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MED627 > Stroke > Flashcards

Stroke Flashcards

1
Q

what is stroke?

A
  • a rapidly developing acute neurological deficit of vascular origin that lasts >24hours or causes death
  • stroke follows heart disease and cancer as the third leading cause of death in developed countries
  • accounts for 10% overall mortality in UK
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2
Q

what are the two types of stroke?

A
  1. ischaemic (85%) - reduced blood flow to particular part of brain followed by occlusion of cerebral artery
  2. haemorrhagic (15%) - due to ruptured blood vessel, commonly associated with high BP and diseases that weaken the arterial wall
    - primary intracerebral haemorrhage 10%
    - subarachnoid haemorrhage 5% - 1/3 of ICH
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3
Q

what is TIA?

A
  • NICE: a stroke that recovers within 24hrs from the onset of symptoms
  • a brief period of cerebral ischaemia may cause a reversible neurological deficit that resolves when the blood flow is restored
  • stroke symptoms lasts less than 24hrs, majority <30mins
  • involvement of retinal blood supply causes temporary blindness in one eye - amaurosis fugax
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4
Q

what are the causes of TIA?

A

caused by inadequate cerebral or ocular blood supply like

  1. arterial thrombosis
  2. low flow
  3. embolism (arterial/cardiac/haematological)
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5
Q

why are TIA’s important?

A
  • 20% of patients with stroke report a preceding TIA
  • to identify and treat if possible high risk individuals (risk factors like hypertension, cholesterol, diabetes etc) to prevent a subsequent more serious event
  • symptoms usually resolves within mins (never lasts >24hrs, by definition) but neuroimaging evidence suggests that permanent damage occurs in 10-20% cases
  • TIA are associated with increased risk of both stroke and heart attacks
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6
Q

what is the ABCD² score and why is it used?

A
  • Prognostic scores to identify people at high risk of stroke after a transient ischaemic attack (TIA) - NICE 2012
  • used for training HR patients and target rapid intervention to HR patients like crescendo TIA (2 or more TIAs in a week) or HR factors like high BP, cholesterol, diabetes, smoking etc.
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7
Q

what does the ABCD score of <4 and >4 signify?

A
  • ABCD < 4 – low risk
    Seen in TIA clinic within 1 week
  • ACBD > 4 – high risk
    Seen in TIA clinic next 24 hrs
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8
Q

what are the treatment options for TIA?

A
  1. Asipirin and ER Dipyridamole - NICE 2012
  2. Clopidogrel monotherapy - RCP 2012
  3. early secondary prevention - BP, DM, cholesterol, smoking, alcohol, weight, exercise
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9
Q

what are the different types of ischaemic stroke?

A
  • classification derived from a multi centre trial of acute stroke treatment (TOAST) 1990 and is widely used in UK stroke trials
  • classified into five group based in the cause
    1. large artery disease/ atherothromboembolism: 25%
    2. small vessel disease: 25%
    3. cardioembolic: 20%
    4. other defined or uncertain cause (like abnormalities if blood coagulation, infectious diseases, arterial damage and inflammatory disorders) : 25%
    5. other: 5%
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10
Q

what is large vessel disease and who is commonly affected?

A
  • ischaemic stroke caused by coagulation of blood within a cerebral vessel termed ins its thrombosis or large artery occlusive disease
  • more common in people of asian and African origin but is increasingly recognised in caucasians
  • artherosclerosis of medium and large arteries(e.g. neck vessels, aorta, coronary arteries) universal in developed countries, as result of lifestyle factors
  • vasculopaths - plaque formation -> inflammation -> thrombosis/ embolism
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11
Q

what are the various mechanisms resulting in large vessel disease?

A
  1. thrombus on lesion causing local occlusion
  2. embolisation of plaque debris or thrombus in distal vessel
  3. small vessel origin occlusion by growth of plaque
  4. severe reduction in diameter of vessel lumen leads to hypoperfusion and infarction of distal “watershed” areas
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12
Q

what are small vessel disease, its two types and its pathology?

A
  • small penetrating arteries of brain affected
  • common cause: arterial hypertension
  • High BP damages arterial walls and its smooth muscle is gradually replaced by collagen termed hyaline arteriosclerosis
  • some cases: necrosis of vessel wall + accumulation of lipid laden foam cells - lipohyalinosis
  • both types of pathology cause arteriosclerosis or hardening of arteries
  • sclerotic vessels are unable to dilation in repose to reduced flow leading to lacunar infarcts
  • often BG or internal capsule damaged
  • important cause of vascular cognitive impairment and dementia
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13
Q

what is cardioembolism?

