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Introduction: Migraine is a neurovascular disorder characterized by recurrent unilateral headaches accompanied by nausea,
vomiting, photophobia and phonophobia. Migraine headache is associated with trigeminal nerve activation and calcitonin gene
-related peptide (CGRP) release from the trigeminovascular system. Various factors have been identified as being migraine
triggers, including foods, stress, hormones, sensory stimuli, and so on. Individuals with migraine are often aware of the things
that serve as triggers for them, since part of migraine management is avoidance of triggers. One of factors on the onset of
migraine is olfactory sensory. This is review article to examine the relationship between headaches and smell disturbance.
And the psychological effects of odors are in this group. Most common causes of smell disturbance are nasal and sinus disease,
upper respiratory infection and head trauma. Smell or taste dysfunction can have a significant impact on quality of life. In
general, the olfactory system regenerates poorly after a head injury. Most patients who recover smell function subsequent to
head trauma do so within 12 weeks of injury. Olfactory dysfunction in some people as loss of smell sense, and in some one the
psychological impact of an increased sense of smell, which affect their quality of life.
Anatomy and Physiology: The human sense of smell depends on the functioning of not only cranial nerve I (olfactory nerve)
but also portions of cranial nerve V (trigeminal nerve). Smell receptors are located within the olfactory neuroepithelium, a
region of tissue found over the cribiform plate, the superior septum and a segment of the superior turbinate. The free nerve
endings of cranial nerve V are located diffusely throughout the nasal respiratory epithelium. The axons (C- and A -delta fibers)
project to the trigeminal sensory nucleus ansl to the spinal, principal and mesencephalic trigeminal nuclei. Nociceptive afferents
descend in the trigeminal tract and terminate in the spinal nucleus .Trigeminal information is relayed to the amygdala from
the trigeminal sensory nuclei via the lateral parabranchial complex. It must be noted that electrophysiological data indicate
that an area of increased trigeminal chemo sensitivity might be located at the anterior third of the septum. Indeed, most
odorant molecules have the propensity to simultaneously stimulate olfactory and trigeminal systems in the nasal cavity. The
trigeminal system provides an important pain -transmitting link from the cranial vasculature to the CNS. In humans, unilateral
stimulation of the trigeminal ganglion results in increased bilateral cortical blood flow, slightly more on the stimulated than
on the contralateral site. This may provide the anatomical link between cerebral neurons and the trigeminovascular system
which is the central communication for the afferent pain to the brainstem and the central aspects of the migraine symptoms.
Several studies indicate that olfactory receptor responses to chemical stimuli can be modified by activation of the trigeminal
nerve. Also in some studies, the results have showed a significant difference in the olfactory threshold at the immediate post
-operative period. Therefore, the injured trigeminal fibers are probably associated with the increase in the olfactory threshold
after the surgery; it has been shown in normosmic subjects that trigeminal stimuli are perceived as more intense when they
were accompanied by olfactory stimulation On the other hand, in a small sample of women with congenital anosmia, nausea
and vomiting of pregnancy occurred in only 1 pregnancy, suggesting that olfaction is a highly selected trigger for nausea and
vomiting of pregnancy. The shared nausea and vomiting experience of hyperemesis gravidarum and migraine headache among
women suggests there is a common mechanism.
Conclusions: Thus, previous trigeminal activation induced an increase in olfactory sensitivity and it must be argued that both
time and intensity of stimulations probably play a role in modulating interactions.
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