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Photophobia in neurologic disorders

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Abstract

Photophobia is a common symptom seen in many neurologic disorders, however, its pathophysiology remains unclear. Even the term is ambiguous. In this paper, we review the epidemiology and clinical manifestations of photophobia in neurological disorders, including primary headache, blepharospasm, progressive supranuclear palsy, and traumatic brain injury, discuss the definition, etiology and pathogenesis, and summarize practical methods of diagnosis and treatment.
R E V I E W Open Access
Photophobia in neurologic disorders
Yiwen Wu and Mark Hallett
*
Abstract
Photophobia is a common symptom seen in many neurologic disorders, however, its pathophysiology remains
unclear. Even the term is ambiguous. In this paper, we review the epidemiology and clinical manifestations of
photophobia in neurological disorders, including primary headache, blepharospasm, progressive supranuclear palsy,
and traumatic brain injury, discuss the definition, etiology and pathogenesis, and summarize practical methods of
diagnosis and treatment.
Keywords: Photophobia, Migraine, Blepharospasm, Progressive supranuclear palsy, Traumatic brain injury, Melanopsin
Background
Photophobia refers to a sensory disturbance provoked by
light. The term photophobia, derived from 2 Greek words,
photo meaning lightand phobia meaning fear, literally
means fear of light. Patients may develop photophobia
as a result of several different medical conditions, related
to primary eye conditions, central nervous system (CNS)
disorders and psychiatric disorders. Since the original lit-
erature described the manifestations of photophobia [1],
many developments have taken place that makes it pos-
sible to establish a more precise picture of photophobia.
In this paper, we will review its presence in neurological
disorders, focusing on the definition, epidemiology, eti-
ology, clinical manifestations, pathogenesis, diagnosis and
treatment.
Definition
In 1934, photophobia was first described and defined by
Lebensohn as exposure of the eye to light definitely in-
duces or exacerbates pain[1]. This definition emphasized
that the core character is pain, but did not specify what
kind of light (e.g., bright light or dim light) caused the
symptom. In fact, photophobia is heterogeneous. Descrip-
tions of photophobia vary among patients, and some of
the heterogeneity comes from the different disorders that
manifest this symptom. For example, some patients with
migraine will deny that pain is a part of the experience at
all but just prefer to be in a darkened room [2]. Thus,
some researchers believe that photophobia involves not
only the pain pathway, but also a limbic system pathway
that superimposes an emotional discomfort leading to
avoidance of light [3, 4]. Due to the evidence from basic
research and the limitations of the earlier definition, Fine
and Digre used the term photo-oculodyniato describe
the pain or discomfort in the eye arising from a light
source that should not be painful or discomforting under
ordinary circumstances [5]. The term photophobiais
defined by Digre and Brennan as a sensory state in which
light causes discomfort in the eye or head; it may also
cause an avoidance reaction without overt pain [6].
Although there is no consensus definition of photophobia
in the field, this definition proposed by Digre and Brennan
seems more encompassing and descriptive.
Etiologic classification
The etiology of photophobia can be subdivided in four
main sections: (1) Orbital and visual pathway pathology
(e.g., ocular disorders, optic nerve and chiasm problems);
(2) Neurological disorders (e.g., primary headache, bleph-
arospasm, traumatic brain injury), (3) Psychiatric disorders
(e.g., agoraphobia, anxiety disorder, depression.); and (4)
Drug-induced photophobia (e.g., barbiturates, benzodiaze-
pines, haloperidol.)
A number of neurologic conditions are associated
with photophobia (Table 1). The most common neuro-
logical conditions encountered are primary headaches,
benign essential blepharospasm (BEB), Progressive
supranuclear palsy (PSP) and traumatic brain injury
(TBI) [7]. This review will focus on photophobia
present in these conditions.
* Correspondence: hallettm@ninds.nih.gov
Human Motor Control Section, National Institute of Neurological Disorders
and Stroke, National Institutes of Health, 10 Center Drive MSC 1428, Building
10, Room 7D37, Bethesda, MD 20892, USA
© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Wu and Hallett Translational Neurodegeneration (2017) 6:26
DOI 10.1186/s40035-017-0095-3
Photophobia in neurologic disorders
Primary headaches
Primary headaches include migraine, tension-type head-
ache (TTH), cluster headache and other trigeminal auto-
nomic cephalalgias, and other less frequent headache
types according to the International Classification of
Headache Disorders, 3rd edition (ICHD-III) [8]. Photo-
phobia is a common and debilitating symptom often
present in migraine and other primary headaches. In a
population-based epidemiological study of primary head-
ache in Croatia in 2014 (n= 2350), up to 40% of patients
reported the symptom [9].
Photophobia is noted in 80%90% of patients with mi-
graine, which is higher than that in other primary head-
aches [10, 11]. Patients with migraine experience the
symptom both during and between the attacks [12], but it
occurs more during the attack than after [13]. Recent
research has shown a clear association between migraine-
related allodynia and photophobia only in chronic
migraineurs [14, 15]. These findings suggest that light
stimulation may contribute to central sensitization of
pain pathways in migraineurs, possibly contributing to
progression into chronic forms. Although the exact
prevalence of photophobia in TTH and cluster head-
ache patients is not precisely known, clinical studies
showed that subjects with TTH and with cluster head-
aches had more light sensitivity than controls [16, 17].
One study showed that patients with TTH had lower
discomfort thresholds to white light than controls, but
had higher thresholds than patients with migraine. It
may explain why photophobia is more common in pa-
tients with migraine than in patients with TTH [18],
and indicates that light sensitivity may be present, but
not noticeable to every patient with TTH. Whether the
symptom can be unilateral or not still remains contro-
versial. Experimental evidence showed that photopho-
bia is bilateral even when the headache is unilateral in
primary headaches [13, 17]. On the other hand, unilat-
eral photophobia has been reported with cluster head-
ache, hemicrania continua, and other trigeminal
autonomic cephalagias [19, 20]. A prospective clinical
study of short-lasting unilateral neuralgiform headache at-
tacks with conjunctival injection and tearing or cranial
autonomic features showed that unilateral photophobia is
present in more than 40% of patients [21]. More work is
necessary to describe the exact clinical features (bilateral
or unilateral) of photophobia by using a more detailed
questionnaire.
