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Phase 2a Revision > Neuro > Flashcards

Neuro Flashcards

1
Q

define infarction

A

obstruction to the blood suply

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2
Q

what is a TIA

A

transient neurological dysfunction secondary to ischaemia without infarction, resolves within 24hrs

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3
Q

what is crescendo TIA

A

2 or more TIAs within a week

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4
Q

typical symptoms of a stroke

A

UNILATERAL

  • sudden limb weakness
  • sudden facial weakness
  • sudden onset dysphasia
  • sudden onset visual or sensory loss
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5
Q

what are the risk factors for a stroke/TIA

A
  • CVD (angina/MI/PVD)
  • previous TIA/stroke
  • AF
  • DM
  • HTN
  • Carotid artery disease
  • Vasculitis
  • thrombophilia (group of conditions where blood clots more easily)
  • Smoking
  • Combined contraceptive pill
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6
Q

What risk tool is used in the community to identify stroke

A

FAST

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7
Q

What risk tool is used in A&E to identify stroke

A

ROSIER - recognition of stroke in emergency room

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8
Q

what risk score is used for a pt with a TIA

A

ABCD2

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9
Q

what does ABCD2 risk score assess

A

assess a pts risk of having a subsequent stroke after having a TIA

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10
Q

What does ABCD2 stand for

A

A - age (>60=1)
B - BP (>140/90=1)
C - clinical features (unilateral weakness =2, dysphasia without weakness = 1)
D - duration (>60mins=2, 10-60mins =1, <10mins=0)
D - diabetes (=1)

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11
Q

what result in ABCD2 indicate high risk

A

a high score = higher risk of pt having a stroke in the following 48hrs

<4 = specialist assessment within 1wk
>3 = specialist assessment within 24hrs
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12
Q

what is the gold standard Ix for ?stroke

A

diffusion-weighted MRI

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13
Q

define stroke

A

disruption of blood supply to the brain, characterised by rapidly developing signs of focal or global disturbance of cerebral functions, lasting for more than 24 hours or leading to death

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14
Q

what are the two types of stroke

A
  • haemorrhagic

- ischaemic

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15
Q

what are the three types of ischaemic stroke

A
  • Cerebral hemisphere infarcts
  • Posterior circulation ischaemia
  • Lacunar infarcts
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16
Q

what are the typical presenting symptoms for a cerebral hemisphere infarct

A
  • Contralateral hemiplegia which is initially flaccid (floppy limb, falls like a dead weight when lifted) and then becomes spastic.
  • Contralateral sensory loss.
  • Homonymous hemianopia.
  • Dysphasia.
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17
Q

what are the typical presenting symptoms for a posterior circulation infarct

A
  • Motor deficits
  • ‘Crossed’ syndromes: ipsilateral cranial nerve dysfunction and contralateral long motor or sensory tract dysfunction.
  • Sensory deficits
  • Homonymous hemianopia.
  • Ataxia, imbalance, unsteadiness, or disequilibrium.
  • Vertigo, with or without nausea and vomiting.
  • Diplopia (ophthalmoplegia).
  • Dysphagia or dysarthria.
  • Isolated reduced level of consciousness can result from bilateral thalamic or brain stem ischaemia.
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18
Q

what motor deficits are seen in posterior circulation infarcts

A
  • weakness
  • clumsiness
  • paralysis
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19
Q

what sensory deficits are seen in posterior circulation infarcts

A

numbness, including loss of sensation or paraesthesia in any combination of extremities, sometimes including all four limbs or both sides of the face or mouth.

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20
Q

what can a complete infarct affecting the pons cause

A

‘locked-in syndrome’

-quadriparesis, loss of speech, but preserved awareness and cognition, and sometimes preserved eye movements

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21
Q

which arteries are commonly affected by strokes in the cerebral hemisphere

A
  • anterior cerebral artery
  • middle cerebral artery
  • posterior cerebral artery
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22
Q

typical symptoms of a stroke in the anterior cerebral artery

A
  • contralateral leg weakness and sensory loss
  • mild/no upper extremity involvement
  • balance problems
  • L-sided = aphasia
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23
Q

typical symptoms of a stroke in the middle cerebral artery

A
  • contralateral face and arm weakness and sensory loss
  • mild/no leg weakness
  • head+eyes deviate toward side of stroke
L-sided = aphasia
R-sided = deficits of spatial perception, apraxia
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24
Q

typical symptoms of a stoke in the posterior cerebral artery

A
  • visual problems
  • prosopagnosia (unable to recognise faces)
  • alexia (inability to read)
  • aphasia
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25
Q

typical symptoms of a vertebrobasilar system stroke

A
  • vertigo
  • nystagmus
  • visual problems
  • facial weakness
  • dysphasia
  • dysarthria
  • loss of pain and temp
  • ipsilateral horner’s syndrome (ptosis, miosis, anhidrosis)
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26
Q

what are the typical differential dx for stroke

A
  • hypoglycaemia
  • TIA
  • brain tumour
  • Subdural haematoma
  • Todd’s palsy
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27
Q

what is Todd’s palsy

A

condition experienced by pts with epilepsy where a seizure is followed by brief period of paralysis (typically unilateral)

