Rarely do intracranial tumours produce headache until

quite large. Raised intracranial

pressure is apparent in the history. Epilepsy is a cardinal
symptom of intracerebral space
occupying lesions, and loss of consciousness should be
viewed very seriously. In all
likelihood, focal neurological signs are present. Problems are
more likely to occur with
slowly growing tumours, especially those in neurologically
"silent" areas of the frontal lobes.
Subtle personality change may result in treatment for
depression, with headache attributed to
it. Investigation may be prompted eventually by non-
response to treatment, but otherwise
some of these can be very difficult to pick up, whilst their
infrequency does not justify
routine brain scanning. Fundoscopic examination is
mandatory at first presentation with
headache, and it is always worthwhile to repeat it during
follow-up.
The signs of fever and neck stiffness usually accompanying
meningitis, in an obviously ill
patient, demand urgent referral to specialist care. Headache
may be generalised or frontal,
perhaps radiating to the neck, and accompanied later by
nausea and disturbed consciousness.

………………………………………………………………………………
………………..INTRA CRANIAL SPACE OCCUPYING LESIONS
DR.Bindu. K BHMS,MD(HOM)

These are lesions which expand in volume to displace normal

neural structures & lead to increase in intra – cranial
pressure.

PATHOLOGY :-
Symptoms are produced due to,
1. Irritation & destruction of brain tissue causing
 neurological phenomena,eg. epilepsy, paralysis.

2. Raised intra cranial pressure:- The rate of increase of

tension depend on the nature of the lesion and its location.
Posterior fossa lesions lead to more rapid rise in tension
than supratentorial lesions.

3. False localizing signs :-

• Neurological phenomena arising from the secondary
effects of lesion like herniation of neural tissue under the
falx-cerebri or downward herniation through tentorium
cerebelli or foramen magnum, pressure effects on other
parts of brain develop.
• Countre – coup effect:- This is pressure effect caused on
the side opposite to the side of lesion when a space
occupying lesion expands. The midline structures such as
brainstem may be pushed towards the opposite free margin
of tentorium cerebelli to give rise to compression of normal
side also.

In addition to this , different lesions may produce symptoms

specific to their nature like fever in case of brain abscess,
signs of meningeal irritation in subarachnoid haemorrhage

Classification of intra cranial space occupying

lesions :-
I. Congenital :- Dermoid, Epidermoid, Teratoma.
II. Traumatic :- Subdural & Extradural haematoma
III. Inflammatory :- Abscess, Tuberculoma, Syphilitic
gumma,fungal Granulomas.
IV. Parasitic :- Cysticercosis, Hydratid cyst, Amebic abscess,
Schistosoma japonicum.
V. Neoplasms

a) Tumors arising from neural structures: Gliomas –

astrocytoma, ependymoma, oligodendroglioma, germinoma,
medulloblastoma.
b) Tumors arising from appendages: Meningioma,
 schwannoma, chondroma, osteoma.
c) Pituitary lesions : Pituitary adenoma, Craniopharyngioma.
d) Vascular lesions : Angioma, Hemangioblastoma,
Papilloma of choroid plexus.
e) Secondary neoplasms.

Clinical features :-
1. Persistent headache not due to any other detectable
cause and unresponsive to medication. This may be due to
focal irritation, displacement of pain sensitive structures or
due to increased intra- cranial tension. If due to increased
intra- cranial tension headache develop rapidly over several
minutes persist for 20-40 minutes and subside quickly. May
awaken the patient from sound sleep 60-70 mts after
retiring and also precipitated by coughing, sneezing,
vomiting etc.

2. Vomiting & visual loss :- projectile vomiting unassociated

with nausea.
3. Papilledema in increased intra- cranial tension.
4. Recent onset behaviour changes.
5. Late onset seizures :- Any type of seizure occuring for the
first time after the age of 15 years should suggest the
possibility of intra cranial space occupying lesions. It is due
to disruption of cortical circuits by tumours that invade or
compress cerebral cortex.
6. Sudden onset of neurological deficits like dementia,
personality changes, gait disorders etc.

