What is Post-Concussive Photophobia?

Jul 26

Photophobia, a sensory disturbance provoked by light, is a common neurological and visual symptom. The most common cause of photophobia is migraine, however other primary headache conditions and impairment of the visual pathways can cause photophobia. Photophobia can be difficult to treat with conventional therapies, and the pain of photophobia can be debilitating.

We very commonly see photophobia as a primary symptom of post-concussion syndrome (1).

How Common is Post-Concussive Photophobia?

Concussions affect 1.8-3.8 million people annually, however the true numbers of concussions are very likely underreported. Approximately 39 million people in the United States experience migraines (12). While photophobia is not a commonly tracked symptom on its own, we can ascertain from this data that it is very common.

In cases of post-concussion syndrome, females show greater sensitivity to sensory stimuli across multiple modalities, including photophobia (11). Photophobia is very common in cases of post-concussion syndrome with comorbid post-traumatic stress disorder (12).

What Causes Post-Concussive Photophobia?

Photophobia is commonly a problem associated with the anterior segments of the eye. Dry eyes, iritis, and uveitis are common causes of photophobia. These are generally easily treated with lubricant drops and medications.

In other cases, photophobia involves a problem with the neurological systems that control pupillary dilation (2). The pupil is the black center of the eye that will either get bigger (dilate) or smaller (constrict) depending on the amount of light in the environment. This reflex allows us to see our environments in bright or low light settings.

Pupillary diameter is under the control of our Autonomic Nervous System (or ANS). The ANS regulates critical involuntary bodily functions including heart rate, blood pressure, breathing, digestion, and a number of other reflexes that are critical to survival. There are two major subcategories to the ANS: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS).

The sympathetic nervous system is responsible for helping us respond quickly and efficiently to potentially harmful stimuli. It generates what is known as the “fight or flight” response. It is responsible for increasing our heart rate, increasing our respiratory rate, turning off digestion and dilating our pupils to take in our visual environment. It can be activated when we are in literal danger, or during stressful times at work, or while stuck in traffic on the way to the airport.

The parasympathetic nervous system is responsible for helping us do the normal functions necessary to continue living during peaceful and calm moments. It is often referred to as the “resting digesting” system. It keeps our heart and respiratory rates stable, maintains appropriate pupil constriction and increases digestive functions.

The balance between these systems is frequently damaged in concussions and other traumatic brain injuries. The central brainstem structures that control the sympathetic and parasympathetic systems are vulnerable to rotational shearing forces seen in concussions and mTBIs. Too much activation of the SNS and not enough inhibition from the PNS is often the cause of photophobia (2).

What are the Symptoms of Photophobia?

Symptoms of post-concussive photophobia are predominantly sensitivity to light, although the severity of this sensitivity differs between patients. Patients may become nauseous and vomit when exposed to bright light. It may trigger headaches or migraines. They are often fatigued and experience “brain fog.” They may have excessive sweating or intermittent pounding heartbeat. Photophobia is also commonly present with phonophobia, or sensitivity to sound.

What Happens in the Brain with Photophobia?

Pupillary dilation is a three-neuron pathway in the brain that is driven by the SNS. It begins in the subcortical region called the hypothalamus, which is a strong emotional center. This is why stress or emotions may make light sensitivity worse. From the hypothalamus, it descends through the midbrain and synapses in the spinal cord between C8-T2 on a main neuron called the center of Budge. The second neuron, known as a preganglionic sympathetic neuron, exits the spinal cord and then ascends through the chest, passing by the top of the lungs, to land on the superior cervical ganglion near the top three cervical vertebrae and the angle of the jaw. The third post-ganglionic neuron travels along the blood vessels in the neck up into the skull then entering the eye sockets where they land on the dilator papillae muscles, causing pupillary dilation (3).

As you can see, this small finding of an enlarged pupil is from a complicated process. Any number of things could go wrong, including neck trauma or brain trauma, to cause issues with this pathway.

One of the most common issues with migraine is what is called multisensory dysfunction, which expresses itself as increased sensory perception of visual, auditory and olfactory sensations. These can become so pronounced as to become painful, becoming what are called sensory allodynias. These sensory disturbances originate from abnormal processing in different cortical areas, including the visual cortex, but recent data suggest that pathological processing may occur at lower levels of the visual pathways, including parts of the brainstem (4).

One of these is the Trigeminovascular complex. Migraine is associated with a brainstem-level inability to suppress glare and light-induced pain, and trigeminal nerve, which maps blood vessels in the dura of the brain appears to be involved in this process. The trigeminal system is also involved in autonomic reflexes that further contribute to pain by promoting vasodilatation in pain-sensitized extra/intracranial vessels (5).

