Pearls cProgressive, subacute cognitive decline can be seen in patients with cerebral amyloid angiopathy-related inflammation (CAARI). c Cognitive decline may be the first and only clinical presentation of CAARI. c Brain MRI and lumbar puncture are warranted in patients with a subacute cognitive decline who have an unremarkable preliminary infectious and metabolic workup.Oysters c Cerebral amyloid angiopathy (CAA) and CAARI should be considered in elderly patients with subacute or rapid cognitive decline. c Subacute cognitive decline in patients with Parkinson disease (PD) can often be misdiagnosed as progression of their parkinsonian symptoms.cSubacute cognitive decline in patients with PD can mimic that which is seen with common infections and metabolic derangements.A 66-year-old man with rest tremor, bradykinesia, and rigidity since July 2017 was diagnosed with idiopathic PD. His parkinsonian symptoms were mild, and he did not require medical therapy. In December 2017, his wife reported a subacute onset of odd behaviors. He left things on the stove, put soup in the oven, stopped reading books, which he usually enjoyed, and stopped responding to texts and emails. His behavioral changes were initially thought to be due to a recent increase to his antidepressant, vortioxetine, from 10 to 20 mg daily. However, his behavior progressed despite a reduction back to 10 mg daily.On initial visit, his Montreal Cognitive Assessment (MoCA) score was 26/30 and examination was revealing for rest tremor, bradykinesia, and rigidity. Seven months later, during his followup visit after his cognitive symptoms started, his MoCA was 19/30; however, his motor symptoms remained unchanged. Initial laboratory studies revealed a within normal range vitamin B 12 , thyroid-stimulating hormone, complete blood count (CBC), comprehensive metabolic panel (CMP), and urinalysis. An MRI brain completed after his cognitive decline revealed substantial bilateral frontal white matter changes, as shown in figure 1. CSF was acellular and revealed normal protein and glucose levels. CSF varicella-zoster virus, herpes simplex virus, Epstein-Barr virus, and cytomegalovirus were all negative. CSF immunoglobulin G index was within normal range and there were no oligoclonal bands. Arylsulfatase A and very long chain fatty acids were also normal. MRI brain was repeated with additional sequences per radiology's request 3 weeks after the initial scan. Repeat MRI revealed increase in edema in the right frontal lobe with mild increase in mass effect and minimal midline shift to the left, shown in figure 2A. There were also numerous bifrontal microhemorrhages, shown in figure 2B.