pediatric neurology lectures: increased intracranial pressure; cerebral edema, brain tumors

PEDIATRIC NEUROLOGY LECTURES: INCREASED INTRACRANIAL PRESSURE;

CEREBRAL EDEMA, BRAIN TUMORS

Assoc. Prof. Ingrid Miron

INCREASED INTRACRANIAL PRESSURESYMPTOMS

• Headaches of recent onset and increasing severity associated with nausea, vomiting, or transient visual obscuration in the older child,

• complaints related by the parents of poor feeding, vomiting, excessive irritability, or lethargy in an infant

• the child with an acute onset of increased ICP presents with stupor or coma.

• Etiologies: trauma, hemorrhage, hypoxic ischemic encephalopathy, diabetic ketoacidosis, CNS infections, and parainfectious encephalopathies

INCREASED INTRACRANIAL PRESSURESYMPTOMS

• Increased ICP on neurologic examination of children less than 3 years of age: an excessive rate of head growth, separated sutures (by palpation or on skull x-ray), and a full or bulging anterior fontanel (in infants).

• Enlargement of the third ventricle in infants results in spontaneous downward deviation of the eyes (sunsetting sign), while enlargement of the lateral ventricles causes pathologically brisk reflexes in the lower extremities.

• In the older child (over 3 years) the cranium becomes nonresilient, and increased ICP is reflected by pressure on the optic nerve sheaths, resulting in papilledema, and pressure on the sixth cranial nerve, causing paresis of the lateral rectus muscle . Ventricular enlargement in the older child causes an impairment of upward gaze, pathologically brisk reflexes, and less commonly, an unsteady gaze.

INCREASED INTRACRANIAL PRESSURE

• computed tomographic (CT) scan or magnetic resonance imaging (MRI) scan are essential to look for surgically correctible lesions. MRI scanning may show more anatomic detail and better visualization of cerebral edema, but CT scanning is entirely adequate in most cases.

• Brain tumors, subdural empyema or brain abscess, epidural, subdural or intraparenchymal hematomas may cause increased ICP from mass effect or obstruction of cerebrospinal fluid (CSF) flow. Most brain tumors in childhood are in the posterior fosa or midline and produce increased ICP by causing obstruction of CSF flow. Hydrocephalus, not associated with an obstructing mass, is also a common cause of increased ICP.


• If the CT or MRI scan shows small ventricles and basal cisterns, the probable diagnosis is cerebral edema. Additional signs include the loss of distinction between gray and white matter and a homogenous appearance of the parenchyma.

• Neurologic deterioration after trauma, hypoxic ischemic encephalopathy, or diabetic ketoacidosis is often associated with increased ICP.

• the child has to be admitted to the intensive care unit and monitors have to be placed for continuous measurement of ICP and arterial blood pressure. The epidural ICP monitors are preffered as there are fewer problems with infections. The ventricular catheter for ICP monitoring has the advantage to allow withdrawal of CSF.

• Particular attention has to be payed to cerebral perfusion pressure (CPP), which is defined as mean arterial pressure minus intracranial pressure and attempt to maintain a CPP greater than or equal to 50 mmHg.

• In general, for brief episodes of increased ICP, we start with mannitol and use intermittent hyperventilation. Morphine is given prior to painful procedures. If this is not successful, pentobarbital coma is considered. Hypothermia is used in some centers. We avoid it because of potential circulatory compromise and increased susceptibility to sepsis.


• Lumbar puncture should be performed - if the etiology for increased intracranial pressure is unknown, particularly when meningitis or encephalitis are considered. If the CT scan has not shown a mass lesion, this procedure is reasonably safe.

• If there is concern about significant increased ICP, the child is sedated prior to the procedure and given mannitol 20 minutes prior to the lumbar puncture. The opening pressure is measured and the CSF is sent for routine analysis. A normal opening pressure suggests either a mistaken diagnosis, such as the confusion of papilledema with papillitis or pseudopapilledema, or possibly resolved increased ICP. If the opening pressure is elevated, the CSF analysis normal, and the child is not encephalopathic, the most likely diagnosis is begin intracranial hypertension (pseudotumor cerebri). If the child is encephalopathic, the most likely diagnosis is a parainfectious noninflammatory encephalopathy such as Reye syndrome. An abnormal CSF formula suggests infectious or neoplastic meningitis or encephalitis.

