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Spontaneous spinal cord infarction is significantly less common than cerebrovascular disease. Because of the tight anatomical distribution of pathways in the cord, small spinal cord infarcts usually give more obvious symptoms and signs than similar lesions in the brain. Large epidemiological stroke studies have generally not included spinal cord stroke and so the incidence of vascular syndromes in the spinal cord is unknown. Management and prevention strategies for spontaneous spinal cord infarcts stem from small case series and case reports. Patient outcomes from spinal cord infarction are better with prompt recognition, timely management and prevention of associated medical complications arising from paraplegia, tetraplegia, neurogenic bladder and bowel dysfunction. The process of rehabilitation following spinal cord infarction is an evolving area.

Strokectomy means surgical excision of infarcted brain tissue post-stroke with preservation of skull integrity, distinguishing it from decompressive hemicraniectomy. Both can mitigate malignant middle cerebral artery (MCA) syndrome but evidence regarding strokectomy is sparse. Here, we report our data and meta-analysis of strokectomy compared to hemicraniectomy for malignant MCA infarction. All malignant MCA stroke cases requiring surgical intervention in a large tertiary centre (January 2012–December 2017,N = 24) were analysed for craniotomy diameter, complications, length of follow-up and outcome measured using the modified Rankin score (mRS). Good outcome was defined as mRS 0–3 at 12 months. In a meta-analysis, outcome from strokectomy (pooled from our cohort and published strokectomy studies) was compared with hemicraniectomy (our cohort pooled with published DECIMAL, DESTINY and HAMLET clinical trial data). In our series (N = 24, 12/12 F/M; mean age: 45.83 ± 8.91, range 29–63 years), 4 patients underwent strokectomy (SC) and 20 hemicraniectomy (HC). Among SC patients, craniotomy diameter was smaller, relative to HC patients (86 ± 13.10 mm, 120 ± 4.10 mm, respectively;p = 0.003), complications were less common (25%, 55%) and poor outcomes were less common (25%, 70%). In the pooled data (N = 41 SC, 71 HC), strokectomy tended towards good outcome more than hemicraniectomy (OR 2.2, 95% CI 0.99–4.7;p = 0.051). In conclusion, strokectomy may be non-inferior, lower risk and cost saving relative to hemicraniectomy sufficiently to be worthy of further investigation and maybe a randomised trial.

This study aimed to identify very early incidence of hemiplegic shoulder pain within 72hours (HSP), how clinical assessment was related to pain at 8-10 week follow-up and explore current standard therapy/management.Observational, prospective.Teaching hospital hyper-acute and follow-up stroke services.121 consecutive patients with confirmed cerebral infarct/haemorrhage recruited within 72hours of stroke onset.N/A.Subjective report of pain severity and aggravating factors: using numerical rating scales and pain questionnaire (ShoulderQ), shoulder abductor and flexor muscle strength (Oxford MRC Scale), Neer's Test of sub-acromial pain, shoulder subluxation and soft tissue shoulder palpation.At initial assessment (72hours), 35% (42/121) reported HSP. At follow-up (8-10 weeks), 44% (53/121) had pain: pain persisted in 32 of the original 42, resolved in 10 and had developed since initial assessment in 21. Pain at follow-up was associated with a statistically significant higher frequency of severe shoulder muscle weakness (MRC grade ≤2) and gleno-humeral subluxation at initial assessment. Soft tissue palpation and Neer's Test detected pain but did not predict development of HSP. 50/121 patients had 140 therapy interventions, particularly targeted to those with a higher HSP risk.This study reports HSP at an earlier time point after stroke than previous publications. Patients with severe arm weakness and/or shoulder subluxation within 72hours are at significantly higher risk of HSP at 8-10 weeks. These data highlight the high incidence of HSP, the non-standardized therapy approach, and can inform sample size calculations for future intervention studies.NCT02574000 (clinicaltrials.gov).

