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neurology > 2. Strokes - TIA, Ischaemic + Haemorrhagic > Flashcards

2. Strokes - TIA, Ischaemic + Haemorrhagic Flashcards

1
Q

What is the definition of TIA?

A

Transient Ischaemic Attack.

A brief episode of transient neurological dysfunction due to temporary focal cerebral ischaemia without infarction.

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2
Q

What is a crescendo TIA?

A

A crescendo TIA is where there are 2 or more TIAs within a week.
-> Carries a high risk of developing in to a stroke.

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3
Q

What is the duration of symptoms in a TIA? How long do these symptoms last in a TIA?

A

Symptoms are maximal at onset:
-> Usually last 5-15 minutes

Classical definition: lasts <24 hours.

Without intervention, 1 in 12 have a stroke within a week.

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4
Q

Explain the pathophysiology of TIA.

A
  1. Cerebral ischaemia
  2. Lack of oxygen + nutrients to the brain
  3. Cerebral dysfunction
  4. In TIA: period of ischaemia = short-lived

= Ischaemia without infarction (the tissue does not die)

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5
Q

What is the main cause of TIA?

A

Atherothromboembolism from the carotid artery
(listen for the carotid bruit!)

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6
Q

Other than atherothromboembolism, name 3 other causes of TIA.

A
  1. Cardioembolism
    - In Atrial Fibrillation
    - After an MI

2, Valve disease/prosthetic valve

  1. Hyperviscosity
    - Polycythaemia
    - Sickle cell anaemia
    - Extremely raised white cell count
    - Myeloma
  2. Hypoperfusion
    - Cardiac dysrhythmia
    - Postural hypotension
    - Decreased flow through atheromatous arteries
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7
Q

Name 5 risk factors for TIA.

A

Risk factors:
- Age - risk increases with age
- Hypertension
- Smoking
- Diabetes
- Obesity
- High alcohol intake

  • Heart disease - valvular, ischaemic or atrial fibrillation
  • Past TIA
  • Raised packed cell volume (PCV)
  • Peripheral arterial disease
  • Polycythaemia vera
  • Combined oral contraceptive pill (since increase risk of clots)
  • Hyperlipidaemia
  • Clotting disorder
  • Vasculitis e.g. SLE, giant cell arteritis is rare risk factor
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8
Q

Describe the epidemiology of TIA.

A
  1. 15% of first strokes are preceded by TIA, they are also a foreshadowing of an MI.
  2. More common in MALES than females (M > F).
  3. Black ethnicity are at greater risk due to their hypertension and
    atherosclerosis predisposition.
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9
Q

For the clinical presentation of a TIA, the features be categorised based on what?

A

Site of the TIA - the arterial territories affected:

  1. Carotid artery (anterior circulation) - 90% of TIAs
  2. Vertebrobasilar artery (posterior circulation) - 10% of TIAs
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10
Q

For a TIA affecting the carotid artery and the anterior circulation, describe the clinical presentation.

A
  1. Hemiparesis
    - Weakness on an entire side of the body
  2. Hemisensory loss
  3. Hemianopic visual loss
  4. Aphasia/Dysphagia
    - Loss of language
  5. Amaurosis fugax
    - Sudden transient loss of vision in one eye
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11
Q

The occurrence of which symptom in TIA is often the first clinical evidence of an ICA stenosis?

A

Amaurosis fugax (sudden transient loss of vision in 1 eye)

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12
Q

What is amaurosis fugax and what causes it?

A

Sudden transient loss of vision in 1 eye (unilateral).

Occurs due to the temporary reduction in the retinal, opthalmic or ciliary blood flow, leading to a temporal occlusion, leading to temporary retinal hypoxia.

“Like a curtain descending.”

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13
Q

For a TIA affecting the vertebrobasilar artery and the posterior circulation, describe the clinical presentation.

A
  1. Diplopia (double vision), vertigo, vomiting
  2. Choking & dysarthria (unclear articulation of speech but
    understandable)
  3. Ataxia - no control of body movement
  4. Hemisensory loss
  5. Hemianopia vision loss
  6. Tetraparesis
    - Muscle weakness affecting all 4 extremities
  7. Loss of consciousness (rare)
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14
Q

What symptoms that occur on their own do not imply a TIA?

A

NOT a TIA if these occur on their own:
- Syncope
- Dizziness
- Temporary loss of consciousness
- Temporary memory loss

Gradual onset – suggests demyelination, tumour, migraine

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15
Q

Investigations for a TIA.

A

Often solely based on its description.

First line: Diffusion weighted CT/MRI
-> if stenosis: to determine extent

Carotid artery doppler ultrasound
-> to look for stenosis/atheroma

Then: MR/CT angiography
-> if stenosis: to determine extent

Bloods:
* FBC - look for polycythaemia
* ESR - raised in vasculitis
* Glucose - to see if hypoglycaemic
* U+Es
* Cholesterol
* INR (prothombin time) - if pt on warfarin

ECG:
-> Look for AF or evidence of MI ischaemia

Echocardiogram/cardiac monitoring
-> to assess for a cardiac cause

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16
Q

What is essential to do in someone who has had a TIA?

