TIA – European Stroke Organisation https://eso-stroke.org the voice of stroke in Europe Thu, 31 Mar 2022 10:25:40 +0000 en-GB hourly 1 https://wordpress.org/?v=6.8.5 Capsular Warning Syndrome: not all TIAs remain the same https://eso-stroke.org/capsular-warning-syndrome-not-all-tias-remain-the-same/ Fri, 01 Apr 2022 05:53:46 +0000 https://eso-stroke.org/?p=21935 <p>The post Capsular Warning Syndrome: not all TIAs remain the same first appeared on European Stroke Organisation.</p>

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Giuseppe Reale, MD1,2; Marco Moci, MD2.

1Fondazione Policlinico Universitario A. Gemelli IRCCS, UOC Neuroriabilitazione ad Alta Intensità

2Università Cattolica del Sacro Cuore – Roma, Dipartimento di Neuroscienze

Transient Ischemic Attack (TIA) is usually characterized by transient focal neurological signs such as speech disturbances, hemiparesis or partial visual loss, without any neuroimaging evidence of cerebral ischemia1,2. Short-term risk of stroke after TIA is high: according to the most used score for assessing such risk, ABCD2 score, the risk of stroke within the first 48 hours ranges from 1% to 8.1%, depending on symptoms, their duration, patients’ age, hypertension and diabetes3. However, not all focal neurological signs are the same. This is the case of Capsular Warning Syndrome (CWS) that constitutes a subgroup of all TIAs. First described by Donnan et al in 1993, CWS consists of acute, transient, stereotypical sensory and/or motor symptoms affecting the face, arm and/or leg. There has to be an absence of cortical signs and it has to occur within a seven-day period after an index TIA4–6.

The most comomn manifestation of CWS is with a pure hemiparesis, the number of episodes mostly ranging between 3 to 10 (even in a single day), their mean duration being about 6 minutes, and appearing in “clusters”4–6. Although CWS is only responsible of 1.5-4.5% of all TIAs, the risk of ischemic stroke is likely high, with an incidence ranging between 17% and 70%. A recent review even showed that 74% of these patients had infarction on neuroimaging, which is far above the 8% risk detectable with ABCD2  score4–6. The ABCD3-I score proposed in 2010 added occurrence of at least two TIAs – a so called ‘dual TIA’ – to the stroke risk score7–9 and this was later validated in a Chinese population. However, when the recurrences of symptoms in a patients with a CWS is regarded as a ‘dual TIAs’, the risk of subsequent stroke is likely underestimated10. Pathophysiological mechanisms that might explain such increased risk of ischemic stroke are still unclear. Several mechanisms might contribute to the ischemic damage, including penetrating small vessel disease, hemodynamic impairment, branch-artery disease, artery-to-artery embolism and peri-infarct depolarization6.

Regarding treatment, dual antiplatelet therapy is the mainstay for all TIAs, CWS included6,11,12. Other potential therapies are matter of investigation, such as intravenous tirofiban (overlap loading Clopidogrel 300 mg and Aspirin 100 mg), which has been suggested as a potential intervention toreduce fluctuations in CWS patients13. When a DWI-FLAIR mismatch on MRI in the acute symptomatic phase is present, choosing thrombolytic therapy is reasonable.

In conclusion, CWS represent a non-neglectable sub-group of TIAs, it is characterized by several episodes of transient subcortical neurological symptoms and has a high risk of stroke progression. Therefore, when evaluating a TIA, suspecting CWS could have a significant impact on patients’ management strategies, especially in terms of monitoring during the early stage.

REFERENCES

  1. Sorensen AG, Ay H. Transient ischemic attack: definition, diagnosis, and risk stratification. Neuroimaging Clin N Am. 2011;21:303–313, x.
  2. Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E, Hatsukami TS, Higashida RT, Johnston SC, Kidwell CS, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. 2009;40:2276–2293.
  3. Johnston SC, Rothwell PM, Nguyen-Huynh MN, Giles MF, Elkins JS, Bernstein AL, Sidney S. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. 2007;369:283–292.
  4. Paul NLM, Simoni M, Chandratheva A, Rothwell PM. Population-based study of capsular warning syndrome and prognosis after early recurrent TIA. Neurology. 2012;79:1356–1362.
  5. Donnan GA, O’Malley HM, Quang L, Hurley S, Bladin PF. The capsular warning syndrome: pathogenesis and clinical features. Neurology. 1993;43:957–962.
  6. Sales C, Calma AD. Stroke warning syndrome. Clinical Neurology and Neurosurgery. 2022;213:107120.
  7. Merwick A, Albers GW, Amarenco P, Arsava EM, Ay H, Calvet D, Coutts SB, Cucchiara BL, Demchuk AM, Furie KL, et al. Addition of brain and carotid imaging to the ABCD2 score to identify patients at early risk of stroke after transient ischaemic attack: a multicentre observational study. Lancet Neurol. 2010;9:1060–1069.
  8. Knoflach M, Lang W, Seyfang L, Fertl E, Oberndorfer S, Daniel G, Seifert-Held T, Brainin M, Krebs S, Matosevic B, et al. Predictive value of ABCD2 and ABCD3-I scores in TIA and minor stroke in the stroke unit setting. Neurology. 2016;87:861–869.
  9. Kiyohara T, Kamouchi M, Kumai Y, Ninomiya T, Hata J, Yoshimura S, Ago T, Okada Y, Kitazono T, Fukuoka Stroke Registry Investigators. ABCD3 and ABCD3-I scores are superior to ABCD2 score in the prediction of short- and long-term risks of stroke after transient ischemic attack. Stroke. 2014;45:418–425.
  10. Song B, Fang H, Zhao L, Gao Y, Tan S, Lu J, Sun S, Chandra A, Wang R, Xu Y. Validation of the ABCD3-I Score to Predict Stroke Risk After Transient Ischemic Attack. Stroke. 2013;44:1244–1248.
  11. Johnston SC, Easton JD, Farrant M, Barsan W, Conwit RA, Elm JJ, Kim AS, Lindblad AS, Palesch YY, Clinical Research Collaboration, Neurological Emergencies Treatment Trials Network, and the POINT Investigators. Clopidogrel and Aspirin in Acute Ischemic Stroke and High-Risk TIA. N. Engl. J. Med. 2018;379:215–225.
  12. Wang Y, Wang Y, Zhao X, Liu L, Wang D, Wang C, Wang C, Li H, Meng X, Cui L, et al. Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic Attack. N Engl J Med. 2013;369:11–19.
  13. Li W, Wu Y, Li X-S, Liu C-C, Huang S-H, Liang C-R, Wang H, Zhang L-L, Xu Z-Q, Wang Y-J, et al. Intravenous tirofiban therapy for patients with capsular warning syndrome. Stroke Vasc Neurol. 2019;4:22–27.