Blepharospasm
Blepharospasm, often called benign essential blepharo-
spasm (BEB), is one of the most common focal dysto-
nias. It is characterized by involuntary orbicularis oculi
muscle spasms that are usually bilateral, synchronous,
and symmetrical [22]. Photophobia is a prominent com-
plaint of patients with blepharospasm. One study dem-
onstrated that patients with blepharospasm were as light
sensitive as patients with migraine between the migraine
attacks, and that both groups were more light sensitive
than controls [23]. In a survey of 316 blepharospasm pa-
tients, 94% reported light sensitivity; ambient lighting
could provoke spasms about half of the time, but bright
light provoked spasms almost all of the time [24]. An-
other study comprising 240 BEB patients showed that
photophobia was present in 25% of patients prior to the
onset of the blepharospasm, and up to 74% patients re-
ported the photophobia at the time of the neurological
examination [25]. Furthermore, photophobia is consid-
ered the second most common factor which can impact
BEB patientsquality of daily life. The mechanism of
photophobia is still elusive. A case-control study studied
the effect of photochromatic modulation with tinted
lenses on the sensory symptoms of photophobia in bleph-
arospasm patients [26]. The results indicated that wave-
length of light exposure may influence the symptoms of
photophobia in addition to the actual light intensity. In
contrast, another study found that the relevant feature for
photophobia is the light intensity and not the wavelength
at least as altered by the FL-41 lens [23]. Whether symp-
toms are better relieved by reducing light in a specific re-
gion of the spectrum or just reducing the net flux is still
controversial.
Progressive supranuclear palsy
Progressive supranuclear palsy (PSP), previously referred
to as Steele Richardson Olszewski syndrome, is a Parkin-
sonian Syndrome. Characteristic features of PSP include
vertical supranuclear gaze palsy and postural instability
with falls. A clinical cohort study of 187 patients with PSP
showed that photophobia occurred in 43% of patients
[27]. Another prospective study showed that photophobia
is significantly more frequent in clinically diagnosed PSP
than corticobasal degeneration (CBD) (100% vs 18%,
p= 0.0002) [28]. These results suggest that the presence
Table 1 Neurological conditions associated with photophobia
Neurological Conditions
Primary headaches (most common in Migraine)
Secondary headaches
Blepharospasm
Progressive supranuclear palsy
Traumatic brain injury
Meningitis
Subarachnoid hemorrhage
Lesions of the thalamus
Wu and Hallett Translational Neurodegeneration (2017) 6:26 Page 2 of 6
of photophobia could be used to help clinicians differenti-
ate the two diseases.
Traumatic brain injury
Traumatic brain injury (TBI) can manifest with visual
dysfunction including deficits in accommodation, ver-
gence movements, versions, and field of vision as well
increased photosensitivity [29, 30]. Photophobia is one
of the most common visual complaints [31]. Studies of
TBI have frequently addressed the issue of photosensi-
tivity and its prevalence. One study showed a preva-
lence of 50% in patients compared with 10% health
controls [32]. Photosensitivity does not only occur in
the acute phase of brain injury, but also in the chronic
phase. However, it is still unclear if photophobia is a
primary or secondary symptom of the brain injury. Fur-
thermore, studies revealed that over years, about half of
the patients reported reduced photosensitivity (i.e., 10%
in the 1st year plus 40% after the 1st year), while 42%
remained the same, 3% increased and 5% waxed and
waned [33]. The decrease in photosensitivity may be a
result of neural repair, neural adaptation and/or com-
pensatory mechanisms.
Mechanism of photophobia
Since light is the cardinal stimulus for photophobia, pho-
toreceptors must be involved. There are at least five differ-
ent types of photoreceptors in humans: three kinds of
cones, rods and ipRGCs. Rods and cones in the outer
retina are the predominant photoreceptor cells of the
mammalian retina. Their high temporal and spatial sensi-
tivity to light forms the basis of image-forming vision. The
intrinsically photosensitive retinal ganglion cells (ipRGC),
which contain the melanopsin photopigment (HUGO
gene symbol OPN4), have been identified in recent years
[34]. The ipRGC cells are atypical retinal photoreceptors
separate from classical rod and cone photoreceptors. Sev-
eral studies demonstrated that ipRGC play an important
role in non-image-forming light effects [35]. The ipRGC
cells send their axons to the suprachiasmatic nucleus and
the Edinger-Westphal nucleus. In the suprachiasmatic nu-
cleus, these cells entrain circadian rhythms [36]. In the
Edinger-Westphal nucleus, they control the pupillary light
reflex [34, 36, 37]. Furthermore, evidence accumulating
from animal models shows that ipRGCs are involved in
photophobia of rod- and cone deficient mice. [38, 39]. In
humans, ipRGCs were implicated in photophobia since
migraine patients who became blind from a complete lack
of rod and cone function still experience photoallodynia
compared with patients with enucleated eyes [40]. Mela-
nopsin, the ipRGC photopigment, has peak sensitivity at
480 nm. Using the photic blink reflex, one study tried to
objectively quantify the ocular sensitivity to red (640 nm)
and blue (485 nm) light in patients with light sensitivity
and normal subjects. The data demonstrated an increased
photic blink reflex to blue light as opposed to red light in
light-sensitive patients [41]. These results suggest that the
melanopsin signaling system may control light aversion
and the ipRGC may be the most important photoreceptor
cell in the pathophysiological mechanism of photophobia.
Although the discovery of the ipRGC cells appear to
make an advancement in understanding the mechanism
of photophobia, how light functions as a pain stimulus
remains elusive. Increasing evidence demonstrates that
at least 3 pathways can transmit this signal to the brain.
The first pathway was described by Okamoto et al. [42].
They investigated the pattern of neuronal activation in
the caudal brainstem after bright light stimulation using
quantitative Fos-like immunoreactivity in anesthetized
rats. The results showed that light activated the trigeminal
brainstem neurons through photoreceptors in the retina
(whether rod, cone or ipRGC), which in turn evoked ocu-
lar vasodilation and activation of pain-sensing neurons on
blood vessels [42]. The second pathway for photophobia is
a direct connection between the ipRGC cells and thalamic
nuclei, which are associated with somatic sensation and
pain [43]. The discovery of this second pathway is particu-
larly significant as the thalamus is an important center for
sensory integration, and has important connections to
somatosensory centers of the cortex [43]. A third pathway
is suggested that does not involve the optic nerve. The
ipRGCs and/or ipRGC-like melanopsin-containing neu-
rons in the iris can contribute to the trigeminal afferents
bypassing the optic nerve [44, 45].
Neuropeptides that enhance synaptic transmission may
play a role in photophobia at multiple levels of the visual
and trigeminal pathways. Two particular candidates are
the calcitonin gene-related peptide (CGRP) and pituitary
adenylate cyclase-activating polypeptide (PACAP), both of
which may play a role in migraine attacks in migraineurs
[46]. These multifunctional peptides are widely distributed
in the nervous system and in addition to their vascular ac-
tions; they are both implicated in modulating nociception.
Pre-clinical studies have linked both neuropeptides to
photophobia. Animal models showed that mice with a
gain-of-function mutation of CGRP receptor, exhibit light
avoiding behavior when they receive injections of calcium
gene-related peptide [47]. Mice lacking PACAP do not de-
velop nitroglycerin-induced light aversion.
