Stroke & TIA

Really long post on a really important topic. Enjoy 🙂


Stroke

Definition: rapid permanent neurological deficit resulting from ischaemic infarction or bleeding into part of the brain, manifesting as rapid onset (e.g. secs-mins) of focal CNS signs and symptoms, lasting > 24h.

Aetiology/ risk factors:

Ischaemic (80%):

-Small vessel occlusion/ microangiopathy or thrombosis in situ

-Carotid disease- atherothromboembolism infarct from carotid artery

– Atherothromboembolism infarct from aortic arch

-Hypotension- if below the autoregulatory range maintaining cerebral blood flow, infarction results in the ‘watershed’ zones between different cerebral artery territories.

Cardiac emboli (post-MI, AF, valve vegetations in endocarditis, prosthetic valves, external cardioversion, paradoxical systemic emboli via venous circulation in patent foramen ovale and septal defects, cardiac surgery e.g. bypass graft, atrial myxoma) = cause in > 30%

Haemorrhagic (75% intracerebral, 25% subarachnoid haemorrhage):

-Hypertension

-Trauma

-Aneurysm rupture

-Anticoagulation, thrombolysis

-Tumour, arteriovenous malformations, vasculitis- (less common)

Other causes: sudden BP drop by ≥ 40mmHg (e.g. in sepsis), carotid artery dissection (spontaneous or from neck trauma or fibromuscular dysplasia), vasculitis, subarachnoid haemorrhage, venous sinus thrombosis, antiphospholipid syndrome, thrombophilia, Fabry’s disease, CADASIL, CARASIL (inherited conditions).

 

Risk factors:

-hypertension, smoking, diabetes, hyperlipidaemia, alcohol

-heart disease (valvular, ischaemic, AF), peripheral vascular disease

-past TIA, carotid bruit

-increased haematocrit, hypercoagulable state (e.g. increased plasma fibrinogen or anti-thrombin deficiency)

-hyperhomocysteinaemia

-OCP, syphilis

Epidemiology: common

Incidence is falling- 1/1000/year- perhaps due to a more rigorous approach to primary prevention

Signs and symptoms:

-Sudden onset, deterioration within seconds, maybe with further progression over hours (rarely days)

-In theory, focal signs relate to distribution of the affected artery.

 

Image result for cerebral artery territories

Anterior Cerebral Artery = frontal and medial part of the cerebrum; Middle Cerebral Artery = lateral part of each hemisphere; Posterior Cerebral Artery = occipital lobe.

Image result for circle of willisAnterior Cerebral Artery= occlusion may cause weak, numb contralateral leg +/- similar, if milder, arm symptoms. Face is spared.

Confusion (frontal lobe)

Bilateral infarction can cause akinetic mutism (tending not to move or speak) from damage to cingulate gyri (part of limbic system)- also a rare cause of paraplegia.

Middle Cerebral Artery = occlusion may cause contralateral hemiparesis, hemisensory loss (especially face & arm), contralateral homonymous hemianopia (due to involvement of optic radiation- quadrantanopia if only superior/inferior radiation), cognitive change including dysphasia (Broca/Wernicke’s area) with dominant hemisphere lesions, and visuospatial disturbance (e.g. cannot dress, gets lost) with non-dominant lesions.

Hemineglect and apraxia (parietal lobe)

Hemineglect is a deficit in attention to and awareness of one side of space, so they will only shave one side of their face and only eat the food on one side of their plate and think they’re finished.

Apraxia is a motor disorder where the person is unable to perform tasks and movements although they can understand what they have to do.

Image result for homunculus

Because of the way in which our body is mapped onto the cerebral hemispheres, occlusion of the MCA is more likely to affect arms and face than legs, because it supplies blood to the lateral part of each hemisphere. Conversely, occlusion of the ACA will affect legs more, as it supplies blood to the medial part of the cerebrum.

 

Posterior Cerebral Artery= occlusion gives contralateral homonymous hemianopia (often with macular sparing)

Carotid Artery= occlusion of internal carotid artery, at worst, causes total fatal infarction of anterior 2/3rds of its hemisphere and basal ganglia. More often, presents like a Middle Cerebral Artery occlusion.