A

NEW NICE Guidance: Refer immediately for assessment to be seen within 24 hours of onset of symptoms.

Assess their risk of having a stroke in the next 7 days - ABCD2 score.

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17
Q

What is the ABCD2 score?

A

It is used in patients who have had TIA’s to assess their risk of stroke in the next 7 days.

  • Age > 60. (1 point)
  • BP > 140/90 mmHg. (1 point)
  • Clinical features: unilateral weakness (2 points), speech disturbance (1 point)
  • Duration of symptoms: > 1h or 10-59 mins. (10 mins+ = 1; 1h+ = 2)
  • Diabetes?

If more than 6 -> refer patient specialist immediately
If more than 4 -> assessed by specialist within 24hr

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18
Q

What specific investigation would you carry out if you suspected that atherosclerosis had caused your patient’s TIA?

A

Carotid artery Doppler ultrasound.
Then: MR/CT angiography.

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19
Q

Name 3 differential diagnoses of a TIA.

A

Until there is a full recovery, it is IMPOSSIBLE to differentiate from a stroke.

  1. Hypoglycaemia
  2. Migraine aura
  3. Focal epilepsy
  4. Vaculitis
  5. Syncope
    - e.g. due to arrhythmia
  6. Retinal bleed
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20
Q

What is the immediate management of a TIA?

A
  1. Immediate loading dose: Aspirin 300mg
    -> For 2 weeks
    -> Then lower dose
  2. Refer to specialist – to be seen within 24h of symptom onset.
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21
Q

What is the long term treatment for a TIA?

A

AAAS
A - Antiplatelet
A - Anticoagulant
A - Antihypertensive
S - Statin

  1. Antiplatelet therapy
    - Standard treatment is Aspirin 75mg daily
    - With modified-release Dipyridamole
    - OR Clopidogrel daily
  2. Anticoagulation
    - e.g. Warfarin
    - For patients with Atrial Fibrillation
  3. Statins
    - e.g. Simvastatin
  4. Control CV risk factors
    - Antihypertensives e.g. ACEi (Ramipril) or ARBs (Candesartan)
    - Improve diet, stop smoking
  5. No driving for at least 4 weeks after a TIA
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22
Q

How does warfarin work to reduce platelet aggregation?

A

Inhibits vitamin K dependent synthesis of clotting factors 2, 7, 9 and 10

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23
Q

What is the surgical treatment for a TIA?

A
  1. Endarterectomy if 70% or more stenosis
    -> Reduces stroke/TIA risk by 75%
  2. Stent e.g. carotid stent
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24
Q

At what point, do symptoms become a stroke rather than a TIA?

A

If they last over 24h.

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25
Q

What is a cerebrovascular accident (CVA)?

A

Another term for a stroke (ischaemic or haemorrhagic)

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26
Q

Define a cerebrovascular accident / stroke.

A

Syndrome of RAPID onset of neurological deficit caused by focal, cerebral, spinal or retinal INFARCTION.

  • Characterised by RAPIDLY DEVELOPING signs of focal or global disturbance of cerebral functions, lasting for MORE THAN 24HRS or leading to death.
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27
Q

What are the main vessels in the anterior cerebral circulation? (6)

A
  1. Posterior communicating
  2. Middle cerebral
    • Anterior choroidal
  4. Internal carotid
  5. Anterior cerebral
  6. Anterior communicating
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28
Q

What main arteries branch off the basilar artery?

A

Source: vertebral artery (posterior inferior cerebellar + anterior spinal arteries are branches)

  1. Anterior inferior cerebellar artery (AICA)
  2. Pontine arteries
  3. Superior cerebellar artery (SCA)
  4. Posterior cerebral arteries - terminal
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29
Q

What are Broca’s & Wernicke’s area?

A

Wernicke = understanding words
Brocas = forming words/speaking

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30
Q

Where is Broca’s area? What is it supplied by?

A

Frontal lobe
Opposite side to dominant hand
Supplied by middle cerebral artery

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31
Q

Where is Wernicke’s area? What is it supplied by?

A

Parietal/temporal lobe
Opposite side to dominant hand
Supplied by middle cerebral artery

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32
Q

What parts of the brain does the anterior cerebral artery supply?

A

Front & top - so frontal cortex and some of the motor cortex (esp upper limbs)

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33
Q

What does the middle cerebral artery supply?

A

Sides of brain including Broca’s, Wernicke’s, motor (esp lower limbs) and sensory

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34
Q

What does the posterior circulation supply?

A

Cerebellum and brainstem

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35
Q

What is the most common artery to have a stroke in?

A

Middle cerebral artery

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36
Q

Describe the epidemiology of strokes.