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]]> Livedo racemosa in Sneddon Syndrome: a mysterious hint to recognise a rare stroke etiology https://eso-stroke.org/livedo-racemosa-in-sneddon-syndrome-a-mysterious-hint-to-recognise-a-rare-stroke-etiology/ Fri, 18 Feb 2022 11:29:40 +0000 https://eso-stroke.org/?p=21653 <p>The post Livedo racemosa in Sneddon Syndrome: a mysterious hint to recognise a rare stroke etiology first appeared on European Stroke Organisation.</p>

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By: Dr. Inna Lutsenko, Specialist, Neurologist, Center for Distance Learning and Advanced Training, Kyrgyz State Medical Academy after I.K.Akhunbaev

twitter: @inna_lutsenko

Sneddon syndrome (SS) is a rare disorder (about 4 patients per million), affecting small and medium-sized blood vessels in mainly young females (1). A typical pattern on the skin, concomitant livedo racemosa (LR), a persistent and pathological form of livedo reticularis, which is caused by intimal thickening of the small deep dermal arteries (2), helps to suspect a rare stroke etiology based on a Sneddon syndrome in young women. Salomon Ehramn, Austrian dermatologist already in 1907 very colorfully described this skin phenomena in his work devoted to vascular lesions in syphilis: “a blue slender tree-branching and “forked lighting” pattern that worsens in cool temperature” (4). Pathogenetic explanation for this pattern is that LR develops due to a permanent focal arteriolar obstruction which produces branching net-like pattern and broken circles-hallmarks of racemosa lesion (5). The pathogenesis of Sneddon syndrome itself is unknown, although the detection of anticardiolipin antibodies in 9 to 42% of SS patients suggested a possible overlap with the antiphospholipid antibody syndrome and an immune-mediated pathogenesis (6). Theories on pathology of Sneddon syndrome postulate a primarily thrombotic focus, a cardio-embolic aetiology caused by associated valvular disease or inherited/acquired endothelial dysfunction (5-7).

In Sneddon syndrome the involvement of many organs is observed: it can manifest with signs of ischemic heart disease, myocardial infarction, cardiac murmurs (7), microthrombosis in the systemic flow, including uttering vessels and leading to obstetric complications as well as endarteritis obliterans in the skin and the kidney.

Common neurological manifestations are ischaemic or haemorrhagic stroke, transient ischaemic attack (TIA), cognitive impairment, headache and epilepsy. Boesch et al. described in their study 13 patients with SS and the development of clinical features over 6 years (8). Neurological symptoms included headache, vertigo, dizziness, loss of concentration, memory disturbances, or emotional dysregulation. In 54 % of this study there was a development of TIA with involvement of the middle cerebral artery territory in 84% (8). In Boesch study, an interesting MRI finding was infarcts involving the cortical and subcortical layers, resembling watershed and embolic infarcts.. Tietjen et al. made an observation that LR is common in persons being treated for migraine, and that migraineurs with LR more frequently report a history of stroke than those without LR, showing an odds ratio (OR) of 4.4 [95% confidence interval (CI) 1.4, 13.9] for stroke within the cohort with LR (9). Brain histopathological reports in persons with Sneddon’s syndrome are limited in number but suggest that a similar non-inflammatory endothelial process may underlie vascular lesions in the brain (10). on histpathological examination leukoencephalopathy, multiple cortical infarcts and fibrosis of the intima of the vessels comprising the circle of Willis were also described (11).

In conclusion, examination of the skin is important to detect rare causes of stroke. Sneddon syndrome, sometimes accompanied with LR and/or aPL antibodies, should be considered in cryptogenic stroke patients.


Livedo racemosa. An erythematous tree branching and forked-lightning pattern on the lower extremities.

P. Samanta D, Cobb S, Arya K. Sneddon Syndrome: A Comprehensive Overview. J Stroke Cerebrovasc Dis. 2019 Aug;28(8):2098-2108. Doi: 10.1016/j.jstrokecerebrovasdis.2019.05.013. Epub 2019 May 31. PMID: 31160219. https://pubmed.ncbi.nlm.nih.gov/31160219/

