Advertisment Polium-B
Indian Journal of Critical Care Medicine
An open access publication of ISCCM™ 
Users online: 904 
     Home | Login 
  About Current Issue Archive Search Instructions Online Submission Subscribe Etcetera Contact  
 »  Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
 »  Article in PDF (873 KB)
 »  Citation Manager
 »  Access Statistics
 »  Reader Comments
 »  Email Alert *
 »  Add to My List *
* Registration required (free) 

  IN THIS Article
 »  Abstract
 »  Introduction
 »  Epidemiology
 »  Risk Factors
 »  Pathophysiology
 »  Clinical Manifes...
 »  Laboratory Inves...
 »  Management
 »  Recommendations ...
 »  Recommendations ...
 »  Recommendations ...
 »  Recommendations ...
 »  Rehabilitation T...
 »  Outcome, Morbidi...
 »  Our Experience a...
 »  Conclusions
 »  Recommendations ...
 »  References
 »  Article Figures
 »  Article Tables

 Article Access Statistics
    PDF Downloaded583    
    Comments [Add]    
    Cited by others 7    

Recommend this journal


 Table of Contents    
Year : 2010  |  Volume : 14  |  Issue : 3  |  Page : 129-140

Cerebrovascular complications in pediatric intensive care unit

1 Department of Pediatrics, Sir Ganga Ram Hospital, New Rajinder Nagar, New Delhi, India
2 Department of Pediatrics, Dr. B. L. Kapoor Memorial Hospital, Pusa Road, New Delhi, India

Date of Web Publication23-Dec-2010

Correspondence Address:
Anil Sachdev
Sir Ganga Ram Hospital, New Rajinder Nagar, New Delhi - 110 060
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-5229.74171

Rights and Permissions

 » Abstract 

Cerebrovascular complications are being frequently recognized in the pediatric intensive care unit in the recent few years. The epidemiology and risk factors for pediatric stroke are different from that of the adults. The incidence of ischemic stroke is almost slightly more than that of hemorrhagic stroke. The list of diagnostic causes is increasing with the availability of newer imaging modalities and laboratory tests. The diagnostic work up depends on the age of the child and the rapidity of presentation. Magnetic resonance imaging, computerized tomography and arteriography and venography are the mainstay of diagnosis and to differentiate between ischemic and hemorrhagic events. Very sophisticated molecular diagnostic tests are required in a very few patients. There are very few pediatric studies on the management of stroke. General supportive management is as important as the specific treatment. Most of the treatment guidelines and suggestions are extrapolated from the adult studies. Few guidelines are available for the use of anticoagulants and thrombolytic agents in pediatric patients. So, our objective was to review the available literature on the childhood stroke and to provide an insight into the subject for the pediatricians and critical care providers.

Keywords: Anticoagulant therapy, cerebrovascular accident, childhood stroke, pediatric intensive care unit, stroke, thrombolytic therapy

How to cite this article:
Sachdev A, Sharma R, Gupta D. Cerebrovascular complications in pediatric intensive care unit. Indian J Crit Care Med 2010;14:129-40

How to cite this URL:
Sachdev A, Sharma R, Gupta D. Cerebrovascular complications in pediatric intensive care unit. Indian J Crit Care Med [serial online] 2010 [cited 2018 Jun 19];14:129-40. Available from:

 » Introduction Top

Cerebrovascular accident in children is more common than was once recognized. It is typically associated with an underlying anatomic anomaly or a systemic disease. The cerebrovascular complications are due to any abnormality of the brain resulting from a pathologic process of the blood vessels, e.g., occlusion of the lumen by a thrombus or embolus, rupture of the vessel, any lesion or altered permeability of the vessel wall and increased viscosity or other change in quality of blood.

This review article is presented since there are few pediatric studies on childhood stroke and clear guidelines are not available to deal with such patients in the pediatric intensive care. A search of publications listed in the electronic databases Pubmed and OVID was conducted using the keywords like stroke, childhood stroke, cerebrovascular accident, thrombolytic therapy and anticoagulant therapy. We preferred to select studies on pediatric stroke particularly and also studies on adults with reference to children. The relevant cross-references from the eligible articles were also searched manually. Some articles were also obtained manually from National Medical Library, New Delhi. The selection of studies was based on study title initially, followed by the abstract and full body text. Two hundred studies were selected on the basis of study title. This was reduced to 130 after abstract search and 65 full text articles were selected and read.

 » Epidemiology Top

It is a general impression that childhood cerebrovascular diseases are more often underdiagnosed as compared to that of the adult population. The overall average annual incidence rate for children through 14 years of age was 2.52/100,000/year. [1] Broderick et al, [2] found an incidence of 2.7 cases/100,000/year, similar to the figure reported previously by Schoenberg and colleagues. [1] In the Canadian Pediatric Ischemic Stroke Registry, [3] incidence of arterial and venous occlusion is estimated to be 1.2/100,000 children/year.

 » Risk Factors Top

Strokes in children occur in conjunction with intracranial infection, arteriovenous malformations (AVMs) or with occlusive vascular diseases secondary to cardiac disease, hematological and metabolic disorders. Central nervous system infections and trauma remain the major causes of stroke in children. Despite extensive evaluation, an etiologic factor or associated conditions remain undetermined in 20-50% of all stroke patients [Table 1]. [4],[5],[6] The incidence of stroke in pediatric cardiac patients is 4% with 75% occurring within the first two years of life. [7]
Table 1 :Risk factors for pediatric cerebrovascular disease

Click here to view

Vascular malformations, including AVMs, aneurysms, and cavernous malformations are the most common surgically treatable risk factors for children with hemorrhagic stroke [Figure 1]. [8],[9] Hematological disorders leading to hyperviscosity syndromes (polycythemia, hyperleukocytosis, and thrombocytosis) can lead to arterial occlusion. [10],[11]
Figure 1 :A vein of Galen malformation

Click here to view

There has been a recent recognition of the importance of hypercoagulable states. Antithrombin III, proteins C and S are naturally occurring anticoagulants whose deficiencies are inherited as an autosomal recessive trait. [12],[13] Autoimmune disorders may lead to cerebrovascular disease through a vasculitis or by inducing a hypercoagulable state. In systemic lupus erythematosus, neurologic involvement is seen in over 50% of patients. [14]

Several inborn errors of metabolism are associated with cerebral infarction. Homocystinuria, due to a defect in methionine metabolism, may present as a thrombotic syndrome due to endothelial damage and increased platelet aggregation. [15] Stroke-like episodes in a nonvascular distribution are seen in mitochondrial encephalomyopathy with lactic acidemia (MELAS). This recently described disorder is due to a mutation of mitochondrial DNA and a tentative diagnosis can be made by the presence of ragged red fibers in skeletal muscle. [16]

Trauma to the neck may predispose to carotid thrombosis. This can be a blunt injury to the neck, intraoral trauma, falling with a pencil in the mouth, or trauma to the cervical spine (chiropractic manipulation).

