Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neurology > Stroke > Flashcards

Stroke Flashcards

1
Q

What is the role of the pre-frontal cortex?

A

Decision and planning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does one calculate CPP?

A

CPP = Mean blood pressure – ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a lentiform bleed?

A

Extradural haematomas - ARTERIAL BLEED

  • Lense shaped depression on scan
  • Usually due to middle meningeal artery bleed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the Monroe-Kellie doctrine?

A

The relationship between ICP, CSF, CPP, blood and brain tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What % of stroke patients have diabetes?

A

20% - 2-4x risk of stroke with diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What % of stroke is associated with AF?

A

16%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What patients are at the highest risk of stroke?

A

Patients that have already had one

15% of patients with untreated AF will have another stroke within a year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a carotid endarterectomy?

A

Surgical procedure to remove build up of fatty deposits in carotid arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is clopidogrel?

A

Prevents platelet function, blocks P2Y12ADP receptor thus preventing cross linking of fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What % of strokes are bleeds?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the roles of the frontal cortex?

A
  • Contralateral movements
  • Broca’s area (dominant hemisphere, which is the left in 96% of people)
  • cortical inhibition of bladder and bowels
  • prefrontal – personality, initiative, sequencing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the roles of the parietal lobes?

A
  • Post central gyrus – sensory cortex
  • Wernicke’s area – receptive, comprehension
  • Handling numbers (dominant hemisphere)
  • non dominant – concepts of body image
  • visual pathways in Meyer’s loop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the roles of the temporal cortex?

A
  • Auditory cortex
  • Learning and memory
  • Olfaction
  • Emotional behaviour
  • Visual pathways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What % of ischemic stroke is due to atheroembolism?

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a lacunar infarction?

A

Most common type of ischemic stroke, due to occlusion of small penetrating arteries that provide blood to deep structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What would be the consequences of a stroke in the posterior circulation?

A
  • Vertigo
  • Ataxia: cerebellar syndrome
  • Isolated hemianopia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a TACI?

A

Total anterior circulation infarct
(top half of circle of Willis)

*Diagnosed when all three are present:

  • hemi motor and sensory deficit: has to be at least 2/3 of face, arms/ legs
  • hemianopia
  • cortical (higher) dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is a PACI?

A

Partial anterior circulation infarct

  • same as a TACI but when 2/3 are present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is a LACI?

A

Lacunar infarct

  • pure motor hemiplegia
  • pure sensory loss
  • Motor and sensory loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is dysarthria?

A

Problem with the muscles, make speaking difficult or impossible – disorder in the motor aspect of speech

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is dysphasia?

A

Inability to generate or comprehend speech

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Broca’s aphasia?

A

Inability to form words correctly – expressive aphasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Wernicke’s aphasia?

A

Receptive aphasia, cant understand speech but can say words without trouble

*due to receptive loss, words said don’t make sense as a sentence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the roles of the frontal lobe?

A
  • Intellectual function
  • Paraxis - Giving instructions in an ordered sequence
  • Bladder continence
  • Saccadic eye movement - Voluntary horizontal eye movements
  • Motor function
  • Expression of language - In dominant lobe (normally left)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the roles of the temporal lobes?

A
  • Memory
  • Smell
  • Hearing
  • Vestibular function
  • Emotion (limbic system)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the role of the parietal cortex?

A
  • Sensory integration - Information on sight/smell etc comes from the other lobes, the parietal lobe interprets this information andintegrates it together
  • Receptive language-Making sense of language
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the most common type of stroke?

A

Lacunar infarct

Often as a result of hypertension, small vessels become thickened and occlude and are prone to blockages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the consequences of an anterior cerebral artery stroke?

A

LEGS Loss of sentation and motor function on the contralateral side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Consequences of a middle cerebral artery stroke

A

ARMS AND FACE - loss of sensory and motor function on the contralateral side

BROCA’S APHASIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Consequences of a posterior cerebral artery stroke

A

Occipital lobe - homonymous hemianopia - loss of the same visual field in both eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Consequences of a basilar artery stroke

A

Locked in syndrome - corticospinal tracts on both sides affected

Vertical eye movements and awareness maintained

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which type of stroke is associated with cranial nerve 7 paralysis?