Patent foramen ovale (PFO) is the most common anatomical cause of an interatrial shunt. It is usually asymptomatic but may cause paradoxical embolism, manifesting as stroke, myocardial infarction or visceral/peripheral ischaemia. PFO is a risk factor for stroke and may be associated with migraine with aura. New evidence suggests PFO closure reduces the risk of recurrent ischaemic stroke in a highly selected population of stroke survivors: those aged 60 years or younger with a cryptogenic stroke syndrome, a large right-to-left shunt, an atrial septal aneurysm and no evidence of atrial fibrillation. They benefit from percutaneous PFO closure in addition to antiplatelet therapy, rather than antiplatelet therapy alone. Current evidence does not support PFO closure in the treatment of migraine.

Background and aim Neutrophil-lymphocyte ratio (NLR) and lymphocyte-monocyte ratio (LMR) are associated with clinical outcomes in malignancy, cardiovascular disease and stroke. Here we investigate their association with outcome after acute ischaemic stroke treated by mechanical thrombectomy (MT). Methods Patients were selected using audit data for MT for acute anterior circulation ischaemic stroke at a UK centre from May 2016–July 2017. Clinical and laboratory data including neutrophil, lymphocyte and monocyte count tested before and 24 h after MT were collected. Poor functional outcome was defined as modified Rankin Scale (mRS) of 3–6 at 3 months. Multivariable logistic regression analyses were performed to explore the relationship of NLR and LMR with functional outcome. Results One hundred twenty-one patients (mean age 66.4 ± 16.7, 52% female) were included. Higher NLR (adjusted OR 0.022, 95% CI, 0.009–0.34, p = 0.001) and lower LMR (adjusted OR − 0.093, 95% CI (− 0.175)−(− 0.012), p = 0.025) at 24-h post-MT were significantly associated with poorer functional outcome when controlling for age, baseline NIHSS score, infarct size, presence of good collateral supply, recanalisation and symptomatic intracranial haemorrhage on multivariate logistic regression. Admission NLR or LMR were not significant predictors of mRS at 3 months. The optimal cut-off values of NLR and LMR at 24-h post-MT that best discriminated poor outcome were 5.5 (80% sensitivity and 60% specificity) and 2.0 (80% sensitivity and 50% specificity), respectively on receiver operating characteristic curve analysis. Conclusion NLR and LMR tested at 24 h after ictus or intervention may predict 3-month functional outcome.

Introduction: Risk factors for neurological complications in sickle cell disease differ in the adult and pediatric populations. Here, we focused on neurological complications in adults with sickle cell disease.Methods: Patients were selected using the audit data from the St George's Hospital Red Cell Database. The genotyping, demographics, clinical data, and investigation findings were collected.Results: A total of 303 patients were enrolled in the study: hemoglobin S homozygosity (HbSS) genotype 56%, hemoglobin S and C coinheritance (HbSC) genotype 35%, and hemoglobin S and β-thalassemia coinheritance (HbSβ) thalassemia genotype 9%; the mean age was 38.8 years (±13.5 SD) with 46% males. The most common neurological complication was cerebrovascular disease (n = 37, 12%) including those with ischemic stroke (10%), cerebral vasculopathy (3%), and intracranial hemorrhage (1%). Ischemic stroke was common among the HbSS genotype compared with other genotypes (8 vs. 1.6%, p = 0.001). Comparing the patients with sickle cell disease who had suffered a stroke to those who had not, there was a higher proportion of intracranial vasculopathy (p = 0.001, in particular, Moyamoya) and cognitive dysfunction (p < 0.0001).Conclusion: Our cohort supports previous reports that the most common neurological complication in adult sickle cell patients is cerebrovascular disease. Strategies to prevent cerebral vasculopathy and cognitive impairment should be explored.