Although less frequent, photophobia has also been reported in tension-type headache, headaches associated with traumatic brain injury, unilaterally in cervicogenic and cluster headache. All of these processes involve the trigeminal nerve, and are considered to be trigeminal autonomic cephalalgias (TACs) (6).

Photohpobia also involves light activation of intrinsically photosensitive retinal ganglion cells in the eye, activation of which has been shown to produce photophobia during migraine headaches (7).

Electrophysiological recordings of dura-sensitive (trigeminovascular) neurons in the thalamus showed that shining light into the contralateral eye induces a large and sustained increase in their activity. These light/dura-sensitive neurons, which are located in the lateral posterior (LP) and posterior (Po) thalamic nuclei, receive input from ipRGCs. In addition, the axons of these thalamic trigeminovascular neurons project to multiple cortical areas including somatosensory (S1/S2) and visual (V1/V2) cortices of the brain. These studies suggest that the convergence of light signals from ipRGCs onto the trigeminovascular thalamo-cortical pathway has the potential to explain how light intensifies the perception of headache during migraine (8).

There is also solid evidence of dysfunction of retinal pathways controlling the pupillary light reflex (PLR) through autonomically-driven midbrain circuits (9).

Quantitative measurement of the pupillary light reflex together with clinical evaluation and psychophysical assessment of photophobia threshold was performed in migraineurs and healthy controls. They showed that abnormal pupillary light reflex was associated with low photophobia thresholds between headaches, and that this abnormality was correlated with migraine severity. The authors conclude that abnormal PLR is central in origin and reflects autonomic maladaptation to chronic light sensitivity. This is consistent with the notion of altered excitability in CNS structures in migraine pathophysiology (10).

Many other systems susceptible to injury fire into the sympathetic nervous system to activate it, as well, an important one being the vestibular system (13). When someone goes from lying to standing, or standing to sitting, gravity pulls blood down towards their feet. There are two systems that tell the brain about the body’s relationship to gravity: pressure receptors in the neck and the vestibular system. The vestibular system is the only system that relays information to the brain about the head’s location relative to its body and relative to gravity. Therefore, it must fire extremely fast so that you get enough blood to the brain during postural changes against gravity.

The brain will normally increase the heart rate to compensate for this blood pressure drop. It does this by telling the SNS to activate, which constricts blood vessels so that blood can be pumped back up to the brain. The vestibular system is commonly injured or damaged during a concussion resulting in these reflexes working improperly, also known as post-concussive dysautonomia.

In some types of dysautonomia, the increase in heart rate is extreme, and thus the heart will beat before it has a chance to properly fill with blood. This leads to even less blood flow to the brain. These patients will sufferer dizziness, often will faint, and frequently are injured as a result of these falls. Others may experience constant headaches, migraines, brain fog, light and sound sensitivity or lightheadedness as a consequence of their dysautonomia. Research also demonstrates that consistently increased blood pressure and demand on the sympathetic nervous system can cause damage to the organs that process blood, such as the heart and kidneys (14).

When the brain does not receive sufficient blood flow, myriad symptoms may present. Your brain requires a great deal of energy to function properly, and when this is disrupted, a host of brain functions are impaired. Simple cognitive tasks become profound challenges, simple physical tasks become exhausting. Emotional regulation can become extremely difficult. Everything your brain does depends on the ability to properly regulate blood flow. When this fails, virtually everything your brain attempts to do can become a struggle (15).

How is Photophobia Usually Treated?

There is no established cure for post-concussive photophobia. Many people find relief from wearing sunglasses and hats, to physically block the light. Some people may be provided with glasses with specific filters to block specific frequencies of light that over-stimulate their brain (16).

How is the NeuroRescue Program Different?

One of the main things your brain does, and maybe even the primary thing, is help you determine where you are in the world. Your brain uses inputs from your inner ear to figure out where your head is in relation to gravity and how it is moving. It uses inputs from your muscles and joints to figure out where your body is in relation to your head and what your body is doing. It uses inputs from your eyes to figure out where your body is in relation to the visual environment.

Your brain needs to put all of that together to make sense of where the world is, and where you are in relation to the world. It needs to be able to localize you effectively in the environment, in order for you to be able to respond to the environment properly.

Your brain organizes all of this information in terms of maps. There is a vestibular map from the inner ear, a proprioceptive map from muscles and joints, a vascular map of your blood flow, a visual map of the world from your eyes, and several others. Your brain needs these maps to be saying largely the same thing about where you are in the world at all times.

