Avoid or seek light - a randomized crossover fMRI study investigating opposing treatment strategies for photophobia in migraine.

BACKGROUND: Photophobia, the aberrantly increased sensitivity to light, is a common symptom in migraine patients and light discomfort is frequently found as a trigger for migraine attacks. In behavioral studies, planned exposure to light was found to reduce headache in migraine patients with photophobia, potentially by increasing habituation to this migraine trigger. Here, we aimed to elucidate neurophysiological mechanisms of light exposure versus light deprivation in migraine patients using functional magnetic resonance imaging (fMRI). METHODS: Ten migraine patients (9 female, age = 28.70 ± 8.18 years) and 11 healthy controls (9 female, age = 23.73 ± 2.24 years) spent one hour on 7 consecutive days exposed to flashing light (Flash) or darkness (Dark) using a crossover design with a wash-out period of 3 months. Study participants kept a diary including items on interictal and ictal photophobia, presence and severity of headache 7 days before, during and 7 days after the interventions. One week before and one day after both interventions, fMRI using flickering light in a block design was applied. Functional activation was analyzed at whole-brain level and habituation of the visual cortex (V1) was modeled with the initial amplitude estimate and the corrected habituation slope. RESULTS: Mean interictal photophobia decreased after both interventions, but differences relative to the baseline did not survive correction for multiple comparisons. At baseline, flickering light induced activation in V1 was higher in the patients compared to the controls, but activation normalized after the Flash and the Dark interventions. V1 habituation indices correlated with headache frequency, headache severity and ictal photophobia. In the Flash condition, the individual change of headache frequency relative to the baseline corresponded almost perfectly to the change of the habituation slope compared to the baseline. CONCLUSIONS: On average, light exposure did not lead to symptom relief, potentially due to the short duration of the intervention and the high variability of the patients' responses to the intervention. However, the strong relationship between visual cortex habituation and headache symptoms and its modulation by light exposure might shed light on the neurophysiological basis of exposure treatment effects. TRIAL REGISTRATION: NCT05369910 (05/06/2022, retrospectively registered).

Blepharospasm With Photophobia Secondary to Midbrain Tuberculoma and Thalamic Infarct.

INTRODUCTION: Blepharospasm is a type of focal dystonia and categorized into primary and secondary forms, based on whether or not a cause can be established. Secondary blepharospasm is uncommon and can be associated with underlying brain lesions. Photophobia is a prominent complaint in blepharospasm patients. We are reporting a case of secondary blepharospasm with photophobia in a patient who had underlying midbrain tuberculoma and thalamic infarcts. This type of presentation has not been reported to the best of our knowledge. CASE REPORT: A 26-year-old man presented to us with the complaint of increased blinking and involuntary closure of both eyes for 1 year. He had a past history of tubercular meningitis 16 years back when he presented with bilateral ptosis, left up gaze palsy and right hemiparesis suggestive of Weber syndrome. His magnetic resonance images of the brain were suggestive of multiple intracranial tuberculomas, thalamic infarcts, and noncommunicating hydrocephalus. Following treatment he recovered significantly with no residual neurological deficit except mild bilateral ptosis. His recent magnetic resonance images of the brain was suggestive of calcified granuloma in the midbrain and chronic left thalamic lacunar infarcts. He was treated with injection Onabotulinum toxin and his symptoms improved significantly. CONCLUSIONS: Our patient had tuberculoma in the midbrain and chronic infarcts in the thalamus, and both lesions may cause blepharospasm and photophobia independently, so it is difficult to ascertain the causative lesion in our patient. However, it is possible that these heterogenous lesions are all part of a single functionally connected brain network and further studies are required to confirm this hypothesis.

Blue light activates pulvinar nuclei in longstanding idiopathic photophobia: A case report.

Numerous pathologies can contribute to photophobia. When considering light transduction alone, photophobia may be triggered through melanopsin pathways (non-image forming), rod and cone pathways (image-forming), or some combination of the two. We evaluated a 39 year old female patient with longstanding idiopathic photophobia that was exacerbated by blue light, and tested her by presenting visual stimuli in an event-related fMRI experiment. Analysis showed significantly greater activation in bilateral pulvinar nuclei, associated with the melanopsin intrinsically photosensitive retinal ganglion cell (ipRGC) visual pathway, and their activation is consistent with the patient's report that blue light differentially evoked photophobia. This appears to be the first demonstration of functional activation of the ipRGC pathway during photophobia in a patient.

The Spectrum of Vestibular Migraine: Clinical Features, Triggers, and Examination Findings.

