PHOTOPHOBIA
Photophobia literally means to have a fear of light; however this is just a symptom of pain in the presence of light. Photophobia is described as a painful response to light.
This is a neuro-ophtalmological disorder, which means the optic nerves are effected along with the brain. So, even though eye disorders commonly involve light sensitivity, photophobia can be caused by a variety of things.
One of the most common ocular conditions that occur with tension headaches, migraines, or TBI’s (Traumatic brain injury’s).
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TBI’s
Photophobia is one of the most common symptoms of concussions and TBI’s. TBI produces cognitive symptoms such as dizziness, vertigo, nausea, irritability, cognitive delays, and vision related symptoms to light-sensitivity. About 40% of individuals with brain injuries experience sensitivity to light. Light sensitivity can show up post-concussion, or 6 months to even years after the concussion occurred.
Cranial Nerve 5- trigeminal CN V
The star of the show is cranial nerve five which is the largest cranial nerve. The trigeminal nuclei and nerves have a crucial role in being a moderator for pain in the eyes and head.
“The trigeminal ganglion’s afferent ophthalmic (V1) branch is responsible for transmitting pain signals of several eye structures, including the cornea, conjunctiva, sclera, and uvea. These structures are richly innervated with nerve fibres and immensely sensitive to pain. Additionally, the optic nerve carries trigeminal afferents within the blood vessels and the dura, which can explain why arteritic anterior ischaemic optic neuropathy and optic neuritis cause pain.1” (Abusamak and Alrawashdeh, p. 87).
(CGRP) Calcitonin gene-related peptide, which is the peptide that is released that cause pain signals in the brain in response to the trigeminal nerve. Located in the trigeminals ganglion, this is triggered by stress, brain vessels, and or inflammation.
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What Causes Photophobia in TBI’s?
With TBIs, photophobia is usually caused by injury to the thalamus, preventing it from getting oxygen. However with concussion light sensitivity multiple areas are dysregulated, Light sensitivity could mean dysregulation in one or all areas. This creates a symptom cascade, meaning a problem in one area could ignite other problems.
Thalamus
The thalamus is in charge of relaying sensory information to the brain. Neurovascular coupling, which happens in the brain and retina become dysregulated, communication pathways are faulty so there isn’t always enough oxygen to be used. Patients are recommended to stay in dark rooms because they have less visual information.
Autonomic Nervous System
The autonomic nervous system is in charge of involuntary system, which involves functions like heart rate, breathing etc. Within light sensitivity, pupils dilate more than needed in a post concussion scenario causing exposure to light causing sensitivity.
Vestibular System
The vestibular system involves the inner ear, sight, and touch. Dysfunction in this area causes the body to become off balance, leading to dizziness and vertigo. The Vestibular system and visual system do not agree which increases optic sensitivity, which in turn creates an overload of sensory information.
Superior Colliculus
The superior colliculus is in charge of visual mapping and coordination, aiding in detecting and locating visual and audio stimuli. This contributes motor functions to orient the head and eyes away/toward a stimulus. This is described sometimes as a looming stimulus which can be perceived as a threat and initiates a response from fear. For example a snake would be processed in the superior colliculi and would orient an individual away from the snake because the snake is perceived as a threat. This can occur without eye movements.
Footnotes:
Abusamak, Mohammad, and Hamzeh Mohammad Alrawashdeh. “Post-Concussion Syndrome Light Sensitivity: A Case Report and Review of the Literature.” Neuro-Ophthalmology 46, no. 2 (n.d.): 85–90. https://doi.org/10.1080/01658107.2021.1983612.
n J., and Matilde Inglese. “The Role of Thalamic Damage in Mild Traumatic Brain Injury.” Journal of Neurotrauma 33, no. 2 (January 15, 2016): 163–67. https://doi.org/10.1089/neu.2015.3965.