Download to read offline
More Related Content
Similar to autoimmune encephalitis types, clinical features.pptx
autoimmune encephalitis types, clinical features.pptx
- 1. Psychiatric manifestations of autoimmuneencephalitis
- 2. We will learn…… •What is autoimmune encephalitis? • Types of autoimmune encephalitis? • PSYCHIATRIC manifestations of autoimmune encephalitis? • Red flag signs to suspect autoimmune encephalitis in patients with psychiatric symptoms? • NMDARE • Limbic encephalitis,Hashimoto encephalopathy • Psychiatric drugs used in treatment • prognosis
- 3. AUTOIMMUNE ENEPHALITIS • Encephalitiswith antibodies to neuronal cell surface/ synaptic antigens are a group of neuropsychiatric disorders in which the antibodies produce neuronal dysfunction by direct interaction with their target antigen. • These disorders can occur with and without a cancer association. • The antibody effects are reversible and although the process of recovery can be prolonged, patients with autoimmune encephalitis often have full or substantial recovery after immunotherapy.
- 8.
- 11.
- 12.
- 14. LIMBIC ENCEPHALITIS • rapiddevelopment of confusion, working memory deficit, mood changes, and often seizures. • The subacute development of short-term memory loss is considered the hallmark of the disorder
- 15.
- 16. Anti-NMDA receptor encephalitis •Anti-NMDA receptor encephalitis is frequently recognisable on clinical grounds and is associated with CSF IgG antibodies against the GluN1 subunit of the NMDA receptor. • Antibodies are highly specific • Predominantly affect young individuals {<45 years} with a female sex predominance of 4:1 • frequency of an underlying tumour varied with age and sex (usually an ovarian teratoma).
- 18. 75% first approachespsychiatrist for help
- 19. Psychiatric phase • Highlyvariable • Delutional thought including paranoid ideation • Perceptual disturbance • Disorganised thoughts and behaviour • Anxiety ,fear,agitation • Cognitive deterioration • Progressive Decline in speech – alogia,echolalia,perseveration • Peadiatric population – manic symptoms,irritability,behavioural outburst,sleep dysfunction,hyperactivity,hypersexuality
- 20. • Seizures cantake place at any time during the disease, but tend to occur earlier in males • the clinical picture at 3–4 weeks after symptom onset was similar in most cases.
- 21.
- 23. INVESTIGATIONS • CSF –lymphocytic pleocytosis,elevated protein,ocb (60%) • MRI BRAIN – 50% Normal.others-medial temporal lobe,frontal,MO • EEG- DYS, Extreme delta brush • Nmda antibody in serum and csf – cell based assay
- 24.
- 25. • Treatment ofteratoma • Quetiapine is an appropriate drug to treat psychosis • ECT ?
- 27. Hashimoto encephalopathy EPIDEMIOLOGY PREVALENCE 1-2/ILAKH MEAN AGE ONSET 45-55YEARS FEMALE>MALE 5:1 CLINICAL FEATURES INVESTIGATION COGNITIVE DYSFUNCTION ANTI TPO -100% SEIZURE ANTI TG – 70% FOCAL DEFICIT EUTHYROID/SUBCLINICAL HYPOTHYROID – > 60% TREMOR CLINICAL HYPOTHYROID -20% MYOCLONUS CSF – MILD PLEOCYTOSIS MILD ELEVATED PROTEIN GAIT DISORDER MRI NORMAL>50% ATAXIA
- 28.
- 29.
