Cerebral Infarction Flashcards

(77 cards)

1
Q

Define stroke

A

A sudden onset of focal or global neurological symptoms caused by ischemia or haemorrhage and lasting more than 24 hours.

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2
Q

Define TIA

A

Term used to describe symptoms which resolve within 24 hours.

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3
Q

How long do most TIAs last?

A

Most resolve within 1-60min

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4
Q

What are the types of stroke cause?

A
  • Ischaemic 85%

- Haemorrhagic stroke 15%

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5
Q

What can cause an ischaemic stroke?

A
  • Large artery atherosclerosis
  • Cardioembolic
  • Small artery occlusion
  • Undermined/cryptogenic
  • Rare causes such as arterial dissection or venous sinus thrombosis
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6
Q

What can cause a haemorrhagic stroke?

A
  • Primary intracerebral haemorrhage

- Secondary haemorrhage such as subarachnoid haemorrhage or AVM

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7
Q

What is the incidence and impact of stroke?

A
  • 2nd- 3rd cause of death in developed countries
  • # 1 cause of disability in adults.
  • 150,000 new strokes/year in UK.
  • 67,000 deaths/year in UK.
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8
Q

What does the risk of stroke increase with?

A

Increases with age

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9
Q

What public campaign is associated with stroke awareness?

A

FAST

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10
Q

What is ischaemia?

A
  • Is the failure of cerebral blood flow to a part of the brain caused by an interruption of the blood supply to the brain.
  • It can be transient (as in TIA) and results in varying degrees of hypoxia (↓oxygen).
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11
Q

What can hypoxia result in?

A
  • Hypoxia stresses the brain cell metabolism. This is especially important in the ischemic penumbra.
  • If prolonged, the hypoxia→anoxia (no oxygen).
  • Anoxia →infarction (complete cell death, leading to necrosis). This is a stroke.
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12
Q

Apart from infarction what other damage can anoxia result in?

A

Oedema, depending on the size +location of the stroke or secondary haemorrhage into the stroke

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13
Q

What is the ischaemic penumbra?

A

Area around the ischaemic core

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14
Q

What is the pathogenesis of ischaemic stroke?

A
  • Disruption/injury to plaque surface
  • Platelet adhesion/aggregation and fibrin formation
  • Platelet-fibrin embolus
  • Total arterial occlusion due to thrombus
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15
Q

What are the non-modifiable risk factors for strokes?

A
  • Previous stroke
  • Being old
  • Being male
  • Having a horrible family history
  • Impaired cardiac function (recent heart attack, atrial fibrillation).
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16
Q

What modifiable risk factors for strokes?

A
  • Hypertension
  • Smoking
  • Cholesterol
  • Diet
  • High BMI
  • Sedentary life style
  • Alcohol
  • Oral contraceptives (+ HRT) with a high estrogen content. Progesterone-only OK
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17
Q

What is the most important modifiable risk factor for stroke?

A

Hypertension

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18
Q

Why is hypertension a risk factor for stroke?

A
  • Stroke risk is related to blood pressure level
  • Chronic hypertension worsens atheroma and affects small distal arteries.
  • Both stroke and hypertension reach major proportions in the elderly.
  • The majority of people with hypertension have it poorly treated.
  • Hypertension is a major risk factor for haemorrhagic strokes as well (~50% of cases).
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19
Q

How does diabetes affect the risk of stroke?

A

Diabetes mellitus increases the incidence of strokes up to 3-fold in both sexes.

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20
Q

How does smoking affect the risk of stroke?

A

Smokers have

  • a 2-fold ↑risk of cerebral infarction.
  • a 3-fold ↑risk of sub-arachnoid haemorrhage.

Some of the increased risk of stroke relates to the complications of cardiac problems.

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21
Q

Why do increased serum lipids increase the risk of stroke?

A

↑serum lipids increase stroke risk due to blood vessel wall atheroma

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22
Q

What increases the deposition on LDL-C in arterial walls?

A
  • ↑plasma level of low density lipoprotein (LDL) results in excessive amounts of LDL within the arterial wall.
  • Hypertension, cigarette smoke, and diabetes contribute to LDL-C deposition in arterial walls.
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23
Q

How does alcohol affect stroke risk?

A
  • Small amounts of alcohol ↓stroke risk .

- Heavy drinking ↑risk 2.5 fold.

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24
Q

How does obesity (especially abdominal) affect stroke risk?

A

Recently identified as an independent risk factor for vascular disease including stroke.

