Simona Dostálová

Isolated REM sleep behavior disorder (iRBD) is associated with impaired colour discrimination, cognitive deficits and morphological changes. This study evaluates whether colour discrimination deficits in iRBD are mediated by cognitive functions or related to dopaminergic denervation and brain morphology. A sample of 73 patients with iRBD and 77 controls underwent neuropsychological assessment, and colour discrimination assessment using the Farnsworth Munsell 100 Hue Test, DAT-SPECT, and MRI. The data were analyzed using multiple regression, mediation analysis, and voxel-based morphometry. Significant between-group differences were found in total colour discrimination as well as in the red-yellow spectrum. The association between iRBD and performance in the yellow-green spectrum was mediated by cognitive functions, as measured by the Montreal Cognitive Assessment. In controls, a positive correlation between the yellow-green spectrum and the left inferior frontal gyrus was observed compared to patients, however, this association was largely driven by a single data point. The performance in the green–blue spectrum was associated with the activity of dopamine transporters in the caudate nucleus. No interactions were found for total colour discrimination in any analysis. The present findings demonstrate a colour vision deficit in iRBD, which is not directly linked to any of the proposed potential explanatory mechanisms.

Objective: To date, very few studies have focused on structural changes and their association with cognitive performance in isolated REM sleep behaviour disorder (iRBD). Moreover, the results of these studies are inconclusive. This study aims to evaluate differences in the associations between brain morphology and cognitive tests in iRBD and healthy controls. Methods: Sixty-three patients with iRBD and thirty-six controls underwent MRI with a 3 T scanner. The cognitive performance was assessed by a comprehensive neuropsychological battery. Based on performance, the iRBD group was divided into two subgroups with (iRBD-MCI) and without mild cognitive impairment (iRBD-NC). The high-resolution T1-weighted images were analysed using an automated atlas segmentation tool, voxel-based (VBM) and deformation-based (DBM) morphometry to identify between-group differences and correlations with cognitive performance. Results: VBM, DBM and the comparison of ROI volumes yielded no significant differences between iRBD and controls. In the iRBD group, significant correlations in VBM were found between several cortical and subcortical structures primarily located in the temporal, parietal, occipital lobe, cerebellum, and basal ganglia and three cognitive tests assessing psychomotor speed and one memory test. Between-group analysis of cognition revealed a significant difference between iRBD-MCI and iRBD-NC in tests including a processing speed component. Conclusions: iRBD shows deficits in several cognitive tests that correlate with morphological changes, the most prominent of which is in psychomotor speed and visual attention as measured by the TMT-A and associated with the volume of striatum, insula, cerebellum, temporal lobe, pallidum and amygdala.

Summary: Little attention has been paid to the long‐term development of idiopathic hypersomnia symptoms and idiopathic hypersomnia comorbidities. The aim of this study was to describe the general health of patients with idiopathic hypersomnia years after the initial diagnosis, focusing on current subjective hypersomnolence and the presence of its other possible causes. Adult patients diagnosed with idiopathic hypersomnia ≥ 3 years ago at sleep centres in Prague and Kosice were invited to participate in this study. A total of 60 patients were examined (age 47.3 ± SD = 13.2 years, 66.7% women). In all participants, their hypersomnolence could not be explained by any other cause but idiopathic hypersomnia at the time of diagnosis. The mean duration of follow‐up was 9.8 + 8.0 years. Fifty patients (83%) reported persisting hypersomnolence, but only 33 (55%) had no other disease that could also explain the patient's excessive daytime sleepiness and/or prolonged sleep. In two patients (3%), the diagnosis in the meantime had changed to narcolepsy type 2, and 15 patients (25%) had developed a disease or diseases potentially causing hypersomnolence since the initial diagnosis. Complete hypersomnolence resolution without stimulant treatment lasting longer than 6 months was reported by 10 patients (17%). To conclude, in a longer interval from the diagnosis of idiopathic hypersomnia, hypersomnolence may disappear or may theoretically be explained by another newly developed disease, or the diagnosis may be changed to narcolepsy type 2. Thus, after 9.8 years, only 55% of the examined patients with idiopathic hypersomnia had a typical clinical picture of idiopathic hypersomnia without doubts about the cause of the current hypersomnolence.

The aim of the present study was to investigate if prospective memory (PM) is impaired in idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD). RBD is a parasomnia characterized by dream enactment and by REM sleep without muscle atonia. iRBD is considered as the initial stage of neurodegeneration with pathological storage of alpha-synuclein. Sixty iRBD patients with polysomnography-confirmed RBD without parkinsonism and dementia and 30 demographically matched normal controls (NC) were enrolled in the present study. Clinical assessment included Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS), dopamine transporter single-photon emission computed tomography (DaT-SPECT) for imaging synapses of dopaminergic neurons in the striatum and a neuropsychological battery with embedded time-based and event-based PM measures. iRBD differed significantly from NC in event-based PM, a number of event-based failures to recall intention and total PM performance (all p < .001) but did not differ in time-based PM and recognition. PM did not contribute to impairment of instrumental activities of daily living in iRBD. Despite being preserved in iRBD in comparison to NC, time-based PM correlated significantly with dopaminergic neuronal loss measured by DaT-SPECT. We show evidence for a differential pattern of PM impairment in iRBD with severe impairment of event-based and concurrent preservation of time-based PM. We theorize that event-based PM impairment in iRBD is caused by severe impairment of retention and recognition mechanisms in episodic memory whereas time-based PM seems to be affected by reduced striatal dopaminergic synapses.

