Intracranial Space Occupying Lesions (SOLs)

Question 1

What are intracranial SOLs?

Answer 1

Focal lesions that take up space (mass effect) and add volume to the cranial cavity leading to an increase in ICP

Question 2

What does SOLs include?

Answer 2

Tumours
Abscesses (and other infective lesions)
Hematomas

Question 3

What usually accompanies SOLs (other than a mass effect)?

Answer 3

Brain edema (this adds to further increase the volume)

Question 4

How would you describe the edema in an intracranial SOL?

Answer 4

Vasogenic - due to disruption of BBB and extravastion of fluid into the extracellular space

Question 5

Describe the clinical presentation of a general (non-localizing) SOL.

Answer 5

Increase in ICP + Brain Herniation –> headache, nausea, vomiting, disturbed consciousness level, papilledema
Seizures

Question 6

Name the clinical presentation of focal (localizing) SOLs.

Answer 6

Signs and symptoms depend on the size and location of the mass.

• Lesion in the motor cortex = contralateral motor dysfunction
• Visual disturbances (e.g. pituitary tumour invading the roof of the sella turcica & impinges on the optic chiasm)
• Behavioural changes due to lesion on frontal lobe

Question 7

List the effects of intracranial SOLs.

Answer 7

Ventricular compression (hydrocephalus)
Midline shift
Increased ICP
Herniation

Question 8

List the presenting symptoms/signs of brain tumours.

Answer 8

Seizures
Worsening vision (visual cortex)
Sensory abnormality
Limb weakness (motor cortex)
Non-focal neurologic disturbances - headache and other signs/symptoms of ICP
Stroke-like fashion as a consequence on intratumoral haemorrhage

Question 9

Name the two types of brain tumours.

Answer 9

Primary - arising from brain tissue

Metastatic - hematogenous spread from a primary tumour elsewhere in the body)

Question 10

Explain what the grading scheme of brain tumours is.

Answer 10

Divides primary tumours into one of four grades.
Grade I = benign
Grade IV = highly aggressive
The higher the grade the worse the prognosis

Question 11

What is the most common type of brain tumour?

Answer 11

Gliomas (tumour of glial cells)

Question 12

List the different types of glial cells.

Answer 12

Astrocytes - support for neurons and axons, form part of BBB, repair following injury to CNS
Oligodendrocytes - myelinate axons in the CNS
Ependymal Cells - line the ventricles and spinal canal

Question 13

What is a neuropil?

Answer 13

Network of axons

Question 14

List the major types of brain tumors.

Answer 14

Gliomas - Astrocytomas, Oligodendrogliomas, Ependymomas
Neuronal and mixed neuronal glial tumours
Embryonal tumors (Medulloblastoma)
Meningeal tumours (Meningiomas)
Others

Question 15

What is the most common primary brain tumor?

Answer 15

Astrocytomas

Question 16

Name the two categories of astrocytomas.

Answer 16

Infiltrating astrocytomas

Non-infiltrating astrocytomas

Question 17

Name the most common non-infiltrating astrocytoma.

Answer 17

Pilocytic astrocytoma (grade I) - most common astrocytoma in children

Question 18

Name the types of infiltrating astrocytomas.

Answer 18

80% of primary brain tumours in adults in the 4th to 6th decades

• Diffuse astrocytoma (grade II)
• Anaplastic astrocytoma (grade III)
• Glioblastoma (grade IV)

Question 19

Describe the gross morphology of the infiltrating astrocytoma.

Answer 19

Poorly defined infiltrative tumours
Expand and distort the invaded brain without forming a discrete mass
Cut surface of tumour is either firm or soft and gelatinous

Question 20

What is the gross morphology and CT of a glioblastoma (infiltrating astrocytoma)

Answer 20

Grade IV - show areas of haemorrhage and necrosis
On CT - ring-like contrast enhancement due to abnormal, abundant tumour vascularization (microvascular proliferation in the periphery) against central tumour necrosis

Question 21

What is the histologic diagnosis of astrocytomas based on?

Answer 21

Pleomorphism
Cellularity
Infiltration

Question 22

What is pleomorphism?

Answer 22

Presence of abnormal appearing astrocytes with variation in their size and shape

Question 23

What is cellularity with regards to a tumor?

Answer 23

Density of the tumour cells within a given volume of tissue compared to normal brain tissue

Question 24

What is infiltration?

Answer 24

Extension of tumour cells into surrounding brain tissue without discrete or sharp interface

Question 25

What is the hallmark of the glioblastoma?

Answer 25

Foci of necrosis and vascular proliferation | alongside pleomorphism, cellularity and infiltration

Question 26

What is palisaded necrosis?

Answer 26

Necrosis in glioblastoma which is characteristically surrounded by viable tumour cell nuclei in a parallel arrangement

Question 27

What causes microvascular proliferation in glioblastomas?

