Diagnosis and management of astute ischaemic stroke

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  1. http://orcid.org/0000-0002-4226-7681Robert Hurfordane,
  2. Alakendu Sekhar2,
  3. Tom A T Hughesiii,
  4. http://orcid.org/0000-0001-9535-022XKeith W Muir4
  1. 1 Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK
  2. ii Department of Neurology, Walton Middle for Neurology and Neurosurgery, Liverpool, U.k.
  3. 3 Department of Neurology, University Hospital of Wales Healthcare NHS Trust, Cardiff, U.k.
  4. 4 Constitute of Neuroscience and Psychology, University of Glasgow, Glasgow, U.k.
  1. Correspondence to Professor Keith W Muir, Institute of Neuroscience and Psychology, University of Glasgow, Glasgow G51 4TF, United kingdom; keith.muir{at}glasgow.air-conditioning.uk

Abstract

Acute ischaemic stroke is a major public health priority and volition become increasingly relevant to neurologists of the hereafter. The cornerstone of effective stroke care continues to be timely reperfusion handling. This requires early recognition of symptoms by the public and first responders, triage to an appropriate stroke centre and efficient assessment and investigation by the attention stroke team. The aim of treatment is to achieve recanalisation and reperfusion of the ischaemic penumbra with intravenous thrombolysis and/or endovascular thrombectomy in accordingly selected patients. All patients should be admitted directly to an acute stroke unit of measurement for close monitoring for early neurological deterioration and prevention of secondary complications. Prompt investigation of the mechanism of stroke allows patients to start advisable secondary preventative handling. Future objectives include improving accessibility to endovascular thrombectomy, using avant-garde imaging to extend therapeutic windows and developing neuroprotective agents to forestall secondary neuronal damage.

  • STROKE
  • CEREBROVASCULAR DISEASE
  • NEUROANATOMY
  • NEUROEPIDEMIOLOGY
  • NEURORADIOLOGY
  • REHABILITATION
  • DYSPHAGIA

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  • STROKE
  • CEREBROVASCULAR DISEASE
  • NEUROANATOMY
  • NEUROEPIDEMIOLOGY
  • NEURORADIOLOGY
  • REHABILITATION
  • DYSPHAGIA

INTRODUCTION

Stroke is the fourth leading crusade of death and the largest cause of adult neurological disability in the Great britain.1 2 The associated socioeconomic brunt is huge; the aggregate cost of stroke, including long-term healthcare, rehabilitation and loss of employment, is estimated to be £25.6 billion per twelvemonth.3 As such, it is one of the key diseases targeted by the National Health Service (NHS) Long Term Programme in England and Wales.4

In contrast to most other countries around the world, stroke medicine in the UK is not the sole preserve of neurologists; indeed, most stroke consultants in the NHS are geriatricians. While stroke medicine is indisputably multidisciplinary, appropriately trained neurologists are well placed to manage stroke and its mimics. In the Britain, the new neurology training curriculum will produce consultants trained in stroke medicine, with the potential to expand the stroke workforce.4 Here, we review the diagnosis and management of acute ischaemic stroke and transient ischaemic attack (TIA) for the practising neurologist.

Service pattern

The introduction of intravenous thrombolysis with recombinant tissue-type plasminogen activator (rtPA, alteplase) to treat acute ischaemic stroke required a revolution in the organisation of stroke care. Recognition that 'time is brain' collection constructive public and prehospital sensation campaigns, such as the 'Face, Arm, Speech, Time' (FAST) test5 and rapid prehospital triage to designated centres.

