David G Bruce1, Melinda E Nelson2, Janet L Mace2, Wendy A Davis2, Timothy M E Davis2, Sergio E Starkstein3. 1. School of Medicine & Pharmacology, University of Western Australia, Crawley, Western Australia, Australia. Electronic address: David.Bruce@uwa.edu.au. 2. School of Medicine & Pharmacology, University of Western Australia, Crawley, Western Australia, Australia. 3. School of Psychiatry & Neuroscience, University of Western Australia, Crawley, Western Australia, Australia.
Abstract
OBJECTIVE: To determine the prevalence, incidence, persistence, likely causes, and consequences of apathy in patients with Type 2 diabetes and to compare the prevalence with a healthy control sample. DESIGN: Cross-sectional comparison of diabetic and nondiabetic samples; longitudinal follow-up of diabetic sample. SETTING: Academic research department. PARTICIPANTS: Non-demented, older patients with long-standing Type 2 diabetes (N = 122) recruited from a community-based cohort study and 69 healthy volunteers. MEASUREMENTS: Clinical assessments of apathy and potential causative conditions, repeated in the diabetic sample after 16.7 ± 2.5 months. Informant rated symptoms from the 14-item Apathy Scale were used to generate apathy diagnoses based on standardized criteria. Cognition was assessed by Mini-Mental State Examination (MMSE) and Clinical Dementia Rating (CDR). RESULTS: The diabetic and comparison samples had the same age and MMSE scores, but the diabetic sample had a higher frequency of depression, cerebrovascular history, and cognitive deficits. Apathy was more prevalent in diabetes (diabetic 13.9% versus control sample 1.4%, p = 0.005) and was independently associated with CDR 0.5 status (OR [95% CI]: 3.66 [1.25-19.70]) and depression (8.48 [2.74-26.21]). In 108 diabetic patients who were followed up, incident apathy occurred in 7.4% of cases, and persisted in 50% of those with baseline apathy. Baseline apathy was independently associated with lnHbA1c levels (β: 0.20, t = 2.29, df = 119, p = 0.024; model R(2) = 0.10) and incident/persistent apathy was associated with greater risk of cognitive decline (6.72 [1.19-37.87]). CONCLUSION: Apathy is a frequent neuropsychiatric syndrome in older patients with Type 2 diabetes, and is associated with poor glycaemic control and cognitive decline.
OBJECTIVE: To determine the prevalence, incidence, persistence, likely causes, and consequences of apathy in patients with Type 2 diabetes and to compare the prevalence with a healthy control sample. DESIGN: Cross-sectional comparison of diabetic and nondiabetic samples; longitudinal follow-up of diabetic sample. SETTING: Academic research department. PARTICIPANTS: Non-demented, older patients with long-standing Type 2 diabetes (N = 122) recruited from a community-based cohort study and 69 healthy volunteers. MEASUREMENTS: Clinical assessments of apathy and potential causative conditions, repeated in the diabetic sample after 16.7 ± 2.5 months. Informant rated symptoms from the 14-item Apathy Scale were used to generate apathy diagnoses based on standardized criteria. Cognition was assessed by Mini-Mental State Examination (MMSE) and Clinical Dementia Rating (CDR). RESULTS: The diabetic and comparison samples had the same age and MMSE scores, but the diabetic sample had a higher frequency of depression, cerebrovascular history, and cognitive deficits. Apathy was more prevalent in diabetes (diabetic 13.9% versus control sample 1.4%, p = 0.005) and was independently associated with CDR 0.5 status (OR [95% CI]: 3.66 [1.25-19.70]) and depression (8.48 [2.74-26.21]). In 108 diabeticpatients who were followed up, incident apathy occurred in 7.4% of cases, and persisted in 50% of those with baseline apathy. Baseline apathy was independently associated with lnHbA1c levels (β: 0.20, t = 2.29, df = 119, p = 0.024; model R(2) = 0.10) and incident/persistent apathy was associated with greater risk of cognitive decline (6.72 [1.19-37.87]). CONCLUSION: Apathy is a frequent neuropsychiatric syndrome in older patients with Type 2 diabetes, and is associated with poor glycaemic control and cognitive decline.
Authors: Amanda E Carlson; Benjamin D Aronson; Michael Unzen; Melissa Lewis; Gabrielle J Benjamin; Melissa L Walls Journal: J Health Care Poor Underserved Date: 2017