In der vorliegenden Arbeit wurde die "laparoskopisch gestützte Zystotomie" als neues Therapieverfahren zur Behandlung der Zystolithiasis bei drei männlichen Pferden erstmals klinisch eingesetzt. Bei dieser Verfahrenstechnik erfolgte die Darstellung, die Vorlagerung und die abschließende Reposition der Harnblase als laparoskopischer Eingriff am rückengelagerten Pferd. Die Zystotomie, die Exstirpation des Urolithen und die Naht der Zystotomiewunde wurden hingegen extrakorporal über eine parainguinale Minilaparotomie durchgeführt. Hierbei zeigte sich, dass dieses kombinierte Operationsverfahren eine spannungsfreie und zeitsparende Mobilisation sowie ausreichende extrakorporale Vorlagerung der Harnblase ermöglichte. Ferner konnte die Laparotomiewunde in ihrem Ausmaß der Größe des zu extrahierenden Urolithen angepasst werden (zwischen 8-10 cm). Auch war die extrakorporale Naht der Zystotomiewunde im Vergleich zur intrakorporalen endoskopischen Naht technisch einfacher, zeitsparender und sicherer. In den vorgestellten Fällen betrug die Operationsdauer definiert als der Zeitraum zwischen der Erstinzision und der Beendigung der Hautnaht 35-40 Minuten. Alle drei Patienten konnten innerhalb von 7 bis 10 Tagen geheilt entlassen werden. Während des Beobachtungszeitraumes von 4 bis 8 Monaten waren die Patienten rezidiv-und symptomfrei. Anhand der Ergebnisse dieser drei klinischen Fälle konnte nachgewiesen werden, dass bei der laparoskopisch gestützten Operationsmethode unter Vermeidung der Negativaspekte die entscheidenden Vorteile der parainguinalen Laparozystotomie und der laparoskopischen Operationstechnik zum Tragen kamen

We studied 75 patients with severe intracranial vertebral artery (ICVA) occlusive disease from the New England Medical Center Posterior Circulation Registry to learn the etiologies and locations of the vascular lesions, the location and patterns of related ischemia and infarctions, and the outcomes. All patients had neuroimaging and vascular studies. Thirty-nine percent of patients had bilateral ICVA lesions. Twenty-four percent also had basilar artery disease and 36% had associated extracranial disease. The most common site of lesions was the distal ICVA after the origin of the posterior inferior cerebellar artery (PICA). Twenty-five percent of patients had only proximal intracranial posterior circulation territory infarcts (medullary and PICA cerebellar); 32% had infarcts that involved other intracranial territories in addition to the proximal territory. We found more distal intracranial territory infarcts resulting mainly from embolism from ICVA lesions than reported previously; this occurred in 17% of all patients. The ICVA was a recipient site for emboli in 8% of patients. Thirteen percent of patients died during follow-up. The outcome was favorable in most surviving patients. Three-fourths of them had no deficit or only slight disability. The patients with distal territory infarcts due to emboli from the ICVA had the worst outcome.

We studied 91 patients with proximal intracranial territory posterior circulation ischemia from the New England Medical Center Posterior Circulation Registry to learn their distribution, underlying cardiovascular causes and long-term outcome. All patients had imaging and vascular studies. Six patients had proximal territory TIAs. Among 85 stroke patients, 52% had infarcts limited to the proximal territory, while 48% also had infarcts in other intracranial posterior circulation territories. Eighty-five percent of proximal territory infarcts were posterior inferior cerebellar artery (PICA) territory cerebellar infarcts and 30% were lateral medullary infarcts. One patient had a hemi-medullary syndrome. Six patients had PICA territory cerebellar and lateral medullary infarcts. The most common vascular lesion in lateral medullary infarct patients was ipsilateral intracranial vertebral artery (ICVA) disease (38% isolated ICVA disease) and in PICA territory cerebellar infarcts, extra-cranial vertebral artery (ECVA) disease (29% isolated ECVA disease). Half of all lateral medullary infarcts were due to a hemodynamic mechanism, most often in situ thrombosis of an ICVA occlusive lesion. Half of all PICA territory cerebellar infarcts were due to intra-arterial embolism and one-fifth to cardiac origin embolism. Embolism was a more frequent cause of proximal territory posterior circulation infarcts than intrinsic ICVA disease. The etiological profiles of lateral medullary and PICA cerebellar infarcts were different. Seventeen percent of all patients died during follow-up (41 months) but mortality related to the acute stroke or new strokes was only 6 percent. The outcome was favorable in the surviving patients; 89% had no or only slight disability.

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