The organisation of stroke care depends upon local geography, simply the implementation of dedicated acute stroke pathways varies widely in the Britain. Comprehensive stroke centres provide all aspects of acute stroke care. Triage of patients eligible for endovascular thrombectomy directly to a comprehensive stroke centre (the 'mothership' model) may ameliorate the likelihood of skillful issue, even if other hospitals are closer. Primary stroke centres are usually smaller centres that initiate intravenous thrombolysis and transfer patients eligible for endovascular thrombectomy to a comprehensive stroke middle, the so-chosen 'drip-and-ship' model.6 Rural hospitals without a stroke squad tin can be linked with stroke centres past telemedicine for thrombolysis calls.7 8 The central attribute of whatever stroke service model is that patients can access specialist expertise, neuroimaging and stroke unit care without delay.ix

The distinction between TIA and stroke cannot exist made while the patient remains symptomatic; therefore, all patients should be assessed rapidly. Patients with a completed TIA (symptom resolution within 24 hours) or pocket-size, non-disabling, stroke crave prompt mechanistic investigation and secondary preventative handling, with good review within 24 hours recommended for all suspected cases.x Organisational models to reach this commonly include rapid-access clinics (effigy 1). The remainder of this article focuses on the assessment and treatment of astute disabling ischaemic stroke.

Diagnosis

Initial history

As with all aspects of neurology, the history is crucial for diagnosis. Even so, in the setting of acute stroke, details demand to be acquired efficiently and focused on answering a few fundamental questions. Collateral history from witnesses or family members is essential every bit the nature of the deficit ordinarily prevents patients themselves from giving a reliable history.

'When was the patient final seen to be well?' Early on decision of whether the patient is within the reperfusion therapy treatment window sets the footstep of subsequent investigations and aids the triage of simultaneous referrals. Symptom onset should be documented as a clock time to avoid defoliation. The fourth dimension recorded for unwitnessed events or 'wake-up' strokes should exist when the patient was definitely last well (rather than when found); the surrogate utilize of an activity can be useful, for example, waking to become to the toilet or successfully using a mobile telephone.

'How quickly did the symptoms develop?' Stroke symptom onset is usually sudden, although notable exceptions include the stuttering nature of capsular warning syndrome, or prodromal symptoms of basilar artery occlusion. Fluctuating severity is common in the early on hours after stroke, and initial improvement may be followed by deterioration, especially among those with intracranial vessel occlusion. More gradual evolution of symptoms may propose alternative diagnoses.

'Is in that location any significant past medical and drug history?' A brief overview of the patient'south groundwork, especially vascular risk factors, will influence the diagnostic decision process; these details can sometimes exist obtained from electronic medical records before the patient'due south arrival. Risk factors associated with ischaemic stroke include cigarette smoking, hypertension, hypercholesterolaemia, diabetes mellitus, cardiac or peripheral vascular disease, and drugs of abuse. A history of carotid stenosis or atrial fibrillation may suggest a crusade.11 Reviewing the listing of medication helps to screen for known relevant diagnoses, take a chance factors for stroke, and whether the patient is taking oral anticoagulation therapy as a potential contraindication to thrombolysis.

Stroke mimics account for at least 20–25% of astute presentations and many of them can be suspected from the history. In ane study, the five most frequent stroke mimics were seizure, syncope, sepsis, migraine and encephalon tumours12; detailed reviews tin be plant in Applied Neurology. 13 14

Posterior circulation strokes are misdiagnosed 3 times more often than anterior apportionment strokes, equally they ofttimes present with non-specific symptoms, including isolated 'dizziness' (vertigo or disequilibrium) or headache.xv Acute onset vertigo or disequilibrium with an boosted posterior circulation symptom should necessitate further cess.

Examination

An overview of the patient can exist made immediately and should focus on the level of consciousness, head and/or gaze deviation, and laterality of purposeful movements. As in any emergency state of affairs, an initial screen of the airway, breathing and circulation and vital signs will establish cardiovascular stability and suitability to go to scan.

