Electrophysiological brain stem investigations in idiopathic narcolepsy

Marx, Jürgen; Hopf, Hanns Christian; Grün, B.; Querings, Kerstin; Dahmen, Norbert

doi:10.1007/s004150050239

Cited by 5 publications

(3 citation statements)

References 35 publications

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“…This is in line with existing literature showing, at least in the cataplexy‐free state, no difference in blink reflex in narcolepsy–cataplexy compared to controls (Khatami et al. , 2007; Marx et al. , 1998).…”

Section: Discussionsupporting

confidence: 93%

“…In our study, blink reflex parameters did not differ between patients and controls. This is in line with existing literature showing, at least in the cataplexy-free state, no difference in blink reflex in narcolepsy-cataplexy compared to controls (Khatami et al, 2007;Marx et al, 1998). In addition, Khatami et al (2007) found that patients with narcolepsy-cataplexy failed to exhibit startle potentiation during unpleasant stimuli, supporting the hypothesis of an amygdala dysfunction in human narcolepsy-cataplexy.…”

Section: Discussionsupporting

confidence: 90%

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Narcolepsy–cataplexy: deficient prepulse inhibition of blink reflex suggests pedunculopontine involvement

Frauscher

Löscher

Ehrmann

et al. 2012

Journal of Sleep Research

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Summary Hypocretin (orexin) deficiency plays a major role in the pathophysiology of narcolepsy–cataplexy. In animal models, hypocretinergic projections to the pedunculopontine nucleus are directly involved in muscle tone regulation mediating muscle atonia – a hallmark of cataplexy. We hypothesized that pedunculopontine nucleus function, tested with prepulse inhibition of the blink reflex, is altered in human narcolepsy–cataplexy. Twenty patients with narcolepsy–cataplexy and 20 healthy controls underwent a neurophysiological study of pedunculopontine nucleus function. Blink reflex, prepulse inhibition of the blink reflex and blink reflex excitability recovery were measured. Blink reflex characteristics (R1 latency and amplitude, and R2 and R2c latency and area under the curve) did not differ between patients and controls (P > 0.05). Prepulse stimulation significantly increased R2 and R2c latencies and reduced R2 and R2c areas in patients and controls. However, the R2 and R2c area suppression was significantly less in patients than in controls (to 69.8 ± 14.4 and 74.9 ± 12.6%, respectively, versus 34.5 ± 28.6 and 43.3 ± 29.5%, respectively; each P < 0.001). Blink reflex excitability recovery, as measured by paired‐pulse stimulation, which is not mediated via the pedunculopontine nucleus, did not differ between patients and controls (P > 0.05). Our data showed that prepulse inhibition is reduced in narcolepsy–cataplexy, whereas unconditioned blink reflex and its excitability recovery are normal. Because the pedunculopontine nucleus is important for prepulse inhibition, these results suggest its functional involvement in narcolepsy–cataplexy.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 90%

Narcolepsy–cataplexy: deficient prepulse inhibition of blink reflex suggests pedunculopontine involvement

Frauscher

Löscher

Ehrmann

et al. 2012

Journal of Sleep Research

View full text Add to dashboard Cite

show abstract

“…However, Overeem et al [28] found no differences in global gray or white matter volumes between patients and controls, suggesting either that narcolepsy is associated with microscopic changes undetectable by VBM or that functional abnormalities of hypocretin neurons do not have any structural correlates. A multimodal electrophysiological investigation showed no relevant brain stem lesions as compared with controls [24].An attempt to utilize quantitative EEG methods for assessing EDS in narcolepsy had been made before by Alloway et al [1], who applied the alpha attenuation test (AAT). In a power spectral analysis of a single EEG lead it was found that mean eyes-closed alpha power was significantly reduced in narcoleptics as compared to normals.…”

Section: Discussionmentioning

confidence: 98%

EEG-tomographic studies with LORETA on vigilance differences between narcolepsy patients and controls and subsequent double-blind, placebo-controlled studies with modafinil

et al. 2004

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The aim of the present study was to identify brain regions associated with vigilance in untreated and modafinil-treated narcoleptic patients by means of low-resolution brain electromagnetic tomography (LORETA). 16 drug-free narcoleptics and 16 normal controls were included in the baseline investigation. Subsequently patients participated in a double-blind, placebo-controlled crossover study receiving a three-week fixed titration of modafinil (200, 300, 400 mg) and placebo. Measurements comprised LORETA, the Multiple Sleep Latency Test (MSLT) and the Epworth Sleepiness Scale (ESS) obtained before and after three weeks' therapy. Statistical overall analysis by means of the omnibus significance test demonstrated significant inter-group differences in the resting (R-EEG), but not in the vigilance-controlled recordings (V-EEG). Subsequent univariate analysis revealed a decrease in alpha-2 and beta 1-3 power in prefrontal, temporal and parietal cortices, with the right hemisphere slightly more involved in this vigilance decrement. Modafinil 400 mg/d as compared with placebo induced changes opposite to the aforementioned baseline differences (key-lock principle) with a preponderance in the left hemisphere. This increase in vigilance resulted in an improvement in the MSLT and the ESS. LORETA provided evidence of a functional deterioration of the fronto-temporo-parietal network of the right-hemispheric vigilance system in narcolepsy and a therapeutic effect of modafinil on the left hemisphere, which is less affected by the disease.

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Increased prevalence of obesity in narcoleptic patients and relatives

Dahmen

Bierbrauer

Kasten

2001

European Archives of Psychiatry and Clinical Neuroscience

131

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Increased Body Mass Indices (BMIs), increased prevalences of non insulin-dependent diabetes and sleep apnoe syndrome have been reported to be associated with narcolepsy. Our objective was to explore and possibly confirm the association of narcolepsy and increased BMI. In addition, we addressed the question whether increased BMIs also occur in relatives of narcoleptic patients. Together with narcolepsy-related clinical parameters we measured body weight and height of 132 narcoleptic patients who agreed to participate in our narcolepsy research program. In addition, 52 first degree relatives of 22 index patients, mostly from multiplex families, were included in the study. Data were compared to published general population surveys, recently conducted in Germany and Switzerland as well as to collective of 104 psychiatric inpatients. Narcoleptic patients had significantly increased BMIs in comparison to general populations or psychiatric controls. BMIs of first degree relatives were lower than those of index patients but significantly higher than those found in the general population. BMIs were not related to symptom severity or to medication status. Thus, the elevated BMIs appeared not to be secondary to behavioral consequences of narcolepsy but may reflect a trait at least partially common to index patients and relatives.

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Electrophysiological brain stem investigations in idiopathic narcolepsy

Cited by 5 publications

References 35 publications

Narcolepsy–cataplexy: deficient prepulse inhibition of blink reflex suggests pedunculopontine involvement

Narcolepsy–cataplexy: deficient prepulse inhibition of blink reflex suggests pedunculopontine involvement

EEG-tomographic studies with LORETA on vigilance differences between narcolepsy patients and controls and subsequent double-blind, placebo-controlled studies with modafinil

Increased prevalence of obesity in narcoleptic patients and relatives

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