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Need to know - stroke

Stroke physician Dr Anthony Rudd answers questions from GP Dr Kathryn Griffith on depression, the importance of blood pressure control, the use of ß-blockers and antiplatelet combinations

Stroke physician Dr Anthony Rudd answers questions from GP Dr Kathryn Griffith on depression, the importance of blood pressure control, the use of ß-blockers and antiplatelet combinations

1. In a patient with previous TIA, can we assume that a completed stroke is likely to be embolic?

41188492No. Most TIAs are ischaemic, although occasionally they are shown to be caused by very small haemorrhages (microbleeds). Someone at risk of ischaemic stroke is likely to be also at risk of haemorrhagic stroke. The risk factors, particularly hypertension, are the same. Also, it has been shown in a large population-based register of stroke in south London that people who have a recurrent stroke often have a different type of stroke the second time around. So it is vital that a stroke happening after a TIA is investigated as rigorously as any other.

The only way to differentiate different stroke subtypes reliably is by brain imaging. If someone is on aspirin or anticoagulation after their TIA and they then have a stroke, they should have these drugs stopped until haemorrhage has been excluded.

2. What proportion of strokes are caused by atrial fibrillation and how hard do you look for paroxysmal AF?

About 25% of people admitted with a stroke will be in atrial fibrillation compared to about 4% in the general population. It is difficult to be certain how many of those in AF actually had their stroke as a result of it but unless there are is an obvious alternative explanation it should be assumed the AF is responsible. The appearances of the infarct on the brain scan can also suggest that a stroke is likely to be embolic – for example, a wedge of ischaemia in the cortex or evidence of multiple territory large vessel infarcts. I don't think we look hard enough for paroxysmal AF. In our unit nearly all patients have their cardiac rhythm monitored for about 24 hours after admission but even that probably results in us missing cases. Where the presentation of the stroke suggests the possibility of embolism, or no other cause is found, I would recommend Holter monitoring.

3. At what point after stroke does tight blood pressure control become important?

It's difficult to answer this because we are still waiting for good research to be published in the area. The current National Clinical Guidelines for Stroke (2004) suggest that starting treatment for hypertension should be delayed until two weeks after the stroke. The rationale for this is that there is concern about lowering cerebral blood flow to the ischaemic penumbra. Nearly every patient with a stroke shows a rise in their blood pressure over the first few days and this may be a physiological response to maintain cerebral perfusion.

There are a couple of studies currently looking at earlier intervention to lower blood pressure and trying to ascertain whether pre-existing blood pressure treatment should be continued after acute stroke, but these will not report for a couple of years.

There is a rational argument that patients whose stroke is caused by primary intracerebral haemorrhage should have their blood pressure controlled more aggressively acutely after stroke and I certainly try and keep their systolic pressures below 200mmHg at all times.

4. ß-blockers have been shown to be less effective at reducing stroke. Would this be an indication for changing therapy and have trials shown that any drugs are particularly good at reducing stroke?

I think the most important factor is how effectively the blood pressure is kept under control rather than the specific drug used to achieve this. It is true that ß-blockers perform less well than other antihypertensives but if a patient's blood pressure is well controlled and they are tolerating the drug without any side-effects then I would be tempted to continue without changing the regime.

The most important trial was the PROGRESS trial, which showed that a combination of a long-acting ACE inhibitor – perindopril – and a thiazide diuretic – indapamide – in combination significantly reduced the risk of stroke recurrence in both hypertensive and non hypertensive patients. My practice is therefore to lower the blood pressure as much as the patient can tolerate without side-effects and not use ß-blockers as first- or second-line treatment.

5. What are the indications for a combination of antiplatelet agents rather than aspirin alone?

Combining aspirin with dipyridamole MR 200mg twice daily has been shown to be more effective than aspirin alone in two randomised controlled trials (ESPS2 and ESPRIT). There was some scepticism after the first industry-sponsored trial but almost identical results were obtained in the investigator-led study published a couple of years ago.

It is therefore my policy – and recommended by the national clinical guidelines – to use aspirin alone for the first couple of weeks and then add dipyridamole long-term.