Objectives\ud To assess the prevalence of high on-clopidogrel platelet reactivity (HCPR) in patients with ischaemic stroke or transient ischaemic attack (IS/TIA), their outcome and genetic basis of on-treatment response variability in IS/TIA patients.\ud \ud Methods\ud We conducted a comprehensive search of PubMed and EMBASE from their inceptions to March 9, 2019. Studies that reported absolute numbers/percentages of HCRP at any time point after IS/TIA onset evaluated with any type of platelet function tests, clinical outcomes and genotyping data were included.\ud \ud Results\ud Among 21 studies of 4312 IS/TIA patients treated with clopidogrel, the pooled prevalence of HCPR was 28% (95%CI: 24–32%; high heterogeneity: I2 = 88.2%, p < 0.001). Heterogeneity degree diminished across groups defined by the HCPR testing method. Clopidogrel non-responder IS/TIA patients had poorer outcome compared to responders (RR = 2.09, 95%CI: 1.61–2.70; p = 0.036; low heterogeneity across studies: I2 = 27.4%, p = 0.210). IS/TIA carriers of CYP2C19*2 or CYP2C19*3 loss of function alleles had a higher risk of HCPR compared to wild type (RR = 1.69, 95%CI: 1.47–1.95; p < 0.001; I2 = 0.01%, p = 0.475).\ud \ud Conclusions\ud This systematic review shows a high prevalence of clopidogrel resistance in IS/TIA and poor outcome in these patients. CYP2C19 polymorphisms may potentially influence clopidogrel resistance.

Background Protein convertase subtilisin–kexin type 9 (PCSK9) inhibitors effectively clear low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C). We evaluated stroke admissions potentially eligible for more intensive cholesterol treatment. Methods Retrospective analysis of consecutive admissions to a hyperacute stroke unit over 5 months in 2017. Records were individually searched. Data were collected on diagnosis, risk factors, and stroke work-up. European Society of Cardiology and European Atherosclerosis Society guidelines for the management of dyslipidaemias were used for screening patients eligible for PCSK9 inhibitors. Results Of 650 patient admissions: 351 (54%) had acute ischemic stroke or transient ischemic attack (TIA), 80 (12%) hemorrhage, and 219 (34%) mimic syndromes. Patients with hemorrhage (n = 80), mimic syndromes (n = 219), and absent LDL-C, or non-HDL-C testing (n = 27) were subsequently excluded. 324 patients with acute ischemic stroke and TIA were further screened for PCSK9-inhibitor treatment eligibility. Forty-one (13%) patients with LDL-C greater than or equal to 1.8mmol/L (≥70 mg/dL) on maximal tolerated statin dose and with concomitant “very high vascular risk” were identified. “Very high vascular risk” was defined as a documented history of cardiovascular disease and/or peripheral arterial disease. Of 41 patients eligible for PCSK9 inhibitors, median age was 82 years (range 53-96); median vascular risk factors were 2 (range 1-5); 7 (17%) had TIA; 13 (31%) had history of preceding cerebrovascular events, 13 (31%) diabetes mellitus, 17 (42%) cardioembolic events, 9 (22%) lacunar syndrome, 11 (22%) symptomatic internal carotid artery stenosis (n = 9 were >70%), and 4 (10%) undetermined aetiology. Eighty-three percent patients eligible for PCSK9 inhibitors also had non-HDL-C values greater than or equal to 2.6 mmol/L. Conclusions Up to 13% of unselected acute ischemic stroke or TIA patients admitted to a hyper-acute stroke unit were potentially suitable for more intensive cholesterol treatment. Our data may act as a useful guide for sample size selection in future stroke trials testing PCSK9 inhibitors.

