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Transient Ischaemic Attacks: Mimics and Chameleons

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Transient Ischaemic Attacks: Mimics and Chameleons REVIEW Transient ischaemic attacks: mimics and chameleons V Nadarajan,1 R J Perry,1 J Johnson,1 D J Werring1,2 1Hyperacute Stroke Unit, UCL ABSTRACT can be associated with infarction on Hospitals NHS Foundation Trust, Suspected transient ischaemic attack (TIA) is a diffusion-weighted MRI; acute ischaemic London, UK 2Stroke Research Group, UCL common diagnostic challenge for physicians in stroke requires urgent treatment within Institute of Neurology, London, neurology, stroke, general medicine and primary minutes, and certainly long before 24 h; UK care. It is essential to identify TIAs promptly and the vast majority of TIAs last well because of the very high early risk of ischaemic Correspondence to under an hour (usually less than 30 min). Dr David Werring, Reader in stroke, requiring urgent investigation and More recently, the American Heart Clinical Neurology and Honorary preventive treatment. On the other hand, it is Association recommended a ‘tissue-based’ Consultant Neurologist, Stroke also important to identify TIA ‘mimics’, to avoid definition of TIA: “a transient episode of Research Group, UCL Institute of Neurology, Queen Square, unnecessary and expensive investigations, neurological dysfunction caused by a London WC1N 3BG, UK; incorrect diagnostic labelling and inappropriate focal brain, spinal cord, or retinal ischae- [email protected] long-term prevention treatment. Although the mia, without acute infarction”.1 This def- pathophysiology of ischaemic stroke and TIA is inition usefully eliminates the 24-h time identical, and both require rapid and accurate limit, but is highly dependent on timely diagnosis, the differential diagnosis differs for access to diagnostic tests (mainly MRI), TIA owing to the transience of symptoms. For which is hugely variable, even in devel- TIA the diagnostic challenge is greater, and the oped countries like the UK. Thus, for the ‘mimic’ rate higher (and more varied), because moment, TIA remains a clinical diagnosis there is no definitive diagnostic test. TIA heralds based around accurate history interpret- a high risk of early ischaemic stroke, and in many ation skills.2 With regard to patient path- cases the stroke can be prevented if the cause is ways, the most important distinction is identified, hence the widespread dissemination not between TIA and stroke, but between of guidelines including rapid assessment and risk TIA and disabling stroke, or between tools like the ABCD2 score. However, these non-disabling stroke (which can be guidelines do not emphasise the substantial managed in an outpatient setting) and challenges in making the correct diagnosis in disabling stroke (which is usually patients with transient neurological symptoms. managed as an inpatient stay). In this article we will mainly consider the Like ischaemic strokes, TIAs are due to common TIA mimics, but also briefly mention locally decreased blood flow to the brain, the rather less common situations where TIAs causing focal neurological symptoms. can look like something else (‘chameleons’). Decreased blood flow results from either embolism into a cerebral supply artery (from the heart, or the great proximal vessels, extracranial or intracranial arter- Definition and pathophysiology ies, usually affected by atherosclerosis), or TIA is defined as temporary focal neuro- in situ occlusion of small perforating logical symptoms resulting from cerebral, arteries; resolution of symptoms probably Open Access retinal—or, very occasionally, spinal— Scan to access more occurs by spontaneous lysis or distal free content ischaemia. The concept of TIA emerged passage of the occluding thrombus or in the 1950s, with the observation by C embolus, or by compensation through Miller Fisher, and others, that ischaemic collateral circulation restoring perfusion stroke often followed transient neuro- into the ischaemic brain area. Rarely, logical symptoms in the same arterial ter- focal hypoperfusion due to critical arter- ritory. An arbitrary maximum duration of ial stenosis can cause TIA, often stereo- 24 h for TIA is now recognised to be typed and related to upright posture. unhelpful—and should be abandoned— To cite: Nadarajan V, Blood pressure and blood oxygenation or Perry RJ, Johnson J, et al. for the following reasons: up to 50% of viscosity may also impact upon the Pract Neurol 2014;14:23–31. TIAs, including brief attacks (minutes), Nadarajan V, et al. Pract Neurol 2014;14:23–31. doi:10.1136/practneurol-2013-000782 23 REVIEW duration and pattern of symptom evolution or modality can help to identify individuals at highest resolution. risk of early ischaemic stroke.15 Specific challenges in diagnosing TIA CLINICAL FEATURES OF TIA The main diagnostic challenge of TIA is that the The key rule here is that symptoms of TIA should symptoms and signs have usually resolved by the time mimic known stroke syndromes, and so depend on of assessment.3 There is no test for TIA: the gold the arterial territory involved. Distinguishing the terri- standard remains assessment as