A

Anterior inferior cerebellar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Posterior cerebral artery stroke consequences

A
  • Visual problems
  • Prosopagnosia (facial recognition)
  • Alexia (inability to read)
  • Aphasia (can’t comprehend spoken words)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Middle cerebral artery stroke

A
  • Contralateral face and arm weakness and sensory loss
  • Mild/ no leg weakness
  • Head and eyes deviated to side of stroke
  • If left-sided (most people are left-dominant) aphasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Anterior cerebral artery stroke

A
  • Contralateral leg weakness and sensory loss
  • Mild/ no upper extremity involvement
  • Balance problems
  • Aphasia if left-sided
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Lacunar infarct

A
  • Pure motor stroke without sensory symptoms
  • Pure sensory stroke without motor symptoms
  • Ataxia (loss of coordination)
  • Absence of higher cortical functions e.g. language, vision, facial recognition
  • Clumsy hand syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Vertebrobasilar stroke

A
  • Vertigo
  • Dizziness
  • Vision problems
  • Facial weakness
  • Dysphagia
  • Dysarthria
  • Loss of pain and temperature sensation
  • Ipsilateral Horner’s syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Which sequence of MRI pick up oedema due to ischaemia?

A

DWI - diffusion weighted imaging

Looks for cytotoxic edema which occurs becayse a lack of ATP causes ion channels to stop working and cells swell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Define a stroke

A

Sudden onset focal neurological deficit of presumed vascular aetiology lasting >24hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Stroke epidemiology

A

3rd commonest killer in UK

£2.8 billion direct care costs

300,000 disabled survivors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Rsik factors for stroke

A

Non-modifiable

  • Age
  • Gender
  • Race
  • FHx

Modiafiable

  • Smoking
  • BP (most important by far for cerebral haemorrhage)
  • AF
  • Hyperlipidaemia
  • Obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What can mimic a stroke?

A

Metabolic: hypoglycaemia

CNS causes: epilepsy, Todd’s paresis, migraine, mass lesion, MS, encephalitis

Functional disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Things that look like something else but is stroke

A
  • Acute confusional state
  • Abnormal movements/ seizures
  • PNS symptoms
  • Acute vestibular syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Causes of stroke

A

Atheromatous disease: 50%

Heart: AF, valve, endocarditis, myxoma: 25%

Small end arteries: 25%

Others: air, fat etc (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

TACS

A

Total anterior circulation stroke

All three of:

  1. Unilateral weakness of arm, leg or face ± sensory deficit
  2. Homonymous hemianopia
  3. Higher cerebral dysfunction e.g. dysphasia, visuospatial disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

PACS

A

Partial anterior circulation stroke

Two of the following:

  1. Unilateral weakness of arm, leg or face ± sensory deficit
  2. Homonymous hemianopia
  3. Higher cerebral dysfunction e.g. dysphasia, visuospatial disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

LACS

A

Lacunar stroke syndrome - most common ischaemic stroke syndrome

One of:

  1. Pure motor stroke
  2. Pure sensory stroke
  3. Sensori-motor stroke
  4. Ataxic hemiparesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

POCS

A

Posterior stroke syndrome

One of:

  1. Cranial nerve palsy + contralateral motor/ sensory deficit
  2. Bilateral motor/ sensory deficit
  3. Conjugate eye movement disorder e.g. gaze palsy
  4. Isolated homonymous hemianopia or cortical blindness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Commonest complications of stroke

A
  • Urinary incontinence (30-65%)
  • Acute confusion
  • Pain
  • Malnutrition (8-35%)
  • Chest infections
  • VTE
  • Epilepsy
  • Pressure sores
  • Aspiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Secondary prevention of stroke

A
  • Clopidogrel 75mg
  • Atorvastatin 40mg
  • Antihypertensives
  • Lifestyle advice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Where would we listen for a carotid bruit?