A
  1. Is the major neurological disease of our time
  2. 3rd most common cause of death worldwide
  3. Death rate of 20-25%
    -> In the UK, someone has a stroke every 3.5 minutes
    -> 1 in 4 people who suffer a stroke die within 1 year
    -> 1 in 2 stroke survivors have permanent disability
  4. Most common in older people
  5. Rare aged <40
  6. M > F
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37
Q

Why may the incidence of strokes be falling?

A

Incidence is falling due to more vigorous approach to risk factors in primary care
I.E. statin use and control of BP

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38
Q

What can cause a stroke?

A
  1. Cerebral infarction due to embolism or thrombosis (85%).
  2. Intracerebral or sub-arachnoid haemorrhage (15%).
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39
Q

What are the 2 main types of stroke?

A
  1. Ischaemic
  2. Haemorrhagic
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40
Q

What is an ischaemic stroke?

A

Blood vessel to/in brain occluded by a clot

Ischaemic strokes occur when the blood supply to an area of brain tissue is reduced, resulting in tissue hypoperfusion.

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41
Q

Give 5 risk factors for an ischaemic stroke.

A

Main ones:
- Male
- Black or Asian
- Increasing age
- Hypertension
- Smoking
- Diabetes mellitus

  • Past TIA
  • Heart disease (valvular, ischaemic)
  • Alcohol
  • Polycythaemia, thrombophilia
  • AF - stasis of blood in poorly contracting atria = thrombus formation
  • Hypercholesterolaemia
  • Combine oral contraceptive pill
  • Vasculitis
  • Infective endocarditis
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42
Q

What is the main cause of an ischamic stroke?

A

Arterial disease and atherosclerosis:
-> Atherothromboembolism
E.g. From Carotid artery

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43
Q

Other than atherosclerosis, name 2 other causes of an ischaemic stroke.

A
  1. Small vessel occlusion by thrombus
  2. Cardioembolism
    -> AF, post-MI, valve disease, infective endocarditis
  3. Hyperviscosity
  4. Hypoperfusion
  5. Vasculitis
  6. Fat emboli from a long bone fracture
  7. Venous sinus thrombosis
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44
Q

What does the clinical presentation of an ischaemic stroke depend on?

A

Depends on the site of the stroke
e.g. ACA, MCA, PCA

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45
Q

What are the common features of an ischaemic stroke?

A
  1. Contralateral sensory loss
  2. Contralateral hemiplegia
  3. Initially flaccid (floppy limb)
    -> Becomes spastic (UMN lesion)
  4. UMN facial weakness (forehead sparing)
  5. Dysphasia
  6. Homonymous hemianopia
  7. Visuo-spatial deficit

Weakness may recover gradually, over days-months.

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46
Q

In an ischaemic stroke, how does the hemiplegia change over time?

A

Initially: flaccid.
Then: becomes spastic as an UMN lesion.

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47
Q

How would an ischaemic stroke of the anterior cerebral artery (ACA) present?

A

Tends to affect feet, legs, up to bowel problems.

  • Leg weakness
  • Sensory disturbance in leg
  • Gait apraxia (a loss of ability to have normal function of the lower limbs such as walking)
  • Truncal ataxia
  • Incontinence
  • Drowsiness (since part of consciousness is in the frontal lobe)
  • Akinetic mutism
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48
Q

What is akinetic mutism?

A

Worst form of ACA stroke.
Decrease in spontaneous speech, “stuporous state”, completely mute and don’t move.

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49
Q

How would an ischaemic stroke of the middle cerebral artery (MCA) present?

A

Tends to be more arm and face.

  • Contralateral arm and leg weakness
  • Contralateral sensory loss
  • Hemianopia
  • Aphasia (inability to understand or produce speech)
  • Dysphasia (deficiency in speech generation)
  • Facial droop
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50
Q

How would a posterior cerebral artery (PCA) stroke present?

A

Visual issues.

  • Contralateral homonymous hemianopia (loss of half the vision of the same side in both eyes)
  • Cortical blindness with bilateral involvement of the occipital lobe branches (eye healthy, but brain issue causing blindness)
  • Visual agnosia (can see, but can’t interpret visual information).
  • Prospagnosia - can’t recognise faces (parietal lobe).
  • Dyslexia, anomic aphasia, colour naming and discrimination problems.
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51
Q

What is visual agnosia?

A

An inability to recognise or interpret visual information.

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52
Q

What is prosopagnosia?

A

An inability to recognise a familiar face.

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53
Q

How would a posterior circulation stroke (vertebral/basilar arteries) present?

A

More catastrophic - due to wide region affected.
-> More likely to get ‘locked in’ in these strokes!!
(Locked-in Syndrome = total paralysis but still have consciousness and their normal cognitive abilities)

  • Motor deficits e.g. hemiparesis or tetraparesis and facial paralysis.
  • Dysarthria (unclear speech articulation) & speech impairment.
  • Vertigo, nausea and vomiting.
  • Visual disturbances.
  • Altered consciousness.
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54
Q

Acute vision loss suggests a stroke in which region?

