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Clinical vignette

An 82 years old patient was referred to the Emergency Department for a sudden left hemiparesis associated with dysarthria. His past history and vascular risk factors included a triple aorto-coronary bypass, arterial hypertension and dyslipidemia under medical treatment.

On admission, the patient was agitated and the neurological examination showed severe dysarthria, left central facial palsy, left homonymous hemianopia, a motor deficit of the upper left limb, discrete sensory deficits on the left hemibody and tactile hemi-extinction (without position sense impairment). NIH Stroke Scale was 10. An MRI was performed at the emergency department (figure 1).

The patient underwent iv thrombolysis. About 6 hours later, the patient presented with an acute-onset movement disorder (video). We performed a new MRI that showed neither new ischemic lesion nor haemorrhagic transformation. The basal ganglia, thalamus, and subthalamic region were intact.

The patient underwent iv thrombolysis. About 6 hours later, the patient presented with an acute-onset movement disorder (video). We performed a new MRI that showed neither new ischemic lesion nor haemorrhagic transformation. The basal ganglia, thalamus, and subthalamic region were intact.

Video: Left hemiballism. Ballism is a hyperkinetic movement disorder, characterized by brisk, fast, flinging and unpredictable high amplitude movement. The movement has some element of rotation and occurs mainly in the proximal segment of the limbs. Its differential diagnosis involves the more common pseudo-choreoathetosis, which results from proprioceptive sensation deficit and appears as a snake-like, principally confined to the distal extremity.

How do you define the movement disorder? Which is the physiopathology? Where is the culprit cerebral lesion? How do you treat it?

Ballism in cerebrovascular diseases

The frequency of post-stroke movement disorders varies from 1% to 4% of all strokes, with both sexes equally affected ^1,2,3. Mean age at onset is typically 60-70 years, but extreme ages can be also affected³. Onset and progression of post-stroke movement disorder is variable, because they can occur immediately at the onset of the acute stroke, or they can be delayed and progressive. Hemiballism showed a prevalence of 0.4%. It is often preceded by hemiparesis and has been described during acute stroke presentation or shortly after². Although various structural lesions have been associated with ballism⁵, damage to the subthalamic nucleus and the pallidosubthalamic pathways appear to play a critical role in its expression. Nevertheless, this anatomical correlation may extend beyond the contralateral subthalamic nucleus, through connecting structures to the adjacent internal capsule. In particular, anterior parietal strokes, without any evidence of involvement of the basal ganglia, thalamus or subthalamic nucleus, have been associated with contralateral hemiballism⁵. In these cases, the pathophysiologic mechanisms implicate the interruption of the parieto-striatal pathways. Indeed, under normal physiologic conditions, the cerebral cortex provides excitatory stimuli to the basal ganglia; thus, lesions involving cortico-striatal fibers may disrupt the balance of basal ganglia circuits.

Treatments

Although usually self-limited, post-stroke ballism can substantially increase morbidity through injury (rhabdomyolysis is a very frequent complication) and impaired coordination. Pharmacological therapy consists of antidopaminergic therapy with neuroleptics, through the block of dopamine receptors. These drugs may cause parkinsonism and tardive dyskinesia. Indeed, tetrabenazine, a dopamine-depleting agent, has become the preferred choice because it does not cause tardive dyskinesia. Clonazepam and sodium valproate have also been used with some success⁷. In a small case series, complete improvement was reported in 45–56% on one or two of these drugs²,⁸. Compared with conditions that result from destruction of the subthalamic nucleus, our patient’s hemiballismus was milder and was successfully treated with tetrabenazine.

Acknowledgments:

Dr Alexandre Kreisler, CHRU Lille, France

References

1. Mehanna R. and Jankovic J. Movement disorders in cerebrovascular diseases. Lancet Neurol 2013; 12: 597–608.
2. Ghika-Schmid F, Ghika J, Regli F, Bogousslavsky J. Hyperkinetic movement disorders during and after acute stroke: the Lausanne stroke registry. J Neurol Sci 1997; 146: 109–16.
3. Alarcon F, Zijlmans JC, Duenas G, Cevallos N. Post-stroke movement disorders: report of 56 patients. J Neurol Neurosurg Psychiatry 2004; 75: 1568–74.
4. Postuma RB, Lang AE. Hemiballism: revisiting a classic disorder. Lancet Neurol 2003; 2: 661–68.
5. Rossetti AO, Ghika JA, Vingerhoets F, Novy J, Bogousslavsky J. Neurogenic pain and abnormal movements contralateral to an anterior parietal artery stroke. Arch Neurol 2003; 60: 1004–06.
6. Young AB, Penney JB. Neurochemical anatomy of movement disorders. Neurol Clin. 1984;2:417-433.
7. Shannon KM. Hemiballismus. Curr Treat Options Neurol 2005; 7: 203–10.
8. Ristic A, Marinkovic J, Dragasevic N, Stanisavljevic D, Kostic V. Long-term prognosis of vascular hemiballismus. Stroke 2002; 33: 2109–11.