A

Angle of the jaw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Arterial supply to the brain

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Sources of intracerebral haemorrhage

A
  • Aneurysm rupture
  • AVM
  • Cavernoma (blood blister/ raspberry cluster of blood vessels, abnormality bleeds into itself)
  • Bleed into infarct
  • Trauma
  • Amyloid angiopathy (amyloid deposits in vessels, vessels are frail and can bleed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is amyloid angiopathy?

A

Accumulation of amyloid protein in blood vessels - increases risk that the vessel will rupture because the proteins cause vessel walls to become more frail

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Commonest site for subarachnoid haemorrhage?

A

Junction of anterior cerebral and anterior communicating arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Clinical presentation of a subarachnoid haemorrhage

A
  • Thunderclap headache
  • Sudden collapse/ coma
  • Seizures
  • 1/3 die within 1st 2hrs
  • Vasospasm can occur leading to ischaemic stroke (for this nimodipine is used, it is a Ca2+ channel blocker than opens vessels and prevents spasms)
57
Q

Risk factors for thrombo-embolic stroke

A
  • HTN
  • Smoking
  • DM
  • Lipid abnormalities
  • Hormones
  • Age
  • Vaculitis
  • AF
  • Endocarditis
  • Valvular heart disease
58
Q

What is Weber syndrome?

A

Midbrain stroke syndrome: causes ipsilateral 3rd nerve palsy and contralateral motor dysfunction

59
Q

Which type of stroke is most common?

A

Ischaemic - 80%

Haemorrhagic - 20%

60
Q

What are the three factors that precipitate thrombosis?

A
  1. Blood stasis
  2. Vessel wall changes
  3. Changes in blood consituency

= VIRCHOW’S TRIAD

61
Q

What is the cause of most ischaemic strokes?

A
  1. Atherosclerosis: either within the vessels in the brain itself or within systemic vessels that embolise
  2. AF: causes cardioembolism
62
Q

Conditions which increase the likelihood of ischaemic stroke

A
  • Inflammatory vascular disease/ vasculitis
  • Collagen vascular disease e.g. Marfan’s
  • Infection
  • Arterial dissection
  • Coagulopathy e.g. polycythemia
63
Q

Consequences of haemorrhagic stroke

A
  • Disruption of BBB
  • Cerebral oedema
  • Neuronal damage
  • Increased ICP
  • Hydrocephalus if haemorrhage occurs into ventricles
64
Q

What is the biggest cause of intracerebral haemorrhage?

A

HTN: small cerebral vessels are weakenes by high pressures

65
Q

What is the Oxford classification of stroke?

A

AKA Bamford classification

  • Divides stroke into 4 categories
    1. Anterior circulation syndromes: either total or partial (MCA and ACA)
    2. Posterior circulation syndrome
    3. Lacunar syndrome
66
Q

Discuss hemispheric dominance

A

Cerebral dominance = term used to describe the lateralisation f brain functions

  • The activity associated with some functions is located in one hemisphere only e.g. speech

Dominant hemisphere = language, mathematical processing, writing

Non-dominant hemisphere = emotion, tone of language, spatial recognition, musical interpretation

Most people = left-sided dominance

**The clinical pattern of higher cortical dysfunction indicates whether the stroke has occurred in the dominant or non-dominant hemisphere

67
Q

Patient has difficulty reading, writing and calculating but they have insight - dominant or non-dominant hemisphere affected by stroke?

A

Dominant - the dominant hemisphere does all the essential, non-arty stuff

68
Q

How to tell if a stroke is ischaemic or haemorrhagic clinically

A

You can’t - typically headache is worse in haemorrhagic stroke but the only way to distinguish is imaging

69
Q

What would the clinical features of a posterior communicating artery aneurysm be?

A

Aneurysm compresses 3rd nerve:

  • Ptosis
  • Restriction of eye movements
  • Pain in eye
  • Dilated pupil (this occurs 1st as parasympathetic fibres encase the motor fibres of the 3rd nerve)
70
Q

Discuss the clinical features of a posterior circulation stroke

A

Involves damage to the area of the brain supplied by the posterior circulation (e.g. brainstem and cerebellum)

One of the following need to be present for a diagnosis of POCS

  1. Cranial nerve palsy and contralateral motor/ sensory deficit
  2. Bilateral motor/ sensory deficit
  3. Conjugate eye movement disorder (inability to move both eyes in the same direction
  4. Cerebellar dysfunction e.g. vertigo, nystagmus
  5. Isolated homonymous hemianopia
71
Q

Are higher cortical functions lost following a lacunar stroke?

