Episode 6: Transient Ischemic Attack

Transient Ischemic Attack (TIA) can be difficult to diagnose. It’s unclear who to work up. It’s challenging if the patient is already taking blood thinners. Dr. Walter Himmel and Dr. Daniel Selchen discuss the key historical and physical examination maneuvers to determine whether patients with neurologic complaints have had a TIA or whether they have had a TIA mimic. They review the 3 best risk stratification rules including the ABCD2 Score to help us determine who needs to be admitted and who needs timely investigations to reduce vascular morbidity and mortality. The reasoning behind which patients require urgent carotid imaging, echocardiograms and advanced imaging such as CT Angiogram is explained, and the best medication choices are reviewed, as well as the indications for Clopidogrel, Aggrenox, Warfarin, Heparin and carotid endarterectomy in the managment of Transient Ischemic Attack. In the second part of the episode, a simple and practical approach to the patient with dizziness is presented, and a discussion on which patients with dizziness need urgent work-up and treatment for vertebrobasilar TIA.

Written Summary and blog post by Dr. Lucas Chartier, edited by Dr. Anton Helman, July 2010

In this episode Dr. Himmel and Dr. Selchen answer questions like: What simple things can we do in the ED for our TIA patients to improve cerebral blood flow? How do we manage blood pressure in the ED after a TIA? What are the limitations of the best stroke risk prediction rules after TIA? How can we differentiate the common TIA and stroke mimics from a true TIA or stroke in the ED? When is IV Heparin indicated for TIA? Why is carotid doppler imaging such an important test? Which patients need an urgent CT Angiogram or MR Angiogram? Which patients with TIA require admission? Which medication is better for stroke prevention after TIA, Clopidogrel or Aggrenox? How good is Warfarin at reducing the risk of stroke in patients with Atrial Fibrillation and TIA? Should we be prescribing antihypertensives for our patients who have had a TIA? When should we suspect carotid or vertebral artery dissection as a cause for TIA? How should we interpret the Dix-Hallpike manoeuvre and the Head-thrust test? How can we differentiate peripheral vs. central causes of vertigo at the bedside? What are the best medications for patients with vertigo? and many more…..

 

TRANSIENT ISCHEMIC ATTACK

Definition of TIA

Classic definition of TIA is neurologic dysfunction caused by focal brain or retinal ischemia lasting < 24 hrs. Recent definition has changed to 1 hr because up to 50% of classically defined TIAs are actually infarcts as shown on MRI

TIA Risk Stratification Scores

ABCD2 score: Combination of California Score and ABCD Score, and most relevant to Emergency Physicians because of 2‐day risk of stroke (as opposed to 90 days or 7 days for the others)

Points Criteria
1 Age > 60
1 Blood pressure > 140 systolic or > 90 diastolic
2 Clinical feature: Unilateral weakness
1 Clinical feature: Speech disturbance
2 Duration of symptoms: > 60min
1 Duration of symptoms: 10-60 min
0 Duration of symptoms: < 10 min
1 Diabetes

Score interpretation:

  • Score 0‐3 = low risk (1% risk of stroke at 48hrs)
  • Score 4‐5 = moderate risk (4% at 48hrs)
  • Score 6‐7 = high risk (8% at 48hrs)

 

Transient Ischemic Attack Key historical features

  • Abrupt onset of focal neurological symptoms, with the features identified by the ABCD2 score;
    • Other relevant features: multiple episodes (eg, crescendo), associated headache or trauma, history of atrial fibrillation or risk for cardioembolic source (mural thrombus, carotid stenosis, patent foramen ovale – PFO)

TIA/CVA Mimics

  • Partial seizure: context is crucial because a Todd’s paresis will occur in the setting of a focal seizure (or generalized with focal onset) with pre‐existing CNS lesion, stroke or tumor (which should be seen on a CT scan)
  • Migraine: migraine‐equivalent visual disturbances may occur – migraine aura without the associated headache; the symptoms are usually positive (scintillating scotomatas, shimmering) and asynchronized (the migraine “marches”, with visual disturbance then a speech or weakness appears) in visual phenomena, versus negative (actual visual loss, obscuration) and synchronized (both visual and motor disturbances simultaneously) in TIA
  • Other diagnoses to consider: Hypoglycemia (it CAN cause focal symptomatology), subdural hematoma, brain tumor, labyrinthitis/neuronitis, transient global amnesia, severe postural hypotension, arrhythmia, cervical disk disease, cerebral venous thrombosis, conversion disorder

 

Key physical exam findings in TIA

Most important are facial droop, pronator drift and abnormal speech

  • Head and neck: pupillary size and EOMs, facial droop and abnormal speech, level of alertness
  • Cardiovascular: heart rate and RHYTHM (eg, a.fib), blood pressure and neck bruits
  • Motor exam (and reflexes, Babinski): Grip strength and big motor groups are too gross examinations; use also finger extension and pronator drift for >10sec
  • Romberg test and gait (including tandem gait)

