144 research outputs found
NEUROPSYCHIATRIC SYMPTOMS OF DEMENTIA AND BIOMARKERS OF NEURODEGENERATION: CSF TAU AND MRI
No full textBackground: Behavioral and psychological symptoms of dementia (BPSD) are a distressful condition. We aimed to investigate the BPSD distribution in subjects with cognitive impairment, and the potential correlations between BPSD and neurodegeneration in terms of cerebrospinal fluid (CSF) tau and brain atrophy. Materials and Methods: One-hundred patients with mild cognitive impairment (MCI) or dementia (Alzheimer’s disease; Dementia with Lewy-body disease, DLB; frontotemporal dementia; vascular dementia) underwent a complete diagnostic workup, including 3T-MRI and/or CT and CSF. Cortical atrophy was assessed i) first with visual rating scales (medial temporal atrophy MTA, posterior atrophy PA and global cortical atrophy-frontal lobe GCA-F scales), ii) secondly with quantitative measures (such as cortical thickness CT and volume V). BPSD were rated using Neuropsychiatric Inventory (NPI), and BPSD clusters were defined according to the European Alzheimer Disease Consortium. Results: Delusions, hallucinations and psychosis cluster were differently distributed among the diagnostic groups (p<0.05, p<0.001, and p<0.05), with DLB patients showing higher scores for hallucinations (vs MCI, p<0.001, and AD, p<0.05) and psychosis cluster (vs MCI, p<0.05). In primary dementias, we found a negative correlation between NPI total score and tau levels (p=0.08), confirmed by beta regression (p<0.01), while a positive non-significant relationship was observed in MCI. Higher GCA-F scores were associated with delusions and apathy (p<0.05, on both hemispheres) and to hallucinations (left: p<0.01, right: p<0.05). GCA-F scores were positively correlated with psychosis cluster (right: p<0.05), and agitation/aggression (left: p<0.05). With regard to the quantitative measures od atrophy, significant correlations were observed for 4 main neuropsychiatric symptoms: delusions, hallucinations, agitation, and apathy. Delusions showed negative correlations with CT and V of frontal areas (dorsolateral and orbital, with a prevalent involvement on the right side) and of areas of the limbic system (anterior and posterior cingulate, isthmus and entorhinal cortex). As well, hallucinations showed an involvement of the frontal lobe (dorsolateral) and the limbic system (anterior and posterior cingulate, isthmus, fusiform gyrus and hippocampus). A decrease in CT and V of the opercular region (insula and temporal pole) and the limbic system (entorhinal, parahippocampal and fusiform cortex and amygdala) was instead correlated with agitation/aggression. Finally, apathy showed a negative correlation with regions of the frontal lobe (dorsolateral, orbital, opercular, precentral and paracentral) insula and the limbic system (anterior cingulate and isthmus). Conclusion: This study provides a real-world overview of the most clinically relevant BPSD occurring in patients attending a memory clinic due to dementing conditions. The gathered evidence suggests that, in a future perspective, CSF biomarkers and visual rating scales for cortical atrophy could be hopefully included in a multidimensional evaluation of demented patients, aimed to predict prognosis and occurrence of BPSD. Moreover, quantitative measures of atrophy suggest that the limbic system cover a paramount role in the their pathophysiology through the dysfunction of the mesolimbic circuitry.Background: Behavioral and psychological symptoms of dementia (BPSD) are a distressful condition. We aimed to investigate the BPSD distribution in subjects with cognitive impairment, and the potential correlations between BPSD and neurodegeneration in terms of cerebrospinal fluid (CSF) tau and brain atrophy. Materials and Methods: One-hundred patients with mild cognitive impairment (MCI) or dementia (Alzheimer’s disease; Dementia with Lewy-body disease, DLB; frontotemporal dementia; vascular dementia) underwent a complete diagnostic workup, including 3T-MRI and/or CT and CSF. Cortical atrophy was assessed i) first with visual rating scales (medial temporal atrophy MTA, posterior atrophy PA and global cortical atrophy-frontal lobe GCA-F scales), ii) secondly with quantitative measures (such as cortical thickness CT and volume V). BPSD were rated using Neuropsychiatric Inventory (NPI), and BPSD clusters were defined according to the European Alzheimer Disease Consortium. Results: Delusions, hallucinations and psychosis cluster were differently distributed among the diagnostic groups (p<0.05, p<0.001, and p<0.05), with DLB patients showing higher scores for hallucinations (vs MCI, p<0.001, and AD, p<0.05) and psychosis cluster (vs MCI, p<0.05). In primary dementias, we found a negative correlation between NPI total score and tau levels (p=0.08), confirmed by beta regression (p<0.01), while a positive non-significant relationship was observed in MCI. Higher GCA-F scores were associated with delusions and apathy (p<0.05, on both hemispheres) and to hallucinations (left: p<0.01, right: p<0.05). GCA-F scores were positively correlated with