Mg/wk) and hydroxychloroquine (200 mg/d). One year later, following an exacerbation of joint symptoms and also the improvement of interstitial lung disease believed to become a systemic complication of RA, his methotrexate dose was elevated to 25 mg/wk (subcutaneously) and leflunomide (10 mg/d) was added. At presentation, he remained on methotrexate and hydroxychloroquine in the similar doses, but leflunomide had been discontinued and sulfasalazine (three g each day) commenced. The only other history of note was an episodeof obstructive cholestasis. He was otherwise well, and also the main carer for his wife. Examination revealed marked visuospatial dysfunction and simultanagnosia. The patient was in a position to study when presented with one particular line of text, but unable to study a paragraph. Object recognition was preserved; having said that, he was unable to describe a picture of a scene. He could not recognize interrupted figures or letters. He had an ideomotor limb apraxia, with impaired gesture copying (e.g., extending the 1st and 2nd digits at appropriate angles). He scored 16/30 on the Bcl-xL Inhibitor Molecular Weight Montreal Cognitive Examination (MoCA), with serious constructional apraxia, becoming unable to draw a cube or clock, performing poorly around the Trail-Making Test (figure, A), and added impairments on vigilance testing and serial 7s, lowered verbal fluency, and impaired delayed recall. There was no dysgraphesthesia or neglect. Speech was intact, and he could fully grasp and follow written commands. There had been no parkinsonian attributes and the remainder on the neurologic examination was typical. Systemic examination revealed bibasal lung crepitations. His admission blood pressure was 128/75 mm Hg. There was no clinical proof of active joint inflammation.Queries for consideration:1. What exactly is your localization at this point two. What’s your differential diagnosis three. What further tests would you performGO TO SECTIONSupplemental data at Neurology.orgFrom the Nuffield Division of Clinical Neurosciences, Oxford University (M.S., W.K., U.G.S.), and the Department of Neuroradiology (W.K.), John Radcliffe Hospital, Oxford, UK. Visit Neurology.org for full disclosures. Funding facts and disclosures deemed relevant by the authors, if any, are provided in the end on the short article. e6 2014 American Academy of NeurologySECTIONOur patient’s marked visuoconstructive deficits but preservation of language suggests dysfunction of predominantly posterior brain regions. Challenges with the Trail-Making Test indicate added frontal-executive involvement. Difficulty in recognizing incomplete letters implies a degree of apperceptive visual agnosia, most typical of ideal hemispheric lesions, while ideomotor limb apraxia is usually seen in left hemispheric injury. The differential diagnosis right after the clinical assessment hence comprised causes of progressive encephalopathy preferentially affecting bilateral occipital and parietal function. In order of likelihood, we thought of a diffusely infiltrating space-occupying lesion prion disease (Heidenhain variant), given the rapid progression; a posterior reversible IL-12 Modulator MedChemExpress leukoencephalopathy syndrome (PRES), either linked with autoimmune illness or drug-induced; progressive multifocal leukoencephalopathy (PML), given the immunosuppression; or cerebral vasculitis related to RA. Demyelinating illness can also present as a diffuse encephalopathy or mimic space-occupying lesions. Nutritional deficiency could also producethis picture; as an example, B12 deficiency can cause selective sp.