 

TIA classification and tests (rule of 4s – 4 types and 4 investigations)

 Types of TIA Appropriate investigations
Cardioembolic (1/4 of TIAs) ECG: Look for a.fib (12‐16% of stroke) and other cardiac problems that might cause embolic phenomena from the heart: CHF, recent MI, left ventricular aneurysm, rheumatoid heart disease, valvular disease); if the ECG looks like acute MI and a severe headache ispresent, think of ICH and SAH
Lacunar (small arteries) TIAs (1/4 of TIAs)

  • Classically: pure motor and pure sensory, or mixed‐motor‐sensory but without cortical findings (below)
Unenhanced CT head: To rule out TIA mimics (tumor, SDH, ICH, SAH – especially given that ASA will be given), and see old strokes
Large arteries in neck, brain (1/4 of TIAs)

  • Cortical findings: aphasia (sometimes mistaken for confusion) means left hemispheric involvement; neglect means right‐hemispheric involvement; visual disturbances (field cuts)
Vascular imaging: Organize for carotid Doppler in the neck 1‐3d maximum, or consider adding CT‐angiogram to CT head (which can assess for intracranial arteries) – see discussion below
Other TIAs (1/4 of TIAs)

  • Intracranial hemorrhages (15%), cryptogenic, clotting diosrders, PFOs
Blood: Accucheck and blood work (CBC, lytes and blood sugar, BUN, Cr, INR)

Other important causes of TIA:

  • Carotid dissection: young patient with no risk factors, especially if associated with trauma or sudden, rapid movement of the neck, neck pain (anterior pain in carotid dissection, posterior pain in vertebral dissection), vertigo or headache
  • Endocarditis: unwell for weeks, flu‐like symptoms, recurring fever, weight loss, and headache

Vascular Imaging (NASCET trial)

  • Essential to organize early imaging (1‐3d max) given that carotid endarterectomy (CEA) performed within 2wks of TIA gives an absolute risk reduction (ARR) of 30%, or a number needed to treat (NNT) of 3 – unparalleled in terms of benefit compared to other treatments we can offer; early treatment is crucial given that the ARR drops to 16% if CEA is performed 2‐4wks after TIA, and close to 0% if after 4 weeks; interestingly, the benefit of early CEA seems to drop in women after3wks, emphasizing the need for prompt treatment
  • Consider CTA if there is no renal dysfunction nor allergies to contrast, especially in a convincing TIA story or concern for dissection (the vascular imaging will be done immediately and admission will be considered, as opposed to a few‐days outpatient management); carotid Doppler, although still good, cannot assess intracranial circulation and is an imprecise measure in certain cases
  • Echocardiography: lower priority test as the yield is low, especially if there is no known cardiac disease; consider it in patients for which there is no explanation of the TIA/stroke

 

Acute TIA management

  • Maximize cerebral blood flow by rehydrating dehydrated patients, and by resisting the urge to rapidly lowering the blood pressure
  • Antiplatelet medications (decreases the risk of stroke – and MI – by 1/4)
  • ASA should almost always be the first option, and given as soon as there is no bleed as confirmed by CT head, with loading dose of 160‐325mg NON‐enteric coated chewed, then 81mg daily
  • In severe ASA allergy, Clopidogrel is the only choice
  • If ASA failure (ensure compliance first), Plavix™ and Aggrenox™ are equally effective and at least as good as ASA, but Plavix™ has a better side‐effects profile
  • Plavix™ (Clopidogrel) should be given either as a loading dose of 300mg (onset of action 6‐7hrs) then 75mg daily, or overlapped with ASA for 3‐4d if no loading dose is given (onset of action 3‐4d); do not combine ASA + Clopidogrel for extended periods as the risks of major bleeding and ICH outweight the benefits (MATCH trial)
  • Aggrenox™ (dipyridamole 200mg + ASA 25mg) should be given BID, but patients should be warned of the frequent severe headaches accompanying the medication, and therefore should be directed to take acetaminophen with the first few doses
  • Heparin should probably never be started by the EP (even in the setting of a.fib), except possibly in crescendo TIAs with suspected critical carotid artery stenosis or tight basilar artery occlusion in consultation with a neurologist

 

Disposition for Transient Ischemic Attack

Admit high‐risk patients with suspicion of large vessel disease, especially if other “soft factors” that would delay care are present: non‐English speaking, no means of transportation, unreliable patient or family, impoverished); other patients can be referred to stroke clinic for prompt assessment

Medications for home

Reduction in blood pressure leads to lower events in the long run, but can be dangerous if performed too rapidly and acutely; it is therefore reasonable to let the patient know to discuss antihypertensive medications with their GP; alternatively, for hypertensive patients in the ED, low‐dose medications can be started (eg, Hydrochlorothiazide 12.5mg, Ramipril 2.5mg or Telmisartan 40mg daily – follow up with the GP for electrolyte monitoring is essential)

