Advanced reading - transient ischaemic attack and stroke prevention
The following article was published in Australian Doctor, Australia’s leading newspaper for general practitioners. It is abridged and re-published here for Itsmyhealth visitors who already have a good understanding of the topic. This article does not replace consultation with your doctor and you should always discuss your treatment and anything you are uncertain about with your doctor.
Epidemiology, risk factors and aetiology
Secondary prevention after stroke or TIA
STROKE and transient ischaemic attacks are intrinsically linked and, although they warrant discussion as separate entities, they have a shared pathophysiological basis that includes them under the single umbrella of cerebrovascular disease.
Stroke is Australia’s second most common killer after coronary heart disease, and a leading cause of disability.1 In 2011, Australians will experience about 60,000 new and recurrent strokes, which equates to one stroke every 10 minutes.2 Strokes cost Australia an estimated $2.14 billion a year, underscoring the magnitude of the adverse public health impact and the need to improve outcome after stroke.3
Ischaemic stroke is defined as the sudden onset of neurological deficit as a result of ischaemia. Transient ischaemic attack (TIA) is defined as a transient neurological event that lasts from less than 24 hours to one that typically lasts less than one hour, and that is not associated with changes on neuro-imaging.4
Within the first 12 months after an initial stroke, 8-12% of patients experience a second stroke, and patients who have TIA have a 5-7% risk of stroke in the following week.5,6 Clearly not only is optimal management of an index event essential, but it is also paramount to address the overall vascular risk to prevent recurrent strokes.
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STROKE aetiology is divided into ischaemic (comprising of athero-thrombotic and embolic), and haemorrhagic. About 85% of strokes are ischaemic, and about 15% are haemorrhagic. In this article we concentrate on the mechanisms underlying ischaemic stroke.
Mechanisms of brain ischaemia include:
- Thrombosis of an artery supplying the brain, related to in-situ processes within that artery.
- Embolic occlusion of a cerebral artery.
- Global hypoperfusion caused by a systemic process such as shock.
It has become more useful to think about the vasculature as a single entity, as there are epidemiological data linking cerebral, coronary and peripheral vessels, and the aetiological risk factors underlying the pathology in them are similar (see box above right).
A recent publication reported the prevalence of common atherosclerotic risk factors in a cohort of patients with stroke or TIA.7 The mean age ± standard deviation was 71 ± 15 years. Of these:
- 15% had previously diagnosed diabetes; 10% were diagnosed with diabetes during admission.
- 62% had previously diagnosed hypertension; another 7% were diagnosed during admission.
- 88% of patients had dyslipidaemia.
- 33% had all three risk factors concurrently.
Clinically the division of strokes into age groups is useful aetiologically. Strokes in young patients (often defined as those under 40) are associated with distinct aetiological factors, in particular, thrombophilic disorders and valvular heart disease. Young patients warrant more extensive investigation to exclude some of these less common conditions.
Risk factors for atherothrombotic stroke
- Age >65
- Diabetes mellitus
- Family history of cerebrovascular events
- History of TIAs
- Involvement of other vascular territories, eg, ischaemic heart disease, peripheral vascular disease
- Thrombophilic conditions
- Extracranial arterial dissection (figure 1)
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STROKE can be subclassified by the pathological process and the vascular distribution affected. Defining the overall pathological process is critical for making decisions regarding thrombolysis and inpatient therapy, and for prognosis.
Identifying the clinical features of a stroke and using the Oxfordshire Ischaemic Stroke Subtypes definitions (table 1) may help identify the vascular distribution of the stroke.8 Unfortunately, interobserver agreement on the vascular territory is at best fair.
Thus, history and physical examination remain important in the clinical diagnosis of strokes. In a community-based study of diagnostic accuracy, clinical diagnosis by primary care physicians practising in an emergency setting had a sensitivity of 92% for stroke and TIA.9
Clinically several factors significantly increase the probability of a stroke being haemorrhagic, including:
- Neck stiffness.
- Seizures accompanying the neurological deficit.
- Diastolic blood pressure >110mmHg.
However, intracerebral haemorrhage and ischaemic stroke can only be reliably differentiated using neuro-imaging, emphasising the need for early referral for non-contrast or advanced modality CT scan or perfusion–diffusion MRI if available (see Investigations, page 22).