A

No - these are sub-cortical strokes that occur due to small vessels disease

No loss of higher cerebral functions

One of the following needs to be present

  1. Pure sensory stroke
  2. Pure motor stroke
  3. Sensori-motor stroke
  4. Ataxic hemiparesis (ataxia = group of disorders that affect coordination, balance and speech
72
Q

Differentials for stroke

A

Graciaa Charlotte So Sassy Haaris Didn’t like

Glucose derrangement

Complicated migraine

Sepsis

Seizures

Hepatic encephalopathy

Drugs

Lesions

73
Q

What is the first investigation done when stroke is suspected?

A

Urgent CT - used to differentiate ischaemic and haemorrhagic stroke or to identify other pathology

74
Q

Does infarction show on CT immediately?

A

No - it takes a few hrs

Early signs are subtle:

  • Cortical sulci lose definition due to oedema
  • Loss of differentiation between grey and white matter due to oedema
  • Occluded MCA appears hyperdense on CT
75
Q

Imagine in haemorrhagic stroke

A

CT - rapidly localises haemorrhage and visualises associated complications e.g. if ventricles are involved

CT angio/ MRI if aneurysm or AVM is suspected

Repeat MRI 6-8 weeks after haemorrhage as tumours/ space occupying lesions can hide under the bleed

76
Q

Why is it important to re-image a brain 6-8 weeks after a haemorrhagic stroke?

A

Space occupying lesions can hide underneath the bleed

77
Q

What are the goals of CT in an acute stroke setting?

A
  1. Exclude haemorrhage
  2. Look for early features of ischaemia
  3. Rule out other intracranial pathologies that may mimic a stroke
78
Q

What is the mainstay imaging technique in acute stroke?

A

Non-contrast CT

79
Q

Other than head CT/ MRI what investigations are important following stroke?

A

ECG: look for arrhythmias that can cause stroke mimic e.g. heart block OR rhythms that precipitate embolism formation e.g. AF

Bloods: Hypoglycaemia, hyperlipidaemia, electrolytes, thrombophilia screen, vasculitis screen

80
Q

Diagnostic approach for acute stroke

A
  1. Assess presentation
  2. Acute stabilisation if needed A-E
  3. Localise lesion: hx and examination
  4. Identify timing of symptom onset: collateral hx?
  5. Identify cause and risk factors
  6. Imaging: urgent CT to exclude haemorrhage
  7. Assess suitability for thrombolysis
81
Q

Other than thrombolysis and thrombectomy, discuss management of acute stroke patients

A

BP: treat if there are HTN related complications e.g. aortic dissection, hypertensive encephalopathy - important not to over manage as decent BP required for function of colateral vessel formation. IV labetalol = 1st line

Glucose control: hyperglycaemia associated with poor outcomes aim for 4-11mmol/L

Nutrition and hydration: hypovolemia can worsen ischaemia and increase delirium, DVT and infection risk

DVT prophylaxis

Seizure prevention: 2% have seizures after stroke

PT: prevent pressure sores, contractures, restore function

Neuropsychiatric

Communication is key

82
Q

What is the overall aim in sichaemic stroke?

A

Salvage to ischaemic penumbra

This is the area of ischaemia around the infarction that is at risk of progressing to infarction but is salvageable if reperfused

83
Q

Discuss thrombolysis in acute stroke

A

Must be given within 4.5hrs of symptom onset

  • ALTEPLASE

**Only used once haemorrhagic stroke has been excluded

84
Q

How do thrombolytic drugs work?

A

E.g. alteplase, streptokinase

  • Convert plasminogen into plasmin which breaks down fibrin
85
Q

Discuss thrombectomy in acute stroke

A

Offere ASAP and within 6hrs symptom onset

86
Q

How is warfarin anticoagulation reversed following haemorrhagic stroke?

