179 research outputs found
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Managerial compensation incentives and merger waves
This paper examines the relation between executive compensation incentives and the nature of merger transactions inside and outside of merger waves. We find that the sensitivity of CEO wealth to firm risk, vega, increases the likelihood of merger transactions outside of waves, but is unrelated to merger frequency inside wave periods. CEOs whose compensation is more closely tied to firm risk make better performing acquisitions when they acquire outside of merger waves, but this is not the case for in-wave deals, suggesting that underperformance of acquiring firms during waves can be attributed in part to ineffective compensation incentives. We also find that the cross-sectional dispersion of acquirersâ returns is higher for in-wave acquisitions relative to acquisitions made outside a wave, suggesting that out-wave acquisitions are characterized by lower uncertainty of future stock price returns. This is again restricted to high vega CEOs during out-wave periods
Incentive compensation vs. SOX: evidence from corporate acquisition decisions
We empirically examine the impact of incentive compensation on the riskiness of acquisition decisions before and after the passage of Sarbanes-Oxley Act (SOX). Controlling for confounding events, firm characteristics and industry fixed effects, we find a substantial change in the relation between equity-related compensation and acquisition risk post-SOX stemming from a previously unidentified shift in the effectiveness of executive stock options to control managerial risk aversion. Not only has incentive compensation failed to offset the adverse impact of SOX on risk-taking activity but it has also significantly altered managerial incentives. The decrease in acquisition risk post-SOX cannot be solely attributed to changes in the structure of executive compensation but it additionally stems from the way managers perceive compensation-based incentives in the new regulatory environment. The results are robust to different measures of acquisition risk and alternative definitions of incentive compensation
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Incentive compensation vs SOX: evidence from corporate acquisition decisions
In this paper, we use the introduction of the Sarbanes-Oxley Act in 2002 to assess the impact of executive option and stock grants on corporate acquisition decisions. Amongst its many innovations, the Sarbanes-Oxley Act (SOX) has limited the value and effect of equity-related compensation. We find strong evidence of a shift in the factors driving acquisitions post-SOX. Specifically, while bid premiums have fell irrespectively of the type of acquirer, highly incentivised managers have become more risk-averse after the passage of the Act. Investors also appear to have recognised the effect of a change in equity-related pay. Both market response to acquisition announcements and post-acquisition performance have been improved after the introduction of SOX but these cannot be attributed to firms that grant high levels of incentive compensation to their managers. Our results are robust to a number of explanatory factors and confounding events in the post-SOX period
Longitudinal thalamic white and gray matter changes associated with visual hallucinations in Parkinsonâs disease
Objective: Visual hallucinations are common in
Parkinsonâs disease (PD) and associated with worse
outcomes. Large-scale network imbalance is seen in
PD-associated hallucinations, but mechanisms remain
unclear. As the thalamus is critical in controlling cortical
networks, structural thalamic changes could underlie
network dysfunction in PD hallucinations.
Methods: We used whole-brain fixel-based analysis
and cortical thickness measures to examine longitudinal
white and grey matter changes in 76 patients with PD
(15 hallucinators, 61 non-hallucinators) and 26 controls
at baseline, and after 18 months. We compared white
matter and cortical thickness, adjusting for age, gender,
time-between-scans and intracranial volume. To assess
thalamic changes, we extracted volumes for 50 thalamic
subnuclei (25 each hemisphere) and mean fibre crosssection (FC) for white matter tracts originating in each
subnucleus and examined longitudinal change in PDhallucinators versus non-hallucinators.
Results: PD hallucinators showed white matter changes
within the corpus callosum at baseline and extensive
posterior tract involvement over time. Less extensive
cortical thickness changes were only seen after followup. White matter connections from the right medial
mediodorsal magnocellular thalamic nucleus showed
reduced FC in PD hallucinators at baseline followed
by volume reductions longitudinally. After follow-up,
almost all thalamic subnuclei showed tract losses in PD
hallucinators compared with non-hallucinators.
Interpretation: PD hallucinators show white matter
loss particularly in posterior connections and in thalamic
nuclei, over time with relatively preserved cortical
thickness. The right medial mediodorsal thalamic
nucleus shows both connectivity and volume loss in
PD hallucinations. Our findings provide mechanistic
insights into the drivers of network imbalance in PD
hallucinations and potential therapeutic targets
Fibre-specific white matter reductions in Parkinsonâs hallucinations and visual dysfunction
Objective: To investigate the microstructural and macrostructural white matter changes that accompany visual hallucinations and low visual performance in Parkinsonâs disease, a risk factor for Parkinsonâs dementia.
Methods: We performed fixel-based analysis, a novel technique that provides metrics of specific fibre-bundle populations within a voxel (or fixel). Diffusion MRI data was acquired from patients with Parkinsonâs disease (n=105, of which 34 low visual performers and 19 hallucinators) and age-matched controls (n=35). We used whole brain fixel-based analysis to compare micro-structural differences in fibre density (FD), macro-structural differences in fibre bundle cross-section (FC) and the combined fibre density and cross-section metric (FDC) across all white matter fixels. We then performed a tract of interest analysis comparing the most sensitive FDC metric across 11 tracts within the visual system.