Moyamoya disease occurs primarily in the Japanese population, and is characterized by progressive stenosis and occlusion of the cerebral arteries at the Circle of Willis. In response to the stenosis, an abnormal network of small collateral vessels develops, creating the characteristic "puff of smoke" appearance on angiograms. Children with Moyamoya disease present with recurrent transient ischemic attacks as well as acute ischemic stroke. In general, there is a progressive neurologic deterioration that is characterized by significant impairment of motor and cognitive function. [17],[18] The majority of cases are idiopathic. Moyamoya syndrome is a disorder with a similar angiographic appearance to Moyamoya disease but is secondary to several slowly progressive occlusive cerebral vasculopathies, such as sickle cell disease, postradiation vasculopathy and neurofibromatosis.

Newborn illnesses that increase the risk of sino-venous thrombosis include asphyxia, dehydration, sepsis, and head and neck disorders, including meningitis. In children, acute illnesses like sepsis or dehydration are present in one-third of the cases of sinus thrombosis. [19] Head trauma or cranial surgery may damage dural sinuses, triggering thrombosis. Chronic systemic inflammatory diseases are the underlying risk factor in 60% of the patients with cerebro-sinovenous thrombosis (CSVT). [20],[21]

 » Pathophysiology Top

Strokes are broadly classified as either hemorrhagic or ischemic, but may also be caused by decrease in cerebral blood flow. [22] Acute ischemic stroke refers to strokes caused by thrombosis or embolism and accounts for 85% of all strokes. Thrombotic strokes can be divided into large vessel disease, including the carotid artery system, or small vessel disease comprising the intracerebral arteries, including the branches of the Circle of Willis and the posterior circulation. The most common sites of thrombotic occlusion are cerebral artery branch points, especially in the distribution of the internal carotid artery. [23] Cerebral hemorrhage [Figure 2] may occur when an artery in the brain tears or bursts, causing blood to spill out. A hemorrhage often happens without warning. In children, it may result from blood vessel defects like aneurysm or an AVM present since birth. Very rarely, it may occur as a result of high blood pressure. [24]
Figure 2 :Extensive cerebral haemorrhage

Click here to view

Loss of perfusion to a portion of the brain initiates the ischemic cascade within seconds to minutes. Within the ischemic cerebrovascular bed, there are two major zones of injury: the core ischemic zone of necrosis and the potentially reversible "ischemic penumbra". Due to inadequate supply and rapid depletion of oxygen and glucose in the core zone, the neurons and the supporting tissues (glial cells) undergo necrosis. The cells in the penumbra zone suffer mild to moderate ischemia due to the presence of collateral circulation. Restoration of perfusion to ischemic penumbra is the earliest goal of treatment of ischemic stroke. [25]

Cellular changes during the ischemic event involve a series of complex metabolic changes. The duration, severity, and the location of focal cerebral ischemia determine the extent of brain function and thus the severity of stroke. Once the blood flow to the neurons diminishes, anaerobic glycolytic pathways are utilized in the affected region and hydrogen ions and lactic acid are produced leading to generation of free radicals, arachidonic acid, nitric oxide and cytokines [Figure 3]. [26],[27]
Figure 3 :Ischemic cascade of cellular damage (NMAD – N-methyl-d aspartate)

Click here to view

 » Clinical Manifestation Top

The signs and symptoms depend on the location and size of the occluded vessel, as well as the patient's age. Anterior circulation strokes are much more common than posterior, and the left cerebral hemisphere is affected more often than the right. [28]

Most children who have suffered a stroke present with hemiparesis with or without seizures. Seizures at the onset of stroke are relatively frequent in children as compared to adults. [29] A prolonged persistent focal deficit following seizures that is inconsistent with Todd paresis raises the possibility of stroke. Gaze palsy or head turning suggests a large supratentorial infarct. If headache is present, arterial dissection or venous thrombosis is the possible cause. Deterioration in the level of consciousness is common in cerebral hemorrhage, large middle cerebral territory infarcts, and posterior fossa strokes, and is an indication for immediate transfer to an intensive care unit with pediatric neurology and neurosurgery facilities available. [30]

The clinical findings of ischemic and hemorrhagic stroke overlap, so a brain imaging study is mandatory to distinguish ischemic stroke from hemorrhage or other structural brain lesions that may imitate stroke. Hemiplegia, headache, seizure or altered levels of consciousness may all herald a potentially reversible or lethal medical or surgical stroke emergency. The time from onset of symptoms to presentation is very useful diagnostically, for example, arteriopathy is more likely to present with a stuttering onset, and "thunderclap" headaches may be indicative of a subarachnoid hemorrhage.

The chance of hemorrhagic stroke is more if a child presents with headache, nausea, vomiting, coma, hemiparesis, seizures and skin lesions. The clinical presentation of acute ischemic stroke more commonly has associated cranial nerve palsy (VII, IX, X, XII, Horner), visual field defects along with hemiparesis, seizures, headache, ataxia and coma. [24]

Middle cerebral artery occlusions commonly produce contralateral hemiparesis, contralateral hypesthesia, ipsilateral hemianopsia and gaze preference towards the side of the lesion. Agnosia is common, and receptive or expressive aphasia may result if the lesion occurs in the dominant hemisphere. Since the middle cerebral artery supplies the upper extremity motor strip, weakness of the arm and face is usually worse than that of the lower limb. [31]

Anterior cerebral artery occlusions primarily affect frontal lobe function and can result in disinhibition and speech perseveration, producing primitive reflexes (e.g., grasping, sucking reflexes), altered mental status, impaired judgment, contralateral weakness (greater in legs than in arms), contralateral cortical sensory deficits, gait apraxia, and urinary incontinence. [32]

Posterior cerebral artery occlusions affect vision and thought process, producing contralateral homonymous hemianopsia, cortical blindness, visual agnosia, altered mental status, and impaired memory. [33]

Vertebrobasilar artery occlusions are notoriously difficult to detect because they cause a wide variety of cranial nerve, cerebellar, and brainstem deficits. [34] These include vertigo, nystagmus, diplopia, visual field deficits, dysphagia, dysarthria, facial hypesthesia, syncope, and ataxia. A hallmark of posterior circulation strokes is that there are crossed findings: ipsilateral cranial nerve deficits and contralateral motor deficits. This is in contrast to anterior strokes, which produce findings on one side of the body only.

