Cephalalgia

The management of medication-overuse headache (MOH) is often difficult and no specific guidelines are available as regards the most practical and effective approaches. In this study we defined and tested a consensus protocol for the management of MOH on a large population of patients distributed in different countries.

The protocol was based on evidence from the literature and on consolidated expertise of the members of the consensus group. The study was conducted according to a multicentric interventional design with the enrolment of 376 MOH subjects in four centres from Europe and two centres in Latin America. The majority of patients were treated according to an outpatient detoxification programme. The post-detoxification follow-up lasted six months.

At the final evaluation, two-thirds of the subjects were no longer overusers and in 46.5% of subjects headache had reverted back to an episodic pattern of headache. When comparing the subjects who underwent out-patient detoxification vs those treated with in-patient detoxification, both regimens proved effective, although the drop-out rate was higher in the out-patient approach.

The present findings support the effectiveness and usability of the proposed consensus protocol in different countries with different health care modalities.

Cluster headache (CH) is well known to show a seasonal predilection; however, the impact of temperature and other meteorological factors on cluster periods (or bouts) has not been established.

This nationwide survey included 758 patients with episodic CH retrieved from the Taiwan National Health Insurance Research Database from 2005 to 2009. Corresponding meteorological recordings were obtained from the Central Weather Bureau. A case-crossover study design was used to investigate the association between cluster periods and meteorological factors.

A total of 2452 episodes of cluster periods were recorded. The cluster periods were most frequent in the autumn and least frequent in the winter. Seasonal changes from winter to spring and from autumn to winter also increased the frequency of cluster periods. The risk of cluster periods increased when there was a higher mean temperature on event days (odds ratio (OR), 1.014, 95% confidence interval (CI), 1.005–1.023, p = 0.003) or within seven to 56 days. Either an increase or a decrease in temperature (0.05℃/day) following a warm period (mean temperature ≥26℃) was associated with the onset of cluster periods. In contrast, a greater increase in temperature (0.15℃/day) following a cold period (mean temperature < 21℃) was needed to evoke cluster periods. No such associations were found following moderate periods (21℃ ≤mean temperature <26℃).

Our study shows that temperature is associated with precipitating or priming cluster periods. The influence depends on the temperature of the preceding periods.

The age of onset of cluster headache (CH) attacks most commonly is between 20 and 40 years old, although CH has been reported in all age groups. There is increasing evidence of CH with early or late onset and a different course of the disorder. The aim of the study was to analyze the influence of the age of onset on clinical features, disorder course, and therapy effectiveness in CH patients.

A retrospective and cross-sectional analysis was performed on 182 CH patients divided into three groups according to the age of onset. The first group consisted of patients with the first CH attack before 20 years of age, the second group was patients with age of onset between 20 and 40 years of age, and the third group was patients with age of onset after 40 years of age. Demographic data, features of CH periods and attacks, and the response to standardized treatment were compared among the groups.

Patients with CH onset after 40 years of age reported a lower number of autonomic features and less frequently had conjunctival injection and nasal congestion/rhinorrhea phenomena during their attacks. Diagnostic delay was the longest in the patients with CH onset before 20 years of age.

The influence of the age of onset of CH is intriguing for further studies and could possibly extend the knowledge about CH pathophysiology. From a clinical point of view, the differences in CH presentation are insufficient to preclude a correct diagnosis and treatment because the same criteria could be applied regardless of patient age.

Headache is one of the most common symptoms after cocaine use.

We investigated headache frequency and characteristics and the correlation between headache and acute cocaine intake in a cross-sectional study in a consecutive series of chronic cocaine users.

Participation rate was 94.1%. Of the 80 subjects enrolled, 72 (90%) reported current headaches, in most cases migraine or probable migraine without aura. Of these 72, 29 (40.3%) had a headache history, whereas 43 (59.7%) reported de novo headache after beginning to use cocaine. After acute cocaine use, a large percentage of users reported headache attacks: 86.2% of previous headache sufferers (migraine or probable migraine without aura in all cases) and 93% of de novo headache sufferers (migraine/probable migraine without aura = 35; episodic tension-type headache = three patients; cocaine-induced headache= two patients). Most subjects reported that when they used cocaine headaches worsened.

Chronic cocaine use frequently seems to worsen or induce headache with migraine or migraine-like characteristics, probably owing to a serotoninergic and dopaminergic system impairment. In headache sufferers, especially those with migraine headaches, clinicians should enquire into possible cocaine use.

