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Clinical Neuroscience > CNS tumours and disease > Flashcards

CNS tumours and disease Flashcards

1
Q

Two types of CNS tumours and examples

A

Primary:
* Gliomas
* Parenchymal
* Meningeal
* Neuronal
* Poorly differentiated - medulloblastoma

Secondary:
* Metastatic - paraneoplastic

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2
Q

Types of gliomas - stromal cell tumours

A

Astrocytic tumours
Oligodendrogliomas
Ependymomas
Colloid cysts of 3rd ventricle

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3
Q

Types of parenchymal CNS tumour - brain tissue

A

CNS lymphomas
Germ cell

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4
Q

Types of meningeal CNS tumour

A

Meningioma

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5
Q

Types of neuronal CNS tumour

A

Ganglion cell tumour
Neuroblastoma

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6
Q

Gliomas - what are they, grading, most common

A

Malignant CNS tumour arising from stroma
Graded 1-5
Astrocytic tumours most common - astrocytomas low–> high grade (80%), glioblastoma multiforme -high grade
Then oligodendrogliomas (20%)
Ependymoma - ventricular system disseminated into CSF

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7
Q

What are lymphomas of CNS?

A

Diffuse large B cell lymphomas
Associated with epstein-barr virus pts

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8
Q

What are germ cell tumours of CNS?

A

Midline tumours - pineal and suprasellar eg germinoma

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9
Q

What are medulloblastomas?

A

20% occur in children
Occur in cerebellum
Very radiosensitive

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10
Q

What are meningiomas?

A

Benign
Derived from arachnoid meningothelial cells
Can cause problems if compress important structures

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11
Q

How can infections enter the CNS?

(4)

A
  1. Direct/local spread - air sinuses, skull fractures, middle ear infections, infected teeth
  2. Haematogenous - arterial blood, retrograde venous through anastomoses of veins to face and venous sinuses of skull
  3. Iatrogenic - lumbar puncture, spinal anaesthesia, surgery
  4. Peripheral nerves - Herpes zoster, viruses
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12
Q

What part of the CNS can infections affect?

(3)

A

Meninges
Aggregates of acute inflammation - can cause abscesses
Brain parenchyma

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13
Q

What is meningitis?

A

Inflammation of leptomeninges - arachnoid and pia mater

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14
Q

Types of meningitis

(4)

A
  1. Acute pyogenic - baterial
  2. Aspetic - viral, immunocompromised?
  3. Chronic - mycotuberculosis, fungi causes
  4. Carcinomastosis - lots small cancer cells spread

+/-septicaemia (bacteria in blood)

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15
Q

Presentation of meningitis

A

Headache
Stiff neck - meningeal irritation
Photophobia
Irritability
Altered consciousness
Focal neurological impairment

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16
Q

Investigations for meningitis

A

CT scan
Lumbar puncture - pressure, neutrophils, glucose lower as bacteria using for food

17
Q

Complications of meningitis

A

Cerebral oedema
Cerebral infarction
Cerebral abscess
Empyema
Epilepsy
Meningoencephalitis - infection of brain and meninges
Septicaemia

18
Q

Pathogen Cause of acute meningitis in each age group

A

Infants - Escherichia coli or group B streptococci
Young adults - Neisseria meningitidis
Older adults - Streptococcus pneumoniae or listeria monocytogenes

19
Q

Pathogen cause of chronic meningitis

A

Tuberculosis mycobacterium

20
Q

Pathogen cause of abscess and empyema

A

Abscess - streptococci and staphylococci
Empyema - polymicrobial (staphylococci, anaerobic gram -ve)

21
Q

What is encepahlitis?

A

Infection of the brain parenchyma - tissue
Usually viral rather than bacterial
Causes neurones death by viruses (viruses cause inclusion bodies)
Lots of lymphocytes present

22
Q

Examples of viruses and which particular lobe of brain they affect

A

Herpes zoster - temporal lobe
Polio - spinal cord motor neurones
Rabies - brainstem

23
Q

Common viruses causing encephalitis

A

Herpes simplex virus - HSV-1 and HSV-2
Cytomegalovirus - foetus and immunocompromised
HIV

24
Q

What are prion diseases and their effects?

