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To characterize and evaluate the estimation of oxygen saturation measured by a wrist-worn reflectance pulse oximeter during sleep.

Sleep is a critical component of health and well-being but collecting and analyzing accurate longitudinal sleep data can be challenging, especially outside of laboratory settings. We propose a simple neural network model titled SOMNI (Sleep data restOration using Machine learning and Non-negative matrix factorIzation [NMF]) for imputing missing rest-activity data from actigraphy, which can enable clinicians to better handle missing data and monitor sleep–wake cycles of individuals with highly irregular sleep–wake patterns. The model consists of two hidden layers and uses NMF to capture hidden longitudinal sleep–wake patterns of individuals with disturbed sleep–wake cycles. Based on this, we develop two approaches: the individual approach imputes missing data based on the data from only one participant, while the global approach imputes missing data based on the data across multiple participants. Our models are tested with shift and non-shift workers' data from three independent hospitals. Both approaches can accurately impute missing data up to 24 hours of long dataset (>50 days) even for shift workers with extremely irregular sleep–wake patterns (AUC > 0.86). On the other hand, for short dataset (~15 days), only the global model is accurate (AUC > 0.77). Our approach can be used to help clinicians monitor sleep–wake cycles of patients with sleep disorders outside of laboratory settings without relying on sleep diaries, ultimately improving sleep health outcomes.Graphical Abstract

The prevalence of artificial light exposure has enabled us to be active any time of the day or night, leading to the need for high alertness outside of traditional daytime hours. To address this need, we developed a personalized sleep intervention framework that analyzes real-world sleep–wake patterns obtained from wearable devices to maximize alertness during specific target periods. Our framework utilizes a mathematical model that tracks the dynamic sleep pressure and circadian rhythm based on the user’s sleep history. In this way, the model accurately predicts real-time alertness, even for shift workers with complex sleep and work schedules (N= 71, t= 13~21 days). This allowed us to discover a new sleep–wake pattern called the adaptive circadian split sleep, which incorporates a main sleep period and a late nap to enable high alertness during both work and non-work periods of shift workers. We further developed a mobile application that integrates this framework to recommend practical, personalized sleep schedules for individual users to maximize their alertness during a targeted activity time based on their desired sleep onset and available sleep duration. This can reduce the risk of errors for those who require high alertness during nontraditional activity times and improve the health and quality of life for those leading shift work-like lifestyles.

Somatosensory reflex epilepsy is induced by repetitive cutaneous contact of a circumscribed body area with a tight time‐lock between somatosensory stimulation and seizure. We describe the case of a 27‐year‐old man with seizures induced by repetitive tapping on the sole of the right foot. Simultaneous video‐EEG monitoring and surface electromyography was performed during a seizure triggered by repetitive tapping on the right sole aspect using a hammer. Stimulation produced a tingling sensation on the right sole that extended to the right lower leg. This was followed by motor Jacksonian march of the right leg. [Published with video sequence onwww.epilepticdisorders.com]

Despite compelling evidence from animal studies indicating hippocampal subfield-specific vulnerability to poor sleep quality and related cognitive impairment, there have been no human magnetic resonance imaging (MRI) studies investigating the relationship between hippocampal subfield volume and sleep disturbance. Our aim was to investigate the pattern of volume changes across hippocampal subfields in patients with primary insomnia relative to controls.

The aim of this study was to assess the effects of oxcarbazepine (OXC) on cognition and psychosocial difficulties in patients with new-onset partial epilepsy.

To investigate differences in cortical thickness in patients with obstructive sleep apnea (OSA) syndrome and healthy controls.

Topiramate (TPM) is a broad-spectrum anticonvulsant used both as an adjunctive treatment and as monotherapy. In this study, the results from a routine therapeutic drug monitoring (TDM) service for TPM are summarized. In addition, factors influencing the variability in serum concentration of TPM and the effects of comedication on serum TPM concentration were investigated.