Answer 27

Proliferation of endothelial cells and capillaries under the effect of VEGF produced by tumour cells

Question 28

What is the second most common tumours of the CNS?

Answer 28

Meningiomas

Question 29

Where do meningiomas occur?

Answer 29

Derived from the meningothelial cells of the arachnoid | They are extraaxial/outside the brain

Question 30

What grade are meningiomas and who do they commonly affect?

Answer 30

Most are benign (grade I) - slow growing/slow infiltrating More common in women Grade I meningiomas become adherent to the dura & impinge upon, but do not invade the underlying brain = symptoms are related to the compression of the area of brain affected by the tumour

Question 31

Describe the gross morphology of meningiomas.

Answer 31

Tumour is adherent to dura Rounded, well circumscribed margins Presses against, but does not invade the brain

Question 32

Describe the microscopic morphology of a meningioma.

Answer 32

Clusters of meningothelial cells in whorled appearance Indistinct cell membranes Central clearing in nuclei Psammoma bodies (calcific spherules) are seen

Question 33

Name the five most common primary sites of brain metastases.

Answer 33

``` Lung (both adenocarcinoma and small cell) Breast carcinoma Skin (melanoma) Kidney (renal cell carcinoma) GIT (adenocarcinoma) ```

Question 34

Describe the appearance of metastatic tumours.

Answer 34

Multiple, well demarcated & may be surrounded by gliosis (hypertrophy/proliferation of glial cells)

Question 35

Where do metastatic tumours arise?

Answer 35

Interface between the gray matter and white matter - this region contains a dense capillary network

Question 36

How do you notice metastatic melanomas?

Answer 36

Brown melanin pigment in the tumour

Question 37

What are the most common pituitary tumors?

Answer 37

Benign adenomas arising in the anterior pituitary (adenohypophysis)

Question 38

How do pituitary adenomas present?

Answer 38

Signs and symptoms of endocrine disturbances | Localized mass effect

Question 39

What is the normal pituitary gland formed of?

Answer 39

``` Anterior pituitary (adenohypophysis) - 80% of the gland, many different types of cells Posterior pituitary (neurohypophysis) - formed of axons and their terminals (derived from neurons located in the hypothalamus) ```

Question 40

Where does the pituitary gland lie?

Answer 40

Within the sella turcica of the sphenoid bone Bound laterally by the cavernous sinuses & superiorly by the sella diaphragma (a dural fold) Optic chiasm lies above the sela diaphragma

Question 41

Where do pituitary adenomas arise from?

Answer 41

Any of the cell types in the anterior pituitary

Question 42

What are functioning pituitary adenomas?

Answer 42

Autonomously produce hormones | Most commonly occuring

Question 43

What are non-functioning pituitary adenomas?

Answer 43

Present as SOLs because they can grow to a larger size before becoming symptomatic Cause symptoms of increased ICP May produce more localizing findings

Question 44

What is the microscopic morphology of pituitary adenomas?

Answer 44

Sheets of monotonous cells with eosinophilic cytoplasm and round to oval nuclei

Question 45

What is the localizing effect of pituitary adenomas?

Answer 45

``` Bitemporal hemianopia (nasal fibres compressed by tumour) May extend laterally into cavernous sinuses & impinge upon cranial nerves III, IV, VI and V1 (opthalamic nerve) and V2 (maxillary nerve) = ophthalmoplegia, dilated pupil, ptosis, partial facial sensory dysfunction Larger lesions could produce brainstem compression/hydrocephalus Acute haemorrhage into an adenoma = severe headache, visual disturbances, pan hypopituitarism (reduced production of pituitary hormones) ```

Question 46

What are the sources of infection for brain abscesses?

Answer 46

Direct implantation due to trauma Extension from paranasal sinusitis or mastoiditis Blood-borne spread from a distant infection (e.g. infective endocarditis) - these abscesses are multiple, located at the gray/white interface (rich capillary network)

Question 47

What are the most common organisms causing brain abscess in immunocompetent vs immunocompromised patients?

Answer 47

Immunocompetent - streptococci/staphylococci | Immunocompromised - broader range of organisms - including fungal and protozoan infections

Question 48

What are the presenting symptoms and signs of brain abscesses?

Answer 48

``` Fever Headache Changes in mental state (drowsiness, confusion) Focal neurological deficits Seizures Nausea and vomiting Neck stiffness ```

Question 49

What is the gross morphology of brain abscesses?

Answer 49

Well circumscribed cavities filled with pus, surrounded by fibrosis (in older lesions) and edema

Question 50

What is the microscopic morphology of brain abscesses?

Answer 50

Early abscess cavity with neutrophils & necrotic debris (suppurative necrosis) without sharp separation from brain tissue Older abscess = granulation tissue and fibrosis

Question 51

What is the treatment for brain abscesses?

Answer 51

Surgical drainage (decrease ICP and provide material for culture) Antibiotic therapy Elimination of the primary site of infection