Brainscape's Knowledge GenomeTM

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


See full index

Neurology STG > Cerebrovascular Disease > Flashcards

Cerebrovascular Disease Flashcards

1
Q

What kind of ages do strokes occur

A

25% of all strokes occur before 65;

Death rate 20-25%

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

What is stroke?

A

Syndrome of rapid onset Cerebral Deficit (Usually Focal) lasting >24hr or leading to
head, with a vascular cause

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

What is a TIA?

A

Brief episode of Neurological Dysfunction due to
temporary Focal Cerebral/Retinal Ischaemia without Infarction; Seconds to minutes for
complete recovery; May precede Stroke

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

Types of Ischaemic stroke

A 
Thrombotic
Large Artery Stenosis 
Small vessel disease
Cardioembolic
Hypoperfusion 
Might be lacunae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Types of Haemorrhagic stroke

A

Intracerebral

Subarachnoid

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

Other causes of stroke

A

Arterial dissection
Venous sinus thrombosis
Vasculitis

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

Pathophysiology of Ischaemic Strokes: Thromboembolism

A

Peripheral Vascular Disease (Including Atherosclerosis) related; Bifurcations (e.g. Arch of Aorta) are particularly affected; Caucasians tend to have more extracranial disease while the
opposite is true for other populations
Thrombosis at site of plaque rupture leads to Embolism or Vessel Occlusion; Large Artery Stenosis typically leads to Embolism

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

Pathophysiology of Ischaemic Strokes: Small Vessel Disease

A

Lacunae infarction of Small Penetrating Arteries that supply the Brain Parenchyma; Pathology is due to Hypertension leading to Occlusive Vasculopathy
(Lipohyalinosis) rather than Thromboembolic disease
o Accumulation of diffuse Ischaemic changes in deep White Matter

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

Pathophysiology of Ischaemic Strokes: Cardioembolic Stroke

A

Atrial Fibrillation and
other Arrhythmias, Valvular disease including
Infective Endocarditis, Wall Motion Abnormalities, DVT if PFO is present; Rarer
causes include Fat Emboli secondary to fracture, Atrial Myxomas, Air Embolism
o Simultaneous Infarction in different vascular territories are very suggestive of proximal source of
Emboli (e.g. Heart, Aorta)

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

Pathophysiology of Ischaemic Strokes: Hypoperfusion

A

Hypoperfusion e.g. In Cardiogenic Shock can
lead to Watershed Infarction (Balint’s Syndrome) in the Parieto-Occipital Area
between MCA and PCA territories

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

Carotid and Vertebral Artery Dissection: Aetiology

A

Accounts for 20% of Strokes under 40yrs; Sequelae of trivial Neck Trauma or Hyperextension
(e.g. Whiplash injury); Thought to be predisposed by occult Collagen disorders e.g. Partial Marfan’s Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Carotid and Vertebral Artery Dissection: Pathophysiology

A

Most dissections occur in Large Extracranial vessels; Blood penetrates Subintimal Vessel wall forming a false lumen; Thrombosis within true lumen due to Thromboplastin release leads to Thrombosis at the site, as well as Thromboembolic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Carotid and Vertebral Artery Dissection: Presentation

A

Pain in Neck/Face; Horner’s Syndrome or Lower Cranial Nerve Palsies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Venous Stroke

A

1% of Stokes; Thrombosis within Intracranial Venous Sinuses E.g. Superior Sagittal Sinus, Cortical Veins especially in Hypercoagulable states (Pregnancy, Dehydration/Alcohol,
Malignancy), Thrombotic disorders
• Cortical Infarction, Seizures and raised ICP can occur

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

TIA: Aetiology

A

Usually due to Microemboli; Different mechanisms than Embolic Stroke; TIAs may be caused by fall in Cerebral Perfusion (Dysrhythmia, Postural Hypotension, Atheroma); Infarction
averted by Autoregulation
o Emboli typically from Cardiac Thrombus or Atheromatous plaque
o Infective Endocarditis and Polycythaemia can cause TIAs
• Tumours and Subdural Haematomas might present similarly to TIA

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

TIA: Management

A

All patients given Aspirin 300mg and referred to TIA clinic and seen within 24hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