Diagnosis and evaluation of photophobia
Generally, the diagnosis of photophobia is established in
the history, along with neurologic and neuro-ophthalmic
examination. However, answering the usual question,
does light bother you,with a noshould not be taken
as indicative of the absence of photophobia [48]. Further
questioning with the use of more detailed closed-ended
questions is needed to detect the symptom and to evaluate
Wu and Hallett Translational Neurodegeneration (2017) 6:26 Page 3 of 6
the severity. Assessment tools for photophobia have been
sparse. Bossini et al. developed and validated a photopho-
bia questionnaire, a self-assessment tool established in
Italian populations [49] (Table 2). It consists of 16 items
investigating psychopathological traits and behavioral sen-
sitivity to light. The questions try to identify specifically
both behaviors that actively avoid light, termed photopho-
bia (items 2, 6, 7, 9, 10, 12, 13, 14) and that actively search
light, described as photophilia (items 1, 3, 4, 5, 8, 11, 15,
16), which have been identified as relevant to the Mediter-
ranean population in clinical practice. For each item the
patient may respond in a dichotomous way (yes or no).
Affirmative answers are rated as 1 and negative ones as 0,
except for item 5 where the scores are reversed (yes = 0,
no = 1). Two scores are obtained by the simple sum of
each item divided by the number of items for each dimen-
sion (8 for photophobia and 8 for photophilia); therefore,
two scores ranging from 0 to 1 identify photophobic and
photophilic behavior, respectively). Recently, Choi et al.
validated a questionnaire in order to assess light aversion
behavior in a reproducible way (Table 3) [50]. Their
questionnaire seems to be a useful method for detecting
photophobia in patients with migraine in Korea. Although
this questionnaire has not been validated in populations
outside Korea, it may be useful to clinical researchers who
are trying to better understand photophobia.
Treatment
Since the mechanism of the photophobia is still not
clear, the pharmacotherapeutic treatment remains un-
known. There is only little evidence that shows that the
systemic medication can relieve the photophobia itself,
but treating the underlying conditions may improve the
associated photophobia, such as migraine preventive or
specific medication (e.g., beta-blockers, calcium channel
blockers, anti-convulsants, CGRP-P) for patients with
migraine associated photophobia [51, 52, 53].
Botulinum neurotoxin (BoNT) is the treatment of
choice for blepharospasm and it also has some efficacy
in migraine headache. However, there is limited informa-
tion for the effect of BoNT on photophobia. A cohort
study showed that injection of onabotulinumtoxinA is
helpful for photophobia associated with TBI [54].
However, the efficacy needs to be further explored in
well-designed studies involving a large population of
patients. More work is necessary to evaluate the efficacy
of the BoNT in the treatment of photophobia in other
conditions as well [54].
Different photoreceptors have different spectral sensitiv-
ity to light. Maximum light sensitivities of human rods
(R), S cones, M cones and L cones are 500 nm, 420 nm,
530 nm and 560 nm wavelength, respectively. The ipRGCs
exhibit their peak sensitivity at 480 nm. There is some
evidence that patients with blepharospasm reported the
Table 2 Photosensitivity Assessment Questionnaire (PAQ)
Photosensitivity Assessment Questionnaire (PAQ)
1. I prefer summer to winter because winter dreariness makes me
sad. (Phi)
2. If I could, I would be happier to go out after dusk rather than during
the day. (Pho)
3. Often in winter, Id like to go to the other hemisphere where it is
summer time. (Phi)
4. My ideal house has large windows. (Phi)
5. I like cloudy days. (Phi)
6. Sunlight is so annoying to me, that I have to wear sunglasses when I
go out. (Pho)
7. I prefer to stay at home on sunny days, even if it is not warm. (Pho)
8. I feel reborn in spring when the days start to become longer. (Phi)
9. Usually strong sunlight annoys me. (Pho)
10. I prefer rooms that are in semi-darkness. (Pho)
11. I prefer sunlight to semi-darkness. (Phi)
12. Looking at a very bright view annoys me. (Pho)
13. I cant stand light reflecting off snow. (Pho)
14. I think summer annoys me because its too bright. (Pho)
15. Sunlight is like therapy for me. (Phi)
16. I prefer walking in the sunlight if the weather is cool. (Phi)
Phi: photophilia; Pho: photophobia
These questions try to identify specifically both behaviors that actively avoid
light, termed photophobia (items 2, 6, 7, 9, 10, 12, 13, 14) and that actively
search light, described as photophilia (items 1, 3, 4, 5, 8, 11, 15, 16), which
have been identified as relevant to the Mediterranean population in clinical
practice. For each item, the patient may respond in a dichotomous way (yes or
no). Affirmative answers are rated as 1 and negative ones as 0, except for item
5 where the scores are reversed (yes = 0, no = 1). Two scores are obtained by
the simple sum of each item divided by the number of items for each
dimension (8 for photophobia and 8 for photophilia); therefore, two scores
ranging from 0 to 1 identify photophobic and photophilic
behaviors, respectively
Table 3 Photophobia questionnaire for patients with primary
headaches (English version of the questionnaire developed by
Choi et al. [51])
1 During your headache, do you feel a greater sense of
glare or dazzle in your eyes than usual by bright lights?
Yes No
2 During your headache, do flickering lights, glare, specific
colors or high contrast striped patterns bother you or
your eyes?
Yes No
3 During your headache, do you turn off the lights or draw
a curtain to avoid bright conditions?
Yes No
4 During your headache, do you have to wear sunglasses
even in normal daylight?
Yes No
5 During your headache, do bright lights hurt your eyes? Yes No
6 Is your headache worsened by bright lights? Yes No
7 Is your headache triggered by bright lights? Yes No
8 Do you have any of the above symptoms mentioned
even during your headache-free interval?
Yes No
The score ranges from 0 (no photophobia) to 8 (severe photophobia)
Wu and Hallett Translational Neurodegeneration (2017) 6:26 Page 4 of 6
best relief of photophobia with the FL-41 lens, which
blocks wavelengths around 480 nm [55]. The use of dark
sunglasses indoors must be strongly discouraged. By wear-
ing dark glasses indoors, patients are dark adapting their
photorecetors and aggravating their sensitivity to light.
These patients should be encouraged to transition to the
use of FL-41 or other tints for indoor light sensitivity [7].
Conclusions
Photophobia is a common symptom seen in many
neurologic disorders. While the underlying mechanism
of photophobia is still elusive, the discovery of ipRGCs
appears to be an advance in understanding. The cal-
cium gene-related peptide receptors (for CGRP and
PACAP)) may be potential targets in the treatment of
headache and photophobia as well. Generally, the diag-
nosis of photophobia is established upon the history,
along with neurologic and neuro-ophthalmic examination.
Since a number of common ophthalmic conditions are as-
sociated with photophobia, patients should be referred to
an ophthalmologist to rule-out or treat these conditions if
the neurologic history and examination fail to suggest a
diagnosis. Furthermore, physicians should be encouraged
to use an assessment tool of photophobia or photophilia
for detecting the symptoms. Wearing specially tinted
spectacles may provide an effective means to relieve the
photophobia.
