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Pathology Term 4 > Week 2 - CNS2 > Flashcards

Week 2 - CNS2 Flashcards

Tumours, Meningitis, Epilepsy, Increased ICP

1
Q

What % of all tumours are CNS tumours?

A

10%

-commonest SOLID tumour in children (2nd to leukemia)

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2
Q

What age are CNS tumours increasingly common?

A
  • double peak

- 1st and 6th decade of life

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3
Q

Where are CNS tumours more likely to be located in adults vs. children?

A

adults –> 70% supratentorial (cerebral hemispheres)
children –> 70% infratentorial (brainstem/cerebellum)

N.B. tentorium = line separating cerebellum from occipital lobe

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4
Q

What % of CNS tumours are metastatic?

A

50-70% (common in adults)

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5
Q

Why are CNS tumours typically of glial cell origin rather than neurons?

A

neurons are NON-DIVIDING CELLS

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6
Q

What are the special features of CNS tumours?

A
  • glial origin (rarely neural)
  • rarely spread outside CNS
  • NO capsule (no collagen tissue present)
  • NO in-situ stage (like epithelial cell malignancies)
  • location NOT type of tumour determines clinical outcome
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7
Q

What is the commonest CNS tumour in adults and children?

A

ASTROCYTOMA - glioma (glioblastoma = high grade)

  • both adults + kids (kids also medulloblastoma - germ cell tumour - v. common)
  • -> 90% in kids (+medulloblastomas); 70% in adults

N.B. in adults commonest cause of CNS tumour = metastasis (breast, lung, colon, melanoma)

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8
Q

What are the clinical features of CNS tumours?

A
  • slow, progressive, chronic, morning headache, crescendo
  • nerve damage –> unilateral* vision defects, anosmia, seizures
  • raised ICP –> headache, vomiting, bradycardia, papilloedema
  • nausea/vomiting –> ICP: medulla oblongata compression
  • bradycardia –> ICP: parasympathetic (vagal) stimulation
  • seizures (convulsions) –> irritation/injury/inflammation
  • drowsiness/obtundation –> brainstem compression
  • personality/memory –> frontal lobe injury
  • changes in speech –> temporal lobe injury
  • limb weakness –> motor area injury
  • balance/ataxia –> cerebellar injury
  • eye movements/vision –> optic tract/occipital lobe injury
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9
Q

What is a low grade vs. high grade glioma?

A

low grade = astrocytoma

high grade = glioblastoma (high grade astrocytoma)

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10
Q

What are the nerve sheath CNS tumours?

A
  • schwanoma (schwann cells)

- neurofibroma

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11
Q

What tumour is common in meninges?

A

meningioma

-commonest CNS tumour but technically not included as a CNS tumour as it is of the meningeal layer covering the CNS

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12
Q

What is the commonest germ cell CNS tumours and what are the others?

A
  • MEDULLOBLASTOMA (incr. in kids)
  • neuroblastoma
  • teratoma
  • neuroma
  • neuroganglioma
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13
Q

What is the commonest INTRACRANIAL tumour?

A

meningioma

  • mostly asymptomatic
  • usually in adults
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14
Q

What is the origin of meningiomas?

A
  • meningeal cells
  • arachnoid granulation fibroblasts within venous sinuses (attached to dura)
  • compresses NOT infiltrates
  • common in females (2:1)
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15
Q

What effect does progesterone have on meningiomas

A
  • stimulates increase in size
  • therefore F:M = 2:1
  • cyclical (menstruation) and pregnancy –> stimulates meningiomas
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16
Q

What are the commonest types of meningiomas?

A

parasagittal meningiomas

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17
Q

What are the features of meningiomas?

A
  • slow growth
  • multiple; asymptomatic commonly*
  • well differentiated and demarcated
  • does not invade brain tissue (benign - rarely malig.)
  • reactive hyperostosis of skull over tumour
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18
Q

What gene mutation is commonly seen in meningiomas?

A

NF2 gene mutation

-50% of meningiomas

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19
Q

What is the commonest histologic subtype of meningiomas?

A
  • psammomatous
  • rounded collection of epithelial-like looking cells (actually from fibroblasts)
  • microcalcification = psammoma bodies
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20
Q

Compare low and high grade commonest glioma in adults?

