Management of TIA. Dr Ali Ali Consultant Stroke and Geriatrics Royal Hallamshire Hospital

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Management of TIA Dr Ali Ali Consultant Stroke and Geriatrics Royal Hallamshire Hospital

Objectives Definition TIA and stroke TIA: Diagnosis & mimics Risk assessment Referral and emergency management Secondary care management

A Journal of the life of Charles Dickens 1869-1870 In 1869 wrote a letter to W.H. Willis MD, mentioning difficulties speaking and moving the foot Jan. 1870 new year s day at Gad s Hill suffering another attack of the foot trouble Jan 23 complains: something the matter with my right thumb and can t write plainly June 8th : writing Edwin Drood and suffers a stroke at Dinner.

Transient Ischaemic Attack (TIA) Concept of TIA gathered in 1950 s Neurologists e.g. Miller Fisher observed that stroke often followed transient neurological symptoms of the same arterial territory. Definition evolved: Transient focal neurological symptoms resulting from cerebral, retinal, or spinal ischaemia. Lasts < 24 hours. NOT USEFUL why?

New definition TIA Vast majority of TIAs last less 1 hour. Up to 50% of TIAs are associated with infarction on diffusion weighted MRI. Acute ischaemic stroke requires urgent treatment within minutes let alone 24 hours. New tissue based AHA definition: A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia, without acute infarction.

TIA Epidemiology 46,000 TIA s annually in the UK. ~ 480 TIA s treated annually in Sheffield. But, ~ 1300 TIA clinic referrals annually in Sheffield. Thus 60% clinic referrals turn out to be alternative diagnosis.

Oxfordshire Community Stroke Project Oxfordshire Community Stroke Project 512 Patients referred for suspected TIA 317 Others 195 (38%) with TIA 52 (10%) Migraine 33 (6%) Vertigo 48 (9%) Syncope 29 (6%) Epilepsy 46 (9%) Poss. TIA 17 (3%) TGA 45 (9%) Funny turn 47 (9%) Other OXVASC 2002

Diagnosing TIA Difficult symptoms resolved when acquiring history. No definitive test for TIA diagnosis remains clinical. Inter-observer agreement between stroke trained and nontrained poor.

Clinical features - History Age & demographics: TIA s are rare in young patients without vascular risk factors. Acute neurology in pregnant females unlikely TIA. Older age more likely TIA less likely mimic.

Clinical features - History Nature of symptoms: Positive: excess of neuronal discharge visual (flashing lights, zig-zags, lines, shapes), sensory (pain, paraesthesia), motor (limb jerking) Negative: loss of neuronal function loss of vision, hearing, sensation or power. TIA negative symptoms mostly arterial territory. Seizure & migraine positive symptoms particularly at the outset.

Clinical features - History Onset & progression: Abrupt onset of maximal symptoms. If multiple symptoms all generally occur together. Gradual offset over minutes. Migraine occurs over minutes to tens of minutes positive symptoms initially may be replaced by negative ones e.g. spreading paraesthesia followed by numbness; visual aura followed by field defect. Seizures progress over seconds usually one functional domain e.g. motor or sensory can be recurrent and stereotyped.

Clinical features - History Duration of symptoms: TIA s nearly always < 1 hr (mostly < 10 mins). Migrainous auras usually 10-30 mins (can be few hours). Seizures usually < 5 mins. Syncope few seconds (unless remains upright). Episodes recurring over some years unlikely TIA.

Unlikely TIA Non-focal symptoms: LOC Dizziness Generalized weakness Mental confusion Loss of vision if associated with reduced LOC Sphincter incontinence

Headache and TIA Mild headache 1/6 TIA. Usually ipsilateral to affected carotid territory. More common in posterior TIA. Think about carotid or vertebral dissection. Bilateral headache TIA unlikely

Migraine Hemiplegic Migraine. Acephalgic Migraine. Opthalmoplegic Migraine. Basillar Migraine. Prolonged Aura. Status migrainosus. Gradual Onset ( > 5 mins) Positive symptoms. Symptom spread over several seconds to minutes. Gradual resolution - minutes to days. Headache not always. Recurrent Stereotyped attacks. Typically young.

Migraine

Migrainous Infarcts Classical Migraine vascular risk factor Migrainous infarction: Infarct during attack where aura lasts > 60 mins More prevalent in: Young women (<45 years) OCP Smokers Account for 0.2-0.5% Ischaemic stroke Most commonly posterior circulation

Seizure Generalised should be easier to identify but can be brief: Confusion, involuntary movements, incontinence. Negative motor symptoms are very rare as a sole manifestation of seizure. Complete speech arrest Seizure > TIA. Recurrent stereotyped events unlikely TIA.