Coumadin to prevent stroke in patients with Atrial Fibrillation:

  • Risk stratification is essential: CHADS Score (CHF, HTN, Age>75, DM, previous Stroke) ≥2 should get warfarin given the benefits – 70% risk reduction in embolic events – and the risks – moderate bleeds (10‐12%), or severe bleeds (2‐3%) requiring hospitalization, transfusion, or causing ICH
  • Remember that older age means higher risk for embolic event, so a 92y.o. woman who everyone is afraid of giving warfarin to is probably the person who would most benefit from it

 

emcases-updateUpdate 2014: Canadian Cardiovascular Society 2014 Guidelines on Atrial Fibrillation with Dr. Ian Stiell’s algorithm for stroke prevention

emcases-updateUpdate 2012: CHADS-Vasc Score to assess need for anticoagulants in atrial fibrillation

 

APPROACH TO VERTIGO IN THE ED

4 types of dizziness (there’s always one that predominates):

  1. Syncope / pre‐syncope: feeling of passing out
  2. Vertigo: hallucination of rotation or linear movement; spinning
  3. Disequilibrium: cannot walk properly, staggering
  4. Non‐specific light‐headedness

4 types of vertigo (based on duration of symptoms):

  1. Less than 60sec: Positional event (MARKEDLY worse with movement)
  2. Minutes (few to 30): If not positional: migraine (in young, low‐risk patients) or TIA/CVA (in older, at‐risk patients)
  3. Many hours: Vestibulopathy, Ménière’s disease
  4. Days: Labyrinthitis, or stroke

Approach to vertigo

The easiest way to rule out an ominous central cause is by ruling in a benign peripheral cause:

  1. BPPV: <1min, normal in between attacks, Dix‐Hallpike positive (see below), Epley maneuver cures it in 50% of cases (see youtube)
  2. Vestibular neuronitis: acute severe constant vertigo, positive head‐thrust manoeuvre (see below)
  3. Ménière’s disease: >20mins to hrs in combination with tinnitus, ear fullness or decreased hearing

Vertigo History

Features suggestive of posterior circulation ischemia: diplopia, ataxia (especially between episodes), dysarthria (slurred speech) and dysphagia – and central cause: non‐positional or bidirectional nystagmus, inability to ambulate, focal neurological deficit and cerebrovascular risk factors

Note: all causes of vertigo can be worsened by head movement

Vertigo Physical examination

  • Unidirectional horizontal nystagmus is usually peripheral in nature, whereas vertical, pure torsional and/or bidirectional nystagmus, limb ataxia and pinprick sensation asymmetry are usually central

Dix Hallpike test:

  • Useful in ruling in BPPV only if CLASSIC response: brief latency of 3‐5 seconds, dramatic response with vertical or rotatory eye movements that stop after 30‐60sec, and fatigability if the test is repeated

Head thrust test:

  • Abnormal test (unilateral latency in eye repositioning when the head is thrust) is indicative of peripheral lesion (eg, vestibular neuronitis with acute, severe and constant vertigo) almost always

 

Go to Episode 45 where Dr. Stuart Swadron explains his approach to Vertigo from North York General’s EMU Conference 2014 and Episode 99 where Dr. Himmel refines his approach to differentiating central from peripheral causes of vertigo.

 

Medications for Vertigo

  • Antihistamines (eg, dimenhydrinate), antidopaminergic (prochlorperazine ‐ Stemetil™), and/or anticholinergic (atropine 0.4‐0.6mg IM or Scopolamine 0.5mg patch) may be tried
  • Serc™ (betahistine) should ONLY be prescribed for Ménière’s disease

Key References

Diener HC, Bogousslavsky J, Brass LM, et al. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. Lancet. 2004;364(9431):331-7.

Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009;40(11):3504-10.

Ferguson G et. al. The North American Symptomatic Carotid Endarterectomy Trial. Stroke. 1999; 30: 1751-1758.

Quinn TJ, Cameron AC, Dawson J, Lees KR, Walters MR. ABCD2 scores and prediction of noncerebrovascular diagnoses in an outpatient population: a case-control study. Stroke. 2009;40(3):749-53.

 

Dr. Selchen, Dr. Helman and Dr. Himmel have no conflicts of interest to declare.

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About the Author:

Dr. Anton Helman is an Emergency Physician at North York General in Toronto. He is an Assistant Professor at the University of Toronto, Division of Emergency Medicine and the Education Innovation Lead at the Schwartz-Reisman Emergency Medicine Instititute. He is the founder, editor-in-chief and host of Emergency Medicine Cases.

One Comment

  1. Tom Wade MD March 5, 2016 at 10:09 am - Reply

    Thanks to all three of you doctors. Outstanding teaching and oustanding show notes and pdf resources. Dr. Hellman every podcast you have produced is worth reviewing by every primary care physician, nurse, nurse practioner, and physician assistant.
    I hope you never stop.

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