Abbreviations
BEB: Benign essential blepharospasm; BoNT: Botulinum neurotoxin;
CBD: Corticobasal degeneration; CGRP: Calcitonin gene-related peptide;
CNS: Central nervous system; ipRGC: Intrinsically photosensitive retinal
ganglion cells; PACAP: Pituitary adenylate cyclase-activating polypeptide;
PSP: Progressive supranuclear palsy; TBI: Traumatic brain injury; TTH: Tension-
type headache
Acknowledgements
Thanks for the assistance of Lu He during the writing of the manuscript. Dr.
Hallett is supported by the NINDS Intramural Program.
Availability of data and materials
Not applicable.
Funding
The work was supported by the National Natural Science Foundation of
China (No.81200981, 81,371,407), the Innovation Program of Shanghai
Municipal Education Commission (No.13YZ026), and the Intramural Program
of the National Institute of Neurological Disorders and Stroke.
Authorscontributions
YW wrote the first draft of the manuscript, MH revised and wrote the final
edition. Both authors read and approved the final manuscript.
Ethics approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
Received: 6 May 2017 Accepted: 29 August 2017
References
1. Lebensohn JE. The nature of photophobia. Arch Ophthalmol. 1934;12:3803.
2. Selby G, Lance JW. Observations on 500 cases of migraine and allied
vascular headache. J Neurol Neurosurg Psychiatry. 1960;23:2332.
3. Ahn AH, Brennan KC. Unanswered questions in headache: so what is
photophobia, anyway? Headache. 2013;53(10):16734.
4. Hattar S, Kumar M, Park A, et al. Central projections of melanopsin-
expressing retinal ganglion cells in the mous e. J Comp Neurol. 2006;
497(3):32649.
5. Fine PG, Digre KBA. Controlled trial of regional sympatholysis in the
treatment of photo-oculodynia syndrome. J Neuroophthalmol.
1995;15(2):904.
6. Digre KB, Brennan KC. Shedding light on photophobia. J Neuroophthalmol.
2012;32(1):6881.
7. Katz BJ, Digre KB. Diagnosis, pathophysiology, and treatment of
photophobia. Surv Ophthalmol. 2016;61(4):46677.
8. The International Classification of Headache Disorders, 3rd edition (beta
version). Cephalalgia, 2013, 33(9): 629808.
9. Cvetkovic VV, Plavec D, Lovrencic-Huzjan A, et al. Prevalence and clinical
characteristics of headache in adolescents: a Croatian epidemiological study.
Cephalalgia. 2014;34(4):28997.
10. Rasmussen BK, Jensen R, Olesen JA. Population-based analysis of the diagnostic
criteria of the international headache society. Cephalalgia. 1991;11(3):12934.
11. Russell MB, Rasmussen BK, Fenger K, et al. Migraine without aura and
migraine with aura are distinct clinical entities: a study of four hundred and
eighty-four male and female migraineurs from the general population.
Cephalalgia. 1996;16(4):23945.
12. Drummond PD, Woodhouse A. Painful stimulation of the forehead increases
photophobia in migraine sufferers. Cephalalgia. 1993;13(5):3214.
13. Vanagaite J, Pareja JA, Storen O, et al. Light-induced discomfort and pain in
migraine. Cephalalgia. 1997;17(7):73341.
14. Lovati C, Mariotti C, Giani L, et al. Central sensitization in photophobic and
non-photophobic migraineurs: possible role of retino nuclear way in the
central sensitization process. Neurol Sci. 2013;34(Suppl 1):S1335.
15. Baykan B, Ekizoglu E, Karli N, et al. Characterization of Migraineurs
having allodynia: results of a large population-based study. Clin J Pain.
2016;32(7):6315.
16. Drummond PDA. Quantitative assessment of photophobia in migraine and
tension headache. Headache. 1986;26(9):4659.
17. Vingen JV, Pareja JA, Stovner LJ. Quantitative evaluation of photophobia
and phonophobia in cluster headache. Cephalalgia. 1998;18(5):2506.
18. Main A, Vlachonikolis I, Dowson A. The wavelength of light causing
photophobia in migraine and tension-type headache between attacks.
Headache. 2000;40(3):1949.
19. Irimia P, Cittadini E, Paemeleire K, et al. Unilateral photophobia or
phonophobia in migraine compared with trigeminal autonomic
cephalalgias. Cephalalgia. 2008;28(6):62630.
20. Cittadini E, Goadsby PJ. Hemicrania continua: a clinical study of 39 patients
with diagnostic implications. Brain. 2010;133(Pt 7):197386.
21. Cohen AS, Matharu MS, Goadsby PJ. Short-lasting unilateral neuralgiform
headache attacks with conjunctival injection and tearing (SUNCT) or cranial
autonomic features (SUNA)a prospective clinical study of SUNCT and
SUNA. Brain. 2006;129(Pt 10):274660.
22. Hallett M, Evinger C, Jankovic J, et al. Update on blepharospasm: report
from the BEBRF international workshop. Neurology. 2008;71(16):127582.
23. Adams WH, Digre KB, Patel BC, et al. The evaluation of light sensitivity in
benign essential blepharospasm. Am J Ophthalmol. 2006;142(1):827.
24. Judd RA, Digre KB, Warner JE, et al. Shedding light on Blepharospasm: a
patientresearcher partnership approach to assessment of photophobia and
impact on activities of daily living. Neuro-Ophthalmology. 2009;31(3):4954.
25. Peckham EL, Lopez G, Shamim EA, et al. Clinical features of patients with
Blepharospasm: a report of 240 cases. European journal of neurology the official
journal of the European Federation of Neurological. For Soc. 2011;18(3):382.
26. Herz NL, Yen MT. Modulation of sensory photophobia in essential
blepharospasm with chromatic lenses. Ophthalmology. 2005;112(12):220811.
27. Nath U, Ben-Shlomo Y, Thomson RG, et al. Clinical features and natural
history of progressive supranuclear palsy: a clinical cohort study. Neurology.
2003;60(6):9106.
Wu and Hallett Translational Neurodegeneration (2017) 6:26 Page 5 of 6
28. Cooper AD, Josephs KA. Photophobia, visual hallucinations, and REM
sleep behavior disorder in progressive supranuclear palsy and corticobasal
degeneration: a prospective study. Parkinsonism Relat Disord. 2009;15(1):5961.
29. Sihlbom C, Van DHI, Lidell ME, et al. Current treatment options in
neurology. Le J Médical Libanais the Lebanese Med J. 2004;52(52):338.
30. Kapoor N, Ciuffreda KJ. Vision disturbances following traumatic brain injury.
Curr Treat Options Neurol. 2002;4(4):27180.
31. Vos PE, Battistin L, Birbamer G, et al. EFNS guideline on mild traumatic brain
injury: report of an EFNS task force. Eur J Neurol. 2002;9(3):20719.