References

  1. Greisenegger E K, Sara L,  Chamorro A, Cervera A, Jimenez‐Escrig A, Rappersberger K, Marik W, Greisenegger S, Stögmann E, Kopp T,  Strom T, Henes J, Joutel A, Zimprich A. A NOTCH3 homozygous nonsense mutation in familial Sneddon syndrome with pediatric stroke.  Journal of Neurology (2021) 268:810–816 https://doi.org/10.1007/s00415-020-10081-5
  2. Sneddon Syndrome: A Case Report Exploring the Current Challenges Faced with Diagnosis and Management. Jonathan Cleavera Mario Teob Shelley Renowdenc Keith Millerd Harsha Gunawardenae Philip Clatworthya. Case Rep Neurol 2019;11:357–368
  3. Tourbah A, Piette JC, Iba-Zizen MT, Lyon-Caen O, Godeau P, Francès C. The natural course of cerebral lesions in Sneddon syndrome. Arch Neurol. 1997 Jan;54(1):53–60.
  4. Ehrmann S. Ein neues Gefassymptom bei Lues. Wien Med Wochenschr 1907;16:777-782.
  5. Samanta D, Cobb S, Arya K. Sneddon Syndrome: A Comprehensive Overview. J Stroke Cerebrovasc Dis. 2019 Aug;28(8):2098-2108. doi: 10.1016/j.jstrokecerebrovasdis.2019.05.013. Epub 2019 May 31. PMID: 31160219.
  6. Bersano A, Morbin M, Ciceri E, Bedini G, Berlit P, Herold M, Saccucci S, Fugnanesi V, Nordmeier H, Faragò G, Savoiardo M, Taroni F, Carriero M, Boncoraglio G B, Perucca L, Caputi L, Parati E A, Kraemer M. The diagnostic challenge of Divry van Bogaert and Sneddon Syndrome: Report of three cases and literature review. Journal of thNeurological Sciences 364 (2016) 77–8 http://dx.doi.org/10.1016/j.jns.2016.03.011 0022-510X/© 2015 Elsevier B.V. All rights reserved.
  7. Kalashnikova L, Nasonov E , Borisenko V, Usman V, Prudnikova L, Kovaljov L,  Kushekbaeva A. Sneddon’s syndrome: cardiac pathology and antiphospholipid antibodies. Clin Exp Rheumatol. Jul-Aug 1991;9(4):357-61.
  8. S M Boesch, A L Plörer, A J Auer, W Poewe, F T Aichner, S R Felber, N T Sepp. The natural course of Sneddon syndrome: clinical and magnetic resonance imaging findings in a prospective six year observation study. J Neurol Neurosurg Psychiatry 2003;74:542–544
  9. Tietjen GE, Al Qasmi MM, Shukairy MS. Livedo reticuaris and migraine: a marker for stroke risk? Headache 2002; 42:352–5.
  10. GE Tietjen, MM Al-Qasmi, P Gunda & NA Herial. Sneddon’s syndrome: another migraine–stroke association? Cephalalgia, 2005, 26, 225–232. doi:10.1111/j.1468-2982.2005.01032.x

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]]> GSSW – Session 5 – Future Research Models https://eso-stroke.org/garmisch-stroke-science-workshop-session-5-future-research-models/ Mon, 29 Nov 2021 06:50:37 +0000 https://eso-stroke.org/?p=20793 <p>The post GSSW – Session 5 – Future Research Models first appeared on European Stroke Organisation.</p>

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By: Ellis van Etten, Bart van der Worp, Mira Katan

twitter: #GSSW @Ellis_van_Etten

ESO Garmisch Stroke Science Workshop 2021

Session 5: Future Research Models

 

The last day of the Garmisch Stroke Science Workshop started with a sessions that focused on future research models. The speakers informed the audience about new technical developments and exciting new frontiers in stroke research. This led to a lively discussions about the benefits, but also potential pitfalls of using these new technologies. This session was hosted by Bart van der Worp and Mira Katan.

The first talk and the keynote lecture of this session, was given by Philippe Ryvlin, professor of Neurology at the University of Lausanne. Professor Ryvlin introduced us to the Human Brain Project (HBP) and explained its broad infrastructure and capacity to model and simulate multiscale human brain networks. He elaborated on the steps leading from a classical input, i.e. MRI, to simulation of brain activity and refining the model by applying it to real data. Objectives for stroke research are to better understand the heterogeneity between patients, predict post-stroke recovery and individualize rehabilitation approaches. He demonstrated a framework for federated analyses that allows for standard analyses and machine learning techniques in larger datasets while ensuring privacy regulations. The FERES project (Federating European REgistries for Stroke), which is an EAN-ESO-HBP initiative, will focus on federating European national stroke registries. All in all, many promising possibilities of the HBP to help advance stroke research and improve stroke care.

Moving on, Jeannette Hofmeijer from the University of Twente introduced us to induced pluripotent stem cells for penumbra research. She pointed out that conventional imaging techniques sometimes show surprisingly normal images of damaged brain tissue, e.g. in the case of hypoxia after cardiac arrest. She pointed out that using the human brain-on-a-chip model provides an unique opportunity to translate findings between animal models and patients by creating a network of different types of brain cells. By inducing metabolic conditions that simulate hypoxia, she and her research group can study reversable and irreversible neuronal processes such as synaptic failure and loss of neuronal network activity. Currently, she is using this exciting technique to study potential treatment strategies for ischemic brain damage and we will hear many more interesting insights from her side in the near future.

The third speaker, Peter Kelly from the Mater University Hospital/University College Dublin and our next ESO President, presented his views on future therapeutic targets for secondary prevention. Prof. Kelly started by showing that the residual risk of cardiovascular complications after ischemic stroke or TIA is still substantial despite current secondary prevention strategies. He discussed the optimal blood pressure target according to the current guidelines and emphasized the need for data on safety and generalisability before we can apply these targets to all stroke patients. As for LDL, we are also in need of stroke specific RCT data reflecting the stroke population that is often older and might have underlying small vessel disease. He introduced the concept of adaptive platform trials, such as the STARMAP study, that can answer several research questions simultaneously by performing multiple randomized comparisons, thereby saving precious time, money, and resources.

