Both authors contributed equally to this work.
Narcolepsy–cataplexy: deficient prepulse inhibition of blink reflex suggests pedunculopontine involvement
Article first published online: 28 APR 2012
© 2012 European Sleep Research Society
Journal of Sleep Research
Volume 21, Issue 5, pages 495–501, October 2012
How to Cite
FRAUSCHER, B., LÖSCHER, W. N., EHRMANN, L., GSCHLIESSER, V., BRANDAUER, E., HÖGL, B. and KOFLER, M. (2012), Narcolepsy–cataplexy: deficient prepulse inhibition of blink reflex suggests pedunculopontine involvement. Journal of Sleep Research, 21: 495–501. doi: 10.1111/j.1365-2869.2012.01016.x
- Issue published online: 25 SEP 2012
- Article first published online: 28 APR 2012
- Accepted in revised form 4 March 2012, received 24 July 2011
- pedunculopontine nucleus
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.