A

Give prothrombin complex concentrate and IV Vitamin K

87
Q

Discuss BP control in patients with acute intracerebral haemorrhage

A

Aims for systolic BP 130-140mmHg within 1hr and maintain for at least 7 days

88
Q

Discuss involvement of SaLT following stroke

A
  • Ensure that patients have swallowing screened by SALT before any oral fluid, medication or food given
  • If admission screen indicates problems ensure patient has specialist assessment within 24hrs and not more than 72hrs afterwards
  • Patients unable to take nutrition, fluid and medication orally should have NG tube inserted and be fed within 24hrs admission unless they’ve had thrombolysis and have oral medication reviewed to amend route of administration
89
Q

Acute ischaemic stroke management

A
  1. Give 300mg aspirin as soon as bleed ruled out
  2. Thrombolysis: only give if <4.5hrs since symptoms began
  3. Thrombectomy: within 6hrs of symptom onset OR within 24hrs if patient known to be well previously and have confrimed total occlusion of proximal posterior circulation
90
Q

Contraindications to thrombolysis

A
  • Previous intracranial haemorrhage
  • Seizure at stroke onset
  • Intracranial neoplasm
  • Suspected subarachnoid haemorrhage
  • Stroke or brain injury in past 3 months
  • Lumbar puncture in last few days
  • GI haemorrhage in past 3 weeks
  • Current bleeding
  • Pregnancy
  • Varices
  • Uncontrolled HTN >200/120
91
Q

Secondary prevention of stroke

A

Continue aspirin until 2 weeks after symptom onset

After 2 weeks start long-term antithrombotic treatment e.g. clopidogrel

92
Q

Carotid endarterectomy for stroke patients

A

Recommended if patient has had a TIA in the carotid territory and they are not severly disabled

Considered if carotid stenosis >70%

93
Q

Acute haemorrhagic stroke management

A

No specific medial treatment for most causes or haemorrhagic stroke

  • Stop all antiplatelet and anticoagulant drugs
  • Correct coagulation deficits
  • Monitor BP
  • Discuss with neurosurgeons: if intraventricular bleed CSF diversion may be needed, ruptured aneurysms may need clipping
94
Q

What is a TIA

A

Transient ischaemic attack, acute symptoms and signs of neurological dysfunction resolve completely within 24hrs

Suggests presence of atherosclerotic disease and high risk of stroke

95
Q

Stroke risk following TIA

A

15% strokes are preceded by a TIA

8-12% 7 days troke risk following TIA

18% 30 day stroke risk following TIA

Secondary prevention, if started within 72hrs, can reduce 90-day stroke risk to 2%

96
Q

Most common cause of TIA

A

Atherosclerosis causing embolism or cardioembolism

97
Q

What is amaurosis fugax?

A

Common TIA syndrome caused by embolism occluding retinal artery, causes painless, rapid loss of vision in on eye ‘like a curtain coming down’

98
Q

What is the ABCD2 cirteria?

A

Used to predict stroke risk following TIA but it is actually poor at discriminating low and high risk and is therefore not used anymore (since 2020)

99
Q

Investigation for TIA

A

Imaging of brain, blood vessels, heart investigations, bloods

Same as acute stroke

100
Q

Management of TIA

A

Overall aim is to reduce risk of stroke

Control risk factors: stop smoking, HTN control, DM control, hyperlipidaemia control

Antiplatelets: aspirin 300mg for 2 weeks then clopidogrel 75mg for life

Warfarin indicated if TIA caused by cardioembolism and patient has risk factors for cardioembolism e.g. prosthetic mechanical valve

101
Q

What is the HASBLED score?

A

Used to estimate the risk of major bleeding for patients on anticoagulation who have AF

Scored from 0-9 with a score closer to 9 meaning bleeding risk is more likely

102
Q

What is the CHADS2 VASC score?