A

commonest glioma = astrocytoma
low grade –> solid, diffuse astrocytoma
high grade –> glioblastoma multiforme* (necrotic, haemorrhagic + highly malignant)

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21
Q

What is pilocytic astrocytoma?

A
  • commonest glioma in children

- ‘pilo’ = hairs (microscopically - cells have long, hairy processes)

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22
Q

What mutations can be found in adult + childhood astrocytomas?

A

Adults –> IDH1 mutation (immunostainng for IDH1 = important diagnostic tool)

Children –> BRAF mutation

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23
Q

What are grade IV astrocytomas AKA?

A

glioblastoma multiforme (GBM)

  • v. necrotic/haemorrhagic and high graded tumours
  • mean survival <1yr
  • commonest astrocytoma in adults (>40yrs)
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24
Q

What mutation is commonly present in glioblastoma multiforme patients?

A
  • mutation on chromosome 10

- 80% of cases

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25
Q

What are the 2 types of glioblastoma multiforme?

A
  1. primary (worst)
    - starts as high grade tumour and rapidly kills pt.
  2. secondary (more common - better prognosis)
    - starts from low grade astrocytomas
    - after many yrs –> high grade malignancy
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26
Q

What are the gross and microscopic features of glioblastoma multiforme?

A

Gross:

  • pleomorphic
  • necrotic (multiforme)
  • haemorrhagic

Micro:

  • pleomorphic cells
  • central necrosis
  • pallisading
  • haemorrhage
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27
Q

How can you differentiate between low grade and high grade (GBM) astrocytomas on MRI?

A

low grade = diffuse margins

high grade = well demarcated (due to rapidly growing tumour); also RING ENHANCEMENT

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28
Q

What is ring enhancement?

A
  • feature of very high grade astrocytoma (GBM)

- peritumoral edema

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29
Q

Where are pilocytic astrocytomas located and what clinical feature do they cause?

A
  • cerebellum
  • abnormal gait
  • *children, slow growth, low grade, BRAF mutation (not IDH1 - adults)
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30
Q

What are the gross and microscopic features of pilocytic astrocytomas?

A

Gross:
-cystic mass with mural nodule

Micro:
-hair-like (pilocytic) astrocytes

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31
Q

What cells are affected in medulloblastomas? and where in the brain do they occur?

A
  • embryonic cells
  • Primitive Neuro Ectodermal Tumour (PNET)
  • located in cerebellum (upper portion –> vermis)

N.B. highly malignant but v radiosensitive

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32
Q

True or False?

CSF seeding and meningeal irritation is common in medulloblastomas

A

True

-can present like meningitis

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33
Q

What is the microscopy of medulloblastoma?

A
  • dark blue, small, blast cells with scanty cytoplasm
  • similar to retinoblastoma, neuroblastoma, nephroblastoma, lung SCC, etc
  • rosettes and neuronal differentiation (embryonic) may be seen
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34
Q

What is infection of the dura known as?

A

pachymeningitis

  • rare
  • following sinusitis, fracture, etc
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35
Q

What is leptomeningitis?

A

infection/inflammation of the arachnoid only

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36
Q

What are the 2 types of meningitis?

A

Acute:

  • septic –> bacterial
  • aseptic –> viral

Chronic:
-fungal, TB, parasitic, etc

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37
Q

What is bacterial meningitis AKA?

A

acute pyogenic meningitis

38
Q

What is the term used when meningitis is combined with infection of the brain?

A

meningoencephalitis

39
Q

What are the causative pathogens for bacterial meningitis in infants, young adults and adults?

A

etiology = breakthrough the blood brain barrier

  • infants –> E. coli
  • young adults –> Neisseria meningitides; S. pneumoniae
  • adults –> S. pneumoniae
40
Q

What is the pathogenesis of neck stiffness in meningitis?

A

-inflammation of meninges is so severe that any movement of the head causes pain due to sensory nerves in the meninges

41
Q

What are the clinical features of meningitis?

A

-acute
-fever
Meningeal irritation:
-headache
-photophobia –> irritation to optic nerves
-clouding of consciousness –> raised ICP
-irritability
-neck stiffness –> severe meningeal inflammation
(-seizures)

*MENINGISM

42
Q

How is meningitis diagnosed?