32. Capo-Aponte JE, Urosevich TG, Temme LA, et al. Visual dysfunctions and
symptoms during the subacute stage of blast-induced mild traumatic brain
injury. Mil Med. 2012;177(7):80413.
33. Truong JQ, Ciuffreda KJ, Han MH, et al. Photosensitivity in mild traumatic
brain injury (mTBI): a retrospective analysis. Brain Inj. 2014;28(10):12837.
34. Ksendzovsky A, Pomeraniec IJ, Zaghloul KA, et al. Clinical implications of the
melanopsin-based non-image-forming visual system. Neurology. 2017;
88(13):128290.
35. Do MT, Yau KW. Intrinsically photosensitive retinal ganglion cells. Physiol
Rev. 2010;90(4):154781.
36. Berson DM, Dunn FA, Takao M. Phototransduction by retinal ganglion cells
that set the circadian clock. Science. 2002;295(5557):10703.
37. Kawasaki A, Kardon RH. Intrinsically photosensitive retinal ganglion cells. J
Neuroophthalmol. 2007;27(3):195204.
38. Johnson J, Wu V, Donovan M, et al. Melanopsin-dependent light avoidance
in neonatal mice. Proc Natl Acad Sci U S A. 2010;107(40):173748.
39. Matynia A, Parikh S, Chen B, et al. Intrinsically photosensitive retinal
ganglion cells are the primary but not exclusive circuit for light aversion.
Exp Eye Res. 2012;105:609.
40. Noseda R, Kainz V, Jakubowski M, et al. A neural mechanism for
exacerbation of headache by light. Nat Neurosci. 2010;13(2):23945.
41. Kardon R. Melanopsin and its role in photophobia. Acta Ophthalmol. 2012;
90(Supplement s249):00.
42. Okamoto K, Thompson R, Tashiro A, et al. Bright light produces
Fos-positive neurons in caudal trigeminal brainstem. Neuroscience.
2009;160(4):85864.
43. Noseda R, Constandil L, Bourgeais L, et al. Changes of meningeal excitability
mediated by corticotrigeminal networks: a link for the endogenous
modulation of migraine pain. J Neurosci. 2010;30(43):144209.
44. Dolgonos S, Ayyala H, Evinger C. Light-induced trigeminal sensitization
without central visual pathways: another mechanism for photophobia.
Invest Ophthalmol Vis Sci. 2011;52(11):78528.
45. Xue T, Do MT, Riccio A, et al. Melanopsin signalling in mammalian iris and
retina. Nature. 2011;479(7371):6773.
46. Rossi HL, Recober A. Photophobia in primary headaches. Headache. 2015;
55(4):6004.
47. Recober A, Kaiser EA, Kuburas A, et al. Induction of multiple photophobic
behaviors in a transgenic mouse sensitized to CGRP. Neuropharmacology.
2010;58(1):15665.
48. Evans RW, Seifert T, Kailasam J, et al. The use of questions to determine the
presence of photophobia and phonophobia during migraine. Headache.
2008;48(3):3957.
49. Bossini L. Sensibilità alla luce e psicopatologia : validazione del
Questionario per la Valutazione della Fotosensibilità (QVF).
Headache. 1988;28:12434.
50. Choi JY. Oh K, Kim BJ, et al. usefulness of a photophobia questionnaire in
patients with migraine. Cephalalgia. 2009;29(9):9539.
51. Sprenger T, Goadsby PJ. Migraine pathogenesis and state of
pharmacological treatment options. BMC Med. 2009;7:71.
52. Edvinsson L, Villalon CM, MaassenVanDenBrink A. Basic mechanisms of
migraine and its acute treatment. Pharmacol Ther. 2012;136(3):31933.
53. Negro A, Lionetto L, Simmac o M, et al. CGRP receptor antagonists: an
expanding drug class for acute migraine? Expert Opin Investig Drugs.
2012;21(6):80718.
54. Yerry JA, Kuehn D, Finkel AG. Onabotulinum toxin a for the treatment of
headache in service members with a history of mild traumatic brain injury:
a cohort study. Headache. 2015;55(3):395406.
55. Blackburn MK, Lamb RD, Digre KB, et al. FL-41 tint improves blink frequency,
light sensitivity, and functional limitations in patients with benign essential
blepharospasm. Ophthalmology. 2009;116(5):9971001.
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Wu and Hallett Translational Neurodegeneration (2017) 6:26 Page 6 of 6
... When photophobia and headache occur together, their consequences are more disabling and treatments may become more difficult. Patients with headache disorders exhibit more severe and frequent photophobia than controls [2]. As reported in a large population-based cross-sectional study (n = 2350), over 40% of patients with headache disorders have suffered from photophobia [3]. ...
... In this review, we summarized photophobic characteristics of the three categories of headache disorders including: (1) primary headaches: migraine, tension-type headache (TTH), and trigeminal autonomic cephalalgias (TACs); (2) secondary headaches: headaches attributed to traumatic brain injury (TBI), meningitis, non-traumatic subarachnoid hemorrhage (SAH) and disorder of the eyes; (3) painful cranial neuropathies: trigeminal neuralgia and painful optic neuritis. We then discussed potential mechanisms for the coexistence of photophobia and headache. ...
Article
Full-text available
Photophobia is present in multiple types of headache disorders. The coexistence of photophobia and headache suggested the potential reciprocal interactions between visual and pain pathways. In this review, we summarized the photophobic characteristics in different types of headache disorders in the context of the three diagnostic categories of headache disorders: (1) primary headaches: migraine, tension-type headache, and trigeminal autonomic cephalalgias; (2) secondary headaches: headaches attributed to traumatic brain injury, meningitis, non-traumatic subarachnoid hemorrhage and disorder of the eyes; (3) painful cranial neuropathies: trigeminal neuralgia and painful optic neuritis. We then discussed potential mechanisms for the coexistence of photophobia and headache. In conclusion, the characteristics of photophobia are different among these headache disorders. The coexistence of photophobia and headache is associated with the interactions between visual and pain pathway at retina, midbrain, thalamus, hypothalamus and visual cortex. The communication between these pathways may depend on calcitonin gene-related peptide and pituitary cyclase-activating polypeptide transmission. Moreover, cortical spreading depression, an upstream trigger of headache, also plays an important role in photophobia by increased nociceptive input to the thalamus.
... Another reported symptom of traumatic brain injury is photophobia (also sometimes referred to as light sensitivity), a state of discomfort or pain in response to light that may also cause light avoidance. [5][6][7] Currently, there are no validated objective tools to quantify photophobia. Therefore, the presence of photophobia is determined almost exclusively by clinical history from patient self-report or questionnaires. ...
... Systematic and narrative reviews were also inspected for additional studies. [5][6][7][8][9][10][11][12][13][14] ...