The National Institute of Health Stroke Scale (NIHSS) is a commonly used classification of stroke severity at the time of presentation.11 It provides a structured neurological examination with diagnostic and prognostic value. This scale is particularly useful in frontline work at EDs and other pre-hospital settings.
There is no reliable way to determine if the abrupt onset of neurological deficits represents reversible ischaemia without subsequent brain damage, or if the ischaemia will result in permanent damage to the brain (ie, a stroke). Therefore, patients presenting with reversible neurological symptoms suggestive of a TIA should be managed with the same sense of urgency as for an established stroke and should be referred urgently for appropriate investigations and management.
Indications for admission to hospital for patients with TIA follow the guidelines set out by The National Institute of Neurological Disorders and Stroke (NINDS) score.11 This is clearly modifiable for individual facilities and the availability of clinical and radiological support services.
In general practice it is useful to be aware of conditions that share signs and symptoms with stroke and that should be included in the differential diagnosis when assessing patients with a suspected stroke. Hypoglycaemia, migraines and seizures may present with some stroke-like features. A known history of cognitive impairment, non-neurological abnormal physical findings, and decreased level of consciousness in patients with suspected stroke should suggest to the clinician that the presentation may not be due to stroke.
A diagnosis of TIA is paramount to decrease the chance of an established stroke developing. On diagnosis of a probable TIA, the ABCD2 score (see box right) is a simple scoring system that can be used to stratify patients who need urgent specialist assessment within 24 hours (ABCD2 score ≥4), and those who are suitable for outpatient assessment if tests can be performed within 48 hours (ABCD2 score <4).14 Patients not admitted for investigation should be reviewed in a TIA clinic if available. If not available, the investigations (described in the next section) should be performed.
People with crescendo TIA (two or more TIAs in a week) should be treated as being at high risk of stroke, even if their ABCD2 score = 3.
Patients who have had a TIA but who present late (more than one week after their last symptom has resolved), should be treated as though they are at lower risk of stroke.
|Table 1: Oxfordshire Ischaemic Stroke Subtypes
|Total anterior circulation infarct (TAC)
- New higher cerebral dysfunction (eg, dysphasia, dyscalculia, visual–spatial disorder) and;
- Homonymous visual field defect and
- Ipsilateral motor and/or sensory defect involving two areas of the face, arm or leg
|Lacunar infarct (LACI)
||Pure motor or pure sensory symptoms, sensorimotor stroke, or ataxic hemiparesis; face–arm and arm–leg syndromes
|Partial anterior circulation infarct (PACI)
- Only two of three TACI components, or
- Higher cerebral dysfunction alone, or
- A motor or sensory deficit more restricted than those classified as LACI (eg, confined to one limb or to face and hand, but not the whole arm)
|Posterior circulation infarct (POCI)
||Any one of the following:
- Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit
- Bilateral motor and/or sensory deficit; disorder of conjugate gaze
- Cerebellar dysfunction without ataxic hemiparesis; isolated homonymous visual field defect
ABCD2 is a prognostic score used to identify people at high risk of stroke after a TIA. It is calculated based on:
A: Age (≥60 years = 1 point)
B: Blood pressure at presentation (≥140/90mmHg = 1 point)
C: Clinical features:
- Unilateral weakness = 2 points
- Speech disturbance without weakness = 1 point
D: Duration of symptoms:
- ≥60 minutes = 2 points
- 10-59 minutes = 1 point
D: Diabetes = 1 point
Total scores range from 0 (lowest risk) to 7 (highest isk)
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DISTINGUISHING bleeding from ischaemia is based on the clinical history and examination. However, corroborating the clinical impression is always necessary by brain imaging that can show subarachnoid or intra-parenchymatous blood, a brain infarct, or no apparent bleeding or infarction.
In patients with acute-onset focal brain symptoms, the absence of bleeding and important non-vascular pathology (eg, neoplasm, abscess) on brain neuro-imaging is usually sufficient to indicate that the problem is brain ischaemia, especially when the patient has risk factors for stroke.
Non-contrast CT images can be acquired rapidly with modern multi-detector scanners and at sub-millimetre image resolution. CT is considered sufficiently sensitive for detecting mass lesions, such as a neoplasm or abscess, as well as for detecting acute haemorrhage. However, it may not be sensitive enough to detect an ischaemic stroke, especially if it is small, acute, or in the posterior fossa (ie, brainstem and cerebellar areas).
