Introduction

All too often a patient presents to hospital saying ‘I thought I was having a stroke but wanted to wait to see what happened’. If not the patient, then the relative or spouse says something similar. This wouldn’t happen with a suspected ‘heart attack’!

It is sobering to acknowledge that one can replace a heart, or part of a heart, but it is still impossible to replace the ‘motherboard’ in the brain. The heart is basically a pump for which one can even offer a mechanical substitute. Conversely, the brain is a super computer that is still not fully understood. It is time to replace the nihilism and think in terms of ‘brain attack’, in much the same way one thinks of ‘heart attack’. To do this underlines the most important message for either heart or brain, namely, ‘Time is of the essence!’ The catchcry for people dealing with stroke is ‘Time is brain’.

What follows is an overview of stroke that offers a clinician’s perspective of management. No message is more important than the need for early presentation. The previously accepted three-hour time window has been expanded to four-and-a-half hours in which to safely offer intravenous tissue-type plasminogen activator (tPA),¹ but sooner is still better.

Atherosclerosis

‘Brain attacks’ and ‘heart attacks’ have a common pathophysiology. An embolus of thrombus dislodges from the surface of an atherosclerotic plaque and becomes lodged downstream to occlude blood flow and hence nutrition distal to the blockage. This accounts for ischaemic strokes, comprising 85% of all strokes (only 15% have haemorrhagic aetiology).²

Atherosclerosis increases with age, hypertension, hyperlipidemia, diabetes and cigarette smoking.² It follows that medical management must address these factors. The thrombus that is dislodged from the plaque was formed consequent to prothrombotic effects involving tissue factor. Activated factor VII with platelet recruitment results in formation of platelet-rich fibrin thrombus, which embolised. Thus antiplatelet agents are important in preventing thrombotic emboli and hence strokes.

Cardiac causes

One of the most common cardiac causes of strokes is atrial fibrillation (AF). It also occurs with rheumatic heart disease, increasing age, hypertension, ischaemia and thyroid disease. AF occurs in approximately 1% of those under 60 years and about 6% in those over 80 years, and the population is ageing.

While there has been an attempt to classify AF into acute and chronic,³ this concept has less relevance to the neurologist/stroke-ologist, whose most important take-home-message concerning AF is the need to prevent emboli. Hence, one must recognise the need for anticoagulation. The actual treatment of AF is supervised by the cardiologist, but anticoagulation with Coumadin® is a high priority for stroke prevention. More recently a new class of anticoagulation drug has emerged.⁴ It is still too early to be certain about the place of dabigatran, but it appears destined to replace Coumadin® as the drug of choice for patients with AF. This remains a question for consultants until there is wider experience.

There are other cardiac causes of emboli, such as micotic emboli, with growths particularly on rheumatic valves. Unless this is appreciated with an index of suspicion for bacterial endocarditis, it may be overlooked. Mercifully this is rare but echocardiography is mandatory in the stroke evaluation. Transoesophageal echocardiogram is preferable, especially in the young stroke patient. Another cause detected by echocardiogram is patent foramen ovale (PFO), which may be under-diagnosed in stroke patients. One study reported in excess of 15% in over 55-year-old cryptogenic stroke patients having PFO with atrial septal aneurysm.⁵ The question of closure of PFOs in stroke patients or those with transient ischaemic attacks (TIAs) is a topic of some debate, which is not yet fully resolved. Evidence suggests an association of PFO with hypercoagulation, especially factor V leiden and prothrombin G20210A genetic mutations.⁶ Often hypercoagulable states travel together to evoke symptoms, such as dehydration or antiphospholipid antibodies in association with prothrombin G20210A mutations. The take-home-message is that the stroke patient deserves a detailed assessment of their hypercoagulable profile. This should have been done while in hospital, but the general practitioner can check to make sure.

Cardiac consideration is not restricted to stroke prevention but also offers a window to predict post-stroke mortality. Conventional heart rate variability measures were not of prognostic value, but abnormal long-term heart rate dynamics do predict post-stroke mortality. They may have value in risk stratification in stroke.⁷

Carotid artery disease

Carotid vessels are a major alternative source of emboli, but management of carotid disease relies on antiplatelet agents rather than full anticoagulation (if surgery is not warranted).

