We have previously shown that during repetitive pattern-reversal stimulation, lasting 2 min, the amplitude of the visual evoked potential (PR-VEP) increases in migraineurs when tested interictally whereas it decreases in healthy control subjects. According to Sappey-Marinier et al. (J Cereb Blood Flow Metab 1992; 12: 584-92) habituation of the PR-VEP in normal subjects is maxima after 12 min, at a time when there is a decrease of stimulation-enhanced lactate levels in the occipital cortex. We have therefore compared PR-VEP during long periods of repetitive stimulation in healthy control subjects (n = 25) and in patients suffering from migraine without (n = 25) and with aura (n = 15) between attacks. During uninterrupted stimulation at 3.1 Hz VEPs were sequentially averaged in blocks of 100 responses for a total duration of 15 min and analysed in terms of latencies and peak-to-peak amplitudes of N1-P1 and P1-N2 peaks. Amplitude changes from the baseline were calculated for each block, by comparison with the first block, and analysed statistically using Zerbe's method. The N1-P1 and P1-N2 amplitudes in the first block tended to be lower in migraineurs than in healthy control subjects. During the 15 min of stimulation, amplitudes of both components progressively decreased in control subjects, but remained stable in both groups of patients. The difference between patients and control subjects proved to be significant (P < 0.05). The neurophysiological data were not correlated with clinical features such as attack frequency or duration of illness. These results are yet another demonstration in migraine of an interictal habituation deficit in cortical information processing, which might favour lactate accumulation in sensory cortices during sustained activation.

The aim of this study was to evaluate the function of pain modulating systems subserving diffuse noxious inhibitory controls (DNICs) in primary headaches. DNICs were examined in 24 migraineurs, 17 patients with chronic tension-type headache (CTTH) and 20 healthy subjects by means of nociceptive flexion RIII reflex and the cold pressor test (CPT) as heterotopic noxious conditioning stimulation (HNCS). The subjective pain thresholds (Tp) and the RIII reflex threshold (Tr) were significantly lower in CTTH vs. controls. In controls a significant inhibition of the RIII reflex was observed during the CPT (-30%, P < 0.05). Conversely, migraine and CTTH patients showed facilitation (+31%, P < 0.05 and +40%, P < 0.01, respectively) of the RIII reflex during the HNCS. This study demonstrates a dysfunction in systems subserving DNICs in both migraine and CTTH. Impairment of endogenous supraspinal pain modulation systems may contribute to the development and/or maintenance of central sensitization in primary headaches.

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Clinical evidence suggests that chronic daily headache (CDH) occurs in association with psychopathologies: previous studies have focused particularly on migraine. To evaluate this association, we studied, using the DSM-IIIR criteria, a population of 88 patients (18M, 70F) affected by CDH (mean duration 7.4 +/- 8.7 years). We documented the presence of a psychiatric disorder in 90% of this population. The most frequent diagnosis was a comorbidity of anxiety and mood disorders. The comorbidity of psychiatric disorders and headache has important implications as far as treatment is concerned.

Neuroimaging studies in cluster headache (CH) patients have increased understanding of attack-associated events and provided clues to the pathophysiology of the condition. They have also suggested stimulation of the ipsilateral posterior inferior hypothalamus as a treatment for chronic intractable CH. After 8 years of experience, stimulation has proved successful in controlling the pain attacks in almost 60% of chronic CH patients implanted at various centres. Although hypothalamic implant is not without risks, it has generally been performed safely. Implantation affords an opportunity to perform microrecordings of individual posterior hypothalamic neurons. These studies are at an early stage, but suggest the possibility of identifying precisely the target site by its electrophysiological characteristics. Autonomic studies of patients undergoing posterior hypothalamic stimulation provide further evidence that long-term stimulation is safe, revealing that it can cause altered modulation of the mechanisms of orthostatic adaptation without affecting the baroreflex, cardiorespiratory interactions or efferent sympathetic and vagal functions. Chronically stimulated patients have an increased threshold for cold pain at the site of the first trigeminal branch ipsilateral to the stimulated side; when the stimulator is switched off, changes in sensory and pain thresholds do not occur immediately, suggesting that long-term stimulation is required to induce sensory and nociceptive changes. Posterior inferior hypothalamic stimulation is now established as a treatment for many chronic CH patients. The technique is shedding further light on the pathophysiology of the disease, and is also providing clues to functioning of the hypothalamus itself.