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28
Q

acute Mx of stroke

A

thrombolysis within 4.5hrs

thrombectomy within 6hrs

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29
Q

what medication is used in thrombolysis

A

alteplase

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30
Q

how does alteplase work

A
  • tissue plasminogen activator

rapidly breaks down clots

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31
Q

what medication is given for strokes

A

aspirin 300mg STAT (within 24hrs) and continued for 2wks

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32
Q

what other treatments are used in the secondary prevention of stroke

A
  • clopidogrel 75mg OD
  • atorvastatin 80mg
  • treat modifiable risks
  • carotid endarterectomy or stenting (if carotid disease present)
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33
Q

who is involved in the stroke rehabilitation MDT

A
  • SALT
  • nutrition and dieitics
  • physio
  • OT
  • social services
  • ophthalmology
  • psychology
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34
Q

when are statins prescribed in stroke pts

A

Do not start statin treatment immediately after an acute stroke but continue statin treatment for people with acute stroke who are already taking statins

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35
Q

what risk assessment is used in the primary prevention of strokes

A

Qrisk3

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36
Q

what does the Qrisk 3 score assess

A

calculates a persons risk of developing a heart attack of stroke in the next 10 years

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37
Q

what does GCS assess

A

level of consciousness

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38
Q

what responses are assessed in the GCS

A
  • eyes (4)
  • verbal (5)
  • motor (6)
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39
Q

GCS eye response levels

A

4 - spontaneous
3 - voice
2 - pain
1 - none

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40
Q

GCS verbal response levels

A 
5 - orientated
4 - confused
3 - inappropriate words 
2 - groans/incoherent sounds
1 - none
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41
Q

GCS motor response levels

A 
6 - voluntary movement
5 - localise to pain
4 - normal flexion
3 - abnormal flexion
2 - extension
1 - none
42
Q

what score is the GCS out of

A

15

43
Q

what GCS score indicates intubation

A

8

44
Q

what are the different types of intracranial haemorrhage

A
  • subdural
  • extra-dural
  • subarachnoid
45
Q

what are the three layers of the meninges

A
  • dura (outer layer)
  • arachnoid
  • pia (inner layer)
46
Q

where is the subdural space

A

between the dura matter and the arachnoid matter

47
Q

where is the arachnoid space

A

between the arachnoid matter and the pia matter

48
Q

what are the different stages of a subdural haemorrhage

A
  • An acute SDH.
  • A subacute SDH (this phase begins 3-7 days after the initial injury).
  • A chronic SDH (this phase begins 2-3 weeks after the initial injury).
49
Q

what are the main causes of a subdural haemorrhage

A
  • tearing of bridging veins

- damaged cortical artery bleeding

50
Q

which groups are at high risk of subdural haemorrghage

A
  • infants (tearing of bridging veins ?shaken baby syndrome)
  • elderly (cerebral atrophy)
  • alcoholics (cerebral atrophy)
51
Q

acute presentation of subdural haemorrhage

A
  • headache
  • wound from trauma
  • LoC (not always present acutely)
52
Q

chronic presentation of subdural haemorrhage

A
  • progressive symtpoms
  • n+v
  • neurological deficit such as focal limb weakness, speech difficulties, increasing drowsiness/confusion or personality changes
  • progressive headache
53
Q

when ?subdural haemorrhage what information is vital to get from the Hx

A
  • anticoagulant use
  • PMHx of bleeding disorders/coagulopathies
  • alcohol intake
54
Q

differentials for ?subdural haemorrhage

A
  • progressive stroke
  • SAH
  • infection (meningitis/encephalitis)
  • tumour

if pt presents confused all the differentials for that!

55
Q

Ix for subdural haemorhage

A
  • FBC, U&E, LFTs
  • Coagulation screen
  • Group and save/cross-match
  • CT head
56
Q

what Ix are included in FBC

A
  • Hb
  • WBC count
  • Platelet count
  • RBC count
  • Haematocrit
  • MCV
  • Mean cell haemoglobin

can also include differential white cell count

  • neutrophils
  • lymphocytes
  • monocytes
  • eosinophils
  • basophils
57
Q

complications of a sub-dural haemorrhage

A
  • seizures
  • Raised ICP
  • Death
  • cerebral oedema
  • coma (coning due to midline shift)
  • permanent neurological damage
58
Q

Mx of subdural haemorrhage

A
  • If small, asymptomatic, acute SDH = observation, serial examinations and serial CT scanning
  • Surgery is needed if there are focal signs, deterioration, a large haematoma, raised intracranial pressure or midline shift
59
Q

what surgery is used in the tx of subdural haemorrhage

A
  • emergency craniotomy and clot evacuation

- burr holes may be considered if there is rapid deterioration

60
Q

what is a extra-dural haemorrhage

A

a bleed into the potential space between the skull and the dura matter

61
Q

which artery is typically affected in an extra-dural haemorrhage

A

middle meningeal artery

62
Q

which region of the brain is typically affected in an extra-dural haemorrhage

A

temporo-parietal region

63
Q

where else can an extra-dural haemorrhage occur

A

in the spinal column

64
Q

which age group is more likely to have an extra-dural haemorrhage

A

adolescents and young adults

65
Q

on a CT scan what shape are subdural haemorrages

A

concave

66
Q

on a CT scan what shape are extra-dural haemorrages

A

convex

67
Q

what is the most common cause of extra-dural haemorrhage

A

trauma (to the skull or spine)

