A systematic approach to the definition of stroke

The 24-hour time-line for symptomsin the current definition of stroke is arbitrary. Moreover, this definition does not include silent stroke, encourage acute stroke therapy and consider dramatic recovery after successful therapy. Silent stroke, which is five times more common than symptomatic stroke, is a risk factor for future stroke and is associated with adverse neurological and cognitive functions. Whilst pathological confirmation remains the gold standard in defining stroke and its underlying etiology, widely available neuroimaging has greatly obviated the need for post-mortem examination. Modern multimodal neuroimaging permits confirmation of infarction and/or hemorrhage in the central nervous system, reveals the location and size of the vascular lesion, excludes the stroke mimics and evaluates the relevant cerebrovascular anatomy. Nevertheless, neuroimaging may be limited to anunenhanced computed tomography of the brain. Furthermore, stroke symptoms may resolve either spontaneously or upon successful thrombolysis despite development of new infarction or hemorrhage. It was timely for the American Heart Association and American Stroke Association to publish an updated definition of stroke in July 2013. This updated definition of stroke incorporates both clinical and tissue criteria and comprises of ten possible definitions of stroke. The latter include silent infarction and silent hemorrhage. One problem of the updated definition is major overlaps among the definitions. Another problem is the non-systematic nature of the definitions. This editorial proposes a comprehensive and systematic approach to the definition of stroke by incorporating the following factors: level of certainty, presence and nature of symptoms, duration of symptoms, pathological types, and underlying etiologies.published_or_final_versio

Clopidogrel and thrombotic thrombocytopenic purpura: Letters to the editor

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Cerebrovascular disease - Advances in management

Recent advances in the diagnosis and treatment of stroke have justified its management as a medical emergency. This article summarises current recommendations for the initial management of major types of stroke with emphasis on acute therapy for ischaemic stroke. Recommendations are based on the results of well-designed clinical trials. An acute stroke care team and an acute stroke unit should be established in all regional hospitals. Diagnosis of stroke must be accurate. General management aims for prevention and treatment of neurological and systemic complications, whereas specific management varies according to the stroke type and the underlying pathogenic mechanisms. For selected patients with ischaemic stroke, intravenous recombinant tissue plasminogen activator or a modified viper venom within 3 hours of onset, or intra-arterial pro-urokinase within 6 hours may improve functional outcomes. Neuro-surgical treatment is indicated for some patients with ischaemic or haemorrhagic strokes. Prevention of recurrence and rehabilitation are the core components of subsequent management.published_or_final_versio

Cerebral perfusion parameters in acute, subacute, or chronic middle cerebral artery territory ischaemia

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Thrombolytic and interventional therapy for acute ischaemic stroke – are we ready in Hong Kong?

Symposium 3 — Symposium on Strokepublished_or_final_versio

Neurological disorders in pregnancy

Pregnant women can present with a wide variety of neurological conditions. Patient data from 1 January 1985 through 31 December 1994 for all deliveries at the Tsan Yuk and Queen Mary hospitals were reviewed to determine the local frequency of various neurological conditions during pregnancy. Conditions including epilepsy, eclampsia, facial nerve palsy, pituitary tumour, cerebrovascular disorders, myasthenia gravis, multiple sclerosis, and non-pituitary intracranial tumours were encountered, in descending order of frequency. The limitations of this retrospective analysis are acknowledged. This paper reviews the current concepts of these conditions and outlines appropriate management.published_or_final_versio

Primary and secondary prevention of stroke

Results from recent clinical trials have shown that stroke is preventable both before and after symptomatic cerebrovascular disease through a change in lifestyle, medical therapy and surgical procedures. Risk factor control, antiplatelet agents, anticoagulation, and carotid endarterectomy have been proven to be effective under appropriate clinical circumstances. In this update, we shall highlight the areas in which scientific evidence is available.published_or_final_versio

Brain injury and neurogenesis after intracerebral haemorrhage in hypertensive rats

