S10 L1 Stroke Flashcards

1
Q

Define stroke?

A

Cerebrovascular accident
Serious life threatening condition that occurs when the blood supply to part of the brain is cut off
Symptoms and signs persist for more than 24hrs

A neurological defect attributed to the an acute foal injury of the central nervous system by a vascular cause, including cerebral infarction, intracerebral haemorrhage (ICH), and subarchnoid haemorrhage
Signs and symptoms persist for more than 24hours

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2
Q

Define TIA?

A

Transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia, wihtout acute infarction
Completely resolve within 24hours

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3
Q

What are the different types of stroke?

A

Ischaemia (85%) → thromboembolic
Haemorrhage (10%) → intracerebral (rupture of vessel in the brain parenchyma), or subarachnoid
Other (15%) → Dissection (separation of walls of artery, can occlude branches), venous sinus thrombosis (occlusion of veins causes back pressure and ischaemia due to reduced blood flow), hypoxic brain injury (post cardiac arrest)

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4
Q

What are the risk factors for stroke?

A
  • Hypertension
  • Smoking
  • Diabetes Mellitus
  • Heart disease → vascular, ischaemic, atrial fibrillation
  • Peripheral arterial disease
  • Post TIA (high early risk of stroke)
  • Carotid artery occlusion, carotid bruit
  • Polycythemia
  • Combined oral contraceptive pill
  • Hyperlipidaemia
  • Excess alcohol
  • Clotting disorders
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5
Q

What are the features of a stroke?

A

Dependent on whether the anterior or posterior circulation are affected and whether it is in the proximal or distal territory

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6
Q

What happens if there is a lesion in the anterior cerebral artery?

A
  • Contralateral lower limb weakness → medial part of the primary motor cortex- lower limb homunculus
  • Contralateral sensory changes in lower limb → medial part of primary sensory cortex- lower limb homunculus
  • Urinary incontinence→ paracentral lobules are affected (most medial part of the motor and sensory cortices and supplies the perineal area
  • Split brain syndrome/ alien hand syndrome →Corpus callosum normally supplied by the ACA
  • Frontal lobe features → personality changes, apraxia changes, coordinate motor activities
  • Apraxia → inability to complete motor planning, often caused by damage to left frontal lobe
  • Dysarthria/aphasia → unusual sign in ACA infarct compare with MCA infarct, may ne related to frontal lobe damage
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7
Q

What happens if there is an infarct in the middle cerebral artery?

A
Supplies a large area of the brain tissue 
Can be occluded at 3 main points 
- Proximal 
- Distal 
- Lenticulostriate
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8
Q

What is the presentation of a patient with a proximal middle cerebral artery defect? Why?

A

Main stem before lenticulostriate arteries
All branches of MCA will be affected - most widespread damage
- Contralateral hemiparesis → Lateral PMC affect but also supplied the IC so descending motor fibres also affected (face, arms, legs affected)
- Contralateral sensory deficits → Lateral PSC affected (face and arms only) if sensory part of IC affected more widespread problem
- Visual field defects → contralateral homonymous hemianopia without macular sparing - both optic radiations affected (parietal and superior temporal)
- If left sided lesion - aphasia - global deficit brocas and wenickes area affected → cannot understand or interpret words (left contains language)
- Contralateral neglect → more commonly right sided parietal lesion as right side has bilateral input, doesn’t acknowledge left side of the world/space (right side has input from both left and right whereas left only has input from right (remember fibres decussate) because it has the main language centre so if you loose the right side of the brain only the left remains and so you are only aware of the right)

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9
Q

What does contralateral neglect lead to?

A

Tactile extinction - if touch each side simultaneously is unable to feel the affected side
Visual extinction - unable to see half of the visual field even the visual fields and retinas are normal
Anosognosia - doesn’t acknowledge that they had a stroke, confabulate to explain disability

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10
Q

What do lenticulostriate occlusions cause?

A

Lacunar strokes
Destruction of small areas of the internal capsule and basal ganglia
- Pure motor- arms, face or legs*
- Pure sensory- arms, face or legs*
- Sensorimotor- mixed caused by boundary between motor and sensory fibres
*if infarct <15mls- very small area affected
Distinguished from proximal MCA as no cortical signs

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11
Q

What is the presentation of a patient with a distal MCA infarct look like?

A

Split into superior and inferior
Superior- lateral frontal lobe
→ Primary motor cortex and Broca’s area
→ Contralateral face and arm weakness and expressive aphasia if the left hemisphere is affected
Inferior - lateral parietal lobe and superior temporal lobe
→ Primary sensory cortex, Wernicke’s area and optic radiations
→ Contralateral sensory changes in face and arms, receptive aphasia if left hemisphere (speak fluently but can’t understand), and contralateral visual defect (homonymous hemianopia as both radiations are damaged)
Occlusions even more distally will have even more specific effects

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12
Q

What is the presentation of someone with posterior cerebral artery occlusion?

