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We hypothesize that OSA reducing sleep quality and producing intermittent hypoxia lowers CSF Aβ42 levels, increases CSF lactate levels, and alters cognitive performances in SCI patients, thus inducing early AD clinical and neuropathological biomarkers changes. Notably, controls as well as OSA-CPAP SCI patients did not show clinical and biochemical AD markers. Therefore, OSA may induce early but possibly CPAP-modifiable AD biomarkers changes.

Background:  Sleep disturbances and excessive daytime somnolence are common and disabling features in adult-onset myotonic dystrophy type 1 (DM1). Methods:  Our study used questionnaires, ambulatory polysomnography and the multiple sleep latency test to evaluate sleep-wake cycle and daytime sleepiness in unselected adult-onset DM1 patients. We recruited 18 patients affected by adult-onset DM1 and 18 matched controls. Results:  Sleep efficiency was <90% in 16/18 patients, and it was significantly reduced when compared with controls. Reduced sleep efficiency was associated with abnormal respiratory events (5/18 patients) and/or periodic limb movements (11/18 patients). The Periodic Limb Movement Index was significantly increased in DM1 versus controls. A significantly lower mean MSLT sleep latency was detected in DM1 versus controls, but it did not reach pathological levels. Conclusions:  Our controlled study demonstrated sleep alterations in unselected consecutive DM1 patients. Periodic limb movements in sleep are commonly associated with sleep disturbance in adult-onset DM1, and it may represent a marker of CNS neurodegenerative processes in DM1

Posterior reversible encephalopathy syndrome (PRES) is a serious adverse event associated with calcineurin inhibitors used for graft-versus-host disease (GVHD) prophylaxis. We compared the incidence of PRES in children with thalassemia (n = 222, 1.4 to 17.8 years old) versus sickle cell disease (SCD; n = 59, 2 to 17 years old) who underwent hematopoietic cell transplantation from HLA-matched siblings or alternative donors and analyzed the risk factors for PRES. Overall, 31 children developed calcineurin inhibitor-related PRES (11%), including 30 patients with seizures and 1 patient without seizures. PRES incidence was significantly higher in SCD patients (22%; 95% confidence interval [CI], 10% to 32%) than in thalassemia patients (8%; 95% CI, 5% to 12%;P = .002). In multivariate analysis, factors associated with PRES were hypertension (hazard ratio [HR], 5.87; 95% CI, 2.57 to 13.43; P = .0001), SCD (HR, 2.49; 95% CI, 1.25 to 4.99; P = .009), and acute GVHD (HR 2.27; 95% CI, 1.06 to 4.85; P= .031). In the entire cohort overall survival (OS) was significantly higher in patients without versus with PRES (90% versus 77%; P = .02). In a subgroup analysis that including matched sibling transplants, OS and disease-free survival (DFS) were similar in thalassemia patients without PRES (92% and 88%, respectively) and with PRES (82% and 73%, respectively), whereas SCD patients with PRES had significantly lower OS (67%) and DFS (67%) than patients without PRES (94% and 94%, respectively; P = .008). Thus, SCD patients had a significantly higher incidence of PRES than thalassemia patients, and hypertension and GVHD were the 2 main risk factors for PRES in patients with hemoglobinopathies. Although PRES did not significantly influence survival in patients with thalassemia, patients with SCD had significantly lower survival after PRES.

Vestibular dysfunction was linked to moderate-to-severe obstructive sleep apnea syndrome (OSAS) patients in literature. However, due to a lack of knowledge among valid and recent implementations conceived to study postural control on static posturography (SP) and vestibulo-ocular reflex (VOR) gain under physiological conditions (video Head Impulse Test; vHIT), the aim of this work was to integrate (i) VOR changes via vHIT implementation, (ii) postural arrangement by studying both classical parameters and frequency spectra (PS) and (iii) correlation between these findings, polygraphic (PG) and subjective scores along Dizziness Handicap Inventory (DHI) and Epworth Sleepiness Scale (ESS). Thus, 32 moderate-to-severe OSAS patients and 32 healthy subjects - studied by using PG, DHI and ESS - underwent vHIT and SP posturographic assessment. Analysis of variance was performed to disclose between-group effects and correlation analysis was implemented between otoneurological, PG, DHI and ESS values. OSAS group demonstrated a significant decay of VOR gain and an increase in both frequency spectra PS values, especially within the low-frequency interval, and in classical posturographic SP parameters. Further, positive and negative correlations between mean SaO and gain and low frequency interval spectra PS were found, respectively. Strengthening previous hypothesis related to brainstem chronic hypoxemia phenomena affecting vestibular network, implementation of these data could generate future attentions (i) for screening under physiological conditions postural and vestibular detriments in OSAS subjects, especially exposed at risk settings, and (ii) among PG parameters, such as mean SaO , to propose further reliable tools in monitoring postural and vestibular decay in these patients demonstrating PG parameters detriments.

