Brain Tumors

Glial Cells…….Neurons
Glial Cells
What Is a Brain Tumor?
Primary vs. secondary:

 May lodge into the ff structures:

Localized vs. invasive
THEY CAN ALSO BE:
WHO GRADING SYSTEM
WHO Histologic Classification of Tumors of
the CNS
1.Tumors of Neuroepithelial Tissue
2.Tumors of Cranial and Spinal Nerves
3.Tumors of the Meninges
4.Tumors of Uncertain Histogenesis
1.Hemangioblastoma from primitive vascular
structures
5.Lymphomas and Hematopoietic Neoplasm
6.Germ Cell Tumor
1.Ex: Germinoma – common in pineal gland area
7.Cysts and Tumor-like lesions
1.Usually in the third ventricle
8.Tumors of the Sellar Regions
9.Local Extension from Regional Tumors
10.Metastatic Tumors
 What Causes a Brain Tumor?

  

Occupational exposures
Common Types of Brain Tumors

A stro cyto m a s co m e in fo u r m a jo r su b typ e s:

 ju ve n ile p ilo cytic a stro cyto m a ( g ra d e 1 )
 fib rilla ry a stro cyto m a ( g ra d e 2 )
 a n a p la stic a stro cyto m a ( g ra d e 3 )
 g lio b la sto m a m u ltifo rm e ( g ra d e 4 )
T h e h ig h e r th e g ra d e , th e m o re a g g re ssive
th e tu m o r.

Age Incidence
 Adults
- Supratentorial: 80-85%
 - Intratentorial: 15-20%
 - Children
- Intratentorial: 60%
 - Supratentorial: 40%

Clinical Presentation

 Slowly
 Progressi

ve
 Tumors
Cerebral Dysfunction
Cerebellar Dysfunction
Increased ICP
Papilledema
Course of Illness
Ancillary Procedures
Treatment of Brain Tumors
The Neurological
Rehabilitation team:
The Rehabilitation Team
The Rehabilitation Team
Common types of brain
tumors
I. GLIOMAS
- Most common primary brain tumor
- 50% of all symptomatic brain tumors
- Incidence increases with advancing age
- Peak in 8th and 9th decades
- No known environmental factors
- No behavioral lifestyle choices
- Ionizing radiation: the only clear risk factor
- Originate from glial cells or their stem cell
precursors
GLIOMAS
 Include:
 a. Astrocytoma
 b. Oligodendroglioma
 c. Ependymoma
 - WHO Classification Basis
 a. Increased cellularity
 b. Nuclear atypia
 c. Endothelial proliferation
 d. Necrosis
A. Astrocytoma
 - Most common glioma
 - Cerebral astrocytoma (more in adults)
- Behavioral changes
 - Seizures
 - Hemiparesis
 - Language difficulty
 - Cerebellar astrocytoma (more in children)
- Hemisphere
 - Ataxia
 - Brain stem (children)
- Pons
 - CN deficits
Grade I:
 Pilocytic Astrocytomas
 Primary in children &
young adults
 Focal astrocytoma may
be associated with:
Grade II:
 Diffuse or Fibrillary
Astrocytoma
 Most common in the
cerebral hemisphere in
young adults
 Low grade or benign
histologically
 Infiltrative – usually a
problem because the
tumor cannot be resected
completely if this is a
characteristic of the
tumor
 Complete resection not
possible
 Latent potential for
malignant transformation

Grade III: Anaplastic Astrocytoma
Grade IV: Glioblastoma multiforme
 Grades III and IV are high-grade gliomas
 20% of all intracranial tumors
 55% of gliomas
 80% of gliomas of the cerebral hemispheres
in adults
 Peak incidence middle to late adulthood
 Males/females = 1.61
 No familial predilection
Anaplastic Astrocytoma
 Have increased pleomorphism, enlarged nuclei
and most importantly, increased
proliferative activity that is reflected as
increased mitotic activity.
 There should be NO necrosis or endothelial
proliferation.
 Presence of either/both is suggestive of worse
biological behavior.
Glioblastoma Multiforme
 CSF seeding:
 Malignant cells in the CSF may form:

