stroke in the young – European Stroke Organisation https://eso-stroke.org the voice of stroke in Europe Fri, 16 Sep 2022 20:09:02 +0000 en-GB hourly 1 https://wordpress.org/?v=6.8.3 25th ESO Summer School – a very special week in Birmingham https://eso-stroke.org/25th-eso-summer-school-a-very-special-week-in-birmingham/ Fri, 16 Sep 2022 20:09:02 +0000 https://eso-stroke.org/?p=24554 <p>The post 25th ESO Summer School – a very special week in Birmingham first appeared on European Stroke Organisation.</p>

]]> .flex_column.av-2ggdaxo-6feee612ba318da298387cff2b80def4{ border-radius:0px 0px 0px 0px; padding:0px 0px 0px 0px; }

By Katarzyna Krzywicka

Follow on Twitter: @kat_krzywicka

Class of 2022 in Birmingham

25th ESO Summer School – a very special week in Birmingham

The 25th ESO Stroke Summer School took place on 5-9 September 2022 in Birmingham, England and was an unforgettable experience – not only because it was a first post-pandemic live (!) Summer School, but also due to very special events taking place in the United Kingdom throughout these five days (announcement of a new Prime Minister, passing of Queen Elisabeth II and appointment of a new King).

In early September, as 50 (aspiring) neurologists from 24 countries gathered in the halls of the University of Birmingham Medical School, the city of Birmingham topped the ranking with a number of stroke enthusiasts per square kilometre. Birmingham, also called “The Heart of England”, temporarily became “The Brain of England” and thanks to fantastic efforts of the organising team – Dr Phil Ferdinand, Professor Christine Roffe, Dr Indira Natarajan, Dr Sissi Ispoglou, Dr Jason Appleton, Dr Don Sims, Dr Girish Muddegowda, all participants of the Summer School enjoyed a delightful mixture of high level stroke education, networking and socialising.

First day was initiated by Professors Gary Ford and Iris Grunwald reminding us about everything we have learned and should know about thrombolysis and mechanical thrombectomy in acute ischaemic stroke. Afterwards, we worked in small groups discussing the importance of venous thromboembolism prevention, oxygen and blood pressure in stroke patients. From Dr Adam Low we learnt about safety considerations of anaesthesia during thrombectomy (always inform the anaesthetist if you expect a complex patient!). Dr Ranjan Sanyal entertained us with an interactive (and very useful!) lecture and provided us with simple algorithm for an often challenging diagnosis in dizzy patients. Dr Sissi Ispoglou triggered a discussion about atypical presentations and underdiagnosis of stroke and Dr Neena Bodasing reminded us of the importance of low-threshold HIV testing and advantages of an opt-out approach. The evening social programme kicked off with a delicious Indian curry dinner (a real Birmingham specialty!).

On a second day, Professors Hanne Christensen and Nikola Sprigg discussed the impact and management of intracerebral haemorrhage. Particularly the difficulty of attaining high quality data and high numbers of patients in intracerebral haemorrhage studies have been highlighted as current problems in the field. An important message was that time is brain – also in intracerebral haemorrhage patients – so do not slow down once you see blood! Consequently, a debate between Dr Adrian Parry-Jones and Dr Jason Appleton on whether elevated blood pressure should be intensively lowered in acute intracerebral haemorrhage patients yielded some unexpected results in voting among the participants – although everyone seemed to agree it should be lowered – the question was – how intensively. Professor David Werring introduced us to cerebral amyloid angiopathy and microbleeds and Mr Edward White took us on a journey from a neurosurgeon’s perspective – arguing that that the guidelines should not be seen as sanctity but that criteria for surgical intervention should be tailored to specific cases. Dr Samer Al-Ali showed us the stroke world from a neuroradiologist’s perspective, and presented a number of interesting cases. Professors Thompson Robinson and Rustam Al-Shahi Salman discussed the role of anti-platelet therapy in both ischemic and haemorrhagic strokes. Professor Joanna Wardlaw introduced us to the small vessel disease – reminding us it is a highly prevalent, important cause of cognitive impairment and very much a dynamic disease. Dr Linxin Li focused on in increased incidence of a young stroke and its possible causes and the scientific part of the day ended with Professor Anita Arsovska giving a comprehensive overview of stroke prevention in women. Evening dinner took place in an Italian restaurant with countless delicious dishes and ended with a luxurious cheese platter.

Third day gave platform to the number of international speakers, also the ESO Executive Committee Members to share their clinical and research interests. Professor Georgios Tsivgoulis gave us an extensive overview of the state of the art of stroke care and frontiers for thrombolysis or thrombectomy (138 slides in 25 minutes challenge?!). Professor Thorsten Steiner gave us perspectives on what future holds for intracerebral haemorrhage. Professor Peter Kelly showed us highly inspiring molecular and imaging approaches to studying inflammation in secondary stroke prevention. Dr Diana Aguiar de Sousa gave us a comprehensive overview of the knowledge about cerebral venous thrombosis (also after COVID-19 vaccination) and future perspectives for this relatively uncommon but highly relevant disease. Professor Martin Dichgans introduced complex but fascinating concepts of genetics in stroke (among others, the use of GWAS) and Dr Else Sandset took us on a personal journey and gave us early career tips (say yes to the opportunities when you are young). Second part of the day was opened by Professors John Camm and Robert Hatala who introduced atrial fibrillation and cardioembolic strokes from a cardiologist’s perspective. Dr Jukka Putaala  discussed the young stroke studies with focus on the cardiac causes of stroke. The day was crowned with a royal steak dinner topped off with an elegant sticky toffee pudding (an absolute highlight according to some).

The focus of the fourth day was life after stroke. Important topics were rehabilitation of the motor function of the limbs – introduced by Professor Nick Ward, management of spasticity – discussed by Dr Sachin Vashistha and balancing the exercise post-stroke to achieve better outcomes (importance of strength and aerobic exercises) – by Dr Ulrike Hammerbeck. After the break, from Dr Joseph Kwan we learned about the holistic approach to stroke care and about how little we know about almost miraculous effects of exercise and diet, we discussed fatigue, depression and anxiety in stroke patients with Professor Gillian Mead, and studied late rehabilitation, reintegration and return to work after stroke (physicians unfortunately rarely encourage patients to return to work…) with Professor Avril Drummond. We also learned from Mr Brin Heliwell about how it is to be a stroke patient – he also gave us recommendation about how we should make our work more meaningful for our patients. After lunch, Professor Silke Walter showed us the progress of work on the Mobile Stroke Unit and the challenges associated with introducing them (price and geographic landscape, just to mention two). Professor Christopher Price explained the pre-hospital stroke assessments, including the newest portable diagnostic technology to help identify large vessel occlusion. Lastly, Dr Deb Lowe, Dr David Hargroves and Dr Ajay Bhalla introduced us to a an integrated approach to Stroke Delivery Networks, Stroke National Audit Program and taught us how to bring change in the stroke field. Last evening was celebrated in the Jewellery Quarter of Birmingham, and dancing to an outstanding live band lasted until late night hours.

