Narcolepsy-cataplexy: deficient prepulse inhibition of blink reflex suggests pedunculopontine involvement
Narcolepsy-cataplexy: deficient prepulse inhibition of blink reflex suggests pedunculopontine involvement
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DOI:
10.1111/j.1365-2869.2012.01016.x
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发表时间:
2012-10-01
影响因子:
4.4
通讯作者:
Kofler, Markus
中科院分区:
文献类型:
--
作者:
Frauscher, Birgit;Loescher, Wolfgang N.;Kofler, Markus
Hypocretin (orexin) deficiency plays a major role in the pathophysiology of narcolepsycataplexy. 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 narcolepsycataplexy. Twenty patients with narcolepsycataplexy 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 narcolepsycataplexy, 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 narcolepsycataplexy.