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Clinical presentation and diagnosis of brain tumors
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©2011 UpToDate®
Clinical presentation and diagnosis of brain tumors
Authors
Eric T Wong, MD
Julian K Wu, MD
Section Editors
Jay S Loeffler, MD
Patrick Y Wen, MD
Deputy Editor
Michael E Ross, MD
Disclosures
Last literature review version 19.3: september 2011 | This topic last updated:
november 11, 2010
INTRODUCTION — Brain tumors are a diverse group of neoplasms arising from
different cells within the central nervous system (CNS) or from systemic tumors that
have metastasized to the CNS. Brain tumors include a number of histologic types with
markedly different tumor growth rates (table 1 and table 2). (See "Classification of brain
tumors" and "Overview of the clinical manifestations, diagnosis, and management of
patients with brain metastases".)
Brain tumors can produce symptoms and signs by local brain invasion, compression of
adjacent structures, and increased intracranial pressure (ICP). In addition to the
histology of the tumor, the clinical manifestations are determined by the function of the
involved areas of the brain. The proper evaluation of the patient with a suspected brain
tumor requires a detailed history, comprehensive neurologic examination, and
appropriate diagnostic neuroimaging studies [1].
The clinical manifestations and diagnosis of primary brain tumors will be reviewed here.
Aspects of the various primary brain tumors are discussed in the specific topics, and the
presentation and approach to patients with brain metastases is presented separately.
(See "Overview of the clinical manifestations, diagnosis, and management of patients
with brain metastases".)
CLINICAL MANIFESTATIONS — Patients with primary or metastatic brain tumors may
present with either generalized or focal signs and/or symptoms (table 3).
Generalized
Headaches — Headache is a common manifestation of brain tumors and is the worst
symptom in about one-half of patients [2]. The headaches are usually dull and constant,
but occasionally throbbing. Severe headaches are infrequent, unless obstructive
hydrocephalus or meningeal irritation is present. The "classic" early morning brain tumor
headache appears to be uncommon. (See "Evaluation of headache in adults".)
Features suggestive of a brain tumor in a patient complaining of headaches include
nausea and vomiting (present in about 40 percent), a change in prior headache pattern,
and an abnormal neurologic examination [2]. In addition, many patients with a brain
tumor report worsening of headache after a change in body position, such as bending
over, or with maneuvers that raise intrathoracic pressure, such as coughing, sneezing, or
the Valsalva maneuver [2]. These activities lead to a period of raised ICP, which
uncommonly can cause a loss of consciousness (see 'Syncope' below).
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The headache can be localizing. In the above series, the typical headache was bifrontal,
but worse on the same side as the tumor [2]. Alternatively, a generalized headache may
result from increased intracranial pressure (ICP), which can arise either from a large
mass or from restriction of cerebrospinal fluid outflow causing hydrocephalus. Increased
ICP may lead to the classic triad of headache, nausea, and papilledema. (See "Evaluation
and management of elevated intracranial pressure in adults".)
Tumor-related headaches tend to be worse at night and may awaken the patient. This
nocturnal pattern is thought to be due in part to transient increases in PCO2, a potent
vasodilator, during sleep. Other possible physiologic explanations include recumbency
and decreased cerebral venous return.
The manifestations of headache in brain tumor patients were illustrated by a
retrospective review of 111 patients with brain tumors, in which headaches were present
in 48 percent of cases with either primary or metastatic disease [2]. The headaches were
tension-type in 77 percent, migraine-type in 9 percent, and other types in 14 percent.
Brain tumor headaches are discussed in more detail elsewhere. (See "Brain tumor
headache".)
Seizures — Seizures are among the most common symptoms of gliomas and cerebral
metastases. Some patients who are seizure-free at diagnosis subsequently develop
seizures [3,4], but routine prophylaxis with anticonvulsant medications is not
recommended. (See "Seizures in patients with primary and metastatic brain tumors".)
The incidence of seizures is higher with primary tumors than with metastatic lesions, and
among patients with primary tumors, seizures are less common with high-grade as
opposed to low-grade gliomas [5,6]. This was illustrated in a review of 1028 patients
with primary brain tumors: the prevalence of seizures was 49, 69, and 85 percent among
patients with glioblastoma (GBM), anaplastic glioma, and low-grade glioma, respectively
[6].
Seizures may be the presenting symptom or develop subsequently. In two large series of
patients with GBM, seizures were the initial manifestation in 18 percent and were present
at the time of diagnosis (for an average of one year) in 29 percent (table 4) [7,8]. The
frequency and onset of seizures in patients with brain metastases was illustrated in a
series of 195 patients, in which seizures were present at diagnosis in 9 percent and
subsequently developed in another 10 percent [4].
