1.

Meningioma

 Gejala klinis (http://emedicine.medscape.com/article/1156552-clinical)

o Meningiomas produce their symptoms by several mechanisms.

They may cause symptoms by irritating the underlying cortex,
compressing the brain or the cranial nerves, producing
hyperostosis [4] and/or invading the overlying soft tissues, or
inducing vascular injuries to the brain. [5] The signs and symptoms
secondary to meningiomas may appear or become exacerbated
during pregnancy but usually abate or improve in the postpartum
period.

 Irritation: By irritating the underlying cortex, meningiomas

can cause seizures. New-onset seizures in adults justify
neuroimaging (eg, MRI) to exclude the possibility of an
intracranial neoplasm.

 Compression: Localized or nonspecific headaches are

common. Compression of the underlying brain can give
rise to focal or more generalized cerebral dysfunction, as
evinced by focal weakness, dysphasia, apathy, and/or
somnolence.

 Stereotypic symptoms: Meningiomas in specific locations

may give rise to the stereotyped symptoms listed in the
Table. These stereotypical symptoms are not
pathognomonic of meningiomas in these locations; they
may occur with other conditions or lesions. Conversely,
meningiomas in these locations may remain asymptomatic
or produce other unlisted symptoms.

Location Stereotypical Symptoms

Parasagittal Monoparesis of the contralateral leg

Subfrontal Change in mentation, apathy or disinhibited behavior, urinary

incontinence

Olfactory groove Anosmia with possible ipsilateral optic atrophy and contralateral
papilledema (this triad termed Kennedy-Foster syndrome)

Cavernous Sinus Multiple cranial nerve deficits (II, III, IV, V, VI), leading to
decreased vision and diplopia with associated facial numbness
Occipital lobe Contralateral hemianopsia

Cerebellopontine Decreased hearing with possible facial weakness and facial

angle numbness

Spinal cord Localized spinal pain, Brown-Sequard (hemispinal cord)

syndrome

Optic nerve Exophthalmos, monocular loss of vision or blindness, ipsilateral

dilated pupil that does not react to direct light stimulation but
might contract on consensual light stimulation; often,
monocular optic nerve swelling with optociliary shunt vessels

Sphenoid wings Seizures; multiple cranial nerve palsies if the superior orbital
fissure involved

Tentorial May protrude within supratentorial and infratentorial

compartments, producing symptoms by compressing specific
structures within these 2 compartments

Foramen Paraparesis, sphincteric troubles, tongue atrophy associated

Magnum with fasciculation

 Vascular: This presentation, although rare, should be

considered. Meningiomas of the skull base may narrow
and even occlude important cerebral arteries, possibly
presenting either as transient ischemic attack (TIA)–like
episodes or as stroke.

 Miscellaneous

 Intraventricular meningiomas may present with

obstructive hydrocephalus.

 Meningiomas in the vicinity of the sella turcica may

produce panhypopituitarism.

 Meningiomas that compress the visual pathways

produce various visual field defects, depending on
their location.

 Rarely, chordoid meningiomas can present with

hematologic disturbances, namely Castleman
syndrome.

o Pemeriksaan Fisik
 The physical findings mirror the aforementioned
symptoms and include signs due to raised intracranial pressure,
involvement of cranial nerves, compression of the underlying
parenchyma, and involvement of bone and subcutaneous tissues
by the meningioma.

 Raised intracranial pressure leads to papilledema,

decreased mentation and, ultimately, to brain herniation.

 Involvement of the cranial nerves may lead to anosmia,

visual field defects, optic atrophy, diplopia, decreased
facial sensation, facial paresis, decreased hearing,
deviation of the uvula, and hemiatrophy of the tongue.

 Compression of the underlying parenchyma may give rise

to pyramidal signs that are exemplified by pronator drift,
hyperreflexia, positive Hoffman sign, and presence of the
Babinski sign. Parietal-lobe syndrome may occur if the
parietal lobes are compressed.

 Compression of the dominant (usually left) parietal

lobe may give rise to Gerstmann syndrome:
agraphia, acalculia, right-left disorientation, and
finger agnosia.

 Compression of the nondominant (usually right)

parietal lobe leads to tactile and visual extinction
and neglect of the contralateral side.

 Compression of the occipital lobes leads to a

congruent homonymous hemianopsia.

 Spinal meningiomas may give rise to a Brown-Sequard

syndrome (ie, contralateral decreased pain sensation,
ipsilateral weakness, decrease in position sense),
sphincteric weakness and, ultimately, complete
quadriparesis or paraparesis.

 Ganas atau nggak (survival rate)

(http://emedicine.medscape.com/article/1156552-overview#a6)

o Benign

o Estimates of the 5-year survival usually range from 73-94%

 Epidemiology (http://emedicine.medscape.com/article/1156552-
overview#a6)

o Meningiomas afflict women more often than men. The male-to-

female ratio ranges from 1:1.4 to 1:2.8.
  The female preponderance may be less pronounced in the
black population than in other groups.