INTRACRANIAL HAEMATOMAS

I. EXTRA DURAL HAEMATOMAS :-

Collection of blood between the dura & the skull due to
injury to the middle meningeal vein, middle meningeal
artery, diploic vein, dural venous sinuses or small vessels
lying between dura and skull. Common site is temporal
fossa.
 Pathogenesis :-
Initial collection of blood in the extradural space causes
stripping of the dura from bone. Symptoms are produced
when symptoms exceed 25 ml in volume. Extent and
location of haematomas are determined by the ease of
stripping of the dura, site of injury, its severity, and
presence of depressed fractures of the skull.

Clinical features :-
1. 1 – 2% persons suffering from head injury develop extra
dural haematoma.
2. Uncommon in children below 3 yrs and in old age –
adherance of dura
To the skull prevents its easy stripping.
3. Progressive deterioration of level of consciousness :-
there may be a period of immediate loss of consciousness,
after that a period of apparent normalcy with clear
consciousness followed by deterioration of mental state.
4. Pupillary changes :- called Hutchinson’s pupillary reaction
– pupil on the side of lesion constricts initially then it dilates
and as intra cranial tension increases the opposite pupil also
dilates.

Investigation :-
CT scan
MRI
Cerebral angiography.

II. SUBDURAL HAEMATOMAS :-

Collection of blood between the dura and the arachnoid.
Usually follow injuries which may be apparently trivial or
even unnoticed. Common causes are bleeding from
superficial veins or venous sinuses. Anticoagulant treatment
predispose to intracranial bleeding and subdural
haematoma. Usual sites are frontal, anterior temporal,&
parietal.
 Pathology :-
Haematoma consists of fluid blood covered on inner and
outer aspects by layers of fibrin. Blood is defibrinated due to
the constant pulsation of the brain. High protein content of
fluid makes it hyperosmotic. So it absorbs fluid from the
surrounding and enlarges leading to increase in intra cranial
tension.

Clinical features :- Manifestation may be acute or chronic

in nature.
Acute : Clinical features are similar to extra dural
hematoma.
Chronic : Dementia, altered behaviour, psychiatric
manifestations or
focal neurological deficits may develop.
In middle aged headache, contralateral hemiplegia,
papilledema and in children vomiting, restlessness.
Irritability, refusal to feed, anaemia, seizures and failure to
thrive are common presenting symptoms.

Investigation :-
CT scan
MRI
Cerebral angiography.

NEOPLASMS OF BRAIN
About 50 % of intracranial tumors are primary neoplasms
and the rest secondary. Out of this 50 – 60 % of primary
brain tumors are gliomas, 25% - meningiomas, 10% -
schwannoma and the remainder others.

Etiology:
1. Exposure to ionizing radiations is the only well
documented enviornmental risk factor.
2. A number of heriditary factors are associated with an
increased risk of brain tumours, eg. Neurofibromatosis type
– I and type – II, Multiple endocrine neoplasia type –I.
3. Genes also contribute to the development of brain
 tumours and other malignancies. There are two classes of
genes namely, tumour suppressor genes and proto
oncogenes. There is over – expression of proto oncogenes in
brain tumours.
Clinical course of brain tumours :-

There are four stages of development of tumour.

Stage I : Initial period of silent growth.
Stage II : Stage of focal syndromes like epilepsy.
Stage III : Increased intracranial tension.
Stage IV : Brain displacement and false localizing signs.

PRIMARY NEOPLASMAS OF BRAIN :

I. Astrocytomas :
Derived from astrocytes. Common sites are cerebrum,
cerebellum, thalamus, pons and optic chiasma. Slow
growing tumour. Most commonly used grading system is
WHO four tired grading system.