Early features of ischaemia on CT include local cortical/gyral swelling and sulcal effacement (narrowing) secondary to cytotoxic oedema. Another early radiological sign is the hyperdense ‘middle cerebral artery sign’, in which a hyperintensity is noted within the lumen of the proximal middle cerebral artery due to thrombotic occlusion of this vessel.
CT has 95-100% sensitivity for detecting subarachnoid blood in the first 12 hours. However, unlike the case for ischaemic stroke, the sensitivity greatly decreases over time as the subarachnoid blood is cleared. The sensitivity of subarachnoid haemorrhage detection by CT drops to about 50% after one week, and haemorrhage is not detectable by CT after a period of about 2-3 weeks.
Ischaemic lesions may become apparent after 48-72 hours. This feature is sometimes used to confirm a stroke in patients with normal non-contrast CT on admission by repeating the CT after 72 hours. This is useful if an MRI or newer advanced CT modalities are not readily available.
Neuro-imaging of vascular territories that may suggest an atherosclerotic aetiology includes:
- Left cerebral hemisphere, supplied by the internal carotid artery and its anterior cerebral artery and middle cerebral artery branches.
- Right cerebral hemisphere, supplied by the anterior circulation (anterior cerebral artery and anterior communicating artery).
- Brainstem or cerebellar territory, supplied by the verte-brobasilar arteries.
- Left posterior hemisphere, supplied by the left posterior cerebral artery.
- Right posterior hemisphere, supplied by the right posterior cerebral artery.
- Small deep hemisphere lesion (lacunar infarct).
CT is considered sufficiently sensitive for detecting mass lesions, such as neoplasm or abscess, as well as for detecting acute haemorrhage.
MRI and perfusion CT
Recent evidence suggests the use of thrombolysis may be beneficial even when used beyond the three hours post-stroke period usually recommended. This has resulted in the use of more sophisticated scanning modalities to try to document a penumbral area (potentially salvageable parenchyma) that may benefit from reperfusion.
These imaging techniques include both diffusion-weighted and perfusion-weighted imaging MRI technologies, and perfusion CT (figures 2-4). The modality chosen is often determined by the resources available in the private sector or the in-hospital radiology service to which the patient is referred.
A recent Cochrane review on advanced imaging modalities showed summary estimates for MRI diffusion weighted imaging were sensitivity 0.99 (95% confidence interval [CI] 0.23 to 1.00) and specificity 0.92 (95% CI, 0.83 to 0.97). The summary estimates for CT were: sensitivity 0.39 (95% CI, 0.16 to 0.69) and specificity 1.00 (95% CI, 0.94 to 1.00).12 The apparently better diagnostic accuracy of MRI compared with CT occurred in patients with a high pre-test probability of stroke. Therefore this may not apply when MRI is used in the broad range of unselected patients presenting with suspected acute stroke usually seen in routine clinical practice.
MRI cannot be performed on people with certain types of implanted devices (eg, pacemakers) or in those with claustrophobia or delirium, as motion in the scanner degrades the image resolution. The increased sensitivity of multimodal MRI sequences (T1- and T2-weighted and fluid attenuated inversion recovery (FLAIR) images [figure 5]) has documented that patients presenting with TIAs have ischaemic lesions in about 50% of cases.
Newer modalities involving perfusion scanning protocols using CT can also identify the potentially salvageable penumbral area and allow experienced clinicians to extend the time window for reperfusion using thrombolysis in carefully selected individuals. Perfusion CT offers both qualitative and quantitative measurements of cerebral blood flow and cerebral blood volume.
There has been recent emphasis on the radiation exposure of CT scans. A 64-slice scanner delivers a mean effective dose from baseline non-contrast CT brain scan of 2.7mSv, while additional CT angiogram and CT perfusion scans take the mean effective dose to 13mSv — about five times the exposure of an unenhanced CT brain. However, in a single CT — even with prolonged exposure to radiation with the new modalities — this is unlikely to be of any clinical relevance. It is not currently an issue that concerns physicians, as CT of the brain involves relatively low radiation exposure.
The volume (ie, size) of the lesions identified by diffusion weighted imaging and perfusion weighted imaging MRI may not only serve a diagnostic purpose but may also predict initial clinical severity, final infarct size and late clinical outcome in anterior-circulation stroke syndromes, thus serving prognostic purpose as well.
