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Biomedical subjects

B Ondze

Publications and source records attributed to B Ondze.

8 recordsLinked to original sources

Sleep architecture, slow wave activity and sleep spindles in mild sleep disordered breathing.

OBJECTIVE: A high degree of sleep fragmentation by arousals related to respiratory events would result in an abnormal distribution of slow wave activity (SWA) and a decrease in sleep spindle density in sleep disordered breathing (SDB) patients when compared to controls. METHODS: Eighteen mild SDB subjects (6 females and 12 males), aged 18-56 years with (5<respiratory disturbance index (RDI)<30/h) were compared to 18 controls (11 female and 7 male) aged 18-52 years. The sleep EEG power density was performed using fast Fourier transform (FFT) analysis and sleep spindle density integrated digital filtering analysis (IDFA). Esophageal pressure monitoring was performed on the third night. RESULTS: Sleep analysis showed a significant higher number of awakenings <1 min and arousal indexes in total sleep time, in non-REM (NREM) sleep and in slow wave sleep (SWS) than in controls. SWA and theta band decreased significantly from the first to the fourth cycle in both subjects. Theta and sigma bands were significantly lower in patients than in controls, in each sleep cycle and during the whole night. Moreover, the temporal course of SWA showed an exponential decay in both patients and controls but the time constant of the curve was significantly slower in patients than in controls. Furthermore, in both groups, the sleep spindle index was significantly lower in both SWS and stage 2 in patients than in controls. CONCLUSIONS: Sleep architecture in mild SDB subjects is characterized by a high degree of sleep fragmentation resulting in a different time course of SWA and a decreased sleep spindle index when compared to controls.

Adolescent↗

Age at onset of narcolepsy in two large populations of patients in France and Quebec.

BACKGROUND: Narcolepsy usually starts around adolescence; however, there is great variability in the clinical presentation of narcolepsy. OBJECTIVE: To determine the age at onset in conjunction with severity of narcoleptic symptoms in two large populations of narcoleptic patients with a similar genetic background. METHODS: Information on age at onset and severity of the condition was obtained in 317 patients with well-defined narcolepsy-cataplexy from Montpellier (France) and in 202 from Montreal (Canada). RESULTS: The mean age at onset was 23.4 years in Montpellier and 24.4 in Montreal. The age at onset was bimodal in two independent patient populations: a first peak occurring at 14.7 years, and a second peak occurring at 35. Age at onset clearly differentiates patients with a positive family history of narcolepsy (early onset) from those without a family history. Other clinical and polygraphic findings may indicate that young age at onset is associated with increased severity of the condition (higher frequency of cataplexy and decreased mean sleep latency on the Multiple Sleep Latency Test). CONCLUSION: Bimodal distribution of age at onset of narcolepsy was found in two independent patient populations. Our data suggest that age at onset is genetically determined.

Adolescent↗

Sleep architecture, slow wave activity, and sleep spindles in adult patients with sleepwalking and sleep terrors.

OBJECTIVES: A very strong SWS intensity reflected by both an increased level of SWA and an abnormal sleep spindles distribution would be responsible for the major difficulty of parasomniac subjects in waking up from SWS, leading to episodes of parasomnia. METHODS: Eleven adult parasomniac subjects, 6 females and 5 males, with sleepwalking (SW) and/or sleep terrors (ST) and 11 age- and sex-matched control subjects underwent polysomnography (PSG) during 2 consecutive nights. After an habituation and selection night followed by a 16 h period of controlled wakefulness, the sleep EEGs of the parasomniac and control subjects were analyzed on the second night by computer-aided visual scoring (integrated digital filtering analysis, IDFA) and spectral analysis (fast Fourier transform, FFT). Throughout the night subject behaviour was controlled and recorded by means of a video infra-red camera and videotape recorder. RESULTS: Fifteen episodes of parasomnia were recorded during the second night in the 11 subjects. Sleep analysis showed significantly (P<0.05) decreased sleep efficiency and stage 2 sleep (absolute values and percentage of total sleep time) and increased (P<0.05) slow wave sleep (absolute values and percentage of total sleep time). Arousal index and wake-time after sleep onset were significantly higher in parasomniac subjects. Sleep fragmentation was mainly concentrated in stages 3 and 4. The slow wave activity (SWA) absolute values averaged during the 2 min immediately preceding an episode of parasomnia were significantly higher than the SWA averaged during 2 min in the same stage 10 min before an episode of parasomnia. Moreover, SWA was higher in the slow wave sleep (SWS) episodes preceding the episode of parasomnia than in the episodes preceding an awakening without an episode of parasomnia. The temporal course of SWA showed a slower exponential decay in both groups, but the time constant of the curve was larger in parasomniacs than in controls. Finally, in control subjects the sleep spindle index increased from the beginning to the end of the night while it was equally distributed in parasomniacs. CONCLUSIONS: An abnormal deep sleep associated with a high SWS fragmentation might be responsible for the occurrence of SW or ST episodes.

