Browsing by Subject "cognitive impairment"

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  • Weichert, I.; Romero-Ortuno, R.; Tolonen, J.; Soe, T.; Lebus, C.; Choudhury, S.; Nadarajah, C. V.; Nanayakkara, P.; Orru, M.; Di Somma, S. (2018)
    What is known and objectiveDrugs with anticholinergic properties increase the risk of falls, delirium, chronic cognitive impairment, and mortality and counteract procholinergic medications used in the treatment of dementia. Medication review and optimisation to reduce anticholinergic burden in patients at risk is recommended by specialist bodies. Little is known how effective this review is in patients who present acutely and how often drugs with anticholinergic properties are used temporarily during an admission. The aim of the study was to describe the changes in the anticholinergic cognitive burden (ACB) in patients admitted to hospital with a diagnosis of delirium, chronic cognitive impairment or falls and to look at the temporary use of anticholinergic medications during hospital stay. MethodsThis is a multi-centre observational study that was conducted in seven different hospitals in the UK, Finland, The Netherlands and Italy. Results and discussion21.1% of patients had their ACB score reduced by a mean of 1.7%, 19.7% had their ACB increased by a mean of 1.6%, 22.8% of DAP naive patients were discharged on anticholinergic medications. There was no change in the ACB scores in 59.2% of patients. 54.1% of patients on procholinergics were taking anticholinergics. Out of the 98 medications on the ACB scale, only 56 were seen. Medications with a low individual burden were accounting for 64.9% of the total burden. Anticholinergic drugs were used temporarily during the admission in 21.9% of all patients. A higher number of DAPs used temporarily during admission was associated with a higher risk of ACB score increase on discharge (OR=1.82, 95% CI for OR: 1.36-2.45, P What is new and conclusionThere was no reduction in anticholinergic cognitive burden during the acute admissions. This was the same for all diagnostic subgroups. The anticholinergic load was predominantly caused by medications with a low individual burden. More than 1 in 5 patients not taking anticholinergics on admission were discharged on them and similar numbers saw temporary use of these medications during their admission. More than half of patients on cholinesterase-inhibitors were taking anticholinergics at the same time on admission, potentially directly counteracting their effects.
  • Jansson, Anu; Karisto, Antti; Pitkälä, Kaisu (2021)
    Background: More than one in three older people in assisted living facilities suffer from loneliness that leads to adverse health outcomes. Group work may have the potential to improve residents' quality of life. Aims/Objectives: The purpose of this feasibility study was to thoroughly describe a facilitated group process and compare its effects on cognitively impaired (n = 6) and cognitively intact (n = 7) lonely resident groups in assisted living facilities. Material and Methods: We used a closed, occupational therapy-oriented group model designed for lonely people. The study used a qualitative, multi-method approach. Material included individual and focus group interviews, observations and the facilitators' field diaries. Results: Loneliness was reflected in diverse ways in both groups. Meaningful activities in mutual interaction played an important role in empowering the participants and enabling the development of the group process. Group processes had similar, parallel steps, from which the participants seemed to benefit. Surprisingly, the cognitively impaired group progressed towards self-direction more quickly than the cognitively intact group. Conclusions: A group process with clearly progressing steps revealed that lonely older people are capable of empowerment and self-direction - despite their frailty and cognitive impairment. Facilitators should be familiar with group processes to enable them to progress effectively.
  • Roitto, Hanna-Maria; Öhman, Hannareeta; Salminen, Karoliina; Kautiainen, Hannu; Laurila, Jouko; Pitkälä, Kaisu H. (2020)
    Objectives: Falls and neuropsychiatric symptoms (NPS) are common among long-term care residents with cognitive impairment. Despite the high prevalence of falls and NPS, little is known about their association. The aim of our study was to explore how NPS, particularly the severity of NPS and specific NPS subgroups, are associated with falls and how psychotropics modify this association. Design: Longitudinal cohort study. Setting and Participants: In total, 532 long-term care residents aged 65 years or older in Helsinki, Finland. Methods: NPS were measured with Neuropsychiatric Inventory (NPI) at baseline. Participants were grouped into 3 groups: no significant NPS (NPI points 0-3), low NPS burden (NPI 4-12), and high NPS burden (NPI >12). The number of falls, injuries, fractures, and hospitalizations were collected from medical records over 12 months following baseline assessment. Results: Altogether, 606 falls occurred during the follow-up year. The falls led to 121 injuries, 42 hospitalizations, and 20 fractures. Falls and injuries increased significantly with NPS burden (P <.001): 330 falls in the high NPS group (n = 184), 188 falls in the low NPS group (n = 181), and 88 falls in the no significant NPS group (n = 167). The risk of falling showed a curvilinear association with NPI total score. Of NPS subgroups, psychosis and hyperactivity were associated with a higher incidence rate ratio of falls, whereas apathy had a protective association even after adjustment for age, sex, and mobility. Affective symptoms were not associated with falls. Psychotropics did not modify the association between NPS burden and falls. Conclusions and Implications: The results of this study show that NPS, especially NPS severity, may predict falls and fall-related negative consequences. Severity of NPS should be taken into account when assessing fall risk in long-term care residents with cognitive impairment. (C) 2020 AMDA - The Society for Post-Acute and Long-Term Care Medicine.
