Neurovascular Disease Flashcards

1
Q

arteriovenous malformation

A

complex tangle of abnormal arteries and veins connected together with fistulas creating a shunt that connects them directly - bypassing the normal capillary network

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2
Q

are AVM congenital?

A

some are, can occur later in life

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3
Q

do AVM cause any problems as they are?

A

they tend to be silent until there is a big problem, can cause a progressive neurological deficit as they steal the blood flow to tissue

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4
Q

what acute problems can AVM cause

A

haemorrhage (1), seizure (2), headache

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5
Q

AVM occuring in which areas of the brain are more likely to caue focla and general seizures

A

frontal lobe - generalised

temporal lobe - focal

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6
Q

investigation of AVM

A

catheter angiography - navigated under x ray guidance

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7
Q

investigation of AVM in acute setting

A

CT angiography is faster than catheter so may be used

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8
Q

what procedure may be performed pre surgery on AVM

A

embolization - decrease blood flow through AVM allowing surgery to take place in a more blood less and controlled way

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9
Q

surgical options for AVM

A
  • open craniotomy
  • stereotactic radiosurgery
  • endovascular coiling
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10
Q

which blood vessels cause SAH

A

circle of Willis (90%), also vertebro basilar circulation

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11
Q

which areas of the blood vessels are high risk sites for damage (SAH)

A

bifurcation

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12
Q

2y damage caused by SAH

A

damage surrounding parenchyma due to haemorrhage, infarcts due to disruption of blood supply

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13
Q

most common place for berry aneurysm

A

bifurcation of anterior cerebral and communicating artery

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14
Q

what are fusiform aneurysms associated with

A

diffuse atheromatous degeneration of arterial wall assoicated with hypertension

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15
Q

are females or males more at risk of aneurysm rupture

A

females

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16
Q

are aneurysms in the posterior or the anterior circulation more likely to rupture

A

posterior

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17
Q

risk factors for aneurysms (and rupture)

A

bigger aneurysm, comorbidities (hypertension, smoking, alcohol), bleeding disorder

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18
Q

name 2 drugs that increase blood pressure

A

cocaine, methamphetamine - inc risk of aneurysm rupture

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19
Q

which connective tissue disease is assoicated with aneurysms

A

ehlers danlos - assoicated with very fragile blood vessels

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20
Q

fibromuscular dysplasia

A

abnormal development of arteries leads to narrowing in some places - this creates a string of beads appearance

found in renal, cerebral and carotid arteries. are prone to haemorrhage, aneurysm etc

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21
Q

what problems can aneurysms cause as they are - think compression

A

can compress specific CN

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22
Q

which CN is at risk of compression from a posterior communicating aneurysm

A

CN III

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23
Q

what is at risk of compresion from an ACOM aneurysms

A

optic chiasm

24
Q

presentation of SAH

A
  • thunderclap headache - sudden onset, vvv severe, occipital typically
  • n and v, collapse, seizures, coma, drowsiness (may persist for days)
25
Q

what symptoms arise in SAH due to irritation of the meninges from blood

A

meningitis - neck stiffness, photophobia, fever, Kernigs sign

26
Q

what is teh diagnostic test for SAH

A

CT

27
Q

SAH: what investigation do you perform if CT is normal, when would you do it and what findings would you expect

A

lumbar puncture - wait at least 12 hours from start of headache to allow time for blood cells to lyse and xanthochromia to develop

CSF has blood in it (circulates in subarachnoid space), blood turns yellow due to breakdown and bilirubin release - xanthochromia

28
Q

management of SAH

A
  • endovascular coiling - block blodo flow into aneurysms by inducing clotting of the aneurysm
  • craniotomy and microsurgical clipping - wide necked aneurysm
29
Q

most common cause of death after SAH treatment

A

re bleeding - 20% occur in the first few days

30
Q

who is at the biggest risk of rebleeding after SAH

A

elderly and hypertensives

31
Q

managmenet of SAH re bleeding

A

surgical clipping or coiling again

32
Q

what problems can vasospasm cause after SAH

A
  • blood products can irritate arterial walls and cause spasm
  • this can cause ischaemia –> focal neurological deficit/altered state of consciousness
33
Q

how long after SAH does vaosospasm occur

A

3-10 days

34
Q

how to confirm diagnosis of vasospasm?

A

angiogram

35
Q

management of vasospasm

A

nimodipine - a Ca channel blocker than relaxes narrowed blood vessels

36
Q

SAH leading to hydrocephalus?

A

communicating - arachnoid granulations are blocked by blood

37
Q

seizures after SAH?

A

yes

38
Q

what is the most common electrolyte disorder after SAH

A

hyponatraemia - either through SIADH or CSWS

39
Q

SAIDH

A

the hypothalamus is stimulated by trauma/ischaemia adn there is excessive release of ADH - increased water reabsorption by the kidneys - this results in fluid retention and dilutional hyponatraemia

40
Q

CSWS

A

for some reason in reponse to brain injury or trauma the kidneys excrete too much Na - fluid follows

41
Q

do SIADH and CSWS create a hypo/eu volaemia hyponatraemia

A

SIADH - euvolaemia hyponatraemia

CSWS - hypovol hyponat

42
Q

does hyponatraemia indicate poor outcome?

A

it may, hyponatraemia can cause a shift in water from the EC to the IC space - worsen cerebral oedema and intracranial hypertension - inc risk of seizures and neurological injury

43
Q

management of hyponatraemia after SAH

A

avoid fluid restriction (normally part of SIADH management)

supplement Na intake

fludrocortisone - aldosterone replacement (increase Na absoprtion)

44
Q

where does the blood accumulate in extradural haematoma

A

between blood and dura

45
Q

what is the most common cause of an epidural haematoma

A

pterion fracture - injures middle meningeal artery which runs over the inner aspect of it

46
Q

what is the classical history of an epidural haematoma

A

young adult sustains closed head trauma - lucid interval (brief loss of consciousness, regain consciousness), then deteriorating state 3-4 hours later as blood accumulates

47
Q

how quickly is the decline in epidural haematoma, and why

A

froma high pressure arterial source, so rapid

48
Q

how does an epidural haematoma appear on ct

A

biconvex shape - midline shift due to pressure

it does not cross teh suture lines as the dura adheres tightly here to the skull

49
Q

where does the blood collect in a subdural haematoma and from which vessels

A

between the dura and arachnoid layer.

the cerebral veins drain blood from the brain out to the dural venous sinuses (located between the 2 layers of dura)

50
Q

why are teh elderly more prone to subdural haematima

A

as you get older, the brain atrophies - the bridging veins are stretched and so are more likely to rupture even with minor trauma

can present acute or be chrnoic

51
Q

what other things cause brain atrophy

A

epilepsy, dementia, chronic alcoholism

52
Q

how does a subdural haematoma present in an acute situation

A

decreased state of consciousness, confusion

53
Q

how does a chronic subdural haematoma present

A

insidiously, progressive headache and confusion

54
Q

if there is a subdural haematoma and it is non fatal, so not treated, what does the blood form on the surface of the brain?

A

a yellow neo-membrane

55
Q

subdural haematoma ct

A

some of the blood may be hypodense (black) if it is chronic

may see acute on chronic

56
Q

what is coup and countercoup, and which often causes the most severe injuries?

A

coup = damage at point of impact

countercoup = damage occuring when brain rebounds and hits back of skull

countercoup

57
Q
A