Liaison and diversion services in South East London: Referral patterns over a 25-year period.

Criminal justice liaison and diversion services identify people with mental health needs and ensure they receive appropriate support. We describe a 25-year period of one such service that deals with a population of 864,540 in South East London that was set up in 1991. We used data from three time periods. A diagnosis of a mental illness was recorded in 70.0-80.3% of court liaison and diversion referrals. The proportion receiving a hospital order declined from 15.4% in 1991/1992 to 1.1% in 2015/2016; 54/199 (27.1%) of referrals to the police liaison and diversion service were detained in hospital. Although the service is designed to support any individual with a mental health issue, these results suggest that it has dealt mainly with people who have severe mental illness. Further research is required to understand how best to benefit a wider range of people with mental health issues who attend the lower (Magistrates') courts, and whether screening for mental disorders can be applied in liaison and diversion settings to aid the implementation of national policy. We also need to understand how disposal decisions are made, and which are most effective.

Analysis of primary visual cortex in dementia with Lewy bodies indicates GABAergic involvement associated with recurrent complex visual hallucinations.

Dementia with Lewy bodies (DLB) patients frequently experience well formed recurrent complex visual hallucinations (RCVH). This is associated with reduced blood flow or hypometabolism on imaging of the primary visual cortex. To understand these associations in DLB we used pathological and biochemical analysis of the primary visual cortex to identify changes that could underpin RCVH. Alpha-synuclein or neurofibrillary tangle pathology in primary visual cortex was essentially absent. Neurone density or volume within the primary visual cortex in DLB was also unchanged using unbiased stereology. Microarray analysis, however, demonstrated changes in neuropeptide gene expression and other markers, indicating altered GABAergic neuronal function. Calcium binding protein and GAD65/67 immunohistochemistry showed preserved interneurone populations indicating possible interneurone dysfunction. This was demonstrated by loss of post synaptic GABA receptor markers including gephyrin, GABARAP, and Kif5A, indicating reduced GABAergic synaptic activity. Glutamatergic neuronal signalling was also altered with vesicular glutamate transporter protein and PSD-95 expression being reduced. Changes to the primary visual cortex in DLB indicate that reduced GABAergic transmission may contribute to RCVH in DLB and treatment using targeted GABAergic modulation or similar approaches using glutamatergic modification may be beneficial.

Clinicians' ability to diagnose dementia with Lewy bodies is not affected by ß-amyloid load.

OBJECTIVE: To investigate whether an increasing load of ß-amyloid and/or neuritic plaques influences the phenotype, and thus the clinical diagnostic accuracy, of dementia with Lewy bodies (DLB). METHODS: A series of 64 subjects with autopsy-proven DLB was studied. Last diagnosis before death was used to determine the clinical diagnostic accuracy of DLB in relation to Lewy body distribution and extent of Alzheimer ß-amyloid and/or neuritic pathology. DLB pathologic diagnosis was made according to consensus criteria, using α-synuclein immunostaining for Lewy body identification. ß-Amyloid immunostaining was used for quantifying ß-amyloid deposits. The Consortium to Establish a Registry for Alzheimer's Disease criteria and Braak stage were applied for semiquantitative grading of neuritic plaque and neurofibrillary tangle pathology. RESULTS: Overall clinical diagnostic accuracy for the entire DLB cohort was high (80%), reflecting the high prevalence of core clinical features (fluctuations [81%], parkinsonism [77%], visual hallucinations [70%]). Lower frequencies of core clinical features of DLB, resulting in lower accuracy of its clinical diagnosis, were associated with decreasing Lewy body distribution (p < 0.0001) and with increasing neuritic plaque pathology (p = 0.035), but not with the number of ß-amyloid plaque deposits. CONCLUSIONS: The likelihood of occurrence of the DLB clinical syndrome is positively related to the extent of Lewy body pathology and negatively related to the severity of Alzheimer neuritic pathology, while ß-amyloid load has no effect.