A

Helps calculate the risk of stroke in patients with AF

  • Congestive heart failure
  • HTN = 1
  • Age >75 = +2
  • DM = 1
  • Stroke or TIA in past = +2
  • Vascular disease = 1
  • Age 65-74 = 1
  • Sex female = 1

Score 1 = consider anticoagulant

Score 2 = recommend anticoagulant

103
Q

Primary prevention of stroke and TIA

A
  • HTN, smoking, DM and hyperlipidaemia: all precipitate atherosclerosis
  • Measure: lifestyle changes, medical treatment of HTN, DM and hyperlipidaemia
  • Use CHADS2VASC score to calculate stroke risk in patients with AF and then give anticuagulant appropriately - this used to be warfarin but recently NICE have recommended the use of DOACs e.g. apixaban, dabigatran, rivaroxaban
104
Q

Imaging for TIA

A

Do not offer CT to patients with suspected TIA

After patient has been seen in TIA clinic, consider MRI to detect the terrioty of ischaemia

Carotid imaging for all who have had a TIA and considered a candidate for carotid endaterectomy

105
Q

What is the ROSIER tool?

A

Recognition of stroke in emergency room

Used to differentiate stroke and stroke mimics - recommended by NICE

Scores range from -2 to 5

Score <0 - unlikely to be a stroke

106
Q

Important to exclude when assessing a suspected stroke patient?

A

Hypoglycaemia

107
Q

What is Todd’s paresis?

A
  • Focal weakness in a part/ all of body following a seizure
  • Usally affects one side and can mimic a stroke
  • Usually lasts <48hrs
  • Can affect speech, gaze and vision
108
Q

Presentation of Todd’s paresis

A

Transient (<48hrs) weakness of a hand, arm or leg following a focal seizure

Weakness can range from mild to complete paralysis

  • Weakness usually occurs when seizure has affected motor cortex
109
Q

Aetiology of Todd’s paresis

A

Idea is that the affected cortex is exhausted/ neurones are exhausted following seizure

110
Q

Management of Todd’s paresis

A

None - rest until paralysis disappears

Used of thrombolytic agents is contraindicated if a seizure has occurred following a stroke

111
Q

What are the functions of the facial nerve?

A

Taste to anterior 2/3 tongue

Supplies stapedius muscle

Muscles of facial expression

112
Q

Difference bwteen UMN and LMN facial nerve palsy

A

UMN: forehead is spared

LMN: whole side of face affected

113
Q

Presentation of a facial nerve palsy

A

Weakness in muscles of facial expression and eye closure: can lead to damage of conjunctiva and cornea

Face sags on affected side

UMN lesion: forehead spared

LMN lesion: whole face affected

114
Q

Causes of UMN facial nerve palsy

A

Stroke, tumours, MS, syphilis, HIV, vasculitis

115
Q

Causes of LMN facial nerve palsy

A

Bell’s

Pregnancy

DM

Local anaesthetic following dental work

Infective: otitis media, HIV, EBV

Trauma: forceps delivery

Neurological: GBS, mononeuropathy e.g. due to DM

116
Q

What is Bell’s palsy?

A

Most common cause of acute LMN palsy

Lifetime risk 1 in 60

Probably due to sichaemic compression f facial nerve within facial canal due to inflammation - this is most commonly due to viral infections (latent herpes simplex type 1)

7% have a recurrence

Higher incidence in those with DM

117
Q

A lesion in which cranial nerve can cause hyperacusis?

A

Facial - innervates stapedius muscle

118
Q

How is Bell’s palsy managed?

A

Steroids: if presenting within 72hrs

Advice re eye care and explain that recovery can take several months

85% recover spontaneously

Consider referral if concern regarding aberrant re–nervation e.g. jaw twitching

Surgery: facial nerve decompression

119
Q

What is Ramsay Hunt syndrome?

A

Facial nerve paralysis + rash affecting ear or mouth

Occurs when herpes zoster becomes reactivated in the geniculate ganglion of the 7th cranial nerve

LMN facial palsy

Pain is a prominent feature

Vesicles seen in the ar, on the hard palate and anterior 2/3 tongue

Deafness, tinnitus and vertigo can also occur

120
Q

Management of Ramsay Hunt syndrome

A

Treat within 72hrs symptom onset with specific antiviral and steroids

Eye pad to protect eye + lubricants

121
Q

When to refer a patient with a facial nerve palsy

A

Worsening neurological features

Features suggesting an UMN cause

Features suggestive of cancer: >6months, head/ neck lesion, hx of cancer, hearing loss on affected side

122
Q

Explain the patterm of motor and sensory function loss in UMN and LMN facial nerve lesions

A

Forehead is supplied by bilateral fibres e.g. thr right forehead is supplied by fibres on the right and left

Lower half of face only supplied by contralateral fibres

123
Q

What are the functions of the oculomotor nerve?