A
  • cerebral blood vessels may be occluded by an embolus
  • embolus is a small piece of coagulated blood (sometimes, fat) that travels in the circulation and lodges in the vascular tree of brain
  • emboli often originate from from heart in association w valve disease or abnormal heart rhythm (called atrial fibrillation)
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14
Q

what are the causes of cardioembolsim?

A
  1. Atrial Fibrillation (LA thrombus) – 80%
  2. Myocardial Infarction (anterior wall) with hypokinetic wall segment/ LV aneurysm
  3. Infective endocarditis
  4. Non-bacterial thrombotic endocarditis
  5. Prosthetic heart valves (mitral)
  6. Paradoxical embolus - PFO, ASD, VSD
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15
Q

what are the obscure (uncertain) causes of ischemic stroke?

A
  1. Arterial dissection and trauma e.g. coughing
  2. Inflammatory vascular disease (GCA, SLE, antiphospholipid syndrome, RhA)
  3. Haematological (thrombophilias, leukaemia, lymphoma, polycythaemia, sickle cell, TTP, DIC)
  4. Peri-operative
  5. Recreational drugs (cocaine, amphetamines)
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16
Q

why is stroke considered as a global and national burden?

A

Global burden cause
- stroke: 2nd most common cause of death WW (after IHD)
- 15 million/ year suffer a stroke
- 5 million die
- 5 million people ;eft permanently disabled;ed
- absolute number of strokes increasing because of increase in ageing population
national burden cause
- approx 150,000 strokes each year in UK
- 3rd leading cause of death in UK
- leading cause of disability
- 20% mortality within 30day
- 1 in 4 < 65 years
- high costs: at least £7 billion per year

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17
Q

what are the major modifiable risk factors of stroke?

A
  1. Hypertension
  2. Smoking
  3. Diabetes
  4. High cholesterol
  5. AF (atrial fibrillation)
  6. IHD (ischemic heart disease)
  7. PVD (peripheral vascular disease, blood circulation disorder that causes the blood vessels outside of your heart and brain to narrow, block, or spasm)
  8. Previous TIA
  9. Obesity
  10. Unhealthy diet
  11. Low socioeconomic status
  12. Psychosocial stress
  13. Excess alcohol use
    - 80% stroke causing factors are modifiable
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18
Q

what are the non-modifiable risk factors of stroke?

A
  1. age
    - stroke uncommon in <40s but does happens even in children
    - risk of stroke doubles each decade after 55
    - 85 years (if lived to): 1/4men, 1/5men
  2. family history - increased risk if 1st degree relative has had
  3. IHD or
  4. stroke <55yrs (men), <65yrs (women)
  5. race - people of African and carribean ethnicity - 2x likely to suffer stroke due to high prevalence of high BP and diabetes but is increasingly being recognised in caucasians
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19
Q

what is the effect if BP on stroke risk?

A
  • for every 10 deaths from stroke - 4 preventable if stroke is treated
  • risk of stroke increases with increase in mean BP
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20
Q

what are the stroke prevention techniques from a population based approach?

A
  • Education regarding healthy life style including:
    1. Increased exercise
    2. Lower salt intake
    3. Better diet - more fruit & vegetables
    4. Reduced cholesterol intake
    5. Reduced alcohol intake
    6. Stop smoking
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21
Q

what is the effect of smoking of stroke?

A
  • smoking doubles the risk of stroke in both men and women

- stopping smoking reduces the risk of CVD close to a non-smoker

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22
Q

how does smoking result in stroke?

A
  1. damages endothelial lining
  2. promotes atheroma
  3. enhances clotting
  4. raises LDL and lowers HDL
  5. raises BP
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23
Q

why is diabetes a significant factor for stroke?

A
  • 170m people affected with diabetes WW and the numbers are increasing
  • diabetes doubles the risk of stroke
  • diabetics have a HR of dying from stroke
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24
Q

what is the effect of cholesterol on stroke?

A
  • high LDL and low HDL - risk factors for IHD
  • causation fro stroke not clear yet
  • pooled data suggests high levels of cholesterol - risk factor for ischaemic stroke but not ICH
  • nevertheless, clinical trials have shown lowering cholesterol in patients w IHD, PVD or prion stroke - prevents further stroke
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25
Q

how is statins beneficial in stroke?

A
  • reduce cholesterol and have effectsoin platelets and vascular endothelium
  • reduce the risk of MI, stroke
  • improves revascularisation by 1/3
  • according to the heart protection study in 2001, 5yrs of statin use prevents major vascular events in
  • 100/1000 previous MI
  • 80/1000 other CHD
  • 70/1000 for diabetes (40+), previous stroke and other PVD
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26
Q

what is the effect of obesity on stroke?