  • Roascio, Monica; Canessa, Andrea; Tro, Rosella; Mattioli, Pietro; Fama, Francesco; Giorgetti, Laura; Girtler, Nicola; Orso, Beatrice; Morbelli, Silvia; Nobili, Flavio; Arnaldi, Dario; Arnulfo, Gabriele (2022)
    Study Objectives Increased phase synchronization in electroencephalography (EEG) bands might reflect the activation of compensatory mechanisms of cognitive decline in people with neurodegenerative diseases. Here, we investigated whether altered large-scale couplings of brain oscillations could be linked to the balancing of cognitive decline in a longitudinal cohort of people with idiopathic rapid eye-movement sleep behavior disorder (iRBD). Methods We analyzed 18 patients (17 males, 69.7 +/- 7.5 years) with iRBD undergoing high-density EEG (HD-EEG), presynaptic dopaminergic imaging, and clinical and neuropsychological (NPS) assessments at two time points (time interval 24.2 +/- 5.9 months). We thus quantified the HD-EEG power distribution, orthogonalized amplitude correlation, and weighted phase-lag index at both time points and correlated them with clinical, NPS, and imaging data. Results Four patients phenoconverted at follow-up (three cases of parkinsonism and one of dementia). At the group level, NPS scores decreased over time, without reaching statistical significance. However, alpha phase synchronization increased and delta amplitude correlations decreased significantly at follow-up compared to baseline. Both large-scale network connectivity metrics were significantly correlated with NPS scores but not with sleep quality indices or presynaptic dopaminergic imaging data. Conclusions These results suggest that increased alpha phase synchronization and reduced delta amplitude correlation may be considered electrophysiological signs of an active compensatory mechanism of cognitive impairment in people with iRBD. Large-scale functional modifications may be helpful biomarkers in the characterization of prodromal stages of alpha-synucleinopathies.
  • Valtonen, Jussi; Karrasch, Mira (2020)
    Polypharmacy is common in patients with a diagnosis of bipolar disorder. Although polypharmacy is known to increase the risk of iatrogenic neurological conditions, the recovery of cognitive function after drug withdrawal has been rarely documented in psychiatric patients using standardized neuropsychological methods. We present a neuropsychological case report of patient SN, a 41-year-old woman who developed a socially and occupationally detrimental condition of cognitive dysfunction likely induced by long-term exposure to lithium and other psychiatric medications. To shed light on SN’s cognitive deficits and their recovery after drug withdrawal, neuropsychological assessments were conducted before, and approximately 2 years after, lithium and other psychiatric drugs were discontinued. Selective cognitive impairments were observed before drug discontinuation in visuomotor speed, visuoperceptual reasoning and delayed visual memory. Partial, but not complete, recovery of function was observed 2 years after drug withdrawal.
