BACKGROUND: Cognitive processing in migraine is characterized by a loss of habituation during the interval and increased latencies in an attack. No studies are available on event-related potentials (ERPs) in cluster headache or chronic paroxysmal hemicrania. OBJECTIVE: To determine the involvement of cognitive processing in cluster headache and chronic paroxysmal hemicrania as measured by ERPs. METHODS: Visually evoked ERPs were measured in 50 patients with episodic cluster headache, 11 patients with chronic cluster headache, and 12 patients with chronic paroxysmal hemicrania. Measurements were performed in the cluster period outside an attack with and without prophylactic medication and not in the cluster period. RESULTS: Latencies of the endogenous ERP components were significantly increased during the cluster period as compared with outside the cluster period and with healthy subjects. In chronic cluster headache, latencies of both endogenous and exogenous components were increased. Medication with prophylactic drugs normalized the ERP latencies in episodic cluster headache; in chronic cluster headache, ERP latencies were decreased without complete normalization. No changes of ERP latencies and amplitudes could be observed in chronic paroxysmal hemicrania. A loss of cognitive habituation as it is known in migraine could not be observed in either cluster headache or chronic paroxysmal hemicrania. CONCLUSIONS: Our data suggest that central structures generating ERPs are involved in the pathophysiology of cluster headache during the cluster period but not outside the cluster period. This is in concordance with recent neuroimaging findings on the central role of the hypothalamus and the right frontal cortex in cluster headache and supports the hypothesis of a central origin of cluster headache. Furthermore, the data suggest that cluster headache and chronic paroxysmal hemicrania are distinct entities.
BACKGROUND: Cognitive processing in migraine is characterized by a loss of habituation during the interval and increased latencies in an attack. No studies are available on event-related potentials (ERPs) in cluster headache or chronic paroxysmal hemicrania. OBJECTIVE: To determine the involvement of cognitive processing in cluster headache and chronic paroxysmal hemicrania as measured by ERPs. METHODS: Visually evoked ERPs were measured in 50 patients with episodic cluster headache, 11 patients with chronic cluster headache, and 12 patients with chronic paroxysmal hemicrania. Measurements were performed in the cluster period outside an attack with and without prophylactic medication and not in the cluster period. RESULTS: Latencies of the endogenous ERP components were significantly increased during the cluster period as compared with outside the cluster period and with healthy subjects. In chronic cluster headache, latencies of both endogenous and exogenous components were increased. Medication with prophylactic drugs normalized the ERP latencies in episodic cluster headache; in chronic cluster headache, ERP latencies were decreased without complete normalization. No changes of ERP latencies and amplitudes could be observed in chronic paroxysmal hemicrania. A loss of cognitive habituation as it is known in migraine could not be observed in either cluster headache or chronic paroxysmal hemicrania. CONCLUSIONS: Our data suggest that central structures generating ERPs are involved in the pathophysiology of cluster headache during the cluster period but not outside the cluster period. This is in concordance with recent neuroimaging findings on the central role of the hypothalamus and the right frontal cortex in cluster headache and supports the hypothesis of a central origin of cluster headache. Furthermore, the data suggest that cluster headache and chronic paroxysmal hemicrania are distinct entities.