WHO grading,
Grade I – Least malignant with excellent prognosis after
surgical excision, eg. pilocytic astrocytoma.
Grade II - Astroblastoma
Grade III - Anaplastic astrocytoma
Grade IV - Glioblastoma multiforme – clinically aggressive
Astrocytomas occur in three forms namely, diffuse or
infiltrating, solid and cystic.

Prognosis :-
Poor prognosis in age over 65 years, poor functional status
in grade III and grade IV astrocytomas.
Low grade astrocytoma :- usually in children, spindle shaped
cell (pilocytic astrocytoma), occurs from cerebellum, well
demarcated, cystic. Complete surgical excision usually
produces long term survival.
High grade astrocytoma :- seen in adults, usually supra –
tentorial, no clearly defined margins, infiltration to white
 matter and metastasis to spine through CSF called drop
metastasis occurs. Usually fatal and total surgical excision is
not possible.
Gliomatosis cerebri :-Rare form with diffuse infiltration of
the brain by malignant astrocytes without a focal enhancing
mass.
Treatment :-whole brain radiation therapy in selected
patients with chemotherapy.

II. Oligodendrogliomas :-
Slow growing tumour compared to astrocytoma. They
contain mixture of cells with astrocytic and oligodendroglial
features called mixed glioma. Usually supratentorial. 50% of
patients with 5 year survival.
25– 34% with 10 year survival. Less infiltrative and
complete surgical excision possible.

III. Ependymoma :-
Arise from spinal cord especially from lumbo-sacral region in
adults and from ventricles especially fourthventricle in
children.
Histologically myxopapillary that is, papillary arrangement of
cells and mucin production. Usually relatively demarcated
from adjucent neural tissue. Metastasis through CSF occurs.
Gross total excision provides 5 year disease free survival in
80% cases.

IV. Germinoma :-
A variety of germ cell tumor arising in midline
structures.Common site within or adjacent to 3rd ventricle.
Due to their location causes features of hypothalamic
dysfunction like diabetes incipedus, visual field defects,
disturbances of memory and hydrocephalus.
Radiosensitive and chemosensitive. 5 year survival in 80%
patients.

V. Medulloblastoma :-
Arise from neural precurssor cells. The most frequent
 malignancy of children. Rapidly growing tumours affecting
vermis of the cerebellum and giving rise to wide spread
metastasis.

VI. Meningioma :-
Arise from arachnoid cells particularly seen in sites having
arachnoid granulations. Those are usually benign and
attached to dura. More common in women. Invades skull
rarely invades brain.
Common sites are along sagital sinus, c-p angle and along
the dorsum of spinal cord.
Treatment : Surgical resection and post – operartive
radiation.

VII. Schwannoma :-
Arise from Schwann cells of nerve roots. Commonly from 8th
cranial nerve and less commonly 5th cranial nerve is
affected. It can arise from any cranial nerve except optic
and olfactory (myelinated by oligodendroglia).
Neurofibromatosis type – II predisposes to vestibular
schwannoma. Neurofibromatosis type – I predisposes to
schwannoma of spinal nerve roots.
Clinical features are progressive unilateral hearing loss,
tinitis, vertigo.
Treatment : Surgical excision.

VIII. Craniopharyngioma :-
Arise from remnants of the pituitary stalk called Rathke’s
pouch
(mesodermal structures from which anterior pituitary gland
is derived). Cystic supracellar tumour and in adults usually
calcified.
Clinical features are growth failure in children, endocrinal
disturbances due to pressure on hypothalamus like diabetes
incipedus, somnolence, obesity, hyperphagia and visual loss.

METASTATIC TUMORS OF BRAIN :-

Common route is through haematogenous.Primary site is
 lung in most of the cases. Usually from carcinoma breast
metastasis occurs to cerebellum and posterior pituitary
gland. Others are GIT malignancies, melanoma, thyroid
cancer, Hodgkin’s lymphoma. In brain the usual site of
metastasis is the grey matter – white matter junction and
border zone between middle cerebral and posterior cerebral
artery distribution. Usually incurable. Palliative therapy and
radiotherapy are the treatment of choice.