psychosis cluster (right: p<0.05), and agitation/aggression (left: p<0.05). With regard to the quantitative measures od atrophy, significant correlations were observed for 4 main neuropsychiatric symptoms: delusions, hallucinations, agitation, and apathy. Delusions showed negative correlations with CT and V of frontal areas (dorsolateral and orbital, with a prevalent involvement on the right side) and of areas of the limbic system (anterior and posterior cingulate, isthmus and entorhinal cortex). As well, hallucinations showed an involvement of the frontal lobe (dorsolateral) and the limbic system (anterior and posterior cingulate, isthmus, fusiform gyrus and hippocampus). A decrease in CT and V of the opercular region (insula and temporal pole) and the limbic system (entorhinal, parahippocampal and fusiform cortex and amygdala) was instead correlated with agitation/aggression. Finally, apathy showed a negative correlation with regions of the frontal lobe (dorsolateral, orbital, opercular, precentral and paracentral) insula and the limbic system (anterior cingulate and isthmus). Conclusion: This study provides a real-world overview of the most clinically relevant BPSD occurring in patients attending a memory clinic due to dementing conditions. The gathered evidence suggests that, in a future perspective, CSF biomarkers and visual rating scales for cortical atrophy could be hopefully included in a multidimensional evaluation of demented patients, aimed to predict prognosis and occurrence of BPSD. Moreover, quantitative measures of atrophy suggest that the limbic system cover a paramount role in the their pathophysiology through the dysfunction of the mesolimbic circuitry
The impact of different goodwill accounting methods on stock prices: A comparison of amortization and impairment-only methodologies
No full textIn March 2020, the IASB issued a discussion paper – ‘Business Combinations – Disclosures, Goodwill and Impairment’ – which discussed, inter alia, whether to introduce a sort of counterreformation of IAS 36 that might lead to the reintroduction of goodwill amortization. Among other things, the IASB, leveraging key findings from academic research, questioned a) the disclosure provided by entities applying IFRS 3 requirements and b) the timing of impairment write-downs and their overal1l magnitude.
The main goal of this study, focusing on a large sample of European listed companies since the adoption of IAS in 2005, is to test the value relevance of goodwill under the current accounting framework and the alternative hypothesis of an amortization regime.
Our findings show that the information provided by listed companies to market investors under the current accounting regime (verification at least annually of the recoverability of the value of the goodwill carrying amount through the impairment test) – the level of goodwill before and post impairment, as well as goodwill write downs – is value relevant and contributes to explain the level of the market to tangible book value multiple. On the contrary, simulating the alternative accounting scenario of goodwill amortization, we found that the information conveyed to market investor would not be value relevant, with the amortization itself added back to the multiple. The results support the current accounting framework and indicate that the best way to improve goodwill accounting is by enforcing present rules.
This study aims to provide a multidimensional contribution to the current debate within the IASB, leveraging the largest database in Europe
Sessualità nelle demenze
No full textFIsiopatologia e clinica dei disturbi della sessualità nelle demenz
The Treatment of Trigeminal Autonomic Cephalalgias: An Overview
No full textTrigeminal autonomic cephalalgias (TACs) are primary headaches that include cluster headache (CH), paroxysmal hemicrania (PH), and short-lasting unilateral neuralgiform headache attacks (SUNHAs) with conjunctival injection and tearing (SUNCT) or cranial autonomic features (SUNA). Hemicrania continua (HC) is another form that has been ascribed to TACs for clinical and pathophysiological reasons. CH is the most common of these syndromes, even if is still comparatively rare, with a lifetime prevalence of around 1 in 1,000. TACs share many aspects from the pathophysiological standpoint: a hypothalamic activation may be involved in all forms initiating the attacks, but differences in attack duration and frequency, and in extent of treatment response distinguish one from the other. This review focuses on the treatments currently available for these headaches according to the most recent guidelines. Due to the low frequency of most TACs, there are little data from randomized controlled trials; therefore, evidence from simple open studies in small case series or single-case observations is reported. Promising results have been recently obtained with novel modes of drug administration, with invasive pericranial interventions and with different strategies such as neurostimulation. There are also some future treatments being studied at present
Headaches in the elderly (Cefaleas en el adulto mayor).
