GP Update TIA and mimics
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Transcript of GP Update TIA and mimics
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24 hour duration outdated Majority last under 30 mins Clinical diagnosis Accurate history interpretation skills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