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Nummular headache (NH) is a primary disorder characterized by chronic pain that is exclusively felt in a small area of the head surface. We describe five patients with circumscribed head pain and sensory dysfunction consistent with NH, who in addition developed colocalized trophic changes. All of them had a round or oval patch of skin depression (1–2 cm in diameter) inside of the painful area (2–4.5 cm in diameter). Three of them also showed hair loss, reddish colour, and local increased temperature. Skin biopsies were performed in three patients, and were not specific for any particular dermatological disease. Local trophic changes may be a clinical feature of NH. Together with pain and sensory disturbances, they could represent a restricted form of complex regional pain syndrome. This should be taken as a possible evolution of the underlying morbid process of NH. [ABSTRACT FROM AUTHOR]

Short-lasting Unilateral Neuralgiform headache attacks with Conjunctival injection and Tearing (SUNCT) is a syndrome predominant in males, with a mean age of onset around 50 years. The attacks are strictly unilateral, generally with the pain persistently confined to the ocular/periocular area. Most attacks are moderate to severe in intensity and burning, stabbing or electrical in character. The mean duration of paroxysms is 1 minute, with a usual range of 10 to 120 seconds (total range 5 to 250 seconds). Prominent, ipsilateral conjunctival injection and lacrimation regularly accompany the attacks. Nasal stuffiness/rhinorrhoea are frequently noted. In addition, there is subclinical forehead sweating. During attacks, there is increased intraocular pressure on the symptomatic side and swelling of the eyelids. No changes in pupil diameter have been observed. Attacks can be triggered mostly from trigeminally innervated areas, but also from the extratrigeminal territory. There are also spontaneous attacks. An irregular temporal pattern is the rule, with symptomatic periods alternating with remissions in an unpredictable fashion. During active periods, the frequency of attacks may vary from <1 attack/day to >30 attacks/hour. The attacks predominate during the daytime, nocturnal attacks being seldom reported. A SUNCT-like picture has been described in some patients with either intra-axial or extra-axial posterior fossa lesions, mostly vascular disturbances/ malformations. In the vast majority of patients, however, aetiology and pathogenesis are unknown. In SUNCT syndrome, there is a lack of persistent, convincingly beneficial effect of drugs or anaesthetic blockades that are generally effective in cluster headache, chronic paroxysmal hemicrania, trigeminal neuralgia, idiopathic stabbing headache (‘jabs and jolts syndrome’), and other headaches more faintly resembling SUNCT syndrome. Single reports have claimed that carbamazepine, lamotrigine, gabapentin, corticosteroids or surgical procedures may be of help. However, caution is recommended when assessing any therapy in a disorder such as SUNCT syndrome, in which the rather chaotic and unpredictable temporal pattern makes the assessment of any drug/therapeutic effect per se a particularly difficult matter. [ABSTRACT FROM AUTHOR]

More than 16 years after the first description of hemicrania continua (HC), its aetiology and pathogenesis remain obscure. Clinically, HC is considered a syndrome with two pivotal characteristics: (i) strictly unilateral (moderate, fluctuating, relatively longlasting) headache; and (ii) absolute response to indomethacin. HC is further characterized by some ancillary, but mostly 'negative', features such as: (iii) relative paucity of accompaniments; and (iv) lack of precipitating factors. The female preponderance is also remarkable, although not diagnostic in the solitary case. Finally, a non-specific, but remarkable feature is the temporal pattern. HC may present as a remitting or chronic (continuous) headache. In HC, unilaterality and absolute response to indomethacin are considered crucial diagnostically. Existing controversy, such as regarding atypical features, particularly the so-called 'HC resistant to indomethacin', is discussed. The nature of hemicrania with negative indomethacin response remains most unclear; it may not belong to the HC cycle at all. Accordingly, we propose that the typical clinical picture of HC, including an absolute response to indomethacin, be termed Hemicrania continua vera. More or less analogous, but indomethacin-resistant, clinical pictures can provisionally be termed Hemicrania generis incerti (of undetermined nature), provided other diagnostic possibilities have been ruled out. The differential diagnosis of HC vs. other unilateral headaches is commented on. Previous attempts at classification of HC into the group chronic daily headache (CDH) are discussed. The only acceptable 'link' of HC with the other headaches classified as CDH is the temporal pattern (which is a non-specific feature). HC is probably pathophysiologically different from the others disorders classified under CDH. Conversely, HC and chronic paroxysmal hemicrania share many common features, including the absolute response to indomethacin. HC should probably be... [ABSTRACT FROM AUTHOR]

Both SUNCT syndrome and idiopathic stabbing headache (ISH) (jabs and jolts syndrome) have to be considered when encountering shortlasting headaches. Since there are no specific tests for these headaches, the differential diagnosis depends entirely upon assessment of the clinical features. These headaches are generally easily distinguishable clinically. There seem to be symptomatic forms of SUNCT. [ABSTRACT FROM AUTHOR]

Fernández-de-las-Peñas C, Cuadrado ML, Arendt-Nielsen L, Simons DG & Pareja JA. Myofascial trigger points and sensitization: an updated pain model for tension-type headache. Cephalalgia 2007. London. ISSN 0333-1024 Present pain models for tension-type headache suggest that nociceptive inputs from peripheral tender muscles can lead to central sensitization and chronic tension-type headache (CTTH) conditions. Such models support that possible peripheral mechanisms leading to pericranial tenderness include activation or sensitization of nociceptive nerve endings by liberation of chemical mediators (bradikinin, serotonin, substance P). However, a study has found that non-specific tender points in CTTH subjects were not responsible for liberation of algogenic substances in the periphery. Assuming that liberation of algogenic substances is important, the question arising is: if tender muscle points are not the primary sites of on-going neurogenic inflammation, which structure can be responsible for liberation of chemical mediators in the periphery? A recent study has found higher levels of algogenic substances, and lower pH levels, in active myofascial trigger point (TrPs) compared with control tender points. Clinical studies have demonstrated that referred pain elicited by head and neck muscles contribute to head pain patterns in CTTH. Based on available data, an updated pain model for CTTH is proposed in which headache can at least partly be explained by referred pain from TrPs in the posterior cervical, head and shoulder muscles. In this updated pain model, TrPs would be the primary hyperalgesic zones responsible for the development of central sensitization in CTTH. [ABSTRACT FROM AUTHOR]