A
  • obesity is associated with metabolic syndrome like hypertension, diabetes, reduced physical activity, high cholesterol levels and reduced insulin sensitivity
  • therefore, is associated with increased risk of stroke
  • waist to hip ratio of >1.0 in men and >0.85 in women associated with 3 fold increase in IHD
  • > 60% adults in USA overweight or obese (BMI >25 overweight, >30 obese)
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27
Q

what is impact of social deprivation on stroke?

A
  • people living in deprived areas 3 times more likely to die from stroke than least deprived
  • this is tribute to high rates of smoking, poor diet, obesity, lack of exercise in socially deprived communities
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28
Q

what is the impact of AF on stroke?

A
  1. NVAF (non-valvular AF) associated w x6 fold increase in stroke
  2. Individual’s risk is compounded by other risk factors e.g. CHF (chronic heart failure), PVD, high BP, elderly, diabetes, female
  3. Treatment options include Aspirin, Warfarin or one of the NAOCs (non-vitamin K antagonist oral anti-coagulant, drug used for NVAF)
  4. CHA2DS2VASc score predicts risk of stroke
  5. HASBLED score predicts individual risk of haemorrhage on treatment
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29
Q

what are the primary prevention techniques for stroke?

A
  • identify HR population
  • regular BP checks of adult population
  • well clinics
  • considering diabetes/high cholesterol/AF
  • asses overall cardiovascular risk prior to treatment
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30
Q

what are the secondary prevention techniques for stroke?

A
  • Rapid assessment of patients with TIA
  • address cardiovascular risk factors
  • BP < 130/80, < 120/80 in diabetics
  • Statin for all patients
  • Antiplatelet – reduces risk by ~ 20% annually -> Clopidogrel or aspirin and dipyridamole combination
  • Warfarin/DOAC (direct oral anti-coagulant, sam as NOAC) for patients in AF
  • Carotid endarterectomy (surgery to correct stenosis in common carotid artery and ICA) for patients with tight symptomatic stenosis - within 7days of symptoms
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31
Q

what are the different types of stroke syndrome?

A

according to the Oxford classification
type with morbidity rates associated
1. Total anterior circulation syndrome (TACS)
2. partial anterior circulation syndrome (PACS)
3. posterior circulation syndrome (POCS)
4. lacunar syndrome (LACS)

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32
Q

what are the morbidity rates associated with different stroke syndrome and

A
  • proportion of patients dying within the first year:
    TACS - 60%
    PACS and POCS - 20%
    LACS - 10%
  • most common cause of death is raised ICP due to brain swelling (cerebral oedema) -> causes herniation of tonsils of cerebellar tonsils compressing the brainstem, referred to as coning
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33
Q

what are the symptoms of TACS, PACS, POCS and LACS?

A

TACS
- new higher cortical dysfunction (e.g. aphasia)
- AND homonymous hemianopia
- AND sensorimotor deficit (affecting 2/3 of face, arm,leg)
PACS
- 2/3 elements of TACS
- OR higher cortical disfunction alone
- OR limited sensorimotor deficit (affecting fewer than 2 of face, arm,leg)
POCS
- CN + crossed sensorimotor deficit
- OR bilateral sensory/motor deficit
- OR disordering of conjugate eye movement
- OR isolated cerebellar dysfunction/field defect
LACS
- pure motor deficit
- OR pure sensory deficit
- OR sensorimotor deficit
- OR ataxic hemiparesis

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34
Q

what are the various causes of rupture of vessels in haemorrhagic stroke?

A
  • excessive pressure - hypertension
  • friable/da,aged vessels: vasculitis, CAA, vascular malformations, moyamoya
  • trauma e.g. trauma SAH
  • malignant tumour
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35
Q

what is the eligibility criteria for thrombolysis?

A
  • treatment is started as early as possible within 4.5 hrs of stroke symptoms onset
  • ICH has been excluded by appropriate imaging techniques
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36
Q

what are the exclusive criteria for thrombolysis?

A
  1. Low NIHSS
  2. Uncertain time of onset
  3. Improving NIHSS at time of review
  4. Haemorrhage on CT
  5. Uncontrolled hypertension
  6. Recent head trauma, neurosurgery or stroke within 3 months
  7. Presentation suggests SAH
  8. History of ICH
  9. known AVM, tumour or aneurysm
  10. Active bleeding
  11. Possible SBE
  12. Surgery in last 14 days (relative to type of surgery)
  13. Recent UGI, urinary haemorrhage
  14. Arterial puncture in a non-compressible site
  15. Pregnancy
  16. Recent lumbar puncture
  17. Actively anticoagulated
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37
Q

what are the immediate symptoms of a stroke? (FAST)

A

Face: one side drooping
Arms: weakness
Speech: difficulty
Time: to call 999

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38
Q

what is NIHSS and why is it used?