History Signs of ↑ ICP

CT scan or IRM scan

Hydrocephalus, Small or normal ventricles Mass lesion Cerebral edema Consult neurosurgeon Known event: Uncertain diagnosis Head trauma Respiratory arrest Diabetic ketoacidosis Lumbar puncture Admit to ICU Monitor BP, ICP Normal ICP ↑ ICP, Abnormal Treat ↑ ICP Normal CSF Normal CSF CSF (see Table 1) Mistaken diagnosis, Infectious or Resolved ↑ ICP neoplastic meningitis Encephalitis Encephalopathy Encephalopathy absent present Pseudotumor Reye syndrome cerebri

INCREASED INTRACRANIAL PRESSURE (↑ ICP) DIFFERENTIAL DIAGNOSIS

RESECTION OF MASS, VENTRICULOPERITONEAL SHUNT

. Treatment of increased intracranial pressure. Supportive therapy Respiratory: PaO2 100-150 PaCO2 25-30 Blood Pressure: to maintain CPP. Head up 300, pancurorium for venous pooling Fluids: restrict, expect IADH Nutrition: protein 1,5 x resting metabolic requirement serum albumin > 3,0 g/dl Specific therapies Manual hyperventilation: rapid brief effect Dexamethasone: loading 1,5 mg/kg, maintenance 0,25 mg/kg q6h (? high dose 6/15 mg/kg) Mannitol 0,25 - 1,5 g/kg over 20-30 min Acetazolamide 100 mg/kg/day + furosemide 1 mg/kg/day Pentobarbital: initial 3 – 10 mg/kg, maintenance 1 – 5 mg/kg/hour blood level 35 – 45 μg/ml Morphine 0,1 mg/kg i.v. q 1-3h, 10 min prior to painful procedures Hypothermia 7% decrease in CMR, CBF per drop of 10 C

IDIOPATHIC INTRACRANIAL HYPERTENSION (PSEUDOTUMOR CEREBRI)

• Pseudotumor cerebri is defined as a diffuse increase in intracranial pressure in the presence of normal cerebrospinal fluid and normal brain imaging.

• Symptoms:• - headache increases with Valsalva maneuver• - vomiting• - diplopia• - visual obscuration• - in young children are also seen somnolence and irritability and bulging

fontanelle.• Signs:• - papilledema• - sixth nerve palsy: nonlateralizing


• Risk factors:• - drugs: tetracycline, birth control pills, vitamin A (increased or decreased),

steroid withdrawal• - endocrinopathy: treatment with growth hormone, with thyroid hormone,

hyperthyroidism, adrenal insufficiency or hyperadrenalism, hypoparathyroidism• - refeeding in malnourished children and those with cystic fibrosis• - iron deficiency anemia.• Differential diagnosis:• - mass lesion• - hydrocephalus• - lateral sinus thrombosis (mastoiditis, otitis media)• - sagital sinus trombosis (systemic lupus erythematosus, polycythemia,

dehydration, hypercoagulable states)• - malignancy (carcinomatosis, gliomatosis cerebri, leukemia)


• Evaluation:• - magnetic resonance imaging of the brain- normal- small ventricles may or may not be present- effacement of cortical sulci may or may not be present• - visual acuity and visual fields – repeat frequently• - lumbar puncture:- increased opening pressure (greater than 200 mmH2O)- normal protein and glucose levels, normal cell count.


• Treatment:• - relieve pressure to preserve vision• - lumbar puncture• - reduce pressure to half the opening pressure• - remove 10-20 ml cerebrospinal fluid, but not below 200 mmH2O • - acetazolamide• - dose of 10-20 mg/kg/day• - can range from 250 mg twice daily to 500 mg twice daily• - failure of lumbar puncture and acetazolamide – try the following:• - prednisone 2 mg/kg (maximum of 60 mg) for 2 weeks• - failure of the above – try the following:• - optic nerve fenestration• - lumboperitoneal shunt (may cause acquired Chiari malformatio or tethered cord)• If this condition is left untreated the increased intracranial pressure may cause optic

atrophy and permanent visual loss.

