Zusammenfassung
Einleitung: Der breiten Anwendung aktueller bildgebender Verfahren zur Klärung der Pathophysiologie
des ischämischen Insults steht ein deutlicher Mangel an frühen prospektiven, standardisierten
funktionellen elektroenzephalographischen Studien gegenüber. Methoden: In der vorliegenden prospektiven Studie wurden 25 konsekutive Patienten mit erstmaliger
akuter, supratentorieller, zerebraler Ischämie ohne Anfallsvorgeschichte untersucht.
Hierzu wurden 12 Stunden nach Symptombeginn 24-stündige Langzeit-EEGs abgeleitet.
Das neurologische Defizit wurde mittels NIH Stroke Scale (NIHSS) und der Behinderungsgrad
mit dem Barthel-Index (BI) zum Zeitpunkt der EEG-Ableitung sowie nach einem Jahr erfasst.
Ergebnisse: Die geblindet durchgeführte EEG-Auswertung ergab drei hierarchische Gruppen: unspezifische
Verlangsamungen (n = 9, Gruppe C), fokale hochgespannte Entladungen (n = 10, Gruppe
B) und epileptiforme Entladungen (n = 6, Gruppe A). Die temporospatiale Evolution
spezifischer, elektrischer Potenzialmuster ermöglichte eine verfeinerte Analyse der
pathophysiologischen Abläufe. Eine deutlich verlangsamte Grundaktivität, die Manifestation
kontralateraler Veränderungen und eine Rhythmisierung des Herdbefundes war positiv
korreliert mit dem Auftreten steilerer Potenziale und epileptiformer Entladungen.
Die EEG-Gruppen unterschieden sich in der NIHSS, im BI sowie bezüglich des Auftretens
epileptischer Anfälle jeweils statistisch hoch signifikant (p < 0,0001). Alle Patienten
der EEG-Gruppe C hatten ein gutes Outcome (NIHSS < 10 bzw. BI > 60) und keiner von
ihnen entwickelte epileptische Anfälle (EA) (positiver Vorhersagewert [PV] 1; 95 %-Konfidenzintervall
[KI]: 0,72 - 1). Alle Patienten der EEG-Gruppe A zeigten ein schlechtes Outcome (NIHSS
> 20 bzw. BI < 20 oder Tod: PV 1; KI 0,61 - 1). 5 der 6 Patienten bekamen EA (PV 0,83;
KI 0,36 - 1). Patienten mit EA wiesen eine signifikant erhöhte Mortalität auf (p <
0,025). Schlussfolgerung: Die vorliegenden Daten unterstreichen die Bedeutung von frühzeitigem EEG-Monitoring
nach akuter, zerebraler Ischämie für ein erweitertes pathophysiologisches Verständnis
ischämieassoziierter Anfälle und prognoserelevanter Faktoren.
Abstract
Introduction: There is substantial lack of well-designed functional electrophysiological studies
with respect to pathophysiology and prognosis after cerebral ischaemia despite increasing
progress in neuroimaging. Methods: We prospectively investigated 25 consecutive patients with acute first-ever supratentorial
ischaemic stroke and no history of epilepsy. 24h-EEG monitoring was started within
12 hours after the onset of symptoms. The neurological deficit was assessed by NIH
Stroke Scale (NIHSS) and Barthel Index (BI) during EEG recording and after 1 year.
Results: Blinded EEG evaluation revealed 3 hierarchical classes: focal slowing (n = 9, group
C), focal high voltage discharges (n = 10, group B) and epileptiform activity (n =
6, group A). Temporo-spatial EEG evolution was illustrated in reproducible time series
and thus allowed a refined analysis of the underlying pathophysiology. Slowing-down
of the background activity, occurrence of contralateral potentials and rhythmic focal
slowing-down seemed to correlate with a higher incidence of high-voltage discharges
and epileptiform activity. The EEG groups differed significantly (p < 0.0001) in NIHSS
BI and in the occurrence of seizures. All patients of group C had a good outcome (NIHSS
< 10, BI > 60) and no one developed seizures (predictive value [pv] = 1; 95 % confidence
interval [CI] 0,72 - 1). In contrast all patients of group A had a poor outcome (NIHSS
> 20, BI < 20 or death; PV 1, CI 0,61 - 1) and 5 of them developed seizures (PV 0,83;
CI 0,36 - 1). Patients with epileptic seizures had a significant higher mortality
(p < 0.025) Conclusions: Our data underline the importance of early post-ischaemic EEG recording both for
understanding pathophysiological mechanisms of post-ischaemic seizures and the prognosis
of acute stroke.
Key words
Acute stroke - EEG - Seizures - Outcome
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Dr. med. E. I. Strittmatter
Neurologische Klinik · Universitätsklinikum Heidelberg
Im Neuenheimer Feld 400
69112 Heidelberg