Although seizures can be either generalized or focal, any seizure focus can cause a
generalized seizure. In patients who have focal seizures, the clinical presentation is
dependent upon the tumor location. As an example, frontal lobe tumors may cause focal
tonic-clonic movements involving one extremity, while seizures originating within the
occipital lobe may cause visual disturbances. Temporal lobe seizures are the most
difficult to diagnose and localize. In this setting, abrupt sudden behavioral changes may
occur with or without typical preseizure auras, such as abnormal smell, taste, or
gastrointestinal symptoms.
Tumor-related seizures are typically repetitive and are stereotyped in a given patient.
The ictal event may be preceded by an aura, which is itself a simple partial seizure, and
followed by postictal sequelae. The postictal phase can be manifested as a period of
fatigue and an urge to sleep. For patients with focal seizures, a postictal paresis (also
known as a Todd's paralysis) may be present. (See "Overview of the management of
epilepsy in adults".)
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Both primary and metastatic brain tumors can cause status epilepticus, which may occur
at the time of tumor diagnosis or subsequently [9]. (See "Status epilepticus in adults".)
Patients who present with seizures usually have smaller primary brain tumors or fewer
metastatic lesions in the brain, compared to those who present with other symptoms.
This is probably because the diagnosis of a seizure is an indication for neuroimaging,
which leads to an earlier diagnosis. (See "Evaluation of the first seizure in adults".)
A seizure should not be confused with a syncopal event that may be caused by an abrupt
increase in ICP. This distinction is important since treatment is different in the two
conditions. Patients with seizures are at risk of subsequent seizures [3,10], and the
treatment is anticonvulsants. In contrast, patients with increased ICP require urgent
corticosteroids, neurosurgical intervention, or both. (See 'Syncope' below and "Overview
of the management of epilepsy in adults" and "Management of vasogenic edema in
patients with primary and metastatic brain tumors".)
Nausea and vomiting — Brain tumors can cause nausea and/or vomiting by
increasing the ICP at the area postrema of the medulla. (See "Approach to the adult with
nausea and vomiting".)
Several characteristics suggest the possibility of tumor-associated emesis, such as
triggering emesis by an abrupt change in body position. More importantly, neurogenic
nausea and vomiting usually occur in the context of other neurologic symptoms such as
headache or focal neurologic deficit; these signs and symptoms may be subtle [11,12].
Syncope — A significant rise in ICP can temporarily cut off cerebral perfusion, leading
to loss of consciousness. Patients with brain tumors are particularly susceptible to this
sequence of events in association with normal plateau waves.
Plateau waves are sustained pressure waves that normally occur within the brain and are
caused by activities that transiently raise the ICP [13,14]. As an example, any Valsalva
maneuver (eg, coughing, sneezing, vomiting) that increases the intrathoracic pressure
can impede jugular venous drainage, leading to a transient increase in ICP.
In the presence of a brain tumor, the baseline ICP may be raised to a level that reduces
brain compliance; in this setting, even a further small increase in intracranial fluid
volume can result in dramatic elevations in ICP. The cerebral perfusion pressure is the
difference between the mean systemic arterial pressure and ICP. Thus, a significant rise
in ICP can temporarily cut off cerebral perfusion, leading to loss of consciousness. (See
"Evaluation and management of elevated intracranial pressure in adults".)
A syncopal episode may simulate a seizure, since patients suffer loss of consciousness
and may have a few tonic-clonic jerks. Identification of plateau wave-related episodes of
loss of consciousness is critical, since these events identify patients who require urgent
corticosteroids and/or neurosurgical intervention to reduce elevated ICP rather than
treatment with an anticonvulsant. (See "Management of vasogenic edema in patients
with primary and metastatic brain tumors", section on 'Glucocorticoids'.)
Cognitive dysfunction — Cognitive dysfunction, which includes memory problems
and mood or personality change, is common among patients with intracranial
malignancy.
Most of the neurocognitive deficits associated with brain tumors are subtle. Patients
often complain of having low energy, fatigue, an urge to sleep, and loss of interest in
everyday activities. They may become abulic and show a lack of spontaneity (table 5).
This pattern of symptoms can be confused with depression. (See "Clinical manifestations
and diagnosis of depression".)
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Because these symptoms lack specificity, they are often recognized in retrospect by the
patient or the treating physician. Thus, consideration should be given to neuroimaging to
rule out a brain tumor in patients without a prior history of depression who experience
new onset of depressive symptoms without obvious cause.
Focal
Weakness — Muscle weakness is a common complaint in patients with brain tumors.
The manifestations may be subtle, particularly in the early stages. For upper motor
neuron lesions, weakness is generally more pronounced in the flexors of the lower
extremities than in the extensors, and more pronounced in the extensors than the
flexors in the upper extremities. Transient weakness may represent a postictal state, as
in Todd's paralysis (see 'Seizures' above). (See "The detailed neurologic examination in
adults", section on 'Upper versus lower motor neuron lesions'.)
