Yellow-Coloured Left Homonymous Visual Hemi-Field after Ischaemic Stroke.

We report a patient's challenging case who suffered two acute ischaemic strokes, first in the right occipital lobe and later in the right dorsolateral thalamus (with affection of the lateral geniculate nucleus) who developed a yellow-tinted left homonymous visual hemi-field. No previously described case matched our peculiar symptom presentation in combination with the described brain lesions. Especially, the visual phenomena of patients with these brain lesions that were up until now described in literature were complex and vivid visual hallucinations. Here, we discuss possible explanations and mechanisms of this visual phenomenon (acquired hemidyschromatopsia, peduncular hallucinosis, focal epilepsy with visual symptoms, visual hallucinations) and in light of the current literature, we argue that the most likely explanation is a form of simple visual hallucination due to release phenomena (Charles Bonnet syndrome)

Untersuchung des Einflusses von SNCA-Rep1 auf das Erkrankungsalter und klinische Parameter bei Patienten mit idiopathischem Parkinson-Syndrom

Von der Feststellung ausgehend, dass Duplikationen und Triplikationen des SNCA-Gens seltene, familiäre Formen der Parkinson-Krankheit verursachen können, wurde die Hypothese abgeleitet, das Risiko für die Parkinson-Krankheit könnte mit der Translationsrate von SNCA steigen (Dosis-Effekt). Konsequenterweise wurden Regionen des Gens untersucht, welche für dessen Expression zuständig sind, sogenannte Promotor-Regionen. Es wurde jedoch schnell klar, dass die meisten genetischen Varianten lediglich die Empfänglichkeit für die sporadische Parkinson-Krankheit erhöhen, aber nicht direkt krankheitsverursachend wirken. Rep1, eine Dinukleotid-Wiederholungssequenz in der Promotor-Region von SNCA, wurde als vielversprechende genetische Variante entdeckt, welche das Risiko, an Parkinson zu erkranken, beeinflussen kann. Es kommt in der hiesigen Bevölkerung in drei häufigen Allelen vor (kurz, mittel, lang), wobei entdeckt wurde, dass das lange Allel das Parkinson-Risiko erhöhe und das kurze Allel dieses senke. Diese Erkenntnis führte zu weiteren Untersuchungen, die prüfen sollten, ob Rep1 auch krankheitsmodifizierende Effekte haben könnte in der Hoffnung, den Krankheitsverlauf von Patienten individualisierter beurteilen zu können. Das Ziel dieser Arbeit war es, das Wissen über diese Effekte zu erweitern. Im Rahmen dieser Arbeit wurden dazu die Rep1-Genotypen von 1.025 Parkinson-Patienten mithilfe der DNA-Fragmentanalyse bestimmt. Anschließend wurde im ersten Teil der Analysen geprüft, ob die einzelnen Patientengruppen verschiedener Genotypen ein unterschiedliches Erkrankungsalter aufweisen. Der zweite Teil konzentrierte sich auf die Frage, ob es Hinweise darauf gibt, dass Rep1 auch klinische Parameter beeinflussen kann. Dazu wurden die Punktwerte von Beurteilungs- und Fragebögen zu motorischen Fähigkeiten, Gedächtnisleistung, depressive Symptomatik sowie die Parkinson-Medikation unter den Genotypen verglichen, einerseits in Querschnittsuntersuchungen, andererseits in longitudinalen Analysen. Diese Studie fand weder im Erkrankungsalter noch in den klinischen Parametern signifikante Unterschiede zwischen den einzelnen Rep1-Genotypen. Mit diesen Ergebnissen konnte mehr Klarheit in die bisherige Datenlage gebracht werden in der Hinsicht, dass die überwiegende Zahl der Hinweise nun darauf hindeutet, dass Rep1 das Erkrankungsalter nicht beeinflusst. Auch ein kognitives Defizit und die Parkinson-Medikation scheinen nicht mit Rep1 zusammenzuhängen. Hingegen bleibt aufgrund der Inkonsistenzen in der Literatur die Rolle von Rep1 bezüglich der motorischen Fähigkeiten und der depressiven Symptomatik ungeklärt. Hierzu werden weitere Studien mit größeren Kohorten notwendig sein, um diese Fragen zu klären. Schließlich bietet diese Arbeit mögliche Erklärungen, weshalb es oft zu widersprüchlichen Ergebnissen in Studien zu Rep1 kommt. Einerseits könnte das Rep1-Assoziationssignal wegen einem hohen Kopplungsungleichgewicht möglicherweise ein SNP-Signal reflektieren und keinen unabhängigen Effekt darstellen. Andererseits wäre es möglich, dass postulierte Effekte des Rep1-Repeats von Umweltfaktoren modifiziert werden, für die in Studien nicht kontrolliert wurde