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25
Why may someone be in a hyper-coaguable state?
- Malignancy | - Genetics
26
What is Broca's area responsible for?
Speech
27
What is the frontal lobe responsible for?
Smell
28
What is the temporal lobe responsible for?
- Intellectual and emotional functions | - Hearing
29
What is the brainstem responsible for?
- Swallowing - Breathing - Heartbeat - Wakefulness center - Other involuntary functions
30
What is the cerebellum responsible for?
Coordination
31
What is Wernicke's responsible for?
Speech comprehension
32
What is the occipital lobe responsible for?
Primary visual area
33
What is the parietal lobe responsible for?
Comprehension of language
34
What is the anterior circulation to the brain?
- 2 x Internal carotid arteries - 2 x Anterior Cerebral Artery (ACA) - 2 x Middle Cerebral Artery (MCA)
35
What is the posterior circulation to the brain?
- 2 Vertebral arteries →1 basilar - 3 pairs of cerebellar arteries - 2 Posterior cerebral artery (PCA)
36
What anastomoses exist in the brain?
- Circle of Willis: via anterior and posterior communicating arteries - Borderzone anastomoses: between peripheral branches of anterior, middle and posterior cerebral arteries
37
Where does the anterior circulation arise from?
Internal carotid arteries
38
What are the symptoms of ACA occlusion?
Contra-lateral - Paralysis of foot and leg - Sensory loss over foot and leg - Impairment of gait and stance.
39
What are the symptoms of MCA occlusion?
Contra-lateral - Paralysis of face/arm/leg - Sensory loss face/arm/leg - Homonymous hemianopia - Gaze paralysis to the opposite side - Aphasia if stroke on dominant (left) side - Unilateral neglect and agnosia for half of external space if non-dominant stroke (usually right side).
40
What triad can occur with disruption of MCA territory?
- Hemiplegia - Homonymous hemianopia - Dysphasia
41
What can disruption of the right hemisphere result in?
``` Left hemiplegia, homonymous hemianopia Neglect syndromes agnosias) -Visual agnosia -Sensory agnosia -Anosagnosia (denial of hemiplegia) -Prosopagnosia (failure to recognise faces) ```
42
What is the circulation to the basal ganglia?
Medial and lateral lenticulostriate arteries from the middle cerebral artery
43
What is absent in a lacunar stroke?
Devoid of cortical signs | E.G. no dysphasia, neglect, hemianopia
44
How can a lacunar stroke present?
- Pure motor stroke - Pure sensory stroke - Dysarthria - clumsy hand syndrome - Ataxic hemiparesis
45
What anatomical structures are involved with the posterior circulation?
- Brain stem - Cerebellum - Thalamus - Occipital and medial temporal lobes
46
What are the symptoms of brainstem dysfunction?
- Coma, vertigo, nausea,vomiting, cranial nerve palsies, ataxia. - Hemiparesis, hemisensory loss - Crossed sensori-motor deficits - Visual field deficits
47
Acute ischaemic stroke therapies should...
- Restore blood supply. - Prevent extension of ischemic damage. - Protect vulnerable brain tissue.
48
What are the treatment options for stroke?
- IV TPA - Stroke unit - Aspirin - Thrombectomy
49
What are the components of a stroke unit?
- Clinical staff - Stroke nurses - Physiotherapists - Speech and Language therapists - Occupational therapists - Dietitian - Psychologist - Orthoptist
50
What are the 4 OCSP stroke classifications?
- Total Anterior Circulation Stroke (TACS) - Partial Anterior Circulation Stroke (PACS) - Lacunar Stroke (LACS) - Posterior Circulation Stroke (POCS)
51
LACS: Motor (≥2/3 face arm leg)
+ or -
52
LACS: Sensory loss(≥2/3 face arm leg)
+ or -
53
LACS: Hemianopia or Dysphasia or Neglect
N/A
54
LACS: Brainstem + or cerebellar signs
N/A
55
PACS: Motor (≥2/3 face arm leg)
+ or -
56
PACS: Sensory loss (≥2/3 face arm leg)
+ or -
57
PACS: Hemianopia or Dysphasia or Neglect
1
58
PACS: Brainstem + or cerebellar signs
N/A
59
TACS: Motor (≥2/3 face arm leg)
+ or -
60
TACS: Sensory loss (≥2/3 face arm leg)
+ or -
61
TACS: Hemianopia or Dysphasia or Neglect
2 (must have hemianopia)
62
TACS: Brainstem + or cerebellar signs
N/A
63
POCS: Motor (≥2/3 face arm leg)
+ or -
64
POCS: Sensory loss (≥2/3 face arm leg)
+ or -
65
POCS: Hemianopia or Dysphasia or Neglect
+ or -
66
POCS: Brainstem + or cerebellar signs
+
67
How do death or dependence rates vary depending on type of stroke?
- TACS 96% - PACS 45% - LACS 39% - POCS 38%
68
What is the strict criteria for TPA use?
- < 4.5 hours from symptom onset. - Disabling neurological deficit. - Symptoms present > 60 minutes. - Consent obtained
69
What is the exclusion criteria for IV TPA?
Anything that increases the possibility of hemorrhage: - Blood on CT scan - Recent surgery - Recent episodes of bleeding - Coagulation problems - BP >185 systolic or >110 diastolic - Glucose <2.8 or > 22mmol/L
70
What does benefit of TPA decline with?
Time
71
What is an effective treatment in symptomatic internal carotid artery stenosis?
Carotid endarterectomy
72
What is the aetiology of stroke?
- Atherosclerotic narrowing - Embolic - cardiac source (atrial fibrillation, recent MI) - Artery to artery embolism - Hypercoaguable state - Arterial dissection - Venous sinus thrombosis
73
How should stroke be investigated?
- Routine blood tests (FBC, glucose, lipids, ESR...) - CT or MRI head scan (infarct vs. hemorrhage) - ECG (?AF, LVH) - Echocardiogram (valves, ASD, VSD, PFO) - Carotid doppler ultrasound (?stenosis) - Cerebral angiogram/venogram (vasculitis?) - Hyper-coagulable blood screen
74
What secondary prevention is there for stroke?
- Anti-hypertensive - Anti-platelets - Lipid lowering agents - Warfarin for AF - Carotid endarterectomy
75
What is the differential diagnosis for stroke?
- Post-ictal states (e.g. Todd’s paralysis) - Hypoglycemia - Intracranial masses - Vestibular disease - Bell’s palsy - Functional hemiparesis - Migraine - Demented patients with UTIs
76
What is the management post-stroke?
- Prevention of stroke recurrence. - Prevention of complications related to stroke. - Rehabilitation. - Re-integration into the community.
77
What are the objectives of stroke care?
- Reduce mortality. - Reduce residual disability amongst survivors. - Improve psychological status of patients and care-givers. - Improve patient / care giver knowledge. - Maximize quality of life.