 Meningiomas are equally distributed between boys and

girls (mksdnya pada anak kecil).

o The incidence increases with age. Ages and corresponding

incidence rates reported from 2002 are as follows:

 Age 0-19 years - 0.12

 Age 20-34 years - 0.74

 Age 35-44 years - 2.62

 Age 45-54 years - 4.89

 Age 55-64 years - 7.89

 Age 65-74 years - 12.79

 Age 75-84 years - 17.04

 Age 85 years and older - 18.86

o The incidence rate varies by race, with blacks having a 1.2-fold

higher incidence than whites (Ostrom QT, Gittleman H, Fulop J, et
al. CBTRUS Statistical Report: Primary Brain and Central Nervous
System Tumors Diagnosed in the United States in 2008-2012.
Neuro Oncol 2015; 17 Suppl 4:iv1.)

 Risk Faktor (https://www.uptodate.com/contents/epidemiology-

pathology-clinical-features-and-diagnosis-of-meningioma)

o Ionizing radiation

 Radiation therapy for malignancy (Radiation therapy for

primary malignancies of the central nervous system,
Radiation therapy for tumors in the head and neck region,
Prophylactic craniospinal irradiation to prevent central
nervous system (CNS) relapse as a component of
treatment for acute leukemia or other malignancy)

o Incidental radiation exposure (Dental radiographs, diagnostic head

computed tomography, atomic bomb exposure)

o Genetic predisposition — A genetic predisposition to meningioma

is best characterized in patients with neurofibromatosis type 2
(NF2) and schwannomatosis. Patients with multiple endocrine
neoplasia type 1 (MEN1) also have an increased risk of
meningioma, although at lower rates compared with
neurofibromatosis.
 o Hormonal factors

o Breast cancer

o Obesity

 gambaran CTscan dan MRI

http://emedicine.medscape.com/article/1156552-workup#c5

https://www.uptodate.com/contents/epidemiology-pathology-clinical-
features-and-diagnosis-of-meningioma

o CT

 They are smooth in contour, adjacent to dural structures,

and sometimes calcified or multilobulated.

 On plain head CT scans, meningiomas are usually dural-

based tumors that are isoattenuating to slightly
hyperattenuating.

 Isointensity with normal surrounding brain may make

diagnosis difficult on a non-contrasted scan, but
intravenous contrast administration results in uniformly
bright enhancement.

 They enhance homogeneously and intensely after the

injection of iodinated contrast material.

 Perilesional edema may be extensive. Hyperostosis and

intratumoral calcifications may be present.

 The tumor compresses the brain without invading it.

 Multiple meningiomas may be difficult to differentiate

from metastasis.

o MRI

 On MRI, a typical meningioma is an extra-axial, dural-based

mass that is isointense or hypointense to gray matter on
T1 and isointense or hyperintense on proton density and
T2 weighted images.

 If a meningioma is suspected, obtaining an enhanced MRI

is imperative.

 Meningiomas enhance intensely and homogeneously after

injection of gadolinium gadopentetate.

 The edema may be more apparent on MRI than on CT

scanning.
  Most meningiomas show a characteristic marginal dural
thickening that tapers peripherally (the "tail" sign)

o Cystic meningiomas may exhibit intratumoral or peritumoral cysts.

The peritumoral cysts may actually represent a gliotic response
and may not necessitate surgical extirpation.

o Endovascular angiography allows the surgeon to preoperatively

determine the vascularization of the tumor and its encroachment
on vital vascular structures.

o Late venous images are important to determine the patency of

the involved dural sinuses.

o Angiographic features of meningiomas include the following:

 Supply from the external circulation

 Mother-in-law blush (which comes early and leaves late)

 Sunburst or radial appearance of the feeding arteries

DD: (https://www.uptodate.com/contents/epidemiology-pathology-
clinical-features-and-diagnosis-of-meningioma)

o lymphoma, plasmacytoma, metastatic carcinoma, melanocytic

neoplasms, solitary fibrous tumor, gliosarcoma, inflammatory
lesions such as sarcoidosis and granulomatosis with polyangiitis,
and infections such as tuberculosis

2. Glioma

a. Astrocytoma

o Gejala klinis
 The type of neurological symptoms that result from an
astrocytoma depends foremost on the site and extent of
tumor growth in the central nervous system (CNS). Onset
of any of the following symptoms should alert the clinician
to the presence of a neurological disorder and indicate a
requirement for further investigation (in particular, with
imaging studies such as magnetic resonance imaging [MRI]
or computed tomography [CT] scan, with and without
contrast):

 Altered mental status

 Cognitive impairment

 Headaches

 Visual disturbances

 Motor impairment

 Seizures

 Sensory anomalies

 Ataxia

 Astrocytomas of the spinal cord or brainstem are less

common. Patients with these neoplasms present with
motor/sensory or cranial nerve deficits referable to the
tumor's location.