A key feature of tumor-related muscle weakness is its frequent responsiveness to highdose dexamethasone, particularly with tumors that are near the motor cortex or its
descending fibers. A response to dexamethasone usually means that the weakness is
caused by edema and not by direct tumor involvement. In such a patient, craniotomy
can be considered to relieve mass effect and lessen the corticosteroid requirement, even
if the patient is not resectable for cure. (See "Management of vasogenic edema in
patients with primary and metastatic brain tumors", section on 'Glucocorticoids'.)
Sensory loss — Cortical sensory deficits (eg, graphesthesia or abnormalities in
stereognosis) can develop in patients whose tumors invade the primary sensory cortex
(table 5). These sensory deficits usually do not respect a dermatomal or peripheral nerve
distribution. (See "The detailed neurologic examination in adults", section on 'Sensory
examination'.)
The type of deficit varies in part with location of the tumor. As an example, visual-spatial
disconnection syndromes can be found in patients with tumors located in the visual
association cortex (see 'Visual spatial dysfunction' below). Some of the other corticallybased sensory deficits include loss of spatial orientation, tingling, and lack of
coordination.
Aphasia — Aphasia is a disorder of language function, not of vocalization, as in
dysarthria or hoarseness. It is a specific sign of a lesion in the dominant hemisphere
(usually left frontal or parietal); in comparison, lesions in the nondominant hemisphere
may produce apraxia, which refers to an inability to perform purposeful movements
(table 5).
Patients who are aphasic may be confused with those who have dementia or other
psychiatric disorders such as psychosis or depression. Subacute psychosis in a patient
without an antecedent psychiatric history is a diagnosis of exclusion that requires
diagnostic neuroimaging studies to rule out an organic cause.
Visual spatial dysfunction — The visual pathway courses through the brain from
the retina and optic chiasm to the occipital poles of the cerebral cortex. Because of its
long course through the brain, the visual pathway can be affected by brain tumors that
involve any of these areas.
• Examination of the retina, particularly the optic discs, is an important component
of the initial examination of a patient suspected of having a brain tumor. The optic
nerve head can be a good measure of ICP, although papilledema is often not
present in the elderly despite an increase in ICP. Although gross papilledema is
easy to diagnose, evolving papilledema can be difficult to recognize. As an
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example, only the medial portion of the optic disk may be blurred initially in early
papilledema. Venous engorgement and the absence of venous pulsations are also
important diagnostic clues. (See "Overview and differential diagnosis of
papilledema".)
• Tumor-related compression of the optic chiasm usually manifests as a bitemporal
hemianopsia. However, there may be a unilateral hemianopsia with a central
scotoma in the contralateral eye in the early stages, particularly when the
compression is on one side. The latter results from partial compression of the
Wilbrand's knee in the contralateral optic nerve. (See "Causes, presentation, and
evaluation of sellar masses" and "Optic pathway glioma".)
• Postchiasmatic lesions also may present with visual abnormalities. Because of the
somatotopic representation of the visual pathways, the more anterior the lesion,
the more asymmetric the hemianopsia.
DIAGNOSTIC NEUROIMAGING — The differential diagnosis of an adult presenting with
signs and symptoms suggesting a brain tumor includes both neoplastic and
nonneoplastic conditions (table 6). Neuroradiologic imaging is the major diagnostic
modality in the evaluation of brain tumors. These studies are critical for preoperative
planning, and they often provide information about the etiology of a mass lesion.
Although neuroimaging cannot definitively establish the specific histology, the
characteristic appearance of dural-based meningiomas often can allow a tentative
diagnosis. Treatment of meningiomas without a histologic diagnosis may be warranted in
carefully selected cases for lesions in a surgically inaccessible location. (See
"Meningioma: Clinical presentation and diagnosis", section on 'Neuroimaging'.)
Magnetic resonance imaging — Gadolinium-enhanced magnetic resonance imaging
(MRI) is usually the only test needed to suggest a brain tumor. MRI may also provide
information that indicates the specific tumor type:
• Malignant gliomas are typically hypointense on T1-weighted images, and enhance
heterogeneously following contrast infusion. Enhancing tumor can be distinguished
from the surrounding hypointense signal of edema on T1-weighted sequences
(picture 1).
• Regardless of the histologic grade, astrocytomas generally show increased T2 and
FLAIR signal intensity; however, some astrocytomas do not manifest contrast
enhancement [15].
• Low grade gliomas generally present as an infiltrating hemispheric lesion that
produce little mass effect. The MRI appearance of focal brainstem gliomas is
discussed elsewhere. (See "Focal brainstem glioma", section on 'Clinical
presentation'.)
In addition to permitting visualization of the tumor and its relationship to the
surrounding normal parenchyma, MRI is also superior to computed tomography (CT) for
evaluation of the meninges, subarachnoid space, and posterior fossa, and for defining
the vascular distribution of the abnormality. (See 'Computed tomography' below.)
