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Neurology > Neuropathology 2 - Demyelination and Dementia > Flashcards

Neuropathology 2 - Demyelination and Dementia Flashcards

1
Q

the brain is viscoeleastic, what does this mean?

A

mechanically behaves like a fluid and a solid

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2
Q

what happens to CSF in raised ICP?

A

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

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3
Q

normal CSF volume?

A

120-150 ml

500ml made per day

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4
Q

CSF made in which ventricles?

A

lateral and 4th

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5
Q

describe CSF fluid?

A 
clear
no neutrophils
very few lymphocytes
very little protein
some glucose
no RBCs
>lymphocytes = infection
>neutrophils = infection/meningitis
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6
Q

what can cause hydrocephalus?

A 
obstruction to flow (tumour, inflammation etc)
decreased reabsorption (post SAH, meningitis etc)
overproduction (choroid plexus tumour - v. rare)
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7
Q

non-communicating hydrocephalus?

A

obstruction to flow within ventricular system

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8
Q

communicating hydrocephalus?

A

obstruction to flow outside ventricular system (e.g in subarachnoid space or arachnoid granulations)

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9
Q

what happens if hydrocephalus occurs before or after closure of cranial sutures?

A

before closure = cranial enlargement

after closure = expansion of ventricles and increase in ICP

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10
Q

what is hydrocephalus ex vacuo?

A

dilation of the ventricular system and a compensatory increase in CSF volume secondary to loss of brain parenchyma (e.g alzheimers)

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11
Q

5 effects of raised ICP?

A

intracranial shifts and herniations - “coning”
midline shift
distortion and pressure on cranial nerves and vital neurological centres
impaired blood flow
reduced consciousness

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12
Q

physiological causes of raised ICP?

A

hypoxia
hypercapnia
pain

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13
Q

4 types of shifts/herniation?

A

subfalcine

tentorial/central

cerebellar

transcervical

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14
Q

describe a subfalcine herniation

A

unilateral/asymmetrical expansion of cerebral hemisphere which displace singulate gyrus under falx cerebri
can compress anterior cerebellar artery, sensory/motor weakness in leg

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15
Q

describe tentorial/central herniation

A

medial aspect of temporal lobe herniates over tentorium cerebelli
compression of CN III (blown pupil and impaired ocular movement)

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16
Q

describe cerebellar herniation

A

displacement of cerebellar tonsils through foramen magnum

compresses resp centres

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17
Q

describe transcervical herniation

A

swollen brain herniates through any weakness in skull (e.g after fracture)

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18
Q

signs of raised ICP?

A

papilloedema
headache (worse on lying down, coughing etc)
nausea and vomiting
neck stiffness

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19
Q

general clinical presentation of brain tumours?

A 
focal symptoms
headache (worse in morning)
vomiting
seizures
visual disturbance 
focal deficit
papilloedema
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20
Q

most common site of brain tumour in adults/children?

A 
kids = below tentorium cerebelli
adults = above
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21
Q

multiple brain tumours are most likely to be what?

A

metastatic

22
Q

how are primary brain tumours graded generally?

A

mitosis
neovascularisation
necrosis
atypia, cellularity etc

23
Q

what secondary feature of brain tumour can be very harmful?

24
Q

most common subtype of brain tumour in adults and children?

A 
adults = astrocytoma
kids = medullablastoma < astrocytoma
25
WHO astrocytoma grading 1-4?
1. eg pilocytic (benign, in kids, cystic) 2. nuclear atypia 3. anaplastic, more nuclear atypia and mitotic activity 4. e.g glioblastoma, extreme nuclear atypia and mitotic activity, neovascularisation 1 doesn't progress to malignant, 2+ all progress
26
what is seen on histology in glioblastoma?
proliferation anaplasia necrosis and palisading neoangiogenesis
27
describe medulloblastoma
poorly differentiated/embryonal occurs in midline of cerebellum very radiosensitive so good survival with treatment
28
what can cause single abscess?
``` local extension (eg from chronic otitis media or mastoiditis) direct implantation (skull fracture etc) ```
29
what can cause multiple abscesses?
usually haematogenous spread(pneumonia, endocarditis) | tend to occur at grey/white matter boundary
30
how is abscess diagnosed?
symptoms of fever, raised ICP and underlying cause CT/MRI showing enhancing lesion aspiration for culture and treatment
31
how is brain abscess managed?
can be difficult due to blood supply aspiration can assist with treatment then weeks of antibiotics
32
classification of head injury?
missile (penetrating) | non-missile (blunt)
33
features of a penetrating head injury?
usually focal damage lacerations in region of brain damage haemorrhage
34
high vs low velocity missile head injury?
high velocity = more damage (cavitation due to low pressure surrounding fast moving projectile)
35
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
36
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
37
pathophysiology of primary and secondary head injury?
primary - impact = injury to neurones, irreversible | secondary injury = haemorrhage, oedema, potentially treatable
38
signs of primary injury?
``` scalp leisons skull fractures surface contusions surface lacerations diffuse axonal/vascular injury petechial haemorrhages ```
39
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
40
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
41
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
42
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
43
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
44
what is seen in diffuse axonal injury?
axonal bulbing
45
3 types of oedema?
cytotoxic (alcohol, hypothermia etc) ionic/osmotic (hyponatraemia, excess water/SIADH) vasogenic (trauma, tumours, infection, encephalopathy)
46
most traumatic intracrnail haematomas are where?
intradural
47
what is a burst lobe?
subdural haemorrhage in continuity with intracerebral haematoma particularly in frontal and temporal lobe
48
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
49
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
50
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 ...
51
describe chronic subdural haemorrhages
less commonly assoc with traumatic injury assoc with brain atrophy composed of liquefied blood/yellow tinged fluid

Neurology (53 decks)

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