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Stroke in Children in Neurology

Stroke in Children in Neurology
Course

Clinical Exposure in Mental Health (OT2316L)

6 Documents
Students shared 6 documents in this course
Academic year: 2022/2023
Listed bookSynopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry
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Stroke in Children in Neurology

Children are not small adults when it comes to the diagnosis of stroke. In contrast to adults, the brain of the fetus or child is rapidly changing in organization and chemical composition. Neurologic functions change with neurologic maturation. The nervous system of a nonverbal relatively spastic newborn is different from that of a school-aged child who has mastered language skills and has purposeful locomotion and prehension. Strokes in children differ from those in adults in three important ways: predisposing factors, clinical evolution, and anatomic site of pathology. Cyanotic heart disease is one of the most common childhood conditions that predisposes to cerebral arterial or venous thrombosis. Leukemia commonly leads to cerebral hemorrhage. In contrast, atherosclerosis and hypertension predispose to stroke in adults.

Most stroke-prone children do not die as a direct result of stroke; they often improve much more than an adult with a comparable lesion because of the abundant collateral circulation or because of the differences in response of the immature brain to the lesion. The infant or young child with a new hemiplegia usually recovers to the point of being able to walk. If a child younger than age 4 years has a stroke, speech is invariably recovered and permanent aphasia does not occur. Children, especially before age 2 years, are more prone to behavioral changes, intellectual impairment, and epilepsy. The anatomic site of the stroke lesion also differs in children. For example, affected children commonly show occlusion of the intracranial portion of the internal carotid artery and its branches, whereas adults more frequently show extracranial occlusions of the internal carotid. Cerebral aneurysms in children usually occur at the peripheral bifurcations of cerebral arteries; in adults, cerebral aneurysms usually circle of Willis.

INCIDENCE

In a well-defined pediatric population in Rochester, Minnesota, the annual incidence of cerebrovascular disease was 2 cases per 100,000 children or about 50% the incidence of primary intracranial neoplasm. This figure did not include conditions associated with birth, infection, or trauma, and there were few African-American children in the study.

Cerebrovascular complications occur in 6% to 25% of patients with sickle cell disease; an untreated child with sickle cell disease has a 67% risk of a second stroke. Premature infants weighing less than 1500 g who require intensive care for more than 24 hours have a 50% incidence of complicating subependymal hemorrhage or intraventricular hemorrhage, intracranial infections, viral or bacterial, may also precipitate vascular complications. Craniocerebral trauma occurs in 3% of children during the first 7 years of life and cerebrovascular complications are common. Sonography, magnetic resonance imaging (MRI), and computed tomography (CT) (Figs. 43 through 43) are changing our concepts of the incidence of these disorders in children.

CLINICAL EVALUATION

A variety of studies should be considered in the evaluation of a child with stroke (Table 43). Selection of tests is guided by the clinical situation. Coagulopathy should be excluded as the cause of vasoocclusive or hemorrhagic infarctions in the new born and young infant. Tissue injury occurs much more frequently from hypoxia and ischemia in the asphyxiated new born. Vasculitis is an uncommon cause of stroke in young children.

The possibility of embolic phenomena is increased with cardiac anomaly, particularly in the presence of a midline defect, which acts as a portal for paradoxic emboli. Older infants and children are susceptible to stroke events when there is a coagulopathy, but they also are more susceptible to vasculitides, which may result from immunologic or infectious causes.

ETIOLOGY

A rigid classification of childhood stroke is not possible because a specific cause (e., sickle cell disease) may cause hemorrhage in one child and thrombosis in another. List is a clinically useful classification and includes occlusive vascular disease caused by thrombus or embolus, congenital anomalies (especially aneurysm or vascular malformation), hemorrhage, blood dyscrasias, and disorders that alter the permeability of the vascular wall. Dural sinus and cerebral venous thrombosis Infections-face, ears, paranasal sinuses, meninges Dehydration and debilitating states Blood dyscrasias-sickle cell, leukemia, thrombotic thrombocytopenia.