A

The posterior cerebral artery (PCA)

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55
Q

What is a lacunar infarct & how does it present?

A

Infarct of the deep penetrating arteries.
Produces an isolated deficit e.g. one hand weakness.
No visual field defect or cortical malfunction.

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56
Q

What is a lacunar stroke? How would a lacunar stroke present?

A
  • Small subcortical stroke that occurs secondary to small vessel disease
    = There is no loss of higher cerebral functions (e.g. dysphasia).

Symptoms (only 1 has to be present to diagnose):
- Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three
- Pure sensory loss
- Ataxic hemiparesis (cerebellar and motor symptoms)

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57
Q

Are the motor symptoms ipsilateral or contralateral to the infarct?

A

Contralateral

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58
Q

A patient presents with leg weakness, incontinence, drowsiness, and some missing sensations in his legs.
In what artery is the ischaemic stroke likely to have occurred?

A

Anterior cerebral artery (ACA)

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59
Q

A patient presents with upper limb weakness and loss of sensory sensation to the upper limb. They also have aphasia and facial drop. Which artery is likely to have been occluded?

A

Middle cerebral artery (MCA).

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60
Q

A patient presents with lower limb weakness and loss of sensory sensation to the lower limb. They also have incontinence, drowsiness and gait apraxia. Which artery is likely to have been occluded?

A

Anterior cerebral artery (ACA).

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61
Q

A patient presents with a contralateral homonymous hemianopia. They are also unable to recognise familiar faces and complain of a headache on one side of their head. Which artery is likely to have been occluded?

A

Posterior cerebral artery (PCA).

62
Q

What is the immediate essential investigation to carry out before you start specific stroke treatments?
Why?

A

Urgent CT head

  1. Distinguishes ischaemic from haemorrhagic
  2. Shows site of infarct
  3. Identifies conditions mimicking a stroke
63
Q

After carrying out a head CT scan, the diagnosis is still uncertain. What is the next investigation to carry out?

A

Diffusion weighted MRI scan

  • More sensitive.
  • CT might be negative in first few hours after infarct.
64
Q

After a head CT scan has been done, what other investigations may be done?

A
  1. Pulse, BP & ECG:
    * Look for AF or MI
    * Be careful about treating high BP, since even a 20% fall may
    compromise cerebral perfusion
  2. Bloods:
    * FBC: look for thrombocytopenia & polycthaemia
    * Blood glucose - to rule out hypoglycaemia
65
Q

What is gold standard for an ischaemic stroke investigation?

A

Diffusion-weighted MRI of the head

66
Q

What is the immediate treatment of an ischaemic stroke?

A

Haemorrhagic stroke must be excluded

  1. Immediate loading dose: Aspirin 300mg
    -> Continued for 2 wks
  2. After 2 wks of aspirin:
    -> Clopidogrel daily long term (antiplatelet therapy)

3.Anticoagulation (e.g. Warfarin) for patients with Atrial Fibrillation

67
Q

Management of a confirmed ischaemic stroke.

A

Thrombolysis therapy:

Can be given up to 4.5 hrs post onset of symptoms

  1. IV Alteplase
    -> Tissue plasminogen activator (tPA)
  2. Clopidogrel 24 hrs after thrombolysis
    -> Antiplatelet therapy
68
Q

When can thrombolysis be given to an ischaemic stroke patient? Why?

A

Must happen within 4.5 hours of symptoms onset.
-> The window in which the benefits outweigh the risks.

69
Q

Give 5 contraindications for thrombolysis for ischaemic stroke treatment.

A
  1. Recent surgery last 3 months
  2. Recent arterial puncture
  3. History of active malignancy (highly vascular thus increased bleeding risk)
  4. Evidence of brain aneurysm
  5. Patient on anticoagulation
  6. Severe liver disease (abnormal clotting)
  7. Acute pancreatitis
  8. Clotting disorder
70
Q

Other than the pharmacological treatment of a confirmed ischaemic stroke, what else should be monitored?

A
  • Maximise reversible ischaemic tissue:
  1. Supplemental O2 therapy
    -> Keep O2 sats > 95%
  2. Blood sugar control
    -> Between 4 - 11 mmol/litre
  3. Ensure hydration
  4. Blood pressure
71
Q

Should you lower BP in stroke generally?

A

No.

This risks reducing the perfusion to the brain - I.E. risks hypoperfusion.

72
Q

What is the surgical treatment in ischaemic stroke? When is suitable to do it?

A

Thrombectomy:
-> Endovascular removal of thrombus

Within 6hrs or if you can prove the tissue is viable.
There is a risk of reperfusion injury so only do if it will be worthwhile.

73
Q

If you are going to do a thrombectomy, how will you find the clot?

A

CT angiogram

74
Q

What non pharmacological treatment options are there for people after a stroke?

