Neuropathology 2 - Demyelination and Dementia Flashcards
the brain is viscoeleastic, what does this mean?
mechanically behaves like a fluid and a solid
what happens to CSF in raised ICP?
some blood +/- CSF must escape from cranium to avoid pressure rise
once this is exhausted, venous sinuses are flattened and there is little - no CSF
therefore any further increase in brain volume causes raised ICP
normal CSF volume?
120-150 ml
500ml made per day
CSF made in which ventricles?
lateral and 4th
describe CSF fluid?
clear no neutrophils very few lymphocytes very little protein some glucose no RBCs >lymphocytes = infection >neutrophils = infection/meningitis
what can cause hydrocephalus?
obstruction to flow (tumour, inflammation etc) decreased reabsorption (post SAH, meningitis etc) overproduction (choroid plexus tumour - v. rare)
non-communicating hydrocephalus?
obstruction to flow within ventricular system
communicating hydrocephalus?
obstruction to flow outside ventricular system (e.g in subarachnoid space or arachnoid granulations)
what happens if hydrocephalus occurs before or after closure of cranial sutures?
before closure = cranial enlargement
after closure = expansion of ventricles and increase in ICP
what is hydrocephalus ex vacuo?
dilation of the ventricular system and a compensatory increase in CSF volume secondary to loss of brain parenchyma (e.g alzheimers)
5 effects of raised ICP?
intracranial shifts and herniations - “coning”
midline shift
distortion and pressure on cranial nerves and vital neurological centres
impaired blood flow
reduced consciousness
physiological causes of raised ICP?
hypoxia
hypercapnia
pain
4 types of shifts/herniation?
subfalcine
tentorial/central
cerebellar
transcervical
describe a subfalcine herniation
unilateral/asymmetrical expansion of cerebral hemisphere which displace singulate gyrus under falx cerebri
can compress anterior cerebellar artery, sensory/motor weakness in leg
describe tentorial/central herniation
medial aspect of temporal lobe herniates over tentorium cerebelli
compression of CN III (blown pupil and impaired ocular movement)
describe cerebellar herniation
displacement of cerebellar tonsils through foramen magnum
compresses resp centres
describe transcervical herniation
swollen brain herniates through any weakness in skull (e.g after fracture)
signs of raised ICP?
papilloedema
headache (worse on lying down, coughing etc)
nausea and vomiting
neck stiffness
general clinical presentation of brain tumours?
focal symptoms headache (worse in morning) vomiting seizures visual disturbance focal deficit papilloedema
most common site of brain tumour in adults/children?
kids = below tentorium cerebelli adults = above
multiple brain tumours are most likely to be what?
metastatic
how are primary brain tumours graded generally?
mitosis
neovascularisation
necrosis
atypia, cellularity etc
what secondary feature of brain tumour can be very harmful?
oedema
most common subtype of brain tumour in adults and children?
adults = astrocytoma kids = medullablastoma < astrocytoma
WHO astrocytoma grading 1-4?
- eg pilocytic (benign, in kids, cystic)
- nuclear atypia
- anaplastic, more nuclear atypia and mitotic activity
- e.g glioblastoma, extreme nuclear atypia and mitotic activity, neovascularisation
1 doesn’t progress to malignant, 2+ all progress
what is seen on histology in glioblastoma?
proliferation
anaplasia
necrosis and palisading
neoangiogenesis
describe medulloblastoma
poorly differentiated/embryonal
occurs in midline of cerebellum
very radiosensitive so good survival with treatment
what can cause single abscess?
local extension (eg from chronic otitis media or mastoiditis) direct implantation (skull fracture etc)
what can cause multiple abscesses?
usually haematogenous spread(pneumonia, endocarditis)
tend to occur at grey/white matter boundary
how is abscess diagnosed?
symptoms of fever, raised ICP and underlying cause
CT/MRI showing enhancing lesion
aspiration for culture and treatment
how is brain abscess managed?
can be difficult due to blood supply
aspiration can assist with treatment
then weeks of antibiotics
classification of head injury?
missile (penetrating)
non-missile (blunt)
features of a penetrating head injury?
usually focal damage
lacerations in region of brain damage
haemorrhage
high vs low velocity missile head injury?
high velocity = more damage (cavitation due to low pressure surrounding fast moving projectile)
what causes a non-missile head injury?
sudden acceleration/deceleration of head
brain moves within the cranial cavity and makes contact with the inner table of the cranium and bony protrusions
what determines force of injury in non-missile head injury?
the contact time
smaller contact time = larger force
- i.e hard objects = small contact time, squishy objects = larger contact time
pathophysiology of primary and secondary head injury?
primary - impact = injury to neurones, irreversible
secondary injury = haemorrhage, oedema, potentially treatable
signs of primary injury?
scalp leisons skull fractures surface contusions surface lacerations diffuse axonal/vascular injury petechial haemorrhages
types of skull fracture?
linear - straight, sharp, due to a large force, likely to have an underlying haematoma
compound - assoc with full thickness scalp lacerations
depressed - most are compound
base of skull - causes bacterial infection as often damage nasopharynx etc causing open fracture
coup vs contra-coup?
injuries on lateral surfaces of hemispheres where brain has hit off internal surface of cranium on impact
coup = occurs at point of impact
contra-coup = directly opposite to area of impact, tend to be worse
why might contra-coup be worse than coup?
denser CSF moves to impact site forcing the brain to the contra-coup side so this impact has higher injury
or could be due to lower pressure
what is diffuse axonal injury?
occurs at moment of injury where shearing strains tear axons at time of injury due to acceleration and deceleration
affects central areas
reduced consciousness and coma
can lead to vegetative state
how does diffuse axonal injury occur?
different parts of the brain can move independently from each other in different directions (e.g right/left hemispheres) causing shearing of connecting axons
what is seen in diffuse axonal injury?
axonal bulbing
3 types of oedema?
cytotoxic (alcohol, hypothermia etc)
ionic/osmotic (hyponatraemia, excess water/SIADH)
vasogenic (trauma, tumours, infection, encephalopathy)
most traumatic intracrnail haematomas are where?
intradural
what is a burst lobe?
subdural haemorrhage in continuity with intracerebral haematoma particularly in frontal and temporal lobe
describe traumatic extradural haematomas and its effects?
usually due to tempero-parietal fracture involving middle meningeal artery
causes rapid decrease in cognition?
minimal immediate damage but causes shift/herniation and compression if untreated
describe subdural haemorrhages?
collection of blood between internal surfaces of dura mater and arachnoid mater
caused by disruption of bridging veins that extend from the surface of the brain into subdural space
describe acute subdural haematoma?
most common head injury in elderly
uni/bilateral
sulci preserved as pressure evenly distributed
swelling of cerebrum on side of haematoma
60% mortality but can be non-fatal and haematoma is liquified over time
…
describe chronic subdural haemorrhages
less commonly assoc with traumatic injury
assoc with brain atrophy
composed of liquefied blood/yellow tinged fluid