A significant number of patients are unable to tolerate dipyridamole because of headache. This can be reduced by starting with just once-daily treatment for a week before increasing to the full maintenance dose – but this is not evidence based. There is no evidence to support the combination of aspirin with clopidogrel, except possibly after carotid stenting and in patients with recurrent TIAs secondary to carotid stenosis. The MATCH trial, which looked at the combination, found an increased risk of intracerebral haemorrhage without any evidence that there was benefit in reducing stroke recurrence.

6. Should we be using statins in much the same way in stroke as CHD and what is the evidence for this? In particular, how do the numbers needed to treat compare?

This information is helpful when we are trying to persuade patients to take yet more medication.

Statins have a definite role in reducing the risk of recurrence after ischaemic stroke. Their role after haemorrhagic stroke is less clear.

The Heart Protection Study and SPARCL are the main trials that have included large numbers of patients with cerebrovascular disease, and the message from both is that lowering cholesterol is beneficial for almost all patients. The number needed to treat from the SPARCL study to prevent one stroke was 46.

The National Clinical Guidelines for Stroke recommend the use of a statin in stroke secondary prevention where the total cholesterol is more than 3.5mmol/l, or LDL cholesterol is more than 2.5mmol/l.

7. What proportion of patients become depressed after a stroke, and what is the best way to assess this when stroke itself can cause emotional lability?

The figures for the incidence of major post-stroke depression vary quite widely in the literature from about 15% to 50%. The reasons for the differences probably reflect the different types of cohorts in the studies.

Diagnosis of depression can be extremely difficult, particularly in patients with communication problems such as dysphasia. Non-dominant hemisphere strokes can also cause diagnostic problems. Patients with right hemisphere damage not uncommonly have monotonous speech and may have difficulty in maintaining eye contact – these problems can be misinterpreted as being caused by depression.

Similarly, emotional lability can be misdiagnosed as depression. This is when patients have their emotions much closer to the surface and cry or indeed in some cases laugh with minimal provocation, without actually feeling particularly sad or happy. Emotional lability is most frequently seen in patients with bilateral hemisphere damage.

The best way of establishing the diagnosis is the same as for any patient – a careful history and examination for the classical features of depression. Where the patient cannot express their feelings, the GP is dependent on a history from the carers, particularly asking about appetite, sleep and interaction with others.

There may be some cases where a pragmatic trial of antidepressants is justified, carefully monitoring the response over a month and stopping treatment if there is little evidence of improvement.

8. What is the best pharmacological treatment for clinical depression after stroke and are there any particular problems we need to look out for with treatment?

The Cochrane review of antidepressant trials after stroke made rather depressing reading itself. There is no evidence that either tricyclics or SSRIs are effective. However, the number of patients included in such trials is small and it could still be that they do have a positive, albeit small, benefit. Patients with minor depression should be monitored for progression and should be helped to increase social interaction and other psychosocial interventions and take more exercise. Patients with severe depression should be offered either an antidepressant, usually an SSRI, or psychological therapy delivered by a trained practitioner.

There are no specific problems with the SSRIs in stroke patients that are not seen in other patients. They should be monitored for side-effects such as drowsiness, confusion, hyponatraemia and anorexia.

9. After discharge, patients – or often their carers – will ask about prognosis and the likelihood of full functional recovery. How can we assess this?

Recovery is fastest in the early weeks after a stroke. But recovery can continue for months or even years, particularly in the areas of sensory and speech deficits.

It's important to strike the right balance between optimism – so that patients and the carers do not give up too easily – and realism – so that patients don't continue with unrealistic expectations, putting their lives on hold pending the miracle recovery.

There is no formula I can give that will enable you to tell your patients what the percentage chance is of recovery. If there is still severe impairment at three months, it is highly unlikely that the patient will make a full recovery. If the deficits are milder, then the possibility remains.

Encourage your patients to continue working hard to improve function, but at the same time to make the best use of what function remains and to be as active in all domains of life as possible.

10. What are the most common post-stroke complications that GPs will encounter, and how should they be managed?

This question should be the subject of an entire textbook. However, the problems that often arise are:

• thromboembolic disease

• mood disturbance (anxiety and depression)

• pain (from localised musculoskeletal problems arising from motor deficits and from central post-stroke pain)

• spasticity, causing joint contractures

• immobility and pain

• infections (particularly chest and urine), again often from immobility

• pressure sores

• fatigue (nearly universal after stroke and often debilitating)

• sexual dysfunction and other relationship problems

• drug side-effects

• constipation and faecal incontinence

• cognitive impairment (dementia occurs in about 25% of patients after stroke).