68
Q

what is the typical presentation of a extra-dural haemorrhage

A

Hx of trauma followed by a lucid period followed by a rapid deterioration in the pt & the conscious level

69
Q

what are the possible signs/symptoms of an extra-dural haemorrhage

A
  • N+V
  • headache
  • Seizures.
  • Bradycardia with or without hypertension, indicates raised intracranial pressure.
  • Evidence of skull fractures, haematomas, or lacerations.
  • Cerebrospinal fluid (CSF) otorrhoea or rhinorrhoea resulting from skull fracture with a tear of the dura.
  • Alteration in level of consciousness with deterioration of the Glasgow Coma Scale (GCS) score.
  • Unequal pupils.
  • Facial nerve injury.
  • Weakness of limbs.
  • Other focal neurological deficits include aphasia, visual field defects, numbness and ataxia
70
Q

how may an extra-dural haemorrhage in the spinal column present

A
  • Weakness.
  • Numbness.
  • Alteration in reflexes.
  • Urinary incontinence.
  • Possibly both urinary and faecal incontinence
71
Q

what reflex happens in response to a raised ICP

A

Cushings Reflex

72
Q

what is Cushings triad

A
  • Hypertension
  • Bradycardia
  • Irregular breathing pattern
73
Q

Ix for an extra-dural haemorrhage

A
  • head CT

- baseline FBC, U&E (?abnormalities in coagulopathy)

74
Q

Mx of an extra-dural haemorrhage

A

ABCDE

  • maintain airway and oxygenation
  • IV fluids to maintain circulation

Mx depends on the size of the haemorrhage and the stability of the pt

75
Q

Mx of a small extra-dural haemorrhage

A

conservative

76
Q

Mx of a large extra-dural haemorrhage

A

burr holes to allow for evacuation of the bleed

77
Q

pharmacologically what can be given for raised ICP

A

IV mannitol

78
Q

what drug class is mannitol in

A

osmotic diuretics

79
Q

how does mannitol work

A

increases plasma osmotic pressure leading to brain dehydration and a decrease in ICP

80
Q

complications of an extra-dural haemorrhage

A
  • permanent or temporary neurological deficits
  • death
  • post-traumatic seizures
  • post-concussion syndrome
81
Q

complications of a spinal extra-dural haemorrhage

A
  • spasticity
  • urinary complications
  • neuropathic pain
82
Q

what is a subarachnoid haemorrhage

A

bleeding into the subarachnoid space between the pia matter and arachnoid matter

83
Q

what is typically found in the subarachnoid space

A

cerebrospinal fluid (CSF)

84
Q

what is the most common cause of a subarachnoid haemorrhage

A

rupture of a berry aneurysm

85
Q

which area of the brain does the anterior cerebral artery supply

A

anteromedial portion of the cerebrum

86
Q

which area of the brain does the middle cerebral artery supply

A

lateral parts of the cerebrum

87
Q

which area of the brain does the posterior cerebral artery supply

A

posterior cerebrum

88
Q

risk factors for SAH

A
  • smoking
  • hypertension
  • cocaine use
  • alcohol
  • marfan’s syndrome
  • FHx
89
Q

what is the characteristic symptom of SAH

A

thunder-clap headache

90
Q

differentials for SAH

A
  • meningitis
  • encephalitis
  • migraine
  • ischaemic stroke
91
Q

when are SAH most likely to occur

A

during strenuous activity

  • weight lifting
  • sex
92
Q

what are the other features associated with SAH

A
  • neck stiffness
  • photophobia
  • visual changes
  • weakness
  • seizures
  • LoC
93
Q

Ix for SAH

A
  • CT head
  • LP (raised RCC & Xanthochromia (yellow colour to the CSF caused by bilirubin))
  • angiography (used to locate source of bleeding once SAH confirmed)
94
Q

early Mx of SAH

A
  • ABCDE
  • stop bleeding with endovascular obliteration by coiling (1st) or clipping (2nd)
  • nimodipine
95
Q

what is nimodipine

A

a calcium channel blocker

96
Q

why is nimodipine given in SAH Mx

A

prevents vasospasm which is a common complication of SAH that can cause brain ischaemia

97
Q

what other Mx may be needed following a SAH

A
  • LP or insertion of a shunt to treat hydrocephalus

- anti-epileptic mediciation (if seizures)

98
Q

How is nimodipine prescribed

A

60mg four-hourly

99
Q

what else needs to be managed after/during a SAH

A

Blood pressure

100
Q

How is blood pressure maintained after a SAH

A
  • Nitroprusside
  • labetolol

BP level should be low enough to prevent re-bleeding and high enough to maintain cerebral perfusion

101
Q

what mean arterial pressure is the aim in raised ICP control

A

MAP 50

Phase 2a Revision (13 decks)

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