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Year 2 - Theme 1 > Stroke symposium > Flashcards

Stroke symposium Flashcards

1
Q

Incidence of stroke in the UK per year

A
  • Over 100,000 people in the UK have a stroke per year
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2
Q

How many neurons die per min in stroke

A
  • 1.9 million neurons die/min in stroke
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3
Q

General symptoms of a stroke

A
  • Sudden onset of focal neurological or monocular symptoms
  • Symptoms and signs should fit within a vascular territory
  • Negative symptoms rather than positive symptoms(
  • Vascular injury often shows negative symptoms
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4
Q

Classic presentation of an ACA infarct

A
  • Predominantly the contralateral lower limb
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5
Q

Classic presentation of left MCA infarct

A
  • Dysphasia, right sided weakness/numbness
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6
Q

Classic presentation of right MCA infarct

A
  • Neglect, left sided weakness/numbness
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7
Q

Classic presentation of brainstem infarct

A
  • May involve diplopia, visual field defect, facial weakness, facial weakness, contralateral limb weakness/numbness, incoordination
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8
Q

Differential diagnosis of bell’s palsy and facial weakness caused by a stroke

A
  • Upper motor neurons, such as a stroke, cause contralateral face weakness sparing the forehead due to the bilateral innervation of the occipitofrontalis muscle
  • While lower motor neuron lesions, such as a facial nerve injury causing bell’s palsy, typically cause weakness involving the whole ipsilateral face
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9
Q

Two types of strokes

A

Ischemic - Either thrombotic or embolic

Haemorrhagic - often due to a rise in blood pressure. Eg from an aneurysm , arterio-venous dysplasia.

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10
Q

First test when a stroke is suspected

A
  • CT scan
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11
Q

What are watershed cerebral infarctions

A
  • Also known as border zone infarcts, occur at the border between cerebral vascular territories where the tissue is furthest from arterial supply and thus most vulnerable to reductions in perfusion
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12
Q

What type of infarct may not always show up immediately on a CT scan

A
  • Ischaemic
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13
Q

How might a haemorrhagic infarct show on a CT scan

A
  • Hypertension bleed
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14
Q

Normal physiological blood flow to the brain

A
  • 50 ml/100g/min
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15
Q

Blood flow level at which electrical function stops

A

<20ml/100g/min

  • Neurones still alive
  • Potentially salvageable
  • Reversible ischaemia limited time
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16
Q

Blood flow level at which neuronal death begins to occur

A

<10ml/100g/min

- Neuronal death within mins - irreversible ischaemia - cerebral infarction

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17
Q

What is the efficacy of thrombolysis for stroke treatment dependent on

A
  • Time
  • Due to neuronal damage over time
  • Length of clot
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18
Q

What is the NIHSS

A
  • NIH stroke scale for quantifying the severity of a stroke
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19
Q

What is vasogenic oedema

A

Vasogenic cerebral oedema refers to a type of cerebral oedema in which the blood brain barrier (BBB) is disrupted (cf. cytotoxic cerebral oedema, where the BBB is intact)

It is an extracellular oedema which mainly affects the white matter via leakage of fluid from capillaries.

20
Q

Where is vasogenic oedema normally seen

A
  • It is most frequently seen around brain tumours (both primary and secondary) and cerebral abscesses, though some vasogenic oedema may be seen around maturing cerebral contusion and cerebral haemorrhage.
21
Q

What is cytotoxic oedema

A
  • Cytotoxic cerebral oedema refers to a type of cerebral oedema, most commonly seen in cerebral ischaemia, in which extracellular water passes into cells, resulting in their swelling.
22
Q

What is dwi imaging

A
  • Diffusion-weighted imaging
  • Diffusion-weighted imaging (DWI) is a form of MR imaging based upon measuring the random motion of water molecules within a voxel of tissue
23
Q

What causes cytotoxic oedema to show up on MRI-DWI sequence

A
  • Cytotoxic oedema of cells leads to restricted diffusion of water molecules, gives high signal on DWI sequence
  • Shows up ischaemia within 20 mins unlike CT scan
24
Q

Vascular risk factors for stroke

A 
· Hypertension 
· Hyperlipidaemia 
· LDL 
· Diabetes 
 Smoking
25
Q

What is virchow’s triad

A
  • Describes the three broad categories of factors that are thought to contribute to thrombosis

