Neurology Flashcards

1
Q

Strokes/cerebrovascular events are either:

A

Ischaemic
Intracranial haemorrhage

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2
Q

Causes of an ischaemic stroke/disruption to blood supply

A

Thrombus/embolus
Atherosclerosis
Shock (hypotension)
Vasculitis

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3
Q

What is a TIA?

A

transient neurological dysfunction secondary to ischaemia WITHOUT infarction

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4
Q

what is the significance of a TIA?

A

often precede a full stroke

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5
Q

what is a crescendo TIA?

A

2 or more TIAs within a week, high risk of developing into a full stroke

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6
Q

presentation of a stroke

A

asymmetrical symptoms

sudden weakness of limbs
sudden facial weakness
sudden onset dysphasia
sudden onset visual or sensory loss

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7
Q

presentation of a stroke

A

asymmetrical symptoms

sudden weakness of limbs
sudden facial weakness
sudden onset dysphasia
sudden onset visual or sensory loss

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8
Q

what is the ROSIER tool?

A

need to exclude hypoglycaemia first ***

tool for recognition of stroke in the emergency room
score >0 = likely stroke

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9
Q

first line radiological investigation for suspected stroke

A

non-contrast CT

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10
Q

management of a stroke

A

300mg of aspirin as soon as haemorrhagic stroke has been excluded

thrombolysis with alteplase - no haemorrhage, within 4.5 hours

thrombectomy

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11
Q

criteria for thrombectomy

A

offer as soon as possible and within 6 hours of symptom onset, as well as IV thrombolysis (if within 4.5 hours) to those with acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation
- via computed tomographic angiography (CTA) or magnetic resonance angiography (MRA)

offer as soon as possible to those who were last known to be well between 6-24 hours, have confirmed occlusion of proximal anterior circulation, potential to salvage brain tissue proven by CT perfusion or diffusion-weighted MRI showing limited core infarct volume

consider thrombectomy with IV thrombolysis (within 4.5 hours) as soon as possible for people last known to be well up to 24 hours previously who have acute ischaemic stroke and confirmed occlusion of proximal posterior circulation & potential to salvage brain tissue

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12
Q

secondary prevention of stroke

A

clopidogrel 75mg (/aspirin plus modified release dipyridamole)

atorvastatin 80mg, but not started immediately due to the risk of haemorrhagic transformation

potential carotid endarterectomy or stenting in patients with carotid artery disease

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13
Q

what is the regional blood supply to the brain?

A

anterior cerebral - anteromedial portion of cerebrum
middle cerebral - lateral portions
posterior cerebral - medial and lateral parts of posterior cerebrum

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14
Q

MDT involved in stroke rehab

A

physiotherapists
nurses
speech and language
dieticians
occupational therapy
social services
psychology
optometry
orthotics

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15
Q

risk factors for intracranial bleeds

A

anticoagulants
head injury
hypertension
aneurysms
brain tumours
ischaemic stroke can progress to haemorrhagic (exacerbated with re-perfusion of alteplase)

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16
Q

presentation of intracranial bleed

A

sudden onset headache
seizures
weakness
nausea/vomiting
reduced consciousness
other sudden onset neurological symptoms

17
Q

causes of an extradural haematoma

A

rupture of the MMA in the temporo-parietal region e.g. fracture of the temporal bone

18
Q

what is an extradural haematoma

A

bleed that occurs between the skull and dura mater
bi-convex shape and don’t cross suture lines

19
Q

presentation of extradural haematoma

A

typical history is a young patient with a traumatic head injury that has an ongoing headache

period of improved neurological symptoms and consciousness (lucid interval) followed by a rapid decline over hours as the haematoma gets large enough to compress the intracranial contents
features of raised ICP

20
Q

what is a subdural haematoma

A

occur between dura and arachnoid layer
crescent shape, not limited by the cranial sutures

21
Q

causes of a subdural haematoma

A

rupture of the bridging veins in the outermost meningeal layer
more common in elderly or alcoholic patients (atrophy in brains making vessels more likely to rupture)

22
Q

presentation of a subdural haematoma

A

Slower onset of symptoms than a epidural haematoma

there may be fluctuating confusion/consciousness

23
Q

principles of management of intracranial bleed

A

CT head
check FBC and clotting, correct any clotting abnormality
admit to specialist stroke unit, potential surgery
consider intubation, ventilation and ICU care if they have reduced consciousness
correct severe hypertension but avoid hypotension

24
Q

what is a subarachnoid haemorrhage

A

involves a bleed into the subarachnoid space, between the arachnoid membrane and the pia mater

25
Q

cause of a subarachnoid haemorrhage

A

traumatic vs spontaneous

spontaneous = ruptured aneurysm (berry/saccular** or fusiform)
arteriovenous malformation
Pituitary apoplexy
Arterial dissection

can be particularly associated with cocaine use & sickle cell anaemia

26
Q

presentation of a subarachnoid haemorrhage

A

sudden onset occipital headache that occurs during strenuous activity e.g. sex, weight-lifting
‘thunderclap’ headache

neck stiffness
nausea & vomiting
photophobia
vision changes
neurological changes e.g. weakness, speech changes, reduced LOC
coma/seizures/sudden death

ECG ST elevation may be seen

27
Q

conditions associated with berry aneurysms

A

adult polycystic kidney disease
Ehlors-danlos syndrome
coarctation of the aorta

28
Q

risk factors for subarachnoid haemorrhage

A

hypertension
smoking
excessive alcohol consumption
cocaine use
FHx

more common in black patients, female, 45-70

29
Q

investigations for subarachnoid haemorrhage

A

CT head - hyperdense in basal cisterns
lumbar puncture if CT is negative, but still a strong suspicion

angiography (CT/MRI) can then be used once confirmed to locate source of bleeding e.g. aneurysm/arteriovenous malformation

30
Q

how does a lumbar puncture help with subarachnoid haemorrhage confirmation?

A

red cell count
xanthochromia

taken at least 12 hours after symptom onset to allow development of xanthochromia
**distinguish between true SAH and a traumatic tap

31
Q

management of subarachnoid haemorrhage

A

high risk of re-bleeding, need prompt intervention (within 24 hours)
most are now treated with a coil by interventional radiologists, minority require a craniotomy and clipping

until aneurysm is treated, need strict bed-rest, well controlled BP, avoid strenuous activity

vasospasm prevented with 21 day course of nimodipine (CCB targeting the brain vasculature), treated with hypervolaemia, induced hypertension, and haemodilution

hydrocephalus = external ventricular drain or long term ventriculo-peritoneal shunt

32
Q

complications of subarachnoid haemorrhage

A

re-bleeding** - 10% of cases, happens in first 12 hours
if re-bleeding suspected e.g. sudden worsening of neurological symptoms, repeat CT scan

vasospasm (delayed cerebral ischaemia) - 7-14 days after

hyponatremia (inappropriate SIADH)
seizures
hydrocephalus
death

33
Q

important predictive factors in SAH

A

level of consciousness on admission
age
amount of blood visible on a CT scan