Cerebral edema• Cerebral edema is frequent complication of neurological

disease processes. While the initial brain swelling seen immediately following head injury is due to cerebral vascular congestion, cerebral edema follows, with a peak of swelling usually evident in 48-96 hours. Cerebral edema can be either localized or generalized, but both contribute to intracranial hypertension if there is not a compensatory drop in CSF and/or intracranial blood volume. Two pathophysiologically distinct types of cerebral edema have been described: vasogenic edema and citotoxic or metabolic edema. A third type, interstitial edema, has also been described.

Cerebral edema - vasogenic• Vasogenic cerebral edema starts locally, around the area of

brain injury, but may spread to become generalized. Vascular damage interrupts the permeability pattern of the blood vessels in the injured area of the brain. There is disruption of the normal blood/brain barrier, with leakage of plasma proteins out of the blood vessels into the extracellular space. This is followed by an osmatic influx of water into the area. Most vasogenic edema fluid accumulates in the white matter of the brain, because of the white matter’s less closely interwoven cellular structures. Vasogenic edema can cause focal neurological deficits as well as disturbances of consciousness. Like a leaking water pipe, the higher the patient’s blood pressure, the greater the potential for vasogenic edema. Nursing actions may need to be directed toward preventing and treating hypertensive episodes.

Cerebral edema - cytotoxic• Cytotoxic cerebral edema refers to the actual

swelling of brain cells. It is more generalized and is thought to be due to some toxic factor that causes destructive alteration of brain cellular elements. While neuronal, glial, and endothelial cells are affected, it occurs most often in the gray matter. It may be due to failure of the sodium pump, a situation that results in abnormal distribution or electrolytes and water across the cell membranes.

Cerebral edema - cytotoxic• occurs as a result of hypoxia and hypercapnia, as seen following

cardiac arrest. • occurs in conditions associated with low serum levels of sodium.

These include the syndrome of inappropriate antidiuretic hormone secretion (SIADH), severe sodium depletion, and water intoxication.

• Brain ischemia can results in both vasogenic and cytotoxic edema. Progressive ischemia causes cytotoxic edema, which leads to brain cell death. This contributes to the disruption of the blood-brain barrier and the formation of vasogenic edema.

• Interstitial or extracellular cerebral edema forms as a result of hydrocephalus with leakage of CSF from the ventricles into the surrounding tissues. This edema may develop as a result of impaired CSF reabsoption in the arachnoid villi.

Cerebral edema: clinical features• signs and symptoms do not always occur in any particular

order• Prompt action is necessary at the first sign of neurological

deterioration if brain herniation is to be prevented. Nausea and vomiting and/or increased restlessness and confusion may be the earliest signs.

• Decreased level of consciousness is usually the first sign of neurological deterioration. This occurs because of compression of the reticular activating system (RAS) located in the diencephalon and brainstem.

• Alteration in respiratory pattern. Abnormal respiratory patterns develop depending on the area of the brain or brainstem being compressed.

Cerebral edema: clinical features• Papillary changes also depend on the area of brain compression. • Midbrain compression affects the third cranial nerve, which may

initially cause the appearance of oval pupil. This can progress to a dilating, nonreactive pupil, usually on the same side as the expanding lesion. Pontine compression causes small, fixed pupils.

• There may be paralysis of eye movements and loss of upward gaze.

• Bilateral dilated and fixed pupils imply bilateral brainstem compression and usually indicate a fatal outcome for the patient.

Cerebral edema: clinical features• Motor deficits• Hemiparesis or hemiplegia occurs as the descending motor fibers passing

through the brainstem are compressed.• Paralysis often begins in a lower extremity, progressing upward to include the

arm and face. Most often the motor deficit is noted on the side opposite the brain pathology as the corticospinal motor fibers have not yet crossed to the opposite side in the medullary region.

• Ipsilateral motor deficits may occur from displacement of the brain medially, compressing the controlateral motor fibers.

• Abnormal posturing may be seen: -flexor or decorticate posturing is due to hemispheric compression of corticospinal tracts.-extensor or decerebrate posturing is due to diencephalic or upper brainstem compression. -medullary compression causes flaccidity in all extremities.

