RESUMO
The trigeminal autonomic cephalalgias (TACs), including cluster headache, paroxysmal hemicrania and SUNCT, are characterized by the cardinal combination of short-lasting unilateral pain and autonomic phenomena affecting the head. Hemicrania continua (HC) shares many clinical characteristics with TACs, including unilateral pain and ipsilateral autonomic features. Nevertheless, HC is separately classified in the revised International Classification of Headache Disorders (ICHD-II). Here, we describe the case of a 45-year-old man presenting an unusual concurrence of different forms of primary headaches associated with autonomic signs, including subsequently ipsilateral cluster headache, SUNCT and HC. This report supports the theory that common mechanisms could be involved in pathophysiology of different primary headache syndromes.
Assuntos
Cefaleia Histamínica/fisiopatologia , Cefaleia/fisiopatologia , Síndrome SUNCT/fisiopatologia , Cefalalgias Autonômicas do Trigêmeo/fisiopatologia , Anti-Inflamatórios não Esteroides/uso terapêutico , Anticonvulsivantes/uso terapêutico , Sistema Nervoso Autônomo/fisiopatologia , Artérias Cerebrais/inervação , Artérias Cerebrais/fisiopatologia , Cefaleia Histamínica/complicações , Cefaleia Histamínica/diagnóstico , Diagnóstico Diferencial , Cefaleia/complicações , Cefaleia/diagnóstico , Humanos , Masculino , Pessoa de Meia-Idade , Síndrome SUNCT/complicações , Síndrome SUNCT/diagnóstico , Resultado do Tratamento , Cefalalgias Autonômicas do Trigêmeo/diagnóstico , Nervo Trigêmeo/fisiopatologiaRESUMO
We explored the effects of valproate treatment on visual cortex excitability changes in migraine with aura patients. Abnormal cortical excitability has been suggested to play an important role in the etiopathogenesis of migraine; in particular, it has been suggested a failure of inhibitory circuits in migraine with aura. Valproate acts as a central GABA agonist and it is reasonable suppose that VPA could modify cortical excitability state. Phosphene threshold (PT) was assessed at baseline and after 1Hz rTMS before and after one month therapy. We found that low-frequency rTMS in drug-free migraineurs decreased PT, while the treatment with the GABA agonist valproate is able to revert the effect of 1Hz rTMS over the occipital cortex. If the paradoxical increasing of PT to 1Hz rTMS is consequent upon the deficiency of intracortical inhibitory circuits in migraine, it seems reasonable to suppose that the effect of valproate is due to a recovery of activity of these circuits.