Prescribing tasks, which involve pharmacological knowledge, clinical decision-making and practical skill, take place within unpredictable social environments and involve interactions within and between endlessly changing health care teams. Despite this, curriculum designers commonly assume them to be simple to learn and perform. This research used mixed methods to explore how undergraduate medical students learn to prescribe in the ‘real world’. It was informed by cognitive psychology, sociocultural theory, and systems thinking. We found that learning to prescribe occurs as a dynamic series of socially negotiated interactions within and between individuals, communities and environments. As well as a thematic analysis, we developed a framework of three conceptual spaces in which learning opportunities for prescribing occur. This illustrates a complex systems view of prescribing education and defines three major system components: the “social space”, where the environmental conditions influence or bring about a learning experience; the “process space”, describing what happens during the learning experience; and the intra-personal “cognitive space”, where the learner may develop aspects of prescribing expertise. This conceptualisation broadens the scope of inquiry of prescribing education research by highlighting the complex interplay between individual and social dimensions of learning. This perspective is also likely to be relevant to students’ learning of other clinical competencies.

Sleep is a pillar of health, alongside adequate nutrition and exercise. Problems with sleep are common and often treatable. Twenty years ago, UK medical school education on sleep disorders had a median teaching time of 15 min; we investigate whether education on sleep disorders has improved. This is a cross-sectional survey, including time spent on teaching sleep medicine, subtopics covered and forms of assessment. Thirty-four medical degree courses in the UK were investigated via a questionnaire. We excluded responses not concerned with general undergraduate education (i.e. optional modules). Twenty-five (74%) medical schools responded. Time spent teaching undergraduates sleep medicine was: median, 1.5 hr; mode, <1 hr; mean, 3.2 hr (SD = 2.6). Only two schools had a syllabus or core module (8%) and five (22%) were involved in sleep disorders research. Despite the above, half of the respondents thought provision was sufficient. Free-text comments had recurring themes: sleep medicine is subsumed into other specialties, obstructive sleep apnea dominates teaching, knowledge of sleep disorders is optional, and there is inertia regarding change. A substantial minority of respondents were enthusiastic about improving provision. In conclusion, little has changed over 20 years: sleep medicine is neglected despite agreement on its importance for general health. Sleep research is the exception rather than the rule. Obstacles to change include views that "sleep is not a core topic" or "the curriculum is too crowded". However, there is enthusiasm for improvement. We recommend establishment of a sleep medicine curriculum. Without better teaching, doctors will remain ill-equipped to recognize and treat these common conditions.

Inventory Nursing Home version (NPI-NH) in 2/5. Network analysis was used to evaluate connectedness of psychopathologic features and a qualitative synthesis distilled recurrent psychopathologic features. Finally, each time point was compared with operationalised diagnoses using an automated classifier and plotted with corresponding symptom complexes over time. Results All had psychiatric features at onset and were seen first by general practitioners or emergency departments. All received an incorrect initial diagnosis (1 neurological, 4 primary psychiatric). Two patients were referred to mental health services and detained while three were admitted to a general hospital. Psychiatric diagnoses spanned psychotic, mood, and stress categories. None had a personal or family history of serious mental illness or substance misuse. Despite the atypicality all were ascribed to non-specific psycho-social aetiologies. Autoimmune encephalitis was then first suspected between 4-28 days from onset (median=21 days) because of the psychopathology (n=2) or development of clear-cut seizures or movement disorder (n=3). 10 consistently reported features were identified: sleep disturbance, nightmares, mixed unstable mood, perplexity, incoherent repetitive speech, musical ±visual hallucinosis, catatonic facies, possession-like/ drugged, dissociative-disorganised, and regressed behaviour.The symptom complex peaked rapidly (within 3 weeks). The peak burden was large and crossed multiple psychopathologic domains. Overall the syndrome is poorly-described by any single primary disorder; mixtures of mixed mood-psychotic-catatonic disorders performed best. Furthermore, it showed clear qualitative and hence diagnostic shifts between onset, peak, and resolution. Conclusions The psychopathology of NMDAR-antibody encephalitis is complex and dynamic, likely contributing to diagnostic difficulties. However, it appears stereotyped between individuals, hence sensitive features can be derived. Inconsistency with psychosis and/or mood disorder constructs and better approximation with 'mixtures of mixtures' suggests specificity is possible but similar studies with primary disorder comparators are needed. As the disease can only be ruled out with cerebrospinal fluid antibody testing the practical implication is that the mental health system needs to embrace lumbar puncture as a routine part of practice in high risk groups.

Design and methods We assessed BDNF levels in 27 PI (DSM V criteria) patients (15 males, 56%) and in 14 controls (6 males, 43%). All subjects underwent 18fluorodeoxyglucose positron emission tomography (18F-FDG PET), brain PET with 13N-ammonium in the morning in wakefulness. Brain PET/CT scanning was performed 30 min. after administration of 250 MBq 18F-FDG. The PET images were statistically analyzed by 3D-SSP method (Z-score) using software package Cortex ID. Results There was no difference in BDNF level in PI patients and control group: 11.9 (8.5; 100) and 12.8 (10.1; 72.8) ng/ ml, respectively (p=0,138). We found a weak association between BDNF level and brain metabolism in the left prefrontal medial lobe (=0.57, p=0.02) and right parietal inferior lobe (=0.52, p=0.039). However, there was no association between BDNF level and 13N-ammonium accumulation which indicate the activity of glutamate synthase.Conclusions Insomnia is not associated with the changes in BDNF levels compared to healthy control subjects, although the relation between brain metabolism and BDNF concentration requires further investigation.

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