Stroke & TIA Flashcards

1
Q

What is a transient ischaemic attack (TIA)?

A

Transient episode of neurological dysfunction caused by temporary focal cerebral, spinal or retinal ischaemia without acute infarction i.e. weak limb, aphasia or loss of vision lasting seconds or minutes with complete recovery. Mostly unilateral

TIA is due to a vascular cause, typically lasts 1 hour

*<24h time limit no longer used

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2
Q

What is a distinguishing sign of TIA?

A

Signs specific to artery territory and presents similar to stroke

Amaurosis fugax
=> sudden transient loss in vision in one eye
=> due to emboli passing through retinal artery
=> often 1st clinical sign of internal carotid artery stenosis

*Global events i.e. syncope or dizziness not characteristic of TIA

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3
Q

What signs are present if TIA occurs in the anterior circulation (carotid system)?

A

Amaurosis fugax

Dysphasia

Hemiparesis

Hemisensory loss

Hemianopic visual loss

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4
Q

What signs are present if TIA occurs in the posterior circulation (verterbrobasilar system)?

A

Diplopia

Vertigo & vomiting

Choking & dysarthria

Ataxia

Hemisensory loss ; Hemianopic visual loss ; Bilateral visual loss

Tetraparesis

Loss of consciousness (rare)

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5
Q

What are the causes of TIA?

A

Atherothromboembolism from CAROTID = main cause
=> listen for bruits

Cardioembolism
=> mural thrombus post MI
=> AF, valve disease, prosthetic valve 
=> Hyperviscosity i.e. polycythaemia, sickle cell anaemia 
=> Vasculitis (rare)
Non-embolic cause of TIA:
=> Cranial arteritis
=> SLE
=> Syhillis 
=> Polyarteritis nodosa
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6
Q

How do you diagnose TIA?

A

Clinical diagnosis

*Consciousness usually preserved

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7
Q

What are the differential diagnosis for TIA?

Which conditions mimic TIA?

A

Two most common stroke mimics:

  1. Hypoglycaemia = always check blood glucose with stroke patient
  2. Migraines with aura

Others:

=> Focal epilepsy / seizure
=> Bell's palsy
=> Mass lesions
=> Syncope
=> Sepsis
=> Seizure / epilepsy
=> Trauma 
=> Overdose
=> Intoxication
=> Hepatic encephalopathy
Rare mimics of TIA:
=> Malignant hypertension 
=> Intracranial tumours
=> Peripheral neuropathy
=> Phaeocromocytoma 
=> Somatisation 
=> MS (paroxysmal dysarthria)
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8
Q

How do you investigate for TIA?

What tests are carried out?

A

=> Carotid doppler ± angiography
Atherosclerosis in carotid artery may be source of emboli => all patients to have urgent carotid doppler unless they are not a candidate for carotid endarterectomy

=> Bloods: FBC, LFT, glucose, cholesterol, U&E, ESR, TFT if in AF

=> Chest Xray

=> ECG if AF

=> Echocardiogram (esp if crescendo TIA because likelihood of cardiac cause)

=> MRI is preferred to determine territory of ischaemia or to detect haemorrhage or alternative pathologies (done on the same day as specialist assessment if possible)

*CT or diffusion-weighted MRI only if clinical suspicion of an alternative diagnosis that can be detected by CT

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9
Q

How do you manage TIA?

You can only treat TIA after doing a full neurological exam and after symptoms have settled.

Prognostic score i.e. ABCD2 is no longer used.

A
  1. Immediate antiplatelet / antithrombotic therapy:
    => Aspirin 300mg for 2 weeks + PPI for gastric cover
    => Then switch to clopidogrel 75mg (secondary prevention)
    => If clopidogrel not tolerated, give aspirin 75mg + slow-release dipyridamole

UNLESS,

i) patient has bleeding disorder or is taking anti-coagulant (needs immediate admission for imaging to exclude a haemorrhage)
ii) patient already on low-dose aspirin => continue current dose until reviewed by specialist
iii) aspirin is contraindicated - discuss management urgently with specialist

  1. Anticoagulation:
    => if cardiac source of emboli
  2. Carotid endarterectomy
    => perform with 2wks of presentation if >55% carotid stenosis and operable risk is low
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10
Q

What is the advice on driving with a single or multiple TIA?