One often overlooked feature of post-concussive photophobia is that these maps usually fail to match. Your eyes, inner ear, and muscles are creating maps that say different things about where your head is in relation to gravity. When you go from lying down to sitting up or standing, problems in these maps can make it difficult for the brain to compensate for the postural shift. If the brain does not understand the position of the head in relation to gravity, it cannot properly control the vascular system to send the appropriate amount of blood to the head (17). We utilize eye movements to activate the various cortical, subcortical and brainstem regions involved in the ANS to improve function and connectivity (18). This results in increased firing of our stress pathways, leading to dilated pupils and light sensitivity.

This is why many patients fail to fully resolve their post-concussive photophobia with most forms of treatment. Without addressing the problems in these maps, it will remain impossible for the brain to properly control blood flow, and the best they can hope for is to gain some control over their symptoms. We would much rather try to address the underlying cause.

We find that by far the most effective way to reduce photophobia is to directly rehabilitate all of the pathways that have been injured in your concussion. We use a wide variety of therapies in this process, all of which are tailored to the unique realities of your case.

All of our therapies are backed by the latest neuroscience research. Our therapies may involve eye exercises designed to improve gaze stability (19), or the ability to successfully hit targets with your eyes (20). They may involve exercises to restore reflexes involving your inner ear, your neck, or both (21). They may include exercises to improve your balance under specific conditions (22). They may involve vision training exercises using specific therapies that integrate several modalities at the same time (23). They may involve things like specific types of electrical stimulation (24), transcranial magnetic stimulation (25), or even specific exercises performed in a virtual reality environment (26). Research shows that taking a multimodal functional neurological approach to treating traumatic brain injuries is extremely effective, and that the effects are lasting (27,28,29).

No two concussion presentations are alike, and the same holds true for the NeuroRescue program. A cookie-cutter approach will be doomed to fail in a condition as complicated as post-concussive photophobia. All of our therapy protocols are tailored to the unique needs of the individual, based on your history, examination findings, and diagnostic testing data.

How does the NeuroRescue Program work?

We design your unique NeuroRescue Program to be among the most comprehensive diagnostic and therapeutic protocols available today. We create individual NeuroRescue Programs based on a comprehensive analysis of every relevant neurological system and pathway, using gold-standard, cutting edge neurodiagnostic technologies and examination procedures and state-of-the-art therapies.

We begin with your Discovery Day, wherein we perform a comprehensive history of not only your condition, but your life on a timeline. This allows us to dive deeply into your case and see all of the factors that led to where you are now. It helps us uncover hidden problems and associated conditions that may be making it difficult for you to move your recovery forward.

Our examination allows us to identify the areas and pathways of your brain that have been impacted by your injury. We begin by precisely quantifying the function of your visual, vestibular, and proprioceptive systems through computerized analysis of your eye movements, your inner ear reflexes, and your balance in a host of different sensory conditions.

We employ technologies including Videooculography and Saccadometry to measure several classes of eye movements. We use Video Head Impulse Testing to measure the function of your inner ear, and Computerized Dynamic Posturography to assess your balance in different sensory conditions.

We use NeuroSensoryMotor Integration testing to evaluate hand-eye coordination and cognition, and Virtualis testing to assess dynamic eye tracking and perception of vertical in a virtual reality environment.

We combine all of this with a comprehensive physical and neurological examination of your sensory, motor, autonomic, and cognitive systems. We also perform a passive tilt table test (3) to assess for dysautonomia. We review any relevant laboratory testing, radiological imaging, and prior neurodiagnostic testing, and integrate that information with our findings.

We use this information to identify which parts of your brain are working properly, which systems are struggling, and the precise point at which your systems fatigue.

We can then design a NeuroRescue Program that is unique and specific to your brain, and yours alone. Your NeuroRescue Program works to rejuvenate and reintegrate the damaged neurons and pathways in your brain. It works to improve energy, endurance, and functional capacity within your fragile systems.

We use our technologies and procedures to not only see what we need to address, but also when it is time to stop and let you rest. We address your impaired neurological function from multiple angles of therapy, and provide metabolic support to improve neurological recovery.

While we cannot bring back neurons that have been lost, your NeuroRescue Program allows us to take the pathways that remain and maximize their efficiency and endurance. And by focusing on the integration of systems, we can do more than just get pathways working better, we can get them working together again. This gives us our best opportunity to get your photophobia under control and return you to living a healthy, vibrant, and fulfilling life.

Your Next Best Step:

Living with post-concussive photophobia can be challenging, but there is hope for recovery and remission. To see if the NeuroRescue Program is right for you, contact one of our patient care coordinators to schedule your Discovery Day.

And remember, it’s never too late to start getting better.