Fifth day focused on the challenges ahead in the stroke field. Together with Professor Hugh Markus we studied the vertebral artery disease, with Professor Terry Quinn – the often overlooked topic of cognition in stroke and about the unmet need of post-stroke cognitive screening testing. Professor Serefnur Ozturk took on a highly relevant topic – inequalities in stroke care among migrants and refugees. Professor Craig Smith shared the considerations about stroke and COVID-19 infection. Although the risk of stroke is small, once it occurs, it appears to be more severe, more likely with multiple large vessel occlusions. The summer school was concluded by passionate Professor Christine Roffe with a talk on clinical benefits of the hyper-acute stroke unit.

All in all, we certainly learned a lot about the current stroke practices and newest research directions, interacted with brilliant stroke experts from around the world (also learned that many of them have attended an ESO summer school earlier in their careers) and became even more enthusiastic about the field. We met fellow young stroke physicians and spent fantastic five days in Birmingham (which has more canals than Venice!).

It was a highly successful summer school with a well-rounded programme which surely will remembered for many years to come.

Thank you to everyone who made it possible!

<p>The post 25th ESO Summer School – a very special week in Birmingham first appeared on European Stroke Organisation.</p>

]]> Transcranial direct current stimulation in stroke neurorehabilitation: have you ever been to electric rehab-land? https://eso-stroke.org/transcranial-direct-current-stimulation-tdcs/ Thu, 27 Jan 2022 19:30:46 +0000 https://eso-stroke.org/?p=21423 <p>The post Transcranial direct current stimulation in stroke neurorehabilitation: have you ever been to electric rehab-land? first appeared on European Stroke Organisation.</p>

]]>

By Vincenza Amoruso, MD – Università Cattolica del Sacro Cuore, Rome

Giuseppe Reale, MD – Fondazione Policlinico Universitario A. Gemelli, Rome

Stroke Neurorehabilitation involves many different approaches. Alongside the “conventional” techniques, there are several “unconventional” treatments, ranging from drugs for recovery (you might want to read the post on fluoxetine), to robotics and invasive and non-invasive brain stimulation.

Transcranial Direct Current Stimulation (tDCS) is a non-invasive brain stimulation technique involving low voltage currents applied to the scalp[1]. Two electrodes generate a 1-2 mA current that flows from the anode to the cathode in order to enhance or diminish neuronal excitability of the brain areas just below the electrodes. In particular, the target area placed under the anode (anodal-tDCS) is excited and the resting membrane potential shifts towards depolarization and shows increased rate of spontaneous neuronal firing. On the opposite, the target area placed under the cathode (cathodal-tDCS) is inhibited and the resting membrane potential shifts towards hyperpolarization with reduced neuronal firing[2;3]. The mechanisms of action underlying the modulation of neuronal activity induced by tDCS are still not well demonstrated[4;5]. Several reports have suggested that tDCS could have an effect on cerebral cells, altering the activity of NMDA and GABA receptors[6]. In particular, anodal tDCS causes a local reduction in the inhibitory neurotransmitter GABA, whereas cathodal stimulation causes a reduction in glutamatergic neuronal activity, which is excitatory[7]. Moreover, tDCS could facilitate the plasticity cellular processes, such as long-term potentiation and long-term depression and changes in protein synthesis and gene expression[8;9;10], and blood flow changes with an increase in oxygen supply on cortical areas as assessed at a neuroimaging study[11].

In the last decades, tDCS has been tested in several medical conditions due to its low cost, ease of application, and safety. Several studies have found that tDCS can improve motor and cognitive functions both in healthy subjects and in various neurological conditions, such as stroke, Parkinson’s disease, multiple sclerosis, and many others[1;5].

Regarding stroke neurorehabilitation, two main tDCS approaches have been studied: stimulation of the affected hemisphere with anodal-tDCS and/or inhibition of the unaffected hemisphere with cathodal-tDCS. The latter approach is thought to reduce interhemispheric inhibition, a well-known phenomenon in which the healthy hemisphere inhibits the contralateral affected hemisphere, slowing the recovery process[12;13]. Recent studies have shown greater clinical efficacy of cathodal tDCS applied on the unaffected hemisphere in improving the performance in activities of daily living in stroke patients[14]. However, the contribution of tDCS in the various phases of recovery post-stroke (acute, sub-acute, and chronic) is still object of study[15].

The most recent review concluded that stroke patients who received tDCS have better clinical outcomes in terms of disability, although no clear improvement in arm and leg function, muscle strength or cognitive abilities has been found[16]. This review included 67 studies involving a total of 1729 adult participants with acute, subacute or chronic ischemic or hemorrhagic stroke. It must be noted that the included studies were quite heterogeneous, investigating different types of stimulation, different treatment durations and different current features. Besides, the stroke etiology was mixed and the control groups received sham tDCS (electrodes placed but no or irrelevant current applied) or an active, different intervention.

In conclusion, future research is needed in this fascinating area to investigate the reproducibility of the aforementioned findings, especially regarding arm and leg function, muscle strength and cognitive abilities (including spatial neglect). This could be done by conducting larger and more homogeneous randomized controlled trials.

The magic carpet waits for you. So don’t you be late!