 CSF seeding implies that GBM can go to the CSF

spaces such as the subarachnoid space &
communicate with the ventricular system
 Extraneural metastasis
- To bone & lymph nodes (very rare) after a
craniotomy
 Pseudopalisading around the necrosis is common
in GBM
 Can cross the midline in a “butterfly”
pattern: this shows the aggressive nature of
this tumor because the midline is composed
of a tough dura
Glioblastoma Multiforme
Imaging: High- and Low-Grade Gliomas
 High-grade or malignant gliomas: appear as
contrast enhancing mass lesions which arise
in white matter & are surrounded by edema
 Low-grade gliomas: typically non-enhancing
lesions that diffusely infiltrate brain
tissue & may involve a large region of
brain
 Low-grade gliomas are usually best appreciated
on T2- weighted MRI scans.
Prognosis of Astrocytomas
 Median survival
 GBM: 1 year
 Anaplastic astrocytoma: 3 years
 Low-grade astrocytoma: 5 years
 Others survive a decade or more
 Most die from transformation of tumor to
higher grade
B. Oligodendroglioma
 Derived from oligodendrocytes or their
precursors
 Oligodendrocytes produce the white matter in
the brain
 5-7% of all intracranial gliomas
 Most often in the 3rd and 4th decades
 Males:females = 2:1
 Found primarily in cerebral hemispheres,
within the brain parenchyma
 Highly infiltrative
 May metastasize distantly in ventricular &
subarachnoid spaces like the GBM (CSF
seeding)
 Round regular “fried-egg” cells
Oligodendroglioma
“fried egg cells of oligodendroglioma”
Prognosis of Oligodendroglioma
 Median Survival
 Low-grade oligodendrogliomas: 8-16 years
 Anaplastic oligodendrogliomas: 5 years
 Tumors that have 1p/19q LOH—best prognosis
 Many pxs die from malignant transformation of
the tumor
C. Ependymoma
 Arise from ependymal cells (an
intraventricular tumor)
 More common in children
 10% pediatric intracranial tumors
 5% of adult intracranial tumors
 Most common in the 4th ventricle
 Ataxia, vertigo, increased ICP
 May grow in brain parenchyma without obvious
attachment to the ventricular system
 Spinal lesions more common in adults
 Intracranial ependymomas predominate in
children
Ependymoma
Histological Characteristics of Ependymoma
Prognosis
 5-year survival: 40-50%
 10-year survival: 47-68%
 Better prognosis:
 Young age
 Infratentorial
 Gross total excision
 Low-grade histology
II. MENINGIOMA
 Second most common primary brain tumor
 Originate from arachnoid cells
(meningoepithelial cap cells normally seen
in arachnoid villi)
 20% of all intracranial tumors (with
asymptomatic cases—40% or more)
 7% of all posterior fossa tumors
 3-12% of cerebellopontine angle tumors
MENINGIOMA
II. MENINGIOMA
 Most diagnosed in 6th % 7th decades
 Female: Male—3:2 to 2:1
 Multiple in 5-15% (NF-2)
 90% intracranial
 10% intraspinal
 Spinal meningioma: 10x in women
 All familial meningiomas occur with NF-2
 Rare in children (more in boys)
- Rare with dural attachments
 - Usually Intraventricular or posterior fossa
 - Commonly with sarcomatous changes
 - Frequently with NF-2

Etiology of Meningioma
Progesterone receptors
- Expressed in 80% of women with meningiomas
 - Expressed in 40% of men with meningiomas

Pathology
 Nodular tumors occasionally meningiomas en
plaque (sheer-like formation)
 Highly vascular
 Encapsulated and attached in the dura (blood
supply from external carotid artery)
 Hyperostosis of adjacent bone (bone
proliferation)
Histological Characteristics
 Benign
 Typical features:
- Whorls of arachnoid cells surrounding a
central hyaline material that eventually
calcifies to form PSAMMOMA BODIES
 - No characteristic cytologic marker
Clinical Manifestations
 Some are asymptomatic—found incidentally by
MRI
 But may have symptoms:
 Tumor location: by compression of underlying
neural structures
 Sites of predilection
diagnosis
diagnosis
 Cranial CT Scan
 Isointense or slightly hyperintense
 Hyperostosis—20%
 Isointense (65%) or hypointense (35%) in T1
and T2
 Gadolinium
 Angiography
 Hypervascular mass