To determine first whether there was a clear relationship between concentrations of the active metabolite of oxcarbazepine (OXC), 10-hydroxycarbamazepine (OHC), and dose adjusted for weight, and second, whether the clearance of OHC was influenced by comedication with enzyme-inducing antiepileptic drugs (EIAED).

To investigate differences in cortical thickness in narcolepsy patients with cataplexy and control subjects.

To investigate differences in brain gray matter concentrations or volumes in patients with obstructive sleep apnea syndrome (OSA) and healthy volunteers.

To investigate the effects of modafinil on regional cerebral blood flow (rCBF) in narcolepsy, we performed 99mTc-ethylcysteinate dimer single photon emission computed tomography (SPECT) before and after modafinil or placebo medication.

To investigate changes in regional cerebral blood flow (rCBF) in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS).

Gelastic seizures have been described in various epilepsies arising from the temporal or frontal lobes, although the most commonly encountered form is related to the presence of an hypothalamic hamartoma. We report a patient with gelastic seizures involving the right parietal lobe. Our patient, a 32‐year‐old man, underwent video‐EEG monitoring, interictal and ictal brain SPECTs during gelastic seizures. Subtraction ictal SPECT co‐registered to MRI (SISCOM), was performed to localize any ictal hyperperfusion during these gelastic seizures. The seizures consisted of brief staring followed by smiling and laughing. Electroencephalography during the gelastic seizures showed rhythmic sharp waves in the right parietal lobe. SISCOM showed ictal hyperperfusion in the right parietal lobe and medial portions of right cerebellum. Our findings suggest that the right parietal lobe may actively participate in the particular epileptogenic network generating gelastic seizures.

BACKGROUND Antiepileptic drugs have been reported to affect cerebral metabolism. We performed 18F-fluorodeoxyglucose positron emission tomography (PET) before and after lamotrigine administration to investigate its effects on cerebral glucose metabolism in patients with drug-naïve idiopathic generalized epilepsy. DESIGN We included patients who were newly diagnosed as having idiopathic generalized epilepsy or who had not taken an antiepileptic drug after the diagnosis was made. Antiepileptic drug 18F-fluorodeoxyglucose PETs were obtained before and after lamotrigine administration in 21 subjects (male-female ratio, 10:11; mean ± SD age, 24.3 ± 2.8 years). The mean lamotrigine dosage was 211.9 mg/d (range, 175.0-275.0 mg/d). For statistical parametric mapping analysis, all PET images were spatially normalized to the standard PET template and then smoothed using a 14-mm full width at half-maximum gaussian kernel. The paired t test was used to compare premedication and postmedication 18F-fluorodeoxyglucoae PET images. RESULTS After lamotrigine administration, cerebral metabolism was decreased in bilateral thalami, bilateral caudate nuclei, the left side of the putamen, the left entorhinal area, bilateral parahippocampal gyri, the right inferior temporal gyrus, the left rectosubcallosal gyrus, bilateral superior frontal gyri, the left middle frontal gyrus, the right precentral gyrus, left pericentral gyri, the right superior parietal lobule, and bilateral substantia nigra at P<.05 corrected for multiple comparisons using the false discovery rate approach. No brain region showed increased metabolism after lamotrigine administration. CONCLUSION This study revealed that lamotrigine treatment reduces glucose metabolism in the thalamus, basal ganglia, and multiple regions of the cerebral cortex in drug-naïve patients with idiopathic generalized epilepsy.Arch Neurol. 2006;63:1282-1286--

