GP Update TIA and mimics Kath Pasco Oct 2015

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

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 True TIA=high risk stroke

Stroke following TIA Risk of stroke following a TIA 10% at 7 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% Stroke following TIA

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 Definite diagnosis can be a challenge

Temporary focal neurological symptoms (cerebral, retinal or rarely spinal ischaemia) 24 hour duration outdated Majority last under 30 mins Clinical diagnosis Accurate history interpretation skills TIA

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 Mechanism

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? Screening of referrals?

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 Role of brain imaging

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

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 Clinical features

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 When TIA is less likely

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

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 Clinical features

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 Speech

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 onset and progression

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 Symptom Duration

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 Precipitating factors/Associated symptoms

Common mimics Migraine with aura Transient Global Amnesia Seizure Amyloid spells Structural brain lesions Haemodynamic TIA Subdural (Demyelination) Common mimics

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

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’ Migraine with aura

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

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 Transient Global Amnesia

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 Amyloid spells

Structural brain lesions Meningiomas ? Associated seizures Gradual onset, stuttering Structural brain lesions

Haemodynamic TIA Limb shaking = hemispheric hypoperfusion Posture BP Recurrent Haemodynamic TIA

After diagnosis Reflect on presentation Reassure – mimic Evaluate vascular health Consider role of medication Further investigations? Driving Functioning After diagnosis

Secondary prevention Express trial Aspirin and clopidogrel Aggressive BP management Statin Treatment from clinic BP monitoring Secondary prevention

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 Best medical therapy

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 Next steps post Express?

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 Timing of carotid surgery

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