INTRODUCTION: Effective treatments for intracerebral haemorrhage (ICH) are awaited to reduce its morbidity and mortality. Hypertension is the most important risk factor for ICH. Neurogenesis following ICH in nomotensive rats has been confirmed. In this study, we used a rat renovascular hypertension (RVHT) model, and investigated the effects of hypertension on the pathophysiological and histological changes, and neural stem cell proliferation after induction of ICH. METHODS: RVHT was achieved by applying a silver clip onto the left renal artery. At 6 weeks after renal artery constriction, the mRNA levels of angiogensin II type 1 (AT1) and type 2 (AT2) receptors in the brain were determined by reverse transcription–polymerase chain reaction. ICH was induced by an intrastriatal injection of bacterial collagenase IV in the left brain in both normotensive and hypertensive rats. Left femoral artery was cannulated for continuous monitoring of blood pressure for 4 hours after the induction of ICH. Haematoma volume was quantified at 24 hours after ICH induction. 5’-Bromo-2’-deoxyuridine (BrdU) was used to label cell proliferation from the 6th day to the 9th day after ICH. Rats were killed at 10 days after ICH. BrdU+ and CD31 (an endothelial cell marker) immunoreactive cells were detected using immunofluorescence. Behavioural tests were performed at 1, 3, 7, 10, and 21 days after ICH. RESULTS: RVHT rats showed up-regulation of AT1 receptor in the brain. Following induction of ICH, both the normotensive and RVHT rats demonstrated an acute hypertensive response. As compared to normotensive rats, RVHT rats demonstrated a larger haematoma volume, and greater deficits at all time-points. However, at 10 days after ICH, more BrdU+ cells were detected over the perihaematoma area of RVHT rats than normotensive rats. Moreover, many BrdU+ cells within the ipsilateral basal ganglia of RVHT rats also co-expressed CD31. CONCLUSION: Renovascular hypertension aggravates histological and functional injury partly via up-regulation of AT1 receptor in the brain. Increased brain injury in hypertensive rats induces increased neural stem cell proliferation and angiogenesis after ICH. Experimental ICH in hypertensive rats is a suitable model for evaluation of pathophysiology and treatment of patients with hypertensive ICH.published_or_final_versionThe 15th Medical Research Conference; Department of Medicine, The University of Hong Kong, Hong Kong, 16 January 2010. In Hong Kong Medical Journal, 2010, v. 16 suppl. 1, p. 53, abstract no. 8

Post-ischaemic treatment with melatonin and calpeptin exerts neuroprotective effects against ischaemia/reperfusion injury in a rat model of focal cerebral ischaemia

INTRODUCTION: Melatonin is a potent antioxidant. Previously, we have demonstrated beneficial effects of pretreatment with melatonin in rodent models of focal cerebral ischaemia. Cerebral ischaemia increases intracellular concentration of calcium ion and activates several calcium-dependent proteases such as calpain. Calpeptin is a novel calpain inhibitor. The aim of this study was to investigate the neuroprotective role of postischaemia

Neuroprotective effects of melatonin and calpeptin in a rat model of focal cerebral ischemia

Introduction: Melatonin is a potent-free radical scavenger and antioxidant. Previously, we have demonstrated beneficial effects of pretreatment with melatonin in mild and severe focal cerebral ischaemia in rodent models. Cerebral ischaemia increases intracellular Ca2+ concentrations, and activates several calcium-dependent proteases including calpain. Pretreatment with calpeptin, a novel calpain inhibitor, has been reported to reduce the cerebral infarct volume. In addition, it also decreases the neuronal apoptosis in hippocampal CA1 sector and improves the behavioural deficit in a rat stroke model. The aim of this study was to investigate the neuroprotective role of a post-ischaemia treatment with melatonin and / or calpeptin, and whether combining the two exerts synergistic or addictive effects in transient focal ischaemic stroke in rats. Methods: Male Sprague-Dawley rats (6-8 weeks) were anaesthetised with sodium pentobarbital to undergo right-sided endovascular middle cerebral artery occlusion (MCAO) for 90 minutes followed by 24 hours of reperfusion before being sacrificed. A single or a combined dose of melatonin (50 μg/kg) and / or calpeptin (50 μg/kg) were given via an intracerebroventricular injection at 10-15 minutes after onset of the reperfusion. Sham group with injection of vehicle only was used as a control group. Neurological behaviour was assessed using Neurological Deficit Scoring System (NDSS) test and cerebral infarction volumes were evaluated by TTCstaining. Results: Infarction volumes and NDSS scores were lower in the calpeptin group but not in melatonin group when compared with the control. The combining effects of melatonin and calpeptin will be studied further. Conclusion: Our results suggest that post-ischaemia treatment with calpeptin but not melatonin at 50 μg/kg protects against focal MCAO model in rats.published_or_final_versio