INVESTIGATIONS :-
In primary brain tumour no increase in ESR and tumor
specific antigen.
In metastatic tumours associated with systemic signs of
malignancy.
Lumbar puncture – Should not be performed in patients with
mass lesion it may precipitatebrain herniation.
CSF : increase opening pressure, elevated protein level, mild
lymphocytic pleocytosis and rarely contains malignant cells.
EEG : to distinguish epileptic seizures produced by focal
lesions and idiopathic epilepsy.
CT Scan, MRI, PET, SPECT

INTRA CRANIAL SPACE OCCUPYING LESIONS

DR.Bindu. K BHMS,MD(HOM)

These are lesions which expand in volume to displace normal neural structures & lead to increase in
intra – cranial pressure.

PATHOLOGY :-
Symptoms are produced due to,
1. Irritation & destruction of brain tissue causing neurological phenomena,eg. epilepsy, paralysis.

2. Raised intra cranial pressure:- The rate of increase of tension depend on the nature of the lesion
and its location. Posterior fossa lesions lead to more rapid rise in tension than supratentorial lesions.

3. False localizing signs :-

• Neurological phenomena arising from the secondary effects of lesion like herniation of neural
tissue under the falx-cerebri or downward herniation through tentorium cerebelli or foramen
magnum, pressure effects on other parts of brain develop.
• Countre – coup effect:- This is pressure effect caused on the side opposite to the side of lesion
when a space occupying lesion expands. The midline structures such as brainstem may be pushed
towards the opposite free margin of tentorium cerebelli to give rise to compression of normal side
also.
 In addition to this , different lesions may produce symptoms specific to their nature like fever in
case of brain abscess, signs of meningeal irritation in subarachnoid haemorrhage

Classification of intra cranial space occupying lesions :-

I. Congenital :- Dermoid, Epidermoid, Teratoma.
II. Traumatic :- Subdural & Extradural haematoma
III. Inflammatory :- Abscess, Tuberculoma, Syphilitic gumma,fungal Granulomas.
IV. Parasitic :- Cysticercosis, Hydratid cyst, Amebic abscess, Schistosoma japonicum.
V. Neoplasms

a) Tumors arising from neural structures: Gliomas – astrocytoma, ependymoma, oligodendroglioma,

germinoma, medulloblastoma.
b) Tumors arising from appendages: Meningioma, schwannoma, chondroma, osteoma.
c) Pituitary lesions : Pituitary adenoma, Craniopharyngioma.
d) Vascular lesions : Angioma, Hemangioblastoma, Papilloma of choroid plexus.
e) Secondary neoplasms.

Clinical features :-
1. Persistent headache not due to any other detectable cause and unresponsive to medication. This
may be due to focal irritation, displacement of pain sensitive structures or due to increased intra-
cranial tension. If due to increased intra- cranial tension headache develop rapidly over several
minutes persist for 20-40 minutes and subside quickly. May awaken the patient from sound sleep
60-70 mts after retiring and also precipitated by coughing, sneezing, vomiting etc.

2. Vomiting & visual loss :- projectile vomiting unassociated with nausea.

3. Papilledema in increased intra- cranial tension.
4. Recent onset behaviour changes.
5. Late onset seizures :- Any type of seizure occuring for the first time after the age of 15 years
should suggest the possibility of intra cranial space occupying lesions. It is due to disruption of
cortical circuits by tumours that invade or compress cerebral cortex.
6. Sudden onset of neurological deficits like dementia, personality changes, gait disorders etc.

INTRACRANIAL HAEMATOMAS

I. EXTRA DURAL HAEMATOMAS :-

Collection of blood between the dura & the skull due to injury to the middle meningeal vein, middle
meningeal artery, diploic vein, dural venous sinuses or small vessels lying between dura and skull.
Common site is temporal fossa.