Lastly, lacunar strokes result from occlusion of the small, perforating arteries of the deep subcortical areas of the brain, accounting for 13-20% of all cerebral infarctions. The most common lacunar syndromes include pure motor, pure sensory and ataxic hemiparetic strokes. These infarcts commonly occur in patients with small vessel disease, such as diabetes and hypertension, and do not lead to impairments in cognition, memory, speech, or level of consciousness. [35]

The clinical features of cerebro-sinovenous thrombosis are subtle and present with diffuse neurologic signs and symptoms such as headache, altered sensorium and papilledema in 90% of patients, while seizures are present in 48% and hemiparesis in 17% only. [36],[37]

 » Laboratory Investigations Top

The sequence of investigations depends on the clinical presentation and the duration of onset of stroke [Table 2]. Magnetic resonance imaging (MRI) is an ideal method to evaluate neonates, infants, and children with suspected cerebral ischemia. MR angiography can confirm vessel patency and define the vascular anatomy. However, the rapid acquisition time and ease of monitoring make computerized tomography (CT) the ideal imaging technique in an unstable patient or a patient in whom acute intracranial hemorrhage is likely. [38]
Table 2 :Laboratory investigations in pediatric strok

Click here to view

 » Management Top

Acute treatment of cerebral ischemia requires an intensive care unit setting. Treatment should be directed to the underlying cause if it is identifiable. CT or MRI scan of the brain is essential to determine whether stroke is ischemic or hemorrhagic. The management is essentially aggressive supportive care to prevent neurological sequelae. [39] [Table 3]
Table 3 :Acute medical management of adult and childhood arterial ischemic stroke

Click here to view


Maintenance of airway, breathing, and circulation are the first priority in any acutely ill child. Studies on oxygenation in childhood arterial ischemic stroke are lacking, but a single consensus guideline from the Royal College of Physicians (RCP) advises that oxygen saturation should be maintained within normal limits. Supplement oxygen by mask or hood should be provided when oxygen saturation is <92%, and endotracheal intubation and mechanical ventilation should be instituted in patients with severe hypoxia and hemodynamic instability. [40],[41]

Blood pressure

Elevated blood pressure should not be treated very promptly within the first days after ischemic stroke. The ischemic penumbra loses autoregulation, and perfusion is directly linked to the mean arterial pressure. Acute elevations in blood pressure are often transient, and spontaneous declines are common. Overzealous treatment of hypertension following arterial ischemic stroke can convert the ischemic penumbra into an infarct. Reduction of blood pressure greater than 20 mmHg has been associated with worse neurological outcomes and larger infarcts, leading to the suggestion that even extreme cases of hypertension should be reduced by only 15% in the first 24 hours. [42]

If antihypertensive therapy is necessary, agents that have a rapid onset and predictable response should be used. If a child presents with hypotension, prompt treatment with fluid boluses and ionotropic vasopressors should be instituted to maintain mean blood pressure. [43]


In patients with acute stroke, fever is not uncommon. Fever should be taken care of with prompt use of antipyretics. Even mild elevations in body temperature consistently worsen the neurologic outcome from ischemic insults. [44],[45] Induced hypothermia is a potential treatment strategy for adult arterial ischemic stroke and it improves outcomes of neonates with hypoxic ischemic encephalopathy. [46]


There is strong evidence that hyperglycemia and hypoglycemia are associated with poor outcomes in adult arterial ischemic stroke studies. [47] A similar recommendation has been made for pediatric stroke. [48]

Hyperglycemia induces a pro-oxidative and proinflammatory state that can cause direct neuronal toxicity and cerebral edema. It is also responsible for procoagulant state and may further affect penumbral area blood supply. Besides lowering blood sugar, insulin has antioxidant and anti-inflammatory effects. Insulin also improves nitric oxide production and results in improved blood circulation to the ischemic areas.

Increased intracranial pressure

Acute management of large-distribution arterial ischemic stroke in children and adults often involves management of increased intracranial pressure secondary to edema and/or mass effect on the ventricles during the first 72-96 hours after a large infarct. The American Heart Association (AHA) suggests decompressive surgery for the seriously affected patients after adequate counseling of the family, [40] while the RCP recommends early neurosurgical referral in children with deteriorating sensorium. Unfortunately, evidence and guidelines in childhood stroke are lacking. [49]

Blood transfusion

For children with sickle cell disease, who have ischemic stroke, exchange transfusion is required to reduce hemoglobin S levels to <30% total hemoglobin, and thereafter, regular transfusion (4-6 weekly) to keep hemoglobin S to <20% is required. [50]

 » Recommendations for Supportive Therapy After Stroke in Children Top

The recommendations are discussed below. [38]

Class I recommendation

The supportive measures include maintenance of normothermia, normoxemia, normoglycemia and control of systemic hypertension (Class I, Level of Evidence C).

Class II recommendation

In children with stroke, it is reasonable to maintain euhydration and treat anemia (Class IIa, Level of Evidence C).

Class III recommendations

  1. There is no role of supplemental oxygen in the absence of hypoxemia (Class III, Level of Evidence C).
  2. There is no evidence suggesting the benefit of prophylactic antiepileptics in the absence of clinical or electrographic seizures in children with ischemic stroke (Class III, Level of Evidence C).
  3. Hypothermia should not be used in children with stroke except in the context of a clinical trial as there are no additional data confirming its safety and efficacy (Class III, Level of Evidence C).