Up to 80% of patients with acute ischaemic stroke have an elevated claret pressure (BP) (≥140 mmHg systolic),sixteen which spontaneously improves over the following week17 –nineteen and is associated with poorer outcomes in both ischaemic stroke and intracerebral haemorrhage.twenty 21 The cause of transient mail-stroke hypertension is unknown, but potential mechanisms include disturbed cognitive autoregulation or non-stroke causes such as urinary retention or psychological stress.22 Pyrexia is also common and could reflect aspiration pneumonia, urinary tract infection or infective endocarditis.23

A focused, rather than extensive, neurological examination should be performed in order to identify the affected vascular territory and to quantify physical impairment using the National Institutes of Wellness Stroke Calibration (NIHSS). Limitations to clinical examination in the hyperacute setting include the immaturity of physical signs (such every bit hypertonia or brisk reflexes) and the degree of patient cooperation. In agitated or dysphasic patients, at that place is a greater reliance on careful observation when assessing limb paresis, center movements or visual fields.

The NIHSS is the nearly commonly used neurological deficit rating scale, with a maximum score of 42 (hypothetical due to several mutually exclusive items). Its advantages include an accredited training and certification arrangement (http://www.nihstrokescale.org/), quick completion time (≤10 min24) and facilitation of communication betwixt team members. It may be used to monitor deficit severity, to identify neurological deterioration and to select patients for reperfusion therapy. Its limitations include the underrepresentation of non-ascendant hemisphere deficits,25 such as apraxia or anosognosia (which may be subtle but potentially significantly disabling), and low sensitivity for posterior circulation deficits.26

Quick recognition of common stroke syndromes increases diagnostic confidence and facilitates an efficient neurological test. Despite limited use in the hyperacute setting, stroke syndromes ofttimes suggest the underlying crusade. Big-vessel stroke syndromes (table 1) propose an atheroembolic cause, whereas lacunar syndromes are classically associated with cerebral small-scale-vessel disease. Lacunar syndromes include contralateral pure motor, pure sensory and sensorimotor damage, the clumsy paw–dysarthria syndrome (which tin also be cortical) and ataxic hemiparesis.

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Table 1

Large-vessel stroke syndromes (assumes left hemispheric dominance)

The 3-step 'HINTS' (Head-Impulse-Nystagmus-Examination-of-Skew) bedside test is often used to assess patients presenting with acute vestibular syndromes and has a high sensitivity (100%) and specificity (96%) for detecting a cardinal cause.xxx 31 Every bit its positive predictive value is only 69%, an isolated abnormal head impulse exam (suggesting unilateral peripheral vestibulopathy) should be interpreted with caution.32

Investigations

Pre-imaging

Rapid neuroimaging is essential for patients with acute stroke. The American Stroke Association guidelines advise that the only necessary prior investigation is a capillary blood glucose,33 which in practise is obtained by paramedics. An intravenous cannula is frequently required for dissimilarity or perfusion imaging sequences, allowing a blood panel to be obtained simultaneously. This would usually include a screen for infection, renal function and, if the patient takes anticoagulants, a coagulation screen. Although many radiology departments crave a recent renal role earlier giving contrast,34 recent studies have questioned the concept of contrast-induced nephropathy.35 36

Imaging

Stroke centres should establish protocols to eliminate delays to neuroimaging, for example, protocolled stroke imaging sequences and priority use of a designated scanner well-nigh to the emergency section.

Neuroimaging in the hyperacute acute stroke setting remains predominantly CT-based.37 A non-contrasted CT scan of head is quick, sensitive and cost-constructive at ruling out intracranial haemorrhage, which is usually sufficient for making thrombolysis decisions.38 However, CT scanning has much lower sensitivity and specificity for astute ischaemia because the cyberspace tissue h2o content (and therefore visual alter in parenchymal attenuation) changes over hours after the onset of ischaemia. Specificity is compromised by the high prevalence of existing ischaemic changes or quondam established infarcts. Signs of acute ischaemia on not-contrast CT include loss of grey–white thing differentiation (eg, at the insular ribbon), hemispheric sulcal effacement, loss of integrity of the lentiform nucleus or hyperdensity within an intracranial artery (the 'dense artery sign'). Early ischaemic changes can be quantified to assess the extent of parenchymal damage using the ten-point Alberta Stroke Program Early on CT Score (ASPECTS).39