Partial Seizures Common TIA mimic: Young or middle aged adults. Antecedent symptoms. Positive neurological symptoms. March of symptoms. Recurrent stereotypical attacks. +/- amnesia of event.

Syncope Transient loss of consciousness & postural tone associated with rapid recovery. Presyncopal symptoms: Faintness Dimming vision Muffling sounds Triggers: - Emotion, fear - Change in posture Pallor, sweating, nausea. TIA extremely unlikely with history of TLOC.

Acute vestibular syndrome Dizziness / giddiness what does this mean? True rotational vertigo vs. presyncope vs. unsteadiness Population-based study only 3% of emergency presentations for dizziness have TIA. Dix-Hallpike & Head-impulse tests are specific but not sensitive. In those with vascular risk factors difficult to determine. Kerber et al 2006

Posterior circulation TIA Unlikely if isolated: Unsteadiness / vertigo Dysarthria Diplopia Drop-attacks Usually at least 2 of these posterior circ. symptoms present in true ischaemia. Weakness Sensory loss confined to one part of face / limb

Other mimics TGA - > 50yrs vascular risk factors temporary loss of laying down new episodic memory procedural memory intact. Ask about features of seizures (lip-smacking, dystonic posturing). Tumours / SOL s stuttering onset over weeks. Functional younger inconsistent history / examination. Amyloid spells / haemorrhagic TIA difficult to differentiate.

Amyloid Spell

What next? Stroke risk? 20% strokes preceded by TIA. 20-30% TIA s will stroke within next 5 years. 10% will stroke within next 3 months. 5% will stroke within next 2 days. How do we risk stratify? Rothwell & Warlow 2005, Gladstone et al 2004

Stroke risk stratification Clinical ABCD2 Imaging MRI DWI Carotid imaging

ABCD 2 score ABCD 2 2 days 7 days 6 8.1% 11.7% 4-5 4.1% 5.9% 0-3 1.0% 1.2% Score < 4 TIA clinic within 1 week Score 4 TIA clinic within 24 hrs Specialist review within 24 hrs

High risk TIA s AF Known carotid stenosis Crescendo TIA s On anticoagulation

Late presentation TIA Presentation > 1 week since symptoms generally treat as low risk.

EXPRESS Trial Rapid access TIA clinic (< 2 days) with diagnostics and treatment initiation vs. standard outpatient referral. Before and after study 1,278 patients.

Amarosis Fugax Eliasziw et al 2004

Emergency treatment Aspirin 300mg stat. Clopidogrel if aspirin intolerant same doses. If already on clopidogrel / prasugrel / ticagrelor continue until seen in TIA clinic. If on dual antiplatelets leave on these. If on warfarin: Therapeutic INR leave until specialist review. INR < 1.5 300mg aspirin.

Emergency treatment If on NOAC omit next dose until specialist review. Statin initiation. Don t worry too much about BP immediately await TIA clinic review unless very high (persistently > 200 mmhg SBP) admit.

TIA clinics Daily TIA clinic. Stroke specialist / neurologist assessment. Access to CT, MRI, carotid imaging on day of assessment.

Neuroimaging in TIA Excludes other causes e.g. SOL MRI and carotid imaging 90 day stroke rates: DWI negative 4.3% DWI positive 11% DWI positive & carotid stenosis 33%

Neuroimaging in TIA CT poor sensitivity. 50% TIA s are DWI positive on MRI scan depends on duration of symptoms:

Antiplatelets Clopidogrel 300mg and then 75mg daily thereafter. or Aspirin 75mg od and dipyridamole MR 200mg bd.

TIA and AF Offer anticoagulant with immediate effect: NOAC Treatment dose LMWH until warfarin therapeutic

Carotid Stenosis Symptomatic carotid stenosis of 50-99% - assessed and referred for intervention (CEA or stenting) to be performed within first 2 weeks.

Carotid stenosis NASCET & ECST Rothwell et al 2004

Secondary prevention BP (target < 130/80) Lipid management (chol < 4, LDL < 2) Diabetes management Smoking cessation / alcohol moderation Exercise management

Conclusion Correct diagnosis is key. Urgent investigation and vascular risk reduction required. Thank you any questions?