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CNS I: Brain Tumour
1
SG5®
A. CEREBRAL OEDEMA (Diffuse Brain Swelling)
 Definition: Excess water in ECF (cerebral parenchyma) which results in increase in
cerebral volume!
 Classification of cerebral oedema:
I. Vasogenic: due to blood-brain barrier (BBB) dysfunction (tight junction
open), leading to increased cerebral vascular permeability
-causes of dysfunction: trauma and tumour
II. Cytotoxic: due to cellular injury to neurone and glia, leading to membrane
integrity lost and Na/K ATPase pump fails
-causes of cellular injury: ischaemia
III. Interstitial: due to damaged ventricular filling in hydrocephalus
CNS I: Brain Tumour
2
SG5®
B. HYDROCEPHALUS
 Definition: Excess water in ventricular system
 Classification of hydrocephalus:
I. Primary hydrocephalus
- Due to:
i. CSF overproduction – due to choroid plexus papilloma
ii. CSF circulation blockage – at foramen of Monro, aqueduct of Sylvius
and foramen of Luschka
iii. CSF reabsorption failure - due to arachnoid granulations
II. Secondary hydrocephalus
- Due to:
i. Loss of brain tissue (hydrocephalus ex vacuo) –due to stroke or
injury which results in shrinkage of brain
III. Congenital hydrocephalus
-Arnold-Chiari malformation:
 Tonsilar herniation
 Elongated brainstem
 Small 4th ventricle
 Tectal beaking (fusion of midbrain)
 Hydrocephalus
CNS I: Brain Tumour
3
SG5®
C. BRAIN TUMOUR (all brain tumours are lethal!)
 Never metastasis
 Always recur locally!
 Small volume of tumour is lethal
 Normal brain function until tumour reaches large size!
 All brain tumours potentially lethal! Irrespective of the grade
 Causes: (causes mostly unknown!)
I. Genetic:
 Tuberous sclerosis
 Neurofibromatosis
 Von Hippel-Lindau syndrome
II. Radiation
III. Familial -relatives
IV. Viral
V. Chemical
VI. Immunosuppresion
 Clinical presentations:
I. Cerebral oedema
II. Neurological deficit- progressive and focal
III. Seizure
IV. Behavioural change
V. RIP (Raised intracranial pressure!)
CNS I: Brain Tumour
4
SG5®
 Classification of CNS tumour:
Cells of origin CNS tumour
Glial cells
-Diffusely infiltrating
-Blend with surrounding brain
-Grow to large size before symptoms appear
-Prognosis:
i. Histological grade
ii. Level of patient disability
iii. Adequacy of resection
astrocytoma, oligodendroglioma (1p19q
deletion), ependymoma, glioblastoma
Arachnoidal cells Meningioma
Nerve sheath cells Schwannoma (unilateral nerve deafness),
neurofibroma
-if bilateral deafness, think of neurofibromatosis
Lymphoreticular cells Lymphoma
Primitive neuroectodermal cells (PNET) Medulloblastoma, neuroblastoma
Pinealoma and pituitary adenoma!
 Development of normal brain tissues and neoplasm of brain tissue
CNS I: Brain Tumour
5
SG5®
a) GLIOMA
1) Astrocytoma
 Classifications:
 Non-infiltrating
-Juvenile pilocytic
-Subependymal giant cell astrocytoma
-Subependymoma
 Infiltrating
-Astrocytoma (low grade) (No mitoses or necrosis)
-Anaplastic astrocytoma (Mitoses)
-Glioblastoma multiforme (Mitoses and necrosis)
 Tx:
 Surgery (resection)
-Craniotomy + maximum safe debulking
-Stereotactic volumetric resection
 Radiotherapy
-Conventional external beam
-Stereotactic radiation
-Proton beam
 Chemotherapy
-Systemic
-Direct (into the tumour):- Gliadel
 Therapeutic resistances:
 Radical resection is difficult
 Radiotherapy constraints
 Tumour heterogeneity
 Blood tumour barrier
CNS I: Brain Tumour
6
SG5®
b) TUMOUR OF ARACHNOIDAL CELLS
1) Meningioma
 Do not invade the brain
 Relatively easy to resect
 Lethal if not treated due to RIP!!!
c) PITUITARY ADENOMA
 Classifications:
 Macroadenoma
-Compress optic nerve bilateral hemianopia
 Microadenoma
-Hypo and hyper secretions
d) CHILDHOOD BRAIN TUMOURS
 more devastating than adult
 70% below tentorium
 Treatments have negative impacts on developing nervous system
 Endocrine effects
 Psychological effects
 Behavioural effects
 Development effects
 Classifications:
i. Cerebellar astrocytoma (morning headache and vomiting)
 Cystic
 Easily resected!
 No need additional therapy
 Excellent long term survival
ii. Brain stem astrocytoma
 Impossible to resect!
