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Abstract
Pediatric stroke – a cerebrovascular event in a child aged 30 days to 18 years – is estimated to occur in 2 to 3 of every 100,000 children in the United States per year. It is now frequently recognized in children, probably because of increased awareness of these conditions by clinicians; the widespread application of noninvasive diagnostic studies such as magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), computed tomography (CT). Long-term outcome for survivors of hemorrhagic and ischemic stroke is nearly the same in children (Nield et al., 2006).
The broad definition of pediatric stroke includes ischemic and hemorrhagic stroke. Ischemic stroke can be further subdivided into arterial ischemic stroke and sinovenous thrombosis, whereas hemorrhagic stroke includes intracerebral and subarachnoid hemorrhage. Stroke is an important cause of mortality and chronic morbidity in children. Cerebrovascular disorders are among the top 10 causes of death in children (Lefond et al., 2009).
Srokes in children arise from numerous causes. Cardiovascular disease and sickle cell disease are the most common etiologies. Congenital heart disease has been reported as the leading cause of childhood stroke (Carlin and Chanmugam, 2002).
Acquired heart diseases, collagen vascular diseases, CNS infections, hematologic and coagulation defects (hemophilias, thrombophilias), CNS vascular anomalies, inborn errors of metabolism (such as mitochondrial encephalopathies and homocystinuria), trauma (leading to vascular dissection), and other illnesses and their treatments (such as cancer and chemotherapy) are general classifications of the conditions that can increase a child’s risk of stroke. Structural vascular anomalies collectively constitute the largest cause of non-traumatic intraparenchymal and subarachnoid hemorrhage in children (Nield et al., 2006).
Several genetic disorders are associated with stroke or conditions that can lead to stroke, such as the association of trisomy 21 syndrome with moyamoya disease .Several Mendelian genetic disorders are associated with ischemic stroke including vasculopathies, metabolic or connective tissue diseases, and disorders of coagulation so genetic counceling is important in evaluation of pedhatric stroke (Gold and Patterson.,2005).
The clinical presentation of stroke may be subtle in a young child, but in the first month of life, seizures, apnea, and persistent hypotonia are the predominant manifestations. Beyond the neonatal period, hemiplegia is the most common initial symptom. Other symptoms include headache, mental status changes, sudden collapse with loss of consciousness, speech disturbances, sensory complaints (numbness or tingling), and cranial nerve or cerebellar deficits (Fullerton et al., 2004).
Not surprisingly, most children with intraparenchymal brain hemorrhage present with pain or symptoms of increased intracranial pressure. Subarachnoid hemorrhage classically produces sudden severe headache, vomiting, meningismus, and alteration of consciousness. The clinical picture may be less distinct in younger children, who can present with unexplained irritability, vomiting, photophobia or seizures (Calder et al., 2003).
A detailed history of illness is necessary to support a diagnosis of stroke. What are the exact symptoms and when did they begin? Inquiries into family history of predisposing factors such as sickle cell disease, prothrombotic conditions, and collagen vascular disease should be made. A thorough physical examination, focusing on the cardiac and nervous systems, will reveal any signs of underlying heart disease (such as a murmur or cyanosis) or neurologic deficits (Nield et al., 2006).
A more in-depth evaluation may include neurologic imaging and vascular, laboratory, and cardiac studies. Not all the studies listed may be necessary to diagnose stroke properly and treat each child (Fullerton et al., 2004).
Non contrast CT is typically the initial diagnostic study because of its wide accessibility. Acute hemorrhage usually is detected by CT. Early ischemia is commonly not detected, but CT perfusion imaging may allow earlier identification of subtle indicators of infarction and clarify the amount of viable tissue. Although an MRI scan of the brain is more sensitive than CT for detecting brain infarction, it is usually much more difficult to obtain quickly (Suzuki et al., 2005).
Laboratory studies are numerous and mostly geared toward trying to identify patients with a hypercoagulable state. Cardiac studies as transthoracic or transesophageal echocardiogram and ECG should be obtained in all pediatric patients to search for previously undiagnosed congenital heart disease (Wiebers et al., 2006).
Addressing the ABCs of life support is the initial treatment of the child after stroke. Securing the airway, monitoring cardiovascular parameters, and controlling seizures are paramount. Immediate transfer to a pediatric ICU is mandatory. Cerebral edema in the first several hours must be managed (Nield et al., 2006).
There is little information about the effectiveness or risks of thrombolytic agents such as recombinant tissue plasminogen activator (rTPA) in children, and there are reports of both dramatic successes and serious hemorrhagic complications from thrombolytic agents. If these agents are to be considered for use in children, they should as a minimum be subject to the same exclusions that apply to adults. Individuals with hemorrhagic infarction or those whose stroke began more than 3 hours earlier are typically excluded (Santos et al., 2006).
The usefulness of anticoagulation in children with cerebral infarction depends on the likelihood a second infarction that might be prevented by treatment and on the risk of inducing a hemorrhage due to anticoagulation. Unfortunately, there currently are no published controlled treatment trials in children, but limited experience with anticoagulants and antithrombotic agents has shown that these agents can be safely used in children (Hofman et al., 2001).
Therapies directed at the inhibition of either platelet or coagulation cascade function play a role in the acute, subacute, and chronic phases of pediatric stroke treatment. Acute exchange transfusion should be considered in children with sickle cell-related AIS (Andrew et al., 2005).
The treatment for hemorrhagic stroke (HS) in children depends on the underlying etiology and the condition of the child. The proper characterization of the cause is essential to determine the best therapy. Guidelines for the treatment of spontaneous intra-cerebral hemorrhage in adults should be considered in children (Broderick et al., 1999).
The outcome of children after stroke varies among studies due to differences in follow-up time, functional measures, stroke type, and population studied. More than 50% of survivors develop some neurologic or cognitive problem, and 5% to 20% of affected children die (Nelson and Lynch, 2004).
It is important for the neurologist to define the child’s post-stroke disabilities and recommend ongoing adjuvant interventions such as speech, occupational, and physical therapies. Close monitoring for the development of seizures is necessary, along with educating the family about the risk of seizures post-stroke (Nield, 2006).