Patient’s responsibility to notify DVLA after stroke / TIA

A
  1. Single TIA
    => must NOT drive for 1 month, don’t need to notify DVLA
  2. Multiple TIA
    => must not drive for 3 months, NEED to notify DVLA
    => may resume driving 3 months after if no further TIA
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11
Q

When do you refer patients for specialist review?

A
  1. If the patient has had more than 1 TIA (‘crescendo TIA’) or has a suspected cardioembolic source or severe carotid stenosis:

=> Discuss the need for admission or observation urgently with a stroke specialist

  1. If the patient has had a suspected TIA in the last 7 days:
    => arrange urgent assessment (within 24 hours) by a specialist stroke physician
  2. If the patient has had a suspected TIA which occurred more than a week previously:
    => refer for specialist assessment as soon as possible within 7 days
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12
Q

What is a stroke?

A

Stroke is a clinical syndrome of vascular origin characterized by rapidly developing signs of focal or global disturbance of cerebral functions over 24 hours or leads to death.

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13
Q

What are the 2 most common types of stroke?

A
  1. Ischaemic stroke (85%) = an episode of neurological dysfunction caused by focal cerebral, spinal, or retinal cell death due to infarction following vascular occlusion or stenosis.
    => Thrombotic from large vessels i.e. carotid
    => Embolic from blood clot, fat, air, AF
  2. Haemorrhagic stroke (15%) = rapidly developing neurological dysfunction due to a focal collection of blood from within the brain parenchyma or ventricular system (intracerebral haemorrhage -10%), or bleeding into the arachnoid space (subarachnoid haemorrhage - 5%) that is NOT caused by trauma.

=> Intracerebral haemorrhage occurs due to small cerebral vessel disease i.e. high BP and in the absence of vascular malformation, aneurysm and other structural causes.

=> Subarachnoid haemorrhage occurs due to rupture of saccular aneurysms = 80%

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14
Q

What is silent stroke?

A

Radiological or pathological evidence of an infarction or haemorrhage not caused by trauma without an attributable history of acute neurological dysfunction attributable to the lesion.

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15
Q

What are the risk factors for stroke?

A
1. Lifestyle factors:
=> Smoking
=> Alcohol misuse and drug abuse
=> Physical inactivity 
=> Poor diet 
  1. Established cardiovascular disease i.e:
    => Hypertension
    => Permanent or paroxysmal AF - 20% of ischaemic strokes
    => Infective endocarditis
    => Valvular disease
    => Carotid artery disease i.e. atheroma / stenosis
    => Congestive heart failure
    => Previous MI
3. Non-modifiable factors:
=> Older age
=> Male
=> Previous TIA/stroke 
=> Family hx
=> Genetic / hereditary factors
4. Other medical conditions:
=> Migraine
=> Hyperlipidaemia 
=> Diabetes
=> Sickle cell disease
=> CKD
=> Ehler's-Danlos syndrome 
=> Marfan's syndrome 
  1. Others:
    => Anti-coagulation
    => Lower level of education
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16
Q

What is the most common cause of stroke?

A

Atrial fibrillation => thrombosis in a dilated left atrium => emboli = the most common cause of stroke

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17
Q

What are the causes of stroke?

A
  1. Small vessel occlusion or thrombosis
    => thrombosis at the site of ruptured mural plaque leads to embolism or occlusion.
  2. Cardiac emboli
    => atrial fibrillation (x5 higher risk)

=> infective endocarditis ; rheumatic & degenerative calcific valve changes

=> congenital valve disorders

=> left ventricular mural thrombus

=> severe hypoperfusion due to MI = infarction in watershed areas especially if there is severe stenosis of proximal carotid vessel

  1. Atherothromboembolism from carotid
  2. CNS bleed due to hypertension, trauma, aneurysm rupture, anticoagulation, thrombolysis

Consider in younger patients:

=> sudden BP drop >40mmHg

=> carotid artery dissection (spontaneous or from neck trauma)

=> Vasculitis

=> Subarachnoid haemorrhage

=> venous sinus thrombus

=> Anti-phospholipid syndrome

=> Thrombophilia

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18
Q

What are the modifiable risk factors for stroke?

