ABSTRACT
INTRODUCTION: The limbic system is critical for memory function and degenerates early in the Alzheimer's disease continuum. Whether obstructive sleep apnea (OSA) is associated with alterations in the limbic white matter tracts remains understudied. METHODS: Polysomnography, neurocognitive assessment, and brain magnetic resonance imaging (MRI) were performed in 126 individuals aged 55-86 years, including 70 cognitively unimpaired participants and 56 participants with mild cognitive impairment (MCI). OSA measures of interest were the apnea-hypopnea index and composite variables of sleep fragmentation and hypoxemia. Microstructural properties of the cingulum, fornix, and uncinate fasciculus were estimated using free water-corrected diffusion tensor imaging. RESULTS: Higher levels of OSA-related hypoxemia were associated with higher left fornix diffusivities only in participants with MCI. Microstructure of the other white matter tracts was not associated with OSA measures. Higher left fornix diffusivities correlated with poorer episodic verbal memory. DISCUSSION: OSA may contribute to fornix damage and memory dysfunction in MCI. HIGHLIGHTS: Sleep apnea-related hypoxemia was associated with altered fornix integrity in MCI. Altered fornix integrity correlated with poorer memory function. Sleep apnea may contribute to fornix damage and memory dysfunction in MCI.
Subject(s)
Cognitive Dysfunction , Diffusion Tensor Imaging , Fornix, Brain , Hypoxia , Humans , Male , Female , Cognitive Dysfunction/etiology , Aged , Fornix, Brain/diagnostic imaging , Fornix, Brain/pathology , Middle Aged , Aged, 80 and over , Hypoxia/complications , Polysomnography , Neuropsychological Tests/statistics & numerical data , White Matter/diagnostic imaging , White Matter/pathology , Magnetic Resonance Imaging , Sleep Apnea Syndromes/complications , Sleep Apnea, Obstructive/complicationsABSTRACT
BACKGROUND: Far from being benign, somnambulistic episodes can be frequent and/or severe and potentially injurious. Episodes may also be accompanied by sleep mentation with variable degrees of retrograde amnesia. The present study investigated how somnambulistic episodes unfold from childhood through adulthood, a topic that remains understudied. METHODS: Adult sleepwalkers with a diagnosis of primary somnambulism and a childhood onset of the disorder (n = 113) were assessed for changes in frequency of their episodes, recall of episode-related sleep mentation and aggressive episodes during childhood, adolescence and adulthood. In addition, sleepwalkers (n = 52) with childhood-onset of sleep terrors were assessed for developmental changes in sleep terror frequency. RESULTS: Results indicate that the frequency of somnambulistic episodes remains unchanged during childhood and adolescence before increasing during adulthood. An opposite trend was observed for sleep terrors. The frequency of aggressive somnambulistic episodes and of sleep mentation associated with somnambulism increased from childhood to adolescence and into adulthood. By contrast, the recall of sleep mentation associated with sleep terrors did not change over time. Additionally, a higher frequency of aggressive somnambulistic episodes predicted a higher frequency of sleep mentation associated with somnambulism. These patterns were similar across men and women. CONCLUSION: Our study demonstrates that in chronic sleepwalkers, sleep mentation associated with somnambulistic episodes increases with age while episodes worsen in frequency and severity from childhood to adulthood. These findings add to the limited literature in the field and provide valuable insights into how key clinical characteristics of somnambulism evolve across the lifespan.
Subject(s)
Night Terrors , Somnambulism , Adolescent , Adult , Child , Female , Humans , Male , Night Terrors/epidemiology , Self Report , Sleep , Somnambulism/diagnosis , Somnambulism/epidemiology , Young AdultABSTRACT
We describe an autosomal-dominant locus for Restless Legs Syndrome (RLS) in a French-Canadian (FC) pedigree. Genome-wide microsatellite scan and linkage analysis were used in this study. The locus maps to chromosome 16p12.1 and spans 1.18 Mega bases. The maximum multipoint LOD scores are of 3.5 over the total of 10 markers. Evidence for the same locus was also found in a smaller FC pedigree sime095. The analysis of the sequence of 8 annotated genes within the region did not reveal any pathogenic mutations. Copy number variation and karyotype analyses did not reveal any chromosomal abnormality in the region. Further analyses of the region are necessary to find the genetic cause of RLS in this family.
Subject(s)
Chromosomes, Human, Pair 16/genetics , Genes, Dominant , Restless Legs Syndrome/genetics , Adolescent , Adult , Aged , Aged, 80 and over , Female , France/ethnology , Genetic Heterogeneity , Genotype , Haplotypes , Humans , Lod Score , Male , Microsatellite Repeats , Middle Aged , Paresthesia/genetics , Pedigree , Pregnancy , Pregnancy Complications/genetics , Quebec/epidemiology , Restless Legs Syndrome/ethnology , Young AdultABSTRACT
A new restless legs syndrome locus on chromosome 14 recently has been reported in one family of Italian origin. Our study aimed to replicate this finding and determine the importance of this locus in the French Canadian population. Markers spanning the region were genotyped in 14 large families and linkage assessed using two-point and multipoint logarithm of odds scores. Possible linkage to this locus was found in one of our kindreds providing support for the existence of this locus and indicating that this locus may be responsible for a small fraction of French Canadian restless legs syndrome.