OBJECTIVE: To assess the ictal symptoms, interictal symptoms, psychiatric comorbidities, and interictal neuro-otologic examination findings in vestibular migraine (VM). METHODS: Retrospective chart review of 491 patients seen from August 2014 until March 2018 at a tertiary neurology referral center for vestibular disorders to identify patients fulfilling the 2012 VM criteria. RESULTS: One hundred and thirty-one patients (105 women) were identified. Mean age of VM onset was 44.3 (±13.7) years. Preceding the onset of vestibular symptoms, most had migraine (57.3%) and motion sickness (61.1%). It was common to have a family history of migraine (50.8%) and episodic vestibular symptoms (28.1%). Common ictal symptoms were triggered (visually induced and head-motion) and spontaneous vertigo, accompanied by photophobia and phonophobia (118/131 [90.1%] patients), nausea (105/131 [80.2%] patients), aural symptoms (79/131 [60.3%] patients), and headache (65/131 [49.6%] patients). Interictally, many experienced visually induced (116/131 [88.6%] patients), head-motion (86/131 [65.6%] patients), and persistent (67/131 [51.1%] patients) dizziness. Psychiatric comorbidities include anxiety (92/131 [70.2%] patients), depression (53/131 [40.5%] patients), insomnia (38/131 [29.0%] patients), phobic disorders (15/131 [11.5%] patients), and psychogenic disorders (11/131 [8.4%] patients). Common triggers were stress (52/131 [39.7%] patients), bright lights (35/131 [26.7%] patients), weather changes (34/131 [26.0%] patients), and sleep deprivation (34/131 [26.0%] patients). Interictal neuro-otologic examination was abnormal in 56/131 (42.7%), usually hyperventilation-induced, head-shaking-induced, vibration-induced, and positional nystagmus. The most common balance-test finding was impaired sharpened Romberg's test (22/130 [16.9%] patients). CONCLUSIONS: In this single center study, we found that VM typically affects women in their 40s, with a personal and family history of migraine. Typical ictal symptoms were triggered and spontaneous vertigo, associated with photophobia and phonophobia, nausea, aural symptoms, and headache. Interictal vestibular symptoms, comorbid psychiatric disorders, and non-specific interictal neuro-otologic findings were common.

Case Report: Ocular Gnathostomiasis in Venezuela Most Likely Acquired in Texas.

A 69-year-old male dentist in Caracas, Venezuela, was referred to our Cornea Clinic with a history of pain, photophobia, and blurred vision on his left eye. Routine biomicroscopic examination with a slit lamp showed a worm in the corneal stroma of his left eye. The worm was surgically removed and was identified morphologically as Gnathostoma binucleatum.

A PET study of photophobia during spontaneous migraine attacks.

BACKGROUND: Photophobia is an abnormal sensitivity to light experienced by migraineurs during attacks. The pathophysiology of photophobia is poorly understood. Nevertheless, 2 facts appear to have a link with photophobia: visual cortex hyperexcitability on the one hand and interactions between visual pathway and trigeminal nociception on the other. METHODS: We used H(2)(15)O PET to study photophobia induced by continuous luminous stimulation covering the whole visual field in 8 migraineurs during spontaneous migraine attacks, after headache relief by sumatriptan and during attack-free interval. The intensity of the luminous stimulation provoking photophobia with subsequent headache enhancement was specifically determined for each patient. RESULTS: We found that low luminous stimulation (median of 240 Cd/m(2)) activated the visual cortex during migraine attacks and after headache relief but not during the attack-free interval. The visual cortex activation was statistically stronger during migraine headache than after pain relief. CONCLUSION: These findings suggest that ictal photophobia is linked with a visual cortex hyperexcitability. The mechanism of this cortical hyperexcitability could not be explained only by trigeminal nociception because it persisted after headache relief. We hypothesize that modulation of cortical excitability during migraine attack could be under brainstem nuclei control.

Photophobia in migraine: an interictal PET study of cortical hyperexcitability and its modulation by pain.

OBJECTIVE: Photophobia is an abnormal sensitivity to light experienced by migraineurs and is perhaps caused by cortical hyperexcitability. In clinical studies, an inter-relation between light perception and trigeminal nociception has been demonstrated in migraineurs but not in controls. The purpose of the study was to verify this interaction by functional imaging. METHODS: The authors used H(2)O(15) positron emitting tomography (PET) to study the cortical responses of seven migraineurs between attacks and the responses of seven matched control subjects to luminous stimulations at three luminance intensities: 0, 600 and 1800 Cd/m(2). All three intensities were both with and without concomitant trigeminal pain stimulation. In order to facilitate habituation, the stimulations were started 30 s before PET acquisitions. RESULTS: When no concomitant pain stimulation was applied, luminous stimulations activated the visual cortex bilaterally in migraineurs (specifically in the cuneus, lingual gyrus and posterior cingulate cortex) but not in controls. Concomitant pain stimulation allowed visual cortex activation in control subjects and potentiated its activation in migraineurs. These activations by luminous stimulations were luminance-intensity-dependent in both groups. Concomitant stimulation by pain was associated with activation of the posterior parietal cortex (BA7) in migraineurs and controls. INTERPRETATION: The study shows the lack of habituation and/or cortical hyperexcitability to light in migraineurs. Moreover, the activation by light of several visual cortex areas (including the primary visual cortex) was potentiated by trigeminal pain, demonstrating multisensory integration in these areas.

Photophobia as the visual manifestation of chiasmal compression by unruptured anterior communicating artery aneurysm. Case report.

A 37-year-old woman presented with photophobia without visual loss associated with chiasmal compression by an unruptured anterior communicating artery (AcomA) aneurysm. She had suffered progressive photophobia for one year. Neuroimaging indicated an AcomA aneurysm attached to the chiasm. Photophobia was resolved following clipping of the aneurysm. AcomA aneurysm should be considered in patients who experience photophobia without visual loss.