St George's Hospital hyperacute neurology service (HANS) is a comprehensive, consultant-delivered service set in a teaching hospital regional neuroscience centre. The service addresses deficiencies in acute neurological care previously highlighted by the Royal College of Physicians and the Association of British Neurologists. HANS adopts a disease-agnostic approach to acute neurology, prioritising the emergency department (ED) management of both stroke and stroke mimics alike alongside proactive daily support to the acute medical unit and acute medical take. Rapid access clinics provide a means to assess ambulatory patients, providing an outlet to reduce the burden of referral from primary care to acute medicine. This paper reports the results from the first year of the service. Admission was avoided in 25% of the cases reviewed in the ED. Compared to historic data, there was a significant improvement in the length of stay for non-stroke disorders while the occupancy of stroke beds by non-stroke cases reduced by 50%. The configuration of this service is replicable in other neuroscience centres and provides a framework to reduce the barriers facing patients who present with acute neurological symptoms.

The objective of this study was to analyse the Neurothrombectomy Network registry of the Neuromed Campus (NMC) of the Kepler University Hospital in Linz (Austria). The data were compared to the results of recently published thrombectomy trials (MR CLEAN, ESCAPE, EXTEND-IA, SWIFT-PRIME, REVASCAT and THRACE). We retrospectively studied 246 patients with acute ischemic stroke who underwent thrombectomy between January 2012 and December 2015 at the NMC in Upper Austria. The main outcome measures were modified Rankin scale (mRS) score 0–2 at 90 days, all-cause mortality and stroke or thrombectomy-related mortality at discharge, as well as 90 days postdischarge. The median age was 70.4 years (IQR 59.9–76.9) and the median NIHSS at admission 16 (IQR 13–20). The thrombolysis in cerebral infarction (TICI) scale 2b–3 recanalization was achieved in 87.4%, 11.0% of the patients died in hospital and an additional 6.1% within 90 days after discharge. After 90 days, 56.5% had a mRS score 0–2. These data suggest that the positive results of thrombectomy reported in several randomized controlled studies can be achieved in routine clinical practice; therefore, the setting of an organized, regional stroke network proved an effective and appropriate method for delivering regional thrombectomy stroke treatment.

Nitrones (e.g. α-phenyl-N-tert-butyl nitrone; PBN) are cerebroprotective in experimental stroke. Free radical trapping is their proposed mechanism. As PBN has low radical trapping potency, we tested Sgk1 induction as another possible mechanism. PBN was injected (100 mg/kg, i.p.) into adult male rats and mice. Sgk1 was quantified in cerebral tissue by microarray, quantitative RT-PCR and western analyses. Sgk1+/+ and Sgk1−/− mice were randomized to receive PBN or saline immediately following transient (60 min) occlusion of the middle cerebral artery. Neurological deficit was measured at 24 h and 48 h and infarct volume at 48 h post-occlusion. Following systemic PBN administration, rapid induction of Sgk1 was detected by microarray (at 4 h) and confirmed by RT-PCR and phosphorylation of the Sgk1-specific substrate NDRG1 (at 6 h). PBN-treated Sgk1+/+ mice had lower neurological deficit ( p +/+ mice. PBN-treated Sgk1−/− mice did not differ from saline-treated Sgk1−/− mice. Saline-treated Sgk1−/− and Sgk1+/+ mice did not differ. Brain Sgk3:Sgk1 mRNA ratio was 1.0:10.6 in Sgk1+/+ mice. Sgk3 was not augmented in Sgk1−/− mice. We conclude that acute systemic treatment with PBN induces Sgk1 in brain tissue. Sgk1 may play a part in PBN-dependent actions in acute brain ischemia.

Current national guidelines advocate intravenous thrombolysis to treat patients with acute ischaemic stroke presenting within 4.5 hours from symptom onset, and thrombectomy for patients with anterior circulation ischaemic stroke from large vessel occlusion presenting within 6 hours from onset. However, a substantial group of patients presents with acute ischaemic stroke beyond these time windows or has an unknown time of onset. Recent studies are set to revolutionise treatment for these patients. Using MRI diffusion/FLAIR (fluid-attenuated inversion recovery) mismatch, it is possible to identify patients within 4.5 hours from onset and safely deliver thrombolysis. Using CT perfusion imaging, it is possible to identify subjects with a middle cerebral artery syndrome who have an extensive area of ischaemic brain but as yet have only a small area of infarction who may benefit from urgent thrombectomy in up to 24 hours. Here, we highlight the recent advances in late window stroke treatment and their potential contribution to clinical practice.