ARTERIAL THROMBOSIS

Cerebral arterial thrombosis in children usually involves the intracranial area of the internal carotid artery, although the cervical portion of the internal carotid artery or a spinal artery may be occluded. Neurologic manifestations vary according to the area involved. As in adults, systemic diseases, including collagen-vascular diseases and arteritis, may cause cerebral thrombosis in children. Cerebral arteritis usually results from bacterial infections, but other infections may also involve cerebral arteries. Herpes zoster ophthalmica and rarely chickenpox may have complicacing vasculitis that causes delayed-onset hemiparesis.

Bacterial pharyngitis, cervical adenitis, sinusitis, or pneumonitis may lead to cerebral arteritides. Mucormycosis infection associated with uncontrolled diabetes may extend from the paranasal sinuses to the arteries in the frontal lobe. Both syphilis and tuberculosis may result in cerebral thrombosis in children and adults. Extrinsic conditions may traumatize or compress the cerebral arteries. Most of these occlusions in children affect the anterior circulation. Vertebrobasilar occlusion may follow cervical dislocations and occlusion of the vertebral artery at the C2 level.

Tumors of the base of the skull, craniometaphyseal dysplasia, and retropharyngeal abscesses may compress cerebral arteries. Sickle cell disease commonly causes thrombosis of large or small

The disorder maximally involves the hand; if it persists, the involved limbs are spastic, short, and atrophic. Seizures, focal or generalized, are often refractory to anticonvulsants. The hemiplegia is usually an isolated episode. Bilateral carotid artery thrombosis with telangiectasia typically presents with headaches before the hemiplegia, and recurrences or alternating hemiplegia is characteristic.

Laboratory Data

Blood count, erythrocyte sedimentation rate (ESR), and urinalysis are normal at the time of thrombosis. The cerebrospinal fluid (CSF) is normal at first, and a mild leukocyte pleocytosis may occur a few weeks later. The electroencephalogram often reveals a slow-wave focus over the involved area. Although skull radiographs are normal when thrombosis occurs, after several years they may show signs of cerebral atrophy with thickening of calvarium, enlargement of the frontal and ethmoid sinuses, and elevation of the petrous pyramid of the temporal bone on the involved side.

CT supplies information about the site and age of Within 24 hours there is a nonhomogeneous decreased-density lesion secondary to edema. By the end of the first week, liquefaction necrosis develops, and the infarct becomes homogeneous with defined margins. At 3 months, the necrotic infarct is replaced by a cystic fluid-containing cavity, and the lesion with sharp margins has the homogeneous density of CSF. Sonography is invaluable in defining cerebral anatomy and hemorrhagic complications in the infant, especially the premature infant. MRI has become an important diagnostic tool in the early diagnosis of ischemic lesions.

Magnetic resonance angiography is useful in defining the major portions of large- and medium- size vessels of the intracranial circulation, magnetic resonance venography is helpful in the diagnosis of venous sinus thrombosis if there are changes in vascular outflow. Diffusion-weighted MR imaging is gaining prominence in diagnostic evaluation. Echo-planar diffusion-weighted MR imaging reveals acute and hyperacute ischemia not seen on conventional spin-echo imaging. Arteriography, when performed early, may demonstrate the thrombosed cerebral artery; later there may be a recanalized vessel or evidence of collateral circulation. Cerebral angiography can usually be performed safely in children of all ages. The patency of other cerebral arteries and the ample collateral circulation in children contrast with the status of the cerebral arteries and collateral circulation in adult stroke patients. Children with sickle cell disease are at greater risk if the level of hemoglobin S is not maintained at a level below 20% by exchange transfusion.

Extracranial Occlusion

Trauma is the most common cause of thrombosis of the cervical portion of the internal carotid artery. Blunt trauma in the paratonsillar area of the oropharynx or direct impact of the carotid artery against the transverse process of the second cervical segment can cause occlusion.

Characteristically, about 24 hours lapse between the traumatic incident and clinical manifestations. Non-traumatic conditions are usually infectious in origin.

