Detection of subthreshold atrophy in crossed cerebellar degeneration via two-compartment mathematical modeling of cell density in DWI: A proof of concept study.

Crossed cerebellar diaschisis (CCD) refers to transneuronal degeneration of the corticopontocerebellar pathway, resulting in atrophy of cerebellum contralateral to supratentorial pathology. CCD is traditionally diagnosed on nuclear medicine studies. Our aim is to apply a biexponential diffusion model, composed of intracellular and extracellular compartments, to the detection of subthreshold CCD on DWI, with the calculated fraction of the intracellular compartment as a proposed measure of cell density. At a voxel-by-voxel basis, we solve for intracellular and extracellular coefficients in each side of the cerebellum and compare the distribution of coefficients between each hemisphere. We demonstrate, in all six CCD cases, a significantly lower contribution of the intracellular compartment to the cerebellar hemisphere contralateral to supratentorial pathology (p < 0.01). In a separate, proof-of-concept case of pontine stroke, we also demonstrate reduced intracellular coefficients in bilateral cerebellar hemispheres, excluding middle cerebellar peduncles (p < 0.01). Our findings are consistent with a decreased intracellular fraction, presumably a surrogate for reduced cellular density in corticopontocerebellar degeneration, despite normal-appearing scans. Our approach allows detection of subthreshold structural changes and offers the additional advantage of applicability to most clinical cases, where only three DWI beta values are available.

Complex imaging features of accidental cerebral intraventricular gadolinium administration.

Gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) is a contrast agent commonly used for enhancing MRI. In this paper, the authors report on 2 cases of postoperative inadvertent administration of Gd-DTPA directly into a ventriculostomy tubing side port that was mistaken for intravenous tubing. Both cases demonstrated a low signal on MRI throughout the ventricular system and dependent portions of the subarachnoid spaces, which was originally believed to be CSF with areas of T1 shortening in the nondependent portions of the subarachnoid spaces, and misinterpreted as basal leptomeningeal enhancement and meningitis. The authors propose that the appearance of profound T1 hypointensity within the ventricles and diffuse susceptibility artifact along the ependyma is pathognomonic of intraventricular Gd-DTPA and should be recognized.