  • Ngandu, Tiia; Lehtisalo, Jenni; Levalahti, Esko; Laatikainen, Tiina; Lindstrom, Jaana; Peltonen, Markku; Solomon, Alina; Ahtiluoto, Satu; Antikainen, Riitta; Hanninen, Tuomo; Jula, Antti; Mangialasche, Francesca; Paajanen, Teemu; Pajala, Satu; Rauramaa, Rainer; Strandberg, Timo; Tuomilehto, Jaakko; Soininen, Hilkka; Kivipelto, Miia (2014)
  • Dove, Abigail (Helsingin yliopisto, 2019)
    Background: Despite the well-established link between diabetes and dementia risk, the impact of prediabetes and diabetes on the prodromal dementia phase remains controversial. In this study, we investigated whether prediabetes and diabetes increase the risk of cognitive impairment–no dementia (CIND) and accelerate its progression to dementia, as well as the possible underlying mechanisms. Methods: In the Swedish National Study on Aging and Care-Kungsholmen (SNAC-K), one cohort of cognitively-intact individuals (n=1,837) and one cohort of individuals with CIND (n=671) aged ≥60 years were followed for up to 15 years. At baseline and each follow-up (every 3 or 6 years), a neuropsychological test battery was administered, and the domains of episodic memory, processing speed, executive function, visuospatial abilities, and language were derived. CIND was defined as having no dementia and cognitive performance ≤1.5 SDs below age group-specific means in at least one cognitive domain. Dementia was diagnosed according to DSM-IV criteria. Diabetes (controlled and poorly-controlled) was diagnosed by physicians through medical assessment, clinical records, and glycated hemoglobin (HbA1c) ≥6.5%. Prediabetes was identified as HbA1c 5.7-6.4% in diabetes-free participants. Clinicians diagnosed heart disease and collected blood samples used to measure C-reactive protein (CRP). Data were analyzed with Cox regression models adjusted for possible confounders. Results: At baseline, in the cognitively-intact cohort, 133 (7%) participants had diabetes and 615 (34%) had prediabetes. During follow-up (mean 9.2 ± 3.0 years [range=2.2-15.5 years]), 544 (30%) individuals in the cognitively-intact cohort developed CIND. Poorly-controlled diabetes (HbA1c ≥7.5%) was associated with 2-times higher risk of CIND (HR 2.0, 95% CI:1.11-3.48) than diabetes-free participants. In the CIND cohort, 84 (13%) had diabetes and 238 (36%) prediabetes. During follow-up (mean 7.7 ± 4.0 years [range=0.2-15.2 years]), 132 (20%) individuals progressed to dementia. Poorly-controlled diabetes was associated with 3-times higher risk of dementia progression (HR 3.3, 95% CI: 1.29-8.33). Furthermore, comorbid heart disease and diabetes was associated with 2.5-times higher risk of progression to dementia (HR 2.5, 95% CI: 1.17-5.47), particularly if the diabetes was poorly-controlled (HR 5.8, 95% CI: 1.72-19.3). Similarly, having elevated CRP levels and diabetes was associated with increased risk of progression to dementia (HR 4.1, 95% CI: 1.15-14.2), especially in participants with poorly-controlled diabetes (HR 13.6, 95% CI: 1.89-98). No associations between prediabetes and CIND were detected in either cohort. Conclusions: Diabetes, especially if poorly-controlled, increases the risk of cognitive impairment and accelerates its progression to dementia. The diabetes-associated progression from CIND to dementia is further exacerbated by the presence of heart disease and elevated levels of systemic inflammation.
  • Hatlestad-Hall, Christoffer; Bruna, Ricardo; Erichsen, Aksel; Andersson, Vebjorn; Syvertsen, Marte Roa; Skogan, Annette Holth; Renvall, Hanna; Marra, Camillo; Maestu, Fernando; Heuser, Kjell; Tauboll, Erik; Solbakk, Anne-Kristin; Haraldsen, Ira H. (2021)
    Understanding and diagnosing cognitive impairment in epilepsy remains a prominent challenge. New etiological models suggest that cognitive difficulties might not be directly linked to seizure activity, but are rather a manifestation of a broader brain pathology. Consequently, treating seizures is not sufficient to alleviate cognitive symptoms, highlighting the need for novel diagnostic tools. Here, we investigated whether the organization of three intrinsic, resting-state functional connectivity networks was correlated with domain-specific cognitive test performance. Using individualized EEG source reconstruction and graph theory, we examined the association between network small worldness and cognitive test performance in 23 patients with focal epilepsy and 17 healthy controls, who underwent a series of standardized pencil-and-paper and digital cognitive tests. We observed that the specific networks robustly correlated with test performance in distinct cognitive domains. Specifically, correlations were evident between the default mode network and memory in patients, the central-executive network and executive functioning in controls, and the salience network and social cognition in both groups. Interestingly, the correlations were evident in both groups, but in different domains, suggesting an alteration in these functional neurocognitive networks in focal epilepsy. The present findings highlight the potential clinical relevance of functional brain network dysfunction in cognitive impairment.