Basal Occlusion Disease without Telangiectasia

The thrombotic lesion involves the arteries of the base of the brain: supraclinoid area of the internal carotid artery, proximal segments of anterior or middle cerebral artery, or basilar artery. The condition is unilateral and does not recur.

Basal Occlusive Disease with Telangiectasia (Moyamoya)

This condition involves the arteries at the brain, is often bilateral, and is associated with prominent telangiectasia, especially in the region of the basal ganglia. Of varied etiology, it may complicate sickle cell disease, bacterial or tuberculous meningitis, or neurofibromatosis; it may also complicate the treatment plans of radiotherapy. Recurrent episodes of thrombosis are common and may result in alternating hemiplegia, epilepsy, and learning disabilities. Neuropsychological testing has demonstrated the benefit of surgical intervention in venting further deterioration of function.

Peripheral Leptomeningeal Artery Occlusions

Branch occlusions of the distal leptomeningeal arteries may occur with diabetes mellitus, sickle cell disease, trauma, infection tumor encasement, or neurocutaneous syndromes. The excellent collateral circulation usually results in rapid recovery from the acute hemiplegia.

Perforating Artery Occlusion

Involvement of the small perforating arteries, most commonly the striate arteries, is seen in children with homocystinuria or periarteritis nodosa. Episodes recur, causing a progressive neurologic deficit with alternating hemiparesis or quadriparesis, subarachnoid hemorrhage, or death.

Treatment

Therapeutic measures may include parenteral fluids, antibiotics when indicated, anticonvulsants, anticoagulants to prevent extension of the thrombus, and variations of the agents to control increased intracranial pressure. Variations of the synangiosis procedure are used to enhance circulation to ischemic areas of the brain in moyamoya. Anastomoses of external carotid to internal carotid arteries are not feasible because the arteries of the child's brain are too small in diameter. Instead, the superficial temporal artery is attached to the surface of the brain, allowing the formation of a rich collateral network, which supplies parts of the brain that would otherwise be ischemic.

MRI is often characteristic in showing multiple infarcts, some of which are hemorrhagic. The lesions become lucent with sharp margins 2 to 3 months later. Diffusion-weighted imaging and fluid attenuated inversion recovery FLAIR MRI studies assist the rapid detection of stroke events. Lesions that conform to a territorial distribution are the sequelae of embolic strokes. Cerebral angiography should be performed in all children with septic emboli. It delineates the occluded artery and may demonstrate mycotic aneurysm.

Treatment

Management of cerebral embolism is primarily symptomatic, including anticonvulsants for seizures. Anticoagulants are rarely used in children. Corticosteroids, in dosages used in the management of cerebral edema, are effective in reversing the pulmonary symptoms of fat embolism.

INTRACRANIAL HEMORRHAGE

Hemorrhagic stroke in children usually results from trauma of bleeding disorders. When these conditions are excluded, intracranial hemorrhage is caused by an arteriovenous malformation or aneurysm.

Signs and Symptoms

The child with subarachnoid hemorrhage usually presents with acute onset of headache, vomiting, stupor or coma, and convulsions. Findings include stiff neck and Brudzinski and Kernig signs. Extensor plantar responses and subhyaloid hemorrhages on funduscopic examination are often noted early. Fever and systemic hypertension are nonspecific findings. Ruptured cerebral aneurysm frequently presents with a catastrophic clinical picture. Bleeding from an arteriovenous malformation is less dramatic and is often associated with focal signs.

Laboratory Data

Blood dyscrasias are identified by appropriate blood studies. Children with bleeding from other causes have polymorphonuclear leukocytosis, normal or moderately elevated ESR, and transient albuminuria and glycosuria. CSF analysis and CT document subarachnoid hemorrhage. Sonography in the infant with an open fontanel and CT at any age are invaluable in the diagnosis of intracranial hemorrhage and its complications. CT may demonstrate arteriovenous malformation or giant cerebral arterial aneurysm. Cerebral angiography is the definitive diagnostic technique for these conditions.