Results: Patients with Parkinsonâs disease hallucinations exhibited macrostructural changes (reduced FC) within the splenium of the corpus callosum and the left posterior thalamic radiation compared to patients without hallucinations. Whilst there were no significant changes in FD, we found large reductions in the combined FDC metric in Parkinsonâs hallucinators within the splenium (>50% reduction compared to non-hallucinators). Patients with Parkinsonâs disease and low visual performance showed widespread microstructural and macrostructural changes within the genu and splenium of the corpus callosum, bilateral posterior thalamic radiations and the left inferior fronto-occipital fasciculus.
Conclusions: We demonstrate specific white matter tract degeneration affecting posterior thalamic tracts in patients with Parkinsonâs disease with hallucinations and low visual performance, providing direct mechanistic support for attentional models of visual hallucinations
Visual dysfunction predicts cognitive impairment and white matter degeneration in Parkinson's disease
Visual dysfunction predicts dementia in Parkinsons disease (PD), but whether this translates to structural change is not known. We aimed to identify longitudinal white matter changes in patients with Parkinsons disease and low visual function and also in those who developed mild cognitive impairment (MCI). We used fixel-based analysis to examine longitudinal white matter change in PD. Diffusion MRI and clinical assessments were performed in 77 patients at baseline (22 low visual function /55 intact vision; and 13 MCI, 13 MCI converters /51 normal cognition) and 25 controls and again after 18 months. We compared micro-structural changes in fibre density, macro-structural changes in fibre bundle cross-section (FC) and combined fibre density and cross-section across white matter, adjusting for age, gender and intracranial volume. Patients with Parkinsons and visual dysfunction showed worse cognitive performance at follow up and were more likely to develop MCI compared with those with normal vision (p=0.008). Parkinsons with poor visual function showed diffuse micro-structural and macro-structural changes at baseline, whereas those with MCI showed fewer baseline changes. At follow-up, Parkinsons with low visual function showed widespread macrostructural changes, involving the fronto-occipital fasciculi, external capsules, and middle cerebellar peduncles bilaterally. No longitudinal change was seen in baseline MCI or in MCI converters, even when the two groups were combined. Parkinsons patients with poor visual function show increased white matter damage over time, providing further evidence for visual function as a marker of imminent cognitive decline
Value creation around merger waves: the role of managerial compensation
This paper examines the relation between executive compensation and value creation in merger waves. The sensitivity of CEO wealth to firm risk increases the likelihood of outâofâwave merger transactions but has no influence on inâwave merger frequency. CEOs with compensation linked to firm risk have better outâofâwave merger performance in comparison to inâwave mergers. We also present evidence that crossâsectional acquirer return dispersion is greater for inâwave acquisitions. Our results suggest that the underperformance of acquiring firms during merger waves can be attributed in part to ineffective compensation incentives, and appropriate managerial incentives can create value, particularly in nonâwave periods
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One size fits all? The effectiveness of incentive compensation in public acquisitions
This paper provides new evidence on the relation between incentive compensation and acquisition performance. We find that higher sensitivity of executivesâ wealth to stock-price changes, Delta, is positively associated with post-acquisition stock-price performance and that higher sensitivity of executivesâ wealth to stock-return volatility, Vega, leads to risk-increasing acquisitions only when the target is a non-publicly listed firm. In public deals, we find no difference in the deal synergies available to acquiring firmâs shareholders between high and low incentivised managers and no relation between incentive compensation and the quality of M&A decisions in terms of risk and stock-price returns. Our results are robust to a number of deal and firm characteristics and to controls for selection bias and endogeneity. Our findings suggest that when a publicly listed firm is acquired, the increased negotiation power of the target and information asymmetry considerations offset the positive impact of incentive compensation on both stock-price performance and risk-taking
Organisational and neuromodulatory underpinnings of structural-functional connectivity decoupling in patients with Parkinson's disease
Parkinson's dementia is characterised by changes in perception and thought, and preceded by visual dysfunction, making this a useful surrogate for dementia risk. Structural and functional connectivity changes are seen in humans with Parkinson's disease, but the organisational principles are not known. We used resting-state fMRI and diffusion-weighted imaging to examine changes in structural-functional connectivity coupling in patients with Parkinson's disease, and those at risk of dementia. We identified two organisational gradients to structural-functional connectivity decoupling: anterior-to-posterior and unimodal-to-transmodal, with stronger structural-functional connectivity coupling in anterior, unimodal areas and weakened towards posterior, transmodal regions. Next, we related spatial patterns of decoupling to expression of neurotransmitter receptors. We found that dopaminergic and serotonergic transmission relates to decoupling in Parkinson's overall, but instead, serotonergic, cholinergic and noradrenergic transmission relates to decoupling in patients with visual dysfunction. Our findings provide a framework to explain the specific disorders of consciousness in Parkinson's dementia, and the neurotransmitter systems that underlie these
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