A

CNIII

Motor functions: majority of extraocular muscles

Parasympathetic: causes pupillary sphincter muscles to contract > this constricts the pupil and causes the lense to become more round/ thicker for near vision

(contraction of the ciliary muscle weirdly causes it to move inward towards centre of eye and this relaxes suspensory ligaments which makes lense more round and thick)

124
Q

Most common causes of CNIII palsy

A
  • Raised ICP causes compression of nerve against temporal bone
  • Posterior communicating artery aneurysm
  • Cavernous sinus infection/ trauma / thrombosis
125
Q

Which cranial nerve is most commonly affected by cavernous sinus thrombosis?

A

Abducens

126
Q

Clinical features of CNIII palsy

A
  • Down and out eye
  • Ptosis
  • Dilated pupil
127
Q

Outline abducens nerve palsy

A

Caused by anything that causes downward pressure on the brainstem e.g. space occupyin lesion

Clinical features: diplopia, eye resting in adduction because it doesn’t have the lateral rectus to oppose the action of the occulomotor nerve which controls the medial rectus

128
Q

What is bulbar palsy?

A

Bulbar palsy refers to a set of signs and symptoms linked to the impaired function of the lower cranial nerves, typically caused by damage to their lower motor neurons or to the lower cranial nerve itself. The impacted cranial nerves are a set of nerves that arise straight from the brainstem and include cranial nerves IX (9), X (10), XI (11), and XII (12).

129
Q

Demographic of patients commonly affected by bulbar and pseudobulbar palsy?

A

Men aged 75+

130
Q

Discuss bulbar palsy

A

LMN problem - think B for bulbar and B for below then think lower

Result of diseases affecting the lower cranial nerves (9-12)

Causes: brainstem stroke, muscle disorders e.g. MND, disease of peripheral nerves supplying the muscles, Guillain Barre

Classified as progressive or non-progressive

Symptoms: think LMN lesion in face and neck

  • Lip tremor
  • Weak and wasted tongue
  • Drooling
  • Absent palatal movement
  • Dysphonia **NOT DYSPHASIA**
  • Speech is slurred, patient can’t pronounce ‘r’ for example
131
Q

Management of bulbar palsy

A

No known treatment - supportive only

Medication to prevent drooling: anticholinergics

Feeding tube if difficulty swallowing

SaLT for help with chewing, swallowing, speaking

132
Q

Prognosis of bulbar palsy

A

Can be fatal in progressive cases, often occurs from 1-3yrs after symptom onset due to aspiration pneumonia

Extensive damage can affect respiratory centre in brainstem leading to inability to breathe

133
Q

What is pseudobulbar palsy?

A

UMN problem: damage along the corticobulbar tract

134
Q

Presentation of pseudobulbar palsy

A

Tongue: unable to move but no wasting

  • Dribbling
  • Dysphonia
  • Dysphagia
  • Absent facial expressions
  • Emotional liability
  • Exaggerate jaw jerk (tap on chin, causes brisk closure of jaw)
135
Q

Cause of pseudobulbar palsy

A

Stroke in internal capsule: corticobulbar tract runs through here - note, has to be bilateral to produce clinical signs

MND

High brainstem tumours

Head injury

136
Q

Management of pseudobulbar palsy

A

*No known treatment for irreversible causes

Supportive: anticholinergics, baclofen for spasticity, PEG tube for dysphagia, SSRIs for emotional liability, SaLT

137
Q

Bulbar vs pseudobulbar palsy

A
138
Q

Symptoms of brainstem stroke

A
  • Cessation of breathing
  • Difficulty chewing, swallowing and speaking
  • Weakness/ paralysis in arms/ legs/ face
  • Difficulty with balance
  • Visual problems
  • Vertigo
  • Locked-in syndrome
  • Coma

Neurology (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions