MYELOPATHY SECONDARY TO AORTOCAVAL FISTULA IN A CAT

A 15-month-old neutered male cat was presented for progressive paraparesis of 3 months' duration and suspected cardiomegaly. Neuroanatomical localization was a T3-L3 myelopathy. On abdominal ultrasound, an anomalous vessel with turbulent blood flow was identified arising from the caudal vena cava. Myelography showed a bilateral ventrolateral extradural spinal cord compression from T12 to L4. Nonselective angiography and contrast-enhanced computed tomography clearly indicated a vascular complex and vena caval aneurysm with an engorged internal vertebral venous plexus. Surgical occlusion of the anomalous vessels was unsuccessful

Partial “targeted” embolisation of brain arteriovenous malformations

The treatment of pial arteriovenous brain malformations is controversial. Little is yet known about their natural history, their pathomechanisms and the efficacy and risks of respective proposed treatments. It is known that only complete occlusion of the AVM can exclude future risk of haemorrhage and that the rates of curative embolisation of AVMs with an acceptable periprocedural risk are around 20 to 50%. As outlined in the present article, however, partial, targeted embolisation also plays a role. In acutely ruptured AVMs where the source of bleeding can be identified, targeted embolisation of this compartment may be able to secure the AVM prior to definitive treatment. In unruptured symptomatic AVMs targeted treatment may be employed if a defined pathomechanism can be identified that is related to the clinical symptoms and that can be cured with an acceptable risk via an endovascular approach depending on the individual AVM angioarchitecture. This review article gives examples of pathomechanisms and angioarchitectures that are amenable to this kind of treatment strategy

The Role of Perfusion Computed Tomography in the Prediction of Cerebral Hyperperfusion Syndrome

Hyperperfusion syndrome (HPS) following carotid angioplasty with stenting (CAS) is associated with significant morbidity and mortality. At present, there are no reliable parameters to predict HPS. The aim of this study was to clarify whether perfusion computed tomography (CT) is a feasible and reliable tool in predicting HPS after CAS.We performed a retrospective case-control study of 54 patients (11 HPS patients and 43 non-HPS) with unilateral severe stenosis of the carotid artery who underwent CAS. We compared the prevalence of vascular risk factors and perfusion CT parameters including regional cerebral blood volume (rCBV), regional cerebral blood flow (rCBF), and time to peak (TTP) within seven days prior to CAS. Demographic information, risk factors for atherosclerosis, and perfusion CT parameters were evaluated by multivariable logistic regression analysis. The rCBV index was calculated as [(ipsilateral rCBV - contralateral rCBV)/contralateral rCBV], and indices of rCBF and TTP were similarly calculated. We found that eleven patients had HPS, including five with intracranial hemorrhages (ICHs) of whom three died. After a comparison with non-HPS control subjects, independent predictors of HPS included the severity of ipsilateral carotid artery stenosis, 3-hour mean systolic blood pressure (3 h SBP) after CAS, pre-stenting rCBV index >0.15 and TTP index >0.22.The combination of severe ipsilateral carotid stenosis, 3 h SBP after CAS, rCBV index and TTP index provides a potential screening tool for predicting HPS in patients with unilateral carotid stenosis receiving CAS. In addition, adequate management of post-stenting blood pressure is the most important treatable factor in preventing HPS in these high risk patients