A
  • Grade and track the severity

- Monitor response to acute treatments

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39
Q

what are the pros and cons of CT in acute stroke?

A 
Pros
- Quick 
- Readily available 24/7
- Sensitive for haemorrhage
- May see a ‘hyperdense vessel’ 
Cons
- Cannot usually diagnose an infarct in the acute phase
- Less sensitive than MRI for picking up other abnormalities (demyelination, mass lesions, microhaemorrhages) and for lacunar and posterior circulation infarcts.
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40
Q

what are the key steps in management of stroke?

A
  1. Investigate the cause (history, examination, bloods, imaging)
  2. Screen and prevent complications (dehydration, aspiration, VTEs, pressure sores, infection, depression)
  3. Establish Secondary Prevention (lifestyle, medical, surgical)
  4. Rehabilitation (physiotherapy, occupational therapy, speech and language therapy
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41
Q

what are the keys steps involved in treatment of stroke?

A
  1. MDT
  2. Lifestyle
  3. medical
  4. surgical
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42
Q

what does the multidisciplinary team (MDT) approach involve?

A
  1. Nursing
    - Analysing clinical status and progress; blood pressure management
    - Administration of medications
    - Nasogastric feeding
    - Preventing pressure sores
  2. Physiotherapy
    - Strength, balance, function
    - Preventing spasticity
    - Chest physiotherapy in infections and sputum clearance
  3. Occupational Therapy
    - Functional assessments and future needs planning
    - Cognitive and mood screening
  4. Speech and Language Therapy
    - Swallowing impairment and prognosis
    - Communication rehabilitation in dysphasias
  5. Dieticians
  6. Orthoptics
43
Q

outline the key steps involved in treatment of acute ischaemic stroke?

A
  • identify stroke or TIA
  • first goal: prevent or reverse brain injury
    = ABCD - patient’s airway, breathing, circulation, diabetes
    = treat hypoglycaemia or hyperglycaemia if identified
  • perform emergency non-contrast head CT to differentiate b/w ischaemic stroke and haemorrhagic stroke
  • treatments to reverse or lessen the amount of infarction and improve clinical outcome (fall into six categories)
44
Q

what are the six categories for treatment of ischaemic stroke?

A
  1. medical support (primary prevention?)
  2. IV thrombolysis
  3. endovascular - IA thrombolysis and mechanical thrombectomy
  4. anti-thrombotic treatments
  5. neuroprotection
  6. stroke and rehabilitation
45
Q

what are the medical support or steps to prevent complications provided in stroke management for acute ischaemic stroke?

A
  1. optimise cerebral perfusion in surrounding ischaemic penumbra - immediate goal
  2. preventing common complication of bedridden patients like infections and DVT w pulmonary embolism
    - pneumatic compression device used to prevent DVT
  3. 5-10% develop cerebral oedema -> brain herniation - water restriction and IV mannitol could be used to raise serum osmolarity
    - combined analysis of 3 RCT of hemicraniectomy show that it markedly reduces mortality and clinical outcomes of survivors are acceptable
  4. dysphagia - a common problem -> malnutrition -> HR of thromboembolism -> nutrition and hydration NG/PEG feeding
  5. spasticity
    - physiotherapy - MDT
    - botox
46
Q

what have the NINDS studies on rTPA shown?

A
  1. NINDS t-PA study in 1995 with 624 patients with acute ischemic stroke showed at 3 months treatment with IV tPA within 3hrs of onset - increases the chances of an excellent recovery by 30% (measured by 4 scales and a global test statistic)
  2. another NINDS study showed despite an increased incidence of symptomatic ICH, treatment with IV rtPA within 3hr of symptom onset in IS improved clinical outcomes as there was a non-significant reduction in mortality and significant 12% absolute increase in the number of patients with only minimum disability
47
Q

what is the use of thrombolytic agent? when was it approved by FDA? and what is the standard care?

A
  • thrombolytic agent given to promote acute recanalisation of occluded artery through lysis of occlusive thrombus
  • approved by the FDA in 1996
  • the only approved treatment of acute stroke
  • standard of care for patients: within 3 hours of symptoms onset
48
Q

what is rTPA?

A
  • rtPA or alteplase is a clot-busting drug used to disperse a clot and return blood supply to the brain
49
Q

what has the ECASS III study shown on IV t-PA?

A

ECASS III studied 821 patients with acute ischaemic stroke b/w 3-4.5hrs from onset with IV tPA (0.9mg/kg)

  • favourable outcomes at 3 months by 52.4% in rTPA group and 45.2% placebo
  • one may be able to select patients beyond the 4.5h window will benefit from thromobolysis using advanced neuroimaging but this is currently under investigation
50
Q

what are the limitations of IV t-PA?