BRIEF SUMMARYCurrent Knowledge/Study Rationale: Vitamin D not only participates in bone metabolism and regulates calcium homeostasis, but also has pleiotropic effects, modulating numerous metabolic processes. Considering that patients with obstructive sleep apnea (OSA) suffer from vitamin D defi ciency and show high serum parathyroid hormone (PTH) levels, we tested the effects of short-term continuous positive airway pressure (CPAP) on serum vitamin D and PTH levels. Study Impact: These fi ndings suggest that short-term CPAP therapy in male patients with OSA determines an increase of serum vitamin D levels. Therefore, the current study provides evidence that OSA seems to be an etiopathogenetic factor involved in vitamin D defi ciency, which may recover after CPAP therapy in male patients. Study Objective:Recent studies report a link between obstructive sleep apnea (OSA) syndrome, low vitamin D levels, and high parathyroid hormone (PTH) concentrations. The aim of the current study is to evaluate the effect of 7-night continuous positive airway pressure (CPAP) therapy on serum vitamin D, PTH, and calcium levels in patients with severe OSA syndrome. Methods: Patients with severe OSA were enrolled into the study and compared to control subjects. Patients with OSA underwent CPAP therapy for 7 nights and were consequently divided into responders (OSA-R, mean residual AHI < 5/h) and nonresponders (OSA-nR, mean residual AHI > 5/h). Serum vitamin D, PTH, and calcium levels were measured at baseline in patients with severe OSA (apnea-hypopnea index > 30/h) and control subjects. Patients with OSA underwent a fi nal morning blood sample after 7-night CPAP therapy. Results: We enrolled 90 patients with OSA into the study (65 OSA-R and 25 OSA-nR) compared to 32 control subjects. At baseline, lower vitamin D and higher PTH levels were detected in the OSA group compared to controls. After 7-night CPAP therapy, male OSA-R patients showed a signifi cant increase in vitamin D levels. Conversely, female OSA-R patients did not show the same increase in vitamin D levels. It was also observed that OSA-nR subjects did not show modifi cations of serum markers after nCPAP-therapy. Conclusions:The study demonstrates that short-term nCPAP treatment is able to promote the recovery of vitamin D homeostasis in male patients with OSA. The mediation of sexual hormones in regulating vitamin D is a possible explanation of the lack of recovery of vitamin D homeostasis in female patients with OSA as it often affects postmenopausal women. Keywords: calcium, CPAP, OSA, PTH, vitamin D Citation: Liguori C, Romigi A, Izzi F, Mercuri NB, Cordella A, Tarquini E, Giambrone MP, Marciani MG, Placidi F. Continuous positive airway pressure treatment increases serum vitamin D levels in male patients with obstructive sleep apnea.

SUMMARYPurpose: The endocannabinoid system is involved in excitatory/inhibitory balance mechanisms within the central nervous system (CNS). Growing evidence shows that its perturbation leads to development of epileptic seizures in experimental models, thus indicating that endocannabinoids play an intrinsic protective role in suppressing pathologic neuronal excitability. Experimental data also demonstrate that the endocannabinoid anandamide (AEA) can antagonize epileptic discharges in hippocampal tissue. The objective of our study was to measure endocannabinoids levels in the cerebrospinal fluid (CSF) of drug-naive patients affected by temporal lobe epilepsy (TLE). Methods: We measured the levels of both AEA and the other endocannabinoid, 2-arachidonoylglycerol (2-AG), in the CSF of drug-naive patients with TLE.Results: A significant reduction of AEA was found in the CSF of patients with compared with healthy controls (epileptic patients = 2.55 ± 1.78 pmol/ml; healthy controls = 11.65 ± 7.53 pmol/ml; n = 9 for both groups, p < 0.01). 2-AG levels, however, were not affected (epileptic patients = 209.5 ± 146.56; healthy controls = 159.6 ± 110.2) (n = 6 for both groups, p = 0.48). Discussion: Our findings seem to be consistent with experimental evidence demonstrating a significant prevention of epileptic seizures induced by endocannabinoids in models of epilepsy. Furthermore, they support the hypothesis that AEA may be involved in its pathogenesis, suggesting a hypothetical primary impairment of the endocannabinoid system in untreated TLE. The actual role of this in vivo dysregulation still remains unclear.

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