REFERENCES

  1. Lefaucheur, J.P., Antal, A., Ayache, S.S., et al. Evidence-based guidelines on the therapeutic use of transcranial direct current stimulation (tDCS). Clin. Neurophysiol. 2017;
  2. Nitsche, M.A., Liebetanz, D., Tergau, et al. Modulation kortikaler erregbarkeit beim menschen durch transkranielle gleichstromstimulation. 2002;
  3. Fritsch B, Reis J, Martinowich K, Schambra HM, Ji Y, et al. Direct Current Stimulation Promotes BDNF-Dependent Synaptic Plasticity: Potential Implications for Motor Learning. Neuron 66, 198–204, April 29, 2010
  4. Stagg CJ, Nitsche MA. Physiological basis of transcranial direct current stimulation. Neuroscientist.17(1):37–53;2014.
  5. Santos Ferreira, I., Teixeira Costa, B., Lima Ramos, et al. Searching for the optimal tDCS target for motor rehabilitation. Journal of neuroengineering and rehabilitation,2019.
  6. Rothwell JC. Plasticity in the Human Motor System. Folia Phoniatr Logop ; 62(4): 153–157;2010.
  7. Stagg, C.J., Best, J.G., Stephenson, et al.Polarity-sensitive modulation of cortical neurotransmitters by transcranial stimulation. J. Neurosci. 29, 5202–5206;2009.
  8. Polanía R, Paulus W, Antal A, et al; Introducing graph theory to track for neuroplastic alterations in the resting human brain : a transcranial direct current stimulation study. Neuroimage.54(3):2287–96; 2011.
  9. Ranieri, F., Podda, M. V.,Riccardi, et al; Modulation of LTP at rat hippocampal CA3-CA1 synapses by direct current stimulation. Journal of neurophysiology, 107(7), 1868–1880; 2012.
  10. Ahn, S. M., Jung, D. H., Lee, H. J.,et al. Contralesional Application of Transcranial Direct Current Stimulation on Functional Improvement in Ischemic Stroke Mice. Stroke, 51(7), 2208–2218; 2020
  11. Zheng X, Alsop DC, Schlaug G. Effects of transcranial direct current stimulation ( tDCS ) on human regional cerebral blood flow. Neuroimage. 58(1):26–33;2011.
  12. Beaulé, V. , Tremblay, S. , & Théoret, H. Interhemispheric control of unilateral movement. Neural Plasticity, 2012,
  13. Boddington, L. J. , & Reynolds, J. Targeting interhemispheric inhibition with neuromodulation to enhance stroke rehabilitation. Brain Stimulation, 10(2), 214–222. 2017.
  14. Elsner B, Kwakkel G, Kugler J, Mehrholz J. Transcranial direct current stimulation (tDCS) for improving capacity in activities and arm function after stroke: a network meta-analysis of randomized controlled trials. J Neuroeng Rehabil. 2017;
  15. Kang N, Weingart A, Cauraugh JH. Transcranial direct current stimulation and suppression of contralesional primary motor cortex post-stroke: a systematic review and meta-analysis. Brain Inj. ; 32(9):1063-1070.2018.
  16. Elsner B, Kugler J, Pohl M, Mehrholz J. Transcranial direct current stimulation (tDCS) for improving activities of daily living, and physical and cognitive functioning, in people after stroke. Cochrane Database Syst Rev. 2020.

<p>The post Transcranial direct current stimulation in stroke neurorehabilitation: have you ever been to electric rehab-land? first appeared on European Stroke Organisation.</p>

]]> Thrombectomy in Childhood Stroke? https://eso-stroke.org/childhoodstroke/ Thu, 20 Jan 2022 20:22:49 +0000 https://eso-stroke.org/?p=21360 <p>The post Thrombectomy in Childhood Stroke? first appeared on European Stroke Organisation.</p>

]]>

By PD Dr. Peter Sporns

Department of Diagnostic & Interventional Neuroradiology, University of Basel

Basel, Switzerland

After publication of the landmark randomised clinical trials in 2015, mechanical thrombectomy has become standard of care for large vessel occlusion stroke in adults.1 However, children were excluded or underrepresented in all these trials and due to the different causes of childhood arterial ischaemic stroke and the smaller anatomy of the child’s vasculature, the results in adults cannot be extrapolated to the paediatric population.

Recently, after several case series and meta-analyses,2,3 the Save ChildS Study provided multicentre evidence for the use of mechanical thrombectomy in children with large vessel occlusion arterial ischaemic stroke.4 In that study, rates of recanalization and adverse events were similar to those seen in the large randomised controlled trials in adults, and the children’s neurological outcomes were generally favourable. However, definitive conclusions could not be drawn given the limitations of the Save ChildS Study, which include the retrospective design and the absence of a control group of patients with large vessel occlusion not treated by mechanical thrombectomy.

Regarding the use of mechanical thrombectomy in children beyond 6 hours from symptom onset, a secondary analysis of the Save ChildS Study provided evidence that thrombectomy can be safe even within a timeframe of up to 24 hours after onset of symptoms, when selected by a mismatch between clinical deficit and infarct.5 In this analysis, outcomes were similar to those in children treated in the Save ChildS Study with an onset of less than 6 hours and were better than those of adult patients in the DAWN and DEFUSE 3 trials.6,7

Another important concern is the size of the affected intra- and extracranial vessels, which can be much smaller than in adult patients. Although there is no specific armamentarium designed for use in children, small-scaled endovascular devices such as stent retrievers can be used within the brain vasculature of small children. However, paediatric vasculopathy is usually not due to atherosclerosis and can involve substantial inflammation, such as in focal cerebral arteriopathy, which presents a different vulnerability towards mechanical manipulation. Thus, for arteriopathies including focal cerebral arteriopathy, moyamoya vasculopathy, and dissection (which are present in about half of childhood arterial ischaemic stroke cases), mechanical thrombectomy can carry an increased risk of injuring an inflamed vessel, expanding an existing dissection, or vasospasm. However, another secondary analysis of the Save ChildS Study including 14 children with arteriopathies observed no dissections or vessel ruptures, but there might have been a selection bias against children with suspected inflammatory arteriopathies, which is underlined by the lower proportion of arteriopathies in the Save ChildS study than in population-based studies.8

Another important question is, whether there is a lower age limit for children to have thrombectomy?9 The most systematic evidence for this question again arises from the results of the Save ChildS Study, in which an analysis grouped by age suggested that the outcome was slightly worse in children aged 0–6 years than in the whole study cohort.8 However, although one might think this finding could be attributed to the selection of thrombectomy devices and size of the catheterised arteries, the same post-hoc analysis showed that neurological outcomes were not associated with any specific device selection.8

The exemplary failure of the prospective randomized Thrombolysis in Pediatric Stroke (TIPS) trial to assess the safety of intravenous tissue-type plasminogen activator in paediatric patients—owing to a recruitment shortage—underlines the challenges both of randomly assigning children with stroke and of studying paediatric stroke in randomised trials.10 Hence, the best possible way to generate higher level evidence for the use of mechanical thrombectomy and to define selection criteria in children, seems to be the implementation of prospective registries, such as the Save ChildS Pro Registry currently underway.11

