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Sem 5 > NS 12: Neuropathology > Flashcards

NS 12: Neuropathology Flashcards

1
Q

3 possible routes for microorganisms to get into the CNS?

A

direct spread e.g. middle ear infection, spread to mastoid process and can cause a temporal lobe abscess, and base of skull fracture.
blood borne- cross BB barrier, e.g. infective endocarditis- streptococccus viridans or staph aureus
iatrogenic- e.g. following lumbar puncture, ventriculo-peritoneal shunts for hydrocephalus, surgery

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2
Q

what is meningitis the inflammation of?

A

meninges- specifically the leptomininges= arachnoid mater and pia mater.

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3
Q

in what 2 ways can meningitis cause death

A

rasied IC pressure

septicaemia- SHOCK- inadequate perfusion to vital tissues

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4
Q

what is seen histologically in the brain with meningitis?

A

neutrophil infiltration= multi-lobed nuclei

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5
Q

causes of meningitis in neonates?

A

E coli

listeria monocytogenes

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6
Q

cause of meningitis in children aged between 2 and 5?

A

Haemophilus influenzae B
less likely now following 5 in 1 vaccine immunisation programme= diptheria, tetanus, polio, pertusis- whooping cough and Hib- H influenzae.

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7
Q

cause of meningitis in those aged between 5 and 30?

A

Neisseria meningitidis

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8
Q

cause of meningitis in those aged over 30?

A

Strep pneumoniae

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9
Q

cause of chronic meningitis

A

M.TB- granulomatous inflammation- caseous necrosis, chronic inflammation= fibrotic meninges- causes nerve entrapment
tends to present with headaches and cranial nerve symptoms, may be weight loss and general malaise due to TB

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10
Q

complications of meningitis?

A

death-swelling within rigid cranium causes raised ICP
cerebral infarction-STROKE, causing neurological defecit
cerebral abscess
subdural empyema
epilepsy- part. in children if brain parenchyma damaged as epileptogenic focus created= origin of high frequency electrical impulses discharged episodically in epilepsy, causing seizures.

systemic- septicaemia

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11
Q

what is infected in encephalitis?

A

the brain parenchyma= neurones, neuronal bodies undergo cell death and get viral inclusions, causing neurone death.

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12
Q

what is encephalitis typically caused by?

A

viral infection

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13
Q

example of a virus which can infect the temporal lobe to cause encephalitis?

A

Herpes virus

tends to occur in children and immunocompromised individuals

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14
Q

what doe the polio virus infect?

A

spinal cord motor neurone cell bodies

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15
Q

what virus causes infection of brainstem?

A

rabies

varicella in children- causes chickenpox, but can cause encephalitis and pneumonitis

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16
Q

what happens histologically with encephalitis?

A

lymphocytic infiltration- chronic inflammatory reaction, lymphocytes form perivascular cuffs.

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17
Q

what inclusions occur with cytomegalovirus infection?

A

Owl’s eye

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18
Q

why are pregnant women told to avoid cats in pregnancy?

A

cats may carry toxoplasma gondii, found in their faces, and infection of the mother=toxoplasmosis, can cause teratogenic effects

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19
Q

when might toxoplasma cause problems?

A

pregnant women= teratogenic effects

immunocompromised- toxoplasma can become uncontrolled and cause encephalitis e.g. in chemotherapy patients.

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20
Q

what are prions?

A

proteins, normal constituents of neuronal synapse

if mutated can cause prion disease= mutated proteins aggregate together and interfere with synaptic transfer.

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21
Q

how can people get a mutated prion protein?

A

ingested
sporadic
inherited

22
Q

how does prion disease come about?

A

mutated prion protein can induce a conformational change in a normal prion protein of the neuronal synapse. can then aggregate together and disrupt neuronal transmission.
aggregates cause neurone death and holes in gray matter= spongiform encephalopathy
prion protein= very stable

23
Q

how is dementia separated from delerium?

A

dementia= no impairment of consciousness

24
Q

why are sulci and gyri more prominent in dementia?

A

have lost cortical neurones- death of neurones is accelerated

25
Q

2 causes of increased neuronal death in alzheimer’s disease?

A

neurofibrillary tangles

senile plaques

26
Q

how do neurofibrillary tangles cause damage in alzheimer’s disease?

A

= IC twisted filament of Tau protein= normal protein which usually binds and stabilises microtubules, but protein becomes hyperphosphorylated so clumping occurs as the proteins stick together, posionous to neurone causing cell death= tauopathy.

27
Q

example of genetic familial cause of alzheimer’s disease, which subsequently occurs early in life e.g. in 30s?

A

Down’s syndrome
3 genes related to amyloid protein on chromosome 21
Amyloid precusor protein (APP) gene,
Presenilin (PS) genes 1 and 2 code for components of
secretase enzyme,
Leads to incomplete breakdown of APP and amyloid
is deposited.

28
Q

how do senile plaques cause damage in alzheimer’s disease?

A

Foci of enlarged axons,synaptic terminals and
dendrites, amyloid deposition in vessels in centre of
plaque.

29
Q

pressure normally exerted by CSF?

A

minimal, up to 10mmHg

coughing can increase it to 20mmHg

30
Q

compensation of brain to raised ICP?

A

less blood sent to brain- reduce blood volume
reduced CSF volume= these 2 take hrs to days
brain atrophy= occurs over much longer time period

rasied ICP only significant if maintained for several mins

31
Q

for what ICP can vascular mechanisms maintain cerebral b.flow?

