Role of morphologic feedback in surf zone sandbar response

Several aspects of feedback mechanisms associated with surf zone sandbar response have been characterized using bathymetric surveys, sampled approximately monthly over a 16-year period at the Army Corps of Engineers' Field Research Facility (North Carolina). The measured bathymetry was alongshore averaged and modeled by the superposition of two Gaussian-shaped sandbars on an underlying planar slope. A third, half-Gaussian-shaped bar represented steepening at the shoreline. The rms error between the measured bathymetry and the profile model was 0.10 m (estimated over 322 different surveys). The model explained 99% of the profile variance that remained after first removing the linear, cross-shore trend from each observed profile. Bar response, which was extracted from the modeled profiles, was compared to a local hydrodynamic forcing variable Γ (Γ was defined as the ratio of the wave height to water depth, evaluated at bar crest locations). At low values of Γ (i.e., nonbreaking conditions), bars migrated onshore, and their amplitude tended to decay. At high values of Γ (i.e., breaking conditions), bars migrated offshore, with relatively little change in amplitude. The transition between onshore and offshore migration occurred at a value of Γ that was consistent with the onset of wave breaking. Bar migration was associated with a stabilizing feedback mechanism, which drove bar crests toward an equilibrium position at the wave breakpoint. However, we observed that the rate of bar response showed no reduction for any nonzero choice of Γ, indicating that bars never reached equilibrium. Systematic bar amplitude decay was observed under nonbreaking conditions. Bar amplitude decay could drive Γ farther away from breaking conditions, allowing further bar amplitude decay. This is a destabilizing feedback mechanism, potentially leading to bar destruction

A simple model for interannual sandbar behavior

Time and length scales of beach variability have been quantified using 16 years of beach surveys sampled at the Army Corps of Engineers' Field Research Facility, located on the U.S. Atlantic coast. Between 50% and 90% of the bathymetric variability at this site was explained by alongshore-uniform response over the approximately 1 km alongshore span of the surveys. Although the incident wave height variance was dominated by frequencies at or higher than 1 cycle/yr, more than 80% of the bathymetric variance at all cross-shore locations was explained by frequencies <1 cycle/yr. Interannual cycles consisting of sandbar formation, migration, and decay contributed to the low-frequency variability. The observed behavior can be explained by a simple, heuristic model. The model assumes that bars migrate toward a wave height dependent equilibrium position. This position was shown to coincide with the wave “breakpoint.” Additionally, the rate of bar response is taken to be variable and was empirically determined to be proportional to the wave height cubed. The net effect of a variable response rate is to shift the expected long-term mean sandbar position offshore, toward the equilibrium position associated with the largest waves. The model explained up to 80% of the observed bar position time series variance and up to 70% of the variance of bar crest velocity time series, which were extracted from three different sandbars. Characteristic bar response times (related to the inverse of the response rate) were found to be long relative to the characteristic timescale of the forcing (1 year in our case). As a result, transient response (i.e., bar position far from equilibrium) tended to persist for many cycles of the forcing. Transient bar behavior appears in the observations when bars formed near the shoreline or when outer bars decayed and inner bars faced a changed wave climate. While the present model is able to explain the evolution of these transients, it does not contain a mechanism for their introduction

Clinicopathologic correlations in 172 cases of rapid eye movement sleep behavior disorder with or without a coexisting neurologic disorder

OBJECTIVE: To determine the pathologic substrates in patients with rapid eye movement (REM) sleep behavior disorder (RBD) with or without a coexisting neurologic disorder. METHODS: The clinical and neuropathologic findings were analyzed on all autopsied cases from one of the collaborating sites in North America and Europe, were evaluated from January 1990 to March 2012, and were diagnosed with polysomnogram (PSG)-proven or probable RBD with or without a coexisting neurologic disorder. The clinical and neuropathologic diagnoses were based on published criteria. RESULTS: 172 cases were identified, of whom 143 (83%) were men. The mean ± SD age of onset in years for the core features were as follows – RBD, 62 ± 14 (range, 20–93), cognitive impairment (n = 147); 69 ± 10 (range, 22–90), parkinsonism (n = 151); 68 ± 9 (range, 20–92), and autonomic dysfunction (n = 42); 62 ± 12 (range, 23–81). Death age was 75 ± 9 years (range, 24–96). Eighty-two (48%) had RBD confirmed by PSG, 64 (37%) had a classic history of recurrent dream enactment behavior, and 26 (15%) screened positive for RBD by questionnaire. RBD preceded the onset of cognitive impairment, parkinsonism, or autonomic dysfunction in 87 (51%) patients by 10 ± 12 (range, 1–61) years. The primary clinical diagnoses among those with a coexisting neurologic disorder were dementia with Lewy bodies (n = 97), Parkinson’s disease with or without mild cognitive impairment or dementia (n = 32), multiple system atrophy (MSA) (n = 19), Alzheimer’s disease (AD)(n = 9) and other various disorders including secondary narcolepsy (n = 2) and neurodegeneration with brain iron accumulation-type 1 (NBAI-1) (n = 1). The neuropathologic diagnoses were Lewy body disease (LBD)(n = 77, including 1 case with a duplication in the gene encoding α-synuclein), combined LBD and AD (n = 59), MSA (n = 19), AD (n = 6), progressive supranulear palsy (PSP) (n = 2), other mixed neurodegenerative pathologies (n = 6), NBIA-1/LBD/tauopathy (n = 1), and hypothalamic structural lesions (n = 2). Among the neurodegenerative disorders associated with RBD (n = 170), 160 (94%) were synucleinopathies. The RBD-synucleinopathy association was particularly high when RBD preceded the onset of other neurodegenerative syndrome features. CONCLUSIONS: In this large series of PSG-confirmed and probable RBD cases that underwent autopsy, the strong association of RBD with the synucleinopathies was further substantiated and a wider spectrum of disorders which can underlie RBD now are more apparent