A
  1. Specialised stroke units.
  2. Swallowing and feeding help.
  3. Physiotherapy.
  4. Home modifications.
75
Q

Give 2 examples of primary prevention of stroke.

A
  1. Treat hypertension
  2. Control DM
  3. Statins for hyperlipidaemia
  4. Regular physical exercise
  5. Smoking cessation
  6. Anticoagulation of patients with rheumatic/prosthetic heart valves on left
76
Q

Give 4 examples of secondary prevention of stroke.

A
  1. Control risk factors:
    - Hypertension
    - Diabetes
    - Hyperlipidaemia
  2. Platelet treatment (lifelong if already had stroke)
    e.g. ASPIRIN + DIPYRIDAMOLE or CLOPIDOGREL
  3. Cholesterol treatment
    -> Like statins e.g. SIMVASTATIN / ATORVASTATIN 80mg
  4. Atrial fibrillation treatment e.g. WARFARIN or new oral anticoagulants
    e.g. PIXIBAN
  5. Carotid endarterectomy or stenting in patients with carotid artery disease
77
Q

What is endarterectomy? What investigation to do for it?

A

To remove atherosclerotic plaques
Doppler ultrasound

78
Q

What is the Bamford classification for ischaemic strokes?

A

For ischaemic stroke, total anterior = 3/3 and partial anterior = 2/3

Hemiplegia
Homonymous hemianopia
Higher cortical dysfunction e.g. speech

79
Q

What screening programme for stroke in the community?

A

FAST

F – Face
A – Arm
S – Speech
T – Time (act fast and call 999)

80
Q

Give 3 differential diagnoses of stroke.

A

Head injury
Hypo/hyperglycaemia
Subdural haemorrhage
Intracranial tumours
Hemiplegic migraine
Epilepsy
CNS lymphoma
Pneumocephalus
Wernicke’s encephalopathy
Hepatic encephalopathy
Mitochondrial cytopathies
Abscesses
Mycotic aneurysm

81
Q

How do you differentiate stroke from Bells Palsy?

A

Stroke = lower face weakness but forehead spared
Bells Palsy = forehead affected

82
Q

What is a haemorrhagic stroke?

A

Sudden bleeding into brain tissue due to rupture of a blood vessel within the brain.

83
Q

What is the main form of haemorrhagic stroke?

A

Intracerebral haemorrhagic stroke

84
Q

What proportion of strokes are due to intracerebral haemorrhages?

A

10-15%.

85
Q

Give 4 risk factors for an intracerebral haemorrhagic stroke.

A
  1. Hypertension
  2. Age
  3. Alcohol
  4. Smoking
  5. Diabetes
  6. Anticoagulation
  7. Thrombolysis
86
Q

What can cause an intracerebral haemorrhagic stroke? Give 4 causes.

A

CNS bleeds due to:
1. Head trauma
2. Secondary to ischamic strokes
3. Carotid artery dissection
4. Cerebral amyloid angiopathy
5. AV malformations

87
Q

Explain the pathophysiology of an intracerebral haemorrhagic stroke.

A
  1. Hypertension
  2. Increased intracranial pressure (ICP)
  3. Puts pressure on skull, brain & blood vessels
    -> stiff + brittle vessels = prone to rupture
    -> micro-aneurysms
  4. Healthy tissue can die
  5. May cause CSF obstruction
    - Hydrocephalus
  6. Leading to Midline shift / Tentorial herniation
  7. Eventually: Coning
  8. Leading to brainstem compression
  9. Death
88
Q

The clinical presentation of a haemorrhagic stroke is similar to an ischaemic stroke.
What might be some pointers in the presentation of stroke, to whether it is due to haemorrhagic or ischaemia?

A

Ischaemic - carotid bruit, AF, past TIA, IHD.

Pointers to haemorrhage:
1. Sudden loss of consciousness
2. Severe headache
3. Meningism
4. Coma within hours

89
Q

What is the first line investigation to do for a suspected haemorrhagic stroke?

A

Urgent CT head
- To differentiate between ischaemic + haemorrhagic stroke

90
Q

Are the investigations the same for ischaemic + haemorrhagic strokes?

A

YES!

91
Q

What is the immediate management of a haemorrhagic stroke?

A

Stop anticoagulants immediately!
- Effects reversed with clotting factor replacement.
- Decision to restart after 1-2 weeks on a case by case basis.

92
Q

Management of a haemorrhagic stroke.

A
  1. Stop anticoagulants - reverse them
    -> For Warfarin: use Vitamin K + Beriplex
  2. Reduce ICP:
    -> Manual decompression of raised ICP
    -> Give diuretic e.g. IV MANNITOL
  3. Control of BP/hypertension
    -> IV drugs
  4. Frequent GCS monitoring
  5. Referred for neurosurgical evaluation if:
    -> Hydrocephalus
    -> Coma
    -> Brainstem compression
93
Q

What are the 4 main haemorrhagic events?