Multimodal CT imaging comprises CT-perfusion and/or CT-angiography, besides as non-contrast CT, aiming to improve and augment case choice for reperfusion therapy. Rapid multimodal CT tin be performed in acute stroke care pathways. Stroke centres need articulate protocols for efficient interpretation to forestall unnecessary delays in giving rtPA.twoscore

CT-angiography of the cervicocranial and intracranial arteries should exist performed urgently to detect intracranial large artery occlusion when endovascular thrombectomy is available. Intracranial large artery occlusion is a marker of poor prognosis in minor stroke and TIA41 and observational bear witness suggests that patients with not-disabling symptoms due to intracranial big artery occlusion may benefit from thrombolysis,42 but a randomised trial is ongoing.43

CT-perfusion sequences can appraise diverse aspects of cerebral perfusion (see give-and-take below), often with automatic software, such as MIStar (Apollo Medical Imaging Technology) or Rapid Processing of Perfusion and Diffusion (RAPID) CT-perfusion (iSchemaView); these technologies ease interpretation by increasing inter-observer reproducibility and ensuring apply of validated thresholds. A comprehensive review of CT-perfusion interpretation has recently been published in Applied Neurology.44

MRI has much greater sensitivity for ischaemia than CT, specially in minor stroke where it tin predict poor short- and long-term outcomes.45 Moreover, comparing different sequences offers an approximate indication of time since onset.46 Rapid stroke MRI protocols typically include diffusion-weighted imaging (DWI), time-of-flight MR-angiogram of the intracranial arteries, T2-fluid-attenuated inversion recovery (FLAIR) and a claret-sensitive sequence such as slope-recalled echo or susceptibility-weighted imaging.47

Principles of acute stroke care

The main objective of acute ischaemic stroke handling is to relieve ischaemic, but feasible, brain tissue by recanalising occluded cerebral arteries and reperfusing the ischaemic penumbra.48 The penumbra is a region of electrically inexcitable, hypoperfused parenchyma surrounding the irreversibly damaged core49 that is temporarily supported past leptomeningeal collateral flow. Failure to recruit or maintain collaterals underlies the highly variable individual speed of evolution of the core; the mechanisms of collateral failure are currently poorly understood.50 Apace declining benefit from reperfusion therapies ('fourth dimension is brain')51 reflects the boilerplate pathophysiological status of failure of collateral back up over several hours. Some people, identified by imaging, maintain collaterals for longer periods, and later reperfusion is beneficial. ⇓Figure 2 offers a structured approach to acute stroke reperfusion; it is an overview of 'best practice' and should exist used in conjunction with local protocols tailored to available services where necessary.

Patients with severely elevated BP (≥185 mmHg systolic or ≥110 mmHg diastolic) are precluded from thrombolysis due to alteplase licensing restrictions; they may require intravenous antihypertensive therapy9 (eg, intravenous labetalol 5–x mg or glyceryl trinitrate l mg in l mL starting at one.5 mL/hr). However, the BP threshold is based on the original alteplase trial inclusion criteria52 and there is no evidence that reducing BP in this context helps clinically; indeed, recent data suggest a complex interaction betwixt reperfusion condition, BP and patient outcome, with 1 study suggesting that lowering BP before reperfusion treatment may exist inappropriate.53

Acute reperfusion strategies

Intravenous thrombolysis

Tissue-type plasminogen activator (tPA) cleaves plasminogen on the surface of thrombi to grade plasmin, a powerful endogenous fibrinolytic enzyme.54 Intravenous rtPA (alteplase) is proven and licenced to improve functional outcome in acute ischaemic stroke up to iv.five hours afterward symptom onset.10 55 The treatment issue is heavily time-dependent: the number needed to treat for excellent functional outcome at i.5 hours is v, compared with nine at iii.0–iv.5 hours.56 The relative benefit of rtPA is not modified by baseline stroke severity or past historic period.56 57

UK guidelines recommend all patients with disabling symptoms should be considered for rtPA treatment within 3 hours of symptom onset, and up to 4.5 hours in those aged nether 80. Patients presenting at 4.5–6 hours should be considered on an individual basis for treatment, recognising that the benefits are smaller than if treated earlier, but that the risks of a worse outcome, including decease, are not increased.58 The United kingdom of great britain and northern ireland performs poorly compared with other countries, both in the proportion of patients receiving rtPA (12% for the past half-dozen years59) and hateful door-to-needle times (52 min last year in England and Walesthreescore); considerable improvements in outcome are achievable if these could exist bettered.