A
  • increased incidence of symptomatic ICH post administration (though it increases the clinical outcome)
  • limited time window - 4.5hours (IST 3 did not reveal any benefits to 6h)
  • many contraindication: <10% of all stroke patients receive IV t-PA
  • the % of vessels reanalysed in unknown
51
Q

why is intra arterial thrombolysis used instead of IV thrombolysis?

A
  • occlusion of large vessels like MCA, ICA and basilar artery involve large clot volume and often fail to open with IV rtPA alone
  • therefore, IA route is used to increase the concentration of drug at the clot and minimise systemic bleeding complications
52
Q

what was the PROACT II trial and its outcomes?

A

PROACT II trial of 180 patients found intrarterial pro urokinase (9mg) with low-dose IV heparin beneficial within 6hrs from symptom onset of large artery occlusion

  • 66% recanalisation rate in pro-UK users
  • 40% favourable outcome
  • no different in mortality b/w pro-UK and placebo
53
Q

when is mechanical thrombectomy used?

A
  • it an alternative or adjunctive treatment for acute stroke in patients who are not eligible for thrombolytics or in those who have failed to achieve vascular recnalisation with IV thrombolytics
54
Q

what are outcomes of MERCI and Pneumbra trial?

A
  • MERCI and multi-MERCI single-arm trials investigating the ability of a novel endovascular thrombectomy device to restore patency of occluded in cranial vessels within 8h of ischaemic stroke symptoms onset found recanalisation of target vessels occurred in 50-60% of berated patients and 60-70%following use of adjuvant endovascular methods at 3months
  • based on this, the FDA approved this as the first device for revascularisation of occluded vessels in AIS even if the patient has given rTPA and that therapy has failed
  • penumbra pivotal stroke trial tested another mechanical device that showed even higher rates of recanalisation and led to FDA clearance of this device as well
  • however, the clinical efficacy of these treatments are not proven yet (CHECK)
55
Q

what is the difference b/w ICH and SAH?

A

ICH (10%) - BV ruptures deep into the tissue within the brain
SAH (5%) - BV ruptures on the brain surface

56
Q

what increases the risk of ICH?

A
  • incidence increases for >55y
  • x2 with each decade after 55y
  • x25 after 80y
  • x23 increases w previous CVA
57
Q

what are the common sites for ICH?

A
  • BG/put/len N/IC/GP - 50% most affected
  • thalamus - 15%
  • brain stem - 1-6% least affected
58
Q

what are the common causes of ICH?

A
  1. acute and chronic hypertension
  2. head trauma: coup and contra coup injury
  3. ischaemic infarction transformation
  4. metastatic brain tumour
  5. coagulopathy: VKA
  6. drug: cocaine, amphetamine
  7. aneurysm (weak arteries -> bulging)
  8. CAA: linked w AD
59
Q

which and why lab and imaging tests are done for ICH?

A
  • blood tests: platelet count and PT (prothrombin)
  • CT: acute focal haemorrhages in supratentorial space
  • MRI: more sensitive for delineating posterior fossa lesion, AVM
  • lumbar puncture should be avoided if patients shows signs of increased ICP as it may induce brain herniation
60
Q

what is acute management of ICH?

A
  • 50% of patients w hypertensive ICH die but others have a good to complete recovery if they survive the initial haemorrhage
  • ICH scoring system is used to predict the mortality rate and clinical outcomes
  • coagulopathy: rapid reversal by infusing prothrombin complex followed by fresh-frozen plasma and vitK
  • if ICH associated with reduced platelet count then transfusion of fresh platelets
  • cerebellar haemotoma >3cm in diamater - surgical evacuation required but if alert w/o focal BS signs and haemotoma <1cm in diameter not required
  • if increased ICP -osmotic agents couple w hyperventilation to lower it
  • these methods will allow enough time to place the ICP (intracranial pressure) monitor
  • once ICP recorded - further hyerpventilation and osmotic therapy can be tailored to keep the cerebral perfusion pressure (MAP-ICP) above 60mmHg
61
Q

what are the studies/clinical trials surrounding the treatment of ICH?

A
  • phase 3 trial of treatment w recombinant factor VIIa reduced hematoma expansion; however, clinical outcomes were not improved, so use of this drug cannot be advocated at present
  • STICH data did not support routine surgical evacuation of supratentorial haemorrhages however, many centres operate on patients with progressive neurological deterioration
62
Q

what are the preventive techniques of ICH?