The impact of early degenerative changes of the cervical spine on pain in adulthood is unknown. The objective was to determine whether degeneration in adolescence predicts headache or neck pain in young adulthood.

As part of a follow-up of schoolchildren with and without headache, 17-year-old adolescents with headache at least three times a month (N = 47) and adolescents with no headache (N = 22) participated in a magnetic resonance imaging (MRI) study of the cervical spine. The same adolescents were re-examined by phone interview at the age of 22 years (N = 60/69, 87%).

Mild disc degeneration at the age of 17 years was common, but was not associated with either frequent or intensive headache or neck pain at the age of 22 years.

Conclusion: Mild degenerative changes of the cervical spine in 17-year-old adolescents cannot be regarded as a cause of future headache or neck pain.

The aim of this article is to investigate whether the nitric oxide (NO) donator diethylenetriamine/nitric oxide (DETA/NO) affects trigeminal sensory processing through the trigeminal ganglion in part by activating trigeminal satellite glial cells (SGCs) and whether this effect is attenuated by the anti-inflammatory compound palmitoylethanolamide (PEA).

DETA/NO was administered to isolated rat trigeminal SGCs in vitro, and injected into the rat trigeminal ganglion in vivo, in the presence or absence of PEA.

Administration of DETA/NO (1000 µM) increased the release of prostaglandin E₂ by SGCs. PEA (1 and 10 µM) significantly attenuated prostaglandin E₂ release. Two intraganglionic injections of DETA/NO (10 mM, 3 µl) or prostaglandin E₂ at a 30-minute interval did not evoke discharge in trigeminal ganglion neurons that innervate the rat jaw-closer muscles, but did reduce the mechanical activation threshold of their peripheral endings by 30%–50%. Intravenous administration of PEA (1 mg/kg) or ketorolac (0.5 mg/kg) prevented DETA/NO-induced afferent mechanical sensitization.

Elevation of NO in the trigeminal ganglion results in the sensitization of the peripheral endings of masticatory muscle nociceptors to mechanical stimulation through a mechanism that involves prostaglandin E₂ release from SGCs. Attenuation of this sensitization by PEA suggests a possible option for acute management of craniofacial pain and headache.

Calcitonin gene-related peptide (CGRP) is a key molecule in migraine pathophysiology. Most studies have focused on CGRP in relation to migraine without aura (MO). About one-third of migraine patients have attacks with aura (MA), and this is a systematic review of the current literature on CGRP and MA.

We performed a systematic literature search on MEDLINE for reports of CGRP and MA, covering basic science, animal and human studies as well as randomized clinical trials.

The literature search identified 594 citations, of which 38 contained relevant, original data. Plasma levels of CGRP in MA patients are comparable to MO, but CGRP levels varied among studies. A number of animal studies, including knock-ins of familial hemiplegic migraine (FHM) genes, have examined the relationship between CGRP and cortical spreading depression. In patients, CGRP does not trigger migraine in FHM, but is a robust trigger of migraine-like headache both in MA and MO patients. The treatment effect of CGRP antagonists are well proven in the treatment of migraine, but no studies have studied the effect specifically in MA patients.

This systematic review indicates that the role of CGRP in MA is less studied than in MO. Further studies of the importance of CGRP for auras and migraine are needed.

Familial hemiplegic migraine (FHM) is a rare monogenic subtype of migraine with aura that includes motor auras. Prophylactic treatment of FHM often has marginal effects and involves a trial-and-error strategy based on therapeutic guidelines for non-hemiplegic migraine and on case reports in FHM.

We assessed the response to prophylactic medication in an FHM family and sequenced the FHM2 ATP1A2 gene in all available relatives.

A novel p.Met731Val ATP1A2 mutation was identified. Attack frequency was reduced significantly with sodium valproate monotherapy (n = 1) and attacks ceased completely with a combination of sodium valproate and lamotrigine (n = 2).

We report dramatic prophylactic effects of sodium valproate and lamotrigine in an FHM2 family, making these drugs worth considering in the treatment of other FHM patients.

Migrainous infarction accounts for 12.8% of ischemic strokes of unusual etiology.

A 59-year-old woman with longstanding migraine with aura experienced what appeared to be migrainous infarction characterized by dysmetropsia and transient Cotard’s syndrome. Imaging demonstrated right temporal-parietal-occipital changes with apparent cortical laminar necrosis.

The spectrum of the pathophysiology of migrainous infarction has not been established; however, cortical spreading depression may explain the appearance of imaging findings that do not obey a vascular territory.