<p>The post Cortical-Striatal Disconnection After Parietal Stroke first appeared on European Stroke Organisation.</p>

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

A 44-year-old woman with no comorbidities was admitted to the emergency due to a slowly progressive vertigo and mild left sensorimotor hemiparesis. She is a mother of three, never-smoker, and exercising frequently. She had just returned from maternal leave and had noticed some minor difficulties in learning new procedures at work. She had no medical history of epileptic seizures or migraine with or without aura.

Toxicology and infection screen were negative and she was normoglycemic and normotensive. On the neurological examination, the patient showed only mild ataxia in left extremities with a sense of numbness and tingling. Initial MRI showed widened perivascular spaces with bilateral multiple older small lacunar infarcts, as well as extensive white matter abnormalities. Also hyperintensity of the anterior temporal lobes was evident in T2 sequences typical to CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy). Arterial imaging remained unremarkable. Diagnosis of CADASIL was later confirmed with genetic testing.

Several single gene mutations have stroke (ischemic and/or hemorrhagic) as their primary or secondary feature, the most common being CADASIL. It is caused by autosomal dominant NOTCH3 mutations on chromosome 19, typically with recurrent lacunar strokes, whilst hemorrhagic strokes are less frequent. Clinical features include migraine with aura, cognitive impairment, mood disorders, and seizures. Migraine is present in up to 40% of patients and stroke occurs typically during the fourth and fifth decade. Diagnosis is based on MRI findings, skin biopsy and/or genetic testing. However, there is no specific treatment for CADASIL.^1,2

CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoence-phalopathy has MRI findings similar to CADASIL, but the disease is caused by a HTRA1 gene mutation encoding for a serine protease. CARASIL usually causes early-onset muscle spasticity, alopecia, lower back pain, and about half of the patients have a stroke or similar episodes before age of forty. As with CADASIL, cognitive impairment, and mood and personality changes develop as the disease progresses. The exact prevalence of CARASIL is unkown.³

Another disease to keep in mind is Fabry disease, which commonly results from a single point mutation of the GLA gene. However, this gene is located on the X chromosome. The mutation leads to a lysosomal alpha-galactosidase deficiency and to a progressive accumulation of glycosphingolipids within lysosomes of cells in various organ systems. Clinical manifestations include ischemic and hemorrhagic stroke, angiokeratoma, acroparesthesias, renal dysfunction, cardiac failure (hypertrophy, restrictive cardiomyopathy, arrhythmias, and valvular heart diseases), hearing loss, tinnitus, vertigo, bowel dysfunction etc. First symptoms are usually experienced in early childhood, but the delay from symptom onset to diagnosis (genetic testing for the GLA gene) can take years due to the rarity of Fabry. However, unlike in CADASIL and CARASIL, a specific treatment with enzyme replacement therapy can prevent/slow down disease progression.⁴ According to prior reviews, Fabry disease may explain up to 1% of all stroke in the young, including 3-5% of cryptogenic strokes.⁵

Furthermore, DNA mutations in mitochondrial genes (in >80% of cases point mutation in mtDNA A3242G) may lead to mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). This should be suspected especially in patients with seizures, focal neurological deficits, migraine-like headaches, and encephalopathy. MELAS patients may also present with cardiac diseases, short stature, diabetes mellitus, muscle weakness, and dementia. Imaging might show lesions that do not follow known arterial territories, especially in parietal and occipital lobes.

In addition to these, several mutations with autosomal inheritance have been identified, including e.g. familial moyamoya (mutations in ACTA2, MTCP1, or RNF213), retinal vasculopathy with cerebral leukodystrophy (RVCL, mutations in TREX1), deficiency of adenosine deaminase 2 (associated polyarteritis nodosa vasculopathy, mutations in ADA2), and homocystinuria (mutations in MTHFR, MTR, MTRR, or MMADHC).

In conclusion, these single gene mutations are not common but should be kept in mind when treating especially patients with early-onset cryptogenic strokes. Although most of them do not have specific treatment, the knowledge of hereditary disease may give patients and their family members reassurance and opportunity to treat other modifiable risk factors early enough.