Vertebrobasilar circulation= supplies cerebellum, brainstem and occipital lobes. Signs may include: hemianopia, cortical blindness, diplopia, vertigo, nystagmus, ataxia, dysarthria, dysphasia, hemi- or quadriplegia, unilateral or bilateral sensory symptoms, hiccups, coma.

Anterior Inferior Cerebellar Artery= occlusion may result in vertigo, ipsilateral ataxia, ipsilateral deafness or tinnitus, ipsilateral facial weakness

Lateral medullary syndrome due to infarction of lateral medulla and the inferior cerebellar surface

 

Pontine Artery: occlusion may cause Locked-in Syndrome due todamage to ventral pons. Patients are unable to move, but retain full cognition and awareness, communicating, e.g. by blinking, electronic boards or special computers.

Basilar Artery: cranial nerve pathology + impaired consciousness (emergency)

Cerebral infarcts (50%): ACA, MCA, PCA occlusion

-contralateral sensory loss

-hemiplegia (unilateral paralysis)- initially flaccid, then becomes spastic (UMN sign)

-dysphasia (speech difficulties)

-homonymous hemianopia (if occipital lobe affected)

-visuospatial deficit

Brainstem infarcts (25%): vertebrobasilar circulation

Wide range of effects including:

-quadriplegia (paralysis of all four limbs and torso)

-disturbances of gaze and vision

-locked-in syndrome (aware but not able to respond)

Lacunar infarcts (25%): occlusion of small penetrating arteries supplying deep structures of brain.

In basal ganglia, internal capsule, thalamus and pons.

5 classic syndromes:

-Ataxic hemiparesis

-Pure motor

-Pure sensory

-Sensorimotor

-Dysarthria (motor speech disorder)/ clumsy hands

Cognition/ consciousness are intact, except in thalamic stroke where there is loss of consciousness, as well as a hemisensory deficit.

 

Pointers to bleeding (haemorrhagic stroke)(unreliable):

-meningism (headache, photophobia, neck stiffness)

-severe headache

-coma within hours

Pointers to ischaemia (ischaemic stroke):

-carotid bruit (suggest carotid disease)

-AF, heart murmurs

-past TIA or ischaemic heart disease

 

Investigations:

-Neurological assessment

CT head– For rapid detection of haemorrhage. Early CT (<6h) will not show infarct but will show haemorrhage. Often normal in lacunar infarcts.

MRI brain– MRI has higher sensitivity for infarction, but less readily available than CT in acute setting. Diffusion-weighted imaging can differentiate between recent (< 2wks) and old strokes.

24hr ECG- look for atrial fibrillation

Echo +/- TOE– look for a cardiac source. May show mural thrombus due to atrial fibrillation or a hypokinetic segment of cardiac muscle post-MI. It may also show valvular lesions in infective endocarditis or rheumatic heart disease. Transoesophageal echo (TOE) is more sensitive than transthoracic.

Carotid Doppler USS +/- CT/MRI angiography– may show stenosis causing reduced cerebral blood flow. Carotid endarterectomy or endovascular carotid artery stenting may be considered.

CT-cerebral angiography– to detect artery dissections or intracranial stenosis

 

Bloods: serum glucose, lipids, homocysteine, coagulation screen (thrombocytopenia? bleeding disorders?), FBC (↑haematocrit-polycythaemia?), blood film (sickle cell disease?)

Hypertension: look for retinopathy, nephropathy, cardiomegaly on CXR. In general, BP is not treated acutely.

Vasculitis: ↑ESR, ANA +ve

-Screen for thrombophilia, antiphospholipid syndrome, genetic disease (CADASIL, Fabry’s disease- x-linked)

Management:

Primary prevention:

-control risk factors

-hypertension

-diabetes

-hyperlipidaemia (statin)

-cardiac disease

-Exercise

-Folate supplements may help to some degree (lower homocysteine levels)

-Smoking cessation

-Lifelong anticoagulation if rheumatic or prosthetic valves on left side and in chronic AF (consider).

Acute (1st hour):

-protect the airway to prevent hypoxia or aspiration

-Pulse, BP, ECG (AF?)

Treating even very high BP may cause harm and compromise cerebral perfusion, as autoregulation is impaired

-If on HRT, stop it

-Blood glucose: aim for 4-11 mmol/L. Treat hypoglycaemia.