A
  1. Intracerebral haemorrhage
  2. Subarachnoid haemorrhage
  3. Subdural haematoma
  4. Extradural haematoma
94
Q

Give 2 primary causes of intra-cerebral haemorrhage.

A
  1. Hypertension -> Berry or Charcot-Bouchard aneurysms -> rupture.
  2. Lobar (amyloid angiopathy).
95
Q

Give 5 secondary causes of intra-cerebral haemorrhage.

A
  1. Tumour.
  2. Arterio-venous malformations (AVM).
  3. Cerebral aneurysm.
  4. Anticoagulants e.g. warfarin.
  5. Haemorrhagic transformation infarct.
96
Q

Give 3 potential complications of Charcot-Bouchard aneurysms.

A
  1. Rupture (haemorrhage).
  2. Thrombosis.
  3. Leakage (microbleeds).
97
Q

Name 3 intra-cranial haemorrhagic events.

A
  1. Extra-dural.
  2. Sub-dural.
  3. Sub-arachnoid.
98
Q

What are the 3 layers of meninges?

A

Outer: dura mater - tough fibrous - periosteal and meningeal

Middle: arachnoid mater: loose connective tissue

Inner: pia mater - thin, tightly adhered to brain

Mnemonic: PADS

99
Q

Where are the dural venous sinuses?

A

Between the 2 layers of dura - the periosteal and meningeal layers

100
Q

What is a subarachnoid haemorrhage (SAH)?

A

Spontaneous bleeding into the subarachnoid space.
-> Space between the pia mater + arachnoid mater
-> Where the cerebrospinal fluid is located

101
Q

Where is the bleeding in a subarachnoid haemorrhage (SAH)?

A

Between the arachnoid and pia mater.
- Where the CSF should be.

102
Q

What is the most common cause of SAH?

A

Rupture of Berry aneurysms

103
Q

List the causes of SAH.

A
  1. Rupture of saccular (Berry) aneurysms - 80%.
  2. AV malformations - 10%.
  3. Idiopathic - 15%.
104
Q

What vessels are most often implicated in SAH?

A

Usually caused by ruptured Berry aneurysm.

Rupture of the junction of the posterior communicating artery with the internal carotid or of the anterior communicating artery with the anterior cerebral artery - in the circle of Willis.

105
Q

What are some common sites for Berry aneurysms?

A
  1. Junction of posterior communicating artery with internal carotid.
  2. Junction of anterior communicating artery with anterior cerebral artery (ACA).
  3. Bifurcation of middle cerebral artery (MCA).
106
Q

What 3 conditions are Berry aneurysms associated with?

A
  1. Polycystic kidney disease
  2. Coarctation of the aorta (narrowing of aorta where ductus arteriosus is)
  3. Connective tissue disorders
    - Ehlers-Danos syndrome
    - Marfan’s syndrome
107
Q

Describe the epidemiology for SAH.

A
  1. Typical age 35-65
  2. Black patients
  3. Female patients
  • Make up 5% of strokes:
    ~50% of people die straight away or soon after.
    ~10-20% more die from re-bleeding within weeks.
    Half the survivors are left with significant disability.
108
Q

List 3 risk factors for SAH.

A
  1. Hypertension
  2. Known aneurysm
  3. Previous aneurysmal SAH
  4. Smoking
  5. Alcohol
  6. Family history
  7. Bleeding disorders
109
Q

Give 5 symptoms of SAH.

A
  1. Sudden onset, excruciating, occipital ‘thunderclap’ headache.
  2. Photophobia.
  3. Reduced conciousness.
  4. Neck stiffness.
  5. Nausea and vomiting.
  6. Sentinel headache:
    * Patient may EARLIER have experience a sentinel headache, due to a small WARNING LEAK of the offending aneurysm (6%).
  7. Speech + vision changes.
110
Q

How would you describe the headache associated with SAH?

A

Thunderclap headache - maximum severity within seconds.
-> like being kicked in the head
-> SEVERE PAIN 12/10!!

111
Q

Give 5 signs of SAH.

A

Signs of meningeal irritation:
1. Neck stiffness
2. Kernig’s sign
-> Unable to extend/straighten patients leg at the knee when the thigh/hip is flexed

  1. Brudzinski’s sign
    -> When patients neck is flexed by doctor, patient will flex their hips & knees
  2. Retinal, subhyaloid & vitreous bleeds = vision changes
    -> Worse prognosis
    -> With/without also papilloedema
  3. Focal neurological signs
    E.g. 3rd nerve palsy
  4. Increased BP
112
Q

Name the first-line and the gold standard investigation for SAH.

A

Brain imaging - head CT
-> Done ASAP
-> Detects >95% of SAH in first 24 hours

113
Q

What do you see on the head CT in SAH?

A

“Star shaped” sign
-> blood pools in ventricle = appears as a white star
-> no clear bleed

114
Q

Apart from CT head, what other investigations might be helpful in SAH?