REFERENCES

  1. Goyal M, Menon BK, van Zwam WH, et al. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials. Lancet (London, England) 2016; 387: 1723–1731.
  2. Sporns PB, Kemmling A, Hanning U, et al. Thrombectomy in Childhood Stroke. J Am Heart Assoc. Epub ahead of print 2019. DOI: 10.1161/JAHA.118.011335.
  3. Bhatia K, Kortman H, Blair C, et al. Mechanical thrombectomy in pediatric stroke: Systematic review, individual patient data meta-analysis, and case series. Journal of Neurosurgery: Pediatrics. Epub ahead of print 2019. DOI: 10.3171/2019.5.PEDS19126.
  4. Sporns PB, Sträter R, Minnerup J, et al. Feasibility, Safety, and Outcome of Endovascular Recanalization in Childhood Stroke: The Save ChildS Study. JAMA Neurol; 77. Epub ahead of print 2020. DOI: 10.1001/jamaneurol.2019.3403.
  5. Sporns PB, Psychogios MN, Straeter R, et al. Clinical Diffusion Mismatch to Select Pediatric Patients for Embolectomy 6 to 24 Hours After Stroke: An Analysis of the Save ChildS Study. Neurology 2021; 96: e343–e351.
  6. Nogueira RG, Jadhav AP, Haussen DC, et al. Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct. N Engl J Med 2018; 378: 11–21.
  7. Albers GW, Marks MP, Kemp S, et al. Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging. N Engl J Med 2018; 378: 708–718.
  8. Sporns PB, Straeter R, Minnerup J, et al. Does Device Selection Impact Recanalization Rate and Neurological Outcome?: An Analysis of the Save ChildS Study. Stroke 2020; 51: 1182–1189.
  9. Sporns PB, Fullerton HJ, Lee S, et al. Current treatment for childhood arterial ischaemic stroke. Lancet Child Adolesc Heal. Epub ahead of print July 2021. DOI: 10.1016/s2352-4642(21)00167-x.
  10. Rivkin MJ, deVeber G, Ichord RN, et al. Thrombolysis in pediatric stroke study. Stroke 2015; 46: 880–885.
  11. Sporns PB, Kemmling A, Lee S, et al. A Prospective Multicenter Registry on Feasibility, Safety, and Outcome of Endovascular Recanalization in Childhood Stroke (Save ChildS Pro). Front Neurol; 12. Epub ahead of print 3 September 2021. DOI: 10.3389/fneur.2021.736092.

Are you interested in learning more about Young stroke? Join the ESO Educational Webinar on 9 February at 18:30 CET.

Programme and Registration

<p>The post Thrombectomy in Childhood Stroke? first appeared on European Stroke Organisation.</p>

]]> Prevent post-stroke epilepsy – Part 2 Do we have interventions? https://eso-stroke.org/prevent-post-stroke-epilepsy-part-2-interventions/ Fri, 05 Mar 2021 06:10:10 +0000 https://eso-stroke.org/?p=18038 <p>The post Prevent post-stroke epilepsy – Part 2 Do we have interventions? first appeared on European Stroke Organisation.</p>

]]> .flex_column.av-1mugykc-ff7ffceb011cd4b6599ba3035435c8c1{ border-radius:0px 0px 0px 0px; padding:0px 0px 0px 0px; }

By Kateriine Orav, Department of Neurology, North Estonia Medical Centre, Tallinn, Estonia

The prevention of post-stroke epilepsy is a rising concern with increasing numbers of post-stroke survivors and patients with post-stroke epilepsy.1  Epileptogenesis after stroke involves the development and extension of tissue capable of generating spontaneous seizures, resulting in the development of epilepsy.2

This process consists of a complex cascade of progressive molecular and cellular alterations that are still poorly understood.3 Currently, there are no treatment options to prevent the development of post-stroke epilepsy but such interventions are urgently needed.2  Having a better understanding of patients who are most at risk and the underlying mechanisms may allow for such strategies to be developed. This post will review some experimental evidence of interventions for epilepsy prevention. For a review of risk factors and biomarkers for developing post-stroke epilepsy see part 1 of this topic.

In animal studies of acquired epilepsies several antiseizure drugs (such as levetiracetam, brivaracetam, topiramate, gabapentin, pregabalin, vigabatrin and eslicarbazepine acetate) have shown antiepileptogenic or disease-modifying effects.4  Of these, levetiracetam has been studied in a clinical trial comparing 12 weeks of administering the drug after stroke compared to placebo, but was stopped due to poor recruitment.5  However, levetiracetam has shown a possible antiepileptogenic effect in trials evaluating it in traumatic brain injury and perioperatively in surgically treated refractory temporal lobe epilepsy.4

Several studies have shown a reduced risk of early seizures and post-stroke epilepsy with statin therapy in patients with ischaemic and haemorrhagic stroke. Statins could have a neuroprotective effect through the reduction of excitotoxicity, suppression of reactive astrogliosis and reduction of blood-brain barrier permeability which may influence epileptogenesis. Some studies have found that this protective effect may vary depending on the lipophilicity and dose of the statin.6  Although the certainty of the evidence is low, these are findings that warrant further investigation.

In addition to statins and antiseizure medicines, some other drugs that are in clinical use have shown antiepileptogenic or disease-modifying effects in animal studies. These include ceftriaxon, losartan, isoflurane and N-acetylcysteine. Repurposing of available drugs could be an attractive strategy to evaluate antiepileptogenic potential.4  Network pharmacology is a recently proposed strategy involving a combination of drugs that target different mechanisms of the epileptogenic network simultaneously.4 For example, the combination of topiramate and levetiracetam has shown some promise in preclinical trials.7

Even though post-stroke epilepsy is the most common form of acquired epilepsy, it has received relatively little academic interest.3  So far there is no evidence to support interventions to prevent post-stroke epilepsy in humans and the ESO guideline for the management of post-stroke seizures and epilepsy recommends against antiseizure therapy for the prevention of post-stroke epilepsy.9 One randomized controlled trial compared four-week treatment with valproate to placebo in 72 patients with intracerebral haemorrhage and did not find significant differences in seizure occurrence after one year.10  Post-traumatic epilepsy is another common preventable epilepsy and currently the large international Epilepsy Bioinformatics Study for Antiepileptogenic Therapy (EpiBioS4Rx) is investigating acute electrical, structural and blood biomarkers in post-traumatic brain injury to identify at risk patient populations and develop techniques to carry out feasible clinical trials of epilepsy prevention therapies in this patient population.8  With an increased burden of stroke and post-stroke epilepsy similar co-ordinated research efforts will be necessary also in the field of post-stroke epilepsy.