Magnetic resonance spectroscopy — Magnetic resonance spectroscopy (MRS) is
increasingly being utilized as a diagnostic technique in patients with suspected brain
tumors [16-19]. This technique may improve the differentiation of locally infiltrative
brain tumors from other types of well-circumscribed intracranial lesions by analyzing the
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chemical composition in an area of interest selected by the radiologist. The three
important spectroscopic signals are N-acetylaspartate, choline, and lactate (table 7):
• N-acetylasparate, a byproduct of the ubiquitous neurotransmitter glutamate,
signals the presence of neurons since it localizes to the synaptic terminals, and is
decreased in gliomas.
• Choline, a component of cell membranes, is increased in tumors.
• Lactate, a product of anaerobic respiration, can be present in necrotic tumor,
infection, or stroke.
MRS cannot differentiate the types of infiltrative or circumscribed lesions, and it cannot
replace histologic diagnosis of malignancy [18]. However, it can help differentiate
between neoplasm and other central nervous system processes [20]. The utility of MRS
was illustrated in a study of 26 patients with intracranial masses who underwent MRI,
proton MRS, and stereotactic biopsy [18]. For patients with gliomas and lymphomas,
pathologic spectra were present outside the area of contrast enhancement, suggesting
infiltration beyond the borders suggested by MRI. In comparison, four circumscribed
tumors (meningioma, pineocytoma, metastasis, and germinoma) showed no pathologic
spectra outside the region of enhancement.
MRS spectroscopy signals are degraded by bone and cerebrospinal fluid. As a result, MRS
is less useful for skull base and periventricular lesions.
Functional MRI — When a region of the brain is activated (eg, the language center
during phonation or the motor cortex when moving a limb), blood flow to that region
increases. Functional MRI (also known as echoplanar MRI) permits the measurement of
differences in blood flow though particular regions of the brain and has several
advantages in patients with brain tumors:
• Functional MRI is an important adjunct in the preoperative planning for patients
whose tumor is located near eloquent areas of the brain [21]. In such areas,
imaging after activation of sensory and motor areas by appropriate stimuli may
permit separation of tumor from normal brain preoperatively (functional brain
imaging) [22,23].
• Functional MRI may permit better resolution of tumor versus surrounding edema at
the tumor borders [24,25].
• Ultrafast acquisition of MRI images by echoplanar imaging is free from motion
artifact and may be useful in patients who are unable to cooperate with standard
MRI scanning [26].
Perfusion MRI — Perfusion MRI is the imaging of blood flow in brain tumors. This is
done either with a bolus of gadolinium as in dynamic contrast MRI [27] or dynamic
susceptibility contrast MRI [28], or with magnetic pulsation of water molecules as they
pass through carotid and vertebral arteries as in arterial spin labeling [29,30]. Increased
perfusion can be seen in newly diagnosed or recurrent brain tumors, usually reflecting
the presence of hypervascularity.
Computed tomography — CT has largely been replaced by cranial MRI as the imaging
modality of choice for brain tumors. However, CT retains utility in selected situations:
• To detect bone or vascular involvement
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• To detect metastases to the skull base, clivus, or regions near the foramen
magnum
• In an emergency situation (eg, an unstable patient with a suspected intratumoral
hemorrhage), when CT can be faster to perform than MRI
• In patients for whom MRI is contraindicated, either because of an iron-containing
implant or because of claustrophobia
PET scans — Positron emission tomography (PET) with fluorodeoxyglucose (FDG) can be
used to detect malignant tumors with high metabolic rates. Such lesions take up greater
amounts of glucose than surrounding tissues or tumors with slower metabolic rates.
FDG-PET may be useful in the following situations:
• To localize the areas of maximum glucose utilization within the tumor. This
information can guide the neurosurgeon to biopsy tumor locations with the most
aggressive biologic behavior [31-33].
• To permit the mapping of functional areas of the brain prior to surgery or radiation,
in conjunction with functional MRI, in order to minimize injury to eloquent areas
[22,34,35].
• To differentiate recurrent tumor from radiation necrosis [36-40].
• To help differentiate high-grade (glucose hypermetabolizing) from low-grade
(glucose hypometabolizing) brain tumors [41,42]. In patients with low-grade
gliomas, FDG-PET images that show diffuse hypometabolism may support a
decision to defer treatment, while the presence of hypermetabolic areas may
indicate a high-grade tumor and signal the need for biopsy or treatment. (See
"Diagnosis and classification of low-grade gliomas".)
Because of high basal uptake of FDG by normal brain tissues, the low signal-to-noise
ratio of FDG-PET may result in false negative data [43], sensitivity of 71 percent and
specificity of 80 percent [40]. As a result, FDG-PET is not an FDA-approved diagnostic
study for evaluating malignancies in the brain, even though it is approved for systemic
malignancies. 18F-fluorothymidine-PET (18F-FLT-PET) has a higher signal-to-noise
radiation than FDG-PET [44]. But its exact utility in the brain tumor population await
further clinical trials.
