Turn Down the Lights! You Are Giving Me a Headache!
Turn Down the Lights! You Are Giving Me a Headache!
Abstract & Commentary
By Dara Jamieson, MD, Associate Professor of Clinical Neurology, Weill Cornell Medical College. Dr. Jamieson reports she is a retained consultant for Boehringer Ingelheim, Merck, and Ortho-McNeil, and is on the speakers bureau for Boehringer Ingelheim.
Synopsis: Light-exacerbated pain occurring during migraine headaches is associated with increased cerebral blood flow in the visual cortex. This activation of retinal ganglion cells by light, present even in blind migraineurs, occurs through posterior thalamic connections.
Sources: Denuelle M, Boulloche N, Payoux P, et al. A PET study of photophobia during spontaneous migraine attacks. Neurology 2011;76:213-218. Brennan, KC. Turn down the lights! An irritable occipital cortex in migraine without aura. Neurology 2011;76:206-207. Burstein R, et al. A neural mechanism for exacerbation of headache by light. Nature Neurosci 2010;13:239-245.
Abnormal neuronal activation in the susceptible brain produces the symptoms of migraine headaches, which include pain as well as sensitivity to movement, light, sound, and smell. Photophobia can be a particularly isolating symptom requiring retreat to a dark environment to avoid exacerbation of the headache pain. Patients with a history of migraine-associated photophobia often wear sunglasses and avoid bright light, even between headaches. Theories of migraine pathophysiology should explain how light can make the headache pain more severe and why migraineurs are disturbed by glare between headaches.
Denuelle et al hypothesized that photophobia during a migraine attack is linked with visual cortex hyperexcitability and trigeminal nociception. In their study, an increasing luminous stimulation was applied to the whole visual field in eight migraineurs, until they experienced photophobia and worsening of headache pain during their migraine attacks. The same luminous stimulation was applied during attack-free intervals as well as after migraine pain relief by a subcutaneous injection of sumatriptan. Functional brain imaging by H2 15O PET in patients with and without headache, and after their headache treatment, was used to measure regional cerebral blood flow (rCBF), which is thought to be highly correlated to synaptic activity. During migraine attacks, luminous stimulation induced activation of the primary visual cortex. After headache pain relief with an injection of sumatriptan, the same luminous stimulation also induced activation of the visual cortex, although the treated patients did not report pain or photophobia. The visual cortex was not activated during the attack-free periods when the patients were stimulated with exactly the same luminous stimulation that had been shown to induce photophobia during a migraine attack. Light-induced activation of rCBF was statistically stronger bilaterally in the visual cortex during migraine headache than after headache relief or during attack-free interval. The results of this study indicate that there is interaction between hyperexcitability of cortical visual pathways and the trigeminal nerve pathways with migraine headaches with photophobia. The data strengthen the hypothesis that modulation of cortical excitability during migraine attack is under cortical and brainstem nuclei control.
Burstein et al found that exacerbation of migraine headache pain by light was preserved in blind individuals who could sense light, even though they had severe degeneration of rod and cone photoreceptors. However, the intensity of headaches in blind individuals with enucleation or severe optic nerve damage was unaffected by light, suggesting that migraine-associated photophobia depends on signals relayed from the retina to the brain via the optic nerve. Using single-unit recording and neural tract tracing in the rat, they identified neurons in the posterior thalamus whose activity was distinctly modulated by light and whose axons projected extensively across layers I-V of somatosensory, visual, and associative cortices. The authors proposed that photoregulation of migraine headache is exerted by a non-image-forming retinal pathway that modulates the activity of thalamocortical neurons.
Commentary
Recent research on the pathophysiology of photophobia buttresses the hypothesis that migraine and its accompanying symptoms are based on vulnerability of specific sets of cortical, diencephalic, and brainstem neurons. Light during a migraine modulates the activity of a subset of trigeminovascular thalamic neurons that receive input from the retina and project to multiple cortical areas. Photophobia during a migraine attack induces visual cortex hyperexcitability, linked to trigeminal nociception. The occipital cortex responds differently to light during a migraine attack compared to between attacks in patients who experience photophobia with their migraine headaches. This persistent disruption in neuronal response indicates that cortical changes remain even after elimination of the migraine pain, removing the symptom but not the cause. However, prominent photosensitivity in migraineurs between headaches, like many aspects of this complex and fascinating neurovascular disorder, still remains unexplained.
Light-exacerbated pain occurring during migraine headaches is associated with increased cerebral blood flow in the visual cortex. This activation of retinal ganglion cells by light, present even in blind migraineurs, occurs through posterior thalamic connections.Subscribe Now for Access
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