The North American Symptomatic Carotid Endarterectomy Trial (NASCET)⁸ found that stroke was reduced by 17% where carotid stenosis exceeded 70%, hence becoming the benchmark for ordering endarterectomy. Some advocate surgical intervention with stenosis as low as 60%, even in asymptomatic patients.⁹ Personal preference favours the higher figure.

Stenting is a viable alternative for cardiac vasculopathy and is becoming a respected alternative to carotid endarterectomy.¹⁰ Its exact place remains undefined with growing popularity. Furlan¹¹ reviewed the SAPHIRE (Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy) trial, which showed that carotid artery stenting was safer than carotid endarterectomy in patients at high surgical risk, because of lower risk of myocardial infarction within 30 days after carotid stenting when compared to surgery. Furlan¹¹ reviewed the EVA-35 Study (Endarterectomy versus Angioplasty in patients with Symptomatic Severe Carotid Stenosis in the same issue of The New England Journal of Medicine), which concluded that stenting was more risky than endarterectomy for 30-day incidence of stroke or death. Carotid endarterectomy is also considered a safer option than is stenting in the elderly.¹²

This underpins the need to investigate for carotid stenosis with tools such as duplex Doppler, CTA or MRA or a combination thereof to decide upon appropriate intervention. The general practitioner may initiate both Doppler studies and CTA—and may bypass the neurologist by referring to the vascular surgeon—although most often will rely on a team, including both neurologist and surgeon.

Hyperlipidemia

The meta-analysis of 90 000 patients from studies assessing the benefits of statins in stroke prevention demonstrated that the reduced risk of stroke was particularly reflected in the lowering of low-density lipoprotein cholesterol levels.¹³ Statins have become a basic component of stroke management.

The recent SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels) trial of 4731 stroke or TIA patients concluded that 80 mg of atorvastatin per day reduced the overall incidence of stroke and cardiovascular events. It was associated with an increased incidence of haemorrhagic stroke.¹⁴ Personal preference favours starting with a lower dosage of statin and titrating to effect by monitoring cholesterol profile.

Transient ischaemic attacks (TIAs)

Perhaps the best way to consider TIAs is to equate them with mini strokes that resolve within a day. There is an even more worrying attitude to TIAs than there is to stroke. Because it has resolved by day’s end and very often much sooner, the attitude to TIA is complacent. A recent study confirmed that hospital admissions of TIA patients to a specialised stroke unit has beneficial effect on short-term outcome,¹⁵ and is preferable to home management and nihilism. Reliance on the ABCD² score does not necessarily increase protection by the theoretical admission of TIAs at greater risk^16,17 (see Table 14.1).

TABLE 14.1 ABCD² scores

This reinforces that stroke and TIA should not be taken lightly—they demand referral to a hospital as a matter of urgency. TIA is a warning of an impending more significant ‘brain attack’ and should be treated with respect. TIA mimics, including syncope, seizure, migraine, vertigo and its causes, encephalopathy of non-vascular origin, multiple sclerosis or even transient global amnesia, may confound the picture. It remains far safer, where doubt exists, to have these assessed in hospital rather than expose the patient to risk of stroke. Many of the mimics are themselves worthy of admission, and there should be no shame in referring them to hospital for assessment.¹⁸

Diagnosis of stroke

Correct diagnosis pre-empts appropriate treatment and, while an established stroke is easily diagnosed, the section on TIA highlights the scope of differential diagnoses. The pathophysiology and anatomical site defines the stroke’s expression, be it motor or sensory deficit, loss of eloquent functions of speech, number manipulation, comprehension, orientation, consciousness or more subtle effects determined by smaller lesions.

The mnemonic ‘FAST’ remains a valuable tool for the general practitioner (see Table 14.2) and may be the start of the diagnostic approaches. The Cincinnati Pre-hospital Stroke Scale (CPSS) was developed to help recognise strokes. It has since been modified to produce the ‘Sudden Symptoms’ and ‘FAST’ mnemonic to assist with early stroke recognition (see Table 14.2). Kleindorder et al¹⁹