Informed consent is rarely possible and should not delay treatment. In ane registry of nearly 2000 patients, a median door-to-needle time of simply 20 min included a consent discussion of less than a infinitesimal61; still if unavailable, treatment should go along in the patient's all-time interests.

Currently, there is lilliputian bear witness to support thrombolysis in patients with non-disabling ischaemic stroke.62 ⇓Table 2 shows the relative and accented contraindications to rtPA. Symptomatic intracerebral haemorrhage is the nigh feared adverse effect of rtPA merely haemorrhage associated with significant neurological deterioration occurs in only approximately i.nine% of treated patients.63 64 Radiological haemorrhagic transformation occurs due to reperfusion and is more than common in people with larger infarcts (who therefore more astringent baseline deficits). Neurological deterioration later rtPA infusion is common only usually reflects the initial ischaemic injury; in one contempo case series, only 1 of 511 patients deteriorated during the rtPA infusion due to intracerebral haemorrhage. Almost deterioration related to intracerebral haemorrhage occurred later the complete rtPA infusion, and deterioration was four times more likely to be due to initial ischaemia rather than to intracerebral haemorrhage.65 Deteriorating patients demand urgent repeat neuroimaging to analyze the cause and rtPA infusion is normally suspended pending imaging.

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Tabular array 2

American Heart Association/American Stroke Association absolute and relative contraindications to handling of acute ischaemic stroke with alteplase

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Table 3

Targets for maintaining homeostasis in acute ischaemic stroke patients

Orolingual angioedema is a recognised complication of rtPA; while most cases are mild and cocky-limiting, severe attacks requiring airway direction can occur in upwardly to 1% of treated patients; people taking ACE inhibitors or those with insular ischaemia are at increased run a risk.69 Stroke centres should develop local protocols with the anaesthetic department for assessing and urgently managing angioedema. Although direction in this setting is not bear witness based, treatment should exist consistent with that of other drug reactions (effigy 3).

Endovascular thrombectomy

Despite the overall benefit of rtPA, the subgroup of patients with large proximal intracranial vessel occlusion (large avenue occlusion; carotid, proximal centre cerebral arteries) have low rates of recanalisation with thrombolysis and only a 25% gamble of a practiced event.seventy 71 Endovascular thrombectomy in add-on to best medical therapy has been proven in nine randomised trials as superior to best medical therapy alone (including intravenous rtPA in the majority of patients) for patients with inductive apportionment large avenue occlusion.72 – 80 The number needed to care for to reach a reduction of one or more points on modified Rankin Scale (mRS) is two.half dozen.81 A detailed guide has recently been published in Practical Neurology.82

Unfortunately, the UK has been slow to provide this service; current endovascular thrombectomy rates are v.5 per 1000 ischaemic strokes in the UK, versus 50 in the United states and Western Europe.59 Parts of the United kingdom, notably Scotland, accept no access to thrombectomy at all. In England and Wales, the NHS Long Term Plan aims for a ten-fold increase by 2022, in part by expanding endovascular thrombectomy training to specialities other than interventional neuroradiology.four

Guidelines from the UK'southward National Constitute of Health and Care Excellence (Overnice) recommend endovascular thrombectomy for patients with disabling acute ischaemic stroke (arbitrarily defined as NIHSS ≥6) due to imaging-proven anterior circulation large-vessel occlusion upwards to vi hours, and posterior apportionment (basilar or posterior cerebral avenue) big-vessel occlusion up to 24 hours after symptom onset.10 Patients with lower NIHSS simply functionally disabling symptoms may also be considered due to the loftier risk of deterioration associated with large-vessel apoplexy.83