Cerebral edema: clinical features• Alterations in blood pressure and pulse• Changes in blood pressure and pulse rate and rhythm are often

seen in progressive compression of the brainstem. As intracranial pressure rises, the brain and brainstem become increasingly more ischemic. Sympathetic stimulation induces a systemic vasoconstriction and an increase in cardiac output, which increases the blood pressure in an effort to perfuse the tight brain. Bradycardia ensues because of pressoreceptor responses and stimulation of the vagal nuclei in the brainstem. Respiratory variations are often seen in combination with the elevating blood pressure and slowing pulse rate. This triad of clinical signs is known as the Cushing response. It is felt to be due to ischemia of the medulla.

BRAIN TUMORS• Brain tumors are the most common solid tumor and the second most common

malignancy in children. Signs and symptoms vary depending on the location.• Incidence: 3 per 100000 children with a peak from the age of 5 to 9 years.• Nonlocalizing signs and symptoms that reflect increasing intracranial pressure:• Symptoms• - irritability• - personality change• - headache• - vomiting especially in the early morning or during sleep• - diplopia (may or may not be localizing) usually sixth nerve palsy• Signs:• - an increase in head circumference• - papilledema (may have a larger blind spot)• - head tilt (incipient tonsillar herniation, fourth nerve palsy)• - sixth nerve paresis (inability to abduct the eye fully on lateral gaze)

BRAIN TUMORSPOSTERIOR FOSSA (INFRATENTORIAL) TUMOR

• Most posterior fossa tumor in children present with signs and symptoms of increased ICP.

• These may be accompanied by either head tilt or truncal ataxia. • The three most common tumors that present with increased ICP are

cerebellar astrocytoma, medulloblastoma, and ependymoma. • These are difficult to distinguish on the basis of history, but :- the cerebellar astrocytoma is likely to present insidiously over 4 to 8

months in an older child (5 to 8 years), - the medulloblastoma commonly produces symptoms dating back less

than 2 months and tends to occur in the younger child (3 to 5 years). - the ependymoma is intermediate in regard to age of onset and duration

of symptoms and may present with vomiting as the most prominent feature.

- Brainstem gliomas in contrast to the other three types of tumors, present with symptoms of brainstem dysfunction in the absence of increased ICP.

POSTERIOR FOSSA (INFRATENTORIAL) TUMOR

• The neurological examination reveals increased ICP in patients with tumors that obstruct the spinal fluid (CSF) pathways.

• Medulloblastomas and ependymomas usually produce an unsteady gait without intentional tremor or dysmetria.

• The brain stem glioma: usually presents with the triad of multiple cranial nerve deficits, cerebellar, and pyramidal track signs in the absence of signs of increased ICP.


• A CT or MRI scan helps distinguish the specific types of tumor. • - the cerebellar astrocytoma, medulloblastoma, and ependymoma produce

enlarged ventricles secondary to obstruction of the CSF pathways. • the cerebellar astrocytoma is often, but not always, cystic in appearance with

a small mural nodule, which may be enhanced by contrast medium. It is most often laterally placed in the cerebellar hemisphere but may be in the midline.

• The meduloblastoma, a midline tumor, is uniformly hyperdense, may be enhanced by contrast medium, and tends to compress the fourth ventricle from behind.

• the ependymoma usually grows within the fourth ventricle and may show flecks of calcification or faint enhancement.

• The CT scan may be normal with brainstem gliomas, but usually shows a low density mass enlarging the brainstem. MRI is probably more sensitive for identifying lesions within the brainstem and for showing brainstem invasion by tumors in or around the fourth ventricle.


• Increased ICP, when present, is managed with ventricular drainage or by placement of a ventriculoperitoneal shunt before direct surgical resection is attempted. This decision requires neurosurgical consultation.

• Complete surgical resection is possible with laterally placed cerebellar astrocytomas. This is rarely accomplished with medulloblastomas or ependymomas and is not attempted with brainstem gliomas.