A
  1. Cerebral angiography
    -> to find the source of the bleed
  2. Lumbar puncture
    -> Done if CT normal but SAH still suspected
  • CSF in SAH is uniformly bloody early on and becomes xanthochromic (yellow) after several hours due to breakdown products of Hb (bilirubin)
  • Xanthochromia presence CONFIRMS SAH!
115
Q

How would the CSF look if you performed a lumbar puncture on a person with SAH?

A

CSF is bloody early on, then becomes yellow due to bilirubin - finding xanthochromia (yellow CSF) confirms SAH

116
Q

What clinical features would indicate you should avoid doing a lumbar puncture and why?

A

Headache, unilateral pupillary dilatation, vomiting, papilloedema, reduced mental state.

These are signs of raised ICP - risk herniation of brain and coning, leading to death.

117
Q

Describe the management for SAH.

A
  1. Referral to neurosurgeon immediately!
  2. IV fluids + BP control
    -> to maintain cerebral perfusion by being well hydrated
    -> aim for BP < 160mmHg
  3. IV/Oral Nimodipine (CCB)
    -> to reduce vasospasms & consequent morbidity from cerebral ischaemia
  4. Endovascular coiling:
    * Preferred to surgical clipping since has lower complication rate where possible
    * Promotes thrombosis and ablation of aneurysm
    * FIRST LINE TREATMENT where angiography shows aneurysm
  5. Surgery
    -> Clipping: Involves cranial surgery and putting a clip on the aneurysm to seal it.
    -> Intracranial stents and balloon remodelling for wide-necked
    aneurysms
  6. Lumbar puncture/drainage, if hydrocephalus develops.
118
Q

Give 2 possible complications of SAH.

A
  1. Rebleeding
  2. Cerebral ischaemia due to vasospasm
    - can result in permanent deficit
  3. Hydrocephalus
    - due to blockage of arachnoid granulations - requires ventricular or lumbar drain
  4. Hyponatraemia
119
Q

Give 2 differential diagnoses of SAH.

A
  1. Migraine
  2. Meningitis
  3. Intracerebral bleeds
  4. Cortical vein thrombosis
120
Q

What is a subdural haemorrhage (SDH)?

A

Bleeding into subdural space.
-> Space between dura mater & arachnoid mater

Due to rupture of a bridging vein.

121
Q

Where is the blood in a subdural haemorrhage (SDH)?

A

Between the dura mater and arachnoid mater

122
Q

What can cause a sub-dural haematoma?

A

Head injury -> vein rupture.

123
Q

Describe the epidemiology/risk factors of SDH.

A
  1. Babies
    - Physical abuse of infant
    - ‘Shaking baby syndrome’
  2. Traumatic head injury
  3. Brain atrophy – bridging veins are more susceptible to rupture
    -> Dementia
    -> Elderly
    -> Alcoholics
    = These people are also more accident-prone and at risk of falls
  4. Along with epileptics
  5. People on anticoagulants
124
Q

Describe the pathophysiology of SDH.

A
  1. Dural metastases OR deceleration due to violent injury
  2. Leads to trauma
  3. Bleeding from bridging veins between the cortex + venous sinuses
  4. Bridging veins bleed and form a haematoma (solid swelling of clotted blood) between the dura and arachnoid
  5. Reduces pressure and bleeding stops

DAYS/WEEKS later
6. The haematoma starts to autolyse due to the massive
increase in oncotic and osmotic pressure
7. H2O sucked into the haematoma -> resulting in the haematoma enlarging
8. Results in a gradual rise in ICP over many weeks
9. Causes the shifting away of midline structures from the side of the clot
10. If untreated: leads to eventual tectorial herniation and coning (brain herniates through foramen magnum - causes significant damage)

125
Q

What causes water to be sucked up into a sub-dural haematoma 8-10 weeks after a head injury?

A

The clot starts to break down and there is a massive increase in oncotic pressure, water is sucked up by osmosis into the haematoma.

126
Q

What is the typical patient history in SDH?

A

Acute - car crash with accelleration-deceleration
Chronic - elderly or alcoholic with trivial fall weeks ago

127
Q

Give 4 symptoms of a SDH.

A
  1. Fluctuating level of consciousness
  2. Drowsiness
  3. Headache
  4. Confusion (may fluctuate)
  5. Insidious physical & intellectual slowing
  6. Personality change
  7. Unsteadiness
128
Q

Give 3 signs of a SDH.

A
  1. Signs of raised ICP
    e.g. headache, vomiting, blurred vision, nausea, seizure and raised BP
  2. Seizures
  3. Localising neurological signs:
    -> Unequal pupils
    -> Hemiparesis
    -> Occur late (often >1 month after injury)
129
Q

What is the first-line investigation for a SDH?

A

Head CT scan

130
Q

What do you see on CT in a SDH?