Lastly, Ivo Jansen from the Academic Medical Centre in Amsterdam gave a presentation about artificial intelligence and the future of imaging. He explained the concept of convolutional neural networks and how this technique cannot only be used to perform classical human tasks, for example spotting an hemorrhage on CT, but also “non-human” tasks that cannot be performed by human assessor. He demonstrated several non-human tasks including vessel segmentation for determining clot characteristics, collateral imaging, and hemorrhage volume quantification. Also pre-hospital triage and treatment planning were mentioned as potential applications. He also pointed out that, although these techniques are very promising, we should keep in mind the risk of bias and the need of enough, good quality training data.

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]]> The Wrong Referral? https://eso-stroke.org/the-wrong-referral/ Fri, 23 Apr 2021 10:36:53 +0000 https://eso-stroke.org/?p=18428 <p>The post The Wrong Referral? first appeared on European Stroke Organisation.</p>

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By Dr Linxin Li, Wolfson Centre for Prevention of Stroke and Dementia, Nuffield Department of Clinical Neurosciences, Oxford University

A case from the TIA clinic


It has been a long time since we last met.

I thought this is an interesting case to share with you.

A man in his late 50s was referred to the TIA clinic and complained of recurrent episodes of transient bilateral sensory disturbance for 2 months.

He described these episodes as sudden onset of numbness from head down to both arms lasting for only seconds. There was no trigger identified and was not position related. They could occur at random times without any warning and usually happen once every few days. There was no loss of consciousness, no speech or visual disturbance and no pain. Usually they were not associated with weakness but there was one occasion, after having a cluster of these sensory disturbances he also noticed left arm weakness lasting for approximately 15 minutes.

He has several vascular risk factors, including being an ex-smoker, history of hypertension and hyperlipidaemia.

On examination, his blood pressure was 160/70mmHg and he was in sinus rhythm. Neurological exam was unremarkable.

What are the possible differentials that have come into your mind? Seizures? Transient focal neurologic episodes? TIAs?

Bilateral sensory disturbance is listed as one of the key features for posterior circulation syndrome by the OCSP classification and this additional episode of arm weakness also raised suspicion of these events being vascular.1 Therefore he went on to have MRI brain, which didn’t show any acute infarct, cerebral microbleed or cortical superficial siderosis. However, the CT angiogram showed a tight stenosis of the intracranial segment of the dominant right vertebral artery.

Posterior circulation TIA due to large artery disease was diagnosed and he was subsequently treated with dual antiplatelet therapy (DAPT) and high dose statins. These transient sensory disturbance has since receded.

TIA and ischaemic stroke with vertebrobasilar (VB) artery stenosis is associated with high risk of recurrence. The risk is highest in those with intracranial VB stenosis, which our patient had, with the 90 day risk of stroke being 33.3%.2

Best medical therapy including DAPT for 90 days and high dose statin is at the moment the recommended approach for patients with intracranial stenosis.3 However, there is scarce data on whether dual antiplatelet therapy should go beyond 90 days. Post hoc exploratory analysis from SAMMPRIS suggested that there might be a signal of benefit for DAPT beyond 90 days without any obvious signal of increased major bleeding.4

The role of stenting in treating VB stenosis overall has also been long debated. Pooled results from three randomised controlled trials (VIST, VAST and SAMMPRIS) found no evidence of benefit of stenting for intracranial stenosis compared to best medical treatment alone, partly due to the high procedural stroke risk. Although stenting for extracranial stenosis might be beneficial, further larger trials are required to determine the treatment effect in this subgroup.5 New imaging markers such as distal flow status might also serve as a useful tool in identifying high-risk patients who might benefit from more aggressive management.6

So the take home messages for today: think about posterior circulation events when patients present with bilateral symptoms. Best medical treatment is the currently recommended treatment option for patients with symptomatic VB stenosis and we are waiting to hear from future trials on stenting vs. best medical treatment especially in extracranial VB stenosis.

 

References

  1. Bamford J, Sandercock P, Dennis M, et al. Classification and natural history of clinically identifiable subtypes of cerebral infarction. Lancet. 1991; 337:1521–1526
  2. Gulli G, Marquardt L, Rothwell PM, Markus HS. Stroke risk after posterior circulation stroke/transient ischemic attack and its relationship to site of vertebrobasilar stenosis. Stroke. 2013; 44: 598-604
  3. MI Chimowitz, MJ Lynn, CP Derdeyn, et al. Stenting versus aggressive medical therapy for intracranial arterial stenosis. N Engl J Med. 2011; 365, 993-1003
  4. Rahman LA, Turan TN, Cotsonis G, et al. Dual antiplatelet therapy beyond 90 days in symptomatic intracranial stenosis in the SAMMPRIS trial. J Stroke Cerebrovasc Dis. 2020: 105254
  5. Markus HS, Harshfield EL, Compter A, et al. Stenting for symptomatic vertebral artery stenosis: a preplanned pooled individual patient data analysis. Lancet Neurol. 2019; 18: 666-673
  6. Amin-Hanjani S, Pandey DK, Rose-Finnell L, et al. Effect of Hemodynamics on Stroke Risk in Symptomatic Atherosclerotic Vertebrobasilar Occlusive Disease. JAMA Neurol. 2016:178-85.