• The diagnosis of braistem glioma is usually made on a clinical basis by the characteristic presentation of multiple brainstem signs in the absence of increased ICP and is confirmed by demonstrating an intrinsic brainstem mass by CT or MRI scanning. In some institutions the diagnosis is confirmed by a small tissue biopsy; often, however, treatment is begun without histologic confirmation.

POSTERIOR FOSSA (INFRATENTORIAL) TUMOR - treatment

• Cystic cerebellar astrocytomas may be completely removed surgically. If residual tumor is thought to be present, local radiation therapy is used.

• Medulloblastoma and ependymoma: subtotal resection is followed by radiation therapy of the entire neuraxis because of the tendency of both these tumors to seed the subarachnoid space. Chemotherapy has begun to show promise in the treatment of medulloblastoma.

• Brainstem gliomas are treated with radiation therapy.


• The prognosis in cerebellar astrocytoma is often good, with complete cures possible.

• Medulloblastomas and ependymomas tend to relapse in 1 to 2 years, in spite of treatment, although more instances of long term survival of children with medulloblastoma are now being seen following a combination of radiation therapy and chemotherapy.

• The prognosis in children with brainstem gliomas still remains poor. Occasional children respond dramatically to the newer radiation therapy protocols. Most, brainstem gliomas, however, have a recurrence within 6 to 12 months.

MIDLINE CEREBRAL TUMORS• they grow in or around the third ventricle. • may present with obstruction of the CSF flow causing signs of increased ICP,

indistinguishable from tumors in the posterior fossa. • some characteristic signs or symptoms caused by involvement of the

surrounding midbrain, thalamic, and hypothalamic structures may be present. • 1. The neurologic examination:- confirms only the presence if increased ICP, or - may provide localizing signs: - paralysis of upward gaze with posterior third ventricle tumors, - the characteristic wasting of diencephalic syndrome in infants with

hypothalamic tumors, or - contralateral hemiparesis or tremor with thalamic tumors.• 2. The CT scan or MRI scan shows enlargement of the ventricular system

when CSF flow is obstructed in or around the third ventricle. Tumors within the third ventricle are usually easily recognized. Thalamic tumors cause displacement of the third ventricle to the controlateral side. Hypothalamic tumors and other low-grade astrocytomas in the structures around the third ventricle can be difficult to visualize on CT scan, but are usually seen on MRI scan.

MIDLINE CEREBRAL TUMORS - imaging

• The CT scan or MRI scan shows enlargement of the ventricular system when CSF flow is obstructed in or around the third ventricle. Tumors within the third ventricle are usually easily recognized.

• Thalamic tumors cause displacement of the third ventricle to the controlateral side.

• Hypothalamic tumors and other low-grade astrocytomas in the structures around the third ventricle can be difficult to visualize on CT scan, but are usually seen on MRI scan.

MIDLINE CEREBRAL TUMORS• Colloid cysts are benign tumors within the anterior third ventricle. • Presenting symptoms may overlap with those of suprasellar and

chiasmatic tumors, which distort the anterior third ventricle from below.

• Colloid cysts occur infrequently in childhood and present with intermittent or progressive signs of increased ICP. This can include sudden loss of consciousness or even death, from acute obstruction of the aqueduct.

• Progressive dementia and endocrine signs, including obesity, weight loss, polyuria, polyphagia or acromegaly, have been reported.

• These tumors are treated either with biventricular shunting, or by surgical removal. The long-term prognosis following removal of colloid cysts is excellent. Less common tumors within the third ventricle are the choroids plexus papilloma or ependymoma.

MIDLINE CEREBRAL TUMORS• Tumors of the posterior third ventricle (pineal region)

are histologically pinealomas, dysgerminomas, or glial tumors of the surrounding structures. A characteristic presentation is paralysis of upward gaze (Parinaud’s syndrome). Additional findings may include bilateral ptosis or impaired accommodation. Less commonly, bilateral hearing loss may be present owing to involvement of the inferior colliculi. Subtotal resection of these tumors is possible and is followed by radiation therapy. Survival is variable, averaging 2 to 5 years, occasionally considerably longer. Treatment depends on tumor histology.