A

Smoking

Diabetes

Hypertension

Dyslipidaemia

Obesity

Alcohol

19
Q

What are the non-modifiable risk factors of stroke?

A

Age

Men under 65 and Women over 65 years more likely to have stroke (due to loss of E2)

South asian and Afro-carribean

Heart disease (valvular, ischaemic, AF)

Peripheral vascular disease

Carotid bruit

Pregnancy

Combined oral contraceptive pill

Increased clotting i.e. high plasma fibrinogen, low antithrombin III

Polycythaemia vera

Family history

20
Q

Which main arteries make up the circle of willis to supply the anterior cerebral circulation and the posterior cerebral circulation?

A

Anterior cerebral circulation => two internal carotid arteries

Posterior cerebral circulation => vertebrobasilar arteries

21
Q

Cerebral infarction

Vessel occlusion => brain ischaemia => neuronal failure => infarction + cell death

The ‘CORE’ is the centre of the stroke - the ischaemic area where hypoxia leads to neuronal damage.
=> Fall in ATM results in release of glutamate => opens calcium channel, releasing free radicals => inflammation, necrosis and apoptotic cell death

A

The ischemic ‘PENUMBRA’ surrounds the ischemic region which is not functioning but is structurally intact.
=> timely revascularisation can help regain function in this area

21
Q

Cerebral infarction

Vessel occlusion => brain ischaemia => neuronal failure => infarction + cell death

The ‘CORE’ is the centre of the stroke - the ischaemic area where hypoxia leads to neuronal damage.
=> Fall in ATM results in release of glutamate => opens calcium channel, releasing free radicals => inflammation, necrosis and apoptotic cell death

A

The ischemic ‘PENUMBRA’ surrounds the ischemic region which is not functioning but is structurally intact.
=> timely revascularisation can help regain function in this area

22
Q

Where does anterior circulation infarcts take place?

What are the associated symptoms?

A
Infarcts in territory of: 
=> internal carotid
=> middle cerebral (MCA)
=> anterior cerebral (ACA)
=> ophthalmic arteries 

Complete MCA infarct = devastating stroke
=> contralateral hemiplegia
=> contralateral hemisensory loss
=> facial weakness - forehead spared in stroke because of bilateral innervation (if whole face affected = bell’s palsy)
=> neglect syndrome
=> aphagia / dysphagia
=> hemianopia
=> initially flaccid limbs (floppy limbs like dead weight) then becomes spastic

Internal carotid strokes = similar picture as MCA strokes

23
Q

What is lacunar infarction?

What area is affect?

What are the symptoms?

A

Lacunes = small infarcts in basal ganglia, internal capsule, thalamus and pons

Hypertension is the major risk factor

Lacunar infarcts often symptomless or:
=> Ataxia hemiparesis
=> Pure motor
=> Pure sensory
=> Sensorimotor
=> Dysarthia/clumsy hand 

*cognition/consciousness intact

24
Q

What are the symptoms of a brainstem infarct?

Brainstem infarct is posterior circulation stroke.

A

Quadriplesia

Disturbance of gaze & vision

Locked in syndrome (aware but unable to respond)

*symptoms depended on assoc. with cranial nuclei.

25
Q

What are the investigations for stroke?

A
  1. Rule out hypoglycaemia first (<3.3.mmol/L) - blood glucose
  2. ECG to exclude arrhythmias
  3. non-contrast CT head to exclude haemorrhage = FIRST LINE

Diagnosis:

1. FAST campaign used by the public 
F = face weakness
A = arms weakness
S = slurred speech
T = time to call 999
  1. ROSIER score used by medical professionals:
    * Exclude hypoglycaemia
  2. Loss of consciousness / syncope => -1 point
  3. Seizure activity => -1 point

New, acute onset of:

  1. Asymmetric facial weakness => +1 point
  2. Asymmetric arm weakness => +1 point
  3. Asymmetric leg weakness => +1 point
  4. Speech disturbance => +1 point
  5. Visual field defect => +1 point
    * STROKE is likely if >0
26
Q

How is suspected acute stroke managed in primary care?