A

Crescent/banana shaped bleeding - all way to midline at each side
acute (white) or chronic (grey) blood

  1. Shows haematoma
    = Crescent-shaped bleeding – BANANA
    -> Crosses suture lines
    -> Unilateral (blood over 1 hemisphere)
  2. Shows midline shift
131
Q

How would you differentiate between an acute + chronic SDH on a CT scan?

A

Acute - hyperdense - ‘white blood’

Chronic - hypodense - ‘grey blood’

  • As the clot ages and protein degradation occurs, it becomes isodense (same colour as brain tissue) and eventually, it becomes hypodense.
132
Q

How would you differentiate between a SDH and EDH on a CT scan?

A

SICKLE/CRESCENT SHAPE DIFFERENTIATES subdural blood
from extradural haemorrhage!!

133
Q

Management for SDH.

A
  1. Assess and manage ABCs, prioritise head CT
  2. Stabilise patient
  3. Refer to neurosurgeons:
    * Irrigation/evacuation via burr twist drill and burr hole craniotomy
  4. Address cause of trauma:
    - Fall due to cataract
    - Arrhythmia
    - Abuse
  5. IV MANNITOL to reduce ICP
134
Q

What is the surgical treatment of a SDH?

A

Irrigation/evacuation via burr twist drill and burr hole craniotomy

135
Q

What is an extradural haemorrhage (EDH)?

A

Bleeding into extradural space:
-> Space between dura mater & skull bone.

Usually after trauma to temple.

136
Q

In an EDH, where is the blood?

A

Between the skull and the dura mater - usually tightly stuck!

137
Q

What is the usual epidemiology of EDH?

A
  1. Young patient with traumatic head injury esp. skull fracture
  2. More common in males
138
Q

What artery is most commonly implicated in an EDH?

A

Middle Meningeal artery rupture
- At the pteron (frontal bone joins parietal bone)

139
Q

What causes an EDH? Give 2 causes.

A
  1. MIDDLE MENINGEAL ARTERY most common.
    -> fractured temporal or parietal bone
    -> causes laceration of middle meningeal artery + vein
  2. Any tear in dural venous sinus.
140
Q

Explain the pathophysiology of an EDH.

A

Trauma to the temporal or parietal bone -> causes laceration of middle meningeal artery & vein -> bleeding from the middle meningeal artery.

141
Q

Describe a typical characteristic history of EDH.

A
  1. Head injury -> blow to side of head
  2. Brief post-traumatic loss of consciousness or initial drowsiness.
  3. Lucid period for a few hours:
    = period of time between traumatic brain injury and decrease in consciousness
    - These vessels bleed slowly
    - Loss of consciousness

Example:
- Walks away from road traffic accident seeming fine, then after a few hours/days, there’s a decrease in GCS from rising ICP.

142
Q

Why do you get a lucid interval in EDH?

A

Because the patient is bleeding very slowly - due to how tightly the dura mater is adherent to the skull.
Venous bleed.

143
Q

Describe the clinical presentation of EDH after the lucid period.

A
  1. Rapidly declining GCS (consciousness level)
  2. Increasingly severe headache
  3. Vomiting
  4. Seizures
  5. Hemiparesis
  6. UMN signs
144
Q

Describe the clinical presentation of EDH after the lucid period + initial symptoms (the worsening of symptoms).

A
  1. Ipsilateral pupil dilation
  2. Bilateral limb weakness
  3. Coma
  4. Deep and irregular breathing
    -> Due to coning (brainstem compression)
  5. Late signs include:
    - Bradycardia
    - Raised BP
  6. Death, if no surgical intervention.
145
Q

What do the ventricles do to prolong survival in someone with an EDH?

A

The ventricles get rid of their CSF to prevent the rise in ICP.

146
Q

What is the first-line investigation for EDH?

A

Head CT

147
Q

What does an EDH look like on CT?

A
  1. Shows haematoma
    = Lens-shaped – LEMON: hyperdense ‘bright white’
    -> Doesn’t cross suture lines (limited by cranial sutures)
    -> Unilateral
  2. Shows midline shift
148
Q

How would you differentiate between an EDH and a SDH on a head CT?

A

EDH: round shape - LEMON

SDH: sickle shaped - BANANA

149
Q

Other than a head CT for a first-line investigation, what other investigation can be done?

A

Skull X-ray
- May be normal or show fracture lines crossing the course of the
middle meningeal artery.

  • Skull fracture increases EDH risk - so anyone with suspected fracture -> do urgent CT!
150
Q

Management of EDH.

A
  1. ABCDE emergency management - assess and stabilise patient
  2. Give IV MANNITOL if increased ICP
  3. Refer to neurosurgery:
    * Clot evacuation +/- ligation of bleeding vessel
  4. Maintain airway via intubation and ventilation in unconscious patient
151
Q

What treatment is contraindicated in all cerebral haemorrhages?

A

Antiplatelets and anticoagulants

neurology (20 decks)

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