Clinicopathologic Features and Magnetic Resonance Imaging Findings in 24 Cats With Histopathologically Confirmed Neurologic Feline Infectious Peritonitis

Crawford, A.H.; Stoll, A.L.; Sanchez-Masian, D.; Shea, A.; Michaels, J.; Fraser, A.R.; Beltran, E.

The fluid-attenuated inversion recovery sequence suppresses signal from the CSF and is highly sensitive for detection of lesions adjacent to or within the ventricles. 17, 18 The high protein concentration of the CSF in FIP may result in incomplete suppression of the CSF signal on FLAIR sequences. [17] [18] [19] In our series, failure of CSF signal suppression, or hyperintense CSF, was apparent in 6 of the 19 cats for which FLAIR sequences were available. Cerebrospinal fluid analysis was performed in 3 of these 6 cats, and each was found to have a markedly increased total protein concentration (2.52, 3.68 and 9.89 g/L). A similar elevation in CSF protein concentration was reported in 8 FIPaffected cats in another study, which found that a concentration of >2 g/L was a distinctive feature of FIP, and no other inflammatory CNS disease group had a mean CSF protein concentration >1 g/L. 9 Ten of the 11 cats in our study in which CSF protein concentrations were measured had concentrations >2 g/L. Interestingly, the 3 cats with the highest total protein concentration (29.9, 28.8 and 25.5 g/L) had full CSF signal suppression on FLAIR. Therefore, CSF signal suppression in FLAIR sequences does not exclude the presence of increased CSF protein concentrations. Other potential causes of CSF hyperintensity in FLAIR sequences include both pathologic changes such as ventricular hemorrhage, ischemia, or ventricular metastatic disease, and nonpathologic factors such as inhalation of 100% oxygen, chemical shift artifact, or magnetic susceptibility artifact. 17, 18 Further studies are warranted to ascertain which other factors affect CSF suppression, or lack thereof, in cats with FIP.