Brain tumours Flashcards

1
Q

How common are primary brain tumours?

A

Incidence 8 per 100,000
10% neoplasms
16th most common adult cancer - disproportionate killer in young adults
2nd most common paediatric cancer below leukaemia
Less than 2% of all malignant tumours but 20% of childhood
Majority supratentorial in adults
In children - majority posterior fossa
Most gliomas - astrocytoma (85-90%), oligodendroglioma (5%)

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2
Q

How common are secondary brain tumours?

A

10x more common than primary brain tumours

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3
Q

Which cancers are secondary brain tumours most likely to metastasise from?

A
Non-small cell (1)
Small cell (2)
Breast (3)
Melanoma (4)
Renal cell (5)
GI (6)
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4
Q

What are gliomas?

A

Neuroepithelial origin seen within hemispheres mostly but also cerebellum, brainstem and cord
Unknown cause
Associated with neurofibromatosis
Spread by direct extension and rarely metastasise outside CNS

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5
Q

What are the 2 types of gliomas?

A

Astrocytomas (85-90%)

Oligodendromas (5%)

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6
Q

What are astrocytomas?

A

Gliomas arising from astrocytes
Grades I-IV
Grade I grows slowly over many years
Grade IV (glioblastoma multiforme) causes death within several months
Usually benign in children and cerebellar

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7
Q

What are oligodenromas?

A
Most common in 40s-50s
Arise from oligodendrocytes
Grow slowly usually over several years
Calcification common
May have seizures
WHO grade II
All IDH-1 mutation positive
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8
Q

What are meningiomas?

A

More common in elderly and women
Benign and arise from arachnoid mater and may grow to large size usually over years pushing into brain
Close to skull - erode bone or cause local hyperstosis
Often occur along intracranial venous sinuses which they may invade - usually below tentorium
Common sites - parasagittal region, sphenoidal ridge, subfrontal region, pituitary fossa, skull base

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9
Q

What are neurofibromas?

A

Schwanomas
Solid benign tumours arising from schwann cells and occur principally in the cerebellopontine angle
May be bilateral in neurofibromatosis type 2

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10
Q

What are ependymomas?

A

Arise from ependymal cells

Line ventricles and spinal cord

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11
Q

What are craniophyaryngiomas?

A

Very often benign tumours

Often diagnosed in younger patients

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12
Q

What can increase your risk of brain tumour?

A
More common in affluent groups
Ionising radiation
Vinyl chloride
Immunosuppression
FHx
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13
Q

What is the WHO grading for primary brain tumours?

A

Grade I - good prognosis, often benign
Grade II - > 5 year prognosis, premalignant tumour
Grade III - prognosis of 2-5 year survival rate, cancer, malignant, active growth, and mitotic activity on microscope
Grade IV - < 1 year survival prognosis, most common phenotype, active growth, mitotic activity and necrosis, vascular proliferation, very malignant

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14
Q

What are the 2 pathways to malignant glioma?

A

Common

Less common

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15
Q

What is the common pathway to malignant glioma?

A

Especially in those under 50-60
Initial genetic error of glucose glycolysis
Mutation of isocitrate dehydrogenase I
Results in build-up of 2-hydroxyglutarate
Triggers genetic instability in glial cells and subsequent inappropriate mitosis - cancer

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16
Q

What is the less common pathway to malignant glioma?

A

More common in those over 50-60
No IDH-1 mutation
Instead have catastrophic genetic mutation
Results in poor prognosis even for low grade tumours

17
Q

Why can tumours lead to a rise in ICP?

A

Intracranial compartment is a complaint system
Initially when tumour is small, there will be no symptoms despite the rising ICP – due to brain being compliant and able to remove CSF from ventricle to spinal cord in order to offset the increase in pressure
Comes a point where no more CSF can be relocated – very sharp and rapid rise in ICP resulting in symptoms and eventually death if nothing done
Rising pressure results in midline shift of brain and herniation through foramen magnum – results in brain damage resulting in local and systemic symptoms

18
Q

What are the 4 cardinal presenting symptoms of brain tumours?

A

Symptoms of raised ICP
Progressive neurological deficit
Seizures
Lethargy/tiredness caused by pressure on the brainstem

19
Q

What are the symptoms of raised ICP?

A

Progressive headache
- Worse on waking from sleep (don’t wee at night so accumulation of fluid)
- Pain so bad it can wake patient up
- Pain increased by coughing, straining and bending forwards (increased venous pressure in brain)
- Sometimes relieved by vomiting – reduces fluids and thus pressure
Drowsiness
+/- vomiting
Papilloedema
- Swelling of optic disc due to obstruction of venous return from retina due to raised ICP
- Loss of crisp optic nerve head margins
- Venous engorgement
- Retinal oedema
- Haemorrhages
Distortion of upper brainstem as midline structures displaced – impairment of consciousness, progressing to coning and death
False localising signs eg 6th nerve lesion, 3rd nerve lesion, hemiparesis

20
Q

What are the symptoms of progressive neurological deficit?

A

Depends on part of brain that is affected
Temporal lobe – dysphasia, amnesia
Frontal lobe – hemiparesis, personality change, Broca’s dysphasia, lack of initiative, unable to plan tasks
Parietal lobe – hemisensory loss, reduction in 2-point discrimination, dysphasia, astereognosis (unable to recognise object from touch alone)
Occipital lobe – contralateral visual defects
Cerebellum – DASHING – Dysdiadochokinesis, Ataxia, Slurred speech, Hypotonia, Intention tremor, Nystagmus, Gait abnormality

21
Q

What symptoms of seizures might indicate tumour?

A

Sinister when of recent onset
Partial/focal seizures more common with tumours
- Motor
- Sensory
- Temporal lobe pattern – olfactory aura or déjà vu or a funny feeling in the gut/stomach a few minutes before and/or during the seizure

22
Q

What are the differentials of brain tumours?

A

Other causes of space-occupying lesions

  • Aneurysm
  • Abscess
  • Cyst
  • Haemorrhage
  • Idiopathic intracranial hypertension
23
Q

What investigations should you do for a brain tumour?

A

CT and MRI
- MRI superior for posterior fossa lesions
- Determine size and location of lesions
- High grade tumours have irregular edges and high growth rate
Blood tests – FBC, U&Es, LFTs, B12 ect
Biopsy via skull burr-hole to determine cancer grade and confirm
Lumbar puncture contraindicated when possibility of mass lesion since withdrawing CSF may provoke immediate coning – herniation of brain through foramen magnum resulting in brainstem compression as it passes through foramen magnum and potential death
PET
CXR – as mets more common than primary

24
Q

How do you treat brain tumours?

A

Surgery to remove mass – if possible or just debulk tumour
Chemotherapy for glioma
- Given at same time as surgery and then for 1st 6 weeks post-op
- Temozolomide
- Not all tumours are sensitive – some tumours have high methyl-guanine-methyl-transferase – an enzyme that reverses the therapeutic effect of temozolomide
- Best to determine if tumour is sensitive before administration – if it has methylated MGMT (enzyme silenced) then sensitive
- Little real value – vincristine, procarbazine and temozolomide
Oral dexamethasone for cerebral oedema
- Most powerful synthetic steroid
- Rapidly improves brain performance in all tumours
- Reduces tumour inflammation/oedema
- Must give no later then 14:00 since keeps patient awake
Can give anticonvulsants for epilepsy eg oral carbamazepine
Radiotherapy if mets