Published 25 February 2009, doi:10.1136/bmj.b616
Cite this as: BMJ 2009;338:b616

Endgames

Case report

An episode of transient neurological symptoms

Colin B Josephson, neurology resident1, Rustam Al-Shahi Salman, MRC clinician scientist and honorary consultant neurologist2, Stephen J Phillips, professor of medicine (neurology)1

1 Department of Medicine, Division of Neurology, Dalhousie University, Halifax, NS, Canada B3H 3A7, 2 Division of Clinical Neurosciences, University of Edinburgh, Edinburgh

Correspondence to: S J Phillips stephen.phillips{at}cdha.nshealth.ca

A 72 year old, right handed man presented with weakness of the right hand and difficulty expressing himself, although he was able to comprehend those around him. The symptoms were maximal at onset and resolved spontaneously within one hour. He had a history of hypertension and type 2 diabetes mellitus. His only drugs were metformin and a thiazide diuretic. His neurological and general examinations were normal, and his blood pressure was 140/90 mm Hg. Computed tomography of his brain was normal.

Questions

1 What is the diagnosis?
2 Where is the lesion, and how might you confirm the diagnosis?
3 What are the immediate goals in evaluation and treatment?

Show Answers

Answers

Short answers

1 Transient ischaemic attack (TIA).
2 Expressive aphasia and right hand weakness localise to the middle cerebral artery territory of the left hemisphere. The diagnosis of a TIA is usually made on the basis of the patient’s history. A relevant hyperintense lesion on the diffusion weighted magnetic resonance imaging (MRI) sequence and a corresponding hypointense lesion on the apparent diffusion coefficient MRI sequence, which indicates ischaemia, can be seen in less than half of patients.
3 Perform a thorough history and physical examination, consider conditions that mimic TIA, and seek an underlying cause of the TIA. The ABCD2 score helps to estimate the early risk of ischaemic stroke and to prioritise subsequent investigations. Perform blood tests (including full blood count, urea and electrolytes, glucose, lipid profile, and erythrocyte sedimentation rate), a chest x ray, an electrocardiogram, and carotid Doppler ultrasound as soon as possible (within one week, at the latest). Start antiplatelet therapy, a statin drug, and an angiotensin converting enzyme inhibitor.

Long answers
The diagnosis
TIA has been defined as "a clinical syndrome characterised by an acute loss of focal cerebral or monocular function with symptoms lasting less than 24 hours and which is thought to be due to inadequate cerebral or ocular blood supply as a result of low blood flow, thrombosis or embolism associated with disease of the arteries, heart or blood."1 Most episodes that last longer than one hour will not resolve in 24 hours, so it has been proposed to change the definition to a brief episode of neurological dysfunction caused by focal brain or retinal ischaemia, with clinical symptoms typically lasting less than one hour and without evidence of acute infarction.2 However, application of this definition is restricted by its need for brain imaging. As both TIA and minor ischaemic stroke carry a considerable risk (about 5%) of stroke recurring within one week,3 4 these conditions should swiftly be distinguished from TIA mimics so that investigation and treatment are appropriate. In this case, although the duration of the symptoms would be consistent with migraine aura, the sudden, rather than gradual, onset of the symptoms, and the patient’s age and medical history, all make TIA the most likely diagnosis.

Confirming the diagnosis
Expressive aphasia and right hand weakness localise to the left middle cerebral artery territory. The nature and location of the lesion can be confirmed by diffusion weighted MRI as soon as 11 minutes after the onset of ischaemia,5 and diffusion weighted MRI sequences can be helpful when there is clinical uncertainty regarding the localisation of the lesion.6 7 Diffusion weighted MRI sequences can detect cytotoxic oedema accurately and are more sensitive to acute ischaemia than either plain computed tomography or T2 weighted MRI.8 Diffusion restricted lesions are detected in only 13-48% of patients within 17 days of onset of TIA,7 9 10 and are associated with an increased risk of recurrent TIA and stroke.11 12 13

Goals of treatment
The priority in management is secondary prevention. For the appropriate patient, carotid endarterectomy is effective, but it requires rapid access to carotid imaging and surgical expertise. It halves the risk of any stroke or death at five years for patients with symptomatic 70-99% carotid stenosis (number needed to treat (NNT)=6) and reduces risk by one quarter for patients with symptomatic 50-69% carotid stenosis (NNT =13).14 The benefit of carotid endarterectomy is greatest when it is done within two weeks of the last ischaemic event and declines rapidly thereafter.15

Antiplatelet agents reduce the risk of vascular events after TIA.16 Thienopyridines (such as clopidogrel) or the combination of aspirin and extended release dipyridamole are marginally superior to aspirin alone,17 18 but aspirin plus extended release dipyridamole seems to be as effective as clopidogrel.19 Because anticoagulants are more effective than antiplatelet agents in preventing ischaemic stroke after TIA in patients with atrial fibrillation,20 routine electrocardiography for any patient presenting with a TIA is essential for detecting atrial fibrillation, although the need for routine echocardiography is controversial.21 22

Blood pressure reduction after TIA is beneficial for secondary prevention; perindopril and indapamide reduced the future risk of stroke by 43%, compared to placebo.23 Statins reduce the risk of recurrent vascular events after TIA.24 25 However, most of the studies of drugs for secondary prevention of ischaemic stroke after TIA enrolled few patients within the early, high risk period.

A prospective, population based, sequential comparison showed an early reduction of subsequent stroke by urgent evaluation and treatment after a TIA or minor ischaemic stroke.26 Compared with delayed assessment, patient evaluation and treatment on the day of the event was associated with improved outcomes (adjusted hazard ratio for recurrent stroke 0.20, 95% confidence interval 0.08 to 0.49). Management included assessment and referral for carotid endarterectomy if indicated, warfarin for patients in atrial fibrillation, and immediate start or adjustment of antiplatelets, statins, and—if the systolic blood pressure was >130 mm Hg—antihypertensive agents. Although not a randomised controlled trial, this study has influenced clinical practice guidelines to advocate rapid evaluation and treatment of patients with TIA and minor ischaemic stroke.27 28

The risk of stroke after TIA may be predicted with the ABCD2 score, which uses the patient’s age, blood pressure, clinical symptoms, duration of the attack, and history of diabetes.29 Although potentially useful as a triaging tool to prioritise access to stroke care services, the ABCD2 score does not provide guidance on treatment and may not be reliable beyond the first week after the TIA.30

Cite this as: BMJ 2009;338:b616

Competing interests: None declared.

Provenance and peer review: Not commissioned; externally peer reviewed.

Patient consent not required (patient anonymised, dead, or hypothetical).

References

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