SPECT imaging — Single photon emission CT (SPECT) utilizes various isotopes to detect
abnormalities in the blood brain barrier. Preoperative SPECT using thallium-201 is useful
to distinguish benign from malignant brain lesions, predict the histologic grade of brain
tumors, and select areas for biopsy [45]. The uptake of 201-Tl is unaffected by steroid
treatment [46].
There appears to be a correlation between early and delayed tumor uptake of 201-Tl and
the subsequent grade of the surgically resected tumor, allowing a distinction between
low- and high-grade astrocytomas [46-49].
DIAGNOSTIC NEUROSURGICAL INTERVENTION — Accurate diagnosis of a brain
tumor requires an adequate tissue sample for histologic study. This may be obtained by
stereotactic biopsy or open surgery.
Corticosteroid use should be avoided prior to biopsy or surgery if either a primary
central nervous system lymphoma or an infectious process is part of the differential
diagnosis. (See 'CNS lymphomas' below.)
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Preoperative assessment — The likelihood that a lesion is metastatic should be
assessed prior to proceeding to biopsy. Brain metastases are more common than
primary brain tumors. Although brain metastases usually present in the context of overt
systemic disease, they can occur as the initial manifestation of a systemic malignancy.
If any aspect of the clinical or neurodiagnostic evaluation suggests that a brain tumor is
a metastatic rather than a primary lesion, systemic evaluation, particularly of the thorax,
should be carried. Neurosurgical intervention in a patient with a presumed brain
metastasis should balance the risks of the procedure versus the potential benefits (ie,
tissue diagnosis, resection of a solitary lesion, relief of neurological symptoms). (See
"Overview of the clinical manifestations, diagnosis, and management of patients with
brain metastases".)
Surgical exploration or biopsy — Technical advances have improved the safety of
both surgical resection and stereotactic biopsy. Improved diagnostic neuroimaging
permits better preoperative localization of the lesion and separation of the lesion from
adjacent normal brain tissue, particularly in eloquent areas of the brain. Techniques such
as intraoperative MRI facilitate improved surgical navigation for lesion biopsy and
resection.
For most patients, tissue for histologic confirmation is obtained at the time of surgical
exploration for resection. In those patients with large, nonresectable lesions or those
whose lesions are in a critical location, stereotactic biopsy is an alternative. In some
patients with a meningioma with a lesion that is either difficult or impossible to access,
the characteristic appearance of a dural-based tumor may be sufficient to permit
treatment. (See "Treatment of benign (WHO grade I) meningioma", section on 'RT alone
for nonresectable meningiomas'.)
Glial tumors — For patients with primary glial tumors, maximum surgical resection is
usually recommended. (See appropriate topic reviews).
There are two exceptions to this approach:
• Low-grade glioma — For patients with low-grade glial tumors, the role of maximal
resection remains uncertain. Retrospective studies suggest that more extensive
tumor resection is associated with delay in tumor progression and malignant
degeneration, as well as improved survival. (See "Management of low-grade
glioma", section on 'Surgery'.)
Immediate surgery is generally required for patients presenting with a large mass
or extensive neurologic symptoms, both to establish the diagnosis and to debulk
the tumor. However, for patients with a small tumor not creating a mass effect and
only transient symptoms or tumors in eloquent cortex, careful observation may be
an alternative to immediate surgery.
• Diffuse pontine glioma — As long as characteristic radiologic features are present,
a tissue diagnosis of a pontine gliomas not required prior to treatment (picture
2) [50]. In equivocal cases, the clinician must weigh the risks of a surgical biopsy
versus the diagnostic uncertainty. (See "Diffuse pontine glioma".)
CNS lymphomas — Patients with primary central nervous system lymphoma are
typically not offered surgical debulking, since the extent of surgical resection does not
influence patient survival. Stereotactic biopsy is usually recommended, providing a high
rate of positive tissue diagnosis with a low rate (<2 percent) of morbidity and mortality.
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Definitive treatment is usually chemotherapy, radiation, or a combination of these
modalities. (See "Clinical presentation, pathologic features, and diagnosis of primary
central nervous system lymphoma" and "Treatment and prognosis of primary central
nervous system lymphoma".)
Corticosteroids should be avoided whenever possible prior to biopsy or surgery if
primary CNS lymphoma is part of the differential diagnosis. These agents are
lymphocytotoxic. A single dose can alter the histopathologic evaluation, and a short
course of treatment may cause the lymphoma to disappear temporarily.
Brain metastases — Biopsy is not necessary for patients with multiple brain
metastases if there is a preexisting primary cancer known to have a propensity for brain
metastases. If, however, a patient has a primary tumor that does not usually
metastasize to the brain (eg, prostate cancer), if there is no known primary, or if
neuroimaging is not typical for metastasis, biopsy may be indicated to define the etiology
of a brain lesion. The importance of biopsy in such situations was illustrated in a
randomized trial of surgery for the treatment of solitary brain metastases, in which 11
percent of patients had a second primary malignancy, inflammatory process, or infection
rather than metastasis [51].