A
  • hypertension: leafing cause of primary ICH
  • therefore, reducing BP
  • eliminate excess alcohol
  • discontinue illicit drug usage e.g. cocaine and amphetamines
  • CAA patients: avoid anti-thrombotic agents
63
Q

when is it used and what is decompressive craniectomy?

A
  • brain surgery that removes a portion of the skull to reduce pressure
  • MCA infarcts -> 20% malignant edema within 2-3days
  • w/o treatment mortality 80%
  • therefore, decompressive craniectomy used, same as hemicraniectomy
64
Q

what is the importance of GCS score in decompressive craniotomies?

A
  • Reddy et al. 2002 reported good outcome in patients of pre-operative GCS score of 8 and above (only 10% mortality) in contrast to, no benefit in patients with GCS less than 8 (70% mortality)
  • early detection and intervention better than late
  • predictor of early brain swelling: CT>50% infarct
65
Q

who is an ideal candidate for decompressive craniotomies?

A
  • young
  • no risk factors
  • early and non-dominant MCA infarct (Right side)
  • a high GCS score w no (or) early signs of herniation
66
Q

what are the two main types of vascular anomalies?

A
  1. congenital vascular malformation

2. acquired vascular lesions

67
Q

what are the different types of congenital vascular malformation?

A
  1. arteriovenous malformations (AVMs) - a shunt b/w arterial and venous system
  2. venous anomalies - result of development of anomalous cerebral, cerebellar or BS venous drainage
  3. capillary telangiectasis - true capillary malformations, seen in
68
Q

what are the features of AVM?

A
  • present headache, seizures (focal in 30%) and intracranial haemorrhage (50%)
  • common in age 10-30
  • Men> women
  • risk of re-reupture is high in first few weeks and 2-4% per year
  • large AVM commonly in MCA
  • large AVM could deplete blood from adjacent normal brain tissue -> venous ischaemia
  • asymptomatic AVM: smaller lesions have higher haemorrhage rate
69
Q

what are the imaging techniques used in AVM?

A
  • MRI better than CT for diagnosis

- conventional x-ray angiogram for evaluating the precise anatomy of AVM

70
Q

what are the treatments for symptomatic and asymptomatic AVM?

A

symptomatic

  • preoperative embolisation to reduce operative bleeding for accessible lesions
  • stereotaxic radiation: alternative to surgery -> slow sclerosis of AVM over 2-3 years
    asymptomatic: surgery as an intervention is currently debatable, a large scale RCT is currently addressing this
71
Q

what is Osler-rendu-weber syndrome?

A

hereditary hemorrhagic telangiectasia with AVM and capillary telangiectasias

72
Q

name two acquired vascular lesions and its features

A
  1. cavernous angiomas
    - tufts if capillary sinusoids in deep hemispheric white matter and BS
    - <1cm and often associated w a venous anomalies
    - bleeding, seizure common
    - surgical resection
    - radiation - no benefit shown yet
  2. dural arteriovenous fistulas
    - acquired connects from a dural artery to dural sinus
    - pulsatile tinnitus and headache
    - fistula may form due. to trauma outmost idiopathic
    - an association b/w fistulas and dural sinus thrombosis
    - fistulas can produce venous sinus occlusion over time from the high pressure and high flow through venous structures
73
Q

what are the causes of SAH?

A
  1. head trauma
  2. berry aneurysm - 70-80%
  3. vascular malformation: AVM (4-5%) or dural arterial venous fistula
    - no cause found in 14-22%
74
Q

what are the symptoms of SAH?

A
  • headache often described by patients as “the worst headache of my life” often with neck stiffness and vomitting
  • hemiparesis, aphasia, abulia
  • LOC ( due to ICP)
  • prodromal symptoms suggests the location of progressive enlarging enraptured aneurysm for e.g. third CN palsy - PCA, ICA, sixth CN palsy - cavernous sinus
  • blood: triple H - hypertension, hemodilution and hypervolemic
75
Q

what is the hunt and hess or world Federation of Neurosurgical Societies classification scheme?

A
  • it is the grading system used for classification of SAH clinical manifestations
  • consists of grade 1-5 based on the hunt and hess scale providing details about the symptoms and WFNS providing the GCS score
76
Q

what are the lab and imaging tests used for SAH?

A
  • hallmark of aneurysmal rupture is blood in CSF
  • 95% cases have enough blood to be seen on non-contrast CT within 72h
  • if scan fails to establish the diagnosis of SAH then lumbar puncture (if no mass lesion or obstructive hydrocephalus)
  • once SAH suspected -> x-ray angiogram to localise and define the anatomical details of aneurysm
  • electrolyte close monitoring as hyponatremia during first 2 weeks following SAH can occur rapidly
77
Q

what are the treatment options for SAH?