 Physical Exam

 A detailed neurological examination is required for

the proper evaluation of any patient with an
astrocytoma. Because these tumors may affect any
part of the CNS, including the spinal cord, and may
spread to distant regions of the CNS, a thorough
physical examination referable to the entire
neuraxis is necessary to define the location and
extent of disease.

 Special attention should be paid to manifestations

of increased intracranial pressure (ICP), such as the
following, to determine the risk of mass effect,
hydrocephalus, and herniation:

o Headache

o Nausea and vomiting

 o Decreased alertness

o Cognitive impairment

o Papilledema

o Ataxia

 Localizing and lateralizing signs, including cranial

nerve palsies, hemiparesis, sensory levels,
alteration of deep tendon reflexes (DTRs), and the
presence of pathological reflexes (eg, Hoffman and
Babinski signs), should be noted. Once neurological
abnormalities are identified, imaging studies should
be sought for further evaluation.

o Ganas atau nggak (survival rate)

http://emedicine.medscape.com/article/283453-overview#a6

 Typical ranges of survival from the time of diagnosis are as

follows:

 Pilocytic astrocytomas (WHO grade I): >10 years

 Low-grade diffuse astrocytomas (WHO grade II) [9]

: >5 years

 Anaplastic astrocytomas (WHO grade III): 2-5 years

 Glioblastoma (WHO grade IV): ~1 year

o Epidemiology (http://emedicine.medscape.com/article/283453-
overview#a6)

 Sex

 No clear sex predominance has been identified in

the development of pilocytic astrocytomas. A slight
male predominance, with a male-to-female ratio of
1.18:1 for development of low-grade astrocytomas,
has been reported. A more significant male
predominance, with a male-to-female ratio of
1.87:1 for the development of anaplastic
astrocytomas, has been identified.

 Age

 In most cases, patients with pilocytic astrocytoma

present in the first 2 decades of life. In contrast, the
peak incidence of low-grade astrocytomas,
representing 25% of all cases in adults, occurs in
people aged 30-40 years. Ten percent of low-grade
 astrocytomas occur in people younger than 20
years; 60% of low-grade astrocytomas occur in
people aged 20-45 years; and 30% of low-grade
astrocytomas occur in people older than 45 years.
The mean age of patients undergoing a biopsy of
anaplastic astrocytoma is 41 years.

o Risk Faktor kalo ada

o CT (http://emedicine.medscape.com/article/336695-overview#a2)

 The appearance of astrocytomas on CT scans partly

depends on their grade. Low-grade astrocytomas typically
appear as homogeneous areas of decreased attenuation.
They are relatively well circumscribed and 20% have
associated calcification. Although low-grade tumors usually
do not enhance, rare tumors demonstrate minimal
enhancement. [13]

 Specific low-grade tumors have imaging characteristics

that can increase the specificity of CT scanning. Pilocytic
astrocytomas often appear as a cystic lesion with an
eccentric mural nodule that strongly enhances after the
administration of contrast agent. Subependymal giant-cell
astrocytomas are typically near the foramen of Monro and
usually occur in patients with tuberous sclerosis.
Pleomorphic xanthoastrocytomas are typically
supratentorial, cortically based masses with strong
heterogeneous enhancement. The adjacent dura and
meninges often enhance, creating the dural-tail
appearance.

 Grade III astrocytomas appear more heterogeneous.

Edema is often appreciated, calcification is rare, and the
enhancement pattern is usually more pronounced.

 Grade IV astrocytomas are even more heterogeneous than

tumors of other grades on CT scans, and they almost
always enhance strongly. Hemorrhage and necrosis are
common, but calcification is not. Extensive edema and
mass effect are usually appreciated. This grade often
involves both hemispheres by spreading by means of the
corpus callosum or commissures.

 With CT scanning, the scarcity of edema and mass effect

with low-grade lesions may make the true extent of
pathology difficult to ascertain. Furthermore, small lesions
may not be visible if contrast material is not used.
 o MRI (http://emedicine.medscape.com/article/336695-
overview#a3)

 Low-grade astrocytomas are typically hyperintense on T2-

weighted images. On T1-weighted images, most low-grade
astrocytomas are hypointense relative to white matter.
Contrast enhancement may be absent or, at best, mild.
Exceptions include the mural nodule of pilocytic
astrocytoma and the strong heterogeneous enhancement
of pleomorphic xanthoastrocytomas. Astrocytomas are
often associated with enhancement of the adjacent dura
and meninges, giving the dural-tail appearance. MRS
typically show an elevated Cho peak and decreased NAA
peak. An elevated Cho-Cr ratio or a depressed NAA-Cr ratio
suggests tumor. This holds true for all high-grade tumors
and many, but not all, low-grade tumors. (Some low-grade
tumors may not have an elevated Cho peak.) Perfusion
MRI studies fail to demonstrate increased rCBV.

