GP UpdateTIA and mimicsKath PascoOct 2015

Outline

Why is it important to diagnose TIA? Challenges of the TIA presentation Common mimics Case discussion Secondary prevention

True TIA=high risk stroke

Essential to identify true vascular event due to very high early risk of ischaemic stroke

15-20% patients with stroke report preceding TIA

Stroke following TIA

Risk of stroke following a TIA

10% at 7 days 15% at 30 days

Express study 2007 (Rothwell et al) identified that investigating and treating high risk patients with TIA could reduce those that go on to have full stroke by 80%

Definite diagnosis can be a challenge

Broad differential Symptoms are transient No definitive test Relies on patient account Inter observer agreement of TIA between stroke

trained and non neurologist is poor

Up to 60% patients referred = mimic Migraine/seizure/syncope

TIA

Temporary focal neurological symptoms (cerebral, retinal or rarely spinal ischaemia)

24 hour duration outdated Majority last under 30 mins Clinical diagnosis Accurate history interpretation skills

Mechanism

Locally decreased blood flow to the brain causing focal symptoms

Embolism (from heart, proximal vessels, extra or intracranial usually affected by atherosclerosis

In situ occlusion of small perforating arteries Resolution occurs spontaneously with lysis and

passage of thrombus or collateral compensation

NB cerebral hypoperfusion due to critical stenosis stereotyped and related to upright posture

Screening of referrals?

Recent discussion at UKSF confirms different practice Aim to see patients with TIA in 24 hours

Challenges in practice Usefulness of ABCD score? Limitations? Brain and vessel imaging same day? Imaging before or after assessment?

Role of brain imaging

Even transient symptoms can show evidence of tissue ischaemia in dwi MRI

Can allow risk modification

Confirm vascular aetiology

Likelihood dwi+ increases with symptom duration

Clinical features

TIA should mimic stroke syndromes ie arterial territory

Some patterns identify territory ie aphasia = left, monocular visual loss = carotid

ischaemia Hemianopia = occipital , diplopia = brainstem

ischaemia

Patients presenting with very transient single syndromes eg isolated vertigo, dysarthria need to consider mimics before diagnosing TIA

Clinical features

Abrupt onset Age and other demographics – ? increase probability

of a cerebrovascular event Nature of symptoms – ‘negative’ vs ‘positive’ Onset and progression Duration Precipitating factors Associated features – headache, loss of awareness

during or after

When TIA is less likely

Rare in young individuals without vascular risk factors (hypertension, IHD, DM, smoking, haem disease)

Pregnancy= transient neurological symptoms often migraine

Seizure and syncope can occur at any age, underlying mechanism will be different

Clinical features

Positive ‘excess’ CNS electrical

discharges Visual – flashing lights,

zigzag shapes, lines, objects

Somatosensory – pain, paraesthesia

Motor – jerking limb movements

Negative loss/reduction of CNS

function loss of vision, power,

hearing, sensation

Clinical features

Seizures and migraine often start with +ve TIAs typically –ve (but may develop +ve) Seizures only rarely cause paresis from the outset

(but may develop post ictal) - sequence of symptom onset is relevant

Speech

Dysarthia Dysphasia

Did they know what words they were trying to say? Were the words you heard the right ones, albeit

slurred

Isolated complete and brief speech arrest (recurrent and stereotyped) probably focal seizure

Symptom onset and progression

TIA - onset abrupt with negative symptoms, all occurring at same time and gradually improve

Migraine aura - onset progresses slowly over minutes to tens of minutes, positive symptoms followed by negative

Eg paraesthesia hand, then to arm to shoulder followed by numbness

Eye – aura across field then field defect Seizure - onset progress in seconds, single domain.

Associated with LOC, recurrent episodes and stereotyped.

Symptom Duration

Migraine – 10-30mins TIA - < 1 hour Seizures – 5 mins Syncope – seconds

TIAs occur over days to weeks, ‘crescendo’ If longer time period will be seizure, syncope,

migraine

Precipitating factors/Associated symptoms

Seizure – hyperventilation, sepsis, altered etoh intake,

Haemodynamic TIA (jerking) may occur on sudden standing, after taking BP meds, following large meal or hot bath

BPPV – head turning

Global features unusual for TIA

Remember mechanism

Tongue biting, muscle pains after event – seizure

Vomiting after migraine Nausea, sweating,

pallor, need to urinate or defecate common post syncope

Common mimics

Migraine with aura Transient Global Amnesia Seizure Amyloid spells Structural brain lesions Haemodynamic TIA Subdural

(Demyelination)

Migraine with aura

Spectrum of severity Acephalic migraine –

aura with minimal headache

Aura reflects cortical spreading depression

Hence spreading onset Visual sx – zigzag

(geometric), ‘like looking through heat haze’, kaleidoscope

Migraine with aura

Can include sensory, motor or speech disturbances Hemiplegic migraine (familial and sporadic types)

Headache can occur in TIA and stroke, often if have history migraine

Concept of Migrainous infarction controversial ‘Secondary migraine’

Transient Global Amnesia

Temporary loss of anterograde episodic memory

Usually aged over age 50

Not uncommon to have vascular risk factors

Symptoms last over several hours

Gap in memory persists Procedural memory

intact, repetition common

Consider seizure – lip smacking, limb posturing

Transient epileptic amnesia TEA antero- and retrograde amnesia, other cognitive functions intact, recurrent episodes

Transient Global Amnesia

Episodes rare Does not increase stroke risk Functional imaging suggests hypoperfusion mesial

temporal lobes

TIA rarely affects memory – posterior circulation bilateral medial temporal lobe structures

So if memory involved likely to be a mimic

Amyloid spells

Cortical leptomeningeal white matter perforators (1mm)

Amyloid deposition within superficial arteries impairs venous drainage. Blood leaks.

Transient focal neurological episode, positive symptoms

? Seizure activity or cortical spreading haemorrhage MRI gradient sequence characteristic sign May be indicator of future ICH Cortical superficial siderosis

Structural brain lesions

Meningiomas ? Associated seizures Gradual onset,

stuttering

Haemodynamic TIA

Limb shaking = hemispheric hypoperfusion

Posture BP Recurrent

After diagnosis

Reflect on presentation Reassure – mimic Evaluate vascular health

Consider role of medication Further investigations? Driving Functioning

Secondary prevention

Express trial Aspirin and clopidogrel Aggressive BP

management Statin Treatment from clinic BP monitoring

Best medical therapy

Optimise vascular health Target known risk factors Review unknown risk factors AF/PAF – immediate anticoagulation

NOAC vs warfarin/clexane Issue immediate treatment

Next steps post Express?

What agent is responsible for risk reduction seen? Benefit from aspirin use in short term but does not

appear sustained after 90 days ? Role of aspirin with ‘funny turn’ Bleeding risk increases with age ? Rotate use of aspirin and clopidogrel in 3 month

cycles to maintain benefit seen

Timing of carotid surgery

When to operate post TIA?

(When to operate post stroke?)

Robust pathway for referral

Urgent imaging and second modality

NTN 6 70-99%, 24 50-69% (variables)

RR less as time passes

End of clinic Often no FU required GP and patient to manage vascular health Commence secondary prevention Where diagnosis unclear offer further review