A
  1. clipped by neurosurgeon - metal clip placed across the aneurysm neck -> eliminating the risk of re-bleeding
    - involves craniotomy and brain retraction which is associated w neurologic morbidity
  2. coiled by endovascular surgeon - platinum coil or other embolic lateral placed within the aneurysm visa a catheter -> tightly packed to promote thrombosis/embolisation (blood clot) and prevent blood from getting into it
78
Q

what happened to the ISAT trial of surgery vs endovascular treatment

A
  • the only propestive RCT trail comparing the two
  • terminated as 24% treated w endovascular therapy died or dependent at 1 year compared to 31% w surgery
  • after 5 years, risk of death was lower for endovascular therapy (coiling) group
  • though risk of re-bleeding was more common in coiling group
79
Q

what are the medical management techniques in SAH?

A
  • ABCD (airway, breathing, circulation, disability)
  • maintain the triple H (hypertension, hypervolemia, hemodilemia)
  • Disability - assign GCS
  • CT (fisher grade)/angiogram/LP
  • managing vasospasm: leading cause of mortality following aneurysm SAH -> Ca2+ channel antagonist
  • treating hydrocephalus: ventricular shunting
  • treating hyponatermia oral salt coupled w normal saline however, care should be taken to not correct is quickly - central pontine myelinosis may occur
  • preventing pulmonary embolus
  • DVT: heparin administered
  • treat ICP (hyperventilation, mannitol, sedation) to prevent ischemia
  • adequate hydration to avoid decrease in BV predisposing brain to ischemia
  • seizure-like symptoms associated w LOC in SAH perhaps related to raised ICP instead of seizures, however, anti-convulsants sometimes gives as prophylactic (preventive) therapy as seizure could promote rebleeding
  • anti-fibrinolytic (anti-coagulant) not routinely prescribed but considered in patients whose aneurysm treatment cannot proceed immediately -> associated w reduced aneurysm rerupture but may increase risk of delayed cerebral infarction and DVT
80
Q

name some stroke mimic conditions, how do they mimic stroke (ischemic/TIA) and how they can be differentiated?

A
  1. seizure: adequate history of no convulsive activity at onset excludes seizures however, ongoing complex partial seizures w/o tonic-clonic activity may mimic stroke
  2. intracranial tumour: present acute neurological symptoms due to haemorrhage, seizure or hydrocephalus, imaging used to distinguish?
  3. brain abscesses: focal neurological signs + associated fever, headache, seizures
  4. migraine: hemiplegic migraine (weakness down one side), sudden headache (SAH) + acephalic migraine (w/o headache) diagnosis difficult - associated w stroke like symptoms - sensory deficit + motor deficit across one limb. migraine diagnosis confirmed: cortical disturbance spreads across vascular boundaries or typical visual symptoms presented + normal MRI
  5. metabolic encepahlotpathy: classically, fluctuating mental status + focal neurological signs but
  6. MELAS: common mitochondria encephala-myopathy - present hemipraesis, hemianopia, cortical blindness
  7. MS
81
Q

what are stroke mimics?

A

conditions with stroke like symtoms w acute onset and cause transient or persistent focal signs

82
Q

how common are stroke mimics?

A
  • Hand et al. 2016
  • > 300 patients presented in hospital w susceptec stroke
  • 31% had stroke mimics in final diagnosis
  • most common: postictal deficit followed sepsis and toxic-metabolic disturbances
  • 42% w a stroke mimic had experienced stroke previously - definite history of focal neurological signs + NIHSS score >10
83
Q

why is it essential to differentiate stroke mimics from stroke?

A
  • time is brain -> correct diagnosis -> timely intiation of appropriate treatment e.g.
  • acute stroke: thrombosis/thombectomy
  • ICH: BP control/surgical intervention
  • seizure: AED
84
Q

what is the significance of imaging in distinguishing stroke and its mimic

A
  • imaging: CT scan as the initial assessment

- chalela et al. 2007 found that MRI has 83% senstivity as compared 26% in CT for diagnosis of any acute stroke

85
Q

why is rosier and baysiean scale used in stroke mimics?

A
  • recognition of stroke in the emergency room (ROSIER) is validated for use in the ER and is more detailed than the FAST
  • of value particularly when screening of admissions is performed by non-specialist staff
86
Q

what is stroke rehabilitation and stroke recovery?

A
  • stroke care aimed to
    1. reduce disability
    2. promote active participation
    3. prevent deterioration
    4. preserve remaining function
    5. train patients to help them achieve their goals
  • stroke recovery: improvements across a variety of outcomes in performance in activity based behavioural measures
87
Q

what are the key mechanisms of stroke recovery?