As with rtPA, the benefit of endovascular thrombectomy is highly time-dependent.84 However, several clinical trials showed favourable outcome of endovascular thrombectomy versus medical management in anterior apportionment large-vessel occlusion beyond 6 hours, although based on small numbers of patients.73 76 85 Ii trials have extended the therapeutic window even further: up to 16 hours in DEFUSE 386 and 24 hours in DAWN87 with CT perfusion or DWI-perfusion imaging with clinical mismatch. These trials demonstrated that imaging can select patients with big artery occlusion whose adept collateral supply makes them likely to benefit from endovascular thrombectomy.

The optimal mode of anaesthesia during endovascular thrombectomy has yet to be adamant; retrospective data suggested that general anaesthesia may be harmful (although potentially biased past patient pick),88 whereas single-centre randomised trials have shown neutral or beneficial effects.89 Multicentre randomised trials are ongoing.82

The complication rates of endovascular thrombectomy are in keeping with other emergency procedures and serious adverse events are rare.90 Although adverse events occur in approximately 15% of patients (including vasospasm, arterial perforation or dissection, device misplacement, symptomatic intracerebral haemorrhage or embolisation to new or target vessel territory), clinical result is not affected overall; the number needed to treat of 2.6 includes these complications.91

Acute stroke unit of measurement and early complications

Guidelines recommend that everyone with astute ischaemic stroke is admitted directly to an acute stroke unit.9 Stroke unit care has an number needed to treat of 17 to avert death or disability, a benefit that is sustained over time without lengthening hospital stays.92 93 Key features of the acute stroke unit include stroke-specific multidisciplinary care (physiotherapy, spoken language and language therapy, occupational therapy) and high nursing ratios.94 95 However, for the past five years, only 58% of patients in England and Wales were admitted to an acute stroke unit within 4 hours.60

Central functions of an acute stroke unit are the prevention of secondary encephalon insults by maintaining physiological homeostasis (table three) and monitoring of neurological status.96 The patient should besides undergo bedside cardiac telemetry if atrial fibrillation has non been confirmed.

Neurological deterioration should prompt urgent repeat neuroimaging; early neurological complications include recurrent ischaemia, cerebral oedema or haemorrhagic transformation. Repeat brain imaging effectually 24 hours following rtPA administration is widely undertaken to inform on intracerebral haemorrhage incidence as a quality of care metric, and visualisation of an infarct may provide prognostic and mechanistically relevant information, but the role for routine repeat imaging is debatable. Once haemorrhagic complications have been excluded at 24 hours, antiplatelet therapy should start, nigh often 300 mg aspirin daily for 2 weeks followed by lifelong clopidogrel monotherapy.

Patients with big book hemispheric infarcts from astute occlusion of the proximal middle cerebral artery or internal carotid avenue are particularly vulnerable to 'malignant' cerebral oedema, with a mortality charge per unit of up to 78%.97 Decompressive hemicraniectomy increases the adventure of survival (number needed to treat of two), but patients are ofttimes left with meaning disability (mRS 4–5 at one twelvemonth in 43% with decompressive hemicraniectomy vs 17% with medical management)98; nonetheless, the great majority rate their quality of life as existence satisfactory despite disability.99 Updated NICE guidance10 has removed the upper age limit for consideration of decompressive hemicraniectomy, in line with trial evidence. The current eligibility criteria are as follows:

  • Surgery may be performed 48 hours from stroke onset

  • Clinical deficits that suggest center cerebral avenue infarction with NIHSS >fifteen

  • Decreased level of consciousness (≥1 on level of consciousness on NIHSS)

  • Infarction of ≥l% of center cerebral avenue territory as seen on CT scanning or infarct book >145 cm3 on DWI

The high incidence of dysphagia after stroke is a gamble factor for aspiration pneumonia and is associated with increased mortality and disability.100 Guidelines recommend that patients receive a bedside swallowing assessment and appropriate accommodation of oral intake to prevent aspiration.10 Although there are no randomised studies to determine whether screening methods ameliorate outcomes,101 observational data propose that delayed assessment is associated with a higher chance of aspiration pneumonia.102 Prophylactic antibiotics have not proven effective.103

