Their detection and diagnosis is of great importance, as immune therapy is a causal, frequently successful form of treatment (5). antibodies in patients with clinically defined autoimmune encephalitis is usually estimated at 6080 %. Figures on cumulative specificity are currently unavailable. == Conclusion == The detection of antineuronal antibodies in patients with the corresponding appropriate symptoms implies the diagnosis of autoimmune encephalitis. Observational studies have shown that rapidly initiated immunosuppressive treatment enhances these patients outcomes. Further studies are needed to determine the positive predictive value of antineuronal antibody detection and to develop further treatment options under randomized and controlled conditions. Acute or subacute disorders of wakefulness (quantitative impairment of consciousness, ICD-10 R40.-) and qualitative impairment of consciousness (confusion, impaired orientation, amnesia syndromes; ICD-10 R41.-) are frequently occurring causes of hospitalization. In a large neurological emergency department, quantitative disorders of consciousness were the cardinal symptom in every fifth patient seen (reduced vigilance 9%, epileptic seizures 11%) (1). Around 20 to 30% of all hospital inpatients, 50% of elderly patients, and up to 70% of rigorous care patients suffer from delirium, i.e., acute deterioration of alertness, organized cognition, memory, attentiveness, and belief (2,e1e3). Particularly with delirium syndromes the causes are unclear and the treatment principally comprises supportive steps, e.g., management WYE-354 of systemic infections or electrolyte shifts (3). Recently an additional differential diagnosis has been described, namely a group of previously unknown immune-mediated forms of encephalitis with autoantibodies against Lepr neuronal antigens (4). These diseases are rare, but can be clearly delineated from noninflammatory causes with the aid of a demanding diagnostic work-up for antibodies. Their detection and diagnosis is usually of great importance, as immune therapy is usually a causal, frequently successful form of treatment (5). Owing to the wide heterogeneity of immune-mediated forms of encephalitis, these diseases demand close interdisciplinary cooperation on the part of neurologists, intensive care specialists, oncologists, pediatricians, gynecologists, and psychiatrists (eBoxes 2and3). == eBOX 2. Case 1. == A 70-year-old woman was admitted to the internal medicine department because she was suspected to have dementia. There was a 4-month history of progressive short-term memory loss with personality changes WYE-354 and WYE-354 repeated erroneous actions. Clinical examination on admission found that the patient was disoriented in place and time, showed attention disorder, sometimes displayed diminished affect, and was intermittently indifferent. She experienced no focal neurological deficits. Clinical chemistry exhibited hyponatremia of 125 mmol/L; the cerebrospinal fluid findings were normal. Neurocranial magnetic resonance tomography showed increased transmission and bilateral thickening of the hippocampus. An autoimmune panel investigation for paraneoplastic antibodies, prompted by the patients weight loss, detected antibodies to LGI1 with a serum titer of 1 1:100. Each day during the patients stay in hospital there were several episodes, each lasting a few seconds, in which she grimaced and waved her arms around bizarrely. A neurologist later classified these events as faciobrachial dystonic seizures (FBDS). On the basis of the clinical and laboratory findings, LGI1-antibody-positive limbic encephalitis was diagnosed. The patient was treated with intravenous steroids (1 g methylprednisolone/day) for WYE-354 3 days, followed by oral prednisolone for 5 months. Immune therapy rapidly resulted in remission of the FBDS and the patients orientation progressively improved. With time, the symptoms resolved completely; however, there was retrograde amnesia for the time spent in the hospital. == eBOX 3. Case 2. == A 21-year-old woman was admitted to the hospital because WYE-354 of progressive personality switch with repeated phases of transient mental distraction. The initial clinical examination found fluctuating disorientation but no focal neurological deficit. The patient subsequently designed a hallucinatory psychosis and both complex focal seizures and generalized seizures occurred. Neurocranial magnetic.