Absence of susceptibility vessel sign and hyperdense vessel sign in patients with cancer-related stroke

Background and aimIdentification of paraneoplastic hypercoagulability in stroke patients helps to guide investigations and prevent stroke recurrence. A previous study demonstrated an association between the absence of the susceptibility vessel sign (SVS) on brain MRI and active cancer in patients treated with mechanical thrombectomy. The present study aimed to confirm this finding and assess an association between the absence of the hyperdense vessel sign (HVS) on head CT and active cancer in all stroke patients.MethodsSVS and HVS status on baseline imaging were retrospectively assessed in all consecutive stroke patients treated at a comprehensive stroke center between 2015 and 2020. Active cancer, known at the time of stroke or diagnosed within 1 year after stroke (occult cancer), was identified. Adjusted odds ratios (aOR) and their 95% confidence interval (CI) for the association between the thrombus imaging characteristics and cancer were calculated using multivariable logistic regression.ResultsOf the 2,256 patients with thrombus imaging characteristics available at baseline, 161 had an active cancer (7.1%), of which 36 were occult at the time of index stroke (1.6% of the total). The absence of SVS was associated with active cancer (aOR 3.14, 95% CI 1.45–6.80). No significance was reached for the subgroup of occult cancer (aOR 3.20, 95% CI 0.73–13.94). No association was found between the absence of HVS and active cancer (aOR 1.07, 95% CI 0.54–2.11).ConclusionThe absence of SVS but not HVS could help to identify paraneoplastic hypercoagulability in stroke patients with active cancer and guide patient care

Changes of migraine aura with advancing age of patients

Abstract Aim Given the similar presentation of migraine aura and acute ischemic stroke, advancing patient age might change the characteristics of migraine with aura (MA) and be clinically important. Clinical data, however, are limited. Experimental studies indicate a decrease in the magnitude of cortical spreading depression (CSD), the pathophysiological correlate of migraine aura, with advancing age. Our study aimed to assess the influence of age on the clinical features of MA. Methods Three hundred and forty-three patients were interviewed using a structured questionnaire. The questions covered the headache characteristics and symptom types including the characteristics of the C-criterion, as defined by the International Classification of Headache Disorders 3rd Edition. The association of age with MA characteristics was assessed. Results The median age was 29 (IQR 28–52) and 235 of the 343 patients were women (69%). Individual symptoms of the C-criterion such as gradual aura spreading over longer than 5 min (P < 0.001), two or more aura symptoms occurring in succession (P = 0.005), duration of at least one MA symptom for longer than 60 min (P = 0.004), and associated headache (P = 0.01) were more frequent in younger patients. The number of symptoms (P = 0.003) including the C-characteristics decreased with increasing age (P < 0.027). Patients with sensory (P < 0.001), motor (P = 0.04) and speech disturbance (P = 0.02) were younger, and older patients with headache had less photophobia (P = 0.04) and phonophobia (P = 0.03). Sensitivity analyses yielded similar results. Conclusion The frequency of typical characteristics of migraine aura and migraine headache including photophobia and phonophobia decreases with advancing patient age. This might have potentially difficult implications for the diagnosis of MA in the elderly

Ischaemic stroke despite antiplatelet therapy: Causes and outcomes.

