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An Overview of Migraine Management for Optometrists

Mar 5, 2020
16 min read
1.2k views

Your patient has come in complaining of flashes of light and zigzag patterns followed by loss of vision. There are plenty of differential diagnosis possibilities—including migraine.

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You are panicking because you just finished a dilated exam and found nothing! You found nothing on a patient who came in complaining of flashes of light and zigzag patterns followed by loss of vision in their right eye. They report no health issues, deny any recent trauma, and they do not take any medications. Oddly enough, now their symptoms are gone and they report they feel fine. Before you refer them to the ER (which you may still need to do), take a moment to consider some differential diagnosis possibilities.

And yes, one of those differentials is migraine.

What is a migraine?

mi·graine (/mÍ, grān/), noun: A torturesome agony in your head that feels as if a hammer is being slammed into your head from the inside of your skull, that can ruin your day or sometimes even week with pain, nausea, and heightened sensitivity to your surroundings.

Or at least that’s how someone who suffers from them might describe them. A more medically accepted explanation of migraine is a hereditary neurological condition that is typically characterized by recurrent moderate to severe headache pain that typically lasts for hours to several days.1

A migraine attack can include up to 4 phases. However, not everyone experiences all four phases, and an individual may experience a different number of phases from one migraine to the next.2 Symptoms vary widely among individuals and can also vary from one attack to the next in the same individual. The most commonly accepted clinical phases are as follows:

  1. Prodrome: This phase is characterized by premonitory symptoms of an impending migraine. It can occur hours or sometimes even days before the peak of a migraine. Common symptoms include but are not limited to fatigue, mood changes, anxiety, excessive yawning, muscle stiffness, food cravings, nausea, and difficulty concentrating.2
  2. Aura: An aura is a sensory disturbance that may precede the migraine headache before the onset of pain. Most auras are visual in nature, but can also manifest as numbness or tingling in the face or extremities, vertigo, olfactory hallucinations, auditory hallucinations, difficulty speaking, or even partial paralysis, to name a few.2,5 Auras are unique to the individual and can vary amongst individual headaches.2 These are transient and generally last anywhere from 5-60 minutes.3 Approximately one-third of individuals who suffer from migraines experience auras.4 However, an aura may not occur with every migraine, and headache pain may not occur with every aura.
  3. Headache: The headache phase includes the actual head pain in a migraine attack. It is the most intense part of the migraine and generally brings on the peak of the suffering. The headache is often described as a debilitating pulsing or throbbing pain that can occur on one side of the head, bilaterally, or begin in one area of the head and progress to another. Migraine sufferers often have heightened sensitivity to lights and sounds during this phase. They also may experience nausea, anxiety and/or depression, temperature sensation changes, or dizziness.5,6 The headache can unfortunately last anywhere from several hours to several days.
  4. Postdrome: At the tail end of a migraine, many migraineurs experience postdrome symptoms before their body completely recovers from the attack. Postdrome symptoms can occur even if an actual headache does not. Symptoms often include malaise, fatigue, muscle aches, scalp tenderness, stiff neck, or mood changes. This phase is sometimes referred to as the hangover phase.5,6

Migraine is a common brain disorder that is much more prevalent than many realize; it affects approximately 10% of the population worldwide, but varies greatly in severity and frequency among individuals.1,7 This disorder is experienced at some point by over 20% of women and over 10% men.6 Migraines are currently the most common neurological cause of disability in the world.7

Of relevance to optometrists, migraines are being investigated as a risk factor in the development of primary open angle glaucoma (POAG). No causal relationship has been identified, but there is statistically significant evidence displaying that those who suffer from migraines have a greater risk of developing POAG compared to those who do not. The mechanisms behind this correlation are not fully understood.8

Pathophysiology and mechanisms of migraines

Despite the high prevalence of migraines, our understanding of the pathophysiology of migraines remains limited and variable. With continuous advances in research, theories on migraines change more than a colored contact lens wearer changes from sterling grey to pure hazel!