Article
Significance: This study reports the prevalence and relative risk of photophobia in patients with traumatic brain injury (TBI). Objectives: This study aimed to conduct a systematic review and meta-analysis to determine the prevalence and relative risk of photophobia in patients with TBI. Data sources: Three databases were used for literature search: PubMed, EMBASE, and Cochrane Library. Study appraisal and synthesis methods: Publications reporting the prevalence of photophobia after TBI in patients of any age were included. A series of meta-regression analyses based on a generalized linear mixed model was performed to identify potential sources of heterogeneity in the prevalence estimates. Results: Seventy-five eligible publications were identified. The prevalence of photophobia was 30.46% (95% confidence interval [CI], 20.05 to 40.88%) at 1 week after the injury. Prevalence decreased to 19.34% (95% CI, 10.40 to 28.27%) between 1 week and 1 month after TBI and to 13.51% (95% CI, 5.77 to 21.24%) between 1 and 3 months after the injury. The rapid decrease in the prevalence of photophobia in the first 3 months after a TBI injury was significant (P < .001). Three months post-TBI, the prevalence of photophobia leveled off to a near plateau with nonsignificant variability, increasing between 3 and 6 months (17.68%; 95% CI, 9.05 to 26.32%) and decreasing between 6 and 12 months since TBI (14.85%; 95% CI, 6.80 to 22.90%). Subgroup analysis of 14 publications that contained control data showed that the estimated risk ratio for photophobia was significantly higher in the TBI than in the control group during the entire 12 months after TBI. Conclusions and implications of key findings: This study demonstrates that photophobia is a frequent complaint after TBI, which largely resolves for many individuals within 3 months after the injury. For some patients, however, photophobia can last up to 12 months and possibly longer. Developing an objective quantitative methodology for measuring photophobia, validating a dedicated photophobia questionnaire, and having a specific photophobia International Classification of Diseases, Tenth Revision code would greatly improve data gathering and analysis.
... Q5. While questions 1-4 had mostly a visuo-motor component, question 5 is primarily targeting the presence of photophobia, which is amongst the most prevalent symptoms post-TBI (Wu and Hallett, 2017) and is a symptom addressed in the BIVSS. Most studies estimate the prevalence of photophobia to be between 30 and 40% in the early stages. ...
Article
Full-text available
Visual disturbances are amongst the most commonly reported symptoms after a traumatic brain injury (TBI) despite vision testing being uncommon at initial clinical evaluation. TBI patients consistently present a wide range of visual complaints, including photophobia, double vision, blurred vision, and loss of vision which can detrimentally affect reading abilities, postural balance, and mobility. In most cases, especially in rural areas, visual disturbances of TBI would have to be diagnosed and assessed by primary care physicians, who lack the specialized training of optometry. Given that TBI patients have a restricted set of visual concerns, an opportunity exists to develop a screening protocol for specialized evaluation by optometrists—one that a primary care physician could comfortably carry out and do so in a short time. Here, we designed a quick screening protocol that assesses the presence of core visual symptoms present post-TBI. The MOBIVIS (Montreal Brain Injury Vision Screening) protocol takes on average 5 min to perform and is composed of only “high-yield” tests that could be performed in the context of a primary care practice and questions most likely to reveal symptoms needing further vision care management. The composition of our proposed protocol and questionnaire are explained and discussed in light of existing protocols. Its potential impact and ability to shape a better collaboration and an integrative approach in the management of mild TBI (mTBI) patients is also discussed.
... Several peripheral sensors in the anterior of the eye contain melanopsin, a photopigment that offers a light transduction mechanism that may lead to pain perception. With a peak wavelength sensitivity of 480 nm, melanopsin-based photoreception can occur in intrinsically photosensitive retinal ganglion cells (ipRGCs) and is increasingly implicated as a source for light-induced pain (28)(29)(30)(31)(32). These ipRGCs can generate their own signal independent of rod and cone involvement in response to light absorption yet can additionally receive or relay input from classical RGCs and support cells (33)(34)(35)(36). ...
Article
Full-text available
Supraspinal mechanisms of pain are increasingly understood to underlie neuropathic ocular conditions previously thought to be exclusively peripheral in nature. Isolating individual causes of centralized chronic conditions and differentiating them is critical to understanding the mechanisms underlying neuropathic eye pain and ultimately its treatment. Though few functional imaging studies have focused on the eye as an end-organ for the transduction of noxious stimuli, the brain networks related to pain processing have been extensively studied with functional neuroimaging over the past 20 years. This article will review the supraspinal mechanisms that underlie pain as they relate to the eye.
Article
A preference for darkness is one of the main associated features in people with migraine, the cause remaining a mystery until some decades ago. In this article, we describe the epidemiology of photophobia in migraine and explain the pathophysiological mechanisms following an anatomical structure. In addition, we review the current management of migraine and photophobia. Ongoing characterization of patients with photophobia and its different manifestations continues to increase our understanding of the intricate pathophysiology of migraine and vice versa . Detailed phenotyping of the patient with photophobia is encouraged.
Article
Background: Although patients with abnormal light sensitivity may present to an ophthalmologist or optometrist for the evaluation of photophobia, there are no previous reviews of the most common causes of this symptom. Methods: We conducted a retrospective chart review of patients who presented to our eye center between 2001 and 2009 primarily for the evaluation of photophobia. We recorded demographics, ocular examination findings, and diagnoses of these patients. Results: Our population included 58 women and 53 men. The mean age at presentation to the clinic was 37 years (range 6 months-94 years). The most frequent cause of photophobia was migraine headache (53.7%), followed by dry eye syndrome (36.1), ocular trauma (8.2%), progressive supranuclear palsy (6.8%), and traumatic brain injury (4.1%). A significant proportion of patients (25.9%) left the clinic without a cause for their photophobia documented by the examining physician (11.7% of adults and 69.4% of children). Conclusions: Photophobia affects patients of all ages, and many patients are left without a specific diagnosis, indicating a significant knowledge gap among ophthalmologists and optometrists evaluating these patients.
Article
Background: Tinted lenses have been used to manage visual discomfort and photosensitivity in patients with migraines, benign essential blepharospasm (BEB) and epilepsy. Objectives: The purpose of this review is to examine the existing clinical research regarding the use of colored filters among patients recovering from traumatic brain injuries. Methods: A review of English articles from PubMed, Embase from embase.com, Web of Science, APA PsycINFO (OVID), Scopus, and Cochrane Central Register of Controlled Trials with publication years from date of inception to June 10, 2021 was performed. Articles were first screened by title and abstract, followed by full-text review. The search strategy resulted in 7819 results. The final analysis included seven articles which discussed the use of tinted lenses in patients post-traumatic brain injury. Results: While there is a paucity of information related to the therapeutic use of tinted lenses to mitigate post-traumatic light sensitivity and migraines, patients will subjectively report improved symptoms, specifically with precision tints or FL-41. Conclusion: Further studies are needed to understand the mechanism of action as well as objective and subjective benefits of tinted lenses in patient post-traumatic brain injury.