No full textRevisione aggiornata della letteratura sulle cefalee, primarie e secondarie, dell'anzian
Dementia and Cerebrovascular Disease.
No full textRapporti fra demenza e patologia cerebrovascolare, in tutti gli aspetti (clinici, biologici, di imaging)
A Call for Drug Therapies for the Treatment of Social Behavior Disorders in Dementia: Systematic Review of Evidence and State of the Art
No full textGrowing evidence supports the presence of social cognition deficits and social behavior alterations in major and minor neurocognitive disorders (NCDs). Even though the ability to identify socio-emotional changes has significantly improved in recent years, there is still no specific treatment available. Thus, we explored evidence of drug therapies targeting social cognition alterations in NCDs. Papers were selected according to PRISMA guidelines by searching on the PubMed and Scopus databases. Only papers reporting information on pharmacological interventions for the treatment of social cognition and/or social behavioral changes in major and/or minor NCDs were included. Among the 171 articles entered in the paper selection, only 9 papers were eligible for the scope of the review. Trials testing pharmacological treatments for socio-emotional alterations in NCDs are poor and of low-medium quality. A few attempts with neuroprotective, psychoactive, or immunomodulating drugs have been made. Oxytocin is the only drug specifically targeting the social brain that has been tested with promising results in frontotemporal dementia. Its beneficial effects in long-term use have yet to be evaluated. No recommendation can currently be provided. There is a long way to go to identify and test effective targets to treat social cognition changes in NCDs for the ultimate benefit of patients and caregivers
Retinal and Cortical Visual Processing Dysfunction in a Case of Mild Cognitive Impairment with Lewy Bodies: A Case Report
No full textThe prodromal stage of Lewy body dementia includes a mild cognitive impairment with visual processing and/or
attention-executive deficits. A clinical presentation with progressive visual loss is indeed seldom reported and can be mislead ing with a posterior cortical atrophy disease. While the neurodegeneration at the occipital cortex can only partially explain
the visual disturbances of Lewy body dementia, more recently a retinal dysfunction has been suggested by preliminary
optical coherence tomography and autoptic findings. Herein, we present a case of a mild cognitive impairment with Lewy
bodies, who presented initially with visual disturbances and signs of both retinal and cortical visual processing dysfunction.
A complete neuropsychological, neurophysiological and brain imaging assessment highlighted a prominent ventral visual
pathway involvement. This report provides first that the prodromal stage of Lewy body dementia can manifest as a primarily
progressive visual loss, second that the involvement of visual pathway, particularly the ventral stream, can be detectable from
the retinal to the cortical level
Potential Contribution of Hypertension to Evolution of Chronic Migraine and Related Mechanisms
No full textAims: To investigate the potential contributions of diastolic and systolic blood pressure (BP) and the circadian rhythm of BP to chronic migraine evolution. Methods: This cross-sectional study included four groups of patients selected based on migraine frequency (high frequency ≥ 10 days per month and low frequency < 10) and on the presence of hypertension. Among-group and pairwise comparisons were carried out to investigate potential neurophysiologic differences in the cerebral vessel reactivity to a nitroglycerin test, in autonomic balance (tilting test), and BP circadian rhythm. Results: A more marked decrease in cerebral blood flow velocity was observed in hypertensive high-frequency migraineurs compared to all other groups (P = .037). Moreover, a smaller decrease in vagal tone was recorded in the orthostatic position in hypertensive subjects, whether they were high- (P = .032) or low-frequency migraineurs (P = .014), with a consistently higher vagal to sympathetic tone ratio (P = .033). Finally, in nonhypertensive subjects, a higher but not significant prevalence of systolic nondippers was detected in high-frequency migraineurs (67%) compared to low-frequency subjects (25%; P = .099). Conclusion: These findings suggest that hypertension may contribute to the chronic evolution of headache with mechanisms shared with migraine; ie, vascular tone alteration and autonomic dysregulation
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