Sometimes MRI shows white-matter hyperintensities. These have recently been associated with an increased risk of subsequent stroke, dementia and death.13
Not all patients with TIA need immediate brain imaging.15 Patients should be assessed by a specialist before a decision on imaging is made. Brain imaging after suspected TIA is recommended when:
- The vascular territory affected is uncertain (anterior or posterior circulation) and the patient is being considered for carotid endarterectomy.
- The pathology underlying the patient’s neurological symptoms is uncertain, eg, alternative diagnoses may include migraine, epilepsy or tumour.
- Intracerebral haemorrhage needs to be excluded, for example, patients taking anticoagulants or with long duration of symptoms (eg, for subdural bleeds symptoms can be for hours, days or weeks).
Because many patients are undergoing non-contrast CT scanning during the early phase of diagnosis, there is a trend to use CT angiography to document vascular pathology. CT angiography not only allows non-invasive assessment of the intracranial and extracranial circulation, but can exclude dissection and arte-riovenous malformations that may present with neurological signs and symptoms.
Duplex Doppler scan
Duplex Doppler examination of the carotid arteries should be carried out as soon as possible (figure 1). This is often limited by the availability of ultrasono-graphic resources. The role of carotid endarterectomy and carotid stenting in the prevention of early stroke recurrence in patients with ipsilateral carotid artery stenosis has increased the urgency of this investigation. The results are given in the form of Doppler velocities in the different carotid territories, and reported as arterial stenosis as a percentage of the normal.
Laboratory investigations recommended for patients diagnosed with probable stroke include blood glucose, serum electrolytes and renal function, FBC including platelet counts, other throm-botic parameters such as INR and activated thrombo-plastin time.
An electrocardiogram is essential to rule out arrhythmias, especially atrial fibrillation, and other findings associated with established valvular heart disease or coronary artery disease.
If any evidence of cardiac disease is present, echocardiography will further delineate the pathology and exclude intracardiac thromboembolic sources. Echocardiography may also point to potential left-to-right shunts and explore the aortic arch for atherosclerotic plaques.
Selected patients may require more intensive investigation, including lumbar puncture, EEG and toxicology screen, usually when an alternative diagnosis is suspected.
Investigations in development
Current studies are focusing on the role of biomarkers in the diagnosis of stroke. Measurement of biomarkers related to the aetiology of cardio-embolic stroke, such as B-natriuretic peptide and D-dimer proteins, or PITX2 and ZFHX3 genes, might in the future guide the early use of other diagnostic tests and accelerate the implementation of optimal secondary prevention.
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DATA from the years 1994-99 suggest that although there do not seem to be significant differences in mortality due to stroke during that period, the ‘recovery time from stroke’ was significantly decreased. Most importantly, the improvement in recovery time was significant in each age group and in each comorbidity and disability stra-tum.14
Tissue plasminogen activator
Currently the only specific approved therapy for acute ischaemic stroke is IV tissue plasminogen activator (tPA) given within 4.5 hours of the onset of symptoms, provided there is no contraindication to tPA. However, tPA use has been limited due to the short treatment window, concerns about the limitations of CT-based diagnosis, and fear of haemorrhage. Advances in neuro-imaging may allow differentiation of the infarct core and the penumbral area (potentially salvageable parenchyma), leading to extension of the therapeutic window.
Much of the literature addresses the use of tPA within three hours of stroke onset, as described in the NINDS trial.15 The 3rd European Cooperative Acute Stroke Study (ECASS III)showed that the extension of the treatment window to 4.5 hours is efficacious and safe in selected patients.16
On the basis of an absolute increase in favourable outcomes of 10% between the tPA alteplase and placebo groups in ECASS III among patients who actually received treatment according to the protocol, the number needed to treat to produce one additional excellent recovery is only 10. The number needed to treat to achieve a measurable advantage in functional outcome score is probably only four.
The introduction of aspirin should probably be delayed for 24 hours after thrombolysis due to increased risk of haemorrhagic transformation of the stroke.
It is important to note that although thrombolysis is an exciting development in the management of acute stroke, most patients will not receive thrombolysis because of delayed presentation or lack of local facilities and expertise, especially in regional and rural centres. Currently fewer than 10% of patients receive thrombolysis.
Extension of the therapeutic window may allow for the development of models of management that would include air or road transport to facilities with throm-bolysis capacity. This may resolve some of the challenges of offering equitable care to regional or rural communities where thrombolysis is not currently available.
