migraine headaches probably arise from a complex interaction of neuronal and vascular factors. stress, fatigue, oversleeping, fasting or missing a meal, vasoactive substance in food, caffeine, alcohol, menses, and changes in barometric pressure and altitude may trigger migrainemedications (reserpine, nitrates, oral contraceptives, and postmenopausal hormones) can also trigger migraine. although still debated, personality features of migraine sufferers include perfectionism, rigidity, and compulsiveness. menstrual migraines appear at the menstrual stage of the ovarian cycle and occur in less than 10% of women. most women with migraines experience attacks in premenstrual period and, for some women, migraine headaches recur at specific times before, after, or during the menstrual cycle.most investigation into the pathophysiology of headache has centered on migraine headache. the best evidence suggests that migraine occurs through dysfunction of trigeminovascular system. neuronal depolarization that spreads slowly across the cerebral cortex is observed during aura phase. magnesium deficiency may contribute to this state. stimulation (by an axon reflex) of trigeminal sensory fibers in the large cerebral and dural vessels causes neuropeptide release with concomitant neurogenic inflammation, vasodilation, and platelet and mast cell activation during the headache phase.sinus headache occurs when infection or blockage of the paranasal sinuses causes inflammation or distention of the sensitive sinus walls. most patients who believe they have sinus headache may actually have migraine headache. pathophysiologic mechanisms at work during migraine headache can produce prominent sinus congestion.although a number of medications can cause headache as a side effect, issues discussed here relate to overuse (rebound) and withdrawal of agents used for analgesia. medication-overuse headaches are a challenging are for clinicians. agents associated with these headaches are acetaminophen, aspirin, caffeine, triptans, opioids, butalbital, and ergotamine formulations. medication-overuse headaches are usually associated with frequent use (more than twice weekly) for 3 moths or longer, and occur within hours of stopping the agent; re-administation provides relief. symptomatology shifts from the baseline headache type to a nearly continuous headache, particularly noticeable on awakening. this continuous headache may be punctuated by periodic headaches of the baseline type; some patients note an increased frequency of their baseline headache type. when medication-overuse headache is suspected, use of offending agents(s) shouls be tapered and subsequently eliminated. most often, this should be done with medical supervision, because use of prescription therapies may be needed to combat the increased headaches that temporarily ensue during the days to weeks of the withdrawal period.

the best evidence suggests that migraine occurs through dysfunction of trigeminovascular system. neuronal depolarization that spreads slowly across the cerebral cortex is observed during aura phase. magnesium deficiency may contribute to this state. stimulation (by an axon reflex) of trigeminal sensory fibers in the large cerebral and dural vessels causes neuropeptide release with concomitant neurogenic inflammation, vasodilation, and platelet and mast cell activation during the headache phase.

sinus headache occurs when infection or blockage of the paranasal sinuses causes inflammation or distention of the sensitive sinus walls. most patients who believe they have sinus headache may actually have migraine headache. pathophysiologic mechanisms at work during migraine headache can produce prominent sinus congestion.

sakit kepala sinus terjadi ketika infeksi atau penyumbatan pada sinus paranasal menyebabkan peradangan atau distensi dinding sinus sensitif. Mekanisme patofisiologis di tempat kerja selama migrain dapat menghasilkan kemacetan sinus menonjol.meskipun sejumlah obat dapat menyebabkan sakit kepala sebagai efek samping, masalah yang dibahas di sini berhubungan dengan berlebihan (Rebound) dan penarikan agen yang digunakan untuk analgesia. agen terkait dengan sakit kepala ini acetaminophen, aspirin, kafein, triptans, opioid, butalbital, dan formulasi ergotamine. sakit kepala obat-berlebihan biasanya berhubungan dengan sering digunakan (lebih dari dua kali seminggu) untuk 3 bulan atau lebih, dan terjadi beberapa jam setelah menghentikan agen; kembali Administation menyediakan bantuan. pergeseran simtomatologi dari jenis sakit kepala dasar untuk sakit kepala hampir terus menerus, terutama terlihat pada kebangkitan. sakit kepala terus menerus ini dapat diselingi oleh sakit kepala periodik dari jenis dasar; beberapa pasien mencatat peningkatan frekuensi dasar jenis sakit kepala mereka. paling sering, ini harus dilakukan dengan pengawasan medis, karena penggunaan terapi resep mungkin diperlukan untuk memerangi meningkatnya sakit kepala yang sementara terjadi selama beberapa hari sampai minggu periode penarikan.