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]]> A TIA mimic which alerts of high intracerebral hemorrhage risk https://eso-stroke.org/a-tia-mimic-which-alerts-of-high-intracerebral-hemorrhage-risk/ Fri, 11 Sep 2020 09:40:59 +0000 https://eso-stroke.org/?p=15832 <p>The post A TIA mimic which alerts of high intracerebral hemorrhage risk first appeared on European Stroke Organisation.</p>

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

Cerebral amyloid angiopathy (CAA) is recognized as a major cause of spontaneous lobar intracerebral hemorrhage, especially in the elderly.1 The development of validated neuroimaging criteria (the Boston criteria) has resulted in CAA being increasingly detected during a person’s lifetime and resulted in greater knowledge about different clinical syndromes related to the cerebrovascular pathological trait. In addition to spontaneous lobar intracerebral hemorrhage and cognitive impairment, transient focal neurological episodes (TFNEs) have been increasingly recognized.2

TFNEs are short (up to 30 min, usually < 5min) often recurrent and stereotyped episodes of unilateral focal disturbances that have a wide spectrum of clinical features. The most common presentation is somatosensory (paresthesias, with or without numbness) or motor deficits but visual or language deficits can also occur. Typically the symptoms spread over a few minutes from one body part to another (often involving the perioral area and upper limb – a cheiro-oral pattern). Most patients present with a combination of symptoms instead of an isolated deficit. In about half of the cases the symptoms can clinically resemble classic TIAs with predominantly negative symptoms such as hemiparesis or aphasia, making TFNEs an important TIA mimic. 3, 4

TFNEs seem to be triggered mostly by superficial cortical hemorrhages (sulcal subarachnoid hemorrhage if acute and cortical superficial siderosis if chronic), which can be a biomarker of advanced CAA, likely caused by repeated episodes of small cortical bleeds into the subarachnoid space from fragile CAA affected vessels.2 The symptoms are thought to be related to the phenomenon of cortical spreading depression caused by electrophysical changes in the cortex.5 However, especially in younger patients, other causes of sulcal subarachnoid hemorrhage should also be considered.

The primary radiologic investigation in patients with TFNEs is MRI, which should include a blood-sensitive sequence. CT can often be negative for superficial cortical hemorrhages and does not allow evaluation for other CAA biomarkers.4

The differentiation of CAA-related TFNEs and TIAs has important treatment implications. Patients with sulcal subarachnoid hemorrhage due to amyloid angiopathy have a higher risk of developing a lobar intracerebral hemorrhage. As many as 50% of TFNE patients developed a symptomatic lobar intracerebral hemorrhage over a median follow-up of 14 months in a European multicenter study.6 Patients with TIAs are routinely treated with antiplatelet medications and increasingly with dual antiplatelet therapy. However, these agents may need to be avoided in CAA patients, unless there is a compelling indication.5

TFNEs are an underdiagnosed entity often mistaken for TIAs or other paroxysmal neurological events such as focal seizures or migraines with aura. Clinicians should have a high yield of suspicion for CAA-related TFNEs in older patients (>55 years old) who present with migratory symptoms and recurrent stereotyped events or other features atypical for TIAs, and refer these patients for a MRI scan including a blood-sensitive sequence.  The clinician who recognizes symptoms related to CAA should consider the use of antithrombotics in these patients with great caution and make appropriate interventions, such as better control of blood pressure, to reduce the risk of intracerebral hemorrhage in this patient group. 5,7

References

  1. Viswanathan A, Greenberg SM. Cerebral Amyloid Angiopathy in the Elderly. Ann Neurol. 2011;70:871–880
  2. Charidimou A, Boulouis G, Gurol ME, et al. Emerging concepts in sporadic cerebral amyloid angiopathy. Brain. 2017; 140: 1829-1850
  3. Charidimou A, Baron JC, Werring DJ. Transient focal neurological episodes, cerebral amyloid angiopathy, and intracerebral hemorrhage risk: looking beyond TIAs. International Journal of Stroke. 2013; 8:105-108
  4. Vales-Montero M, García-Pastor A, Iglesias-Mohedano AM, et al. Cerebral amyloid angiopathy-related transient focal neurological episodes: A transient ischemic attack mimic with an increased risk of intracranial hemorrhage. Journal of the Neurological Sciences. 2019; 406: 116452
  5. Charidimou A. Cerebral amyloid angiopathy-related transient focal neurological episodes (CAA-TFNEs): A well- defined clinical-radiological syndrome. Journal of the Neurological Sciences. 2019; 406: 116496
  6. Charidimou A, Peeters A, Fox Z, et al. Spectrum of Transient Focal Neurological Episodes in Cerebral Amyloid Angiopathy. Multicentre Magnetic Resonance Imaging Cohort Study and Meta-Analysis. Stroke. 2012;43:2324-2330
  7. Stanton JED, Chandratheva A, Wilson D, et al. Clinical features distinguish cerebral amyloid angiopathy‐associated convexity subarachnoid haemorrhage from suspected TIA. Journal of Neurology. 2020; 267:133–137

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]]> ESJ Comment: Symptomatic carotid stenosis: time to relax? https://eso-stroke.org/esj-comment-symptomatic-carotid-stenosis-time-to-relax/ Wed, 10 Jun 2020 08:06:30 +0000 https://eso-stroke.org/?p=14584 <p>The post ESJ Comment: Symptomatic carotid stenosis: time to relax? first appeared on European Stroke Organisation.</p>

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Comment Author: Linxin Li, Wolfson Centre of Prevention of Stroke and Dementia, Nuffield Department of Clinical Neurosciences, Oxford University, UK

Original Article: : den Brok, M. G., Kuhrij, L. S., Roozenbeek, B., van der Lugt, A., Hilkens, P. H., Dippel, D. W., & Nederkoorn, P. J. (2020). Prevalence and risk factors of symptomatic carotid stenosis in patients with recent transient ischaemic attack or ischaemic stroke in the Netherlands. European Stroke Journal. https://doi.org/10.1177/2396987320932065

Stroke incidence has fallen in high-income countries in the last four decades and the trend of declining has been maintained in recent years,1,2  largely due to better control of blood pressure and the use of preventative drugs, such as statins. However, a previous systematic review suggested that among the different aetiological subtypes of ischaemic stroke, there was an increase of cardioembolic stroke in whites and an increase of large artery atherosclerosis in Asians.3 Less is known about the current estimates of symptomatic carotid stenosis in predominantly White population.

