ImportanceAutoimmune encephalitis misdiagnosis can lead to harm.ObjectiveTo determine the diseases misdiagnosed as autoimmune encephalitis and potential reasons for misdiagnosis.Design, Setting, and ParticipantsThis retrospective multicenter study took place from January 1, 2014, to December 31, 2020, at autoimmune encephalitis subspecialty outpatient clinics including Mayo Clinic (n = 44), University of Oxford (n = 18), University of Texas Southwestern (n = 18), University of California, San Francisco (n = 17), University of Washington in St Louis (n = 6), and University of Utah (n = 4). Inclusion criteria were adults (age ≥18 years) with a prior autoimmune encephalitis diagnosis at a participating center or other medical facility and a subsequent alternative diagnosis at a participating center. A total of 393 patients were referred with an autoimmune encephalitis diagnosis, and of those, 286 patients with true autoimmune encephalitis were excluded.Main Outcomes and MeasuresData were collected on clinical features, investigations, fulfillment of autoimmune encephalitis criteria, alternative diagnoses, potential contributors to misdiagnosis, and immunotherapy adverse reactions.ResultsA total of 107 patients were misdiagnosed with autoimmune encephalitis, and 77 (72%) did not fulfill diagnostic criteria for autoimmune encephalitis. The median (IQR) age was 48 (35.5-60.5) years and 65 (61%) were female. Correct diagnoses included functional neurologic disorder (27 [25%]), neurodegenerative disease (22 [20.5%]), primary psychiatric disease (19 [18%]), cognitive deficits from comorbidities (11 [10%]), cerebral neoplasm (10 [9.5%]), and other (18 [17%]). Onset was acute/subacute in 56 (52%) or insidious (>3 months) in 51 (48%). Magnetic resonance imaging of the brain was suggestive of encephalitis in 19 of 104 patients (18%) and cerebrospinal fluid (CSF) pleocytosis occurred in 16 of 84 patients (19%). Thyroid peroxidase antibodies were elevated in 24 of 62 patients (39%). Positive neural autoantibodies were more frequent in serum than CSF (48 of 105 [46%] vs 7 of 91 [8%]) and included 1 or more of GAD65 (n = 14), voltage-gated potassium channel complex (LGI1 and CASPR2 negative) (n = 10), N-methyl-d-aspartate receptor by cell-based assay only (n = 10; 6 negative in CSF), and other (n = 18). Adverse reactions from immunotherapies occurred in 17 of 84 patients (20%). Potential contributors to misdiagnosis included overinterpretation of positive serum antibodies (53 [50%]), misinterpretation of functional/psychiatric, or nonspecific cognitive dysfunction as encephalopathy (41 [38%]).Conclusions and RelevanceWhen evaluating for autoimmune encephalitis, a broad differential diagnosis should be considered and misdiagnosis occurs in many settings including at specialized centers. In this study, red flags suggesting alternative diagnoses included an insidious onset, positive nonspecific serum antibody, and failure to fulfill autoimmune encephalitis diagnostic criteria. Autoimmune encephalitis misdiagnosis leads to morbidity from unnecessary immunotherapies and delayed treatment of the correct diagnosis.

Calcium pyrophosphate deposition (CPPD) disease is a crystal arthropathy primarily affecting peripheral joints, most commonly the wrist and the knees. However, CPPD in the cervical spine is a rare entity. This report describes a case of CPPD of the cervical spine which presents with symptoms of neck pain and brachalgia. A 62-year-old woman presented with left-sided upper limb and neck pain. MRI scanning revealed a low signal abnormality within the C6 and C7 vertebrae, and the possibility of lymphoma was raised. The patient was recalled for gadolinium-enhanced scans which showed perivertebral and marrow enhancement. Fine-needle aspirate histology initially suggested a spindle cell tumour or lymphoma. However, CT-guided biopsy showed positively birefringent crystals, confirming CPPD. CPPD of the spine is a rare differential of nerve impingement in the cervical spine when MRI scanning perivertebral signal enhancement. Furthermore, CPPD of the spine can mimic malignancy.

IntroductionDecompressive hemicraniectomy is a lifesaving measure in malignant middle cerebral artery infarction; however, this leaves patients with a skull defect. There is variability of helmet use in this patient group across Britain. We aimed to examine whether (1) specialist physiotherapist were more confident mobilising a patient with hemiparesis and skull defect than a non-specialist physiotherapist (2) non-specialist and specialist physiotherapists would be more comfortable mobilising this patient with a helmet as opposed to without a helmet.MethodsWe carried out a cross-sectional online survey of specialist physiotherapists and non-specialist physiotherapists in Britain. Recruitment was through mailing lists. Physiotherapists were asked to rank their confidence level on a 5-point Likert scale of mobilising an example patient with and without a helmet. They were also asked about the number of additional therapists needed to safely mobilise the patient.Findings96 physiotherapists completed the survey; 44 were specialists and 52 were non-specialists. Specialist physiotherapists felt more comfortable mobilising patients (mean difference = 0.68, p < 0.001). Non-specialist physiotherapists felt significantly more comfortable mobilising patients with a helmet (mean difference = 0.96, p value < 0.001), as did specialist physiotherapists (mean difference = 0.68, p value < 0.001). There was no difference in confidence level arising from helmet use between the two groups (p = 0.72).ConclusionsUse of helmets may allow specialist and non-specialist physiotherapists to feel more comfortable when mobilising stroke patients post-decompressive hemicraniectomy. Consideration should be made by hospitals and health systems for the provision of helmets this patient group, to maximise functional gains.