The management of patients with brain metastases is dependent upon the overall
condition of the patient, as well as the number, size, and location of brain metastases.
The management of patients with brain metastases is discussed separately. (See
"Treatment of brain metastases in favorable prognosis patients" and "Treatment of brain
metastases in poor prognosis patients".)
Neuropathology — Histologic examination of the biopsy specimen remains the most
important component of the diagnostic evaluation of brain tumors. A smear or frozen
section can be performed in the operating room for a preliminary interpretation of the
histologic subtype. With this information, the neurosurgeon can make a decision whether
or not to proceed with a more extensive resection.
A definitive diagnosis requires examination of the permanent tissue sections stained by
hematoxylin and eosin. Important information may be derived additional analyses that
include the following:
•
•
•
•
Proliferative index, using the MIB-1 monoclonal antibody
Immunohistochemical stains
Electron microscopy may be necessary to ascertain the correct diagnosis
Molecular markers (eg, deletions for chromosome 1p/19q or the presence or
absence of promoter methylation of the DNA repair enzyme O6-methylguanineDNA methyltransferase [MGMT])
Caution should be exercised in interpreting the tissue diagnosis when the tissue is
derived only from a biopsy specimen. This is particularly true for glial tumors, because
regional heterogeneity and sampling error may underestimate the histologic grade of
malignancy [52].
In patients suspected of having a primary central nervous system lymphoma,
corticosteroid use should be avoided prior to biopsy, as these drugs are lymphocytotoxic
and can affect the histopathologic evaluation. (See "Clinical presentation, pathologic
features, and diagnosis of primary central nervous system lymphoma", section on
'Diagnosis'.)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education
materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are
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written in plain language, at the 5th to 6th grade reading level, and they answer the four
or five key questions a patient might have about a given condition. These articles are
best for patients who want a general overview and who prefer short, easy-to-read
materials. Beyond the Basics patient education pieces are longer, more sophisticated,
and more detailed. These articles are written at the 10th to 12th grade reading level and
are best for patients who want in-depth information and are comfortable with some
medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you
to print or e-mail these topics to your patients. (You can also locate patient education
articles on a variety of subjects by searching on “patient info” and the keyword(s) of
interest.)
• Basics topics (see "Patient information: Brain cancer (The Basics)")
• Beyond the Basics topics (see "Patient information: Primary low-grade glioma in
adults" and "Patient information: High-grade glioma in adults" and "Patient
information: Meningioma")
SUMMARY — Brain tumors can produce symptoms and signs by local brain invasion,
compression of adjacent structures, and increased intracranial pressure (ICP). In
addition to the histology of the tumor, the clinical manifestations are determined by the
function of the involved areas of brain. The proper evaluation of the patient with a
suspected brain tumor requires a detailed history, a comprehensive neurologic
examination, and appropriate diagnostic neuroimaging studies.
Although newer imaging techniques often provide information suggesting a specific
histology, an adequate tissue sample should generally be obtained, either at the time of
neurosurgical resection or by stereotactic biopsy, to optimize treatment.
Use of UpToDate is subject to the Subscription and License Agreement.
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GRAPHICS
WHO classification of brain tumors
Tumors of neuroepithelial tissue
Astrocytic tumors
Pilocytic astrocytoma
Subependymal giant cell astrocytoma
Pleomorphic xanthoastrocytoma
Diffuse astrocytoma
Anaplastic astrocytoma
Glioblastoma
Gliomatosis cerebri
Oligodendroglial tumors
Oligodendroglioma
Anaplastic oligodendroglioma
Oligoastrocytic tumors
Oligoastrocytoma
Anaplastic oligoastrocytoma
Ependymal tumors
Subependymoma
Myxopapillary ependymoma
Ependymoma
Anaplastic ependymoma
Choroid plexus tumors
Choroid plexus papilloma
Atypical choroid plexus papilloma
Choroid plexus carcinoma
Other neuroepithelial tumors
Astroblastoma
Chordoid glioma of the third ventricle
Angiocentric glioma
Neuronal and mixed neuronal-glial tumors
Dysplastic gangliocytoma of cerebellum (Lhermitte-Duclos)