Obstructive sleep apnoea (OSA) is a condition leading to excessive daytime sleepiness. The aim of the study was a) to study course of daytime sleepiness in patients with OSA and b) to find the most important nocturnal polysomnography parameters influencing daytime sleepiness in OSA. The cohort consisted of forty-five patients (6 women, 39 men) diagnosed with OSA. All patients underwent polysomnography, Multiple Sleep Latency Test (MSLT) and rated subjectively their daytime tendency to sleep with the Epworth Sleepiness Scale. Sleep latency was significantly longer at 15:00 and at 17:00 hours compared to previous tests. A significant negative correlation was found between the mean of the MSLT sleep latency and a number of awakenings, the apnoea/hypopnoea index and oxygen desaturation index values. The study showed the sleep latency prolongation at 15:00 and 17:00 hours respectively and confirmed connection of excessive daytime sleepiness to fragmentation of nocturnal sleep and OSA severity.

OBJECTIVE: To explain the effect of craniofacial relations on the development of the sleep apnoea syndrome (SAS) in acromegaly, and to elucidate how the activity of acromegaly affects the severity of SAS. DESIGN: Prospective observational study. METHODS: Cephalometry and sleep ventilation measurements were performed in 26 acromegalic men and in 96 men with SAS. RESULTS: SAS was found in 20 acromegalic men. Compared with non-acromegalic men with SAS, patients with acromegaly and SAS were found to have: enlargement of almost all linear dimensions; increased angle indicating mandibular protrusion; increased difference between maxillary and mandibular protrusion; articular angle decrease; soft palate lengthening; and pharyngeal airway space (PAS) enlargement in the palatal and uvular-tip planes. A comparison of acromegalic men with and without SAS revealed no significant difference in the craniofacial skeleton, although there was a narrowing of the minimal PAS (MinPAS) and of PAS in the uvular-tip plane in patients with SAS. SAS was more frequent in the patients with active acromegaly. MinPAS in the patients with active acromegaly was narrower than in those without disease activity. CONCLUSION: Skeletal abnormalities in acromegalic men with SAS were different from those in SAS patients without acromegaly. Upper airway narrowing due to changes in pharyngeal soft tissues takes a more relevant share in the development of SAS in acromegalic men than skeletal anomalies.

The prevalence of sleep apnea syndrome (SAS) in acromegaly is high. Consequences of SAS are serious and are associated with increased morbidity and mortality. The aim of this study was to assess the relative frequency and predictive factors for SAS in a group of patients with acromegaly (n=55). The presence of SAS was evaluated using the Polymesam device. Hormonal and clinical examination consisted of assessment of growth hormone, insulin-like growth factor I plasma levels, body mass index (BMI), neck circumference, age, sex, treatment modes of acromegaly and ear, nose and throat (ENT) examination. The relative frequency of SAS in our group of patients with acromegaly was 75%. Independent predictors of SAS were: increased activity of acromegaly, higher age and neck circumference. No association between SAS and BMI and ENT findings was observed. The role of gender was controversial.

Craniofacial abnormalities which predispose to pharyngeal obstruction can be detected by cephalometry. The aim of the present study was to compare cephalometric findings of the patients with sleep apnoea syndrome (SAS) with those of healthy population. The SAS patients (23 females, 96 males) and normal population (36 females, 50 males) were examined by cephalometry. In the group of females with SAS following significant differences were observed: elongation of the soft palate (p < 0.001), narrowing pharyngeal airway space (p < 0.001), mandibular retrognathism (p < 0.05), micrognathism of the mandible (p < 0.001), dorsocaudal rotation of the mandible (p < 0.01), increased lower gonion angle (p < 0.001) and the articular angle (p < 0.05), increased anterior facial height (p < 0.05), narrowing the depth of bony framework of the nasopharynx (p < 0.001), decreased depth of the upper face (p < 0.01) and decreased length of the cranial base (p < 0.01). In the group of males with SAS, following significant differences were observed: elongation of the soft palate (p < 0.001), narrowing pharyngeal airway space (p < 0.001), decreased depth of the maxilla (p < 0.001), decreased angle of the cranial base (p < 0.01), decrease saddle angle (p < 0.01), decreased depth of the upper face (p < 0.01), increased lower gonion angle (p < 0.01), increased articular angle (p < 0.001) and increased anterior and posterior facial height (p < 0.001). There are important differences in orofacial skeleton and soft tissue of the nasopharynx measured by cephalometry in the patients with sleep apnoea compared to normal population.