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Overview of Intracranial Tumors

By Roy A. Patchell, MD, MD, Chair of Neurology; Chair of Neurology, Barrow Neurological Institute; University of Arizona - Phoenix

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Intracranial tumors may involve the brain or other structures (eg, cranial nerves, meninges). The tumors usually develop during early or middle adulthood but may develop at any age; they are becoming more common among the elderly. Brain tumors are found in about 2% of routine autopsies.

Some tumors are benign, but because the cranial vault allows no room for expansion, even benign tumors can cause serious neurologic dysfunction or death.


There are 2 types of brain tumors:

  • Primary tumors: Originate in the brain either in the brain parenchyma (eg, gliomas, medulloblastomas, ependymomas) or in extraneural structures (eg, meningiomas, acoustic neuromas, other schwannomas)

  • Secondary brain tumors (brain metastases): Originate in tissues outside the brain and spread to the brain

Brain metastases are about 10 times more common than primary tumors.

Pearls & Pitfalls

  • Brain metastases are about 10 times more common than primary brain tumors.

Type of tumor varies somewhat by site (see Common Localizing Manifestations of Brain Tumors) and patient age (see Common Tumors).

Common Localizing Manifestations of Brain Tumors

Tumor Site


Common Primary Tumor Types*

Anterior corpus callosum

Cognitive impairment



Basal ganglia

Hemiparesis (contralateral), movement disorders


Brain stem

Unilateral or bilateral motor or sensory loss, cranial nerve deficits (eg, gaze palsies, hearing loss, vertigo, palatal paresis, facial weakness), ataxia, intention tremor, nystagmus

Astrocytoma (most often juvenile pilocytic astrocytoma)

Cerebellopontine angle

Tinnitus and hearing loss (both ipsilateral), vertigo, loss of vestibular response to caloric stimulation

If tumor is large, ataxia, loss of facial sensation and facial weakness (both ipsilateral), possibly other cranial nerve or brain stem deficits

Acoustic neuroma




Ataxia, nystagmus, tremor, hydrocephalus with suddenly increased intracranial pressure




2nd cranial (optic) nerve

Loss of vision

Astrocytoma (most often juvenile pilocytic astrocytoma)

5th cranial (trigeminal) nerve

Loss of facial sensation, jaw weakness


Frontal lobe

Generalized or focal (contralateral) seizures, gait disorders, urinary urgency or incontinence, impaired attention and cognition and apathy (particularly if tumor is bilateral), hemiparesis

Expressive aphasia if tumor is in dominant hemisphere

Anosmia if tumor is at base of lobe




Eating and drinking disorders (eg, polydipsia), precocious puberty (especially in boys), hypothermia


Occipital lobe

Generalized seizures with visual aura, visual hallucinations, hemianopia or quadrantanopia (contralateral)



Parietal lobe

Deficits in position sensation and in 2-point discrimination (contralateral), anosognosia (no recognition of bodily defects), denial of illness, hemianopia (contralateral), generalized or focal seizures, inability to perceive (extinguishing of) a contralateral stimulus when stimuli are applied to both sides of the body (called double simultaneous stimulation)

Receptive aphasia if tumor is in dominant hemisphere



Pineal region

Paresis of upward gaze, ptosis, loss of pupillary light and accommodation reflexes, sometimes hydrocephalus with suddenly increased intracranial pressure

Germ cell tumor

Pineocytoma (rare)

Pituitary or suprasellar region

Endocrinopathies, monocular visual loss, headache without increased intracranial pressure, bitemporal hemianopia


Pituitary adenoma

Pituitary carcinoma (rare)

Temporal lobe

Complex partial seizures, generalized seizures with or without aura, hemianopia (contralateral), mixed expressive and receptive aphasia or anomia




Sensory impairment (contralateral)


*Similar manifestations may result from brain parenchymal metastases or from tumors around the dura (eg, metastatic tumors; meningeal tumors such as meningiomas, sarcomas, or gliomas) or skull lesions (eg, granulomas, hemangiomas, osteitis deformans, osteomas, xanthomas) that compress the underlying brain.

Common Tumors

Age Group




Cerebellar astrocytomas and medulloblastomas


Gliomas of the brain stem or optic nerve


Congenital tumors*

Neuroblastoma (usually epidural)

Leukemia (meningeal)




Primary lymphomas

Gliomas of the cerebral hemispheres, particularly glioblastoma multiforme, anaplastic astrocytoma, low-grade astrocytoma, and oligodendroglioma

Bronchogenic carcinoma

Adenocarcinoma of the breast

Malignant melanoma

Any cancer that has spread to the lungs

*Congenital tumors include craniopharyngiomas, chordomas, germinomas, teratomas, dermoid cysts, angiomas, and hemangioblastomas.