Although the mechanisms behind migraines are still a source of debate, today the most widely accepted theory regards migraines as a neurovascular disorder. We won’t give you an actual migraine by going into every detail, but know that the current theory suggests migraines involve trigeminal nerve activation. In essence, the theory proposes that migraine attacks begin with dysfunction of the brainstem nuclei (including the hypothalamus, thalamus, and cortex) that are involved in sensory function.4,7,9

This activated neuronal dysfunction may then spread to the trigeminal nerve fibers and trigeminal vascular system, given their close proximity to the thalamus. Convergence of the cervical and trigeminal afferent nerves may also explain why neck pain sometimes occurs with migraines. As the neuronal dysfunction spreads, neuropeptides are released, which in turn cause inflammation and pain in the associated cranial nerves and vessels.4,7,9 One of the main neuropeptides thought to be involved in migraines is calcitonin gene-related peptide (CGRP), which is the target of many new migraine prevention therapies.

Recall from anatomy class that the three major branches of the trigeminal nerve are the ophthalmic, maxillary, and the mandibular divisions. The ophthalmic branch is affected in migraines very often. Therefore, you will often have migraine patients who may describe a pain or pressure sensation behind their eyes.9 There are certainly a number of differentials to consider with these complaints, but migraines should always be one of them.

Migraine auras are also believed to be neuronal in nature, followed by vascular changes. Several studies have concluded that the aura in the migraine sequence is associated with reduced cerebral blood flow and a wave of neuronal depolarization across the cortex. This is known as cortical spreading depression (CSD). Visual auras appear to correlate to the movement of CSD across the cortex.7,9

You likely have heard of “migraine triggers.” These are certain stimuli or circumstances that consistently give someone a migraine. Triggers are different for everyone, and are sometimes difficult to identify. Not everyone has known or specific triggers. The following is a non-comprehensive list of common migraine triggers1,4-6:

  • Stress
  • Changes in sleep patterns
  • Caffeine withdrawal
  • Changes in hormone levels
  • Drinking alcohol
  • Bright or fluorescent lights
  • Loud or shrill sounds
  • Strong odors
  • Missed meals
  • Foods with tyramine or MSG

So what about ocular migraines?

Ocular migraine is a loose term that includes any component of migraines that includes visual sensory symptoms. This can include migraines with auras or the experience of just an aura with no headache. It can also include retinal migraines. The triggers and predisposing factors of ocular migraines are thought to be the same as any migraine.3

Visual disturbances that occur in ocular migraines commonly present as the following3-5:

  • Flashes of light
  • Zigzag patterns or geometrics shapes (often described as kaleidoscope patterns)
  • Complete loss of vision in one eye
  • Tunnel vision, field loss (hemianopia), or blind spots (scotoma)
  • Flickering lights or scenery
  • Visual Snow
  • *Please note this is not a comprehensive list and many have unique auras not mentioned on this list!

So think about migraine before you tell your patient to lay off of the psychedelics!

Retinal migraines are a rare type of migraine with aura. It is often difficult to differentiate between a retinal migraine and another migraine with aura. A retinal migraine is more likely to be unilateral and have more intense visual sensory changes. Symptoms frequently include flickering lights or visual snow, decreased vision, or complete loss of vision. Again, symptoms can occur with or without an actual headache. While they can occur at any age, the majority of initial cases begin in the second decade of life.3 A suspected rare complication of retinal migraines is retinal artery occlusion, but data on this is limited and still being explored.3,10

As with all migraines, the theories behind retinal migraine are also controversial. The theories that have gained the most support suggest that vasospasms occur within the retinal vasculature, or that CSD occurs in the retina as it may in the cortex as well.3,7,9

Remember, migraine is still a brain disorder, even with its visual side effects.

That was a lot of information. What does this mean for optometrists?

Most importantly, you need to remember that ocular migraine is a diagnosis of exclusion!

As optometrists, we do not diagnose or medically treat migraines. However, many patients will walk into our office with visual or ocular symptoms associated with migraines or one of their differentials. Therefore, we do need to be able to recognize the signs and symptoms of migraine, and rule out its more adverse masqueraders.

Some differentials we need to consider in any type of ocular migraine are amaurosis fugax, transient ischemic attack or stroke, giant cell arteritis, increased intracranial pressure, occipital epilepsy, optic neuritis, orbital apex mass, angle closure glaucoma, anterior ischemic optic neuropathy, uveitis, scleritis, posterior vitreous detachment, and retinal detachment.3

The optometrist serves to guide patients to the appropriate care when it comes to ocular migraines or one of their differentials. In order to do this, we need to take a good history and do a thorough exam. Ask about location and duration of symptoms. Inquire about personal or family history of migraines, any changes in lifestyle or medications, and if the patient has had any exposure to common migraine triggers. Take special note of cholesterol and carotid issues, history of stroke, hypertension, diabetes, and smoking and drinking habits.

