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It is estimated that there are 55 million people living with dementias globally. With so few effective treatments available for dementias, it is vital that services optimise the management of risk factors for patients to slow their disease progression as much as possible. Commonly prescribed medications with anticholinergic effects can cause iatrogenic cognitive impairment and lead to faster decline in people living with dementia. United Kingdom (UK) national guidelines recommend minimising their use when assessing people with suspected dementia or during medication reviews of people with dementia. We proposed to audit how many people were being referred to memory assessment services in two UK locations with a significant anticholinergic burden, which medications were responsible, and whether this impacted on diagnosis.
Methods:
We developed an audit tool based on national guidelines to gather data on the age, gender, medications, diagnosis and cognitive impairment of the first 50 patients assessed in the Memory Assessment Services in Wolverhampton and Walsall in 2022. We used the anticholinergic effect on cognition scale (AEC) to measure patients’ anticholinergic burdens and identify the most frequently prescribed medications.
Results:
We collected data from 30 patients from Wolverhampton and 20 patients from Walsall. Across the two locations, only 10% presented with a significant anticholinergic burden, with 24% having some anticholinergic burden that was not considered significant. Every patient with a significant anticholinergic burden was later diagnosed with dementia.
Most of the anticholinergic medications that were prescribed are generally prescribed for psychiatric or neurological indications and the most frequently prescribed drug was amitriptyline.
Conclusion:
The prescription of anticholinergic medications was not as prevalent as predicted in our sample. It may be that anticholinergic medication are less prescribed for physical illnesses as alternatives that do not cross the blood-brain barrier are available. Psychogeriatricians are well placed to review the anticholinergic medications that are commonly prescribed during the assessment of suspected dementia, due to their familiarity with these medications. In response to our findings, we plan to update our memory clinic assessment tools to highlight the need for clinicians to review patients’ anticholinergic burden during assessment.
Cannabis has been associated with poorer mental health, but little is known of the effect of synthetic cannabinoids or cannabidiol (often referred to as CBD).
Aims
To investigate associations of cannabis, synthetic cannabinoids and cannabidiol with mental health in adolescence.
Method
We conducted a cross-sectional analysis with 13- to 14-year-old adolescents across England and Wales in 2019–2020. Multilevel logistic regression was used to examine the association of lifetime use of cannabis, synthetic cannabinoids and cannabidiol with self-reported symptoms of probable depression, anxiety, conduct disorder and auditory hallucinations.
Results
Of the 6672 adolescents who participated, 5.2% reported using of cannabis, 1.9% reported using cannabidiol and 0.6% reported using synthetic cannabinoids. After correction for multiple testing, adolescents who had used these substances were significantly more likely to report a probable depressive, anxiety or conduct disorder, as well as auditory hallucinations, than those who had not. Adjustment for socioeconomic disadvantage had little effect on associations, but weekly tobacco use resulted in marked attenuation of associations. The association of cannabis use with probable anxiety and depressive disorders was weaker in those who reported using cannabidiol than those who did not. There was little evidence of an interaction between synthetic cannabinoids and cannabidiol.
Conclusions
To our knowledge, this study provides the first general population evidence that synthetic cannabinoids and cannabidiol are associated with probable mental health disorders in adolescence. These associations require replication, ideally with prospective cohorts and stronger study designs.
Deficits in social cognition (the ability to recognise and understand emotions, intentions and actions in oneself and in others) have been found in people with post-traumatic stress disorder (PTSD). Few studies so far have examined whether social cognitive ability impacts on PTSD recovery. Here we present a protocol and preliminary data for a study that aims to evaluate whether pre-treatment social cognitive deficits are associated with treatment outcomes following trauma-focused therapy for PTSD.
Method
The protocol was developed after discussion with Patient and Public Involvement (PPI) groups, and a battery of social cognitive tasks was trialled on 20 participants without PTSD. The final protocol was then developed using information and feedback from these preliminary studies. We aim to recruit 60 individuals who are about to start a trauma-focused therapy for PTSD within the two tertiary PTSD services. Social cognition (measured using a variety of tasks including Reading the Mind in the Eyes Task and the Reflective Functioning Questionnaire) and potential confounders (including severity of trauma history, attachment and verbal IQ) are assessed at baseline, prior to the start of therapy. PTSD symptom severity (measured using the PCL-5) and daily functioning (measured using the WSAS) are assessed pre and post-treatment. The primary aim of the study is to examine whether baseline social cognition is associated with the degree of improvement in the PCL-5.
Result
So far 29 participants have been recruited and consented. 6 participants have completed follow-up assessments. The study has been adapted for the COVID-19 pandemic so participants can complete the tasks remotely. Preliminary results show a moderate negative correlation between baseline social cognitive abilities and baseline PTSD symptom severity (Spearman's correlation -0.30) and functional abilities (Spearman's correlation -0.42).
Conclusion
Development of our study in collaboration with PPI and preliminary testing of measures suggests it is likely that it will be feasible for us to conduct this study in this patient group. Baseline preliminary results show/suggest a moderate correlation between PTSD symptom severity and social cognitive impairment. Our main analyses, when completed, will help to determine whether social cognitive ability is associated with recovery from PTSD.
Clozapine is used in the management of treatment-resistant schizophrenia and is effective in reducing aggression; however a subgroup of patients is poorly responsive. For violent patients in this group, there is limited literature on the use of strategies to augment clozapine with other agents. Here we present a case series of 6 schizophrenia patients, within a high-security hospital, who have a history of serious violence and who were treated with clozapine augmented with amisulpride.
Methods
We reviewed case notes and health records for evidence of violence/aggression and positive factors such as engagement in activities, and Clinical Global Impression (CGI) scores were formulated. We also examined metabolic parameters before and after augmentation.
Results
All 6 of the patients showed clinical improvement in symptoms and a reduction in their risk of violence to others. Five patients had a reduction in number of violent/aggressive incidents, and all patients showed improvement in engagement in occupational, vocational, and/or psychological work. Metabolic parameters were largely unchanged except for 1 patient whose Body Mass Index (BMI) increased. Five patients reported side effects as unchanged or improved.
Conclusion
These schizophrenia patients with a history of violence showed clinical improvement and reduced aggression and violence with amisulpride augmentation of clozapine. To our knowledge, this is the first report of an antiaggressive benefit of this combination in forensic psychiatric patients. Further studies are warranted to establish the efficacy and anti-aggressive effects of amisulpride augmentation of clozapine.
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