Pathogenesis :-
Initial collection of blood in the extradural space causes stripping of the dura from bone. Symptoms
are produced when symptoms exceed 25 ml in volume. Extent and location of haematomas are
determined by the ease of stripping of the dura, site of injury, its severity, and presence of
depressed fractures of the skull.

Clinical features :-
1. 1 – 2% persons suffering from head injury develop extra dural haematoma.
2. Uncommon in children below 3 yrs and in old age – adherance of dura
To the skull prevents its easy stripping.
3. Progressive deterioration of level of consciousness :- there may be a period of immediate loss of
consciousness, after that a period of apparent normalcy with clear consciousness followed by
deterioration of mental state.
4. Pupillary changes :- called Hutchinson’s pupillary reaction – pupil on the side of lesion constricts
initially then it dilates and as intra cranial tension increases the opposite pupil also dilates.

Investigation :-
CT scan
MRI
Cerebral angiography.

II. SUBDURAL HAEMATOMAS :-

 Collection of blood between the dura and the arachnoid. Usually follow injuries which may be
apparently trivial or even unnoticed. Common causes are bleeding from superficial veins or venous
sinuses. Anticoagulant treatment predispose to intracranial bleeding and subdural haematoma.
Usual sites are frontal, anterior temporal,& parietal.

Pathology :-
Haematoma consists of fluid blood covered on inner and outer aspects by layers of fibrin. Blood is
defibrinated due to the constant pulsation of the brain. High protein content of fluid makes it
hyperosmotic. So it absorbs fluid from the surrounding and enlarges leading to increase in intra
cranial tension.

Clinical features :- Manifestation may be acute or chronic in nature.

Acute : Clinical features are similar to extra dural hematoma.
Chronic : Dementia, altered behaviour, psychiatric manifestations or
focal neurological deficits may develop.
In middle aged headache, contralateral hemiplegia, papilledema and in children vomiting,
restlessness. Irritability, refusal to feed, anaemia, seizures and failure to thrive are common
presenting symptoms.

Investigation :-
CT scan
MRI
Cerebral angiography.

NEOPLASMS OF BRAIN
About 50 % of intracranial tumors are primary neoplasms and the rest secondary. Out of this 50 –
60 % of primary brain tumors are gliomas, 25% - meningiomas, 10% - schwannoma and the
remainder others.

Etiology:
1. Exposure to ionizing radiations is the only well documented enviornmental risk factor.
2. A number of heriditary factors are associated with an increased risk of brain tumours, eg.
Neurofibromatosis type – I and type – II, Multiple endocrine neoplasia type –I.
3. Genes also contribute to the development of brain tumours and other malignancies. There are
two classes of genes namely, tumour suppressor genes and proto oncogenes. There is over –
expression of proto oncogenes in brain tumours.
Clinical course of brain tumours :-

There are four stages of development of tumour.

Stage I : Initial period of silent growth.
Stage II : Stage of focal syndromes like epilepsy.
Stage III : Increased intracranial tension.
Stage IV : Brain displacement and false localizing signs.

PRIMARY NEOPLASMAS OF BRAIN :

I. Astrocytomas :
Derived from astrocytes. Common sites are cerebrum, cerebellum, thalamus, pons and optic
chiasma. Slow growing tumour. Most commonly used grading system is WHO four tired grading
system.

WHO grading,
Grade I – Least malignant with excellent prognosis after surgical excision, eg. pilocytic astrocytoma.
Grade II - Astroblastoma
Grade III - Anaplastic astrocytoma
Grade IV - Glioblastoma multiforme – clinically aggressive
Astrocytomas occur in three forms namely, diffuse or infiltrating, solid and cystic.