Thrombolytic therapy

Tissue plasminogen activator (tPA) is used acutely in adult arterial ischemic stroke as a profibrinolytic agent, for lysing intracerebral clots and thereby restoring blood flow to compromised regions of the brain [Table 4]. These patients are now routinely given systemic tPA when presenting within 3 hours of stroke onset. [51] A dose of 0.9 mg/kg (maximum 90 mg) is used, with 10% of the dose given as a bolus over the first minute, and the remaining dose given as a 1-hour infusion.
Table 4 :Antithrombotic management of adult and childhood arterial ischemic stroke

Click here to view

There is currently no evidence to support the use of thrombolytic agents such as tPA in the acute treatment of pediatric arterial ischemic stroke. A prospective study by Browne et al, [52] using 0.5 mg/kg/hour systemic recombinant tPA for 6 hours concurrently with heparin (10 U/kg/hour) and fresh frozen plasma supplementation prior to recombinant tPA infusion, reported complete resolution of thrombosis in 13 of 20 children (65%), partial resolution in 4 patients (20%), and no response in 3 patients (15%). Zenz et al, [53] reported a dose of 0.5 mg/kg/hour for the first hour followed by 0.25 mg/kg/hour until clot lysis occurred or treatment had to be stopped because of bleeding complications. Complete clot lysis was achieved in 16 of 17 pediatric patients within 4-11 hours after the start of treatment. At this time, there is no evidence to suggest that there is an advantage of local over systemic thrombolytic therapy in children with thrombotic complications. [54] Thrombolytic therapy has been reported to have significant bleeding complications in children (68%) and blood transfusion is required in 39%. [55] Before thrombolytic therapy is used, the correction of other concurrent haemostatic problems such as associated thrombocytopenia or vitamin K deficiency is advisable. In case of major bleeding, discontinuation of thrombolytic agent and administration of cryoprecipitate and other blood components are needed. [38]

 » Recommendations for Thrombolytic Therapy for Childhood Stroke Top

The recommendations are discussed below. [38]

Class II recommendation

In children with CVST, thrombolytic therapy with tPA can be considered (Class IIb, Level of Evidence C).

Class III recommendation

Thrombolytic therapy is not recommended for children with acute ischemic stroke outside a clinical trial (Class III, Level of Evidence C). However, there was no consensus about the use of tPA in older adolescents who otherwise meet standard adult tPA eligibility criteria.

Antiplatelet aggregation

The Joint Guideline Statement from the AHA and the American Academy of Neurology (AAN) recommends that aspirin should be given within 24-48 hours of stroke onset in most patients (Level of Evidence grade A). [40] The administration of aspirin as an adjunctive therapy, within 24 hours of the use of thrombolytic agents, is not recommended (grade A). Aspirin should not be used as a substitute for other acute interventions, especially t-PA (grade A). A low dose of 1-5 mg/kg/day for platelet aggregation inhibition has been proposed. [56] Pediatric doses of aspirin are not based on studies of the effect on platelet function in pediatric patients.

Ticlopidine and clopidogrel selectively inhibit ADP-induced platelet aggregation, via the inhibition of the P2Y 12 receptor. The antiplatelet effect of ticlopidine and clopidogrel is additive to that of aspirin. [57] There has been no reported use in children, and dosage recommendations are unknown.

 » Recommendations for Aspirin Use in Children with Stroke Top

The recommendations are discussed below. [38]

Class II recommendations

  1. To prevent recurrence of acute ischemic stroke in children, aspirin can be used, except in cases where the underlying cause of stroke is sickle cell disease, severe hypercoagulable disorder and all those children who are at increased risk for embolization (Class IIa, Level of Evidence C).
  2. A dose of 3-5 mg/kg/day is adequate for stroke prevention in children (Class IIa, Level of Evidence C). If dose-related side effects occur, then, a dose reduction to 1-3 mg/kg may be considered (Class IIb, Level of Evidence C).
  3. In children taking aspirin for stroke prevention, it is reasonable to vaccinate for varicella and annually with influenza vaccine to reduce the risk of Reye's syndrome (Class IIa, Level of Evidence C). During the period of varicella and influenza infection, it is reasonable to withhold aspirin (Class IIa, Level of Evidence C).


Heparins, including unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH), are the principal agents used in the acute phase of anticoagulant therapy for arterial ischemic stroke. Based on the high rates of prothrombotic abnormalities, cardioembolic stroke and vascular dissection in childhood arterial ischemic stroke, American College of Chest Physicians' (ACCP) guidelines [58] recommend treatment with UFH or LMWH for 5-7 days. However, this recommendation remains controversial, and the RCP recommends initial treatment of childhood arterial ischemic stroke with aspirin 5 mg/kg until an indication for anticoagulation is found. [62] Parenteral anticoagulants should not be prescribed until a brain imaging study has excluded the possibility of a primary intracranial hemorrhage. [59] UFH doses are age dependent, with younger children requiring greater average doses (20 U/kg/hour) than older children and adults; similar observations have been made for LMWHs. Bolus dosing of UFH is typically avoided in arterial ischemic stroke. In children, heparin therapy is monitored most accurately by antifactor Xa activity. For UFH, the therapeutic range is 0.35-0.7 antifactor Xa activity U/ml, whereas for LMWH, the therapeutic range is 0.5-1.0 U/ml. Side effects of UFH include bleeding, osteoporosis, and heparin induced thrombocytopenia. [60] Burak et al, [61] administered enoxaparin to eight children with stroke and concluded that the LMWH was a safe and effective alternative to heparin for children. Anticoagulants also are being explored as an adjunct to thrombolytic therapy.

 » Recommendations for LMWH in Children with Stroke Top

The recommendations are discussed below. [38]

Class I recommendations

For long-term anticoagulation, LMWH can be used in all children with substantial risk of recurrent cardiac embolism, CVST, and selected hypercoagulable states (Class I, Level of Evidence C).

Class II recommendations

The administration of LMWH or UFH may be considered in children for up to 1 week after an ischemic stroke, pending further evaluation to determine the cause of the stroke (Class IIb, Level of Evidence C).

 » Recommendations for the Use of Warfarin in Children with Stroke Top

The recommendations are discussed below. [38]

Class II recommendations

For long-term anticoagulation, warfarin can be used in all children with substantial risk of recurrent cardiac embolism, cervico-cephalic arterial dissection, CVST, and selected hypercoagulable states (Class IIa, Level of Evidence C).

