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 migraine
medications (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.