1) Hypercoaguable state
2) Vascular wall injury
3) Circulatory stasis

26
Q

5 subtypes of ischaemic stroke

A
  • Large artery atherosclerosis
  • Cardioembolism
  • Small vessel occlusion
  • Stroke of other determined etiology
  • Stroke of undetermined etiology
27
Q

Features of speech and language therapy in stroke care

A

· Initial screen of swallow on admission. Then, if indicated, specialist assessment by SLT no more than 72 hours after admission. Considerations of NBM/NG/PEG with consultant.
· Swallow therapy at least 3 times a week
· Initial language/speech screen within 72 hours of symptoms
· Follow up language therapy – at least 45 mins a day
· MDT working and support
· Discharge Planning and ESD
· Handover to rehab or community teams

28
Q

Features of community care for stroke care

A

· Follow up assessment of communication and swallow
· Usually at the patient’s home
· 3-4 months of therapy, usually 1-2 times a week.
· Working alongside the patient’s family, carers, nursing home staff
· Support in getting back to community activities and work
· Link to community support e.g. Say Aphasia, befriending scheme
· 6 month review and offer
- further treatment if appropriate

29
Q

What is aphasia

A
  • Impairment of language, affecting the production or comprehension of speech and the ability to read or write
30
Q

What is dysarthria

A
  • difficult or unclear articulation of speech that is otherwise linguistically normal
  • Due to loss of control of the muscles used to make the sounds of speech eg lips, tongue, soft palate, larynx
  • Speech can sound slurred or unintelligible
31
Q

What is apraxia of speech

A
  • is a motor disorder caused by damage to the brain (specifically the posterior parietal cortex) in which the individual has difficulty with the motor planning to perform tasks or movements when asked, provided that the request or command is understood and the individual is willing to perform the task.
32
Q

What is dysphagia

A

An impairment at any of the 4 stages of swallowing:

  • Pre-oral
  • Oral
  • Pharyngeal
  • Oesophageal
33
Q

What can dysphagia lead to

A
  • Aspiration pnemonia
  • Malnutrition
  • Dehydration
  • Choking and death
34
Q

How is dysphagia assessed for

A
  • Assessed at bedside via observation and palpation and/or through instrumental techniques such as videofluroscopy or fiberoptic endoscopic evaluation of swallow(FEES)
35
Q

How can we help with dysphagia

A
  • Adaption of posture
  • Environmental changes eg reducing distractions
  • Modifying diet and fluids
  • Educating family/carers
  • Compensatory strategies
  • Swallow rehab exercises
  • Adaptive equipment
36
Q

What are the risk factors for dysphagia

A
  • Poor positioning
  • Reduced dentition
  • Comorbiditieseg COPD, frailty, alertness, cognition
37
Q

What is aphasia

A
  • Aphasia is an impairment of language, affecting the production or comprehension of speech and the ability to read or write.
  • Aphasia is always due to injury to the brain-most commonly from a stroke, particularly in older individuals.
38
Q

Expressive difficulties of aphasia

A
  • Word finding difficulties
  • Non-fluent output
  • Short, staggered sentences
  • Difficulty with past/present, he/she may miss words out
39
Q

Receptive difficulties of aphasia

A
  • Long muddled sentences
  • Use of non-words eg ‘ploof’ for ‘dog’
  • Unable to understand what others are saying
  • May not be aware of impairment
40
Q

Damage to what regions of the brain causes cognitive communication disorders

A
  • Results from damage to frontal regions of the brain(predominantly right-sided)
  • The frontal lobes are particularly important for cognitive communication skills because of their role in the brain’s ‘executive functions’ including planning, organisation, flexible thinking and social behaviour
41
Q

How does hypertension increase risk of stroke

A

shearing forces - endothelial injury, and prothrombotic state

42
Q

How does hyperlipidaemia increase risk of stroke

A
  • Lipid accumulation in foamy macrophages
43
Q

How do LDLs increase risk of stroke

A

LDL - oxidised to free radicals - promote inflammation

44
Q

How does diabetes increase risk of stroke

A

Diabetes - promotes prothrombotic state, facilitates platelet adhesion

45
Q

How does smoking increase risk of stroke

A

Smoking - prothrombotic state, platelet activation and adhesion, endothelial injury

Year 2 - Theme 1 (30 decks)

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