Prescribing pharmacotherapy for older individuals with an intellectual disability (ID) is a complex process, possibly leading to an increased risk of prescription errors. The objectives of this study were (1) to determine the prevalence of older individuals with an intellectual disability with at least one prescription error and (2) to identify potential risk factors for these prescription errors (age, gender, body mass index (BMI), frailty index, level of intellectual disability and living situation). The study population consisted of 600 older (≥ 50 years) individuals with an ID using one or more drugs who were randomly selected from the study cohort of the Healthy Ageing and Intellectual Disability (HA-ID) Study. The medication used at the time of measurement was screened for errors by a hospital pharmacist/clinical pharmacologist and a Master's student pharmacy using consensus methodology. Participants with one or more prescription errors were compared to participants without prescription errors by multivariate logistic regression to identify potential risk factors. The prevalence of individuals with one or more prescription errors was 47.5% (285 of 600 individuals; 95% confidence interval (CI) 43-52%). Relevant errors, defined as errors that actually do require a change of pharmacotherapy, were identified in 26.8% of the individuals (161 of 600 individuals; 95% CI 23-30%). Higher age (adjusted odds ratio (OR adj) 1.03; 95% CI 1.01-1.06), less severe intellectual disability (moderate: OR adj 0.48; 95% CI 0.31-0.74 and severe: OR adj 0.56; 95% CI 0.32-0.98), higher BMI (OR adj 1.04; 95% CI 1.01-1.08), higher frailty index (0.39-0.54: OR adj 2.4; 95% CI 1.21-4.77 and ≥ 0.55: OR adj 3.4; 95% CI 1.03-11.02), polypharmacy (OR adj 8.06; 95% CI 5.59-11.62) and use of medicines acting on the central nervous system (OR adj 3.34; 95% CI 2.35-4.73) were independently associated with the occurrence of prescription errors. Interventions targeted to high risk patients should be designed and implemented to improve pharmacotherapy in older individuals with an intellectual disability.
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http://dx.doi.org/10.1016/j.ridd.2013.02.005 | DOI Listing |
Mol Psychiatry
January 2025
Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, China.
To understand the neural mechanism of autism spectrum disorder (ASD) and developmental delay/intellectual disability (DD/ID) that can be associated with ASD, it is important to investigate individuals at an early stage with brain, behavioural and also genetic measures, but such research is still lacking. Here, using the cross-sectional sMRI data of 1030 children under 8 years old, we employed developmental normative models to investigate the atypical development of gray matter volume (GMV) asymmetry in individuals with ASD without DD/ID, ASD with DD/ID and individuals with only DD/ID, and their associations with behavioral and clinical measures and transcription profiles. By extracting the individual deviations of patients from the typical controls with normative models, we found a commonly abnormal pattern of GMV asymmetry across all ASD children: more rightward laterality in the inferior parietal lobe and precentral gyrus, and higher individual variability in the temporal pole.
View Article and Find Full Text PDFEMBO J
January 2025
Department of Biochemistry and Cellular Biology, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, 187-8502, Japan.
AUTS2 syndrome is characterized by intellectual disability and microcephaly, and is often associated with autism spectrum disorder, but the underlying mechanisms, particularly concerning microcephaly, remain incompletely understood. Here, we analyze mice mutated for the transcriptional regulator AUTS2, which recapitulate microcephaly. Their brains exhibit reduced division of intermediate progenitor cells (IPCs), leading to fewer neurons and decreased thickness in the upper-layer cortex.
View Article and Find Full Text PDFMed Sci Law
January 2025
Department of Psychological Medicine, University of Otago, Wellington, New Zealand.
Epilepsia
January 2025
Department of Epilepsy Genetics and Personalized Medicine, Danish Epilepsy Center, Dianalund, Denmark.
Objectives: Developmental and epileptic encephalopathies (DEEs) caused by pathogenic variants in SCN8A are associated with difficult-to-treat and early-onset seizures, developmental delay/intellectual disability, impaired quality of life, and increased risk of early mortality. High doses of sodium channel blockers are typically used to treat SCN8A-DEE caused by gain-of-function (GoF) variants. However, seizures are often drug resistant, and only a few patients achieve seizure freedom.
View Article and Find Full Text PDFActa Neurobiol Exp (Wars)
January 2025
Laboratory of Animal Models, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene is a critical tumor suppressor that plays an essential role in the development and functionality of the central nervous system. Located on chromosome 10 in humans and chromosome 19 in mice, PTEN encodes a protein that regulates cellular processes such as division, proliferation, growth, and survival by antagonizing the PI3K‑Akt‑mTOR signaling pathway. In neurons, PTEN dephosphorylates phosphatidylinositol‑3,4,5‑trisphosphate (PIP3) to PIP2, thereby modulating key signaling cascades involved in neurogenesis, neuronal migration, and synaptic plasticity.
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