Stroke services have been centralised in several countries in recent years. Diagnosing acute stroke is challenging and a high proportion of patients admitted to stroke units are diagnosed as a non-stroke condition (stroke mimics). This study aims to describe the stroke mimic patient group, including their impact on stroke services. We analysed routine clinical data from 2,305 consecutive admissions to a stroke unit at St George's Hospital, London. Mimic groupings were derived from 335 individual codes into 17 groupings. From 2,305 admissions, 555 stroke mimic diagnoses were identified (24.2%) and 72% of stroke mimics had at least one stroke risk factor. Common mimic diagnoses were headache, seizure and syncope. Medically unexplained symptoms and decompensation of underlying conditions were also common. Median length of stay was 1 day; a diagnosis of dementia (p=0.028) or needing MRI (p=0.006) was associated with a longer stay. Despite emergency department assessment by specialist clinicians and computed tomography brain, one in four suspected stroke patients admitted to hospital had a non-stroke diagnosis. Stroke mimics represent a heterogeneous patient group with significant impacts on stroke services. Co-location of stroke and acute neurology services may offer advantages where service reorganisation is being considered.

Hearing disturbances are not commonly reported in stroke or transient ischemic attack. We describe a case of a 60-year-old man with fluctuating brainstem ischemia with basilar artery thrombosis where the patient has consistently described hearing "white noise," bilaterally becoming progressively louder over 10 minutes that prevented him from hearing surrounding noise including the radio. These episodes were transient and preceded episodes of hemiparesis or reduced conscious level. We correlate this to the sequential imaging findings from the patient. We discuss how this case provides in vivo evidence for localization of auditory hallucinations in the context of the auditory pathways and their blood supply, and review 25 previous cases of auditory hallucinations and possible mechanisms.

Summary Objectives Audits in the United Kingdom and other countries show that only a small proportion of eligible stroke patients receive thrombolysis. Providing 24-hour thrombolysis cover presents major challenges in both infrastructure and staffing. One model for improving access is to provide out-of-hours cover in a regional centre but this may present problems including greater delays to hospital admissions. Design Evaluation of the introduction of a ‘hub-and-spoke’ model of thrombolysis to increase access to thrombolysis for patients in south west London. One-year data are presented. Setting A network in south-west London comprised of a hub hospital and three district ‘spoke’ hospitals. Participants All suspected stroke admissions to a regional stroke centre. Main outcome measures Thrombolysis rates for acute stroke. Results Increased out-of-hours thrombolysis rates were achieved with only a small increase in stroke admissions (approximately 10%) in the hub hospital. Thrombolysis rates increased from 1.2 per 100 stroke admissions for the local daytime service to 6 per 100 admissions for the regional service. Most patients thrombolysed were not local to the hub hospital. Only 1 in 4 patients considered for thrombolysis was thrombolysed, in line with previous data. Ten percent of all thrombolysis calls were not stroke but represented stroke mimics. Median length of stay was 6 days (target was 3 days). Fifty percent of the thrombolysed patients from spoke hospitals were discharged directly home. Conclusions In an urban area, a hub-and-spoke thrombolysis model increased access to thrombolysis without resulting in a marked increase in overall stroke admission numbers for the hub hospital. Proactive plans to repatriate patients back to district hospitals are required, and repatriation protocols have to prioritize regional patients over other targets in spoke hospitals to facilitate capacity in the hub hospital.

Patients who are face, arm, speech test (FAST) positive may have a stroke mimic diagnosis. Careful attention to the speed of onset of symptoms is paramount. Magnetic resonance imaging is helpful in supplementing the clinical assessment.