A

Abnormal cellular protein acummulations leading to cell injury in and out of cell eg:
* Neurone cell death
* Synapse loss
* Microvacuolations - spongiform sponge like brain (holes)
* Lack of inflammation

Called an infection because it spreads to neighbouring cells

25
Q

Cause of prion disease

A

Can be sporadic
Familial
Iatrogenic - contaminated equiptiment, blood transfusions
Or ingested

26
Q

Types of prion disease

A
  • Creutzfeldt-Jakob disease (CJD) and variant CJD
  • Scrapies (sheep)
  • Bovine spongiform encephalopathy (BSE mad cow diease)
27
Q

What occurs to proteins in prion disease?

A

Normally proteins in brain are rich in alpha helices
Initiation - Prion disease is ingested, inoculated or there is a random mutation causing conformational change to a new protein structure - beta pleated sheet
Problem with beta pleated sheet is they are resistant to destruction by proteolysis
Propagation - new protein forces surrounding proteins to undergo conformational change to alpha helices to beta pleated sheet
Aggregation - these then aggregate forming amyloid plaques and spongiform (holey) brain

28
Q

What are some features of Creutzfeld Jakob prion disease?

A
  • Usually occurs >70yrsd old
  • Rapidly progressive dementing illness - unlike slower onset of alzheimers
  • Subtle changes in memory
  • Definitive diagnosis is made during post mortem exam
  • Often brain looks normal +/-brain atropy and ventricular enlargement
29
Q

What are some features of variant Creutzfeld Jakob disease?

A
  • Affects young adults
  • Slower progression
  • Starts with behavioural issues
  • Due to exposure to prion disease in cattle (BSE) - meat? burgers? blood transfusions?
  • Prolonged incubation period - 15 yrs
30
Q

what causes neurodegenerative diseases?

A

Loss of neurones
Accumulation of protein aggregates

31
Q

Effects of neurodegenerative diseases

A

Hippocampus and cortex - cognitive changes, alteration in memory, behaviours and language
Basal ganglia - movemement disorders (hypo/hyperkinetic)
Cerebellum - ataxia loss of co-ordination
Motor neurones can also be affected

32
Q

When does Alzheimer’s disease occur?

A

3% of 65-74 year olds - then increases after this
Often sporadic - 90%
Can be familial causing earlier onset - 5-10%

33
Q

What occurs to proteins in Alzheimer’s disease?

A
  • Alpha beta plaques form and neurofibrillary tangles (tau proteins)
  • This causes neuronal damage –> loss of neurones, cortical atrophy and shrunked brain
  • Can effect frontal, temporal and parietal lobes especially
34
Q

How do plaques and tangles form in Alzheimers?

A

Either Amyloidogenic pathway or non-amyloidogenic pathway

Amyloidogenic:
* Transmembrane protein on chromosome 21 cleaved to alpha beta monomer (by beta and gamma secretase)
* These clump forming alpha beta oligomers, then aggregates then amyloid fibrils = plaques and tangles
* Alpha beta Oligomers can become hyperphosphorylated by kinases forming Tau aggregates = plaques and tangles and neuronal damage

Non-amyloidogenic:
* Alpha secretase and gamma secretase cleave

35
Q

Why is the fact the protein causing Alzheimers is located on chromosome 21 importnat?

A

In Trisomy 21 - down syndrome there is increase prevalance of Alzheimers due to presence of more of this protein

36
Q

Signs and symptoms of Alzheimers

A

Impaired intellectual function
Impaired memory
Altered mood and behaviour
Disorientated

37
Q

Cause of Parkinson disease

A

Loss of substanstia nigra dopaminergic neurones - Mickey mouse eyebrows lose pigment in midbrain
Causing hypokinesia
Lewy body’s seem to be involved - alpha synuclein neuronal inclusions

38
Q

4 features of Parkinsons disease

A

Rigidity
Bradykinesia
Instability
Tremor

39
Q

Cause of Huntington’s disease

A

Autosomal dominant
CAG tricnucleate repeat expansion - polyglutamine produced
This is then broken down to intranuclear aggregates of huntington protein = cell injury and death, fibrosis (gliosis)

Clinical Neuroscience (24 decks)

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