A
  1. Immediate emergency admission to acute stroke facility
  2. DO NOT start anti-coagulation or anti-platelet until haemorrhage is excluded
  3. A-E exam until transferred to stroke unit
    => give supplemental O2 if sats <95% + no contraindication
27
Q

What is the management of acute stroke?

A
  1. Thrombolysis with alteplase
    => within 4.5h of onset of stroke symptoms
    => best result within first 90 mins
    => haemorrhage definitely excluded post CT head

IV Alteplase 0.9mg/kg to a max of 90mg => agent of choice
=> 10% of total given as bolus and 90% given as an infusion
=> monitor v closely - as high risk of bleeding

Always do CT/MRI 24h post-lysis to monitor for bleeds

28
Q

What are the absolute and relative contraindication to thrombolysis?

A
1. Absolute:
=> Previous intracranial haemorrhage
=> Seizure at onset of stroke
=> Intracranial neoplasm
=> Suspected subarachnoid haemorrhage
=> Stroke or traumatic brain injury in preceding 3 months
=> Lumbar puncture in preceding 7 days
=> Gastrointestinal haemorrhage in preceding 3 weeks
=> Active bleeding
=> Pregnancy
=> Oesophageal varices
=> Uncontrolled hypertension >200/120mmHg

Relative:
=> Concurrent anticoagulation (INR >1.7)
=> Haemorrhagic diathesis
=> Active diabetic haemorrhagic retinopathy
=> Suspected intracardiac thrombus
=> Major surgery / trauma in the preceding 2 week

29
Q

What is thrombectomy?

When is it used?

A

NICE recommend a pre-stroke functional status of less than 3 on the modified Rankin scale and a score of more than 5 on the National Institutes of Health Stroke Scale (NIHSS)

  1. Offer thrombectomy as soon as possible and within 6 hours of symptom onset, together with intravenous thrombolysis (if within 4.5 hours), to people who have:
    => acute ischaemic stroke and
    confirmed occlusion of the proximal anterior circulation shown in computed tomographic angiography (CTA) or magnetic resonance angiography (MRA)
  2. Offer thrombectomy as soon as possible to people who were last known to be well between 6 hours and 24 hours previously (including wake-up strokes):
    => confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA and
    => if there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume
  3. Consider thrombectomy with intravenous thrombolysis (if within 4.5 hours) as soon as possible for people last known to be well up to 24 hours previously (including wake-up strokes):
    => who have acute ischaemic stroke and confirmed occlusion of the proximal posterior circulation (that is, basilar or posterior cerebral artery) demonstrated by CTA or MRA and
    => if there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume
30
Q

What is the secondary prevention in stroke?

A
  1. Clopidogrel is first line (NICE) in people who have had an ischaemic stroke
  2. Aspirin + MR dipyridamole is now recommended after an ischaemic stroke only if clopidogrel is contraindicated or not tolerated
  3. If the cholesterol is > 3.5 mmol/l patients should be commenced on a statin. Many physicians will delay treatment until after at least 48 hours due to the risk of haemorrhagic transformation
  4. Atrial fibrillation: anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days after the onset of an ischaemic stroke
31
Q

Stroke management: other issues

FLUID MANAGEMENT

A
  1. Fluid management

Regular assessment for fluid status must be undertaken to ensure patients remain normovolaemic

The NICE guidelines recommend assessing the hydration of all patients with acute stroke on admission, with regular review during their stay

Greater than 80% of patients who cannot swallow post stroke will recover within 2-4 weeks

However, it is important to manage fluids in this immediate post-event period as hypovolaemia can worsen the ischaemic penumbra, as well as increase risk of other complications i.e. infection, DVT, constipation and delirium