A

Lumbar puncture (CSF)

  • increased pressure
  • increased WBCs/neutrophils
  • increased proteins
  • decreased glucose –> in bacterial as bacteria use up the glucose!
43
Q

What type of bacteria is Neisseria meningitides and how is it transmitted?

A
  • gram negative, aerobic, encapsulated diplococci

- transmitted via contact, schools, congregations, etc

44
Q

What % of people are healthy carriers for Neisseria meningitides?

A

10%

45
Q

What are the features of meningococcal meningitis and what is the characteristic feature?

A
  • begins as throat infection
  • headache
  • RASH* –> petichial/ecchymosis, non-blanching rash
  • drowsiness
  • confusion
  • convulsions/seizures
46
Q

Which meningococcal serotype is the most common?

A

serotype B

-vaccine now available for students :)

47
Q

What type of bacteria is responsible for streptococcus meningitis? and what % of the population have it as a commensal?

A

gram positive, aerobic, diplococci

–> 40% population = commensal

48
Q

True or false?

clinical features of streptococcal meningitis include meningism plus rash

A

False

-NO rash in strep meningitis, rash IS present in meningococcal meningitis

49
Q

Which age group is most affected by acute viral meningitis and what is the commonest causative virus?

A
  • more common in young (<5yrs)

- enterovirus –> coxsackie B virus

50
Q

What is the peculiarity of viral meningitis with regards to clinical features?

A
  • can be asymptomatic

- v. mild –> v. severe

51
Q

Describe the CSF features in viral meningitis?

A
  • clear (aseptic)
  • increased proteins
  • increased lymphocytes
  • NORMAL glucose –> virus does NOT use glucose (c.f. bacterial meningitis)
52
Q

What is the only microscopic finding supportive of viral meningitis?

A

perivascular lymphocyte cuffing

53
Q

What is the commonest cause of fungal meningitis?

A

Cryptococcus neoformans

-increased in immunosuppressed (AIDS) pts.

54
Q

What are the features of fungal meningitis?

A
  • thick, fibrotic exudate over meninges
  • mucoid exudate in ventricles –> hydrocephalus
  • small cysts in parenchyma (soap bubble lesions)
  • specifically in basal ganglia
55
Q

What % of AIDS pts have CNS involvement and how do they typically present?

A
  • 80%

- present as progressive dementia

56
Q

What cells in the CNS does HIV infect?

A

microglial cells –> glial nodules + multinucleate giant cells

57
Q

Which herpes virus is the most common in herpes encephalitis and what are the clinical features?

A

HSV-1

  • children/young adults
  • marked necrosis/destruction of inferior frontal/anterior temporal lobes due to virus –> memory, mood, and behavioural abnormalities result
58
Q

If CSF from a lumbar puncture appeared opalescent with ‘cobweb-like’ structures what is suspected?

A

TB –> meningitis

59
Q

What characteristic imaging finding is present in brain abscess?

A
  • ring enhancement (same as glioblastoma multiforme)

- peritumoral oedema

60
Q

What are the acute and chronic complications of meningitis?

A

acute: -oedema, raised ICP, herniation, ischaemia/infarction –> death
chronic: -epilepsy, hydrocephalus, abscess

61
Q

What is epilepsy?

A
  • abnormal, recurrent, spontaneous neuronal firing

- manifests clinically by changes in motor, sensory, behavioural +/or autonomic function

62
Q

What is ictus?

A

period of seizure

63
Q

What is a key feature of epilepsy that differentiates it from other causes of seizures?

A

stereotypic nature:

  • preceded by aura (subjective sensation –> pt can tell they are about to have a seizure)
  • postictal state (drowsiness, confusion, etc)
64
Q

Where are the most seizure-prone areas of the brain?

A

temporal lobe + hippocampus

65
Q

What is the commonest etiology of epilepsy?

A

idiopathic

66
Q

What is the pathogenesis of epilepsy?

A

-decreased inhibition of neurotransmission due to defective GABA neurons (gamma aminobutyric acid = major inhibitor of neurotransmission)

67
Q

How is epilepsy diagnosed?

A
  • MRI
  • CT
  • interictal EEG** –> abnormal spikes of neuronal activity in between seizure activity
68
Q

What is the commonest subtype of epilepsy?

A

complex partial epilepsy

  • partial = localised to one area of brain (INCR. TEMPORAL)
  • complex = altered LOC/behaviour

**SECOND COMMON = GRAND MAL (TONIC CLONIC)

69
Q

Outline subtypes of epilepsy

A

Partial: -seizure activity starts on one brain area

  • simple –> retains awareness
  • complex –> altered awareness/behaviour

Generalised: -seizure involves whole brain with ALOC

  • tonic clonic –> grand mal/convulsion
  • absence –> petit mal/staring fit
  • atonic/tonic –> drop attack
  • myotonic –> sudden muscle jerksq
70
Q

What is status epilepticus?

A
  • > 30 mins seizure OR from which a person does NOT regain consciousness
  • convulsive or non-convulsive
71
Q

What is the normal ICP and what is it comprised of?

A

5-10mmHg

-blood, brain, CSF

72
Q

What is the Monro-Kellie doctrine?

A

“the sum of the intracranial volumes is constant and therefore an increase in any one of these compartments must be offset by an equivalent decrease in the other two”

73
Q

What is the clinical definition of increased ICP?

A

> 20mmHg for >5mins

74
Q

What is cerebral perfusion pressure (CPP) and what is the normal level?

A

CPP = mean arterial pressure - intracranial pressure
CPP = MAP - ICP
-normal >50mL/100g/min

75
Q

What level of CPP is clinically defined as ischaemia?

A

<20mL

76
Q

What are the common causes of increased ICP?

A
  • cerebral oedema
  • congestion (inflammation, infection - meningitis)
  • hydrocephalus (block in CSF flow)
  • mass (tumour)
77
Q

What are the common clinical features of increased ICP?

A
  • headache, vomiting + visual disturbances

- depressed consciousness

78
Q

What is Cushing’s triad?

A
  • increased BP (hypertension)
  • decreased pulse (bradycardia)
  • irregular breathing

*v. severe injury involving the BRAINSTEM

79
Q

What are the 4 common types of herniation?

A
  1. Subfalcine/Cingulate
    - common; headache + contralateral leg weakness
  2. Transtentorial: central
    - thalamus and midbrain push towards 4th ventricle
    - small but reactive pupil; drowsiness; ALOC; agitation
  3. Transtentorial: temporal/uncal
    - CN III injury; ipsilateral dilated pupil; decreased LOC
  4. Tonsillar
    - obtundation; decerebrate posture; cardiorespiratory arrest (brainstem affected) **MOST SEVERE!
80
Q

What is the commonest type of herniation and what is the most severe type?

A

commonest = subfalcine/cingulate herniation

most severe = tonsillar

81
Q

What is the pathogenesis of contralateral leg weakness in subfalcine/cingulate herniation?

A
  • subfalcine herniation of cingulate gyrus causes block of ACA –> more infarction, oedema and further raised ICP
  • clinically (due to ACA block) –> contralateral leg weakness (hemipariesis)
82
Q

What is the typical Tx for central herniation?

A

craniectomy to relieve pressure (remove portion of skull)

83
Q

True or False?

dilated pupil with normal LOC is not herniation

A

True

84
Q

What are duret haemorrhages?

A
  • small areas of bleeding in midbrain/upper pons

- caused by compression of central veins due to cerebellar/tonsillar herniation

85
Q

What is the definition of hydrocephalus?

A

excess CSF in brain

86
Q

Where is CSF produced?

A

choroid plexus within ventricles of brain

87
Q

Through what does the CSF travel through to reach the subarachnoid space?

A

Foramen luschke and magendie

-absorbed back in arachnoid villi in venous sinuses

88
Q

What are the 3 major types of hydrocephalus?

A
  1. obstructive/non-communicating
    - obstruction to CSF flow –> dilatation of part of CSF space
  2. non-obstructive/communicating
    - excess CSF due to lack of absorption, infections/inflammations
  3. compensatory
    - secondary dilatation due to brain atrophy
89
Q

Cyclical pain is typically seen in which CNS tumour?

A

meningioma

90
Q

What are brain abscesses typically surrounded by?

A

scar tissue

Pathology Term 4 (6 decks)

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