Intracranial Space Occupying Lesions (SOLs) Flashcards

1
Q

What are intracranial SOLs?

A

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

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2
Q

What does SOLs include?

A

Tumours
Abscesses (and other infective lesions)
Hematomas

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3
Q

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

A

Brain edema (this adds to further increase the volume)

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4
Q

How would you describe the edema in an intracranial SOL?

A

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

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5
Q

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

A

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

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6
Q

Name the clinical presentation of focal (localizing) SOLs.

A

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
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7
Q

List the effects of intracranial SOLs.

A

Ventricular compression (hydrocephalus)
Midline shift
Increased ICP
Herniation

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8
Q

List the presenting symptoms/signs of brain tumours.

A

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

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9
Q

Name the two types of brain tumours.

A

Primary - arising from brain tissue

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

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10
Q

Explain what the grading scheme of brain tumours is.

A

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

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11
Q

What is the most common type of brain tumour?

A

Gliomas (tumour of glial cells)

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12
Q

List the different types of glial cells.

A

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

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13
Q

What is a neuropil?

A

Network of axons

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14
Q

List the major types of brain tumors.

A

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

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15
Q

What is the most common primary brain tumor?

A

Astrocytomas

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16
Q

Name the two categories of astrocytomas.

A

Infiltrating astrocytomas

Non-infiltrating astrocytomas

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17
Q

Name the most common non-infiltrating astrocytoma.

A

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

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18
Q

Name the types of infiltrating astrocytomas.

A

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

  • Diffuse astrocytoma (grade II)
  • Anaplastic astrocytoma (grade III)
  • Glioblastoma (grade IV)
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19
Q

Describe the gross morphology of the infiltrating astrocytoma.

A

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

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20
Q

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

A

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

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21
Q

What is the histologic diagnosis of astrocytomas based on?

A

Pleomorphism
Cellularity
Infiltration

22
Q

What is pleomorphism?

A

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

23
Q

What is cellularity with regards to a tumor?

A

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

24
Q

What is infiltration?

A

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

25
Q

What is the hallmark of the glioblastoma?

A

Foci of necrosis and vascular proliferation

alongside pleomorphism, cellularity and infiltration

26
Q

What is palisaded necrosis?

A

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

27
Q

What causes microvascular proliferation in glioblastomas?

A

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

28
Q

What is the second most common tumours of the CNS?

A

Meningiomas

29
Q

Where do meningiomas occur?

A

Derived from the meningothelial cells of the arachnoid

They are extraaxial/outside the brain

30
Q

What grade are meningiomas and who do they commonly affect?

A

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

31
Q

Describe the gross morphology of meningiomas.

A

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

32
Q

Describe the microscopic morphology of a meningioma.

A

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

33
Q

Name the five most common primary sites of brain metastases.

A
Lung (both adenocarcinoma and small cell) 
Breast carcinoma 
Skin (melanoma) 
Kidney (renal cell carcinoma) 
GIT (adenocarcinoma)
34
Q

Describe the appearance of metastatic tumours.

A

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

35
Q

Where do metastatic tumours arise?

A

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

36
Q

How do you notice metastatic melanomas?

A

Brown melanin pigment in the tumour

37
Q

What are the most common pituitary tumors?

A

Benign adenomas arising in the anterior pituitary (adenohypophysis)

38
Q

How do pituitary adenomas present?

A

Signs and symptoms of endocrine disturbances

Localized mass effect

39
Q

What is the normal pituitary gland formed of?

A
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)
40
Q

Where does the pituitary gland lie?

A

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

41
Q

Where do pituitary adenomas arise from?

A

Any of the cell types in the anterior pituitary

42
Q

What are functioning pituitary adenomas?

A

Autonomously produce hormones

Most commonly occuring

43
Q

What are non-functioning pituitary adenomas?

A

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

44
Q

What is the microscopic morphology of pituitary adenomas?

A

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

45
Q

What is the localizing effect of pituitary adenomas?

A
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)
46
Q

What are the sources of infection for brain abscesses?

A

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)

47
Q

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

A

Immunocompetent - streptococci/staphylococci

Immunocompromised - broader range of organisms - including fungal and protozoan infections

48
Q

What are the presenting symptoms and signs of brain abscesses?

A
Fever
Headache
Changes in mental state (drowsiness, confusion) 
Focal neurological deficits
Seizures
Nausea and vomiting
Neck stiffness
49
Q

What is the gross morphology of brain abscesses?

A

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

50
Q

What is the microscopic morphology of brain abscesses?

A

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

51
Q

What is the treatment for brain abscesses?

A

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