TIA: Presentation

A

Sudden loss of function usually lasting minutes or hours; Hemiparesis (affecting the Motor Cortex) and Aphasia (affecting Wernicke’s/Broca’s/Arcuate Fasciculus) are the commonest
Consciousness is typically preserved during TIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Amaurosis Fugax

A

Sudden transient unilateral
loss of sight due to transient loss of Ophthalmic
supply; Might be a sign of Internal Carotid Artery
Stenosis Preceding Hemiparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

TIA: What else should be investigated for

A

Carotid Artery Bruit, Atrial Fibrillation, Valvar
Heart Disease or recent MI should be investigated
for;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

TIA: Underlying conditions

A

Atheroma, HTN, Postural Hypotension,Bradycardia/HF, DM

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

TIA: Rare causes

A

Arteritis, Polycythaemia,

Neurosyphilis, HIV, Antiphospholipid Syndrome

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

Cerebral Infarction: Pathophysiology

A

Following Vessel Occlusion, Brain Ischaemia occurs followed by Infarction; Infarcted area surrounded by swollen area (Ischaemic Penumbra) which is non-functioning but structurally
intact; Can regain function with neurological recovery
• Hypoxia leads to Neuronal damage; Fall in ATP, release of Glutamate; Opening of Calcium Channels and Free Radicals leading to Inflammatory damage, Necrosis and Apoptosis

23
Q

Cerebral Infarction: Morbidity and Mortality

A

25% of patients die within 2 years; 10% within first month; Higher early mortality with
Haemorrhagic stroke; Coma, Conjugate Gaze Deficit, Hemiplegia are poor prognostic indicators; Preventable deaths include Aspiration
• Recurrent Strokes are common (10% within first yr); 30 – 40% of Stroke patients alive at 3yrs

24
Q

Cerebral Infarction: Commonest Sites

A

Most commonly in Internal Capsule following Thromboembolism of MCA (Takes 80% of Anterior Circulation supply); Similar clinical picture in Internal Carotid Artery Occlusion

25
Q

Cerebral Infarction: Presentation

A

o Contralateral Hemiplegia/Hemiparesis with Facial Weakness; Aphasia if Dominant Hemisphere is affected; Weak limbs are at first Flaccid and Areflexic
o Consciousness is usually preserved; Rarely Epileptic seizure occurs at onset; Reflexes return after several days of onset and become hyperreflexia; Extensor Plantar Response appears (Babinski’s)
o Weakness is maximal at first and recovery occurs gradually over the long term

26
Q

Brainstem Syndromes: Weber’s

A

Contralateral Hemiparesis, Oculomotor Palsy

27
Q

Brainstem Syndromes: Ventral Pontine Syndrome

A

(Millard-Gubler) – Contralateral Hemiparesis, Ipsilateral CNVI Palsy, Ipsilateral CNVII Palsy

28
Q

Brainstem Syndromes: Bilateral Ventral Pontine Syndrome

A

Locked in syndrome

29
Q

Brainstem Syndromes: Reticular Formation

A

Coma

30
Q

Brainstem Syndromes: Lateral Medullary Syndrome

A

(Wallenberg’s) – Acute Vertigo, Cerebellar Signs, Horner’s Syndrome,
Contralateral Spinothalamic loss, Ipsilateral Facial sensory loss

31
Q

Brainstem Syndromes: Medial Medullary Syndrome

A

(Dejerine’s) – Contralateral Dorsal Column modalities loss, Ipsilateral Tongue Weakness, Contralateral
Hemiparesis/Hemiplegia

32
Q

Lacunar Infarction Presentation

A

Lacunae Infarction – Infarction <1.5cm3
Hypertension is commonly present; Minor strokes (Pure motor, Pure sensory, Sudden
Unilateral Ataxia, Sudden Dysarthria with clumsy hand)

33
Q

Hypertensive Encephalopathy

A

Cerebral Oedema causing Severe Headaches, Nausea and Vomiting; Agitation, Confusion, Fits and Coma occurs if HTN not treated
o Papilloedema due to Ischaemic Optic Neuropathy or following multiple acute infarcts; MRI shows Oedematous White Matter in Parieto-Occipital Regions

34
Q

Vascular Dementia

A

Multiple Lacunae or larger Infarcts cause Generalised Intellectual loss often seen in advanced Cerebrovascular disease; Late stage presents as Dementia,
Pseudobulbar Palsy, Shuffling gait (Marche à petits pas)