Neurologic dysfunction may result from the following:

  • Invasion and destruction of brain tissue by the tumor

  • Direct compression of adjacent tissue by the tumor

  • Increased intracranial pressure (because the tumor occupies space within the skull)

  • Bleeding within or outside the tumor

  • Cerebral edema

  • Obstruction of dural venous sinuses (especially by bone or extradural metastatic tumors)

  • Obstruction of CSF drainage (occurring early with 3rd-ventricle or posterior fossa tumors)

  • Obstruction of CSF absorption (eg, when leukemia or carcinoma involves the meninges)

  • Obstruction of arterial flow

  • Rarely, paraneoplastic syndromes (see Paraneoplastic Syndromes)

A malignant tumor can develop new internal blood vessels, which can bleed or become occluded, resulting in necrosis and neurologic dysfunction that mimics stroke.

Benign tumors grow slowly. They may become quite large before causing symptoms, partly because often there is no cerebral edema. Malignant primary tumors grow rapidly but rarely spread beyond the CNS. Death results from local tumor growth and thus can result from benign as well as malignant tumors. Therefore, distinguishing between benign and malignant is prognostically less important for brain tumors than for other tumors.

Symptoms and Signs

Symptoms caused by primary tumors and metastatic tumors are the same. Many symptoms result from increased intracranial pressure:

  • Headache

  • Deterioration in mental status

  • Focal brain dysfunction

Headache is the most common symptom. Headache may be most intense when patients awake from deep non-REM sleep (usually several hours after falling asleep) because hypoventilation, which increases cerebral blood flow and thus intracranial pressure, is usually maximal during non-REM sleep. Headache is also progressive and may be worsened by recumbency or the Valsalva maneuver. When intracranial pressure is very high, the headache may be accompanied by vomiting, sometimes with little nausea preceding it. Papilledema develops in about 25% of patients with a brain tumor but may be absent even when intracranial pressure is increased. In infants and very young children, increased intracranial pressure may enlarge the head. If intracranial pressure increases sufficiently, brain herniation occurs (see Brain herniation.).

Deterioration in mental status is the 2nd most common symptom. Manifestations include drowsiness, lethargy, personality changes, disordered conduct, and impaired cognition, particularly with malignant brain tumors. Generalized seizures may occur, more often with primary than metastatic brain tumors. Impaired consciousness (see Coma and Impaired Consciousness) can result from herniation, brain stem dysfunction, or diffuse bilateral cortical dysfunction. Airway reflexes may be impaired.

Focal brain dysfunction causes some symptoms. Focal neurologic deficits, endocrine dysfunction, or focal seizures (sometimes with secondary generalization) may develop depending on the tumor’s location (see Common Localizing Manifestations of Brain Tumors). Focal deficits often suggest the tumor’s location. However, sometimes focal deficits do not correspond to the tumor’s location. Such deficits, called false localizing signs, include the following:

  • Unilateral or bilateral lateral rectus palsy (with paresis of eye abduction) due to increased intracranial pressure compressing the 6th cranial nerve

  • Ipsilateral hemiplegia due to compression of the contralateral cerebral peduncle against the tentorium (Kernohan notch)

  • Ipsilateral visual field defect due to ischemia in the contralateral occipital lobe

Some tumors cause meningeal inflammation, resulting in subacute or chronic meningitis (see Meningitis).


  • T1-weighted MRI with gadolinium or CT with contrast

Early-stage brain tumors are often misdiagnosed. A brain tumor should be considered in patients with any of the following:

  • Progressive focal or global deficits of brain function

  • New seizures

  • Persistent, unexplained, recent-onset headaches, particularly if worsened by sleep

  • Evidence of increased intracranial pressure (eg, papilledema, unexplained vomiting)

  • Pituitary or hypothalamic endocrinopathy

Similar findings can result from other intracranial masses (eg, abscess, aneurysm, arteriovenous malformation, intracerebral hemorrhage, subdural hematoma, granuloma, parasitic cysts such as neurocysticercosis) or ischemic stroke.

A complete neurologic examination, neuroimaging, and chest x-rays (for a source of metastases) should be done. T1-weighted MRI with gadolinium is the study of choice. CT with contrast agent is an alternative. MRI usually detects low-grade astrocytomas and oligodendrogliomas earlier than CT and shows brain structures near bone (eg, the posterior fossa) more clearly. If whole-brain imaging does not show sufficient detail in the target area (eg, sella turcica, cerebellopontine angle, optic nerve), closely spaced images or other special views of the area are obtained. If neuroimaging is normal but increased intracranial pressure is suspected, idiopathic intracranial hypertension (see Idiopathic Intracranial Hypertension) should be considered and lumbar puncture see Lumbar Puncture (Spinal Tap) done.

