8.3 neuropathology Flashcards
how can microorganisms gain entry into the CNS?
Direct spread (from middle ear, basal skull fracture, even through ethmoid bone)
blood borne in sepsis of infective endocarditis
latrogenic (post neurosurgery, ventriculoperitoneal shunt, lumbar puncture)
what is a sign of septicaemia in meningitis?
a non blanching rash = meningococcal septicaemia
what are the causative organisms of meningitis in different age groups?
Neonates - E. coli, L. monocytogenes
2-5 yrs - H influenza type B
5-30 yrs - N meningitides
over 30 yrs - S. pneumoniae
what are the properties of chronic meningitis?
caused by M tuberclosis
granulomas
meningeal fibrosis
cranial nerve entrapment
bilateral adrenal haemorrhage can be a complication
what are the complications of local meningitis?
- death due to raised intracranial pressure
- cerebral infarction (stroke)
- cerebral abscess
- subdural empyema
- epilepsy (due to direct irritation of brain)
under what circumstances can you get systemic effects resulting from meningitis?
if you have septicaemia
what is encephalitis and its usual causative organism?
inflammation of brain parenchyma and not meninges (but can occur as a complication of meningitis)
usually viral. it kills neurones causing inflammation
NB: Herpes affects temporal lobe
what is inflamed in meningitis?
the leptomeninges
what is a prion? and how can it mutate?
a normal constituent of synapse function
mutation can be sporadic, familiar or ingested
will then interact with normal prion protein to undergo a post translation conformational change to form a very stable structure
(isn’t susceptible to immune damage as seen as a self antigen)
what is prion disease?
when mutated prions aggregate together which destroy neurones and create holes in the grey matter
brain takes on a sponge like appearance = spongiform encephalopathies
(e.g mad cow disease)
what is Alzheimers disease (dementia)?
loss of cortical neurones
leads to cortical atrophy and decreased brain weight
damage caused by neurofibrillary tangles and plaques
how can neurofibrillary tangles and plaques cause damage in Alzheimers dementia?
tangles
- twist tau protein
- tau normally binds to microtubules
- hyperphosphorlylation = tangle
plaques
- foci of enlarged axons, synaptic terminals and dendrites
- amyloid deposition in centre of plaque associated with vessels
- trisomy 21 associated with Alzheimers disease
what is normal intracranial pressure and how is it maintained?
0-10mmHg is normal
coughing/straining can increase it to 20mmHg
compensatory mechanisms in place to compensate for ant rise
- reduced blood and CSF volume
- brain atrophy if chronically elevated
how do space occupying lesions affect the brain?
deforms or destroys surrounding brain
displaces midline structures e.g loss of symmetry, midline shift
can cause brain herniation
what types of herniations can space occupying lesions in the brain cause?
subfalcine herniation
- cingulate gyrus is pushed under free edge of faux cerebri
- can become ischaemic due to compression of anterior cerebral artery
tentorial herniation
- medial temporal lobe is pushed down through the tectorial notch ( free edge of tentorium cerebella)
- can compress ipsilateral oculomotor nerve and ipsilateral cerebral peduncle = ipsilateral third nerve palsy and contralateral UMN signs int he limbs
- a mode of death