References:

  1. Thurman DJ, Begley CE, Carpio A, et al. The primary prevention of epilepsy: A report of the Prevention Task Force of the International League Against Epilepsy. Epilepsia. 2018 May;59(5):905-914. doi: 10.1111/epi.14068
  2. Pitkänen A, Roivainen R, Lukasiuk K. Development of epilepsy after ischaemic stroke. Lancet Neurol. 2016 Feb;15(2):185-197. doi: 10.1016/S1474-4422(15)00248-3.
  3. Zelano J, Holtkamp M, Agarwal N, et al How to diagnose and treat post-stroke seizures and epilepsy. Epileptic Disord. 2020 Jun 1;22(3):252-263. doi: 10.1684/epd.2020.1159.
  4. Klein P, Friedman A, Hameed MQ, et al. Repurposed molecules for antiepileptogenesis: Missing an opportunity to prevent epilepsy? Epilepsia. 2020 Mar;61(3):359-386. doi: 10.1111/epi.16450.
  5. van Tuijl JH, van Raak EP, de Krom MC, et al. Early treatment after stroke for the prevention of late epileptic seizures: a report on the problems performing a randomised placebo-controlled double-blind trial aimed at anti-epileptogenesis. Seizure. 2011 May;20(4):285-91. doi: 10.1016/j.seizure.2010.12.012.
  6. Nucera B, Rinaldi F, Nardone R, et al. Statins in primary prevention of poststroke seizures and epilepsy: A systematic review. Epilepsy Behav. 2020 Nov;112:107400. doi: 10.1016/j.yebeh.2020.107400.
  7. Schidlitzki A, Bascuñana P, Srivastava PK, et al. Proof-of-concept that network pharmacology is effective to modify development of acquired temporal lobe epilepsy. Neurobiol Dis. 2020 Feb;134:104664. doi: 10.1016/j.nbd.2019.104664.
  8. Vespa PM, Shrestha V, Abend N, et al. The epilepsy bioinformatics study for anti-epileptogenic therapy (EpiBioS4Rx) clinical biomarker: Study design and protocol. Neurobiol Dis. 2019 Mar;123:110-114. doi: 10.1016/j.nbd.2018.07.025.
  9. Holtkamp M, Beghi E, Benninger F, et al. European Stroke Organisation. European Stroke Organisation guidelines for the management of post-stroke seizures and epilepsy. Eur Stroke J. 2017 Jun;2(2):103-115. doi: 10.1177/2396987317705536.
  10. Gilad R, Boaz M, Dabby R, Sadeh M, Lampl Y. Are post intracerebral hemorrhage seizures prevented by anti-epileptic treatment? Epilepsy Res. 2011 Aug;95(3):227-31. doi: 10.1016/j.eplepsyres.2011.04.002.

<p>The post Prevent post-stroke epilepsy – Part 2 Do we have interventions? first appeared on European Stroke Organisation.</p>

]]> Prevent post-stroke epilepsy – Part 1 Can we identify those at high risk? https://eso-stroke.org/prevent-post-stroke-epilepsy-part-1-can-we-identify-those-at-high-risk/ Fri, 26 Feb 2021 07:47:19 +0000 https://eso-stroke.org/?p=17980 <p>The post Prevent post-stroke epilepsy – Part 1 Can we identify those at high risk? first appeared on European Stroke Organisation.</p>

]]> .flex_column.av-1mugykc-ff7ffceb011cd4b6599ba3035435c8c1{ border-radius:0px 0px 0px 0px; padding:0px 0px 0px 0px; }

By Kateriine Orav, Department of Neurology, North Estonia Medical Centre, Tallinn, Estonia

In 2019 the WHO, in collaboration with the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE) emphasized the importance of prevention in their global report on epilepsy.1  Stroke is one of the most common preventable causes of epilepsy, especially in older adults.

With increasing numbers of stroke survivors the number of patients with post-stroke epilepsy is expected to increase.2  Post-stroke epilepsy is associated with long-term disability and up to 25% of cases may become resistant to antiepileptic drugs.3

Post-stroke epilepsy develops in up to 12% of stroke patients and may develop with a latency of years after the primary insult.4  This may allow for interventions to prevent epileptogenesis, the process of acquiring a predisposition for seizures, in high risk patients.  We will review risk factors and biomarkers of post-stroke epilepsy today, and a second post will look into possible antiepileptogenic interventions.

Common risk factors for post-stroke epilepsy are younger age (<65 years), haemorrhagic stroke, alcohol use, cortical involvement (especially areas like the parieto-temporal cortex, supra marginal gyrus, superior temporal gyrus), and more severe stroke.3  In addition, viable islands of spared tissue and partly destroyed areas within a cortical infarction region have been associated with post-stroke epilepsy.5

While seizures during the first week after stroke do not warrant a diagnosis of epilepsy, the occurrence of early seizures considerably increases the risk of developing post-stroke epilepsy.3  However, a significant amount of early seizures are purely electrographic hence underrecognized.  Studies using continuous electroencephalographic monitoring in the acute phase have shown a prevalence as high as 14.6% for early seizures and 2.6% for non-convulsive status epilepticus after ischaemic stroke and up to a third in patients with haemorrhagic stroke.6

Interestingly, some studies have associated reperfusion therapy with early seizures and epileptiform activity on EEG. Possible proconvulsant mechanisms of tPA include the reperfusion/hyperperfusion syndrome, secondary cortical infarction from distal embolisation, haemorrhagic transformation and possible neurotoxic effects. However, by decreasing the severity of stroke, an important risk factor for post-stroke epilepsy, reperfusion therapies could also decrease the risk of post-stroke epilepsy.7  A possible association between reperfusion therapy and post-stroke epilepsy remains to be answered.

