange blood transfusion ompared with simple transfusion for first overt stroke is assoiated with a lower risk of subsequent stroke: a retrospetive ohort study of 137 hildren with sikle ell anemia. J Pediatr 2006;149: Janjua N, Nasar A, Lynh JK, et al. Thrombolysis for ishemi stroke in hildren: data from the nationwide inpatient sample. Stroke 2007;38: Sträter R, Kurnik K, Heller C, et al. Aspirin versus low-dose low-moleular-weight heparin: antithromboti therapy in pediatri ishemi stroke patients: a prospetive follow-up study. Stroke 2001;32: King AA, White DA, MKinstry RC, et al. A pilot randomized eduation rehabilitation trial is feasible in sikle ell and strokes. Neurology 2007;68: Ganesan V, Kirkham FJ. Stroke and erebrovasular disease in hildhood. International Child Neurology Assoiation and MaKeith Press, In press. 48. Stroke Unit Trialists Collaboration. Organised inpatient (stroke unit) are for stroke. Cohrane Database Syst Rev 2007;(3):CD Drug and Therapeutis Bulletin (DTB) Your key soure of unbiased, independent advie For over 45 years DTB has been an independent, indispensable part of evidene-based linial pratie. DTB offers healthare professionals detailed assessment of, and pratial advie on, individual mediines and other treatments, groups of treatment and the overall management of disease. DTB is now also available online at browse or searh all DTB ontent from the latest issue bak to alerting, sophistiated searhing, RSS feeds and full text links from ited referenes interative servies suh as My Folders for quik aess to artiles that you have viewed previously and My Searhes to save and re-use useful searhes omment online on any DTB artile To subsribe, or for further information, please visit Arh Dis Child 2008;93: doi: /ad

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