Desmoplastic infantile astrocytoma/ganglioglioma
Dysembryoplastic neuroepithelial tumor
Gangliocytoma
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Clinical presentation and diagnosis of brain tumors
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Ganglioglioma
Anaplastic ganglioglioma
Central neurocytoma
Extraventricular neurocytoma
Cerebellar liponeurocytoma
Papillary glioneuronal tumor
Rosette-forming glioneuronal tumor of the fourth ventricle
Paraganglioma
Tumors of the pineal region
Pineocytoma
Pineal parenchymal tumor of intermediate differentiation
Pineoblastoma
Papillary tumor of the pineal region
Embryonal tumors
Medulloblastoma
CNS primitive neuroectodermal tumor (PNET)
Atypical teratoid / rhabdoid tumor
Tumors of cranial and paraspinal nerves
Schwannoma (neurilemoma, neurinoma)
Neurofibroma
Perineurioma
Malignant peripheral nerve sheath tumor
Tumors of the meninges
Tumors of meningothelial cells
Meningioma
Mesenchymal tumors
Adipose tissue: Lipoma, angiolipoma, hibernoma, liposarcoma
Fibrous tissue: Solitary fibrous tumor, fibrosarcoma, malignant fibrous histiocytoma
Smooth muscle: Leiomyoma, leiomyosarcoma
Skeletal muscle: Rhabdomyoma, rhabdomyosarcoma
Cartilage: Chondroma, chondrosarcoma
Bone: Osteoma, osteosarcoma, osteochondroma
Vasculature: Hemangioma, epithelioid haemangioendothelioma,
hemangiopericytoma, anaplastic hemangiopericytoma, angiosarcoma, Kaposi
sarcoma
Ewing sarcoma - PNET
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Clinical presentation and diagnosis of brain tumors
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Primary melanocytic lesions
Diffuse melanocytosis
Melanocytoma
Malignant melanoma, meningeal melanomatosis
Other neoplasms related to the meninges
Hemangioblastoma
Lymphomas and hematopoietic neoplasms
Malignant lymphomas
Plasmacytoma
Granulocytic sarcoma
Germ cell tumors
Germinoma
Embryonal carcinoma
Yolk sac tumor
Choriocarcinoma
Teratoma
Mixed germ cell tumor
Tumors of the sellar region
Craniopharyngioma
Granular cell tumor
Pituicytoma
Spindle cell oncocytoma of the adenohypophysis
Reproduced with permission from: Louis DN, Ohgaki H, Wiestler OD, Cavenee WK. WHO
Classification of Tumours of the Nervous System. IARC Press, Lyon 2007. Copyright © 2007
IARC Press.
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WHO* classification of primary brain tumors according to
histology
Most common tumors
Grade (WHO)
Astrocytic tumors
Pilocytic
1
Astrocytoma (diffuse, infiltrative, fibrillary)
2
Anaplastic
3
Glioblastoma
4
Oligodendroglial tumors and mixed gliomas
Oligodendroglioma, well differentiated
2
Anaplastic oligodendroglioma
3
Mixed oligodendroglioma/astrocytoma•
2
Mixed anaplastic oligodendroglioma/anaplastic astrocytoma•
3
Glioblastoma with oligodendroglioma component
4
Ependymal tumors
Myxopapillary ependymoma
1
Ependymoma
2
Anaplastic
3
Choroid plexus tumors
Choroid plexus papilloma
1
Choroid plexus carcinoma
3
Neuronal and mixed neuronal-glial tumors
Ganglioglioma
1-2
Central neurocytoma
2
Filum terminale paraganglioma
1
Dysembryoplastic neuroepithelial tumor (DNET)
1
Pineal parenchymal tumors
Pineocytoma
2
Pineoblastoma
4
Embryonal tumors
Medulloblastoma
4
Supratentorial primitive neuroectodermal tumor (PNET)
4
Atypical teratoid/rhabdoid tumor
4
Menigeal tumors
Meningioma
Atypical, clear cell, chordoid
1
2
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Clinical presentation and diagnosis of brain tumors
Rhabdoid, papillary, or anaplastic (malignant)
Page 18 of 27
3
* WHO: World Health Organization.
• Mixed tumors that consist of oligodendroglioma/anaplastic astrocytoma or anaplastic
oliogodendroglioma/astrocytoma are usually graded according to the highest grade component,
although there is no consensus from the WHO on this issue. Data from Pathology and Genetics
- Tumors of the Nervous System, Kleihues, P, Cavenee, WK (Eds), International Agency for
Research on Cancer, Lyon 2000.
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Neurologic presentation of brain tumors
Generalized
Focal
Headaches
Seizures
Seizures
Weakness
Nausea/vomiting
Sensory loss
Depressed level of consciousness
Aphasia
Neurocognitive dysfunction
Visual spatial dysfunction
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Initial symptoms in 565 patients with grade III or IV malignant
glioma
Symptom
Grade III, percent
Grade IV, percent
Headache
53
57
Seizure
56
23
Memory loss
26
39
Motor weakness
25
36
Visual symptoms
23
21
Language deficit
22
36
Cognitive changes
22
39
Personality changes
11
27
Change in consciousness
11
18
Nausea and vomiting
8
15
Sensory deficit
5
12
Papilledema
5
5
Data from Glioma Outcomes Project, Chang, SM, et al, JAMA 2005; 293:557.