Once the patient is admitted there are factors that promote short- and medium-term survival. One of the main determinants of good outcomes after stroke is being admitted to a stroke unit during the acute-stroke-phase. The most important organisational factor is to be assessed early by a stroke team.
The stroke specialist’s multidisci-plinary team plays an active role in the evaluation of patients’ needs. It is important for GPs to know that patients who are not admitted to hospital may still benefit from the expertise of the individuals in the stroke care team and the GP may have to co-ordinate this to ensure the patient receives best care.
Preventing aspiration by adequate swallowing assessments and feeding protocols is an important part of early stroke management.
Rehabilitation is an integral part of successfully reintroducing an individual into the community after a stroke. Factors leading to patients’ perception of successful rehabilitation include:
- Being treated with humanity.
- Being acknowledged as individuals.
- Having their autonomy respected.
- Having confidence and trust in professionals.
- Dialogue and exchange of infor-mation.25
These principles should be extended to the patient’s interactions in general practice.
Treatments in development
Neuro-protective therapies such as the use of magnesium, statins, and induced hypothermia are being explored.
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CHADS2 VAS score for the use of warfarin
Congestive heart failure (score = 1)
Hypertension (score = 1)
Age (>75 score = 2)
Diabetes (score = 1)
Stroke and/or TIA (score = 2)
Vascular disease (score = 1)
Age (65-74 score = 1)
Sex (female gender score =1)
SECONDARY prevention of recurrent events after a stroke or TIA focuses on risk reduction and the introduction of antiplatelet or antithrombotic therapy.
Aspirin-based therapy remains the mainstay of prevention in atherothrombotic stroke. Aspirin in a daily dose of 160-300mg initiated within 48 hours of symptom onset results in a net decrease in morbidity and mortality due to acute ischaemic stroke. The main body of evidence for this recommendation comes from the International Stroke Trial and the Chinese Acute Stroke Trial.17,18 Overall, the numbers needed to treat are relatively large. However, the benefits outweigh the small but measurable risk from aspirin therapy.
The combination of dipyri-damole and aspirin (Asasan-tin) has been recommended as first-line therapy by several guidelines. The relatively poor tolerability of full-dose dipyridamole (because of headaches, flushing, gastrointestinal side effects and dizziness) reduces the compliance rate. This can be improved by slow up-titra-tion to the full dose over several days. Although low-dose dipyridamole is better tolerated than full-dose treatment, there is no evidence that low-dose dipyri-damole is effective.
Clopidogrel is a powerful platelet inhibitor with a well-established role in coronary artery disease. In the setting of secondary prevention of stroke, the CAPRIE study showed a reduced incidence of stroke in those treated with clopidogrel versus aspirin (number needed to treat 200 per annum).19 However, this beneficial effect was limited to those with peripheral vascular disease.
The MATCH study showed that the addition of clopidogrel to aspirin reduced the risk of ischaemic stroke (absolute risk reduction 1.0%) but this benefit was counteracted by an increase in bleeding (absolute risk increase 1.3%).20 There was no benefit from the addition of clopidogrel to aspirin in the CHARISMA Study.21
Clopidogrel is thus recommended for patients with aspirin intolerance or allergy, or for those who cannot tolerate dipyridamole.
An important and common drug interaction between proton-pump inhibitors and clopidogrel reduces the conversion of clopidorgel to its active metabolite, due to decreased CYP2C19 activity. Pantopra-zole is free of this interaction and is the preferred PPI when co-prescribing with clopidogrel.
Warfarin remains the gold standard for therapy in patients who have AF and meet the risk–benefit criteria of the new CHADS2 VAS score. This is a comprehensive score taking into account the factors shown in the box above. A score of zero recommends the use of aspirin or nothing, a score of 1 the use of aspirin or warfarin, and a score >1 the use of warfarin for secondary prevention of stroke in patients with A F.
The new guidelines place additional emphasis on the risk of bleeding with the mnemonic HASBLED (Hypertension, Abnormal liver and/or renal function, previous Stroke, previous Bleeding problems, Labile INR results, Elderly >65 years, and Drugs that may increase the risk of bleeding or alco-hol).22
Many of the so-called low-risk patients may actually benefit from the use of a vitamin K antagonist such as warfarin.
