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ZusammenfassungPräsentiert werden magnetresonanztomographische Befunde von drei Hunden nach Kohlenmonoxidvergiftung. Im ersten und zweiten Fall umfassten die Befunde Veränderungen im Nucleus caudatus auf beiden Seiten und im ersten Fall auch im Putamen als bilateral symmetrische, diffuse, homogene, in T2 und FLAIR hyperintense, in T1 hypointense Läsionen. Eine Kontrastmittelaufnahme zeigte sich nicht. Beim dritten Hund fanden sich sowohl multiple bilateral symmetrische in T2 und FLAIR hyperintense Läsionen als auch schlecht abgrenzbare Areale in der grauen Substanz im Frontal-, Parietal- und Okzipitallappen. Beide Colliculi caudales, Globus pallidus, Substantia nigra und der mittlere Thalamus stellten sich bilateral symmetrisch hyperintens in T2 und FLAIR dar und nach intravenöser Kontrastmittelapplikation kam es zu einer mittelgradigen Anreicherung.

Background Studies in animal models, in which internal hydrocephalus has been induced by obstructing the cerebrospinal fluid pathways, have documented an up-regulation of the concentrations of aquaporin-4 (AQP4) in the brain. In this study, the concentrations of aquaporin-1 (AQP1), AQP1, AQP4 and interleukin-6 (IL-6) were determined in the CSF of dogs with idiopathic communicating hydrocephalus before and after the reduction of intraventricular volume following ventriculo-peritoneal shunt (VP-shunt) treatment. Results The concentrations of AQP4 and IL-6 were increased in the cerebrospinal fluid of dogs with hydrocephalus compared to controls. Both parameters significantly decreased after surgical treatment, accompanied by decrease of ventricular size and the clinical recovery of the dogs. AQP1 was not detectable in CSF. Conclusions Brain AQP4 up-regulation might be a compensatory response in dogs with hydrocephalus. Future determination of AQP4 at the mRNA and protein level in brain tissue is warranted to substantiate this hypothesis.

Background Acetazolamide is recommended for the reduction of cerebrospinal fluid production in canine internal hydrocephalus. The efficacy of the drug in terms of alleviation of the clinical symptoms and the restoration of normal ventricular volume has not been documented. We hypothesize that acetazolamide inadequately improve clinical signs and has no effect on the ventricular volume. Six dogs with internal hydrocephalus underwent neurological examination and were examined by magnetic resonance imaging, on the day of the diagnosis, after treatment with acetazolamide directly before surgery, and 6 weeks after implantation of a vetriculo-peritoneal shunt due to lack of improvement after medical therapy with 10 mg/kg acetazolamide three times daily (TID). The ventricular volume in relation to the total brain volume was determined on each occasion. The changes in relative ventricular volume and of the neurological status were assessed and compared. Results McNemar’s test revealed no significant differences in clinical symptoms before and after medical treatment (P > 0.05). However, clinical symptoms changed significantly after surgical treatment (P = 0.001). The ventricle-brain ratio was not significantly changed after therapy with acetazolamide (P > 0.05); however, after subsequent shunt implantation, it was significantly reduced (P = 0.001). Conclusion Acetazolamide (10 mg/kg TID) showed no effects on clinical signs or ventricular volume in dogs with internal hydrocephalus. After subsequent ventriculo-peritoneal shunting, the dogs had a significantly reduced cerebral ventricular volume and five out of six dogs had no abnormal findings in neurological examination.