 No surrounding edema

 Grade III astrocytomas often invade structures without

destroying them, causing their ill-defined borders. The
mass is inhomogeneous and bright on T2-weighted images.
Surrounding edema and/or tumor infiltration is usually
appreciated. Enhancement is usually seen. Perfusion MRI
demonstrates increased relative cerebral flow volume.

 Grade IV astrocytomas (GBM) are usually discovered as

bulky disease, and necrosis is a hallmark of this grade.
These lesions usually enhance peripherally, in a nodular
and irregular manner, and they cause a large amount of
mass effect and edema. These tumors often cross the
corpus callosum, giving them a typical butterfly shape.
Areas of hemorrhage and necrosis are common, and
spectroscopy demonstrates high Cho, high lactate, high
lipid, and low NAA values. Short–echo time (TE) studies
demonstrate an absent or low myo-inositol peak. Perfusion
studies demonstrate elevated rCBV.

i. Grade I

ii. Grade II

iii. Grade III

iv. Grade IV

b. Oligodendroglioma
 Gejala klinis (http://emedicine.medscape.com/article/1156699-
clinical)

o Like other intracranial space-occupying lesions,

oligodendrogliomas present with focal cerebral
dysfunction, depending on location, and rarely as
increased intracranial pressure.

o Most oligodendrogliomas present as a single lesion in the

cerebral hemispheres.

o Typically, they are cortical or subcortical; they rarely are

found in deep gray structures, and occasionally they may
be primarily intraventricular.

o Rarely, they can occur infratentorially or in the spinal cord.

o Occasionally they may be multifocal, like other gliomas.

o The most common presenting symptom is seizure,

observed at diagnosis in as many as half of patients. As
many as 80% of patients have seizures at some time during
their illness.

o Depending on the location of the tumor, the seizure can be

simple partial, complex partial, or generalized.

o Previously undiagnosed oligodendrogliomas may be

identified with medically refractory epilepsy.

o Occasionally patients with oligodendrogliomas are brought

to medical attention for headache, symptoms of increased
intracranial pressure, or focal neurological deficits.

o Tumors that arise within the ventricles may cause

obstructive hydrocephalus and are more likely to
disseminate through the cerebrospinal fluid (CSF). Rarely,
they can metastasize outside the nervous system,
especially the anaplastic oligodendroglioma.

o In long-surviving patients with 1p/19q co-deletion,

indolent leptomeningeal disease may be a complication of
oligodendroglioma, which may have implications for the
treatment. [2, 3]

o Occasional patients present with strokelike transient

ischemic attacks or with intracerebral hemorrhage.

o Physical exam

Physical findings depend on the location of the tumor.

  Frontal, parietal, and temporal lobe tumors most
commonly present with seizures. Seizures may be
simple, complex partial, and even generalized.

 Frontoparietal tumors may present with

hemiparesis and sensory neglect.

 Sensory neglect is pronounced in right

hemispheric lesions.

 Temporal lobe tumors rarely may present

with visual field defects, although patients
may be unaware of hemianopsia.

 Rare intraventricular oligodendroglioma may

present with signs and symptoms of increased
intracranial pressure such as headache, visual
disturbance, and papilledema.

 Posterior fossa oligodendrogliomas are uncommon.

However, well-documented cases are described in
children and may present with cerebellar ataxia
and increased intracranial pressure.

 Ganas atau nggak (survival rate)

http://emedicine.medscape.com/article/1156699-overview#a6

o The morbidity and mortality profile for oligodendrogliomas

is much better than for astrocytic tumors. However, it also
depends on tumor location and pressure effects, as with
any other intracranial lesion. The median survival from
initial diagnosis of all low-grade oligodendrogliomas (LGOs)
is 4-10 years, but it is only 3-4 years for anaplastic
oligodendrogliomas.

 Epidemiology (http://emedicine.medscape.com/article/1156699-
overview#a6)

o Sex

 Oligodendrogliomas occur in both sexes, with a

male-to-female predominance of 2:1.

o Age

 Oligodendrogliomas may be diagnosed at any age

but occur most commonly in young and middle-
aged adults, with a median age at diagnosis of 40-
50 years. In children, only 6% of gliomas are
diagnosed as oligodendrogliomas.
 Risk Faktor kalo ada

 gambaran CTscan dan MRI

o CT (http://emedicine.medscape.com/article/342958-
overview#a2)

 CT scans reveal a hypodense, reasonably well-

demarcated mass with moderate surrounding
edema.

 Intratumoral calcification is common, and

hemorrhage is noted occasionally.

 As with contrast MRI, the tumor does not enhance

unless it is behaving unusually aggressively or has
an anaplastic astrocytic component.