 MR Angiography & Venography

Growth Rate of Meningioma
 Less than 1 cm per year (very slow growth but
can recur)
 Tumor doubling time: 1.27 to 14.35 years
Surgery
 Complete excision may cure many meningiomas
 The extent of resection is the most important
in determining recurrence
 For recurrence: reresection
Radiation Therapy
 Residual tumor after surgery
 Recurrent tumor
 Atypical or malignant histology
III. TUMORS OF THE PITUITARY GLAND
 Third most common primary
 brain tumor
 Often asymptomatic
 Incidence at autopsy:
 1.7 – 24%
 Most common in adults in
 the 3rd and 4th decade
 10% incidence in children & adolescents
 Not hereditary except MEN-1 (multiple
endocrine neoplasia)
Pathology
 Microadenoma
- Less than 1cm
 - Symptoms due to excess hormone secretion (or
hyperfunctioning)

 Macroadenoma
- More than 1cm
 - Symptoms due to compressing normal pituitary
gland and neural structure causing
hypofunctioning

Pathology
 Endocrine Active (Secretory)
- Prolactinoma

- Growth hormone

- ACTH: Cushing’s Syndrome

 - FSH and LH
 - Endocrine Inactive (Non-secretory or null
cell adenoma)
 - 10% mixed secretory tumor
Histological characteristics:
 Almost all are histologically benign
 Pituitary CA: rare
 Macroadenomas
 Pituitary Carcinoma

Macroadenomas
 May invade dural bone
 May infiltrate surrounding structure
 Locally invasive pituitary adenomas are nearly
always histologically benign
 Pleomorphism and mitotic figure insufficient
for diagnosis of carcinoma (may be seen in
benign adenomas)
 Invasive character independent of growth rate
Pituitary Carcinoma
Highly invasive
Rapidly growing & anaplastic
Unequivocal diagnosis relies on
presence of distant metastasis

Clinical Manifestations of Tumors of
the Pituitary Gland
 Compression of neural and vascular structures
 Headache
 Hypopituitarism
 Visual symptoms

 Papilledema is rare
 May enlarge with pregnancy
 5% of pituitary adenoma present with pituitary
apoplexy
Clinical Manifestations of Tumors of
the Pituitary Gland
 Optic chiasm
- Between hypothalamus & sella turcica
 - When this is compressed → bitemporal
hemianopsia
 Optic nerve
- When this is compressed → ipsilateral
blindness
 Optic tract
- When this is compressed → contralateral
homonymous hemianopsia
 Diaphragma sella
- The dura that covers sella turcica
 As tumor grows forward to the sella →
compress the basal dura → headache →
affected pain-sensitive intracranial
structures
VISUAL FIELD PATHWAYS
bitemporal hemianopsia
IPSILATERAL BLINDNESS
contralateral homonymous hemianopsia
Hypothalamus + thalamus
 - Form the lateral wall of the 3rd ventricle
 - Any pathology in the ventricular system will
cause accumulation of CSF proximal to the
block → hydrocephalus
Suprasellar region – region of the
hypothalamus
 An example of a suprasellar tumor is a
craniopharyngoma in children & adults
 A craniopharyngoma can compress the third ventricle &
cause the ff: (hydrocephalus with signs of increased
ICP)
 - Headache
 - Vomiting
 - Papilledema
 Nowadays, pituitary adenoma usually does not grow until
the region of the hypothalamus because visual
problems prompt consult & diagnosis.
 Papilledema is also rare because it manifests late in
the course of the tumor. Before that happens, patient
must have been diagnosed already
 Obstructive hydrocephalus: rare because of diagnosis at
visual problem level
Pituitary Apoplexy
 - Hemorrhage or infarction of pituitary
adenoma
 - Sudden onset of headache, nausea, vomiting,
visual loss, diplopia, altered mental status
 - Diagnosis by CT or MRI
 - Treatment emergency surgery
Diagnosis
 - X-ray – will show you ballooning of the
sella turcica
 - Cranial MRI
- Best way to evaluate pituitary pathology
Treatment
Video on Endoscopic Transsphenoidal
Surgery