A

Somatosensory and visual dysfunction typical

  • Contralateral homonymous hemianopia (with macular sparing due to collateral supply from MCA)
  • Contralateral sensory loss due to damage to thalamus
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13
Q

What happens if you get a cerebellar infarct?

A

Symptoms- nausea, vomiting, headache, vertigo/dizziness
Ipsilateral cerebellar signs - DANISH
- Dysdiadochokinesis
- Ataxia
- Nystagmus
- Intention tremor
- Slurred speech
- Hypotonia
Possible ipsilateral brainstem sign since cerebellar arteries supply the brainstem a they loop round to the cerebellum
Possible ipsilateral Horner’s syndrome- sympathetic damage- Partial ptosis (droopy eyelid), miosis (constricted pupil) and anhydrosis (lack of sweating)
Contralateral sensory signs- spinothalamic tract lateral in brainstem
- contralateral due to decussation at lower levels

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14
Q

What is the presentation of brainstem strokes?

A

Typical features
- Contralateral limb weakness
- Ipsilateral cranial nerve signs
→ Damage to corticospinal tracts (above decussation level at the pyramids of the medulla) and damage to the CN nuclei on the same side

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15
Q

What happen in basilar artery occlusion?

A

Vessel supplies brainstem - important centres - occlusion can lead to death
Occlusion in different parts has different effects
- Proximal and distal

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16
Q

What happens if the distal (superior) basilar artery is occluded?

A
  • Visual and oculomotor deficits (some branches supply the oculomotor nuclei, also prevent blood into PCA so affects occipital cortex)
  • Behavioural abnormalities
  • Somnolence (strong desire for sleep), hallucinations, dreamlike behaviours (important centres for sleep regulation)
  • Motor dysfunction often absent if the cerebral peduncles can get blood from PCA which are filled by posterior communicating arteries
17
Q

What happens if the proximal (inferior) basial artery is occluded?

A

At level of pontine branches
Embolus in basilar artery can occlude pontine branches on each
Can cause catastrophic deficits
- Locked in syndrome
- Complete loss of movement of limbs however preserved ocular movement - eyes still move because midbrain is getting supply from PCAs via posterior communicating arteries
- Preserved consciousness (maybe because midbrain reticular formation is still intact)

18
Q

How are strokes classified?

A

Bamford/Oxford classification
Clinical tool used to quickly diagnose strokes
4 areas:
1- TACS- total anterior circulation strokes
→ all 3 of- (1) unilateral weakness (+/- sensory deficit) of face, arm and leg, (2) homonymous hemianopia, (3) higher cerebral dysfunction (dysphasia/aphasia, visuospatial disorder)
2- PACS- partial anterior circulation strokes
→ only 2 of above
3- POCS- posterior circulation strokes
→ cranial nerve palsy and contralateral motor/sensory deficit, bilateral motor/sensory deficit, conjugate eye movement disorder, cerebellar dysfunction, isolated homonymous hemianopia (with macular sparing)
4- LACS- lacunar syndrome
→ one of the following- pure sensory deficit, pure motor deficit, senori-motor deficit, ataxic hemiparesis

19
Q

What are the main principles for emergency treatment of stroke?

A

Two main principles

  • are they within the window for thrombolysis (<4hours)- only for infarction
  • do a CT head to determine if it is a bleed (if bleed cannot proceed with thrombolysis)
20
Q

What acute imaging is done for a stroke?

A

CT
→ Ischaemic area of brain not visible early on- as infarct becomes more established the ischaemic area will become hypodense
→ A bleed will show up as bright white area, maybe with mass effect
MRI
→ Sometimes performed
→ Ischaemia shows up as a high signal area

21
Q

What is the rule of 4?

A
4 rules about brainstem strokes
1. 4CN above the pons
→ CNI, II, III, IV
2. 4 Motor nuclei 
→ (all a subdivision of 12)
→ CN III, IV, VI, XII
3. 4 'midline' Ms
→ Motor pathway (corticospinal tract)
→ Medial leminiscis (dorsal columns)
→ Medial longitudinal fasciculus 
→ Motor nuclei (III, IV, VI, XII)
4. 4 'side/lateral' Ss
→ Spinocerebellar pathway 
→ Spinothalamic pathway 
→ Sensory nucleus (mainly 5- V, VII, IX, X, XI)
→ Sympathetics