 Oligodendrogliomas are the brain tumors with the

highest frequency of calcification. CT scanning must
be performed before and after the injection of
contrast material to avoid missing the presence of
calcifications. Typically, a round or oval, well-
limited, and fairly large peripheral lesion is
revealed. The tumor matrix is either
hypoattenuating or isoattenuating and occasionally
hyperattenuating because of tumoral hemorrhage
or calcification.

 Calvarial erosion in association with slow-growing,

peripherally located oligodendrogliomas is
occasionally noted. Calvarial erosion also appears
to be independent of the tumor grade. Contrast
enhancement is sometimes difficult to visualize
because of the presence of calcification.

 Tumoral calcification, seen in approximately 40% of

patients, is better defined on CT scans than on
MRIs. It seems to have no direct correlation with
the tumor grade.

o MRI (http://emedicine.medscape.com/article/342958-
overview#a3)

 MRI (with and without gadolinium) is the preferred

modality.

 T1 images generally demonstrate a hypointense or

mixed hypointense and hyperintense mass.
 T2 images reveal a hyperintense mass with or
without surrounding edema.

 With contrast administration, the LGO generally

does not enhance, while an anaplastic
oligodendroglioma does enhance. These tumors
also tend toward calcification.

 A number of features on neuroimaging can suggest

a diagnosis of an oligodendroglial tumor or provide
information about the possible status of
chromosomes 1p and 19q. These include:
(https://www.uptodate.com/contents/clinical-
features-pathology-and-prognostic-factors-for-
oligodendroglial-tumors)

 Low-grade oligodendroglial tumors – On

MRI, typical low-grade tumors show
increased signal intensity on T2-weighted
images without enhancement [3]. On CT,
these tumors appear as low-density masses
without enhancement. Calcifications are
suggestive, but not specific, for
oligodendrogliomas and oligoastrocytomas,
and may be more frequent in tumors with
1p/19q co-deletion [4].

 Anaplastic oligodendroglial tumors – On

MRI and CT, most anaplastic
oligodendroglial tumors are characterized
by some contrast enhancement, which
presumably reflects microvascular
proliferation. However, the absence of
contrast enhancement does not exclude an
anaplastic tumor and some patchy contrast
enhancement can be observed in low-grade
tumors [4].

 1p/19q co-deleted tumors – Findings on

MRI may suggest the presence of 1p/19q
co-deletion in oligodendroglial tumors [4].
Contrast enhancement of 1p/19q co-
deleted tumors is often patchy and
homogeneous, as opposed to the ring-like
enhancement with necrosis typically seen in
high-grade (grade IV) tumors without
1p/19q deletion. In addition, tumors with
the 1p/19q co-deletion often have indistinct
borders and mixed signal intensity on T1-
 and T2-weighted images, whereas tumors
without 1p/19q co-deletion typically have a
distinct border and a uniform signal on T1-
and T2-weighted images

c. Ependymoma

 Gejala klinis (http://emedicine.medscape.com/article/277621-

clinical#b4)

o The clinical history associated with ependymomas varies

depending upon the age of the patient and the location of
the lesion. The duration of symptoms prior to diagnosis
usually varies from 1-36 months; most patients have
symptoms from 3-6 months.

o For children with masses in the fourth ventricle, a history of

progressive lethargy, headache, nausea, and vomiting may be
experienced secondary to increased intracranial pressure
from obstructive hydrocephalus. As the tumor extends along
the floor of the fourth ventricle, it may cause multiple cranial-
nerve palsies (primarily VI-X), as well as cerebellar
dysfunction.

o For those children who present prior to closure of cranial

sutures, enlarging head circumference secondary to
obstructive hydrocephalus also may be part of the clinical
history.

o Supratentorial ependymomas may be associated with

increased intracranial pressure manifested as headache,
nausea, vomiting, and cognitive impairment. Headaches can
vary in intensity and quality and are frequently more severe
in the early morning or upon first awakening.

o Changes in personality, mood, and concentration can be early

indicators or may be the only abnormalities observed.
Seizures are a presenting symptom in 20% of patients, and
focal neurologic deficits may also be prominent.

o Spinal ependymomas are usually associated with a history of

progressive neurologic deficit related to involvement of
ascending or descending nerve tracts, exiting peripheral
nerves, and pain that correlates with the level of the lesion.

o Dissemination of the tumor through the cerebrospinal fluid

(CSF) is observed in fewer than 10% of patients at diagnosis
when ependymoblastomas are excluded. The incidence is
higher with infratentorial ependymomas than with
supratentorial tumors (9% vs 1.6%).
o Physical exam

 Intracranial ependymoma findings are as follows:

 Neurologic symptoms and signs affecting patients with

intracranial ependymoma can be either general or focal,
and they reflect the location of the tumor.

 At the time of diagnosis, the most common signs of

infratentorial ependymomas include papilledema and
ataxia. Nystagmus is present in 40-50% of patients at the
time of diagnosis.