soon as possible by a tory is important to guide further investigation and clinical expert. The diagnosis relies heavily on the secondary prevention. Some common patterns of patient’s account of their history and on expert inter- presentation (eg, hemiparesis) are not very helpful in pretation of that history. Interobserver agreement for distinguishing the arterial territory, as they can occur the diagnosis of TIA between different stroke-trained with both anterior and posterior circulation TIAs. – physicians and non-neurologists is poor.4 7 As in Others can be more localising: for example, aphasia stroke, in some patients a collateral history may be or transient monocular visual loss suggest carotid ter- essential. ritory ischaemia, while bilateral limb weakness, vertigo, hearing loss, haemianopia or diplopia are fea- tures of vertebrobasilar (brainstem) ischaemia. TIAs Subsequent stroke risk and importance of accurate due to perforating artery disease should mimic a diagnosis known lacunar syndrome (most often hemisensory or Patients with a diagnosis of TIA have an increased risk hemimotor symptoms affecting the face, arm and leg); of future ischaemic stroke. Fifteen per cent to 30% of moreover, such ‘lacunar’ TIAs may be recurrent and ischaemic strokes are preceded by TIA symptoms, “ 8 stereotyped over a short period (days) as in the cap- often on the same day. A meta-analysis found a ” 9 sular warning syndrome . Increased awareness of cumulative early risk at 7 days of 5.2%. The risk of symptoms means that patients can now present with stroke is highest within the first 24 h,10 so prompt 11 very restricted transient syndromes, including isolated and accurate diagnosis is critical ; misdiagnosis can vertigo, dysarthria or hemisensory disturbance: in expose patients to unnecessary investigation and long- such cases, clinicians should consider other causes term secondary prevention treatment, as well as 12 before diagnosing TIA. anxiety. Abrupt onset of maximal symptoms predicts a final The ABCD2 score (which includes age, blood pres- diagnosis of TIA,12 but there is no evidence for a stat- sure, clinical features, duration and diabetes) is a istical difference between duration of symptoms in popular clinical prediction tool used to identify those patients with TIA and mimics.14 These findings may patients with suspected TIA at high risk of developing 3 of course be rather circular, since sudden symptoms early ischaemic stroke, but may not always be used are part of the usual criteria for diagnosis of TIA, and appropriately. It is of limited practical relevance in part of what makes a mimic is its similar time course modern stroke clinical practice, since the aspiration is to TIA. Nevertheless, other key aspects of the history to see all patients with suspected TIA within 24 h. that are useful to help identify TIA from mimics are — The ABCD2 is not designed as and should not be as follows: — used as a diagnostic instrument, although a high ▸ Age and other demographic data: is there a high a priori ABCD2 score may predict subsequent stroke, in part probability of a cerebrovascular event? because such patients are more likely to have had a ▸ ‘ ’ ‘ ’ 31314 Nature of the symptoms: positive versus negative ? TIA rather than a mimic. The ABCD2 score ▸ Onset and progression does not include other known predictors of high ▸ Duration stroke risk, including carotid disease, recurrent TIAs ▸ 15 Precipitating factors and evidence of tissue damage on MRI. Finally, the ▸ Associated symptoms, for example, headache, loss of validity of the ABCD2 score in the hands of general awareness, during or after the attacks practitioners and other non-stroke doctors may be limited and is not extensively studied. Age and other demographic data TIAs are rare in young people without vascular risk Role of brain imaging in TIA factors (eg, hypertension, ischaemic heart disease, dia- Even transient deficits can be associated with evidence betes mellitus, smoking, haematological disease, etc). of persistent tissue ischaemia on diffusion-weighted In otherwise healthy pregnant women, transient imaging (DWI). In those cases, positive DWI supports neurological symptoms are a common reason for a clinical diagnosis of TIA. In early series, 35–67% of neurological referral, but are often related to patients with TIAs had restricted diffusion suggesting migraine. Seizures and syncope occur at all ages, cerebral ischaemic injury.16 The likelihood of a DWI although the underlying causes may differ. Syncope is lesion increases with symptom duration. Recent risk more common in women, but seizures have no sex scores incorporating DWI suggest that this imaging predilection. TIAs are more common in men at 24 Nadarajan V, et al. Pract Neurol 2014;14:23–31. doi:10.1136/practneurol-2013-000782 REVIEW younger ages, but the sex difference reduces after the gradually progress up the arm to the shoulder, trunk, menopause. and then the face and leg, frequently followed by numbness. In the visual domain, a visual aura may Nature of the symptoms migrate across the field and be followed by a visual ▸ Positive symptoms indicate an ‘excess’ of central nervous field defect.
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