Magnetic resonance imaging (MRI) is as good as, if not better than, X-ray Computed Tomography (CT) for providing useful information about cerebral infarction [1±3]. In particular, newer techniques such as diffusion weighted imaging are very sensitive to the earliest changes of cerebral ischaemia but are not widely available because of hardware limitations [4]. Most centres, therefore, continue to rely on T2-weighted images to recognize the early ischaemic lesion. Most MRI studies emphasize changes that occur acutely; much less is known about the sub-acute changes that occur. Previous observations have established that changes in T2-weighted imaging occur within the ®rst 24 h after the onset of infarction and it has been assumed that these changes persist inde®nitely in permanent infarcts. Here, we report on two patients in whom we found the surprising and intriguing observation that the T2 of the region of infarction returned to normal, or near normal, about 12 days after the onset of stroke but then became abnormal again a few days later.

High quality stroke management is based on doing the simple things well and may greatly improve long-term patient outcome. This article provides a straightforward approach to managing stroke patients.

Background and Purpose— Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS) patients with carotid stenosis were randomized between endovascular treatment and endarterectomy. The rates of residual severe stenosis and restenosis and their contribution to recurrent symptoms was unclear. Methods— Endovascular patients were treated by balloon angioplasty alone (88%) or stenting (22%). Patches were used in 63% of endarterectomy patients. Carotid stenosis was categorized as mild (0% to 49%), moderate (50% to 69%), severe (70% to 99%), or occluded, using standardized Doppler ultrasound criteria at the examination closest to 1 month (n=283) and 1 year (n=347) after treatment. Recurrent cerebrovascular symptoms during follow-up were analyzed. Results— More patients had ≥70% stenosis of the ipsilateral carotid artery 1 year after endovascular treatment than after endarterectomy (18.5% versus 5.2%, P =0.0001). Residual severe stenosis was present in 6.5% of patients at 1 month after endovascular treatment. Between 1 month and 1 year, restenosis to ≥70% stenosis occurred in 10.5% of the endovascular group. After endarterectomy, 1.7% had residual severe stenosis at 1 month, and 2.5% developed severe restenosis. The results were significantly better after stenting compared with angioplasty alone at 1 month ( P P =0.02), but most were transient ischemic attacks and none were disabling or fatal strokes. There were no recurrent symptoms in the 9 endarterectomy patients with ≥70% stenosis at 1 year. Conclusions— Carotid stenosis 1 year after endovascular treatment is partly explained by poor initial anatomical results and partly by restenosis. The majority of patients were treated by angioplasty without stenting. Further randomized studies are required to determine whether newer carotid stenting techniques are associated with a lower risk of restenosis. The low rate of recurrent stroke in both endovascular and endarterectomy patients suggests that treatment of restenosis should be limited to patients with recurrent symptoms, but long term follow up data are required.

The primary deficit in acute ischaemic stroke is one of impaired blood flow. Part of the cerebral circulation is occluded either by in situ thrombosis, or embolism from the heart or a more proximal artery (for example, the ipsilateral internal carotid artery). Angiographic studies of the cerebral circulation in acute stroke demonstrate occluding thrombus in up to 80% of patients.1 The aim of thrombolytic therapy therefore is to lyse an occluding thrombus or embolus and reduce the volume of cerebral tissue irreversibly damaged. Such an approach is of course successfully employed in the treatment of acute myocardial infarction.2 However a major complication of thrombolysis in stroke is cerebral haemorrhage which could offset any beneficial effects. Here we review the available evidence for thrombolysis in acute stroke and suggest imaging methods that could be used to aid future selection of patients who are most likely to benefit from such treatment. Data from animal stroke models confirm that cerebral blood flow can be restored to near normal levels after administration of recombinant tissue plasminogen activator (rtPA)3 and that thrombolysis results in smaller infarcts and improved neurological function.4-6 Comparison of streptokinase with rtPA suggested that, although their effectiveness in producing thrombolysis was comparable, streptokinase was less clot specific and animals treated with it had increased frequency and severity of cerebral haemorrhage.7 Animals treated with rtPA had the same frequency of cerebral haemorrhages as those treated with saline but the proportion of large haematomas was increased.6 In humans, thrombolytic therapy was first tried over 40 years ago but was largely abandoned due to excess mortality from major haemorrhagic complications.8 When computed tomography became widely available interest in the use of thrombolysis returned, leading to several larger randomised controlled trials. A dose escalation study using rtPA reported that …

