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Amodal completion (AC) is analyzed, by looking at its historical roots and persisting conceptual difficulties. Looking at the origin of the concept, it becomes clear that it is not equivalent to perception of occluded parts. The role of fragment incompleteness is discussed, to clarify that it cannot be taken as a necessary factor for eliciting AC. The standard view of AC, depicted as a set of processes that extrapolate from veridically represented image fragments, is evaluated and rejected on the basis of evidence that AC modifies also modal parts. The theoretical importance of AC phenomena and their potential to reveal the inner forces of perceptual organization are emphasized, with specific reference to the minimum principle. Instances in which AC might be expected but does not occur are examined, to define the limits of such an integrative process.

Carotid intima-media thickness (cIMT) is considered a risk factor for and predictor of cerebrovascular disease. In this study, we explored the contribution of cIMT to cognitive impairment (CI) in dialysis patients and the role of cerebral small vascular disease (CSVD) and brain atrophy in this process.

Cognitive function was assessed using a comprehensive cognitive test battery. CSVD and brain volume were assessed by magnetic resonance imaging, and cIMT was measured by ultrasonography. Multivariable analysis and mediation were used to explore the relevant relationships among cIMT, CI, CSVD and brain volume.

Seventy-three dialysis patients were enrolled. BI-1347 cell line Approximately 54.8% were diagnosed with increased cIMT. The increased cIMT group was older and had lower serum albumin and creatinine levels than the normal cIMT group. There was no difference in the CSVD prevalence between the different cIMT groups. Patients in the normal, unilaterally and bilaterally increased cIMT subgroups demonstrated a gradual decrease in brain-matter volume and degenerate cognitive function. cIMT was related to cognitive function and gray-/white-matter volume. Increased cIMT was associated with a significantly increased risk of a reduced Mini Mental State Examination/Montreal Cognitive Assessment score and Trail A/B time delay. Mediation analysis showed that CI was mediated by brain-matter volume but not by CSVD.

Increased cIMT was an independent risk factor for impairment of global cognitive function, memory, and executive function. The impact of cIMT on cognition was not induced by CSVD but by brain atrophy. cIMT may be a useful tool for screening patients at high risk of CI in the dialysis population.

Increased cIMT was an independent risk factor for impairment of global cognitive function, memory, and executive function. The impact of cIMT on cognition was not induced by CSVD but by brain atrophy. cIMT may be a useful tool for screening patients at high risk of CI in the dialysis population.The standard treatment of Sudden Sensorineural Hearing Loss is based on oral steroids. In addition, intratympanic steroid is currently used in patients who fail to respond to oral treatment. The aim of the present study was to evaluate, in patients affected by SSHL, factors that influence the response to systemic and intratympanic steroid treatment. A retrospective analysis was conducted on 149 patients, all treated with systemic steroids. Moreover, patients not responsive to systemic therapy were treated with intratympanic steroids as salvage therapy. Auditory gain was assessed through the recovery rate at the discharge and after 30 days. Statistical analysis demonstrated that patients with delayed treatment and down-sloping auditory curve presented a poor recovery. Linear and stepwise regression showed that hypertriglyceridemia and hyperglycemia were negative prognostic factors. The prognosis of SSHL is affected by hyperglycemia and hypertriglyceridemia suggesting that a microvascular dysfunction within the cochlea could impair hearing recovery. Intratympanic steroid treatment was used as salvage treatment, however in patients with poor prognostic factors or at risk for side effects, it could be used in association with systemic treatment.The three modes of auditory stimulation (air, bone and soft tissue conduction) at threshold intensities are thought to share a common excitation mechanism the stimuli induce passive displacements of the basilar membrane propagating from the base to the apex (slow mechanical traveling wave), which activate the outer hair cells, producing active displacements, which sum with the passive displacements. However, theoretical analyses and modeling of cochlear mechanics provide indications that the slow mechanical basilar membrane traveling wave may not be able to excite the cochlea at threshold intensities with the frequency discrimination observed. These analyses are complemented by several independent lines of research results supporting the notion that cochlear excitation at threshold may not involve a passive traveling wave, and the fast cochlear fluid pressures may directly activate the outer hair cells opening of the sealed inner ear in patients undergoing cochlear implantation is not accompanied by threshold elevations to low frequency stimulation which would be expected to result from opening the cochlea, reducing cochlear impedance, altering hydrodynamics. The magnitude of the passive displacements at threshold is negligible. Isolated outer hair cells in fluid display tuned mechanical motility to fluid pressures which likely act on stretch sensitive ion channels in the walls of the cells. Vibrations delivered to soft tissue body sites elicit hearing. Thus, based on theoretical and experimental evidence, the common mechanism eliciting hearing during threshold stimulation by air, bone and soft tissue conduction may involve the fast-cochlear fluid pressures which directly activate the outer hair cells.A 70-year-old man presented to the emergency department with blood hypotension associated to a sudden paraplegia and thermalgesic analgesia. He had an history of colic and prostatic adenocarcinoma, hypertension and non-dialyzed Chronic Kidney Disease (CKD) related to an idiopathic membranous glomerulonephritis type 1 discovered 9 years ago. Magnetic resonance imaging confirmed a diagnosis of Spinal Cord Infarction (SCI). Few months later, he presented a blurred vision due to central Retinal Vein Occlusion (RVO), which was improved by Anti-VEGF therapy. This is the first reported case of a concomitance of retinal vascular event and SCI highlights the links between the central nervous system and retinal vascularization despite separate involvement of the two events in the arterial and venous systems. Additionally, CKD worsened the risk of cardiovascular incidents by induced oxidative stress, thrombophilia, chronic inflammation, and endothelial dysfunction. SCI occurrence indicates severe vascular dysfunction and elevates the risk of additional vascular disorders.