To investigate postoperative changes in the cerebral glucose metabolism of patients with mesial temporal lobe epilepsy (MTLE), statistical parametric mapping (SPM) analysis was performed on pre- and postoperative 18F-fluorodeoxyglucose PET (FDG-PET) images. We included 28 patients with MTLE who had undergone surgery and had been seizure-free postoperatively (16 had left MTLE and 12 right MTLE). All patients showed hippocampal sclerosis by pathology or brain MRI. FDG-PET images of the 12 right temporal lobe epilepsy patients were reversed to lateralize the epileptogenic zone to the left side in all patients. Application of the paired t-test in SPM to pre- and postoperative FDG-PETs showed that postoperative glucose metabolism decreased in the caudate nucleus, the pulvinar of the thalamus, fusiform gyrus, lingual gyrus and the posterior region of the insular cortex in the hemisphere ipsilateral to resection, whereas postoperative glucose metabolism increased in the anterior region of the insular cortex, temporal stem white matter, midbrain, inferior precentral gyrus, anterior cingulate gyrus and supramarginal gyrus in the hemisphere ipsilateral to resection. No significant postsurgical changes in cerebral glucose metabolism occurred in the contralateral hemisphere. Subtraction between pre- and postoperative FDG-PET images in individual patients produced similar findings to the SPM results, and additionally showed that postoperative glucose metabolism increased in the anterior thalamus in 12/28 patients (42.8%). SISCOM (subtraction ictal–interictal SPECT co-registered to MRI) performed in 17 patients showed ictal hyperperfusion in the ipsilateral temporal lobe, including the temporal stem white matter, midbrain, insular cortex and cingulate gyrus, bilateral basal ganglia and thalami, and multiple small regions in the frontoparietal lobes during seizures. This study suggests that brain regions showing a postoperative increase in glucose metabolism appear to represent the propagation pathways of ictal and interictal epileptic discharges in MTLE, whereas the postoperative decrease in glucose metabolism may be related to a permanent loss of afferents from resected anterior–mesial temporal structures.

It has been hypothesized that hypothalamus is involved in narcolepsy. The relative difference between cerebral glucose metabolism of 24 narcoleptic patients and 24 normal controls was studied using 18F‐fluorodeoxy glucose positron emission tomography. Patients with narcolepsy showed significantly reduced cerebral glucose metabolism in bilateral rectal and subcallosal gyri, the medial convexity of right superior frontal gyrus, bilateral precuneus, right inferior parietal lobule, and in left supramarginal gyrus (uncorrected p< 0.001). Bilateral posterior hypothalami and mediodorsal thalamic nuclei showed hypometabolism with significance at the level of corrected p< 0.05, with small volume correction. This study showed cerebral glucose hypometabolism of the hypothalamus‐thalamus‐orbitofrontal pathways in the narcoleptic brain. Ann Neurol 2004

Neurocognitive impairment is one of the daytime symptoms of obstructive sleep apnea (OSA). We proposed to use tract-specific statistical analysis (TSSA) to investigate whether there are fiber tract abnormalities in OSA, which may be undiscovered using voxel-based approaches, and whether such tract-specific disruptions in brain connectivity are associated with neuropsychological deficits in patients with untreated OSA.

A 22 year-old woman suffered from recurrent episodes of hypersomnia, apathy, and hyperphagia. The symptoms occurred 3 to 4 times per year, and each attack lasted 2 to 3 weeks. 99mTc-ethylcysteinate dimer brain single photon emission computed tomography (SPECT) was performed during symptomatic and asymptomatic periods. To localize brain regions with perfusion changes during symptomatic period, asymptomatic SPECT was subtracted from symptomatic SPECT. The subtracted SPECT showed significant hypoperfusion in the left hypothalamus, bilateral thalami, basal ganglia, bilateral medial and dorsolateral frontal regions, and left temporal lobe during the symptomatic period. These cerebral hypoperfusion areas support the diencephalic hypothesis and clinical symptoms of Kleine-Levin syndrome.

To localize cerebral perfusion differences during cataplexy, brain SPECT subtraction was performed between cataplexy and baseline awake period or REM sleep in patients with narcolepsy. During cataplexy, subtracted SPECT showed hyperperfusion in right amygdala, bilateral cingulate gyri, basal ganglia, thalami, premotor cortices, sensorimotor cortices, right insula, and brainstem, and hypoperfusion in prefrontal cortex and occipital lobe. This result suggests that cataplexy is produced by the activation of amygdalo-cortico-basal ganglia–brainstem circuit.