Surgical intervention

Surgical decompression has been reported in children presenting in coma with large ischemic middle cerebral infarcts, which are almost always fatal if managed conservatively. Similar intervention is required for a large cerebellar infarction leading to brain stem compression and hydrocephalus. [38]

Prevention of Stroke

The mechanisms and risk factors for arterial ischemic stroke in children are not well understood at present. The primary prevention is well established in few well-defined causes of arterial ischemic stroke, such as sickle cell disease, congenital cardiac lesions and hypercoagulable disorders.

  1. In sickle cell disease, all the children between 2 and 16 years should have Transcranial Doppler study once in a year (Class IIa, Level of Evidence B). Borderline and mildly abnormal studies may be repeated in 3-6 months. Children with abnormal results should receive periodic transfusions to reduce the percentage of sickle hemoglobin (Class I, Level of Evidence A). [38]
  2. All children with congenital heart lesions, especially complex heart lesions, should be repaired both to improve cardiac function and to reduce the subsequent risk of stroke (Class I, Level of Evidence C). [38]
  3. Children with hypercoagulable disorders are at a risk of stroke only in the setting of an additional risk factor. However, it is reasonable to evaluate for elevated serum homocysteine levels and the more common prothrombotic states, and to start folate, vitamin B6, or vitamin B12 if homocysteine is found to be elevated. [38]

 » Rehabilitation Techniques Top

Early evaluation of physical and cognitive disability is the key to prevent avoidable complications and to plan rehabilitation, which should involve a multidisciplinary team. [62],[63],[64] Constraint therapy may be adapted for children and appears to be associated with improved function of a hemiparetic hand. Improvement occurs over a prolonged period of time, and late deterioration is rare. The child and family should be encouraged to express their main concerns about re-integration to the home, community and school environments and to have these concerns addressed. [65],[66]

 » Outcome, Morbidity and Mortality Top

Between 20 and 40% of children die after a stroke. [67],[68],[69],[70],[71],[72] The mortality is higher for the hemorrhagic (about a third) than for ischemic stroke (up to 20%, with about half related to the underlying systemic illness rather than the stroke itself). Death during the acute phase is predicted by the level of consciousness on admission. Recurrent stroke occurs in 6-15% of children and mortality is higher in this group. [71],[73],[74] Intractable intracranial hypertension is a major predictor of poor outcome in patients with large intracerebral or intracerebellar hemorrhage and massive hemispheric or cerebellar infarction. Between 50 and 80% of surviving children have neurological sequelae, most commonly hemiparesis. [70],[71],[75],[76],[77],[78],[79] Neurological outcome appears to be better for those with hemorrhage, CVST, and posterior circulation stroke. [72],[80],[81] Other problems include neuropsychological deficits, poor attention, behavioral problems, and poor quality of life. [82],[83],[84],[85],[86] Predictors of poor neurological, cognitive, and behavioral outcome include systemic disease, multiple risk factors, infarct size, cortical involvement, thromboembolism, and Moyamoya. [87],[88],[89]

 » Our Experience at Sir Ganga Ram Hospital Top

In the year 2009, from January to December, there were 794 admissions in the 12-bedded PICU. Of these, 135 cases had primary non-traumatic central nervous system ailment and only 15 cases presented with stroke. There were nine patients with arterial ischemic stroke and six had hemorrhagic stroke. Central nervous system infection was the predominant risk factor for ischemic stroke in six patients, two had severe dehydration and electrolyte imbalance, and one each with cyanotic heart disease and l-asparaginase induced stroke. There were three cases of hemorrhagic stroke due to malignancy and one each of AVM, middle cerebral artery aneurysm and late hemorrhagic disease of the newborn. Neuroimaging was done in all cases for the diagnosis and to differentiate ischemic from hemorrhagic stroke. All patients received supportive therapy, LMWH and aspirin for ischemic stroke while interventional neurosurgical procedures were done in three cases of hemorrhagic stroke. Thrombolytic therapy was not used in any case.

 » Conclusions Top

Intensive supportive management and rehabilitation techniques are critical components in the management of children with stroke to optimize outcomes. The pathophysiology and outcomes of adult stroke differ significantly from those in children. The therapeutic management currently remains similar, largely because of the paucity of evidence from devoted pediatric observational studies and clinical trials. The use of anticoagulants and thrombolytic agents has been insufficiently investigated in childhood stroke, resulting in a lack of guidance. Dedicated pediatric studies are critically necessary to establish a key evidence for the multifaceted management in childhood stroke.

