A migraine is a complex neurological disorder characterized by recurrent attacks of moderate to severe head pain, often throbbing or pulsating. It also brings a host of other symptoms, such as heightened sensitivity to light, sound, or touch, indicating a temporary disruption in the brain’s sensory processing. A less commonly discussed manifestation of this neurological disturbance is the profound impact a migraine can have on the senses of taste and smell. This sensory disruption confirms the disorder involves widespread brain changes extending beyond the pain centers.
Sensory Alterations: Defining Taste and Smell Changes
The combined senses of taste and smell are often grouped together as chemosensation, and both can be dramatically altered during a migraine attack. One common olfactory change is hyperosmia, which is an overwhelming sensitivity or heightened sense of smell. Odors that are normally tolerated, such as perfume, food, or cleaning products, can become intensely irritating or repulsive. This intense aversion to smells is medically termed osmophobia, and it is reported by a large percentage of people who experience migraines.
Some people also report experiencing phantosmia, where they perceive odors that are not physically present in the environment. These phantom smells can sometimes precede the onset of the migraine headache, acting as an olfactory aura. Such perceived scents are frequently unpleasant, often described as smelling smoke, burning rubber, or chemical fumes.
Taste perception can also be distorted, a condition known as dysgeusia, where people report an unpleasant or altered taste in their mouth. This taste is frequently described as metallic or sour. In less common instances, a temporary loss of the ability to taste, called ageusia, can occur. These distortions highlight how the underlying neurological event can interfere with the brain’s ability to interpret chemical signals.
Neurological Basis for Chemosensory Effects
The reason migraines disrupt taste and smell lies in the activation of specific neurological pathways within the brain and face. A primary player in this process is the trigeminal nerve (Cranial Nerve V), which transmits sensory information from the face, including the nasal and oral cavities. This nerve is involved in the pain pathway of nearly all migraine attacks, forming the trigeminovascular system.
Activation of the trigeminal nerve’s sensory endings by certain irritants or internal processes can trigger the release of Calcitonin Gene-Related Peptide (CGRP). CGRP is a potent neuropeptide that causes blood vessel dilation and initiates the inflammatory pain signals associated with migraine. Since the trigeminal nerve handles both pain and nasal sensory input, its activation can lead to headache pain and simultaneous heightened sensitivity to smells.
The sensory changes are also linked to Cortical Spreading Depression (CSD), considered the neurophysiological correlate of a migraine aura. CSD is a slowly propagating wave of intense neural activity followed by a period of suppressed activity that moves across the brain’s cortex. When this wave passes through brain regions processing sensory input, it can momentarily disrupt their function, causing temporary distortions in taste and smell perception.
Fluctuations in neurotransmitter levels, particularly serotonin, are strongly implicated in migraine pathophysiology. Serotonin receptors are present on the trigeminal nerve endings and cranial vessels. Changes in serotonin concentration influence the excitability of these nerves. A low serotonin state may facilitate the activation of the trigeminovascular pathway, contributing to the neurological hypersensitivity that results in altered chemosensation.
Symptom Timing Relative to Migraine Phases
Altered sensations of taste and smell can occur across the four phases of a migraine attack.
Prodrome Phase
During the prodrome phase, which can begin hours before the headache, a person may notice subtle changes. This is often when hyperosmia (heightened sense of smell) or osmophobia (intolerance to odors) first manifests, signaling the impending attack.
Aura Phase
If the sensory disturbance occurs during the aura phase, typically just before or concurrently with the headache, it may be perceived as phantosmia (a phantom smell). The aura is a transient neurological event, and these hallucinations result from the propagating wave of CSD passing through the sensory cortex.
Headache and Postdrome Phases
The most intense taste and smell alterations, such as metallic taste or acute osmophobia, commonly occur during the headache phase. As the attack subsides, a person enters the postdrome phase, sometimes called the “migraine hangover.” Lingering sensitivities or a continued dullness of taste may persist before the nervous system fully returns to its baseline function.