In this issue of the European Stroke Journal, Melina GHE den Brok and colleagues reported up-to-date data on the prevalence and risk factors of ipsilateral extracranial internal carotid artery (ICA) stenosis in patients with recent transient ischaemic attack (TIA) or ischaemic stroke from a retrospective multi-centre study in the Netherlands.4

Among all 938 patients with a recent TIA or ischaemic stroke in the ICA territory, 883 (94.1%) that had carotid imaging were included. The degree of ICA stenosis was first measured using predominantly duplex ultrasonography (58%), followed by computed tomography angiography (CTA-13.8%) and magnetic resonance angiography (MRA-1.1%). ICA stenosis was defined as atherosclerotic luminal narrowing in the proximal extracranial ICA or at the location of the carotid bifurcation and the degree of stenosis was determined using the NASCET criteria.

What are the key findings?

  • Of all 883 patients (mean age 70 years), 110 (12.5%) had an ICA stenosis of 50-99%, with an additional 46 (5.2%) patients having an occlusion.
  • The prevalence of any ICA stenosis of 50-100% was higher in men (23.4% vs. 10.6% in women) and in whites (21.8% vs. 11.7% in non-whites).
  • Risk factors for ≥50% ICA stenosis included age, male sex, retinal ischaemia and current smoking.

Although it is difficult to reliably compare the current estimates to previous studies given the difference in study characteristics, the prevalence of 12.5% found in this study seemed to be lower than reported in historical cohorts (ranging from 12-25%), which also coincided with a high proportion of patients being on statins (39.2%) premorbidly. Whilst the findings are encouraging, there is perhaps still room for improvement. It is particularly worth noting that a third of patients with 50-100% stenosis were smokers and one in five had history of peripheral vascular disease.

As the authors concluded, the prevalence of symptomatic ICA appeared to be falling in recent years but it is not time to relax yet. With the aging population, we will need to work even harder to maintain the current trend. Moreover, the higher prevalence of stenosis in whites is intriguing and future studies will be needed to explore this more thoroughly.

References

  1. Feigin VL, Lawes CM, Bennett DA, Barker-Collo SL, Parag V. Worldwide stroke incidence and early case fatality reported in 56 population-based studies: A systematic review. Lancet Neurology. 2009;8:355-369
  2. Li L, Scott CA, Rothwell PM. Trends in stroke incidence in high-income countries in the 21st century, Stroke. 2020; 51: 1372-1380
  3. Ornello R, Degan D, Tiseo C, Di Carmine C, Perciballi L, Pistoia F, et al. Distribution and temporal trends from 1993 to 2015 of ischemic stroke subtypes: A systematic review and meta-analysis. Stroke. 2018; 49:814-819
  4. den Brok MGHE, Kuhrij LS, Roozenbeek B, van der Lugt A, Hilkens PHE, Dippel DWJ, et al. Prevalence and risk factors of symptomatic carotid stenosis in patients with recent transient ischaemic attack or ischaemic stroke in the Netherlands. European Stroke Journal. Epub 09/06/2020. DOI: 10.117/2396987320932065

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]]> Antihypertensive drugs: morning or evening? https://eso-stroke.org/antihypertensive-drugs-morning-or-evening/ Fri, 15 Nov 2019 06:20:33 +0000 https://eso-stroke.org/?p=12531 There is emerging evidence in favour of evening vs. morning dosing in patients with diagnosed hypertension. Many questions remain to be answered before we can confidently change the timing of all our patients taking antihypertensive medication.

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By Dr Linxin Li, Centre for Prevention of Stroke and Dementia, Nuffield Department of Clinical Neurosciences, Oxford University

This week, in the TIA clinic we have a 75-year old patient coming back for his 1-year follow-up. He is currently taking all the prescribed secondary prevention medication including two antihypertensive drugs. He has brought back his home blood pressure readings recorded over the preceding months, which consistently showed that despite relatively well-controlled blood pressure during the day, he has late evening spikes. An Ambulatory Blood Pressure Monitor (ABPM) was also fitted which suggested that he has a non-dipper pattern during sleep.

What does this mean? Should we treat his blood pressure differently, for example by changing the timing of these blood pressure medications?

It was suggested more than 4 decades ago that in healthy individuals, blood pressure follows a circadian pattern, where it starts to drop from late evening onwards, reaching a nadir around midnight and then rises up again just after awakening in the morning.1 However, this pattern can change with increasing age or occurrence of cardiovascular disease.2 With the use of ABPM, this phenomenon together with its variation is now more accurately defined and individuals who have a fall of >10% in systolic and diastolic blood pressure in the night compared to their daytime readings are defined as “normal dippers”, whereas individuals with a nocturnal fall <10% are “non-dippers” and those with a paradoxical rise at night are “reverse dippers”.2 Numerous studies have since suggested that disappearing of the relative day vs. night blood pressure ratio is associated with increased risks of cardiovascular events.3 Moreover, emerging evidence also showed that reversing the “non-dippers/reverse dippers” by switching the antihypertensive medication from first thing in the morning to the evening is possible and may reduce future risks of cardiovascular disease without an increase in adverse effects in high risk population.4

So yes, the nocturnal blood pressure pattern of our patient does matter and it is perhaps worth a trial to switch his antihypertensive drugs to the evening to see if we can better control his blood pressure.