Non-convalescent patients with ischaemic stroke are at loftier risk of deep vein thrombosis.104 Prophylaxis with low-molecular-weight heparin is not recommended due to the hazard of haemorrhagic transformation,ix although some studies have shown no significant additional risk.105 Intermittent pneumatic compression devices are effective (compared to compression stockings) at reducing the chance of deep vein thrombosis and are recommended for all non-ambulatory stroke patients.9 106

Future directions

There is a wealth of active clinical inquiry in stroke medicine, driven by the significant public health implications of this common and socioeconomically impactful affliction. A item priority in the Uk is to meliorate systems that reduce onset-to-needle times, increase access to endovascular thrombectomy and admission rates to astute stroke units. Audits, including the Sentinel Stroke National Audit Programme (SSNAP), measure the processes and structure of stroke care and use these information to drive improvements.

Mobile stroke units with in-built CT scanners and telemedicine links with stroke centres are associated with earlier thrombolytic delivery and improved clinical issue in urban settings but are resource intensive and their optimal deployment depends on accurate prehospital triage.107

Alternatives to alteplase that are more fibrin-specific may be safer, more effective and may increase the therapeutic window. However, desmoteplase did non improve functional outcome compared with placebo in astute ischaemic patients 3–ix hours subsequently symptom onset.108 Although tenecteplase has not proven superior to alteplase in minor ischaemic stroke patients109 (a trial in patients with non-disabling symptoms due to large-vessel occlusion is ongoing43), it doubled recanalisation rates in pre-endovascular treatment of strokes from large-vessel occlusion with improved functional effect.110 In improver, the single bolus administration of tenecteplase may be advantageous for drip-and-ship thrombectomy service pathways.

Ongoing trials are investigating the efficacy of endovascular thrombectomy in patient subgroups, including basilar artery occlusion (BASICS111), low NIHSS (MOSTE112 and ENDOLOW113), or low ASPECTS score (TESLA,114 TENSION115 and IN EXTREMIS112). The optimal prehospital service pathway is another unanswered question, and mothership and baste-and-ship models are also being compared in a multicentre trial.116

Multiple preclinical and clinical studies to prevent secondary neuronal injury following ischaemic stroke take been unsuccessful, and to appointment there are no show-based neuroprotective agents.117 Although the neuroprotectant nerinetide did not improve outcomes in endovascular-treated patients compared with placebo in one recent randomised trial, secondary subgroup analyses suggest farther investigation may be warranted in patients not treated with alteplase.118 Translational studies of neuroprotective therapies may be aided by novel tissue cyberbanking of thrombi extracted by endovascular thrombectomy.119 The CHARM trial aims to appraise whether glibenclamide (BIIB093) improves functional outcome in patients with malignant encephalon oedema.120

CONCLUSION

Stroke medicine is a varied and chop-chop developing field that provides the opportunity to offer life-changing treatments to patients affected by the leading cause of neurological disability. Stroke care volition have increasing relevance for neurologists of the futurity and as a specialty we have a lot to offer, in detail with diagnostic expertise. As, we may need to develop our skills farther, for example, through managing acutely unwell patients with general medical issues on the acute stroke unit or past learning how to perform mechanical thrombectomy.

Central points

  • Stroke is a public health priority and prompt specialist intervention significantly reduces the burden of death and inability.

  • Nosotros need effective systems in place for prehospital recognition and advisable triage of suspected acute stroke.

  • Patients with non-disabling stroke or TIA should exist assessed within 24 hours.

  • Reperfusion with intravenous thrombolysis and/or endovascular thrombectomy are highly constructive therapies, merely time-dependent.

  • All patients should be treated in an astute stroke unit of measurement, for monitoring to detect and act on physiological insults including brain oedema, and for investigating promptly to let initiation of mechanism-advisable secondary preventative treatments.

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