Migraine, which affects more than 20% of people at some point in their lives, is considered the most common disabling brain disorder.1,2 It is a type of primary headache, meaning that the pain is due to the headache condition itself, not secondary to another cause, such as sinusitis.1 When chronic, it may severely impair a person’s ability to accomplish everyday activities. 

Migraine has a strong genetic component, and the majority of people living with migraine are women.1,2 In addition, women older than 45 years of age with a history of migraine have a higher incidence of major cardiovascular disease.1,3 

In our last column, we reviewed the basics of primary and secondary headaches, as well as the epidemiology, pathophysiology and diagnostic guidelines for migraine headache disorders.3 Here, we focus on how optometrists can work with other members of the health care team to bring relief to these patients. 

Migraine Aura

Migraine attacks may present with or without preceding aura (Table 1). When present, most auras are visual, commonly consisting of floaters, flashes, zigzag patterns and blind spots. Patients often report a severe, unilateral, throbbing or pulsing pain, which may be accompanied by visual alterations and photophobia.1,2

This is one patient’s approximation of the zig-zag visual disturbance experienced as a migraine aura. According to the patient, it moves and vibrates, expanding and slowly fading away over the course of about 20 minutes.

For some individuals, the typical aura is always followed by the migraine headache. For others, however, the attacks with aura are followed by a less distinct headache, or even no headache. Finally, a number of patients have, exclusively, the typical aura without headache.1,4 There are several sub-types of migraine with aura, as well as episodic syndromes that may be associated with migraine.4 

In cases where an aura occurs for the first time after age 40, or when the aura symptoms consist exclusively of negative phenomena (e.g., hemianopia), or if the aura is either prolonged or very short, clinicians should rule out other causes, such as transient ischemic attacks.1,2 

Eye care clinicians should be on the lookout for two forms of headache that require a more specific diagnosis and directly involve the eye and visual system:

Table 1. Types of Migraine1,4

Migraine without aura (previously known as a common migraine)
Recurrent headache with attacks lasting four to 72 hours. Unilateral location, pulsating quality, moderate to severe intensity, aggravation by routine physical activity and association with nausea, photophobia, phonophobia or a combination of all three.
Migraine with aura (previously known as a classic, complicated, ophthalmic, hemiplegic or aphasic migraine)
Recurrent attacks lasting minutes. Unilateral, fully reversible visual, sensory or other central nervous system symptoms that develop gradually and are usually followed by headache and associated migraine symptoms.
Chronic migraine
Headache occurring on 15 or more days per month for more than three months, which has the features of migraine headache on at least eight days per month.

Retinal migraine, a form of migraine with aura, is a rare cause of transient monocular visual loss. It is characterized by repeated attacks of unilateral visual disturbances, including scintillations, scotomata or blindness, all associated with the headache. Researchers have noted cases of permanent monocular visual loss associated with retinal migraine.4 Appropriate investigations are required to exclude other causes of transient monocular blindness (Table 2).

The term ophthalmoplegic migraine is a misnomer in that it is likely not a variant of migraine but rather a recurrent cranial neuralgia. A more appropriate name might be “ophthalmoplegic cranial neuropathy” or “ophthalmoplegia with migraine-like headache.”5,6  

Table 2. Differential Diagnosis of Transient Monocular Vision Loss7

  • Orbital/ocular ischemia (ophthalmic artery)
  • Retinal ischemia (central retinal artery and its branches, central retinal vein)
  • Optic nerve ischemia (short posterior ciliary arteries/ophthalmic artery)
  • Choroidal ischemia (posterior ciliary arteries)
  • Hyphema
  • Angle closure glaucoma
  • Retinal detachment
  • Papillitis
  • Optic nerve compression
  • Uhthoff’s phenomenon (demyelination)

Symptoms, Triggers and Treatments

The United Kingdom’s National Institute for Health and Care Excellence provides published guidelines on the diagnosis and treatment of migraine, and both the American Headache Society and American Academy of Neurology have expert consensus guidelines.1,2,5 In general, three approaches exist to managing migraine: lifestyle and trigger management, acute treatments (administered during an attack or exacerbation of chronic pain) and preventive treatments (medication or other interventions designed to reduce the tendency to experience attacks).

Lifestyle. Many patients find that lifestyle adjustments such as regularizing meals and sleep can reduce the frequency of their attacks. Patients should avoid triggering factors that precipitate a migraine attack, such as fatigue, lack of sleep, stress, certain foods and use of vasodilating agents.1,2 To help patients better avoid triggers, clinicians can suggest patients use a daily diary to document the headaches and daily activities that might have triggered them. Patients may need to reduce or discontinue any medications that exacerbate their headaches such as oral contraceptives and hormone replacement therapy.1,2,5

