Male, 64 years old, with intracerebral hemorrhage, assess for etiology. Predominantly T1 isointense and T2 hypointense signal within the left thalamus is compatible with the known evolving late acute left thalamic hematoma. The thalamus is expanded and there is moderate edema in the surrounding parenchyma which tracks into the basal ganglia and parietal lobe as well as down into the midbrain. This hematoma results in fairly significant generalized mass-effect with midline shift to the right of up to 9 mm and effacement of the left quadrigeminal plate cistern. The midbrain is distorted as well. Allowing for differences in technique, the overall size of the hematoma is probably not increased.Also seen is partially T1 hyperintense and T2 hypointense material within the ventricular system compatible with intraventricular extension of hemorrhage. This hemorrhage is evident throughout the ventricular system with associated ventricular dilatation. Again, allowing for differences in technique, there has probably not been a significant change in ventricular size. T2 hyperintensity rimming the ventricles is compatible with transependymal CSF flow. A right frontal approach ventriculostomy is redemonstrated.Scattered areas of restricted diffusion are seen throughout the cerebral hemispheres. Many of these are associated with mild susceptibility, but some are not, and it does not seem likely that they could be accounted for entirely by blood induced artifact. In particular, some of them show a fairly vascular morphology, for example within the anterior left temporal lobe. The background brain demonstrate fairly extensive patchy periventricular T2 hyperintensity which may reflect chronic microvascular ischemic disease. Scattered foci of susceptibility are also seen, some but not all of which are probably chronic.On dedicated vascular images, no definite vascular lesion is seen in the vicinity of the left thalamus to account for the hemorrhage. The left PCA is displaced by mass effect, but it remains patent throughout. No definite high grade vascular stenosis is seen, though some degree of atherosclerotic irregularity is suspected within the cavernous ICAs. Flow related signal within the left sylvian MCA branches is uniformly reduced compared to the right, though this is felt to be an artifact of technique as normal signal recovers in all vessels at the same slice level. No aneurysms are detected within the limits of technique. A prominent right PCOM artery is seen. The ACOM artery and left PCOM arteries are not well seen.
A large left thalamic hematoma with intraventricular extension is redemonstrated. There has been no significant interval change in the size of the hematoma, nor of the quantity of intraventricular blood or degree of ventricular dilatation. No definite vascular lesion is seen underlying the thalamic hematoma.Scattered areas of restricted diffusion are seen throughout the cerebral hemispheres, some of which are vascular in morphology and/or too large to be accounted for by minimal associated susceptibility. Given these findings, the possibility of an embolic phenomenon with secondary hemorrhage should be considered. Vasospasm and vasculitis would be additional but less likely etiologies.