One step further – given that the activity of the renin-angiotensin-aldosterone system, which is important in blood pressure regulation, peaks during sleep, should we give blood pressure medication to all our patients in the evening irrespective of their nocturnal blood pressure pattern anyway?

There is emerging evidence in favour of evening vs. morning dosing in patients with diagnosed hypertension. The Monitorización Ambulatoria para Predicción de Eventos Cardiovasculares (MAPEC) study was the first trial to compare in 2156 hypertensive patients a regimen of bedtime vs. morning dosing. After a median follow-up of 5.6 years, they showed that compared with morning dosing, the bedtime regimen was associated with reduced prevalence of non-dipping and a 64% lower risk of cardiovascular events.5 More compelling evidence comes from the recent Hygia Chronotherapy Trial, which randomised in a primary care setting 19,084 hypertensive patients with a mean age of 60.5 years to bedtime vs. morning dosing. They found that during a median follow-up of 6.3 years, compared to usual morning dosing, bedtime dosing significantly increased nocturnal dipping and almost halved the risks of major cardiovascular event. The result was also consistent for reducing stroke risk (hazard ratio=0.51).6

Although promising, many questions however remain to be answered before we can confidently change the timing of all our patients taking antihypertensive medication. Does the observed effect apply in secondary prevention? What about at older ages? Does different drug class have a different effect? What about the long-term effect on cognition?

Another ongoing trial – The Treatment In Morning versus Evening (TIME) study might soon shed light on some of these questions.7 But before that, antihypertensive drugs: morning or evening? This remains a question.

 

References

  1. Millar-Craig MW, Bishop CN, Raftery EB. Circadian variation of blood-pressure. Lancet 1978; i: 795-97
  2. Mahabala C, Kamath P, Bhaskaran U, et al. Antihypertensive therapy: nocturnal dippers and nondippers. Do we treat them differently? Vasc Health Risk Manag 2013; 9:125-133
  3. Fagard RH, Thijs L, Staessen JA, et al. Night-day blood pressure ratio and dipping pattern as predictors of death and cardiovascular events in hypertension. J Hum Hypertens 2009;23:645–53.
  4. Hermida RC, Ayala DE, Mojón A, et al. Influence of time of day of blood pressure-lowering treatment on cardiovascular risk in hypertensive patients with type 2 diabetes. Diabetes Care 2011;34:1270–6.
  5. Hermida RC, Ayala DE, Mojón A, et al. Influence of circadian time of hypertension treatment on cardiovascular risk: results of the MAPEC study. Chronobiol Int 2010;27:1629–51.
  6. Hermida RC, Crespo JJ, Dominguez-Sardina M, et al. Bedtime hypertension treatment improves cardiovascular risk reduction: the Hygia Chronotherapy Trial. Eur Heart J 2019;  doi: 10.1093/eurheartj/ehz754.
  7. Rorie DA, Rogers A, Mackenzie IS, et al, Methods of a large prospective, randomised, open-label, blinded endpoint study comparing morning versus evening dosing in hypertensive patients: the Treatment In Morning versus Evening (TIME) study. BMJ open 2016; http://bmjopen.bmj.com/content/6/2/e010313

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]]> Sometimes Age Doesn’t Matter https://eso-stroke.org/sometimes-age-doesnt-matter/ Fri, 23 Aug 2019 06:16:40 +0000 https://eso-stroke.org/?p=11857 By Dr Linxin Li, Centre for Prevention of Stroke and Dementia, Nuffield Department of Clinical Neurosciences, Oxford University, UK Mr X was referred to our TIA clinic last month. He is in his late-60s. Although retired, he has remained active in life. He has known history of hypertension, hyperlipidaemia and has smoked 18-20 cigarettes/day for […]

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By Dr Linxin Li, Centre for Prevention of Stroke and Dementia, Nuffield Department of Clinical Neurosciences, Oxford University, UK

Mr X was referred to our TIA clinic last month. He is in his late-60s. Although retired, he has remained active in life. He has known history of hypertension, hyperlipidaemia and has smoked 18-20 cigarettes/day for over 40 years.

He presented with two clear-cut transient episodes of right arm weakness. The first event was approximately 2 weeks prior to the clinic appointment when he suddenly noticed that he couldn’t lift the right arm to his face whilst relaxing in the living room. His face or leg was not affected and there was no visual disturbance or speech difficulty. The “dead” arm was back to normally in about five minutes. Then one week prior to the clinic, he had another similar episode when cooking in the kitchen. Again, he suddenly felt that his right arm was weak which resolved in five minutes.

In clinic, his blood pressure was raised at 150/95 mmHg. Neurological exam was unremarkable and he was in sinus rhythm. MRI brain did not show any acute infarct but Carotid Doppler confirmed a stenosis of 60% of the left internal carotid artery at the bifurcation. There was no intracranial stenosis.

So far, all seemed to be straight-forward in terms of aetiology: large artery atherosclerosis in relation to smoking and uncontrolled hypertension/hyperlipidaemia. He was subsequently discharged on standard secondary prevention and was seen by the vascular team with carotid endarterectomy (CEA) scheduled for the following week.

Unfortunately, the story then had a sharp turn.

Two days after being treated in the TIA clinic whilst still waiting for CEA, he presented to the emergency department again with acute onset complete right hand weakness. This time the symptom persisted and considering he is right-handed and is still very active, he was thrombolysed. Mr X recovered well the next day with a normal CT scan. The vascular team was informed about this new admission and came to review him before discharge.

Then, the true story emerged.

It turned out that the most recent episode occurred after a “big party” and on direct questioning, it became apparent that Mr X took cocaine during the party. Moreover, he also used cocaine prior to both of the two initial presentations. Consequently the vascular team felt that the vasoconstriction/spasm associated with the cocaine use was probably contributing more to the recurrent TIAs rather than the <70% smooth stenosis and the CEA was cancelled. Mr X was advised to stop smoking and stop using cocaine. He has not had any recurrence since.