 » References Top

1.Schoenberg BS, Mellinger JF, Schoenberg DG. Cerebrovascular disease in infants and children: A study of incidence, clinical features, and survival. Neurology 1978;28:763-8.   Back to cited text no. 1
2.Broderick J, Talbot T, Prenger E, Leach A, Brott T. Stroke in children within a major metropolitan area: The surprising importance of intracerebral hemorrhage. J Child Neurol 1993;8:250-5.   Back to cited text no. 2
3.Deveber GA, Adams M, Andrew M. Canadian pediatric ischemic stroke registry. Can J Neurol Sci 1995;22:S24.  Back to cited text no. 3
4.Nicolaides P, Appleton RE. Stroke in children. Dev Med Child Neurol 1996;38:172-180.  Back to cited text no. 4
5.Mancini J, Girard N, Chabrol B. Ischemic cerebrovascular disease in children: Retrospective study of 35 patients. J Child Neurol 1997;12:193-9.  Back to cited text no. 5
6.Kerr LM, Anderson DM, Thompson JA, Lyver SM, Call GK. Ischemic stroke in the young: Evaluation and age comparison of patients six months to thirty-nine years. J Child Neurol 1993;8:266-70.  Back to cited text no. 6
7.Roach ES, Riela AR. Pediatric Cerebrovascular Disorders. 2nd ed. New York: Futura; 1995. p. 359.  Back to cited text no. 7
8.Johnston IH, Whittle IR, Besser M, Morgan MK. Vein of galen malformation: Diagnosis and management. Neurosurgery 1987;20:747-58.   Back to cited text no. 8
9.Menezes AH, Graf CJ, Jacoby CG, Cornell SH. Management of veinof Galen aneurysms: Report of two cases. J Neurosurg 1981;55:457-62.   Back to cited text no. 9
10.Portnoy BA, Herion JC. Neurological manifestations in sickle-cell disease - with a review of the literature and emphasis on the prevalence of hemiplegia. Ann Intern Med 1972;76:643-52.  Back to cited text no. 10
11.Balkaran B, Char G, Morris JS, Thomas PW, Serjeant BE, Serjeant GR. Stroke in a cohort of patients with homozygous sickle cell disease. J Pediatr 1992;120:360-6.  Back to cited text no. 11
12.Vomberg PP, Breederveld C, Fleury P, Arts WF. Cerebral thromboembolism due to antithrombin III deficiency in two children. Neuropediatrics 1987;18:42-4.   Back to cited text no. 12
13.Koh S, Chen LS. Protein C and S deficiency in children with ischemic cerebrovascular accident. Pediatr Neurol 1997;17:319-21.  Back to cited text no. 13
14.Montes de Oca MA, Babron MC, Bletry O, Broyer M, Courtecuisse V, Fontaine JL, et al. Thrombosis in systemic lupus erythematosus: A French collaborative study. Arch Dis Child 1991;66:713-7.  Back to cited text no. 14
15.Selhub J, Jaques PF, Bostom AG, D'Agostino RB, Wilson PW, Belanger AJ, et al. Association between plasma homocysteine concentrations and extracranial carotid-artery stenosis. N Engl J Med 1995;268:877-81.  Back to cited text no. 15
16.Schoffner JM. Mitochondrial myopathy diagnosis. Neurol Clin 2000;18:105-23.  Back to cited text no. 16
17.Suzuki J, Kodama N. Moyamoya disease: A review. Stroke 1983;14:104-9.  Back to cited text no. 17
18.Golden G. Cerebrovascular disease. In. Pediatric neurological diseases. Ed. Swaiman K. CV Mosby, St Louis. 1989, pp 603-617.  Back to cited text no. 18
19.Deveber G, Andrew M. Cerebral sinovenous thrombosis in children. N Engl J Med 2001;345:417-23.  Back to cited text no. 19
20.Lin CC, Lui CC, Tain YL. Thalamic stroke secondary to straight sinus thrombosis in a nephrotic child. Pediatr Nephrol 2002;17:184-6.  Back to cited text no. 20
21.Keane S, Gallagher A, Ackroyd S, McShane MA, Edge JA. Cerebral venous thrombosis during diabetic ketoacidosis. Arch Dis Child 2002;86:204-5.  Back to cited text no. 21
22.Garcia JH, Ho Khang-Loon, Pantoni L. Pathology in Barnett. In: Henry JM, Mohr JP, Stein BM, Yatsu FM, editors. Stroke Pathophysiology, Diagnosis and Management. 3rd ed. Philadelphia, PA: Churchill Livingston; 1998.   Back to cited text no. 22
23.Tresher WH. Ischemic stroke syndromes in childhood. Pediatr Ann 1992;21:374-83.  Back to cited text no. 23
24.Yamamoto H, Bogousslavsky J, van Melle G. Different predictors of neurological worsening in different causes of stroke. Arch Neurol 1998;55:481-6.   Back to cited text no. 24
25.Hakim AM. Ischemic penumbra, the therapeutic window. Neurology 1998;51:S44-6.   Back to cited text no. 25
26.Becker KJ. Inflammation and acute stroke. Curr Opin Neurol 1998;11:45-9.   Back to cited text no. 26
27.Hademenos GJ, Massoud TF. Biophysical mechanisms of stroke. Stroke 1997;28:2067-77.  Back to cited text no. 27
28.Abram HS. Vascular Disease. In: David B, editor. Child and Adolescent Neurology. St. Louis: Mosby; 1998. p. 271-93.  Back to cited text no. 28
29.Yang JS, Park YD, Hartlage PL. Seizures associated with stroke in childhood. Pediatr Neurol 1995;12:136-8.   Back to cited text no. 29
30.Pappachan J, Kirkham FJ. Cerebrovascular disease and stroke. Arch Dis Child 2008;93:890-8.  Back to cited text no. 30
31.Hacke W, Schwab S, Horn M, Spranger M, De Georgia M, von Kummer R. Malignant middle cerebral artery territory infarction: Clinical course and prognostic signs. Arch Neurol 1996;53:309-15.  Back to cited text no. 31
32.Brust CM, Chamorro A. Anterior cerebral artery diseases. In: Mohr JP, Choi DW, Grotta JC, Weir B, Wolf PA, editors. Stroke Pathophysiology, Diagnosis and Management. 4th ed. Philadelphia, PA: Churchill Livingston; 2004. p. 101-11.  Back to cited text no. 32
33.Sean I, Savitz MD, Louis R, Caplan MD. Verterbrobasilar disease. N Engl J Med 2005;352:2618-26.  Back to cited text no. 33
34.Rosman NP, Wu JK, Caplan LR. Cerebellar infarction in the young. Stroke 1992;23:763-6.  Back to cited text no. 34
35.Baumgartner RW, Sidler C, Mosso M, Georgiadis D. Ischemic lacunar stroke in patients with and without potential mechanism other than small-artery disease. Stroke 2003;34:653-9.  Back to cited text no. 35
36.Samuel J, Fernandes CM. Lateral sinus thrombosis (a review of 45 cases). J Laryngol Otol 1987;101:1227-9.  Back to cited text no. 36
37.Leker RR, Steiner I. Features of dural sinus thrombosis simulating pseudotumor cerebri. Eur J Neurol 1999;6:601-4.  Back to cited text no. 37
38.Roach ES, Meredith R, Golomb MR, Adams R, Biller J, Daniels S, et al. Management of stroke in infants and children. Stroke 2008;39:2644-691.  Back to cited text no. 38
39.Castillo J. Deteriorating stroke: Diagnostic criteria, predictors, mechanisms and treatment. Cerebrovasc Dis 1999;9:1-8.   Back to cited text no. 39
40.Adams HP Jr, del Zoppo G, Alberts MJ, Bhatt DL, Brass L, Furlan A, et al. Guidelines for the early management of adults with ischemic stroke: A guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Circulation 2007;115:e478-534.   Back to cited text no. 40
41.Treib J, Grauer MT, Woessner R, Morgenthaler M. Treatment of stroke on an intensive stroke unit: a novel concept. Intensive Care Med 2000;26:1598-611.  Back to cited text no. 41
42.Castillo J, Leira R, Garcia MM, Serena J, Blanco M, Davalos A. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke 2004;35:520-6.  Back to cited text no. 42
43.Konstantinos Spengos K, Tsivgoulis G, Zakopoulos N. Blood pressure management in acute stroke. Eur Neurol 2006;55:123-35.  Back to cited text no. 43
44.Ginsberg MD, Busto R. Combating hyperthermia in acute stroke: A significant clinical concern. Stroke 1998;29:529-34.  Back to cited text no. 44
45.Correia M, Silva M, Veloso M. Cooling therapy for acute stroke. Cochrane Database Syst Rev 2000;CD001247.  Back to cited text no. 45
46.Thoresen M, Whitelaw A. Therapeutic hypothermia for hypoxic-ischaemic encephalopathy in the newborn infant. Curr Opin Neurol 2005;18:111-6.   Back to cited text no. 46
47.Baird TA, Parsons MW, Phanh T, Butcher KS, Desmond PM, Tress BM, et al. Persistent poststroke hyperglycemia is independently associated with infarct expansion and worse clinical outcome. Stroke 2003;34:2208-14.   Back to cited text no. 47
48.Monagle P, Chan KC, Deveber G, Malmberg K. Pediatric thromboembolism and stroke. 1st ed. Hamilton, ON: B.C. Decker; 2006.  Back to cited text no. 48
49.Lee MC, Frank JI, Kahana M, Tonsgard JM, Frim DM. Decompressive hemicraniectomy in a 6-year-old male after unilateral hemispheric stroke: Case report and review. Pediatr Neurosurg 2003;38:181-5.  Back to cited text no. 49