Prognosis :-
Poor prognosis in age over 65 years, poor functional status in grade III and grade IV astrocytomas.
Low grade astrocytoma :- usually in children, spindle shaped cell (pilocytic astrocytoma), occurs
 from cerebellum, well demarcated, cystic. Complete surgical excision usually produces long term
survival.
High grade astrocytoma :- seen in adults, usually supra – tentorial, no clearly defined margins,
infiltration to white matter and metastasis to spine through CSF called drop metastasis occurs.
Usually fatal and total surgical excision is not possible.
Gliomatosis cerebri :-Rare form with diffuse infiltration of the brain by malignant astrocytes without
a focal enhancing mass.
Treatment :-whole brain radiation therapy in selected patients with chemotherapy.

II. Oligodendrogliomas :-
Slow growing tumour compared to astrocytoma. They contain mixture of cells with astrocytic and
oligodendroglial features called mixed glioma. Usually supratentorial. 50% of patients with 5 year
survival.
25– 34% with 10 year survival. Less infiltrative and complete surgical excision possible.

III. Ependymoma :-
Arise from spinal cord especially from lumbo-sacral region in adults and from ventricles especially
fourthventricle in children.
Histologically myxopapillary that is, papillary arrangement of cells and mucin production. Usually
relatively demarcated from adjucent neural tissue. Metastasis through CSF occurs.
Gross total excision provides 5 year disease free survival in 80% cases.

IV. Germinoma :-
A variety of germ cell tumor arising in midline structures.Common site within or adjacent to 3rd
ventricle. Due to their location causes features of hypothalamic dysfunction like diabetes incipedus,
visual field defects, disturbances of memory and hydrocephalus.
Radiosensitive and chemosensitive. 5 year survival in 80% patients.

V. Medulloblastoma :-
Arise from neural precurssor cells. The most frequent malignancy of children. Rapidly growing
tumours affecting vermis of the cerebellum and giving rise to wide spread metastasis.

VI. Meningioma :-
Arise from arachnoid cells particularly seen in sites having arachnoid granulations. Those are usually
benign and attached to dura. More common in women. Invades skull rarely invades brain.
Common sites are along sagital sinus, c-p angle and along the dorsum of spinal cord.
Treatment : Surgical resection and post – operartive radiation.

VII. Schwannoma :-
Arise from Schwann cells of nerve roots. Commonly from 8th cranial nerve and less commonly 5th
cranial nerve is affected. It can arise from any cranial nerve except optic and olfactory (myelinated
by oligodendroglia). Neurofibromatosis type – II predisposes to vestibular schwannoma.
Neurofibromatosis type – I predisposes to schwannoma of spinal nerve roots.
Clinical features are progressive unilateral hearing loss, tinitis, vertigo.
Treatment : Surgical excision.

VIII. Craniopharyngioma :-
Arise from remnants of the pituitary stalk called Rathke’s pouch
(mesodermal structures from which anterior pituitary gland is derived). Cystic supracellar tumour
and in adults usually calcified.
Clinical features are growth failure in children, endocrinal disturbances due to pressure on
hypothalamus like diabetes incipedus, somnolence, obesity, hyperphagia and visual loss.

METASTATIC TUMORS OF BRAIN :-

Common route is through haematogenous.Primary site is lung in most of the cases. Usually from
carcinoma breast metastasis occurs to cerebellum and posterior pituitary gland. Others are GIT
malignancies, melanoma, thyroid cancer, Hodgkin’s lymphoma. In brain the usual site of metastasis
is the grey matter – white matter junction and border zone between middle cerebral and posterior
cerebral artery distribution. Usually incurable. Palliative therapy and radiotherapy are the treatment
of choice.

INVESTIGATIONS :-
 In primary brain tumour no increase in ESR and tumor specific antigen.
In metastatic tumours associated with systemic signs of malignancy.
Lumbar puncture – Should not be performed in patients with mass lesion it may precipitatebrain
herniation.
CSF : increase opening pressure, elevated protein level, mild lymphocytic pleocytosis and rarely
contains malignant cells.
EEG : to distinguish epileptic seizures produced by focal lesions and idiopathic epilepsy.
CT Scan, MRI, PET, SPECT