 Supratentorial lesions often present as hemiparesis,

sensory loss, visual loss, aphasia, and cognitive
impairment.

 Cervical/thoracic ependymoma findings are as follows:

 Patients with spinal tumors in the upper segments of the

cervical cord can present with pain or paresthesia in the
occipital or cervical region, stiffness of the neck, and
weakness and wasting of neck muscles.

 Below the lesion, a spastic tetraplegia or hemiplegia and

weakness of the ventrolateral region may occur.

 Cutaneous sensation may be affected below the lesion

with concurrent involvement of the descending
trigeminal nucleus.

 When considering radicular symptoms associated with

cervical tumors, note that nerve roots in the cervical
region exit above the pedicle of the like-numbered
vertebra. Anatomically, the cervical nerve root exits in
close relation to the undersurface of the pedicle through
the neural foramen.

 Characteristic findings associated with various cervical

and upper thoracic levels are outlined as follows:

 C4 (paralysis of the diaphragm)

 C5 (atrophic paralysis of the deltoid, biceps, supinator

longus, rhomboid, and spinate muscles): The upper arms
hang limp at the side. The sensory level extends to the
outer surface of the arm. The biceps and supinator
reflexes are lost.

 C6 (paralysis of triceps and wrist extensors): The forearm

is held semiflexed, and a partial wrist drop is present.
 The triceps reflex is lost. Sensory impairment extends to
a line running down the middle of the arm slightly to the
radial side.

 C7 (paralysis of the flexors of the wrist and of the flexors

and extensors of the fingers): Efforts to close the hands
result in extension of the wrist and slight flexion of the
fingers (ie, preacher's hand). The sensory level is similar
to that of the sixth cervical segment but slightly more to
the ulnar side of the arm.

 C8 (atrophic paralysis of the small muscles of the hand

with resulting clawhand [main-en-griffe]): Horner
syndrome, unilateral or bilateral, results from lesions at
this level and is characterized by the triad of ptosis, small
pupil (ie, miosis), and loss of sweating on the face.
Sensory loss extends to the inner aspect of the arm and
involves the fourth and fifth fingers and the ulnar aspect
of the middle finger.

 T1: Lesions rarely cause motor symptoms because this

nerve root provides little functional innervation of the
small hand muscles. Other signs of cervical tumors
include nystagmus, especially with tumors in the upper
segment. This condition is presumably caused by damage
to the descending portion of the median longitudinal
fasciculus. Horner syndrome may be found with
intramedullary lesions in any portion of the cervical cord
if the descending sympathetic pathways are affected.

 Thoracic ependymoma findings are as follows:

 Unlike the cervical or lumbar region of the cord, where

motor dysfunction is easily discernible, tumors in the
thoracic region are localized more by the sensory
examination.

 Determining the location of lesions in the upper half of

the thoracic cord by testing the strength of intercostal
muscles is difficult.

 The Beevor sign, in which the umbilicus moves upward

when the supine patient attempts to flex the head on the
chest against resistance, can be used to localize lesions
below T10.

 Abdominal skin reflexes usually are absent below the

lesion.

 Lumbar ependymoma findings are as follows:

  The location of a lumbar lesion can be deduced easily
from the patient's root level of sensory loss and
associated motor weakness.

 Radicular pain and weakness are associated with nerve

root compression. In the lumbar region, the nerve root
exits below and in close proximity to the pedicle of its
like-numbered vertebra with the intervertebral disc
space situated well below the pedicle.

 Tumors that compress only the first and second lumbar

segments cause loss of the cremasteric reflexes. The
abdominal reflexes are preserved, while knee and ankle
jerks are increased.

 If the tumor affects the third and fourth segments of the

lumbar cord and does not involve the roots of the cauda
equina, weakness of the quadriceps, loss of the patellar
reflexes, and hyperactive Achilles reflexes occur. More
commonly, lesions at this level also involve the cauda
equina with resulting flaccid paralysis of the legs as well
as loss of knee and ankle reflexes.

 If the spinal cord and cauda equina are affected

concurrently, spastic paralysis of one leg with increased
ankle reflexes ipsilaterally and flaccid paralysis with loss
of reflexes contralaterally may occur.

 Ganas atau nggak (survival rate)

(http://emedicine.medscape.com/article/277621-overview#a6)

o Depending on the patient population, the reported 10-year

overall survival rate for ependymoma can vary from 45-55%.

o The current 5-year survival rate for patients with intracranial

ependymomas is approximately 50%, when rates from
children and adults are combined.

o Stratification based on age reveals 5-year survival rates of

76% in adults and 14% in children.