Craniopharyngioma/Rathke’s
pouch tumour – tumour of
pituitary gland of embryonic
tissue
4C’s
 Childhood
-growth retardation and
blindness
 Cystic
 Calcified
 Cholesterol in cyst
CNS I: Brain Tumour
7
SG5®
 Consequences:
-Major neurological defects
-Obstructive hydrocephalus
 Low grade
 Palliative care indicated
iii. Medulloblastoma (PNET)
 Pluripotent stem cell
 Divergent differentiation

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Cns i brain tumours

  • 1. CNS I: Brain Tumour 1 SG5® A. CEREBRAL OEDEMA (Diffuse Brain Swelling)  Definition: Excess water in ECF (cerebral parenchyma) which results in increase in cerebral volume!  Classification of cerebral oedema: I. Vasogenic: due to blood-brain barrier (BBB) dysfunction (tight junction open), leading to increased cerebral vascular permeability -causes of dysfunction: trauma and tumour II. Cytotoxic: due to cellular injury to neurone and glia, leading to membrane integrity lost and Na/K ATPase pump fails -causes of cellular injury: ischaemia III. Interstitial: due to damaged ventricular filling in hydrocephalus
  • 2. CNS I: Brain Tumour 2 SG5® B. HYDROCEPHALUS  Definition: Excess water in ventricular system  Classification of hydrocephalus: I. Primary hydrocephalus - Due to: i. CSF overproduction – due to choroid plexus papilloma ii. CSF circulation blockage – at foramen of Monro, aqueduct of Sylvius and foramen of Luschka iii. CSF reabsorption failure - due to arachnoid granulations II. Secondary hydrocephalus - Due to: i. Loss of brain tissue (hydrocephalus ex vacuo) –due to stroke or injury which results in shrinkage of brain III. Congenital hydrocephalus -Arnold-Chiari malformation:  Tonsilar herniation  Elongated brainstem  Small 4th ventricle  Tectal beaking (fusion of midbrain)  Hydrocephalus
  • 3. CNS I: Brain Tumour 3 SG5® C. BRAIN TUMOUR (all brain tumours are lethal!)  Never metastasis  Always recur locally!  Small volume of tumour is lethal  Normal brain function until tumour reaches large size!  All brain tumours potentially lethal! Irrespective of the grade  Causes: (causes mostly unknown!) I. Genetic:  Tuberous sclerosis  Neurofibromatosis  Von Hippel-Lindau syndrome II. Radiation III. Familial -relatives IV. Viral V. Chemical VI. Immunosuppresion  Clinical presentations: I. Cerebral oedema II. Neurological deficit- progressive and focal III. Seizure IV. Behavioural change V. RIP (Raised intracranial pressure!)
  • 4. CNS I: Brain Tumour 4 SG5®  Classification of CNS tumour: Cells of origin CNS tumour Glial cells -Diffusely infiltrating -Blend with surrounding brain -Grow to large size before symptoms appear -Prognosis: i. Histological grade ii. Level of patient disability iii. Adequacy of resection astrocytoma, oligodendroglioma (1p19q deletion), ependymoma, glioblastoma Arachnoidal cells Meningioma Nerve sheath cells Schwannoma (unilateral nerve deafness), neurofibroma -if bilateral deafness, think of neurofibromatosis Lymphoreticular cells Lymphoma Primitive neuroectodermal cells (PNET) Medulloblastoma, neuroblastoma Pinealoma and pituitary adenoma!  Development of normal brain tissues and neoplasm of brain tissue
  • 5. CNS I: Brain Tumour 5 SG5® a) GLIOMA 1) Astrocytoma  Classifications:  Non-infiltrating -Juvenile pilocytic -Subependymal giant cell astrocytoma -Subependymoma  Infiltrating -Astrocytoma (low grade) (No mitoses or necrosis) -Anaplastic astrocytoma (Mitoses) -Glioblastoma multiforme (Mitoses and necrosis)  Tx:  Surgery (resection) -Craniotomy + maximum safe debulking -Stereotactic volumetric resection  Radiotherapy -Conventional external beam -Stereotactic radiation -Proton beam  Chemotherapy -Systemic -Direct (into the tumour):- Gliadel  Therapeutic resistances:  Radical resection is difficult  Radiotherapy constraints  Tumour heterogeneity  Blood tumour barrier
  • 6. CNS I: Brain Tumour 6 SG5® b) TUMOUR OF ARACHNOIDAL CELLS 1) Meningioma  Do not invade the brain  Relatively easy to resect  Lethal if not treated due to RIP!!! c) PITUITARY ADENOMA  Classifications:  Macroadenoma -Compress optic nerve bilateral hemianopia  Microadenoma -Hypo and hyper secretions d) CHILDHOOD BRAIN TUMOURS  more devastating than adult  70% below tentorium  Treatments have negative impacts on developing nervous system  Endocrine effects  Psychological effects  Behavioural effects  Development effects  Classifications: i. Cerebellar astrocytoma (morning headache and vomiting)  Cystic  Easily resected!  No need additional therapy  Excellent long term survival ii. Brain stem astrocytoma  Impossible to resect! Craniopharyngioma/Rathke’s pouch tumour – tumour of pituitary gland of embryonic tissue 4C’s  Childhood -growth retardation and blindness  Cystic  Calcified  Cholesterol in cyst
  • 7. CNS I: Brain Tumour 7 SG5®  Consequences: -Major neurological defects -Obstructive hydrocephalus  Low grade  Palliative care indicated iii. Medulloblastoma (PNET)  Pluripotent stem cell  Divergent differentiation