Conversely, over-hydration can also complicate matters by leading to cerebral oedema, cardiac failure and hyponatraemia, therefore it is important to regularly review fluid status in these patients

Recommendations for management:
=> Oral hydration is preferable in all patients who are able to safely swallow

=> Intravenous hydration may be necessary otherwise - currently recommend isotonic saline without dextrose

32
Q

Stroke management: other issues

GLYCAEMIC CONTROL

A
  1. Glycaemic control

=> Closely monitor and control blood sugar, particularly if they are nil by mouth due to concerns regarding swallowing safety post stroke, and/or in diabetics

=> Post stroke, patients with hyperglycaemia have increased mortality

=> NICE recommend maintaining a blood sugar level between 4 and 11 mmol/L in people with acute stroke

=> Hypoglycaemia also needs to be managed appropriately, as alone it can cause neuronal injury as well as mimic stroke-related neurological deficits

33
Q

Stroke management: other issues

FEEDING ASSESSMENT and MANAGEMENT

A
  1. Feeding assessment and management:

All patients presenting with acute stroke must be screened for safe swallowing function prior to further oral intake, as dysphagia is common after stroke

This is to reduce the risk of aspiration and subsequent complications. Assessment should be prior to any oral intake of food, fluids, and/or medications

If there are any concerns regarding swallowing, the NICE guidelines recommend specialist assessment of swallowing
=> within 24 hours of admission and not greater than 72 hours after

Prior to assessment is undertaken, a patient should remain nil by mouth to prevent complications

Recommendations for patients unsafe for oral intake:
=> Patients should receive nasogastric tube feeding, ideally within 24 hours of admission, unless they have had thrombolytic therapy

=> If nasogastric tube feeding is not tolerated, patients should be considered for a nasal bridle tube/gastrostomy instead

=> Medications need to be assessed to determine if formulations are available for nasogastric feeding, or if conversion to subcutaneous or intravenous forms are required

=> Nutritional support may be required for patients at risk of malnutrition post stroke, whether a result from dysphagia, poor oral health or reduced ability to self-feed due to weakness or paralysis

34
Q

Stroke management: other issues

DISABILITY SCALES

A
  1. Disability scales:
    Stroke can result in a number of complications and subsequent disability, therefore disability scales are often used as a measure of functional decline post event and subsequent improvement after medical intervention
    Disability, often measured in terms of functional status (notably, basic activities of daily living), is often the leading cause of morbidity after stroke
    After a patient is medically stabilised after a stroke, they may require transfer to a rehabilitation team for ongoing treatment depending on their level of disability
    Disability is most commonly measured using the Barthel index (BI), an outcome measure for stroke
    Describes 10 tasks, and is scored according to amount of time or assistance required by the patient for each given task
    Tasks: feeding, moving from wheelchair to bed, personal toileting, getting on/off toilet, bathing, walking on level surface, ascending/descending stairs, dressing, controlling bowels and controlling bladder
    The total score is from 0 to 100, with 0 being completely dependent, and 100 being completely independent
    This index should be used to assess the functional status of a patient post stroke, and to monitor their improvement with ongoing rehabilitation to regain independence after the event
35
Q

What anti-platelet agent is initiated once haemorrhage has been ruled out?

A

=> High dose Aspirin 300mg orally or rectally as soon as haemorrhage stroke rules out and thrombolysis contraindicated

OR

=> On day 2 after a second CT scan post thrombolysis

=> Continue high dose aspirin 300mg for 2 weeks

36
Q

Highlights of acute stroke management:

A
  1. Protect the airway => avoids hypoxia + aspiration
  2. Maintain homeostasis => glucose between 4-11mmol/L
  3. Screen swallow => till then nil by mouth but keep hydrated
  4. CT/MRI within 1h => essential if thrombolysis considered or high risk of haemorrhage
  5. Anti-platelet agents (aspirin 300mg) once haemorrhagic stroke ruled out
  6. Thrombolysis or Thrombectomy
  7. Admit to a high acute stroke unit (HASU) => improves outcomes + saves lives + reduces long-term disability
  8. Rehabilitation => start early post stroke to maximise improvement and prevent complications
  9. Nurse queries:
    *in acute initial stage = don’t treat HTN because likely to make ischaemia worse if BP drops
    If massively elevated, consult senior advice (lobetalol?)