Article
Purpose To evaluate the visual photosensitivity threshold and objective photosensitivity luminance in healthy eyes, thereby providing a normative dataset that will lead to a better understanding of diseases causing photophobia. Methods This was a prospective cross-sectional study. Emmetropes whose visual acuity was better than 0.18 logMAR (6/9) with no other ocular abnormality were included. Headache Impact Test-6 and visual light sensitivity questionnaires were administered. Visual photosensitivity threshold was measured subjectively using the ocular photosensitivity analyser. Objective photosensitivity luminance was assessed manually by evaluating videos recorded using an infrared camera and noting the intensity of light at the first squeezing reflex. Results Seventy five normal subjects (age range, 7–71 years) were included. Median age was 32.7 years (inter-quartile range, 20.3–47.9 years). Forty (53.3%) were males. Median Headache Impact Test score was 38 (inter-quartile range, 36–42) and visual light sensitivity questionnaire score was 11 (inter-quartile range, 8–15). Mean (standard deviation) right eye, left eye and binocular visual photosensitivity threshold was 3.34 (0.78), 3.33 (0.81) and 3.37 (0.78) loglux, respectively. There was a significant negative correlation of visual light sensitivity questionnaire scores with right eye, left eye and binocular visual photosensitivity thresholds, and positive correlation of age with binocular visual photosensitivity thresholds. Mean (standard deviation) right eye, left eye and binocular objective photosensitivity luminance was 3.25 (0.55), 3.35 (0.47) and 3.15 (0.52) loglux, respectively. Age was only positively correlated with binocular objective photosensitivity luminance, and there was no correlation between age and right eye or left eye objective photosensitivity luminance. Conclusions The study characterised, for the first time, objective photosensitivity luminance and established normative data for both visual photosensitivity threshold and objective photosensitivity luminance. The data will help in understanding the pathophysiology of diseases causing photophobia, monitoring the disease progression and evaluating treatment modalities.
Article
Visual discomfort is related to the statistical regularity of visual images. The contribution of luminance contrast to visual discomfort is well understood and can be framed in terms of a theory of efficient coding of natural stimuli, and linked to metabolic demand. While color is important in our interaction with nature, the effect of color on visual discomfort has received less attention. In this study, we build on the established association between visual discomfort and differences in chromaticity across space. We average the local differences in chromaticity in an image and show that this average is a good predictor of visual discomfort from the image. It accounts for part of the variance left unexplained by variations in luminance. We show that the local chromaticity difference in uncomfortable stimuli is high compared to that typical in natural scenes, except in particular infrequent conditions such as the arrangement of colorful fruits against foliage. Overall, our study discloses a new link between visual ecology and discomfort whereby discomfort arises when adaptive perceptual mechanisms are overstimulated by specific classes of stimuli rarely found in nature.
Article
B-cell maturation antigen (BCMA) has become a key target for antibody-drug conjugates, bispecific antibodies, chimeric antigen receptor T-cell therapies, and other immunotherapies in multiple myeloma. Some of these agents such as belantamab mafodotin and idecabtagene vicleucel have already received regulatory approval in the United States. Although BCMA has generally been considered to be expressed almost exclusively in plasma cells with a low likelihood of on-target off-tumor toxicity, there has been a range of unusual neurotoxicity observed across the spectrum of BCMA immunotherapies. In certain cases, these unusual neurotoxicity presentations have led to patient death or withdrawal of agents from further development. Our review summarizes the literature in this field and highlights the possibility of on-target toxicities due to neural expression of BCMA. We draw attention to the need for further investigation of these toxicities. This risk becomes increasingly important as BCMA targeted therapies are brought to earlier lines of treatment.
Article
Full-text available
Headaches are often under-diagnosed in adolescents. The aim of this study was to examine the one-year prevalence of primary headaches among high school students in the city of Zagreb, the capital of Croatia. This was a population-based, cross-sectional study. A total of 2350 questionnaires consisting of questions on demographic data, the presence and clinical characteristics of headaches were distributed among students in eight high schools; 2057 (87.5%) questionnaires were eligible for analysis. The mean age of the students was 17.2 ± 1.2 years; 50.2% were female. The prevalence of recurrent headache was 30.1% (620/2057), girls 35.1%, boys 25.2%. Among students with headache, 291 (46.9%) had migraine, and 329 (53.1%) had tension-type headaches (TTHs). The mean frequency of headaches was 5.66 per month in girls and 4.42 in boys; mean duration of a headache attack was 8.94 hours in girls and 8.37 hours in boys (NS). Unilateral headache was present in 31.6%, throbbing quality in 22.6%, dull in 34.4% of students; 22.4% had severe intensity and 70.3% moderate. Nausea was present in 4.0% always and in 14.7% frequently (girls 18.8%), photophobia in 41.3%, phonophobia in 63.2%, osmophobia in 23.9% (NS among genders). Almost 30% of students were disabled and stayed at home, more frequently boys. Girls (33.4%) were more likely to take drugs for every attack; number per month was 3.7. The results of this study showed that the prevalence of migraine among adolescents in Croatia was 16.5% for girls and 11.8% for boys; the prevalence of TTH was 18.4% for girls and 13.4% for boys. The prevalence of self-reported headache among high school students in Zagreb is relatively high. Significant gender differences in frequency and clinical characteristics were observed. Primary headaches among adolescents are an important public health problem and should receive more attention from school and health authorities.
Article
Since the discovery of the non-image-forming visual system, tremendous research efforts have been dedicated to understanding its mechanisms and functional roles. Original functions associated with the melanopsin system include the photoentrainment of circadian sleep-wake cycles and the pupillary light reflex. Recent findings, however, suggest a much broader involvement of this system in an array of physiologic responses to light. This newfound insight into the underlying function of the non-image-forming system has revealed the many connections to human pathology and attendant disease states, including seasonal affective disorder, migraine, glaucoma, inherited mitochondrial optic neuropathy, and sleep dysregulation of aging. In this review, the authors discuss in detail the clinical implications of the melanopsin system.
Article
Photophobia, an abnormal intolerance to light, is associated with a number of ophthalmic and neurologic conditions. In the presence of normal neurologic and ophthalmologic examinations, the most common conditions associated with photophobia are migraine, blepharospasm, and traumatic brain injury. Recent evidence indicates that the intrinsically photosensitive retinal ganglion cells play a key role in the pathophysiology of photophobia. Although pharmacologic manipulation of intrinsically photosensitive retinal ganglion cells and the neural pathways that mediate photophobia may be possible in the future, current therapies are directed at the underlying cause of the photophobia and optical modulation of these cells and pathways.
