ObjectiveTo determine the prevalence, nature and predictors of prescribing errors (PEs) in three mental health hospitals.SettingInpatient units in three National Health Service (NHS) mental health hospitals in the North West of England.ParticipantsTrained clinical pharmacists prospectively recorded the number of PEs in newly written or omitted prescription items screened during their routine work on 10 data collection days. A multidisciplinary panel reviewed PE data using established methods to confirm (1) the presence of a PE, (2) the type of PE and (3) whether errors were clinically relevant and likely to cause harm.Primary outcome measuresFrequency, nature and predictors of PEs.ResultsOf 4427 screened prescription items, 281 were found to have one or more PEs (error rate 6.3% (95% CI 5.6 to 7.1%)). Multivariate analysis revealed that specialty trainees (OR 1.23 (1.01 to 1.51)) and staff grade psychiatrists (OR 1.50 (1.05 to 2.13)) were more likely to make PEs when compared to foundation year (FY) one doctors, and that specialty trainees and consultant psychiatrists were twice as likely to make clinically relevant PEs (OR 2.61 (2.11 to 3.22) and 2.03 (1.66 to 2.50), respectively) compared to FY one staff. Prescription items screened during the prescription chart rewrite (OR 0.52 (0.33 to 0.82)) or at discharge (OR 0.87 (0.79 to 0.97)) were less likely to be associated with PEs than items assessed during inpatient stay, although they were more likely to be associated with clinically relevant PEs (OR 2.27 (1.72 to 2.99) and 4.23 (3.68 to 4.87), respectively). Prescription items screened at hospital admission were five times more likely (OR 5.39 (2.72 to 10.69)) to be associated with clinically relevant errors than those screened during patient stay.ConclusionsPEs may be more common in mental health hospitals than previously reported and important targets to minimise these errors have been identified.

Patients with multiple sclerosis (MS) have an increased risk of developing depression as compared with healthy subjects and patients with many other chronic neurological conditions. The observation that depressive symptoms can precede the onset of neurological symptoms suggests that depression may be related to early disease-specific processes. Several pathogenic mechanisms have been proposed to explain the etiology of depression in patients with MS. This article reviews the current evidence for the contribution of lesional, autoimmune, iatrogenic, and psychosocial factors. It appears that the etiology of depression is multifactorial and varies in individual patients with MS.

Patients with multiple sclerosis (MS) have an increased risk of developing depression as compared with healthy subjects and patients with many other chronic neurological conditions. The observation that depressive symptoms can precede the onset of neurological symptoms suggests that depression may be related to early disease-specific processes. Several pathogenic mechanisms have been proposed to explain the etiology of depression in patients with MS. This article reviews the current evidence for the contribution of lesional, autoimmune, iatrogenic, and psychosocial factors. It appears that the etiology of depression is multifactorial and varies in individual patients with MS.

Huntington's disease (HD) is a neurodegenerative disease associated with cognitive deficits. Cognitive dysfunction may be present in the early stages of the disease, even before the onset of motor symptoms. The cognitive dysfunction includes executive dysfunction, psychomotor symptoms, visuospatial deficits, perceptual deficits, memory loss and difficulty learning new skills. Acetylcholinesterase inhibitors have shown good effect in the treatment of other types of dementia and it is postulated that it might delay cognitive decline in HD. We reviewed the evidence for Acetylcholinesterase inhibitors in the treatment of cognitive decline and dementia associated with Huntington's disease. We identified 6 articles that investigated the role of Acetylcholinesterase inhibitors for treatment of cognitive deficits in Huntington's disease. Following the review, the authors concluded that there is limited evidence for the use of Acetylcholinesterase inhibitors for cognitive impairment in HD.