Urgent CT/MRI if:

High risk of haemorrhage (low Glasgow Coma Scale score, signs of raised ICP, severe headache, meningism, progressive symptoms, known bleeding tendency or anticoagulated)

Thrombolysis considered (need to make sure it is not a haemorrhagic stroke)

Cerebellar stroke (cerebellar haematomas may need urgent referral for evacuation)

Unusual presentation (alternative diagnosis?)

-Otherwise imaging can wait (aim < 24h)

-Diffusion-weighted MRI is most sensitive for an acute infarct, but CT helps rule out primary haemorrhage and is more available.

Consider thrombolysis for ischaemic stroke if onset of symptoms 4.5h (earlier the better so hurry up)          

Thrombolysis should be considered if an expert team is in place and the patient is seen within 4.5 hours and no contraindication exists. Reperfusion is with IV recombinant tissue plasminogen activator e.g. Alteplase (0.9mg/kg over 1h).

-Always do CT 24h post-thrombolysis to identify bleeds. Do not give aspirin in first 24h.

Contraindications: major infarct or haemorrhage on CT; mild/non-disabling deficit; recent birth, surgery, trauma, or artery or vein puncture at uncompressible site; past CNS bleed; arterio-venous malformations or aneurysm; severe liver disease, varices or portal hypertension; seizures at presentation; anticoagulants or INR > 1.7, low platelets (<100 x109/L), BP 220/130

-Nil by mouth: only if swallowing attempts might lead to choking. Keep hydrated but do not overhydrate (risk cerebral oedema).

Anti-platelets-aspirin (300mg): give once haemorrhagic stroke is excluded

→Take to a specialist stroke unit. Specialist stroke units have better results in rehabilitation than on a general medical ward.

 

Secondary prevention (prevent further strokes):

-Control risk factors: hypertension, diabetes, hyperlipidaemia, cardiac disease; exercise and stop smoking.

-Several large studies show benefit of lowering BP and cholesterol, even if not raised.

-Antiplatelets after stroke- Clopidogrel monotherapy is best. Alternatively- aspirin, slow-release dipyridamole.

Assuming no primary haemorrhage on CT.

-Anticoagulants after stroke from AF- start warfarin if indicated, 2wks after stroke (if small, from 7-10 days). Use antiplatelets until anticoagulated, if anticoagulated already, replace with antiplatelet for 1wk.

-Carotid endarterectomy within 2 weeks of stroke may reduce risk of further stroke and may be considered, but carries significant peri-operative risk.

Post-stroke care:

Early management:

→Watch patient swallow and if signs of aspiration, make nil by mouth until assessed by speech therapist. Use IV fluids, then semi-solids and avoid early nasogastric tubes.

→Avoid falls and damaging patient’s shoulder through careless lifting.

→Ensure good bladder and bowel care through frequent toileting, avoiding early catheterisation which may prevent return to continence.

→Position to minimise spasticity, with help from physiotherapy. Botulinum toxin injections are helpful for focal spasticity.

Time taken to sit up and to transfer from lying to sitting is a good measure of progress of physio/occupational therapy.

→If pseudo-emotionalism/emotional lability, tricyclics or fluoxetine may help.

-Requires a multidisciplinary approach, including:

-Speech therapist- assess swallowing difficulties

-Physiotherapist and occupational therapist

-Dietician

-Specialist nurse

→Explore end-of-life decisions.

Complications:

-Cerebral oedema (raised ICP and local compression)

-Immobility, constipation

-Aspiration pneumonia, UTI

-Pressure sores (turn over regularly and keep dry-consider catheter)

-DVT

-Contractures (permanent shortening of muscle or joint, usually in response to prolonged hypertonic spasticity)

-Depression

-Death

Prognosis: Overall mortality- 60,000/year

UK mortality- 20% at 1 month, then ≲ 10%/year

Full recovery- ≤ 40%

-Good nursing on stroke unit, antiplatelet agents and prompt intervention are key to prognosis.


 

Transient Ischaemic Attack (TIA)

Definition: sudden onset of focal CNS phenomena due to temporary occlusion of part of the cerebral circulation, usually by emboli, with symptoms lasting < 24h (often much shorter).

Aetiology/ risk factors:

-Atherothromboembolism from the carotid is the chief cause.