 Epidemiology (http://emedicine.medscape.com/article/277621-
overview#a6)

o Race

Grade II and III ependymoma are more common in black

Americans than white Americans. [25]

o Sex
 The incidence of ependymoma is approximately equal in
males and females.

o Age

Ependymomas generally present in young children with a

mean age of diagnosis of 4 years, yet 25-40% of patients are
younger than 2 years. Spinal ependymomas are most
common in patients aged 15-40 years, most of which are of a
myxopapillary subtype. Intracranial tumors are seen more
often in children, particularly in the infratentorial
compartment.

 Risk Faktor kalo ada

(https://www.uptodate.com/contents/ependymoma)

o The etiologic factors responsible for the development of

ependymoma are not known. A link to exposure to simian
virus 40 was postulated based upon identification of the virus
in tumor tissue. However, a causal relationship has not been
confirmed, and SV40 is no longer considered either a risk
factor or an etiologic agent in the development of
ependymoma. (See "Risk factors for brain tumors", section on
'Viral infection'.)

o There is an increased association of intramedullary spinal

cord ependymoma in patients with neurofibromatosis type II
(NF2) [3,4], although abnormalities in the NF2 gene have not
been identified in the majority of sporadic ependymoma
patients

 CT

o The CT appearance is often hyperdense with homogeneous

enhancement; cysts and calcifications are common. The
presence of calcifications within a tumor located in the fourth
ventricle is highly suggestive but not diagnostic of
ependymoma.
(https://www.uptodate.com/contents/ependymoma)

o Intracranial ependymomas are typically isodense on

unenhanced CT scans with minimal to moderate
enhancement upon contrast administration. Calcification can
be noted on unenhanced CT scans in approximately one half
of cases. Cyst formation is common in these tumors, and
foraminal spread can be observed in posterior fossa lesions
through the foramina of Luschka and Magendie.
(http://emedicine.medscape.com/article/277621-
workup#c4)
  MRI (https://www.uptodate.com/contents/ependymoma)

o On MRI, these tumors have a hypointense appearance on T1,

and are hyperintense on T2 or proton density images;
gadolinium enhancement is usually prominent (image 1A-D)
[31].

o Extension into the foramen of Luska is commonly observed.

o Spinal ependymoma
(http://emedicine.medscape.com/article/277621-
workup#c4)

 Most intramedullary tumors are isointense or slightly

hypointense to the surrounding spinal cord on T1-
weighted images. Often, only subtle spinal cord
enlargement is evident. T2-weighted images are more
sensitive because most tumors are hyperintense to the
spinal cord on these pulse sequences. T2 studies are not
particularly specific and may not distinguish the solid
tumor from polar cysts. Nearly all intramedullary
neoplasms enhance on T1-weighted contrast
examinations.

 Ependymomas usually demonstrate uniform contrast

enhancement and are located symmetrically within the
spinal cord. Polar cysts are identified in the majority of
cases, particularly in the setting of cervical or
cervicothoracic tumors. Heterogeneous enhancement
from intratumoral cysts or necrosis can also be observed.

 In some cases, contrast enhancement of a cystic

ependymoma may be minimal. In these cases,
distinguishing these tumors from intramedullary
astrocytomas is difficult.

 DD: (https://www.uptodate.com/contents/ependymoma)

The differential diagnosis for tumors that present in the posterior

fossa includes medulloblastoma, astrocytoma, and brainstem or
choroid plexus tumors. In the supratentorial location, glial
tumors, embryonal tumors (ETs), and choroid plexus carcinoma or
papilloma should be considered.

d. Mixed Oligoastrocytoma

 Gejala klinis

o
  Ganas atau nggak (survival rate)

 Epidemiology

 Risk Faktor kalo ada

 gambaran CTscan dan MRI

o menyerap kontras apa ga

o hyper/hypo intense/dense

o lokasi nya bisa dimana aja

o ciri khas lain (tidak menyebrang falx, ada edema perifocal

ato ga)

3. Schwannoma

 Gejala klinis (https://www.uptodate.com/contents/vestibular-

schwannoma-acoustic-neuroma)

Symptoms associated with vestibular schwannoma can be due to cranial

nerve involvement, cerebellar compression, or tumor progression.

o Cochlear nerve — Symptomatic cochlear nerve involvement

occurred in 95 percent of patients [18]. The two major symptoms
were hearing loss and tinnitus. Hearing loss was present in 95
percent but only two-thirds of these patients were aware of this
limitation. The hearing loss was usually chronic, with an average
duration of about four years. Occasionally, vestibular
schwannomas can present with sudden sensorineural hearing loss.

Tinnitus was present in 63 percent with an average duration of

three years [18]. The incidence of tinnitus was higher in hearing
than in deaf patients but was also present in 46 percent of deaf
patients.

o Vestibular nerve — Involvement of the vestibular nerve occurred

in 61 percent of patients [18]. Affected patients frequently
acknowledged having unsteadiness while walking, which was
typically mild to moderate in nature and frequently fluctuated in
severity. True spinning vertigo was uncommon because these slow
growing tumors cause gradual rather than acute asymmetries in
vestibular function. In this setting, the central vestibular system
can often compensate for the gradual loss of input from one side.