References: 

1. Desmond DW et al. The natural history of CADASIL: a pooled analysis of previously published cases. Stroke 1999;30(6):1230–1233.
2. Donato D et al. Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) as a model of small vessel disease: update on clinical, diagnostic, and management aspects. BMC Med 2017;15(1):41-017-0778-8.
3. Fukutake T. Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL): from discovery to gene identification. J Stroke Cerebrovasc Dis 2011;20(2):85-93.
4. Zarate YA et al. Fabry’s disease. Lancet 2008;372(9647):1427-1435.
5. Shi Q et al. Prevalence of Fabry disease in stroke patients–a systematic review and meta-analysis. J Stroke Cerebrovasc Dis 2014;23(5):985-992.
6. El-Hattab AW et al. MELAS syndrome: Clinical manifestations, pathogenesis, and treatment options. Mol Genet Metab 2015;116(1-2):4-12.

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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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European Stroke Organisation Department to Department Visit Program 2018- Visit Report

Awardee: Mariana Dias
Period of the visit: 1 January 2019 – 28 June 2019

During my 6 months stay at Vall d’Hebron University Hospital Stroke Unit I had the opportunity to experience and learn different areas and technics. I have spent 1 month on the Stroke Unit, 1 month on Neurossonology, 2 months on Stroke Echoscopy, 1 month with the Stroke Code team on emergency department and 1 month doing scientific research.

During the period on the Stroke Unit I participated on the daily ward rounds and I had the opportunity to participate in the clinical discussions about the patients under the supervision of Dr. Marta Rubiera. This Stroke Unit has nine monitored beds, eight of them with 72-hour telemetry, with one stroke nurse dedicated for two patients.

During the Neurossonology rotation I had the opportunity to improve the technique of carotid and vertebral artery Doppler and transcranial Doppler. With the supervision of Dr. David Rodríguez-Luna and Dr. Noelia Rodriguez Villatoro I performed about ten exams every day that were always discussed and integrated with the patient’s clinical history. I also had the opportunity to learn how to monitor carotid or vertebral artery stent stenosis, to detect right-to-left shunt with transcranial Doppler and to interpret contrast enhanced carotid Doppler to study unstable atherosclerotic plaques.

For the two months that I have stayed on Stroke Echoscan I learned how to perform this technique and the advantages to have Neurologists with experience in this area. This technique is specially directed to detect potential stroke causes such as akinetic left ventricular segment, mitral valve stenosis and aortic arch atherosclerosis. With the supervision of Dr. Jorge Pagola and Dr. Jesus Juega I performed 66 exams to the patients admitted on the Stroke Unit and I had the opportunity to do a 3-days course of basic echocardiography with accreditation from the Spanish Cardiology Society. The Echoscan team is also in charge of the extended cardiac monitoring with wearable devices and I had the opportunity to see the advantages and limitations of these devices.

For the month that I have joined the Stroke Code team I had the opportunity to learn strategies to improve the hyperacute phase care. I have participated on the decisions regarding the patient diagnosis and treatment and observed the endovascular treatment on the angio-suite. I really appreciated the chance to observe the inclusion of patients on acute phase trials such as TASTE, TEMPO and THALES. I was also inspired by the workflow improvement strategies conducted at this center for example the direct transfer to angio-suite stroke code.

For the scientific research period I had the opportunity to work with colleagues from different countries with the orientation of Dr. Carlos Molina, Dr. Marc Ribó and Dra. Marta Rubiera. Our research was focused on the subject arterial blood pressure and thrombectomy and we are still collaborating in order to publish our findings. I also had the chance to work with two engineers doing their master in 3d printed thrombectomy models for endovascular treatment training.

During all the stay I also had the opportunity to attend the multidisciplinary meetings with the radiology, department scientific meetings and Catalunya Stroke Units meetings. I also had the privilege to be invited to the presentation of the thesis of Dr. Noelia Rodríguez Villatoro regarding the treatment options of hyperacute treatment of extracranial internal carotid artery tandem lesions.

I am truly grateful to professor Carlos Molina, Dr. Marc Ribó, Dr. Marta Rubiera and all the Stroke Unit Team for all the knowledge and opportunities that were given to me during these six months. I had the chance to be inspired by a team of Neurologists with challenging ideas that contributed to my formation as a Neurologist.

Finally, I am grateful for the support of the ESO for granting me this amazing opportunity.

Are you eligible for a Department to Department Visit?

You can apply if you meet the below qualifications. The application deadline is 28 February but we encourage potential applicants to be proactive about setting up a potential visit prior to the deadline.