BACKGROUND Ischaemic stroke may occur despite antiplatelet therapy (APT). We aimed to investigate frequency, potential causes and outcomes in patients with ischaemic stroke despite APT. METHODS In this cohort study, we enrolled patients with imaging-confirmed ischaemic stroke from the Swiss Stroke Registry (01/2014-07/2022). We determined the frequency of prior APT, assessed stroke aetiology (modified TOAST classification) and determined the association of prior APT with unfavourable functional outcome (modified Rankin Scale score 3-6) and recurrent ischaemic stroke at 3 months using regression models. RESULTS Among 53,352 patients, 27,484 (51.5%) had no prior antithrombotic treatment, 17,760 (33.3%) were on APT, 7039 (13.2%) on anticoagulation and 1069 (2.0%) were on APT + anticoagulation. In patients with a history of ischaemic stroke/TIA (n = 11,948; 22.4%), 2401 (20.1%) had no prior antithrombotic therapy, 6594 (55.2%) were on APT, 2489 (20.8%) on anticoagulation and 464 (3.9%) on APT + anticoagulation. Amongst patients with ischaemic stroke despite APT, aetiology was large artery atherosclerosis in 19.8% (n = 3416), cardiac embolism in 23.6% (n = 4059), small vessel disease in 11.7% (n = 2011), other causes in 7.4% (n = 1267), more than one cause in 6.3% (n = 1078) and unknown cause in 31.3% (n = 5388). Prior APT was not independently associated with unfavourable outcome (aOR = 1.06; 95% CI: 0.98-1.14; p = 0.135) or death (aOR = 1.10; 95% CI: 0.99-1.21; p = 0.059) at 3-months but with increased odds of recurrent stroke (6.0% vs 4.3%; aOR 1.26; 95% CI: 1.11-1.44; p < 0.001). CONCLUSIONS One-third of ischaemic strokes occurred despite APT and 20% of patients with a history of ischaemic stroke had no antithrombotic therapy when having stroke recurrence. Aetiology of breakthrough strokes despite APT is heterogeneous and these patients are at increased risk of recurrent stroke

Ischaemic stroke despite antiplatelet therapy: Causes and outcomes

BACKGROUND Ischaemic stroke may occur despite antiplatelet therapy (APT). We aimed to investigate frequency, potential causes and outcomes in patients with ischaemic stroke despite APT. METHODS In this cohort study, we enrolled patients with imaging-confirmed ischaemic stroke from the Swiss Stroke Registry (01/2014-07/2022). We determined the frequency of prior APT, assessed stroke aetiology (modified TOAST classification) and determined the association of prior APT with unfavourable functional outcome (modified Rankin Scale score 3-6) and recurrent ischaemic stroke at 3 months using regression models. RESULTS Among 53,352 patients, 27,484 (51.5%) had no prior antithrombotic treatment, 17,760 (33.3%) were on APT, 7039 (13.2%) on anticoagulation and 1069 (2.0%) were on APT + anticoagulation. In patients with a history of ischaemic stroke/TIA (n = 11,948; 22.4%), 2401 (20.1%) had no prior antithrombotic therapy, 6594 (55.2%) were on APT, 2489 (20.8%) on anticoagulation and 464 (3.9%) on APT + anticoagulation. Amongst patients with ischaemic stroke despite APT, aetiology was large artery atherosclerosis in 19.8% (n = 3416), cardiac embolism in 23.6% (n = 4059), small vessel disease in 11.7% (n = 2011), other causes in 7.4% (n = 1267), more than one cause in 6.3% (n = 1078) and unknown cause in 31.3% (n = 5388). Prior APT was not independently associated with unfavourable outcome (aOR = 1.06; 95% CI: 0.98-1.14; p = 0.135) or death (aOR = 1.10; 95% CI: 0.99-1.21; p = 0.059) at 3-months but with increased odds of recurrent stroke (6.0% vs 4.3%; aOR 1.26; 95% CI: 1.11-1.44; p < 0.001). CONCLUSIONS One-third of ischaemic strokes occurred despite APT and 20% of patients with a history of ischaemic stroke had no antithrombotic therapy when having stroke recurrence. Aetiology of breakthrough strokes despite APT is heterogeneous and these patients are at increased risk of recurrent stroke