Article
The attempts so far made to explain the mechanism of photophobia fail to account adequately for all the phenomena observed. Photophobia is a common symptom, sometimes the dominant complaint, and a fuller knowledge of the underlying factors not only is of theoretical importance, but is a prerequisite for rational therapy. In current usage the term photophobia is loosely applied to two quite different sensations. By true photophobia one means that exposure of the eye to light definitely induces or exacerbates pain. In the keratoconjunctivitis that follows exposure to ultraviolet rays the photophobia may be of such degree that looking at a white paper occasions pain ; even moonlight may cause distress, and though the lids are closed the bright light of a lamp cannot be tolerated.¹ On the other hand, the so-called photophobia induced by dazzling is simply uncomfortable vision, based either on diffusion of light through the
Article
Objective: Allodynia reflects the clinical correlate of central sensitization but it is usually neglected in clinical headache management. We aimed to report the prevalence and previously unnoticed associations of allodynia in migraineurs by a nationwide face-to-face questionnaire-based study by physicians. Methods: A total of 5323 households were examined for headache according to the diagnostic criteria of International Classification of Headache Disorders-II. Detailed headache features, premonitory signs, demographics, socio-economic status and hormonal status of females were analyzed regarding to the presence of allodynia in patients with definite migraine. Results: Allodynia was present in 61.1% of migraine sufferers in the general population of Turkey. The duration and severity of attacks (P<0.0001), photophobia (P=0.001), phonophobia and also osmophobia (P<0.0001), as well as premonitory signs (P=0.018) showed significant associations with allodynia. Migraineurs with aura or family history of migraine reported more often allodynia in comparison to those without (P=0.001 and P=0.028, respectively). Allodynic migraineurs had a higher rate of physician consult and high levels of MIDAS reflecting increased burden of headache. Furthermore, migraineurs with allodynia had high probability of attacks close to menses. Migraine improved during pregnancy, but it worsened after menopause or during oral contraceptive use in patients experiencing allodynia when compared those without allodynia. Discussion: The duration, severity and disability of migraine attacks, photophobia, phonophobia and osmophobia, as well as premonitory signs showed significant associations with allodynia in the general population. Moreover, migraineurs with aura or family history of migraine reported more often allodynia and allodynic migraneurs were more sensitive to hormonal changes. Allodynia which seems to indicate higher tendency to sensitization should be implemented in daily headache practice to predict the prognosis and high levels of migraineous involvement.
Article
Photophobia is a debilitating feature of many headache disorders. Clinical and preclinical research has identified several potential pathways involved in enhanced light sensitivity. Some of these structures include trigeminal afferents in the eye, second-order neurons in the trigeminal nucleus caudalis, third-order neurons in the posterior thalamus, modulatory neurons in the hypothalamus, and fourth-order neurons in the visual and somatosensory cortices. It is unclear to what degree each site plays a role in establishing the different temporal patterns of photophobia across different disorders. Peptides such as calcitonin gene-related peptide and pituitary adenylate cyclase-activating polypeptide may play a role in photophobia at multiple levels of the visual and trigeminal pathways. While our understanding of photophobia has greatly improved in the last decade, there are still unanswered questions. These answers will help us develop new therapies to provide relief to patients with primary headache disorders. © 2015 American Headache Society.
Article
Objective Post-traumatic headache (PTH) of the migraine type is a common complication of mild traumatic brain injury (including blast injuries) in active duty service members. Persistent and near-daily headache occur. Usual preventive medications may have unacceptable side effects. Anecdotal reports suggest that onabotulinum toxin A (OBA) might be an effective treatment in these patients.Methods This study is a real-time retrospective consecutive case series of all patients treated with OBA at the Concussion Care Clinic of Womack Army Medical Center, Ft. Bragg, NC, between August 2008 and August 2012. Clinical treatment and pharmacy records were corroborated with the electronic medical records in the Armed Forces Health Longitudinal Technology Application to determine demographics, current headache and treatment characteristics, and clinical and occupational outcomes.ResultsSixty-four subjects (63 male) with mean age of 31.3 + 7.5 (range 20-59) years were evaluated and treated. Blast injuries were most common (n = 36; 56.3%) and 7 patients (11%) reported a prior history of headache. Most patients (36; 56.3%) described more than 1 headache type and 48 (75%) patients had continuous pain. The most prevalent treating diagnosis was mixed continuous headache with migraine features on more than 15 days per month (n = 26; 40.6%). The mean time from injury to the first injections was 10.8 + 21.9 (1-96) months. Forty (62.5%) patients received the Food and Drug Administration-approved chronic migraine injection protocol. Forty-one (64%) patients reported being better. Two patients discontinued for side effects. Twenty-seven (41%) remained on active duty.Conclusions We demonstrate that active duty military patients with headaches related to concussions may benefit from treatment with OBA. Further studies are indicated.
Article
Purpose Photosensitivity is common in patients known to have migraine headaches, in patients following traumatic brain injury, in patients with certain CNS pathology and in inflammatory disorders of the eye. However, it is a subjective complaint and difficult to substantiate and treat. Recently, we have taken advantage of a primitive reflex, the photic blink reflex, to objectively quantify the eye’s sensitivity to light. Methods Patients with light sensitivity and normal subjects were tested using red (640nm) and blue (485nm) Ganzfeld, full field light, one second in duration, over a 6 log unit range of intensity (0.5 log unit steps). Time-stamped, computerized recording of the orbicularis and procerus/corrugator muscle EMG were quantified using the maximum root mean squared (RMS). Results The photic blink reflex appeared to show similar response characteristics as the pupil light reflex, having both a transient response to photopic red and blue light and a sustained response to high intensity blue light. Patients with light sensitivity showed an exaggerated EMG response to light compared to normals. Conclusion The sustained EMG response to bright blue light provides evidence for a melanopsin mediated photic blink reflex. The photic blink reflex, as measured by the electromyogram, appears useful for quantifying light sensitivity and its response to treatment.
Article
Primary objective: To determine whether photosensitivity (PS) changes over time and, if so, what factors may be related to the change; furthermore, to determine whether tint density changes over time, all in mild traumatic brain injury (mTBI). Design and methods: A retrospective analysis of 62 patient records (aged 18-40 years) with mTBI and PS was conducted. All charts were obtained from the SUNY/College of Optometry clinics from 2004-2011. Results: Fifty per cent demonstrated reduced PS over time, with most occurring after year 1 post-injury (40%). Promotion of PS reduction appears to be associated with the lack of spectacle tint usage (p = 0.01) and the use of contact lenses (p = 0.03). Inhibition of PS reduction appears to be associated with tinted lenses (p = 0.06), hyperacusis (p = 0.03), dry eye (p = 0.04), migraines (p = 0.03) and loss of consciousness at the time of injury (p = 0.05). Concerning tint density changes over time, 71% (p = 0.002) maintained the same degree over time, while 27% (p = 0.002) reduced and 2% waxed and waned. Conclusion: Neural adaptation to PS appears to be a long-term process. Tint usage may act to inhibit this adaptive process, while the use of contact lenses may act to promote it. These findings may provide guidance in the clinical management of photosensitivity in the mTBI population.