Neuropathology Flashcards
(32 cards)
What are the 3 routes by which microorganisms can gain entry to the CNS?
- Direct Spread from a physical breach- e.g. middle ear infection, base of skull fracture
- Blood-borne - sepsis, infective endocarditis
- Iatrogenic (by medical professionals) - e.g. V-P shunt, surgery, lumbar puncture
What is meningitis, what are the consequences of it if left untreated?
Meningitis is inflammation of the leptomeninges (pia + arachnoid mater). Can occur with/ without septicaemia
Untreated causes rapid influx of oedema, neutrophil influx causes pus → raises ICP leading to death if not quickly treated
What are the main causative organisms of meningities in the age groups:
Neonates
2-5 years
5-30 years
Over 30s
Neonates - E.coli, L. monocytogenes
2-5 years - H. influenzae type B (HiB) - vaccinated against
5-30 years - N. Meningitides types A,B+C
Over 30s - S.pneumoniae
What organism causes chronic meningitis?
What are the effects of having chronic meningitis?
Mycobacterium Tuberculosis
- Granulomatous inflammation
- Fibrosis of the meninges
- Nerve entrapment
- facial nerve palsy
- headache
What are the some the local and systemic complications of meningitis
Local:
- Death (swelling raises ICP)
- Cerebral infarction → neurological deficit
- Cerebral abcess
- Subdural empyema → chronic pus
- Epilepsy
Systemic: if associated with speticaemia
What is Encephalitis?
Inflammation of the parenchyma (not the meninges) in the brain - affects neuronal cell bodies
What type of microorganisms cause encephalitis affecting different areas of the brain:
- Neuronal cell death
- Temporal lobe
- Spinal cord motor neurones
- Brain Stem
Mainly viral not bacterial
- Neuronal cell death - inclusion bodies (build up of virus)
- Temporal lobe - Herpes Virus
- Spinal cord motor neurones - Polio
- Brain Stem - Rabies
How do you treat encephalitis?
Often self limiting in young patients as long as they’re not immunocompromised
What are prions?
Prions are proteins we all have that are a part of synpases
What is prion disease?
- Mutation in prion proteins that are either sporadiac, familial or ingested
- Mutated PrP interacts with normal PrP to induce post translational conformational change
- Makes an extremely stable striucture that aggregates and cannot be elimited
- Causes neuronal death and holes in grey matter → spongiform encephalopathies
Name some types of spongiform encephalopthies
- Scrapie in sheep
- BSE in cows
- vCJD- Variant Creutzfeld- Jacob Disease - strongly associated with BSE
- Kuru in tribes of New Guinea
There are 2 forms of vCJD, classic and variant. What are the different clinical features of each?
Why is prion diease not classed as infection?
- Infectious agents should not be found in healthy organisms which prions are
- Microorganisms must be isolated and grown in pure culture- proteins cannot be grown
What is dementia?
Name the most common types
Aquired global impairment of intellect, reason and personality without impairment of conciousness
- Alzehimer’s (50%)- Sporadic/ Familial, Early/ Late
- Vascular dementia (20%)
- Lewy body
- Pick’s disease (Fronto-temporal dementia)
What happens to the brain in Alzheimer’s Disease?
- Brain undergoes an exggerated aging process
- Loss of cortical neurones
- decreased brain weight- greater sulci/ gyri definition
- cortical atrophy (thinner cortex)
- Neurofibrillary tangles and senile plaques cause increased neuronal damage
What are neurofibrillary tangles?
- Found in Alzheimer’s Disease
- Intracellular twisted filaments of Tau protein
- Tau, normally binds and stabilies microtubules
- Tau becomes hyperphospharylated and starts to aggregate
- Cell can’t function and produce energy → death
What are senile plaques?
- Plaques found in Alzheimer’s Disease
- Foci of englarged axons, synaptic terminals and dendrites
- Amyloid deposition in vessels in the centre of the plaque- buolds up around blood vessels causing ischemia
- Look like balls of cotton wool
What is the link between amyloid deposition and chromosome 21?
- Down’s syndrome (trisomy 21) will have early onset AD
- Mutation in 3 genes on trisomy 21 throught to be ivolved
- Amyloid precursor protein (APP) gene
- Presenlin genes 1 and 2 make secretase (enzyme that breaks down amyloid)
- Leads to incomplete breakdown of APP and amyloid is deposited
What is normal brain ICP?
0-10 mmHg
(may increase to 20mmHg during coughing and straining)
What compensatory mechanisms happen to maintain noraml brain ICP?
- Recued blood volume
- Reduced CSF volume
- Spatial → brain atrophy (if raised ICP is chronic)
Mechanisms work as long as ICP is <60 mmHg
If ICP raises too much it will cause herniation. What are the different types of herniation?
- Subfalcine
- Tentorial
- Tonsilar
Explain what happens in a subfalcine herniation
- The cingulate gyrus on the same side of the SoL is pushed under the free edge of the falx cerebri
- Causes ischemia of medial parts of the frontal & parietal lobes and the corpus callosum due to compression of the anterior cerebral artery → infarction
What happens in tentorial herniation?
- The uncus (medial part of the parahippocampal gyrus) is pushed through the tentorial notch
- Can cause damage to the occulomotor nerve (on the same side)
- Occlusion of blood flow in posterior cerebral and uperior cerebrallar arteries
- Frequently fatal due to secondary haemorrhage into the brainstem (Duret Haemorrhage- of the midbrain & pons)
What happens in tonsilar herniation?
- Cerebellar tonsisl are pushed into the foramen magnum compressing the brainstem
- Early on- blood can’t get to brain so systemic blood pressure rises to compensate
- After time- brainstem herniation depresses cardio respiratory centres
- Cushing’s reflex : High BP and Bradycardia