Stroke is defined as rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 h or longer or leading to earlier death, with no apparent cause other than of vascular origin. Transient ischaemic attack (TIA) is defined identically except that the symptoms and signs resolve within 24h [1]. There is no fundamental difference between a TIA and a stroke except for the duration. Stroke is therefore a syndrome with numerous symptoms and signs; it has different aetiologies and the prognosis can vary enormously. Disability may be considered by some to be a worse outcome than death since stroke can affect every aspect of normal life, from higher mental functions such as intelligence, personality and expression to more mundane tasks such as toileting, dressing and feeding. The extremely wide definition of stroke and the enormous variety of outcomes has made the conduct of clinical trials in stroke and the choice of outcome measures problematic. In spite of this, there is more information available from clinical trials to facilitate evidence-based practice in stroke than in any other neurological discipline. In this chapter, we discuss the major issues, problems and solutions derived from the most important multicentre trials of cerebrovascular disease.

Acute stroke treatment using aspirin and/or heparin was studied in the International Stroke Trial (IST) and Chinese Acute Stroke Trial (CAST) which randomised over 40,000 patients altogether. Combining the results demonstrated that aspirin (150-300 mg) given within 48 h of the onset of stroke produced a small but significant improvement in outcome (death or dependency) 4 weeks to 6 months after stroke of about 1 patient per 100 treated. There was a significant reduction in recurrent ischaemic stroke of similar degree, which was not associated with significant increase in cerebral haemorrhage. Therefore, aspirin should be used as early secondary prevention against recurrent stroke, after excluding cerebral haemorrhage by scanning the patient. Heparin does not improve clinical outcome after stroke even in patients in atrial fibrillation. It decreased recurrent ischaemic stroke significantly in IST, but at the cost of a significant increase in cerebral haemorrhage. Low molecular weight heparins and heparinoids have not proved any more beneficial. Therefore, heparin does not appear to be a useful routine therapy in acute stroke. The use of heparin should, therefore, be limited to patients at high risk of deep vein thrombosis or early recurrence.

Background and Purpose — 1 H MR spectroscopy can be used to study biochemical changes occurring in the brain in stroke. We used it to examine the relationship between metabolite concentration ( N -acetyl aspartate [NAA], lactate, cholines and creatines), size of infarct, clinical deficit, and 3-month clinical outcome in patients with middle cerebral artery (MCA) territory infarction. Methods —Thirty-one patients with acute MCA territory infarction were recruited within 72 hours of the onset of symptoms. Single-voxel short echo time stimulated echo acquistion mode spectroscopy was used to obtain metabolite data from the infarct core. Metabolite concentrations were determined with use of variable projection time domain-fitting analysis. Infarct size was determined with T2-weighted images. Patient outcome groups at 3 months were “independent,” “dependent,” or “dead.” Results —All patients (100%; 95% CI 75% to 100%) who had an infarct >70 mL did poorly. Eighteen of 20 patients (90%; 95% CI 68% to 99%) with a core NAA concentration 7 mmol/L did well. Combining these results showed that all patients who had an initial infarct volume >70 mL did poorly, irrespective of the NAA concentration. Of those patients with infarcts 7 mmol/L did well (88%; 95% CI 47% to 100%), whereas those with a lower NAA concentration did poorly (80%; 95% CI 44% to 97%). There was no association between other metabolite concentrations and outcome. Conclusions —Infarct volume and NAA concentration can together predict clinical outcome in MCA infarction in humans.

Stroke has become a major NHS priority. Daniel Davies and colleagues look at a career in the area