Treatment

The management of intracranial hemorrhage varies with the cause of the hemorrhage. Repeated lumbar punctures, mannitol, and corticosteroids are often used, but their effectiveness is

controversial. Ruptured intracranial aneurysms require good nursing care, and unless the child is comatose or there is a medical contraindication, surgical extirpation offers the best prognosis. Except in cases of mycotic aneurysms, the occurrence of a second hemorrhage shortly after the initial hemorrhage is uncommon in children. Arteriovenous malformations should be surgically removed. Whenever possible. Embolization may be used preoperatively to reduce the size of the malformation or to treat inaccessible lesions. Traumatic arteriovenous fistulas are treated by ligation of the fistula, embolization, or the implantation of detachable balloons.

METABOLIC DISORDERS

MELAS is a mitochondrial disorder associated with two identifiable mitochondrial DNA mutations. MELAS is characterized by four criteria: a stroke like episode before age 40 years; encephalopathy characterized by seizures, dementia, or both; lactic acidosis; and ragged red fibers in the muscle biopsy. Some patients with MELAS have features of other mitochondrial disorders.

Homocystinuria (cystathionine synthetize deficiency) is an autosomal recessive inherited disorder featuring elevated serum methionine and homocystine concentrations and excessive urinary excretion of homocystine. Cerebral arterial occlusive disease and venous thrombosis occur in this condition.

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Stroke in Children in Neurology

Course: Clinical Exposure in Mental Health (OT2316L)

6 Documents
Students shared 6 documents in this course

University: University of Perpetual Help System DALTA

Was this document helpful?
Stroke in Children in Neurology
Children are not small adults when it comes to the diagnosis of stroke. In contrast to
adults, the brain of the fetus or child is rapidly changing in organization and chemical
composition. Neurologic functions change with neurologic maturation. The nervous system of a
nonverbal relatively spastic newborn is different from that of a school-aged child who has
mastered language skills and has purposeful locomotion and prehension. Strokes in children
differ from those in adults in three important ways: predisposing factors, clinical evolution, and
anatomic site of pathology. Cyanotic heart disease is one of the most common childhood
conditions that predisposes to cerebral arterial or venous thrombosis. Leukemia commonly leads
to cerebral hemorrhage. In contrast, atherosclerosis and hypertension predispose to stroke in
adults.
Most stroke-prone children do not die as a direct result of stroke; they often improve much more
than an adult with a comparable lesion because of the abundant collateral circulation or because
of the differences in response of the immature brain to the lesion. The infant or young child with
a new hemiplegia usually recovers to the point of being able to walk. If a child younger than age
4 years has a stroke, speech is invariably recovered and permanent aphasia does not occur.
Children, especially before age 2 years, are more prone to behavioral changes, intellectual
impairment, and epilepsy. The anatomic site of the stroke lesion also differs in children. For
example, affected children commonly show occlusion of the intracranial portion of the internal
carotid artery and its branches, whereas adults more frequently show extracranial occlusions of
the internal carotid. Cerebral aneurysms in children usually occur at the peripheral bifurcations
of cerebral arteries; in adults, cerebral aneurysms usually circle of Willis.
INCIDENCE
In a well-defined pediatric population in Rochester, Minnesota, the annual incidence of
cerebrovascular disease was 2.52 cases per 100,000 children or about 50% the incidence of
primary intracranial neoplasm. This figure did not include conditions associated with birth,
infection, or trauma, and there were few African-American children in the study.
Cerebrovascular complications occur in 6% to 25% of patients with sickle cell disease; an
untreated child with sickle cell disease has a 67% risk of a second stroke. Premature infants
weighing less than 1500 g who require intensive care for more than 24 hours have a 50%
incidence of complicating subependymal hemorrhage or intraventricular hemorrhage,
intracranial infections, viral or bacterial, may also precipitate vascular complications.
Craniocerebral trauma occurs in 3% of children during the first 7 years of life and cerebrovascular
complications are common. Sonography, magnetic resonance imaging (MRI), and computed
tomography (CT) (Figs. 43.1 through 43.4) are changing our concepts of the incidence of these
disorders in children.

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