Letter to the EditorDear Sir:Post stroke neuropsychiatric syndrome is common.1 Many patients after stroke experience depression, cognitive impairment, personality change, psychosis, apathy, and anxiety. Mania can also be a consequence of stroke but is not common.2 "Mania" is described as a distinct period of abnormally and persistently elevated, expansive, or irritable mood, lasting at least 1 week in the Diagnostic and Statistical Manual of Mental Disorder-V.3 Mania seems to be observed more frequently with the right side brain lesions. 4 Here, we report a professional artist whose painting style dramatically changed with manic illness from a recent stroke. Informed consent for this report was obtained.A 58-year-old Korean man who had worked in Russia as a professional painter visited the emergency room due to a sudden onset of dysarthria and left side weakness, which were noted when he woke up in the morning. He did not have any other vascular risk factors except for smoking. On neurologic examination, dysarthria, left facial palsy and left hemiparesis (motor grade IV/IV) were observed. Left side sensory change and sensory extinction were noted, but prosopagnosia was not observed. With ophthalmologic examination, corrected visual acuity was 0.8/0.8 on near card test, visual field defect was not observed on manual test and achromatognosia was not noted. The brain magnetic resonance imaging revealed a territorial ischemic lesion with proximal occlusion of the inferior division of the right middle cerebral artery ( Figure 1A). Cardioembolic source was not found on the transthoracic echocardiogram, transesophageal echocardiogram and holter monitoring. An antiplatelet drug and statin were prescribed.When he visited our outpatient clinic 2 weeks after the symptom onset, although his neurological deficits were much improved, he became very erratic, aggressive, talkative, hyperenergetic, and lost the desire to sleep with an increased goal directed activities such as staying up all night and continuously drawing art pieces consisting of a human face. Furthermore, his wife noted that his style of painting was absolutely transformed. We compared the paintings he drew after his stroke with some of his paintings from Russia on his website before the stroke ( Figure 1B, C). His previous artwork showed complementary and subtle color schemes, with well-defined heads and figures using sharp lines. The paintings were ordered with an austere simplicity. On the other hands, his new artwork showed a drastic change in the artistic style. The drawings are complex, disrupted and disorganized with splattering of words and phrases (in more than one language). Use of color became broader and more overt.After starting carbamazepine 100 mg twice daily as a mood stabilizer, his mood slightly improved; however, he was still talkative, and his paintings were still awkward, complex and disorganized.Here, we reported the case of a professional painter who showed changes in his artistic style and behavior after an ischemic stroke. There have be...

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Creutzfeldt-Jakob disease (CJD) is the most common prion disease in humans. Once formed by unknown cause, PrP sc can make the normal cellular PrP (PrP c) transform into the pathogenic PrP sc in a cascade. Consequent extensive neuronal loss causes dementia, involuntary movement, psychosis, and incoordination. The criteria for clinical diagnosis include cerebrospinal fluid (CSF) biomarkers (e.g., 14-3-3 protein and t-tau), specific magnetic resonance image (MRI) finding, electroencephalography (EEG), and clinical symptoms. 1 Recently, in vitro protein misfolding amplification system, the real-time quakinginduced conversion assay (RT-QuIC), for the detection of PrP sc in CSF was developed and showed ultra-high sensitivity and specificity, amending the diagnostic criteria. 2 Here, we report the case of a patient without obvious clinical symptoms of sporadic Creutzfeldt-Jakob disease (sCJD) except rapidly progressive cognitive decline and a positive RT-QuIC assay who was not CJD. An age 54 Korean female visited the clinic with progressive cognitive decline for 2 months. Her daughter noticed this when the patient, who is a storekeeper, had problems with calculations at the register. She also misplaced things and spent time searching for them. Also, she had difficulty verbally expressing herself and sometimes could not understand what others were saying. She graduated from high school in 12 years. Her medical history was unremarkable. A month ago, she was admitted to a university hospital for evaluation. On neuropsychological evaluation, visual and verbal memory, frontal/executive function and calculation impairment were noted. Her Mini-Mental State Examination was 23, Clinical Dementia Rating scale 1 (sum of box 4). Brain MRI did not show any lesion even on diffusionweighted images (DWIs) (Fig. 1A). EEG showed mild cerebral dysfunction but no periodic sharp wave complexes. CSF analysis showed five white blood cells with normal chemistry. Autoimmune antibodies and tumor markers were negative. CSF 14-3-3 protein was weakly positive; and total tau (t-tau) level was elevated to 1,206 pg/mL. Additionally, RT-QuIC assay tested positive. Flutemetamol (18F) positron emission tomography showed elevated cortical amyloid uptake (Fig. 1B). She was discharged with a diagnosis of sCJD with superimposed Alzheimer's disease. Donepezil 5 mg was started. However, a month after discharge, she was stable without signs of aggravation. For a second opinion, she visited Asan Medical Center. EEG, and brain MRI DWI did not show abnormal findings. In CSF analysis, 14-3-3 protein was weakly positive, t-tau level increased to 1,336 pg/mL, p-tau to 144.7 pg/mL, and amyloid