Cardioembolism: post-MI, AF, valve vegetations in endocarditis, prosthetic valves, external cardioversion, paradoxical systemic emboli via venous circulation in patent foramen ovale and septal defects, cardiac surgery e.g. bypass graft, atrial myxoma

-Hyperviscosity: polycythaemia, sickle cell anaemia, increased white cell count, myeloma

-Vasculitis (rare cause): cranial arteritis, PAN, SLE, syphilis

Epidemiology: incidence- 0.4/1000/year

15% of first strokes are preceded by TIAs so good management is important. (Also foretell MIs)

Signs and Symptoms:

-there is sudden onset of focal neurological deficit with symptoms maximal at onset and usually lasting 5-15 minutes. Gradual progression of symptoms suggests a different pathology.

-attacks are single or many

-features of TIA mimic those of a stroke in the same arterial territory, may be same or different for each TIA

Carotid Territory:

Amaurosis fugax

-Aphasia

-Hemiparesis

-Hemisensory loss

-Hemianopic visual loss

Vertebrobasilar Territory:

-Diplopia, vertigo, vomiting

-Choking and dysarthria

-Ataxia

-Hemisensory loss

-Hemianopic or bilateral visual loss

-Tetraparesis

-Loss of consciousness (rare)

 

-global events (e.g. syncope, dizziness) are not typical

-multiple highly stereotyped attacks suggest a critical intracranial stenosis

-limb-shaking TIAs may be mistaken for a focal motor seizure

Signs of cause:

carotid bruit

-hypertension

-heart murmur from valve disease

-atrial fibrillation

Fundoscopy during TIAs may show retinal artery emboli.

Investigations:

Diagnosis of a TIA is clinical.

Aim to find cause and define vascular risk. Remember, the goal is to prevent a future stroke.

Bloods: serum glucose, lipids, homocysteine, coagulation screen (thrombocytopenia? bleeding disorders?), FBC (↑haematocrit-polycythaemia?), blood film (sickle cell disease?)

ECG– atrial fibrillation?

Echocardiogram– May show mural thrombus due to atrial fibrillation or a hypokinetic segment of cardiac muscle post-MI. It may also show valvular lesions in infective endocarditis or rheumatic heart disease.

Carotid Doppler +/- angiography– may show stenosis causing reduced cerebral blood flow. Carotid endarterectomy or endovascular carotid artery stenting may be considered.

CT or diffusion-weighted MRI– any existing infarcts? bilateral suggests cardioembolism

Hypertension: look for retinopathy, nephropathy, cardiomegaly on CXR.

Vasculitis: ↑ESR, ANA +ve

-Screen for thrombophilia, antiphospholipid syndrome, genetic disease (CADASIL, Fabry’s disease- x-linked)

Management:

ABCD2 Scoring System

≥ 6 -strongly predicts stroke

≥ 4 – should be assessed by a specialist within 24h

All patients with a suspected TIA should be seen within 7 days.

Age ≥ 60 yrs = 1

BP ≥ 140/90 mmHg = 1

Clinical features

Unilateral weakness = 2

Speech disturbance without weakness = 1

Duration of symptoms

≥ 1h = 2

10-59 mins = 1

Diabetes =1

-Control cardiovascular risk factors: hypertension (lower cautiously, aim for < 140/85), hyperlipidaemia, diabetes, smoking

Antiplatelets: preferably clopidogrel (75mg/d) or alternatively, aspirin (300mg/d- 75mg/d after 2wks) + dipyridamole (200mg/12h)

-Warfarin: if cardiac emboli (e.g. AF, mitral stenosis, recent big septal MI)

-Carotid endarterectomy: if 70% stenosis a the origin of the internal carotid artery and operative risk is good. Surgery should de within 2 weeks of first presentation. Operating on stenosis of 50-70% may be valuable depending if the team has a low perioperative stroke and mortality rate. Endovascular carotid artery stenting is an alternative if surgery is not suitable.

Image result for carotid endarterectomy

Image result for endovascular carotid artery stenting

-Avoid driving for 1 month. Inform DVLA (UK) only if multiple attacks in short period or residual deficit.

Complications:

-stroke

Prognosis:

-90 day risk of stroke  = 2% in those treated within 72h of TIA

= 10% in those treated by 3 weeks

-combined risk of stroke and MI ~9%/yr

-mortality is ~3x that of a TIA-free matched population

References: Cheese & Onion, Rapid Medicine, Kumar & Clarke’s

 

 

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