MIDLINE CEREBRAL TUMORS• Hypothalamic tumor (usually in infants): characteristic symptom complex

designated the diencephalic syndrome. These children show marked wasting of subcutaneous fat, alert and often euphoric facies, and hyperkinesis.

• Vomiting is frequent.• Neurologic signs are limited to bilateral optic atrophy and nystagmus caused

by decreased visual acuity.• Older children with hypothalamic tumors are more likely to show growth

retardation or obesity. Radiation therapy usually provides palliation of symptoms, sometimes for several years.

• Thalamic tumors • signs of increased ICP owing to displacement of the third ventricle• focal signs including contralateral tremor or hemiparesis • less commonly, athetosis, dystonic posturing, or rigidity.• Impaired sensation is rare. These tumors may occasionally be partially

resected, but are most often treated with radiation therapy. The prognosis is poor.

SUPRASELLAR AND CHIASMATIC TUMOR

• Suprasellar and optic chiasm tumors often have in common the following presenting symptoms: visual defects, signs or symptoms of endocrine or hypothalamic dysfunction, and symptoms of increased intracranial pressure (ICP).

• Assessing the degree of decreased visual acuity and ploting visual field defects are often difficult in young children.

• Tumors of the optic chiasm may extend to either or both optic nerves, causing virtually any combination of unilateral or bilateral decreased acuity or field defect.

SUPRASELLAR AND CHIASMATIC TUMOR

• Craniopharyngiomas characteristically compress the optic chiasm, producing bitemporal hemianopia. Optic atrophy is found with both types of tumors. Endocrine dysfunction (specifically growth retardation and sexual infantilism) is commonly seen with craniopharyngiomas. Chiasmal gliomas, by contrast, produce little or no endocrine change early in the course; if changes are present, they are usually those of precocious puberty.

SUPRASELLAR AND CHIASMATIC TUMOR• Neurodiagnostic studies help distinguish the types of tumors in this region. • Skull x-ray studies with optic foramen views are particularly useful. Chiasmal

gliomas characteristically produce deformities of the anterior clinoid processes and frequently cause enlargement of one or both optic foramina.

• Plain skull films in addition may reveal suprasellar calcifications, frequently seen in craniopharyngiomas.

• The CT scan is limited in demonstrating chiasmal gliomas owing to the proximity of the tumor to bone unless the study is perfomed with metrizamide to highlight the subarachnoid space around the tumor.

• Craniopharyngiomas are easily visualized, may be partially cystic, and often show contrast enhancement or calcification. Craniopharyngiomas and large optic chiasm tumors show deformation and obstruction of the anterior third ventricle.

• Small chiasmal gliomas may be identified only by pneumoencephalography. • MRI scanning would be expected to demonstrate craniopharyngiomas easily

and may be of value in diagnosing even small chiasmatic tumors. Experience with this modality is still limited

SUPRASELLAR AND CHIASMATIC TUMOR• Optic chiasm gliomas cannot be resected; • the treatment consists of radiotherapy, • occasionally with an adjunctive

ventriculoperitoneal shunt to relieve obstruction of the third ventricle.

• The prognosis in children with chiasmal gliomas varies considerably. In the majority of cases the tumor is slow growing, and long term survival is common. In a minority of patients, however, the tumor shows rapid growth with invasion of surrounding structures and death within 1 year.

SUPRASELLAR AND CHIASMATIC TUMOR• The treatment of craniopharyngioma in most cases involves craniotomy with

subtotal and rarely total resection of the tumor• Preoperative endocrine evaluation is mandatory, although findings in most studies

are normal• Cortisone replacement is routinely given preoperatively regardless of the endocrine

status.• Total excision is possible only when the tumor is not adherent to major cerebral

vessels, the optic chiasm, or the hypothalamus.• The tumor is relatively radioresistant. • The immediate postoperative period is frequently stormy, with diabetes insipidus

and potentially severe fluid and electrolyte disturbances• Panhypopituitarism is common postoperatively and requires appropriate

replacement therapy. • The prognosis following complete resection of this tumor is excellent, for endocrine

abnormalities can be managed readily. Subtotal resection usually results in recurrence; however, this tumor may be slow growing and survival for many years is possible. Ultimately compromise in vision and tumor extension to the hypothalamus or laterally to the temporal lobes results in increasing morbidity.