There are validated clinical tools to predict the 5-year seizure risk after stroke, such as the SeLECT score for ischaemic stroke and CAVE score for haemorrhagic stroke.3  The SeLECT score considers early seizures and the severity, aetiology and location of stroke to predict the risk of late seizures, while cortical involvement, age <65 years, volume >10mm and early seizures are included in the CAVE score.3

However, to increase the predictive accuracy of the above clinical tools it will be important to incorporate biomarkers. EEG could be a promising tool as EEG abnormalities have been shown to predict the development of epilepsy in the first year after stroke, independent of stroke severity.6  Recently, several blood biomarkers have also been described.8  The collaborative EU-funded EpiTarget project focused on identifying biomarkers of epileptogenesis, including  proteins and RNAs in biofluids as well as imaging techniques.9  Even though most of the findings require further research before they could have any clinical influence, an important step has been made towards a better understanding of epileptogenesis. Only if we can identify patients at high risk for post-stroke epilepsy with reasonable accuracy will we be able to study antiepileptogenic interventions adequately.5

References:

  1. World Health Organization. Epilepsy: a public health imperative. 2019 Retrieved from: https://www.who.int/mental_health/neurology/epilepsy/report_2019/en/
  2. Thurman DJ, Begley CE, Carpio A, et al. The primary prevention of epilepsy: A report of the Prevention Task Force of the International League Against Epilepsy. Epilepsia. 2018 May;59(5):905-914. doi: 10.1111/epi.14068
  3. Feyissa AM, Hasan TF, Meschia JF. Stroke-related epilepsy. Eur J Neurol. 2019 Jan;26(1):18-e3. doi: 10.1111/ene.13813
  4. Graham NS, Crichton S, Koutroumanidis M, et al. Incidence and associations of poststroke epilepsy: the prospective South London Stroke Register. Stroke. 2013 Mar;44(3):605-11. doi: 10.1161/STROKEAHA.111.000220.
  5. Pitkänen A, Roivainen R, Lukasiuk K. Development of epilepsy after ischaemic stroke. Lancet Neurol. 2016 Feb;15(2):185-197. doi: 10.1016/S1474-4422(15)00248-3.
  6. Zelano J, Holtkamp M, Agarwal N, et al How to diagnose and treat post-stroke seizures and epilepsy. Epileptic Disord. 2020 Jun 1;22(3):252-263. doi: 10.1684/epd.2020.1159.
  7. Bentes C, Brigo F, Zelano J, Ferro JM. Reperfusion therapies and poststroke seizures. Epilepsy Behav. 2020 Mar;104(Pt B):106524. doi: 10.1016/j.yebeh.2019.106524.
  8. Abraira L, Santamarina E, Cazorla S, et al. Blood biomarkers predictive of epilepsy after an acute stroke event. Epilepsia. 2020 Oct;61(10):2244-2253. doi: 10.1111/epi.16648.
  9. Pitkänen A, Henshall DC, Cross JH, et al. Advancing research toward faster diagnosis, better treatment, and end of stigma in epilepsy. Epilepsia. 2019 Jul;60(7):1281-1292. doi: 10.1111/epi.16091.

<p>The post Prevent post-stroke epilepsy – Part 1 Can we identify those at high risk? first appeared on European Stroke Organisation.</p>

]]> ESO-WSO Conference 2020 – A Virtual Poster Walk with Dr. Li https://eso-stroke.org/eso-wso-conference-2020-a-virtual-poster-walk-with-dr-li/ Mon, 09 Nov 2020 18:26:11 +0000 https://eso-stroke.org/?p=16786 <p>The post ESO-WSO Conference 2020 – A Virtual Poster Walk with Dr. Li first appeared on European Stroke Organisation.</p>

]]> .flex_column.av-pxfofs-f8cffa300d0abe60229a0238b37e998b{ border-radius:0px 0px 0px 0px; padding:0px 0px 0px 0px; }
/in , /by

By Dr Linxin Li, Wolfson Centre for Prevention of Stroke and Dementia, Oxford University, UK

I visited the E-Poster gallery first thing this morning and was almost overwhelmed by the width and depth of excellent science there! Although we were not able to discuss face-to-face this time, many authors have indicated they are available either through email or in the chat room so I hope you do get into contact.

Given the apparent increase, “young stroke” captures a lot of attention this year. Kivela et al. from Finland used a unique population-based birth cohort and studied PREGNANCY AND BIRTH COMPLICATIONS IN ASSOCIATION WITH EARLY ONSET STROKE IN THE OFFSPRING DASH THE NORTHERN FINLAND BIRTH COHORT 1966 STUDY.  They showed that bleeding and low weight gain during pregnancy were associated with increased stroke risk in offspring, highlighting that pregnancy complications may have long-lasting influence on stroke risk.

Small vessel disease remains an area of growing interest. Jung et al. from Korea performed a very elegant study to look at INDIVIDUAL RISK DETERMINATION WITH PATHOPHYSIOLOGICAL TYPING OF CEREBRAL WHITE MATTER SIGNAL ABNORMALITIES and showed that white matter hyperintensities can be classified into three distinct phenotypes: Type I – multiple, small lower-contrast lesions predominantly in the deep white matter; Type II – large, patch lesions in the periventricular white matter and type III – higher-contrast lesions mostly restricted to the juxtaventricular white matter. Their study offers a new tool to study the associations of white matter hyperintensities and proposed underlying pathophysiology.

Another interesting study that caught my eye was presented by Khan et al from Japan. INCREASE IN AMBIENT TEMPERATURE PARAMETERS IS ASSOCIATED WITH LOWER INCIDENCE OF STROKE IN A JAPANESE POPULATION: TAKASHIMA STROKE REGISTRY, JAPAN, 1988-2010. The authors found that an increase in temperature was associated with lower risk of any stroke, especially for individuals at older ages. The signal seems to be particularly prominent for intracerebral haemorrhage and for subarachnoid haemorrhage.

In addition to studies presenting their results, there are also exciting posters detailing the design of several ongoing trials. I very much look forward to hearing the diagnostic yield of ECG-gated cardio-aortic CTA in the acute phase of ischaemic stroke from the MIND THE HEART trial and if routine monitoring also helps to detect atrial fibrillation in patients with otherwise known aetiology from the STROKE AF trial.

I hope I have given you a flavour of the posters we have. The gallery is still open so please grab a drink and enjoy!