In your complete dilated exam, check for both anterior and posterior inflammation, optic nerve head appearance, the presence of any plaques or emboli, retinal pallor, vascular abnormalities, angle grades and intraocular pressure, or vitreous or retinal detachments.

If your ocular exam is unremarkable and the patient’s symptoms are ambiguous, do not hesitate to send these patients to the ER immediately. Many of the symptoms of migraine overlap with more dire situations and you may very well save your patient’s life. Be particularly wary of patients who are beyond their fourth decade of life and have any type of vision loss or state they have a terrible headache, especially if they have no personal history of any kind of migraines. These patients should be referred immediately for imaging to rule out more serious conditions. Establish a working relationship with a local neurologist and neuro-ophthalmologist for suspected neurological emergencies. As always, you also want to have a network of available ophthalmologists to consult with in the event of any ocular emergencies or uncertainties.

Migraine treatment

Our ability to treat migraines with medications is limited. Prescribing medications for these patients is out of our jurisdiction.

However, we can certainly help to alleviate our patient’s symptoms if they have visual migraine triggers, and we need to be aware of ocular side effects from common migraine treatment medications.

When it comes to migraine, not all lights are created equally. Bright fluorescent lights and electronic screens can sometimes trigger or exacerbate migraine attacks. Research on light-filtering glasses is still developing, but is showing some promise to migraine suffers with light triggers and photophobia. Some studies display that rose-tinted “migraine glasses” significantly decrease the number of migraine days for sufferers who are triggered by harsh or fluorescent lights. These glasses use the FL-41 tint, which is believed to filter wavelengths of light that are more likely to trigger migraine, particularly in the 400-500 nm range.11

We have all heard the controversial buzz around blue light blocking glasses. Whether or not they significantly reduce computer eyestrain is yet another subject of debate. However, it has been proven that excessive exposure to blue light disrupts our circadian rhythms and melatonin regulation.13 As we know now, regular sleep and hormone regulation is crucial for migraineurs. Studies have shown that amber-colored lenses have improved quality of sleep and melatonin regulation in those with heavy blue light exposure.14 So it is not a bad idea to recommend these lenses to your migraine patient who has a lot of screen time, and any improvement in eyestrain is an added bonus!

Those who prescribe medication for migraines may treat migraines both acutely and preventatively. Common medication types that are prescribed for the acute treatment of migraines are triptans, NSAIDS, steroids, ergot derivatives, and antiemetics.15 Common treatments used prophylactically in migraines are CGRP inhibitors, beta-blockers, calcium-channel blockers, OnabotulinumtoxinA (Botox), SPG Nerve Block, tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin norepinephrine reuptake inhibitors, and anticonvulsants.16

Be mindful of the ocular complications many of these medications may cause. Just about all of these medications may cause or exacerbate dry eye syndrome in our patients. Botox injections near the eyes can cause droopy lids, diplopia, and lid swelling.17 Serotonin reuptake inhibitors cause mydriasis and are associated with a greater increase in developing glaucoma.18 Topiramate (a very commonly used antiepileptic used in the prophylaxis of migraines) is known to cause acute angle closure via choroidal effusion.19

Can we wrap this up before I get a migraine?

Migraine is a common and debilitating neurovascular condition that plagues people across the world. To those who suffer from them, it is far more than “just a headache.” Remember that migraineurs suffer emotionally as well as physically; the condition affects quality of life, productivity, and at times is physically unbearable.

Migraines often present with visual or ocular symptoms that bring patients into our office. As optometrists, it is crucial for us to be mindful of not only the signs and symptoms of migraines, but their more deleterious differentials as well. Our job is to direct patients to the appropriate care and testing, sometimes on an emergency basis. With established migraineurs we can help to address lifestyle changes that mitigate the effects of migraine. Be aware of the ocular concerns associated with migraines and their treatments. Keep lines of communication open with other members of the patient’s medical team. As optometrists, we are part of a team effort to ensure a patient’s wellbeing is maximized.