Physicians or researchers born in 1980 or after – with an interest in the field of stroke. Applicants must be ESO members (Junior membership application is available here). In the selection process, we have a special emphasis on applicants from European low-middle income countries, interested in improving the stroke pathways and care in their institutions and six grants per year are reserved for this purpose.

More information: https://eso-stroke.org/eso-department-department-visit-programme/

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Controversies in Stroke I

By: Prof. Anita Arsovska, MD, PhD, University Clinic of Neurology, Medical Faculty, University “Ss Cyril and Methodius”, Skopje, Republic of North Macedonia, FESO, FEAN, SAFE Board Member

The 23^rd of May started with a very exciting and interactive morning session from 08:15-09:45 in the Gold Room,  entitled Controversies in Stroke I, chaired by Martin Dichgans (Germany) and Turgut Tatlisumak ( Sweden). The session started with a burning question: Intravenous thrombolysis before endovascular trombectomy? Yes or no? And than Yvo Roos (The Netherlands) tried to convince the audience to answer yes, providing an overview from the recent studies and own experience. He actually concluded that the answer is still coming and that we need to wait and see the results of DIRECT-MT (expected at ISC 2020) and MrClean No-IV and other trials expected later that year, however in the meantime, we need to include patients in trials or stick to the current evidence….IVT+IMT.

Afterwards, Urs Fischer (Switzerland) in a very charming way gave an excellent lecture entitled IVT before EVT? Not Always! He personally disclosed that he actually loves thrombolysis and it is the drug that he loves the most, however, first we have to answer the following questions: Preinterventional reperfusion: how often and how good? Is IVT plus MT better than MT alone in IVT eligible patients? Which patients should be included in trials? Does one approach fit all? Quoting the latest studies including his own rich experience, he concluded that IVT is currently the standard of care in all patients with LVO, IVT should only be skipped in the framework of well designed RTCs, and only patients with low probability of early recanalization after IVT and immediate access to direct MT should be included.We need an initiative to tailor stroke treatment strategies in the future (precision medicine).

The session continued with the second topic : Restarting oral anticoagulation after ICH – No (Roland Veltkamp, Germany) and Yes (Karin Klijn, The Netherlands). Dr. Veltkamp stated that there is limited evidence that would support restarting someone with an OAC-related ICH on an OAC and that we need to personalize therapy election and shared decision making as best preventive approach. His “opponent” Dr. Klijn, after presenting current evidence, concluded that we should recommencing OAC in high risk ischemic event; microbleeds have no influence; if AF: OACs are preferable over Vit K antagonists; there should be no rush (unless very igh risk ischemia), probably best after 7-8 weeks, it is still unsure if NOACs are safe to be started sooner and we need to randomize our patients in the multiple RTC’s that are ongoing/starting soon.

The third topic elaborated : Extending the window for reperfusion therapy- Do we need perfusion imaging-yes (“defended” by Henry Ma, Australia) and no- presented by Götz Thomalla from Germany. Basically, Dr. Ma presented the benefits of the perfusion imaging, that can identify the ischemic core- poor outcome and risk of haemorrhage, identify the ischemic penumbra- potential benefit, exclude stroke mimics and provide precision medicine, concluding that yes, we do need perfusion imagiing to extend the reperfusion time window for reperfusion. On the other hand, Dr. Thomalla presented a more practical approach, firstly asking the audience if at their stroke center, they have perfusion imaging available for acute stroke imaging 24/7? The actual situation is that 45% had it only during office hours or not at all, 38% had CT perfusion, 11% had CT perfusion and MRI and only 4% had MRI and perfusion imaging. He later asked also a very useful question: At your stroke center, which CT perfusion parameter do you use to define the ischemic core? And surprisingly, the majority of the participants did not know (45%), and the rest of them had doubts between absolute or relative cerebral blood flow of volume. After detailed overview of current studies and evidence, he concluded that perfusion imaging is valuable for research and helpful as diagnostic tool in acute ischemic stroke; there is uncertainty as to the optimal perfusion parameters and thresholds, there are limitations to quantification of ischemic core by CT perfusion, we do not need perfusion imaging to guide MT in extended or unknown time of symptom onset or to guide IVT in unknown symptom onset, penumbral imaging requiring perfusion is only needed to guide IVT on kknown late time window; for the vast majority of patients, we do not need perfusion imaging to guide reperfusion treatment with IVT or MT and Stroke centers must have perfusion imaging available 24/7 but should not waste time in doing perfusion imaging in the majority of patients in whom it is not required!

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