A
  1. adaption
  2. regeneration
  3. neuroplasticity
88
Q

describe the adaptation mechanism in stroke recovery and the problems associated w it?

A
  • adaptation is the reliance on alternative physical movements or devices to compensate for post stroke deficits. e.g. training left hand in right hemiplegia, using a stick or shower chair and using a prism in hemianopia
  • however, the major problem is learned disuse phenomenon as result of adaptation
  • it is harmful to the recovery process as patients do not use their affected limb cause they have redeveloped habits to complete taks bypassing the affected limb, despite having the capacity to use it
89
Q

what is regeneration

A
  • the growth of damaged tissues in the brain: a limited process
  • characterised w sprouting of neurones (mainly dendrites)
90
Q

what is the neuroplasticity

A
  • The dynamic potential of the brain to reorganize itself in response to training, injury, rehabilitation, pharmacotherapy, electrical and magnetic stimulation, and stem cell and gene therapy
  • rewiring or development of new networks: key in stroke recovery (day 3-18)
91
Q

what is diaschisis?

A
  • a focal lesion can lead to changes in brain function far away from the lesion (cortical infarct can lead to enhanced contra-lesional cerebellar activity
92
Q

what drives the neuroplasticity in stroke recovery?

A
  1. task specific goals rather than general movements in rehab intervention
  2. challenging and interesting tasks to maintain the individuals attentions
  3. repetition of tasks through multiple attempts
93
Q

what are the key points in predicting stroke recovery?

A
  • motor recovery starts proximally (for e.g. shoulder -> elbow -> wrist -> fingers)
  • EPOS study suggested recovery of upper limb at 6m could be predicted by - shoulder abduction + finger extension
  • if present after 2 days: good outcome in 98%
  • if not present by day 9: only 14% will have good outcome
94
Q

which functions have better recovery and which have slower recovery?

A
  • better recovery: swallowing, facial movement, gait due to bihemispheric involvement
  • slower recovery: language, spatial attention, dominant hand movement due to lateralisation
95
Q

what factors hinder the stroke recovery?

A
  1. natural history of stroke: recovery plateaus in 3-6m
  2. depression
  3. medication - BZD
  4. comorbidities - C spine disorders
96
Q

what are the advantages of

  1. gait training w rhythmic acoustic pacing receptive training
  2. aerobic exercises and muscle strength training?
A
  1. better stride length + better walking speed

2. physical deconditioning + cardiac comorbidity - use it or lose it??

97
Q

what is the mirror therapy and the mechanism behind it?

A
  • patient gets the visual that the limb in the mirror (affected limb) is fully functional
  • works through by enhancing connections b/w visual input and the pre-motor area
  • however, weak evidence for tis effectiveness
98
Q

outline few device based therapies in stroke recovery?

A
  • robotic arms and bodyweight supported treadmill

- however, not superior to currently used therapies

99
Q

what is contrast induced therapy?

A

the unaffected extremity constrained w a device (mitt) which forces the patient to use the affected side in task specific and receptive methods
- this prevents learned disuse phenomenon which reduces recovery

100
Q

how is electric stimulation techniques used in stroke recovery and what is its advantage?

A
  • electrical stimulation to muscle of interest to produce desired movements
  • proved effective by RCT
  • receptive stimulation improves motor function
  • pro: portable and can be used at home
101
Q

what is melodic intonation therapy?

A
  • dominant hemisphere: language
  • non-dominant: singing and melody (+ language capable)
  • since patients retains the ability to sing and melody - it helps w speech recovery, tone vocalisation, vocal output
  • helpful in expressive aphasia to improve language production
102
Q

what is the significance of dysphasia is stroke recovery?

A
  • common neurological deficit in stroke

- Bhogal SK et al. 2003: total hours of therapy directly related to outcome

103
Q

how significant is post stroke depression?

A
  • very common (30%)
  • patients do worse in stroke recovery compared w no depression patients even if the severity is similar
  • manifestations as fatigue, reduced motivation, concentration and attention
104
Q

what are the non-usual causes of stroke?

A
  1. vasculitis: inflammation and necrosis of BV wall
  2. arterial dissection: carotid artery
  3. infections: HIV, vasculitis, vasculopathy, syphilis
  4. cerebral venous sinus thrombosis
  5. anti-phospholipid anti-body syndrome: promote venous and arterial thrombosis
  6. toxicity: cocaine (vasoconstrictor)
  7. CAA: deposition of beta amyloid in BV walls
  8. degenerative - moya moya (puff of smoke) refers to appearance of angiography, premature large vessel arteriopathy
  9. metabolic: EMLAS, MERRF

MED627 (6 decks)

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