=> BP usually drops after alteplase - If BP still high a week or so post stroke then manage

  1. Aspiration common post stroke - aspiration pneumonia
    => if pyrexial give paracetamol but first do a swallow assessment
    => check if can cough, lick lips, head control => then call SALT team
37
Q

How to follow-up a person who has had stroke / TIA?

A

*Secondary preventative measures are initiated at diagnosis in secondary care.

  1. Arrange follow up in primary care:
    => on discharge,
    => at 6 months,
    => at least annually afterwards

to review health, social care needs (i.e. access to benefits, community participation, housing, and return to work), ongoing risk factors, and secondary prevention.

Arrange review of carers of people with stroke at 6 months and then annually to assess their health and social care needs.

  1. Offer information on stroke, TIA, and vascular risk factors to people with stroke or TIA and their family/carers:
    => Patient information is available from the Stroke Association.
  2. Provide advice about driving if appropriate.
  3. Provide advice about returning to work if appropriate.
  4. Offer verbal and written information about medication for secondary prevention, including:
    => Reasons for medications.
    => How and when to take it.
    => Common adverse effects.
38
Q

What lifestyle measures are required to be put in place post stroke?

A

Encourage physical activity every day:

=> Individualized exercise programs (which may include muscle strengthening, balance, and coordination activities) for people with stroke should be prescribed, delivered, and monitored by the rehabilitation team.

Advise smokers to stop smoking and non-smokers to avoid passive smoking:
Options to help with smoking cessation include referral to an NHS Stop Smoking Service, drug treatment, and written patient information.

Advise the person to eat a healthy balanced diet to help reduce cardiovascular disease (CVD) risk — they should aim to:
=> Eat at least five portions of fruit and vegetables (from a variety of sources) per day and two portions of oily fish per week.

=> Reduce intake of saturated fats.

=> Keep salt intake low — salt should not be added at the table, and processed foods should be kept to a minimum.

=> Advise people who drink alcohol to keep consumption within the recommended limits:
Alcohol intake should be limited to 14 units a week, spread over at least 3 days.

=> Advise against routine dietary supplementation with:
B vitamins or folate; vitamins A, C, or E; selenium; and calcium with or without vitamin D unless required for other medical conditions.

39
Q

Review medications used in secondary prevention

A

Antiplatelet therapy is initiated by secondary care on diagnosis of ischaemic stroke or TIA without paroxysmal or permanent atrial fibrillation for long-term vascular prevention:
=> The standard treatment is clopidogrel 75 mg daily.

=> Aspirin 75 mg daily with modified-release dipyridamole 200 mg twice daily may be used if clopidogrel cannot be tolerated.

=> Modified-release dipyridamole 200 mg twice daily may be used if both clopidogrel and aspirin are contraindicated or cannot be tolerated.

=> Aspirin 75 mg daily may be used if both clopidogrel and modified-release dipyridamole are contraindicated or cannot be tolerated.

Unless contraindicated, treatment with statin (such as atorvastatin 20–80 mg daily) will be offered at diagnosis of ischaemic stroke or TIA by secondary care.

If this reduction is not achieved within 3 months, consider adherence, diet, lifestyle, and increasing dose (if appropriate) — discuss with a stroke specialist if unsure.

Statin treatment should be avoided in people with primary intracerebral haemorrhage unless advised for other indications.

Anti-hypertensive drugs
Treatment for hypertension following stroke or TIA should be initiated by secondary care following diagnosis

Anticoagulant drugs will be initiated in secondary care for people with ischaemic stroke or TIA and paroxysmal, persistent, or permanent atrial fibrillation or atrial flutter once intracranial bleeding and other contraindications (such as uncontrolled hypertension) are excluded.
Treatment in people with TIA will start immediately on diagnosis once imaging has excluded haemorrhage.