There are plenty of other problems that can arise as well. The most important factor in managing them is to identify them in the first place.

Stroke patients – particularly those who have been left with significant residual impairments – may be housebound, often fail to report symptoms because they think there is little that is likely to help and often have a very fatalistic attitude. The primary care team therefore needs to adopt a very proactive approach and then work collaboratively with secondary care to ensure the best possible care is provided.

11. CHD has had a massive investment with the NSF and numerous NICE guidelines. Why has stroke been neglected? And, in your opinion, which aspects of primary care stroke management should be prioritised?

Stroke is beginning to catch up. NICE guidelines on acute stroke and TIA will be published in July, and last December the Department of Health in England published its National Stroke Strategy. This contains a radical agenda for stroke over the next 10 years and is accompanied by the promise of £105m to help with its implementation over the next three years.

Why has stroke not had the attention it deserves? I suspect it is because the average age of a stroke patient is 75 and we live in a very ageist society.

I think there should be three priorities. First, to improve the public's knowledge of how to prevent stroke and how to recognise it. Second, to ensure secondary prevention is optimised and maintained long-term.

We have performed very badly in this area. For example, in the last National Audit of Stroke, less than a third of patients with known AF were admitted on warfarin and about half of patients with previous stroke who were being admitted with a further event were not taking any anti-thrombotic.

Perhaps even more important than my first two priorities is the role of primary care in co-ordinating and delivering longer-term rehabilitation and support to the patient and their families. Secondary care services tend to abandon patients after discharge from hospital. This is an area where the expertise of primary care can make a huge difference to patients' lives.

12. A recent study from Finland has suggested that listening to music improves recovery after stroke. What do you think the mechanism is for this and could it be used in the UK?

This was a very small study and I think does need to be replicated with a larger scale controlled trial. I would not be surprised if music did have a positive benefit. There are very few of us who are not moved emotionally by some form of music and one of the major problems after stroke is an element of sensory and emotional deprivation resulting from people being cut off from their friends, colleagues, work and leisure activities.

Stimulating the brain is the basis of the conventional therapies. Physiotherapy, for example, clearly works and does so – at least in part – through repetitive stimulation of neurones, encouraging dendritic sprouting and opening of new pathways in the brain to allow function to be resumed.

I suspect that music might have its effect in similar ways in addition to having a positive effect on mood and general wellbeing. Even the British might benefit!

13. A Mediterranean diet has been shown to be beneficial in coronary heart disease. Does it have the same benefit in reducing stroke?

The evidence in stroke is much less strong than in heart disease, but I suspect this is more to do with less research being performed rather than a lack of benefit. The disease process causing ischaemic heart disease and ischaemic stroke is very similar and it would be surprising if there was much difference in the effect of dietary modification.

The National Stroke Guidelines therefore recommend that people should eat at least two portions of fish each week, one of which should be oily and eating five or more portions of fruit and vegetables per day. Advice also needs to be given about limiting salt and saturated fat intake and reducing meat intake. Personally I also supplement that with a couple of units of high quality wine.

Dr Anthony Rudd is stroke physician at Guy's and St Thomas' Hospital London, chair of the NICE acute stroke and TIA guidelines development group and chair of the Intercollegiate Stroke Working Party at the Royal College of Physicians

Competing interests: None declared

What I will do now What I will do now

Dr Kathryn Griffiths responds to the answers to her questions

• Even if a patient has had a previous TIA, it is important to rule out a haemorrhagic stroke with brain imaging.
• In AF, only a scan can prove the stroke is an infarct and likely to be embolic and related to the AF. Some patients will need Holter monitoring to rule out paroxysmal AF.
• It's important to have tight BP control even though this isn't reflected in the QOF.
• The choice of agents is not as important as good control, but ß-blockers should not be first-line agents.
• We need to be aware that recovery is fastest in the early weeks but can continue for months or years.

Dr Kathryn Griffith is a GP in York|

thp Stroke

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