Laboratory examinations and treatment.

<p>CSF: cerebrospinal fluid; OB: oligoclonal band, NMO-IgG: neuromyelitis optica immunoglobulin; AQP4 Ab: aquaporin-4 antibody; EP: evoked potential; VEP: visual EP; BAEP: brainstem auditory EP; SSEP: somatosensory EP; INF: β-interferon; ND: not done; NA: not available.</p

Pathology of a biopsied tumefactive brain lesion (patient #4).

<p>It shows some characteristic features of demyelination include hypercellularity and reactive gliosis (a: haematoxylin-eosin), abundant foamy macrophages (b: CD 68 antibody; for macrophage), myelin loss (c: Luxol-fast blue; for myelin), and “relative” axonal preservation (d: Bodian; for nerve fibers).</p

Fluid attenuated inversion recovery (FLAIR) magnetic resonance images (a, b) of another patient #7.

<p>They show multiple hyperintensity lesions over juxtacortical area of left medial temporal lobe and bilateral basal ganglion (caudate nucleus and putamen). Pons and cerebellum are also involved.</p

Magnetic resonance image findings (location, size and enhancement).

<p>PV: periventricular white matter; JC: juxtacortical; IC: internal capsule; BG: basal ganglion (caudate, putamen, globus pallidum).</p><p>S: small, ≤2 cm; M: middle, 2–5 cm; L: large, >5 cm;</p>*<p>enhancement.</p><p>ND: not done; C: cervical cord; T: thoracic cord; s: short, <3 segments; l: long, ≥3 segments.</p>a<p>lesions during the first attack are underlined.</p>b<p>Only spinal lesion without brain lesion noted during the first attack; her large brain lesion was noted during the second attack.</p

General characteristics and clinical neurologic symptoms and signs.

<p>Motor: focal limbs or facial weakness; Mental: impaired cognition; Sensory: hypsthesia, hyperesthesia; Cb: cerebellar dysfunction-incoordination; BS: brainstem sign-diplopia, bulbar sign; VF: visual field defect; Sz: seizure; ON: optic neuritis; ANS: autonomic-orthostatic hypotension, urine/stool/sexual dysfunction; EPS: extrapyramidal tract-involuntary movement; EDSS: extended disability status score; RR: relapsing-remitting.</p>a<p>Times of attack.</p>b<p>The number means the neurological symptoms and signs during the time of attack.</p>c<p>Average EDSS.</p

Higher Particulate Matter Deposition in Alveolar Region Could Accelerate Body Fat Accumulation in Obstructive Sleep Apnea

We conducted a cross-sectional study to investigate associations of particulate matter (PM) of less than 2.5 μm in aerodynamic diameter (PM2.5) and PM deposition with nocturnal changes in body composition in obstructive sleep apnea (OSA) patients. A bioelectric impedance analysis was used to measure the pre- and postsleep body composition of 185 OSA patients. Annual exposure to PM2.5 was estimated by the hybrid kriging/land-use regression model. A multiple-path particle dosimetry model was employed to estimate PM deposition in lung regions. We observed that an increase in the interquartile range (IQR) (1 μg/m3) of PM2.5 was associated with a 20.1% increase in right arm fat percentage and a 0.012 kg increase in right arm fat mass in OSA (p < 0.05). We observed that a 1 μg/m3 increase in PM deposition in lung regions (i.e., total lung region, head and nasal region, tracheobronchial region, and alveolar region) was associated with increases in changes of fat percentage and fat mass of the right arm (β coefficient) (p < 0.05). The β coefficients decreased as follows: alveolar region > head and nasal region > tracheobronchial region > total lung region (p < 0.05). Our findings demonstrated that an increase in PM deposition in lung regions, especially in the alveolar region, could be associated with nocturnal changes in the fat percentage and fat mass of the right arm. PM deposition in the alveolar region could accelerate the body fat accumulation in OSA

sj-docx-1-dhj-10.1177_20552076231205744 - Supplemental material for Machine learning approaches for predicting sleep arousal response based on heart rate variability, oxygen saturation, and body profiles

Supplemental material, sj-docx-1-dhj-10.1177_20552076231205744 for Machine learning approaches for predicting sleep arousal response based on heart rate variability, oxygen saturation, and body profiles by Chih-Fan Kuo, Cheng-Yu Tsai, Wun-Hao Cheng, Wen-Hua Hs, Arnab Majumdar, Marc Stettler, Kang-Yun Lee, Yi-Chun Kuan, Po-Hao Feng, Chien-Hua Tseng, Kuan-Yuan Chen and Jiunn-Horng Kang, Hsin-Chien Lee, Cheng-Jung Wu, Wen-Te Liu in DIGITAL HEALTH</p

Data_Sheet_1_Associations between risk of Alzheimer's disease and obstructive sleep apnea, intermittent hypoxia, and arousal responses: A pilot study.docx

ObjectivesObstructive sleep apnea (OSA) may increase the risk of Alzheimer's disease (AD). However, potential associations among sleep-disordered breathing, hypoxia, and OSA-induced arousal responses should be investigated. This study determined differences in sleep parameters and investigated the relationship between such parameters and the risk of AD.MethodsPatients with suspected OSA were recruited and underwent in-lab polysomnography (PSG). Subsequently, blood samples were collected from participants. Patients' plasma levels of total tau (T-Tau) and amyloid beta-peptide 42 (Aβ42) were measured using an ultrasensitive immunomagnetic reduction assay. Next, the participants were categorized into low- and high-risk groups on the basis of the computed product (Aβ42 × T-Tau, the cutoff for AD risk). PSG parameters were analyzed and compared.ResultsWe included 36 patients in this study, of whom 18 and 18 were assigned to the low- and high-risk groups, respectively. The average apnea–hypopnea index (AHI), apnea, hypopnea index [during rapid eye movement (REM) and non-REM (NREM) sleep], and oxygen desaturation index (≥3%, ODI-3%) values of the high-risk group were significantly higher than those of the low-risk group. Similarly, the mean arousal index and respiratory arousal index (R-ArI) of the high-risk group were significantly higher than those of the low-risk group. Sleep-disordered breathing indices, oxygen desaturation, and arousal responses were significantly associated with an increased risk of AD. Positive associations were observed among the AHI, ODI-3%, R-ArI, and computed product.ConclusionsRecurrent sleep-disordered breathing, intermittent hypoxia, and arousal responses, including those occurring during the NREM stage, were associated with AD risk. However, a longitudinal study should be conducted to investigate the causal relationships among these factors.</p