References

  1. Hildreth, CJ, et al. "Migraine Headache." JAMA. 2009;301(24):2608. doi:10.1001/jama.301.24.2608
  2. Silberstein SD, et al. "Migraine Aura and Prodrome" SEMINARS IN NEUROLOGY. 1995; 15(2).
  3. Khalili, YA, et al. “Retinal Migraine Headache” Treasure Island (FL): StatPearls Publishing; 2020 Jan.
  4. Hansen, J.M., Charles, A. “Differences in treatment response between migraine with aura and migraine without aura: lessons from clinical practice and RCTs.” J Headache Pain 20, 96 (2019). https://doi.org/10.1186/s10194-019-1046-4
  5. Viana, M., Tronvik, E.A., Do, T.P. et al. “Clinical features of visual migraine aura: a systematic review. “J Headache Pain 20, 64 (2019). https://doi.org/10.1186/s10194-019-1008-x
  6. Weatherall, MW. “The Diagnosis and Treatment of Chronic Migraine.” Ther Adv Chronic Dis. 2015 May; 6(3): 115–123 doi: 10.1177/2040622315579627
  7. Puledda, F, et al. “An update on migraine: current understanding and future directions.” J Neurol. 2017; 264(9): 2031–2039. doi: 10.1007/s00415-017-8434-y
  8. Chang, X, et al. “Migraine as a risk factor for primary open angle glaucoma.” Medicine (Baltimore). 2018 Jul; 97(28): e11377. doi: 10.1097/MD.0000000000011377
  9. Peter J Goadsby. “Pathophysiology of Migraine.” Ann Indian Acad Neurol. 2012 Aug; 15(Suppl 1): S15–S22. doi: 10.4103/0972-2327.99993
  10. Gutteridge, IF, et al. “ Branch Retinal Artery Occlusion During a Migraine Attack” Clin Exp Optom. 2007 Sep;90(5):371-5.
  11. Hoggan, RN, et al. “Thin-film optical notch filter spectacle coatings for the treatment of migraine and photophobia. J Clin Neurosci. 2016 Jun;28:71-6. doi: 10.1016/j.jocn.2015.09.024.
  12. Good, Pa, et al. “The use of tinted glasses in childhood migraine.” Headache. 1991 Sep;31(8):533-6.
  13. Noseda, R, et al. “Migraine photophobia originating in cone-driven retinal pathways.” Brain. 2016 Jul; 139(7): 1971–1986. doi: 10.1093/brain/aww119
  14. Burkhart K, et al “Amber lenses to block blue light and improve sleep: a randomized trial.” Chronobiol Int. 2009 Dec;26(8):1602-12. doi: 10.3109/07420520903523719.
  15. Antonaci, F, et al. “Recent advances in Migraine therapy” Springerplus. 2016; 5: 637. doi: 10.1186/s40064-016-2211-8
  16. Agostoni, E.C., Barbanti, P., Calabresi, P. et al. “Current and emerging evidence-based treatment options in chronic migraine: a narrative review.” J Headache Pain 20, 92 (2019). https://doi.org/10.1186/s10194-019-1038-4
  17. Basar, E, et al. “Use of Botulinum Neurotoxin in Ophthalmology” Turk J Ophthalmol. 2016 Dec; 46(6): 282–290. doi: 10.4274/tjo.57701
  18. Chen, VC, et al. “Effects of selective serotonin reuptake inhibitors on glaucoma: A nationwide population-based study.” PLoS One. 2017; 12(3): e0173005. doi: 10.1371/journal.pone.0173005
  19. Aminlari, A, et al. “Topiramate Induced Acute Angle Closure Glaucoma.” Open Ophthalmol J. 2008; 2: 46–47. doi: 10.2174/1874364100802010046
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About Amrita Kaur, OD

Dr. Amrita Kaur is an optometrist practicing in Pittsburgh, PA. She is a 2016 graduate of the Pennsylvania College of Optometry at Salus University. In the exam room she enjoys a challenging neuro or posterior segment case, pediatric exams, and getting to know her patients. Outside of the exam she enjoys painting, drawing, tennis, writing for NGO of course, and a good cup of tea! 


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