<p>The post ESO-WSO Conference 2020 – A Virtual Poster Walk with Dr. Li first appeared on European Stroke Organisation.</p>

]]> FESO Interview with Annette Fromm https://eso-stroke.org/feso-interview-annette-fromm/ Mon, 27 Apr 2020 06:50:48 +0000 https://eso-stroke.org/?p=13905 <p>The post FESO Interview with Annette Fromm first appeared on European Stroke Organisation.</p>

]]> .flex_column.av-pxfofs-f8cffa300d0abe60229a0238b37e998b{ border-radius:0px 0px 0px 0px; padding:0px 0px 0px 0px; }

/in /by

To qualify as a FESO, members must demonstrate scientific quality and a willingness to actively volunteer in ESO. There are no age requirements, but FESO must meet minimum standards. FESO receive additional benefits, including participation in the Council of Fellows. Visit our website for more information on how to distinguish yourself as a FESO.

We hope you enjoy getting to know the Fellows who participate in the 2020 interview series and thank them in advance for taking the time to share with our readers.

For the April issue of the ESO member newsletter, we present Annette Fromm, MD PhD MSc (Stroke) FESO, Bergen Stroke Research Group, Center for Neurovascular Diseases, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Annette is a graduate of the ESO supported, European Master Programme in Stroke Medicine and active in ESO and the Norwegian Stroke Organisation. In addition to being an FESO, she is a member of the WISE working group and participated in the ESO national society stroke meetings as the Secretary of the Norwegian Stroke Organisation.

What are your main fields of interest in stroke medicine and research?


My clinical work is mainly focused on the field of acute stroke treatment and monitoring, including the implementation of new evidence into clinical practice. I largely enjoy the tight collaboration with specialists from all medical fields related to neurovascular medicine at our hospital, in order to continuously improve routines and standard procedures. The last months we have been working a lot on the adaptation of our acute stroke pathways and stroke investigation procedures in light of the additional challenges related to the COVID-19 pandemic.

Neurosonology is a subject of special interest to me. I am truly amazed by the various opportunities the available methods deliver both regarding acute phase monitoring options, causal and preventive investigation options, and the possibility to visualize and understand complex hemodynamic contexts impacting further decision making.

As member of the Bergen Stroke Research Group, the research I am involved in is diverse, combining the fields of acute stroke treatment and prehospital alert, Neurosonology, secondary prevention and the wide field of young stroke.


What is the role of ESO in facilitating and promoting the projects you are coordinating or where you are involved?


ESO has gained worldwide recognition as one of the leading stroke societies, with a profile of responsibility, trustworthiness and passion for the field. I understand ESO as a great platform for exchange and collaboration between researchers and clinical practitioners. The work on and continuous renewal of guidelines and expert opinions based on newly gathered knowledge is especially important to me, providing a valuable foundation to follow, re-think or improve own research questions.


What do you expect from ESO in the future to support research?


I expect ESO to keep its open and including profile, as the ESO society makes multicenter and international cooperation and networking easy, pushing the stroke field further in many directions. Possibly ESO may function as an umbrella society for large scale international research proposals, utilizing the enormous professional variety among its members, and being able to involve a large number of research institutions worldwide.


What do you think a mentor should do to support the projects and the career of a mentee and, conversely, what should a mentee expect from a mentor?


A mentor should be open to new ideas of the mentee, help to adjust and support them, guide professional development, encourage self-reflection, suggest alternative directions and, if possible, provide a network to follow those.

A mentee may benefit from several mentors covering the mentee`s need for guidance in different areas of their development. The mentee may bring along curiosity and passion, and should be encouraged to ask for guidance and mentorship whenever needed.

<p>The post FESO Interview with Annette Fromm first appeared on European Stroke Organisation.</p>

]]> Reversible cerebral vasoconstriction syndrome and stroke https://eso-stroke.org/reversible-cerebral-vasoconstriction-syndrome-and-stroke/ Thu, 23 Apr 2020 06:20:14 +0000 https://eso-stroke.org/?p=13798 <p>The post Reversible cerebral vasoconstriction syndrome and stroke first appeared on European Stroke Organisation.</p>

]]> .flex_column.av-pxfofs-f8cffa300d0abe60229a0238b37e998b{ border-radius:0px 0px 0px 0px; padding:0px 0px 0px 0px; }
/in , /by

By Dr Nicolas Martinez-Majander,  Department of Neurology, Helsinki University Hospital, Finland

A 38-year-old man was admitted to our hospital with a thunderclap headache and a transient left upper limb paresis. He was a non-smoker with no comorbidities or prior medications. He also reported having such headaches repeatedly during the previous two weeks, always associated with physical exercise. Initial non-contrast CT showed no ischemia or intracranial hemorrhage. However, on CT angiography we saw multiple arterial abnormalities with smooth narrowings followed by abnormal dilated segments especially in the more distal branches. There were no abnormalities of cerebrospinal fluid (CFS), and aneurysmal subarachnoid haemorrhage and infections of central nervous system were considered unlikely.  Toxicology and infection screen were negative and the patient remained normoglycemic, normotensive, and no epileptic seizures emerged. Brain MRI the second day, however, revealed a small ischemic lesion in the right MCA territory. The patient was suspected of suffering from reversible cerebral vasoconstriction syndrome (RCVS) and treatment with nimodipine was started. In a control imaging at four weeks CT angiography abnormalities had resolved completely and the patient had a full recovery.

RCVS (sometimes also called Call-Fleming syndrome) is a vasculopathy syndrome with segmental constrictions of cerebral arteries that should resolve within three months.1 Typical symptoms and findings include a thunderclap headache, often with a paroxysmal occurrence. However, there are exceptions since up to 20% of cases can have only subacute headaches that are less severe and reoccur over the course of several weeks.2 Patients can develop intracranial hemorrhage, ischemic disturbance of the cerebral circulation, hypertensive encephalopathy (PRES) or epileptic seizures as complications. Associated symptoms might include focal neurological deficits, nausea, and vomiting.