Adult↗

EEG arousals and awakenings in relation with periodic leg movements during sleep.

It is known that periodic leg movements are frequently accompanied by full awakenings or by signs of EEG arousals. The time relationship of these EEG arousals with leg movements varies from patient to patient. They may precede or follow leg movements or occur simultaneously. It is not clear whether these arousals trigger leg movements or, alternatively, whether both EEG arousals and leg movements are separate expressions of a common pathophysiological mechanism. We investigated the temporal relationship of five EEG arousals, such as alpha activity, K-complexes, spindles, K-alpha, K-spindle activities and awakenings, with leg movements in 10 periodic leg movement patients. These EEG arousals were considered to be associated with leg movements if they occurred 10 s before/after or simultaneously with the onset of right or left tibialis muscle EMG potentials. It was found that 49.19% of EEG arousals occurred before leg movements, 30.61% occurred simultaneously and 23.18% occurred just after leg movements. The number of EEG arousals was significantly higher in the 10 s preceding leg movement than simultaneously or in the 10 s following. Alpha activity was the phenomenon associated most frequently with leg movements, irrespective of its temporal organization and was significantly higher during the 10 s preceding movement. Spindle and K-spindle activities were significantly higher before leg movement, whereas K-complex activity was significantly more frequent during leg movements. The number of awakenings was significantly higher after leg movements than simultaneously. These results indicated that leg movements are not primary, but rather are a phenomenon associated with an underlying arousal disorder.

Adult↗

Are periodic leg movements during sleep (PLMS) responsible for sleep disruption in insomnia patients?

On the basis of polygraphic findings, it has been suggested that periodic leg movements during sleep are not responsible for sleep impairment (Lugaresi et al., 1972). However, for some authors it is an important cause of insomnia (Guilleminault et al., 1975; Coleman, 1982). Thus, the relationship between periodic leg movements during sleep, sleep disruption and the complaint of patients is particularly complex. We investigated the macro- and micro-structure of sleep with and without leg movements in 10 PLMS patients complaining of insomnia to clarify whether periodic leg movements are responsible for sleep disruption. The total sleep time without periodic leg movements was significantly longer than sleep time with leg movements. Sleep time without leg movements was longer than sleep time with leg movements in stage 2, slow wave sleep (SWS) and rapid eye movement (REM) sleep. Short lasting awakenings were significantly more frequent during periodic leg movements associated sleep whilst long lasting awakenings were equally frequent during sleep with and without periodic leg movements. The percentage of the four electroencephalogram (EEG) activities (delta, theta, alpha and spindles) did not show any significant difference between periodic leg movements associated and not associated with sleep stages and total sleep time. The lack of significant differences in both the macro- and micro-structure of sleep and EEG activity content regarding the association with movements confirm the hypothesis that periodic leg movements did not primarily cause sleep disturbance.

Adult↗

Idiopathic hypersomnia.

Identification of idiopathic hypersomnia dates back 20 years only. It typically consists of prolonged nocturnal sleep, great difficulty waking up in the morning or at the end of a nap, and constant or recurrent excessive daytime sleepiness. Complete and incomplete forms are encountered. Twenty-three subjects fulfilling ICSD criteria are reported with clinical, polysomnographic and immunogenetic data. Considering differential diagnosis is an important step in the diagnosis of idiopathic hypersomnia. Idiopathic hypersomnia is much less frequent than narcolepsy. A strong genetic component is suggested by the high proportion of familial cases. No association with HLA has been evidenced to date.

Adolescent↗

Hypersomnia associated with mood disorders: a new perspective.

Thirty-six subjects affected with hypersomnia associated with mood disorders, 31 with a diagnosis of dysthymia, 4 with a diagnosis of bipolar disorder and one with a diagnosis of major recurrent depression underwent standardized polysomnographic procedures including night 1, MSLT and night 2 (uninterrupted). 36.1% of these subjects had a reduced or intermediate mean sleep latency on the MSLT and 13.8% slept over 9 hr at night. In addition 17 of these subjects underwent prolonged polysomnography during day 2. In comparison with eight subjects affected with idiopathic hypersomnia, mean sleep latency on the MSLT was significantly longer and total sleep time during night 2 and during night 2 plus day 2 was significantly lower in subjects affected with hypersomnia associated with mood disorders. It is concluded that a positive diagnosis of hypersomnia associated with a mood disorder requires both behavioral observation and polysomnography. Among these subjects there may be subjects with well-documented hypersomnia and subjects with anergia facilitating or mimicking sleep.

Adult↗

[Benign multiple sclerosis with childhood onset].

We report a case of multiple sclerosis which began at the age of 12 years. Clinical symptoms at onset were acute, regressive cerebellovestibular ataxia and optic neuritis. Twenty-four years later vertigo, motor and sensory deficit of the right lower limb and grand mal seizures developed. CSF and MRI were suggestive of multiple sclerosis. The patient is now free of neurological symptoms with an 8 years' follow-up.

Child↗