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Mental status examination terminology
abulia: loss of initiative, willpower, or drive
acalculia: inability to calculate
agnosia: inability to recognize one or more classes of environmental stimuli, even
though the necessary intellectual and perceptual functions are intact
agraphia: inability to write
alexia: inability to read for comprehension
amnesia: inability to retain new information
anomia: inability to name objects or think of words; in practice, often used as a
synonym for dysnomia
anosognosia: inability to recognize one's own impairment
anterior aphasia: acquired language disorder in which verbal output is nonfluent
aphasia: literally, a complete loss of language function, but in practice, used as a
synonym for dysphasia
aphemia: complete loss of the ability to speak, but retained comprehension and
writing ability
apraxia: inability to perform a previously learned set of coordinated movements
even though the necessary component skills (including intellect, language function,
strength, coordination, and sensation) remain intact
Broca's aphasia: acquired language disorder characterized by nonfluent verbal
output with omission of relational words (prepositions, conjunctions, articles, and
minor modifiers) and abnormal prosody, impaired repetition, and relatively intact
comprehension
conduction aphasia: acquired language disorder characterized by prominent
impairment of repetition, relatively intact comprehension, and verbal output that is
fluent but contains literal paraphasias
delirium: an acute confusional state characterized by clouded, reduced, or shifting
attention, often associated with sensory misperception or disturbed thinking
dementia: acquired impairment of memory and at least one other cognitive
function, without clouding of the sensorium or underlying psychiatric disease
dysnomia: difficulty naming objects or finding the desired words
dysphasia: acquired disorder of language not due to generalized intellectual
impairment or psychiatric disturbance
expressive aphasia: acquired language disorder in which verbal output is nonfluent
fluent: an adjective used to describe verbal output that is normal to excessive,
easily produced, with normal phrase length (five or more words) and normal prosody
fluent aphasia: acquired language disorder in which verbal output is fluent
Gerstmann's syndrome: the constellation of (1) agraphia, (2) acalculia, (3) rightleft confusion, and (4) finger agnosia; classically associated with lesions in the
angular gyrus of the dominant hemisphere (but the subject of endless debate)
jargon: verbal output that contains so many literal paraphasias that the words are
unrecognizable
nonfluent: an adjective used to describe verbal output that is sparse, with only one
to four words per phrase
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nonfluent aphasia: acquired language disorder in which verbal output is nonfluent
paraphasia: a substitution error in which the word produced is similar in sound or
meaning to the intended word. A literal or phonemic paraphasia is a sound
substitution error resulting in production of a word that is phonemically related to the
intended word (eg, "greed" or "greeb" instead of "green"). A semantic or verbal
paraphasia is a word substitution error in which the word produced is semantically
related to the intended word (eg, "blue" instead of "green")
posterior aphasia: acquired language disorder in which comprehension is impaired
prosody: the rhythm and tempo of speech
prosopagnosia: inability to recognize faces
receptive aphasia: acquired language disorder in which comprehension is impaired
transcortical aphasia: acquired language disorder in which the ability to repeat is
intact
Wernicke's aphasia: acquired language disorder characterized by markedly
impaired comprehension and repetition, with verbal output that is fluent but
contaminated by numerous paraphasias or, in severe cases, jargon
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Clinical presentation and diagnosis of brain tumors
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Differential diagnosis of a brain mass
Primary brain tumors
Glioma
Meningioma
Pituitary adenoma
Vestibular schwannoma
Primary central nervous system lymphoma
Other
Metastatic brain tumors
Vascular disease
Cerebral hemorrhage
Vascular anomaly
Hypertensive
Intratumoral
Cerebral infarct
Embolus
Thrombosis
Infections
Abscess
Viral infection
Progressive multifocal leukoencephalopathy
Inflammatory
Multiple sclerosis
Post-infectious encephalomyelitis
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Clinical presentation and diagnosis of brain tumors
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Glioblastoma multiforme
Left: Axial T1-weighted MRI showing edematous right temporal lobe
with loss of sulci and gray-white demarcation. Right: after gadolinium
infusion, a circular 2.5 cm x 2.5 cm area of irregular contrast
enhancement in the left temporal lobe (arrow). Courtesy of Harry
Greenberg, MD.
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Clinical presentation and diagnosis of brain tumors
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MR spectroscopy parameters
Brain process
N-Acetylaspartate
Choline
Lactate
Neoplasm
↓
↑
↑
Infarction
↓
↓
↑
Infection
↓
-
↑
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Diffuse pontine glioma
Upper left panel: axial T1 weighted MR image with contrast;
upper right panel: axial T2, weighted MR image; lower left
panel: T1 weighted sagittal MR image with contrast; lower right
panel: magnetic resonance spectra of a patient with a diffuse
pontine glioma (see arrows).
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Clinical presentation and diagnosis of brain tumors
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