The most nondescript vertiginous sensations, such as brief tilting

or veering, can suggest the presence of a vestibular schwannoma.
The decision whether to obtain an MRI for a patient with these
 symptoms depends upon clinical judgment, with no good data in
the literature about the likelihood that someone with such
symptoms harbors a schwannoma. (See "Pathophysiology,
etiology, and differential diagnosis of vertigo".)

o Trigeminal nerve — Trigeminal nerve disturbances occurred in 17

percent of patients [18]. The most common symptoms were facial
numbness (paresthesia), hypesthesia, and pain. The average
duration of symptoms was 1.3 years; the symptoms usually
occurred after hearing loss had been present for more than two
years and vestibular symptoms for more than one year. (See
"Trigeminal neuralgia".)

o Facial nerve — The facial nerve was involved in 6 percent of

patients [18]. The primary symptoms were facial paresis and, less
often, taste disturbances (due to nervus intermedius impairment).
Xerophthalmia, paroxysmal lacrimation, and xerostomia can also
be seen [19].

o Tumor progression — Other presenting signs can be the result of

tumor progression, leading to pressure on adjacent posterior fossa
structures. Very large tumors can press on the cerebellum or
brainstem and result in ataxia. Brainstem compression, cerebellar
tonsil herniation, hydrocephalus and death can occur in untreated
cases. The functions of the lower cranial nerves can also become
impaired, leading to dysarthria, dysphagia, aspiration, and
hoarseness.

 Ganas atau nggak (survival rate)

 Epidemiology (https://www.uptodate.com/contents/vestibular-
schwannoma-acoustic-neuroma)

o The median age at diagnosis is approximately 50 years

o The tumors are unilateral in more than 90 percent of cases [5],

affecting the right and left sides with equal frequency. Bilateral
vestibular schwannomas are primarily limited to patients with
neurofibromatosis type 2

 Risk Faktor (https://www.uptodate.com/contents/vestibular-

schwannoma-acoustic-neuroma)

o NF2

o Childhood exposure to low-dose radiation for benign conditions of

the head and neck

o Patients with a history of parathyroid adenoma may have an

increased risk for developing vestibular schwannomas
 o use of cellular telephones.

 gambaran CTscan dan MRI

o CT (http://emedicine.medscape.com/article/336141-overview#a3)

 On nonenhanced CT scans, most schwannomas are

isoattenuating relative to brain parenchyma. Calcification
or areas of hemorrhage are rare. On contrast-enhanced CT
scans, the enhancement pattern is typically homogeneous.
[2]

 Bone-window images can demonstrate remodeling of the

adjacent skull base, such as expansion of the IAC by
vestibular schwannomas and expansion of the facial canal
by facial schwannomas. Expansion of the jugular foramen
by CN IX, CN X, or CN XI schwannomas can also be seen.
See the image below.

 Thin-collimation CT imaging of the skull base can be helpful

in evaluating bone destruction. This finding is useful in
differentiating jugular foramen schwannomas from
paragangliomas

 CT findings can be false-negative in small lesions.

Occasionally, a false-positive diagnosis occurs because a
streak artifact in the cerebellopontine angle cistern mimics
a lesion.

o MRI (http://emedicine.medscape.com/article/336141-
overview#a4)

 Similar to CT imaging, MRI tends to depict schwannomas

as homogeneous masses. [1, 10, 18, 19] Schwannomas are
typically isointense or slightly hypointense relative to gray
matter on T1-weighted images and slightly hypointense to
CSF on T2-weighted images. Gadolinium enhancement is
typically homogeneous, although larger schwannomas can
show areas of cystic degeneration and heterogeneous
signal intensity; these findings are based on increased
numbers of areas with Antoni type B histologic features.

 High-resolution, thin-section, heavily T2-weighted, 3-

dimensional (3-D) sequences have been used to look for
acoustic neuromas. On images obtained with these
sequences, individual nerves in the cistern and internal
auditory canal (IAC) can be visualized as linear filling
defects in the bright CSF. Small masses can be identified
without the use of an intravenously administered contrast
agent.
o DD (http://emedicine.medscape.com/article/336141-
overview#a4)

 Glossopharyngeal, vagus, or accessory nerve schwannomas

are rare and difficult to distinguish from one another. The
tumors are classified on the basis of their growth patterns:
Type A lesions grow predominantly intracranially, type B
lesions grow predominantly at the jugular foramen, and
type C lesions grow predominantly extracranially. CT scan
and MRI characteristics are similar to those of other
schwannomas. In contrast to the more common
paragangliomas in this region, schwannomas expand but
do not infiltrate the adjacent bone. Unlike paragangliomas,
which infiltrate and erode adjacent bone, schwannomas
smoothly expand the bone and leave an intact cortical
margin.