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Delirium
Published in Henry J. Woodford, Essential Geriatrics, 2022
A diagnosis of possible autoimmune encephalitis requires all three of the following:44Subacute onset (less than three months) of memory impairment, altered level of consciousness, lethargy or personality change, or psychiatric symptoms (e.g. mood disorders or hallucinations)At least one of:New focal neurological findingsSeizures not explained by a known seizure disorderCSF white blood cell count > 5 per mm3MRI features suggestive of encephalitisReasonable exclusion of alternative causes
Case 11
Published in Andrew Solomon, Julia Anstey, Liora Wittner, Priti Dutta, Clinical Cases, 2021
Andrew Solomon, Julia Anstey, Liora Wittner, Priti Dutta
Autoimmune encephalitis is an increasingly recognised non-infective form of encephalitis that may present to both physical and psychiatric medical services. A range of antibody and CSF-based diagnostics are still in development with improving recognition amongst specialists in the field.
Rabies and other lyssaviruses
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Thiravat Hemachudha, Jiraporn Laothamatas, Henry Wilde
Autoimmune encephalitis is not uncommon. As many as 25% of 103 patients with encephalitis were associated with immune causes. The patients may present as viral-like encephalitis with fever, behavioral change, psychosis, abnormal CSF pleocytosis with or without characteristic MRI features of neuromyelitis optica or anti-NMDA receptor antibody encephalitis (limbic encephalitis) (Figure 13.20, anti-NMDA) [152].
Autoimmune Encephalitis and Related Disorders of the Nervous System
Published in Brain Injury, 2023
“Autoimmune Encephalitis and Related Disorders of the Nervous System” provides an impressively comprehensive coverage of the entire spectrum of autoimmune encephalitides and associated immune-driven disorders of – predominantly – the central nervous system. The initial section provides a very effective overview of these conditions, covering the historical context of their discovery, how best to recognize autoimmune encephalitis clinically and an approach to immune mechanisms causing autoimmune encephalitis. The second section delves more deeply into these immunological mechanisms and the effect of autoantibodies on the nervous system. The third section then catalogs each of the autoimmune encephalitides and related diseases in encyclopedic detail, in each case covering clinical features, diagnostic investigations and treatment. The final section details the more controversial end of the autoimmune encephalitis-associated spectrum, including the intersection between neurological and psychiatric manifestations. This text is vividly brought to life by both insightful clinical vignettes and high-quality images interspersed throughout.
Dipeptidyl-peptidase-like protein 6 encephalitis treated with immunotherapy
Published in Baylor University Medical Center Proceedings, 2021
Lan Ye, Margret Schnegelsberg, Mark Obermann
The treatment strategy for autoimmune encephalitis is a stepwise escalation of immunotherapy. First-line therapy involves corticosteroids, intravenous immunoglobulins, and plasma exchange. Corticosteroids broadly inhibit the inflammatory process. A couple of patients were reported to nearly completely recover within months to years after corticosteroid therapy.4,9 Rituximab is one of the most commonly used second-line agents in autoimmune encephalitis.10 It appears to be effective in multiple autoimmune encephalitis, including DPPX encephalitis.11,12 However, in our case, responses to both corticosteroid therapy and rituximab were unsatisfactory. The relatively late treatment could be a reason. The patient came to us 2 years after symptoms began, but the average time to disease peak is reported to be 8 months after onset.4 Moreover, the patient was switched to rituximab rather late, after 8 months of corticosteroid treatment with one plasma exchange. Although rituximab can deplete B cells peripherally, which is a major contributor to autoimmune disease, it cannot permeate the blood-brain barrier.12
A case of anti-VGKC antibody encephalitis and prolonged encephalopathy despite spontaneous resolution of imaging abnormalities
Published in Journal of Community Hospital Internal Medicine Perspectives, 2020
Victoria Novoselova, Vikas Kumar, Niranjan N. Singh, Alexandre Lacasse
Autoimmune encephalitis is a group of inflammatory brain conditions with diverse clinical, laboratory, and imaging presentation. Anti-VGKC antibody encephalitis is a relatively common autoimmune encephalitis. Although previously was described in other AE such as anti-α-amino-3-hydroxy-5-methyl-4-isoxa- zolepropionic acid receptor (AMPAR) encephalitis [1] and NMDA-R encephalitis, a clinical presentation consistent with severe encephalopathy seem unusual with anti-VGKC antibody encephalitis [2]. Hyperammonemia is a well-known cause of severe encephalopathy and can be seen in patients with cirrhosis, infections with urea-producing bacteria, small intestinal bacterial overgrowth syndrome, recent surgery such as lung transplant, bariatric surgery, ureterosigmoidoscopy, and as a side effect of drugs [3,4,5].