Antithrombotic treatment in people with recurrent TIA or stroke should be the same as for those with a single event

40
Q

How to optimise management of co-morbidity?

A

Diabetes mellitus

Hypertension

Obstructive sleep apnoea
People with stroke or TIA should be screened for obstructive sleep apnoea with a valid clinical screening tool. Refer anyone suspected of having sleep apnoea for a respiratory/sleep medicine assessment.

Heart failure

Obesity
Refer people who are overweight or obese to a weight management service if appropriate.

Manage other risk factors appropriately, such as:
Contraception
Do not offer pre-menopausal women with stroke or TIA the combined oral contraceptive pill.
Consider progestogen-only and non-hormonal contraceptive methods instead.

Hormone replacement therapy (HRT)
Advise post-menopausal women with ischaemic stroke or TIA who wish to start or continue HRT on the risks and benefits of treatment.

Influenza
Arrange annual influenza immunizations.

41
Q

Advice on driving and work after a stroke

A

Discuss the exclusion period and the person’s responsibility to notify the Driver and Vehicle Licencing Agency (DVLA) after stroke or TIA

People who have had a stroke must not drive for 1 month but may not need to notify DVLA. Driving may resume after 1 month if there has been satisfactory clinical recovery.

DVLA does not need to be notified unless there is residual neurological deficit 1 month after the episode and, in particular: visual field defects, cognitive defects, impaired limb function.

Refer people with persisting cognitive, language, or motor disability after stroke who wish to return to driving for on-road screening and evaluation

Inform people who wish to drive after stroke about eligibility for disabled concessions (for example the Blue Badge scheme)

If the person wishes to return to work after stroke:
Discuss the need for assessment for return to work with the rehabilitation team.
The person can be referred through the job centre to a specialist in employment for people with disability or to the specialist vocational rehabilitation team if extra support or advice is needed.

42
Q

The Oxford Stroke Classification

Criteria assessed:
1. Unilateral hemiparesis ± hemisensory loss of face, arm and leg

  1. Homonymous hemianopia
  2. Higher cognitive dysfunction e.g. dysphasia
A
  1. Total anterior circulation infarct (TACI, 15%)
    => involves middle and anterior cerebral arteries
    => all 3 of the above criteria present
  2. Partial anterior circulation infarcts (PACI, 25%)
    => involves smaller arteries of anterior circulation e.g. upper or lower division of MCA
    => 2 of above criteria present
  3. Lacunar infarct (LACI, 25%)
    => involves perforation arteries around internal capsule, thalamus and basal ganglia
    => presents with 1 of the following:
    i) unilateral weakness/deficit of face and arm, arm and leg or all 3
    ii) pure sensory stroke
    iii) ataxic hemiparesis
4. Posterior circulation infarct (POCI, 25%)
=> involves vertebrobasilar arteries
=> presents with one of the following:
i) cerebellar or brainstem symdromes
ii) loss of consciousness 
iii) isolated homonymous hemianopia
43
Q
  1. Anterior cerebral artery
    => Contralateral hemiparesis and sensory loss, lower extremity > upper
  2. Middle cerebral artery
    => Contralateral hemiparesis and sensory loss, upper extremity > lower
    Contralateral homonymous hemianopia
    Aphasia
  3. Posterior cerebral artery
    Contralateral homonymous hemianopia with macular sparing
    Visual agnosia
A
  1. Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain)
    => Ipsilateral CN III palsy
    Contralateral weakness of upper and lower extremity
  2. Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)
    => Ipsilateral: facial pain and temperature loss
    Contralateral: limb/torso pain and temperature loss
    Ataxia, nystagmus
  3. Anterior inferior cerebellar artery (lateral pontine syndrome)
    => Symptoms are similar to Wallenberg’s (see above), but:
    Ipsilateral: facial paralysis and deafness
  4. Retinal/ophthalmic artery
    => Amaurosis fugax
  5. Basilar artery
    => ‘Locked-in’ syndrome