Impairment of Trigeminal Sensory Pathways in Cluster Headache

Abstract

Cluster headache (CH) typically presents in clusters of attacks of intense (peri)orbital, unilateral pain. The distribution of the pain implies involvement of central and/or peripheral trigeminal pathways. These can be investigated by means of trigeminal somatosensory evoked potentials (TSEP) and blink reflexes (BR). We aimed to relate functional changes in trigeminal sensory pathways to the presence of cluster periods. TSEP and BR were performed in 28 episodic CH patients during a cluster period and repeated in 22 outside a cluster period. TSEP latencies (N1, P1 and N2) and amplitude (N1-P1 and P1-N2) and BR latencies (R1, R2 ipsilateral and R2 contralateral) were compared between sides, during and outside a cluster period and with healthy control data ( n = 22). During a cluster period, N2 TSEP latencies were longer on the symptomatic side compared with the non-symptomatic side (27.2 ± 3.0 ms vs. 26.3 ± 3.4 ms, P = 0.02), and compared with the same side outside the cluster period (26.7 ± 3.1 ms vs. 25.1 ± 3.0 ms, P = 0.01). N1, P1 and N2 latencies on the symptomatic side in patients during the cluster period (14.8 ± 2.3 ms, 20.4 ± 2.5 ms and 27.2 ± 3.0 ms, respectively) were significantly longer than those of healthy controls (13.4 ± 1.9 ms, 18.8 ± 2.4 ms and 25.0 ± 2.6 ms, respectively, P < 0.03). Outside the cluster period, N1 latencies of both sides (15.3 ± 2.8 ms symptomatic side and 15.4 ± 2.6 ms asymptomatic side) were longer compared with controls (13.4 ± 1.9 ms, P < 0.04). TSEP amplitudes and BR latencies revealed no significant differences. We conclude that abnormalities of the afferent trigeminal pathway are present in patients with cluster headache, most prominent during the cluster period, and on the symptomatic side. This seems primarily due of changes within the higher cerebral regions of the system.