Radiographic clues to the type of tumor, mainly location (see Common Localizing Manifestations of Brain Tumors) and pattern of enhancement on MRI, may be inconclusive; brain biopsy, sometimes excisional biopsy, may be required. Specialized tests (eg, molecular and genetic tumor markers in blood and CSF) can help in some cases; eg, in patients with AIDS, Epstein-Barr virus titers in CSF typically increase as CNS lymphoma develops.


  • Airway protection

  • Dexamethasone for increased intracranial pressure

  • Mannitol for herniation

  • Definitive therapy with excision, radiation therapy, chemotherapy, or a combination

Patients in a coma or with impaired airway reflexes require endotracheal intubation see Tracheal Intubation. Brain herniation due to tumors is treated with mannitol 25 to 100 g infused IV, a corticosteroid (eg, dexamethasone 16 mg IV, followed by 4 mg po or IV q 6 h), and endotracheal intubation. Mass lesions should be surgically decompressed as soon as possible.

Increased intracranial pressure due to tumors but without herniation is treated with corticosteroids (eg, dexamethasone as for herniation above or prednisone 30 to 40 mg po bid).

Treatment of the brain tumor depends on pathology and location (for acoustic neuroma, see Acoustic Neuroma). Surgical excision should be used for diagnosis (excisional biopsy) and symptom relief. It may cure benign tumors. For tumors infiltrating the brain parenchyma, treatment is multimodal. Radiation therapy is required, and chemotherapy appears to benefit some patients.

Treatment of metastatic tumors includes radiation therapy and sometimes stereotactic radiosurgery. For patients with a single metastasis, surgical excision of the tumor before radiation therapy improves outcome.

End-of-life issues

If brain tumors are expected to soon be fatal, end-of-life issues should be considered (see The Dying Patient).

Cranial Radiation Therapy and Neurotoxicity

Radiation therapy may be directed diffusely to the whole head for diffuse or multicentric tumors or locally for well-demarcated tumors. Localized brain radiation therapy may be conformal, targeting the tumor with the aim of sparing normal brain tissue, or stereotactic, involving brachytherapy, a gamma knife, or a linear accelerator. In brachytherapy, radioactive stable iodine (125I3) or iridium-192 (192Ir4) is implanted in or near the tumor. Gliomas are treated with conformal radiation therapy; a gamma knife or linear accelerator is useful for metastases. Giving radiation daily tends to maximize efficacy and minimize neurotoxicity damage to normal CNS tissue (see Acute radiation syndromes (ARS)).

Degree of neurotoxicity depends on

  • Cumulative radiation dose

  • Individual dose size

  • Duration of therapy

  • Volume of tissue irradiated

  • Individual susceptibility

Because susceptibility varies, prediction of radiation neurotoxicity is imprecise. Symptoms can develop in the first few days (acute) or months of treatment (early-delayed) or several months to years after treatment (late-delayed). Rarely, radiation causes gliomas, meningiomas, or peripheral nerve sheath tumors years after therapy.

Acute radiation neurotoxicity

Typically, acute neurotoxicity involves headache, nausea, vomiting, somnolence, and sometimes worsening focal neurologic signs in children and adults. It is particularly likely if intracranial pressure is high. Using corticosteroids to lower intracranial pressure can prevent or treat acute toxicity. Acute toxicity lessens with subsequent treatments.

Early-delayed neurotoxicity

In children or adults, early-delayed neurotoxicity can cause encephalopathy, which must be distinguished by MRI or CT from worsening or recurrent brain tumor. It occurs in children who have received prophylactic whole-brain radiation therapy for leukemia; they develop somnolence, which lessens spontaneously over several days to weeks, possibly more rapidly if corticosteroids are used.

After radiation therapy to the neck or upper thorax, early-delayed neurotoxicity can result in a myelopathy, characterized by Lhermitte sign (an electric shock-like sensation radiating down the back and into the legs when the neck is flexed). The myelopathy resolves spontaneously.

Late-delayed neurotoxicity

After diffuse brain radiation therapy, many children and adults develop late-delayed neurotoxicity if they survive long enough. The most common cause in children is diffuse therapy given to prevent leukemia or to treat medulloblastoma. After diffuse therapy, the main symptom is progressive dementia; adults also develop an unsteady gait. MRI or CT shows cerebral atrophy.

After localized therapy, neurotoxicity more often involves focal neurologic deficits. MRI or CT shows a mass that may be enhanced by contrast agent and that may be difficult to distinguish from recurrence of the primary tumor. Excisional biopsy of the mass is diagnostic and often ameliorates symptoms.

Late-delayed myelopathy can develop after radiation therapy for extraspinal tumors (eg, due to Hodgkin lymphoma). It is characterized by progressive paresis and sensory loss, often as a Brown-Séquard syndrome (ipsilateral paresis and proprioceptive sensory loss, with contralateral loss of pain and temperature sensation). Most patients eventually become paraplegic.

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