50.Stroke and central nervous system disease: The management of sickle cell disease. National Institute of Health. Bethesda, MD: Publication No. 02-2117. 2002.  Back to cited text no. 50
51.The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995;333:1581-7.  Back to cited text no. 51
52.Browne M, Newall F, Campbell J, Savoia HF, Monagle P. Thrombolytic therapy with tissue plasminogen activator (tPA), analysis of safety and outcome in children. J Thromb Haemost 2003;1:P1488.   Back to cited text no. 52
53.Zenz W, Muntean W, Beitzke A, Zobel G, Riccabona M, Gamillscheg A. Tissue plasminogen activator (alteplase) treatment for femoral artery thrombosis after cardiac catheterisation in infants and children. Br Heart J 1993;70:382-5.  Back to cited text no. 53
54.Monagle P, Phelan E, Downie P, Kaufman SL, Martin LG, Gilarsky BP Local thrombolytic therapy in children. Thromb Haemost 1997;78:504.  Back to cited text no. 54
55.Gupta AA, Leaker M, Andrew M, Massicotte P, Liu L, Benson LN, et al. Safety and outcomes of thrombolysis with tissue plasminogen activator for treatment of intravascular thrombosis in children. J Pediatr 2001;139:682-8.  Back to cited text no. 55
56.Coull BM, Williams LS, Goldstein LB, Meschia JF, Heitzman D, Chaturvedi S, et al. Anticoagulants and antiplatelet agents in acute ischemic stroke. Stroke 2002;33:1934-42.  Back to cited text no. 56
57.Lecompte TP, Lecrubier C, Bouloux C. Antiplatelet effects of the addition of acetylsalicylic acid 40 mg daily to ticlopidine in human healthy volunteers. Clin Appl Thromb Hemost 1997;3:245-50.   Back to cited text no. 57
58.Monagle P, Chan A, Massicotte P, Chalmers E, Michelson AD. Antithrombotic therapy in children: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:645S-87S.  Back to cited text no. 58
59.Sherman DG. Antithrombotic and hypofibrinogenetic therapy in acute ischemic stroke: What is the next step? Cerebrovasc Dis 2004;17:138-43.   Back to cited text no. 59
60.Schmugge M, Risch L, Huber AR, Benn A, Fisher JE. Heparin-induced thrombocytopenia-associated thrombosis in pediatric intensive care patients. Pediatrics 2002;109:E10.  Back to cited text no. 60
61.Burak CR, Bowen MD, Barron TF. The use of enoxaparin in children with acute, nonhemorrhagic ischemic stroke. Pediatr Neurol 2003;29:295-8.  Back to cited text no. 61
62.Royal college of physicians, Pediatric stroke Working group. Stroke in childhood: Clinic guidelines for diagnosis, management and rehabilitation; 2004.   Back to cited text no. 62
63.Sacco RL, Adams R, Albers G, Alberts MJ, Benavente O, Furie K, et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: A statement for healthcare professionals from American Heart Association /American Stroke Association council on stroke: Co-sponsored by the council on cardiovascular radiology and intervention: The American Academy of neurology affirms the value of this guideline. Circulation 2006;113:e409-49.  Back to cited text no. 63
64.Paediatric Stroke Working Group, Royal College of Physicians of London. Stroke in childhood: clinical guidelines for diagnosis management and rehabilitation.  Back to cited text no. 64
65.Willis JK, Morello A, Davie A, Rice JC, Bennett JT. Forced use treatment of childhood hemiparesis. Pediatrics 2002;110:94-6.  Back to cited text no. 65
66.Charles JR, Wolf SL, Schneider JA, Gordon AM. Efficacy of a childfriendly form of constraint-induced movement therapy in hemiplegic cerebral palsy: A randomized control trial. Dev Med Child Neurol 2006;48:635-42.  Back to cited text no. 66
67.Lanska MJ, Lanska DJ, Horwitz SJ, Aram DM. Presentation, clinical course, and outcome of childhood stroke. Pediatr Neurol 1991;7:333-41.  Back to cited text no. 67
68.Higgins JJ, Kammerman LA, Fitz CR. Predictors of survival and characteristics of childhood stroke. Neuropediatrics 1991;22:190-3.  Back to cited text no. 68
69.Keidan I, Shahar E, Barzilay Z, Passwell J, Brand N. Predictors of outcome of stroke in infants and children based on clinical data and radiologic correlates. Acta Paediatr 1994;83:762-5.  Back to cited text no. 69
70.Eeg-Olofsson O, Ringheim Y. Stroke in children: Clinical characteristics and prognosis. Acta Paediatr Scand 1983;72:391-5.  Back to cited text no. 70
71.Lanthier S, Carmant L, David M, Larbrisseau A, de Veber G. Stroke in children: The coexistence of multiple risk factors predicts poor outcome. Neurology 2000;54:371-8.  Back to cited text no. 71
72.Blom I, De Schryver EL, Kappelle LJ, Rinkel GJ, Jennekens-Schinkel A, Peters AC. Prognosis of haemorrhagic stroke in childhood: Along-term follow-up study. Dev Med Child Neurol 2003;45:233-9.  Back to cited text no. 72
73.Strδter R, Becker S, von Eckardstein A, Heinecke A, Gutsche S, Junker R, et al. Prospective assessment of risk factors for recurrent stroke during childhood-a 5-year follow-up study. Lancet 2002;360:1540-5.  Back to cited text no. 73
74.Ganesan V, Prengler M, Wade A, Kirkham FJ. Clinical and radiological recurrence after childhood arterial ischemic stroke. Circulation 2006;114:2170-7.  Back to cited text no. 74
75.DeVeber GA, MacGregor D, Curtis R, Mayank S. Neurologic outcome in survivors of childhood arterial ischemic stroke and sinovenous thrombosis. J Child Neurol 2000;15:316-24.  Back to cited text no. 75
76.Chabrier S, Husson B, Lasjaunias P, Landrieu P, Tardieu M. Stroke in childhood: Outcome and recurrence risk by mechanism in 59 patients. J Child Neurol 2000;15:290-4.  Back to cited text no. 76
77.Ganesan V, Hogan A, Shack N, Gordon A, Isaacs E, Kirkham FJ. Outcome after ischaemic stroke in childhood. Dev Med Child Neurol 2000;42:455-61.  Back to cited text no. 77
78.Pavlovic J, Kaufmann F, Boltshauser E, Capone Mori A, GubserMercati D, Haenggeli CA, et al. Neuropsychological problems after paediatric stroke: Two year follow-up of Swiss children. Neuropediatrics 2006;37:13-9.  Back to cited text no. 78
79.Salih MA, Abdel-Gader AG, Al-Jarallah AA, Kentab AY, Al-Nasser MN. Outcome of stroke in Saudi children. Saudi Med J 2006;27:S91-6.  Back to cited text no. 79
80.De Schryver EL, Blom I, Braun KP, Kappelle LJ, Rinkel GJ, Peters AC, et al. Long-term prognosis of cerebral venous sinus thrombosis in childhood. Dev Med Child Neurol 2004;46:514-9.  Back to cited text no. 80
81.Ganesan V, Chong WK, Cox TC, Chawda SJ, Prengler M, Kirkham FJ. Posterior circulation stroke in childhood: Risk factors and recurrence. Neurology 2002;59:1552-6.  Back to cited text no. 81
82.Hogan AM, Kirkham FJ, Isaacs EB. Intelligence after stroke in childhood: Review of the literature and suggestions for future research. J Child Neurol 2000;15:325-32.  Back to cited text no. 82
83.Max JE, Mathews K, Manes FF, Robertson BA, Fox PT, Lancaster JL, et al. Attention deficit hyperactivity disorder and neurocognitive correlates after childhood stroke. J Int Neuropsychol Soc 2003;9:815-29.  Back to cited text no. 83
84.Max JE, Mathews K, Lansing AE, Robertson BA, Fox PT, Lancaster JL, et al. Psychiatric disorders after childhood stroke. J Am Acad Child Adolesc Psychiatry 2002;41:555-62.  Back to cited text no. 84
85.Friefeld S, Yeboah O, Jones JE, deVeber G. Health-related quality of life and its relationship to neurological outcome in child survivors of stroke. CNS Spectr 2004;9:465-75.   Back to cited text no. 85
86.Delsing BJ, Catsman-Berrevoets CE, Appel IM. Early prognostic indicators of outcome in ischemic childhood stroke. Pediatr Neurol 2001;24:283-9.  Back to cited text no. 86
87.Ganesan V, Ng V, Chong WK, Kirkham FJ, Connelly A. Lesion volume, lesion location, and outcome after middle cerebral artery territory stroke. Arch Dis Child 1999;81:295-300.  Back to cited text no. 87
88.Boardman JP, Ganesan V, Rutherford MA, Saunders DE, Mercuri E, Cowan F. Magnetic resonance image correlates of hemiparesis after neonatal and childhood middle cerebral artery stroke. Pediatrics 2005;115:321-6.  Back to cited text no. 88
89.Hurvitz EA, Beale L, Ried S, Nelson VS. Functional outcome of paediatric stroke survivors. Pediatr Rehabil 1999;3:43-51.  Back to cited text no. 89