HEMISPHERIC CEREBRAL TUMORS

• Most children with tumors of the cerebral hemispheres present with a combination of symptoms, including:

- personality change- headaches, - less commonly: unilateral motor weakness, aphasia, or a sensory or visual

deficit - seizures are a common presenting symptom in children with these tumors.

They may be focal or generalized in type, and can be present for many years before the diagnosis of tumor is made.

• A neurologic examination: evidence of increased ICP including papilledema or sixth nerve paresis.

• The most common focal findings are: controlateral hyperreflexia, extensor plantar response (Babinski), or spasticity, with or without associated motor weakness (hemiparesis).

• Visual field defects or sensory deficits may be demonstrated.


• Neurodiagnostic studies are usually helpful in making the diagnosis of cerebral hemisphere tumors.

• The electroencephalogram often shows a focal slow wave abnormality in the region of the tumor. Focal paroxysmal activity (spike or sharp wave) is a less reliable indication of a mass lesion.

• A CT scan or a MRI scan usually reveals the location of the tumor if it is larger than 1 cm. Larger lesions produce distortion or displacement of the third or lateral ventricles. Many of these tumors show contrast enhancement.

• Very small tumors presenting with seizures may be missed on initial scanning. Refractory focal (partial) seizures or the onset of new focal neurological deficits in a patient with seizures should impose promptly repeated studies.


• The treatment of cerebral hemisphere tumors usually begins with a craniotomy and subtotal resection of the tumor mass.

• Because these are mostly infiltrating glial tumors, total resection is rarely possible.• Steroids (to reduce inflammation) and anticonvulsant medication are commonly given before

surgery. • Anticonvulsant medication is usually required for a long period.• Decisions about additional therapy are made in conjunction with the neurosurgeon, oncologist,

and radiation oncologist. The most common hemispheric tumor of childhood is the glioma, the majority being low grade. Cystic tumors may be completely resected with a resultant cure. Solid gliomas can be only partially resected. For the low grade glioma, radiation therapy has not been proven effective, though most authorities recommend local radiation. For higher grade tumors, a combination of whole brain radiation and chemotherapy is recommended. Patients with low grade solid gliomas have a 30 to 50% five-year survival rate, and those with glioblastoma multiforme have a less than 5% five-year survival rate. The other tumors are much less common. Both the choroids plexus papilloma and the oligodendroglioma can often be completely resected. No additional therapy is necessary. Approximately one-third of ependymomas grow in the lateral ventricle. Spinal metastasis may occur with high grade ependymomas, thus craniospinal radiation should be given. Low grade tumors are less likely to metastasize, and radiation is given only to the tumor bed. The five-year cure rate is approximately 30%. Meningiomas in children are often sarcomatous. Complete resection is possible only occasionally. When partial resection is carried out, radiation therapy is necessary.

HEMISPHERIC CEREBRAL TUMORS• Decisions about additional therapy are made in conjunction with the neurosurgeon,

oncologist, and radiation oncologist. • The most common hemispheric tumor of childhood is the glioma, the majority being low

grade. • Cystic tumors may be completely resected with a resultant cure.• Solid gliomas can be only partially resected.• For the low grade glioma, radiation therapy has not been proven effective, though most

authorities recommend local radiation.• For higher grade tumors, a combination of whole brain radiation and chemotherapy is

recommended. Patients with low grade solid gliomas have a 30 to 50% five-year survival rate, and those with glioblastoma multiforme have a less than 5% five-year survival rate.

• The other tumors are much less common. Both the choroids plexus papilloma and the oligodendroglioma can often be completely resected. No additional therapy is necessary.

• Approximately one-third of ependymomas grow in the lateral ventricle. Spinal metastasis may occur with high grade ependymomas, thus craniospinal radiation should be given. Low grade tumors are less likely to metastasize, and radiation is given only to the tumor bed. The five-year cure rate is approximately 30%.

• Meningiomas in children are often sarcomatous. Complete resection is possible only occasionally. When partial resection is carried out, radiation therapy is necessary.

pediatric neurology lectures: increased intracranial pressure; cerebral edema, brain tumors

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