These patients also tend to be younger than average patients with stroke and may have less cardiovascular risk factors. However, more than half the cases occur postpartum, after exposure to adrenergic or serotonergic drugs, or other triggers such as immunosuppressive drugs (tacrolimus and cyclophosphamide) and illicit drugs (cocaine, ecstasy, and marijuana).3

The onset of headache itself is usually triggered by e.g. physical exertion, sex, and sneezing. Transient or persistent neurological deficits are reported in 8-43% of cases, and up to one third of patients present with an intracranial haemorrhage, most frequently convexity subarachnoid haemorrhage (SAH) that is usually smaller than aneurysmal SAHs. The prevalence of intracerebral bleedings and ischemic strokes are estimated to be around 12-20% and 6-39%, respectively.4,5

Diagnostic work-up should include at least brain CT/MRI, CT/MR angiography of cerebral arteries and a lumbar puncture. Arterial imaging should be repeated if suspicion of RCVS is strong and the initial CTA/MRA remains unremarkable. It should also be repeated later to confirm that the arterial abnormalities are indeed reversible within 12 months. Transcranial doppler can be used in the follow-up of the arterial vasoconstriction as well. Also in RCVS, there might be slight abnormalities in the CSF sample, such as presence of small numbers of white blood cells (usually less than 10/ml), elevated protein levels, and erythrocytes (with SAHs caused by vasoconstriction).6 Diagnostic criteria for RCVS have been proposed previously,7,8 and the most important differential diagnoses include aneurysmal SAH, cervical artery dissection, cerebral venous thrombosis, migraine, and primary angiitis of the central nervous system (PACNS).

Treatment of RCVS included pain relief, blood pressure management especially in cases with intracranial haemorrhage, and treatment of seizures if present. Vasoactive agents (if used prior to RCVS) should be paused or stopped. Thus far, since RCVS is often self-limiting and since there are no randomized controlled trials showing superiority of any specific agents, treatment is still empirical guided by observational studies and expert opinions. Nimodipine is the most commonly used calcium channel blocker, but also verapamil and magnesium sulfate can be considered. These agents can be discontinued after resolution of symptoms and/or angiographic findings. The overall prognosis of RCVS is good and long-term morbidity and mortality low, mainly determined by the occurrence of stroke.1

References:

  1. Ducros et al. Reversible cerebral vasoconstriction syndrome. Lancet Neurology 2012;11:906-917.
  2. Robert T et al. Reversible cerebral vasoconstriction syndrome identification of prognostic factors. Clin Neurol Neurosurg 2013;115:2351–2357.
  3. Singhal AB et al. Postpartum angiopathy and other cerebral vasoconstriction syndromes. Neurocrit Care 2005;3:91-97.
  4. Singhal AB et al. Reversible cerebral vasoconstriction syndromes: analysis of 139 cases. Arch Neurol 2011;68:1005–1012.
  5. Ducros A et al. Hemorrhagic manifestations of reversible cerebral vasoconstriction syndrome: frequency, features, and risk factors. Stroke 2010; 41:2505–2511.
  6. Ducros A et al. The clinical and radiological spectrum of reversible cerebral vasoconstriction syndrome. A prospective series of 67 patients. Brain 2007;130:3091–3101.
  7. Headache classification subcommittee of the International Headache Society. The international classification of headache disorders. Cephalalgia. 2004;24:1-160.
  8. Calabrese LH et al. Narrative review: reversible cerebral vasoconstriction syndromes. Ann Intern Med. 2007;146:34-44.

<p>The post Reversible cerebral vasoconstriction syndrome and stroke first appeared on European Stroke Organisation.</p>

]]> Non-HDL-cholesterol in the young -is it worth worrying? https://eso-stroke.org/non-hdl-cholesterol-in-the-young-is-it-worth-worrying/ Thu, 27 Feb 2020 11:42:03 +0000 https://eso-stroke.org/?p=13619 <p>The post Non-HDL-cholesterol in the young -is it worth worrying? first appeared on European Stroke Organisation.</p>

]]> .flex_column.av-pxfofs-f8cffa300d0abe60229a0238b37e998b{ border-radius:0px 0px 0px 0px; padding:0px 0px 0px 0px; }
/in , /by

By Antje Schmidt-Pogoda, Fachärztin für Neurologie, Klinik für Neurologie mit Institut für Translationale Neurologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, Gebäude A1, 48149 Münster

Only recently, the treat stroke to target trial has demonstrated the benefit of aggressive LDL-cholesterol lowering for secondary stroke prevention.1 Depending on the overall cardiovascular risk and LDL-cholesterol levels, Current European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) guidelines also recommend LDL-cholesterol lowering for primary prevention of cardiovascular disease.

However, in young and otherwise healthy people, cholesterol levels are rarely determined. If increased, would this be worth worrying anyway?

A recent risk-evaluation and risk-modelling study from the Multinational Cardiovascular Risk Consortium sheds light on this important issue: Worrying about cholesterol is in fact worth it – even at young age.2 The study included data from almost 400 000 individuals with a maximum follow-up of 43.6 years (median 13.5). The mean age of participants was 51 years with one third at age<45 years. The primary composite endpoint of atherosclerotic cardiovascular disease was defined as the occurrence of a coronary heart disease event or ischemic stroke.

The study results show progressively higher 30-year cardiovascular disease event rates for increasing non-HDL-cholesterol categories (from 7·7% for non-HDL-cholesterol <2·6 mmol/L to 33·7% for ≥5·7 mmol/L in women and from 12·8% to 43·6% in men; p<0·0001).

In women, a non-HDL value of 2.6 to 3.7 mmol/l was associated with a 10% increase in long-term risk of cardiovascular disease. The hazard ratio was significant with a 95% confidence interval of 1.0 to 1.3. A non-HDL value of over 5.7 mmol/l increased the long-term risk by 90% (hazard ratio 1.9; 1.6 to 2.2) and was most marked at age<45 years (hazard ratio 4.3; 3.0-6.1).

The risk was similar for men: the hazard ratios were 1.1 (1.0 to 1.3) for non-HDL cholesterol from 2.6 to 3.7 mmol/l and 2.3 (2.0 to 2.5) for a non-HDL value of over 5.7 mmol/l. Again most prominent at age<45 years (4.6, 3.3-6.5)!

These long-term calculations show that younger people are at risk even with slightly elevated cholesterol levels. The authors attribute this to an accumulating effect. Altogether, these findings pronounce that elevated non-HDL-cholesterol levels should be taken seriously in the young.

  1. Amarenco P, Kim JS, Labreuche J, Charles H, Abtan J, Bejot Y, et al. A comparison of two ldl cholesterol targets after ischemic stroke. N Engl J Med. 2019
  1. Brunner FJ, Waldeyer C, Ojeda F, Salomaa V, Kee F, Sans S, et al. Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium. Lancet. 2019

<p>The post Non-HDL-cholesterol in the young -is it worth worrying? first appeared on European Stroke Organisation.</p>

]]>