Illicit drug use is normally perceived as behaviour of the young and as a result substance abuse is usually only reserved into a standard history taking for younger patients. However, illicit drug use is reported to be increasing in persons over the age of 65 years in Europe,1 with cocaine and heroin being the two mostly abused substances.2 Whilst this phenomenon is largely under-recognised, it probably reflects the ageing of the general population with people using drugs continuing to do so when they get older and could also be related to the baby boomer generation.3

Numerous case series and cohort studies have suggested a causal link between acute cocaine use and strokes in young adults.4,5 The proposed mechanisms included vasospasm, hypertensive surge causing altered cerebral autoregulation, cerebral vasculitis, enhanced platelet aggregation and cardiac arrhythmia,6 all of which may still be relevant at older ages. It is also possible that with higher frequency of underlying comorbidities at older ages, cocaine as well as other illicit drugs could act as the last straw.

To conclude, it probably no longer holds true that the use of illicit drugs is restricted to the young. As clinicians, we should also increase our awareness of the issue at older ages as it may impact both the diagnosis and the management of our patients.

Sometimes, age doesn’t really matter!

 

Reference

  1. European Monitoring Centre for Drugs and Drug Addiction, Substance Use among Older Adults: A Neglected Problem, 2008 Lisbon, European Monitoring Centre for Drugs and Drug Addiction. 4
  2. Arndt S, Clayton R, Schultz SK. Trends in substance abuse treatment 1998–2008: increasing older adult first-time admissions for illicit drugs. Am J Geriatr Psychiatry. 2011; 19: 704–711.
  3. Beynon CM. Drug use and ageing: older people do take drugs! Age Ageing. 2009; 38: 8-10
  4. de los Ríos F, Kleindorfer DO, Khoury J, et al. Trends in substance abuse preceding stroke among young adults: a population-based study. 2012; 43: 3179–3183.
  5. Cheng YC, Ryan KA, Qadwai SA, et al. Cocaine use and risk of ischemic stroke in young adults. Stroke. 2016; 47: 918-922

Treadwell SD, Robinson TG

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]]> ESOC 2019: Trainsient Ischemic Attack https://eso-stroke.org/esoc-2019-trainsient-ischemic-attack/ Thu, 23 May 2019 15:26:07 +0000 https://eso-stroke.org/?p=11013 The session trainsient ischemic attack took place at 14.45-16.15. The chairs were Prof Marcel Arnold and Prof Ursula Schulz. The first talk was transient neurological attacks are they actually TIAS? Prof Ewoud van Dijk mentioned nonfocal transient neurological attacks (TNS) has 23% DWI lesions whereas TIAs has 31% DWI lesions. Majority of these lesions in […]

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The session trainsient ischemic attack took place at 14.45-16.15. The chairs were Prof Marcel Arnold and Prof Ursula Schulz. The first talk was transient neurological attacks are they actually TIAS? Prof Ewoud van Dijk mentioned nonfocal transient neurological attacks (TNS) has 23% DWI lesions whereas TIAs has 31% DWI lesions. Majority of these lesions in TNS are multiple small lesions. And confusion and isolated hemihypoesthesia are the most common symptoms. 1/3 of patients has transient cognitive impairment after TIA and increased 5 year risk of dementia. The second speaker was Prof Werner Hacke with the topic TIA as a marker of future vascular risk in AF. He focused that in newly diagnosed AF patients a history of TIA is associated with an increased risk of one year mortality and stroke. This excess risk is almost exclusively attributable to a history of stroke or a history of both stroke and TIA while history of TIA only is a much weaker predictor. This weak predictive power of history of TIA is probably caused by the low reliability of establishing the diagnosis of TIA retrospectively specifically if the diagnosis is made by non neurologists.  Every practice most AF patients are evaluated by non neurologists who may have difficulties in diagnosing TIA. He mentioned a newer risk calculator such as Garfield AF risk score that only assess a history of stroke may be preferable to the old risk scores.

Prof Kristina Szabo talked about Imaging in suspected TIA how much is needed? Retrospective US study in 2017 done by Chatarvedi on 7889 patients reported that 85% of the patients had CT or MRI only within 2 days of TIA and 49% had only CT. Increased odds of CT performance is older than 80 years, prior stroke and history of AF , but CT is unremarkable in 90% of patients. Increased odds of MRI performance is diplopia, symptom duration more than 6 hours. But also the percentage of clinical diagnosis of TIA with diffusion weighted MRI is 30-70%. DWI positive patients in TIA have higher rate of prior AF or AF diagnosed during the hospital stay. She mentioned that DWI positivity and vessel pathology convey useful. When MRI is not avaliable non contrast CT plus vessel imaging are alternative methods of choice. Use whichever techniques are more quickly available at your institution.

The next speaker was Prof Eleni Korompoki with the title of screening for AF after TIA. The prevalence of AF in TIA patients is 0-27%. Almost 50% of TIA has undetermined etiology. Recommendations for prolonged monitoring after TIA is needed even prolonged event recording rarely performed (16%). AF detection rate in unselected TIA patients is 3% and in selected TIA patients is 7%, detection rate of AF is higher in selected patients with TIA. AF prevalence in TIA increases with age. Prospective studies are needed to inform patient selection, optimal timing and duration of monitoring specifically in TIA patients.

The last speaker was Prof Pierre Amarenco talked about long term outcome following TIA. Contemporary long term risk is 12% with steady increase after 10 days.  Disabling stroke risk is 8% at 5 years. Stroke patients with ipsilateral atherosclerotic stenosis have higher absolute risk than the others.

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