35
Q

Binswanger’s Disease

A

Widespread low attenuation in Cerebral White Matter usually with Dementia, TIA, Strokes in HTN patients

36
Q

Visual Cortex Infarction

A

– Hemianopia Visual

Loss and Cortical Blindness

37
Q

Watershed Infarction (Balint’s Syndrome)

A

Following prolonged periods of low perfusion;Leads to Cortical Visual loss, Memory loss, Intellectual Impairment; Vegetative state or Minimally Conscious state might follow

38
Q

Immediate Management of Acute Stroke

A

FAST Recognition – Facial Weakness, Arm
Weakness, Speech (Difficulty, Slurring), Time
• Admission without delay; Imaging, Care and
Investigation; Airway protection post-Stroke
• Routine Bloods (FBC, ESR, INR, Lipids), CXR, ECG, Carotid Doppler, MRA
• Source of embolism to be sought; Carotid Bruit,
Atrial Fibrillation, Valvular Lesion, Endocarditis,
Previous Embolism/TIA; BP assessment
o Brachial BP from both sides; >20mmHg
difference suggests Subclavian Stenosis
• Thrombolysis should be used immediately if
Ischaemic stroke is confirmed

39
Q

Stroke Imaging: Non contrast Ct

A

Demonstrate

Haemorrhage immediately; Cerebral Infarction not detected or subtle changes only

40
Q

Stroke Image: MRI

A

MRI shows changes early in Infarction; Shows

full extent of damaged area/Penumbra

41
Q

Stroke Imaging: DW MRI

A

Detect Cerebral Infarction
immediately but also accurate as CT for
Haemorrhagic stroke

42
Q

Stroke Imaging: MRA/CTA

A

MRA or CTA after acute imaging – Confirm surgically accessible Arterial Stenoses

43
Q

Stroke Imagine: Carotid Doppler and Duplex scanning

A

Carotid and Vertebral Stenosis and Occlusion

44
Q

Thrombolysis

A

Age >18, Measurable Neurological deficit, Imaging and Clinically consistent with Acute Ischaemic Stroke, Timing of onset well-established; up to 4.5hrs after onset

45
Q

Thrombolysis: History Exclusion Criteria

A

Stroke/Head Trauma in 3/12, Previous Haemorrhagic Stroke, Major surgery 2/52, GI/GU bleeding 3/52, MI 3/12, LP 1/52,

46
Q

Thrombolysis: Clinical Exclusion Criteria

A

Rapidly improving Stroke syndrome, Minor/Isolated signs, Symptoms suggestive of SAH, Acute MI/Dressler’s Syndrome, Severe HTN,
Pregnancy/Lactation, Active Bleeding/Trauma

47
Q

Thrombolysis: Laboratory Exclusion Criteria

A

Thrombocytopaenic, Severely Hypo/Hyperglycaemic, INR >1.7 if on Warfarin, Elevated aPTT if on Heparin

48
Q

Long Term Management of Stroke: Antiplatelet

A

Dual Antiplatelets (Aspirin and Clopidogrel) for 2 weeks, then continue Clopidogrel lifelong

49
Q

Long Term Management of Stroke: Antihypertensives

A

– Primary and Secondary Stroke prevention; Transient HTN following
stroke does not usually need treatment unless DBP >100mmHg; BP should be lowered slowly
to avoid sudden fall in perfusion

50
Q

Long Term Management of Stroke: Internal Carotid Endarterectomy

A 
For Post-
Stroke/TIA, ICA Stenosis >70%;
Endarterectomy has 3% mortality but reduces
risk of further Stroke/TIA by 75%
o Percutaneous Transluminal
Angioplasty/Stenting as an alternative
51
Q

Long Term Management of Stroke: PT

A

Relieve spasticity and use of walking aids;

52
Q

Long Term Management of Stroke: SALT+OT

A

Speech therapy; NG or PEG tube if unsafe swallow; OT – Home adaptations

53
Q

Long Term Management of Stroke: pharmacotherapy

A

Pharmacotherapy to relieve spasticity (E.g. Baclofen, Botulinum Toxin)

54
Q

Stroke Prognosis

A

One third of patients return to independent mobility, one third have disability requiring
institutional care; If language is intelligible at 3 weeks, good prognosis for speech

Neurology STG (15 decks)

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