A

Vascular mechanisms maintain cerebral
blood flow as long as ICP <60mmHg

*t occur, and survival instinct- try and get brain below heart to get blood into it.

32
Q

what structures stop the brain from moving, causing problems with raised ICP in expanding SOLs?

A

rigid skull
falx cerebri
tentorium cerebelli= infolded layers of the meningeal layer of the dura mater

33
Q

causes of raised ICP?

A 
tumour
haematoma
abscess
infarction= oedema of surrounding tissues
=expanding focal lesions
infection e.g. meningitis, encephalitis= inflammatory
oedema
trauma
= global increase in brain mass
34
Q

what is subfalcine herniation?

A

cingulate gyrus pushed under free edge of falx cerebri
occurs on same side of mass
compromises blood flow through anterior cerebral artery from ICA, so ischaemia of medial parts of the frontal
and parietal lobe and corpus callosum= infarction

35
Q

false localising sign in tentorial herniation?

A

pupil dilation= makes you think lesion on 1 side of brain e.g. stroke, when in fact whole brain experiencing increase in ICP.

36
Q

what happens in tentorial hernitation?

A

uncus pushed through tentorial notch
Damage to the occulomotor nerve on the same
side
Occlusion of blood flow in posterior cerebral and
superior cerebellar arteries
Frequently fatal because of secondary haemorrhage
into the brainstem, resulting in Duret haemorrhage
Common mode of death in those with large brain
tumours and intracranial haemorrhage, and meningitis and encephalitis, brainstem centres compressed so ptnt stops breathing.

37
Q

prodromal features in ptnt with raised IC pressure?

A

headache- worse on walking, lying down and 1st thing on a morning
vomiting
papilloedema- optic disc swelling

38
Q

what happens in acute phase of raised ICP?

A

Occulomotor nerve compression = dilation of the pupil
Compression of the brain stem = coma

alongside, getting compression of cerebral peduncles= hemiparesis, and compression of vital bstem structures causing apnoea and cardiac arrest.

39
Q

what happens in coning?

A

cerebellar tonsils pushed into foramen magnum, compressing brainstem

40
Q

what would very high BP and weak pulse indicate in a patient previously experiencing headaches worse on a morning and walking, and vomiting?

A

Cushing’s reflex following raised ICP compressing brainstem centres
very high BP as body trying to pump blood to brain, and bradycardia

41
Q

most common benign tumour of brain?

A

meningioma

42
Q

origin of malignant tumours in brain which originate in brain?

A

astrocytes
astrocytoma (grade 1 to grade 4) grade 1= well differentiated, 4=anaplastic
– Spread along nerve tracts and through sub arachnoid
space often presents with a spinal secondary
*malignant of brain never metastasise to out of CNS

43
Q

most common tumour in brain?

A

result of metastasis

common metastases to brain= breast cancer, lung cancer, bladder cancer, kidney cancer

44
Q

why are MRIs done following new onset epilepsy?

A

check for brain tumours- causing a focus

45
Q

primary damage in head trauma?

A

physical damage to brain:
Focal damage
– Bruising and laceration of the brain as it hits the
inner surface of the skull
– Tearing of blood vessels and nerves as the brain
moves causing haemorrhage and blood is an irritant to brain, causes vasoconstriction.

Diffuse
– Direct tearing to axons - Diffuse Axonal Injury (DAI)
white matter and grey matter accelerate and decelerate at different times

46
Q

types of damage in focal damage when primary damage occurs in head injury?

A 
coup= focal damage at site if impact
contrecoup= damage on opposite side of brain, often of greater severity
47
Q

what happens with diffuse injury (diffuse axonal injury DAI) in primary damage in head trauma?

A

Micro-tears to axons at sites of differing densities of
brain substance e.g. junction of white and gray
matter
Tearing of nerves and small vessels
Tearing of the pituitary stalk
Severity proportional to the degree of force
(especially rotational), often persistent vegetative
state
Heals by gliotic scarring- damage is permanent*

48
Q

how does a stroke differ from a TIA?

A

TIA- symptoms last for <24 hrs, and complete recovery occurs following this time.
stroke= residual neurological defecit e.g. difficulty moving, difficulty with speech.

49
Q

what do lacuna infarcts commonly affect?

A

basal ganglia

50
Q

2 different types of haemorrhagic strokes?

A 
intracerebral haemorrhage (10%)
SAH (5%)
51
Q

characteristics of IC haemorrhagic strokes?

A

Associated with hypertensive vessel
damage
Charcot-Bouchard aneurysms, artery usually around basal ganglia
May be assoc. with deposition of amyloid around cerebral
vessels in the elderly
May be inherited
Produces space occupying lesion – RICP

52
Q

characteristics of SA haemorrhagic strokes?

A

Rupture of ‘berry’ aneurysms
Pathogenesis poorly understood
– Male sex-inherited
– Hypertension- aneurysm more likely to burst if high BP
– Atheroma
– Links to other diseases
Sited at branching points in the Circle of Willis

occur at base of brain, high pressure arterial blood

thunderclap headache
sentinel headache- occur before big headache= intermittent bleeding of aneurysms before rupture
Loss of consciousness
Often instantly fatal
Arterial spasm - ischaemia and infarction

Sem 5 (35 decks)

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