- 30. Treatment of psychiatricsymptoms
- 33. Prognosis • anti-NMDAR encephalitisoften has a good outcome if appropriate treatment such as immunotherapy or tumor removal are carried out in time • 45% of patients had residual symptoms such as memory deficits, speech disturbances and especially psychiatric symptoms, which may still affect the quality of life of these patients. • It is suggested that around 25% of the patients with anti-NMDAR encephalitis are left with memory, cognitive, and motor deficits • The mild deficits symptoms such as poor attention, behavioral disinhibition, and sleep dysfunction during the recovery period may be due to the frontal-lobe dysfunction
- 34. • What isautoimmune encephalitis? • Types of autoimmune encephalitis? • PSYCHIATRIC manifestations of autoimmune encephalitis? • Red flag signs to suspect autoimmune encephalitis in patients with psychiatric symptoms? • NMDARE • Limbic encephalitis,Hashimoto encephalopathy • Psychiatric drugs used in treatment • prognosis
- 35. TAKE HOME MESSAGE •Isolated psychiatric episodes are rare but can occur as initial onset or relapse of anti-NMDAR encephalitis. • Recognition of these episodes is important because they respond to immunotherapy. • In patients with new-onset psychosis, having a history of encephalitis, subtle neurological symptoms, and/or abnormal results on ancillary tests should prompt screening for NMDAR antibodies
- 36. REFERENCES • Psychiatric Symptomsof Patients With Anti-NMDA Receptor Encephalitis,Wang et al • A clinical approach to diagnosis of autoimmune encephalitis,Graus et al • Autoimmune psychosis: an international consensus on an approach to the diagnosis and management of psychosis of suspected autoimmune origin,Pollack et al • Long-Term Treatment of Hashimoto’s Encephalopathy,Marshall et al • Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study • Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study
Editor's Notes
- #5 Intra cellular synaptic –GAD,AMPHIPHYSIN Autoimmune encephalitis syndromes are different from the classical paraneoplastic encephalitis in which the associated antibodies target intracellular neuronal proteins – t cell mediated cell damage - irreversable
- #8 The weight loss and severe diarrhea occur, on average, 4 months before the onset of neurological symptoms and can result in extensive evaluations for a primary gastrointestinal disorder. The triad of weight loss, cognitive dysfunction, and symptoms of CNS hyperexcitability should raise the suspicion for anti-DPPX encephalitis. The encephalitis is chronic and progresses over months (median 8 months to disease peak). The myenteric plexus is enriched in DPPX receptors
- #15 CSF analysis shows mild-to-moderate lymphocytic pleocytosis (usually less than 100 white blood cells per mm3) in 60–80% of patients, and elevated IgG index or oligoclonal bands in approximately 50% of cases. Among all immunological subtypes of limbic encephalitis, patients with LGI1 antibodies present with a lower frequency of CSF pleocytosis (41%) or elevated CSF protein concentrations (47%) and rarely have intrathecal IgG synthes
- #16 antibody status is not needed to consider limbic encephalitis as having a definite autoimmune origin because immune-mediated limbic encephalitis can occur without detectable autoantibodies Measurement of autoantibodies, however, remains important for two reasons: their presence clarifies the immunological subgroup of limbic encephalitis, with comorbidities, tumour association, and prognosis that might differ according to the autoantibody
- #17 ranging from 0–5% in children younger than 12 years, to 58% in women older than 18 years (usually an ovarian teratoma). Disorder identified first 2007,media attention – Susannah calahann – brain on fire
- #18 Relapse 25% 85% of patients who make a full recovery have executive dysfn,impulsivity
- #19 Dd- psychosis,mania,schizophrenia
- #20 abnormal movements (orofacial, limb, or trunk dyskinesias} NORMALLY EXCITATORY GLUTAMATE STIMULATES NMDA receptor in the interneuron ,resulting GABA release – which tonic inhibit dopamine release Hypoactive nmda receptor ,loss of tonic inhibition resulting hyperdopaminrgia in mesolimbic pathway –positive symptoms
- #23 anti-NMDA receptor encephalitis, affects 20% of patients with herpes simplex encephalitis, and manifests with new-onset choreoathetosis (predominantly in children)79,80 or psychiatric symptoms (mainly in adults and teenagers) a few weeks or, rarely, months after the viral infection.