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2], [Table 3], [Table 4]

This article has been cited by
1 Evaluation, Identification, and Management of Pediatric Strokes in the Emergency Department Using a Pathway Algorithm
Hicks, V.J. and Black, L.M.
Journal of Emergency Nursing. 2013; 39(2): 132-137
2 Experience of pediatric stroke from a tertiary medical center in North India
Kalita, J. and Goyal, G. and Misra, U.K.
Journal of the Neurological Sciences. 2013; 325(1-2): 67-73
3 Evaluation, Identification, and Management of Pediatric Strokes in the Emergency Department Using a Pathway Algorithm
Victor Jerome Hicks,Lisa M. Black
Journal of Emergency Nursing. 2013; 39(2): 132
[Pubmed] | [DOI]
4 Experience of pediatric stroke from a tertiary medical center in North India
Jayantee Kalita,Gourav Goyal,Usha Kant Misra
Journal of the Neurological Sciences. 2013; 325(1-2): 67
[Pubmed] | [DOI]
5 Management of a massive pediatric cerebral infarct with mass effect
Singh, P. and Poddar, B. and Singh, R.K.
Indian Journal of Pediatrics. 2012; 79(12): 1658-1660
6 Management of a Massive Pediatric Cerebral Infarct with Mass Effect
Parikshit Singh,Banani Poddar,R. K. Singh
The Indian Journal of Pediatrics. 2012; 79(12): 1658
[Pubmed] | [DOI]
7 Awareness of stroke in adults and pediatrics among Fayoum University hospital workers and medical students
El Sherbiny, N., Ghaffar, H.A., El-Mously, S.
Egyptian Journal of Neurology, Psychiatry and Neurosurgery. 2011; 48(3): 235-240


Print this article  Email this article
Online since 7th April '04
Published by Wolters Kluwer - Medknow