Male, 74 years old, with cognitive decline and poorly defined lesion in the left temporal lobe on prior exam. Image quality is slightly reduced by motion artifact. Furthermore, the patient was unwilling to receive IV contrast and therefore only noncontrast imaging was obtained.T2 hyperintensity is redemonstrated within the left amygdala and hippocampal head. As before, this abnormal tissue seems to contain one or two small cystic spaces. There is no associated mass effect. No susceptibility or restricted diffusion is seen. Cystic spaces in the adjacent temporal stem likely represent dilated perivascular spaces. No significant change is seen in the size or morphology of this abnormal tissue when compared to both prior examinations.Elsewhere in the brain, numerous foci of white matter T2 hyperintensity are redemonstrated, similar in number and distribution to the prior exam. No evidence of parenchymal edema or mass effect is seen. No acute intracranial hemorrhage or any abnormal extra-axial fluid collections are detected. The ventricular system is normal in size and morphology.
Abnormal signal involving the left amygdala and hippocampal head is again seen without significant interval change. Notably, this lesion is associated with no mass effect or other concerning secondary features.The lesion remains nonspecific, but given the absence of mass effect and its stability dating back to January 2015, chronic sequela of prior parenchymal injury or inflammation is favored over an active inflammatory or neoplastic process. If continued follow-up is desired on clinical grounds, a longer interval (at least 6-12 months) would probably be appropriate.Elsewhere, numerous foci of cerebral white matter signal abnormality are seen which statistically most likely reflect chronic small vessel ischemic disease. No definite acute intracranial abnormalities are seen.