A recent systematic review confirmed the underuse of oral anticoagulation therapy for patients with real-world AF with an elevated risk of stroke, with only 60-70% of eligible patients treated with warfarin.23
The ACTIVE study recruited patients in AF at high risk of stroke who could not take warfarin. The addition of clopidogrel to aspirin reduced the risk of stroke by 0.9% per annum and increased the risk of major bleed by 0.7% per annum.24
Symptomatic extracranial internal carotid artery stenosis poses a high short-term risk of ischaemic cerebral stroke, as high as 20-30% in the first three months. Carotid revascularisation is an integral part of the preventive strategy in patients who meet the current criteria for revascularisation. The criteria for intervention include symptomatic carotid artery stenosis ≥70% (peak systolic velocity >210cm/s).
The procedures currently available include surgical carotid endarterectomy (CEA), carotid artery angio-plasty and stenting. Studies have suggested the benefit of CEA or stenting diminishes with the time from the index event, emphasising the need for urgent referral to a vascular surgeon if the patient meets the criteria for intervention.
There is an ongoing debate about the role of these two procedural alternatives. A recent systematic review concluded that carotid endarterectomy was superior to carotid artery stenting for short-term outcomes but the difference was not significant for intermediate-term outcomes. This difference in benefit was mainly for non-disabling stroke.25 During the peri-procedural period, there was a higher risk of stroke with stenting and a higher risk of MI with endarterectomy.
The management of patients with asymptomatic high-grade carotid stenosis (figure 6) has been a topic of active debate, with proponents on both sides. In 2009 the European Society of Vascular Surgery published guidelines recommending CEA in asymptomatic men under 75 with 70-99% stenosis, if the perioperative stroke and death rate is <3%. CEA should be considered in younger, fit women. Transcranial Doppler showing micro-emboli may help risk-stratify this cohort to a higher-risk group and thus more likely to benefit from CEA.
As medical therapy improves, the annual rate of stroke in medically treated patients may well drop to under 1% and the risk:bene-fit ratio for CEA may well change in favour of optimal medical therapy in asymptomatic patients.
Physicians should keep in mind that other common clinical interventions, including blood pressure control, lipid lowering, glucose control in dysglycaemia, and smoking cessation, are each about three times more effective than aspirin at preventing future stroke.
The target-driven management of hypertension in patients after cerebrovascu-lar events is the single most important treatable risk factor for recurrent stroke, with about 60% of strokes attributed to hypertension. A recent meta-analysis has shown an average decrease in blood pressure of 5.8 mmHg reduced the incidence of stroke by 42% over a 2-5-year follow-up.26
BP targets for cerebrovas-cular disease have not been specifically defined, but it is not unreasonable to use established a BP target of ≤140/90mmHg. The BP should be lowered gradually over several months to minimise side effects, including hypotensive symptoms due to failure of autoregulation of cerebral blood flow. The choice of antihypertensive should be individualised to the patient’s comorbidities, with diuretics, ACEIs, ARBs and calcium-channel block-ers being favoured.
Smoking-cessation programs should be encouraged, as the patient’s health will significantly benefit beyond its effect on stroke prevention.
A meta-analysis has shown the benefit of statins in reducing the rates of stroke and cardiovascular events is independent of cholesterol levels. Given early benefits in trials of acute coronary syndromes, statin initiation during hospitalisation for first ischaemic stroke of atherosclerotic origin is probably justified and may also increase the rates of long-term use.
Falls make up a significant number of complications after stroke. The only intervention shown to be effective in reducing falls is vitamin D for female stroke survivors in an institutional setting.
Ongoing support for carers
It is important to appreciate the toll that a stroke places not only on the patient’s wellbeing, but also on their family and carers. Studies have demonstrated that the stress places family carers at risk for developing depression, poor quality of life and health problems. They need support and links with community-based stroke support groups. Social workers or community health nursing facilities may need to be accessed to ensure appropriate management of the family and avoid carer burnout.
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- Johnson SC, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet 2007; 369:283–92.
- Mangset M, et al. ‘We’re just sick people, nothing else’: ... factors contributing to elderly stroke patients’ satisfaction with rehabilitation. Clinical Rehabilitation 2008; 22: 825-35.
- Marler JR, et al. Early stroke treatment associated with better outcome: the NINDS rt-PA stroke study. Neurology 2000; 55:1649-55.
- Tyrrell P, et al. Diagnosis and initial management of transient ischemic attack. Clinical Medicine 2010; 10:164-67.
- Yew, K, Cheng, E. Acute stroke diagnosis. American Family Physician 2009; 80:33-40.
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