Table 3. Acute Migraine Treatment Options1,2,5

  • Paracetamol (1g)
  • Aspirin (900mg to 1200mg)
  • Ibuprofen (400mg to 800mg)
  • Naproxen (250mg to 500mg)
  • Triptans
    • Sumatriptan (50mg to 100mg orally, 10mg to 20mg nasally, 6mg subcutaneously)
    • Almotriptan (12.5mg)
    • Eletriptan (40mg to 80mg)
    • Frovatriptan (2.5mg)
    • Naratriptan (2.5mg to 5mg)
    • Rizatriptan (5mg to 10mg orally or sublingual melt)
    • Zolmitriptan (5mg to 10mg orally or sublingual melt, 5mg nasally)
  • Combinations
    • Sumatriptan (50mg) and naproxen (250mg to 500mg)

    (All of the above are taken alone or with domperidone (10mg orally) or an alternative antiemetic)

  • Vagal nerve stimulation
  • Single-pulse transcranial magnetic stimulation

Acute management. Combination analgesics containing aspirin, caffeine and acetaminophen are an effective first-line abortive treatment for migraine. Ibuprofen at standard doses is also effective for acute migraine treatment.1,2 As opposed to analgesics, triptans and ergotamines are more migraine-specific classes of medications (Table 3). 

Acute treatment is most effective when given within 15 minutes of pain onset and when pain is mild.2 Antiemetics (e.g., chlorperazine or promethazine) can be used to treat the emesis associated with acute migraine attacks.

 Preventative medication. Some form of medication or other treatment is almost always necessary for those with chronic migraine. Roughly 3% to 13% of migraine sufferers are using preventive therapy, although research suggests the need is much greater, with estimates that 38% of patients with migraine would benefit from a preventive agent (Table 4).1,2,5

Table 4. Preventive Treatments for Chronic Migraine1,2,5

Starting DoseTarget Dose
First line
   - Propranolol
   - Metroprolol
   - Atenolol
Angiotensin blockers
   - Candesartan
   - Amitriptyline
   - Nortriptyline
   - Dosulepin

10mg TID
25mg BID
25mg once daily

4mg once daily

10mg at night
10mg at night
25mg at night 

40mg to 80mg TID
100mg BID
100mg BID

12mg to 16mg once daily

75mg to 100mg at night
75mg to 100mg at night
75mg to 100mg at night
 Second line
   - Topiramate
   - Sodium valproate
toxin A (Botox)

12.5mg at night
200mg at night
5mg once daily
31 small injections of 5
units each placed at
prescribed locations over
the forehead

50mg to 100mg BID
400mg to 800mg BID
5mg to 10mg once daily 
(vitamin B2)
Magnesium citrate
(or taurate)
 400mg daily

600mg daily

The goals of preventive therapy are to reduce attack frequency, severity or duration, improve responsiveness to acute attacks and reduce general disability. Many medications are used to treat migraine prophylactically, including antiepileptic drugs, beta and calcium channel blockers, several subtypes of antidepressants and some antihypertensives, as well as supplements, herbs and vitamins.8

Many prophylactic meds for migraine work by inhibiting cortical spreading depression (CSD), which is considered the basis of migraine aura.8 Others have antiadrenergic or serotonin modulatory effects, or enhance the effect of the neurotransmitter gamma-aminobutyric acid, leading to a decrease in neuronal firing.

In addition, a 2002 survey shows that more than 85% of patients suffering from migraine headache use complementary and alternative medicine (CAM)—such as herbal agents, deep breathing and meditation, yoga and progressive relaxation—and 60% felt the CAM provided some relief.9 Biofeedback and behavioral changes are frequently part of the care for a migraine patient, for example. 

Studies have demonstrated the effectiveness of the herb butterbur (Petasites hybridus) in preventing migraines.10 Patients on butterbur require monitoring of liver enzymes.10 

Other natural supplements such as riboflavin (vitamin B2), coenzyme Q10, melatonin and magnesium appear to be effective and well tolerated for migraine prophylaxis as well.8,11-13

A basic working knowledge of the common primary headaches is key to properly diagnosing patients with migraine. A comprehensive ophthalmic workup with ancillary testing such as threshold perimetry and cranial nerve evaluation can help the optometrist rule out more serious secondary headache syndromes. Having a game plan for managing these patients will ensure they get the relief they need. Comanaging migraine sufferers with neurologists and other headache specialists can confirm the diagnosis and provide a substantial number of acute and preventive treatment options that can improve the lives of our patients. 

1. Weatherall MW. The diagnosis and treatment of chronic migraine. Therapeutic Advances in Chronic Disease. 2015;6(3):115-23. 
2. Hildreth CJ, Lynm C, Glass RM. Migraine headache. JAMA. 2009;301(24):2608. 
3. Pelino CJ, Pizzimenti JP. Not just another headache. Rev Optom2017;154(7):86-7.
4. Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia. 2013;33(9):629-808. 
5. Estemalik E, Tepper S. Preventive treatment in migraine and the new US guidelines. Neuropsychiatr Dis Treat. 2013;9:709-20.
6. Chakravarty A, Mukherjee A. Ophthalmoplegic migraine: A critical analysis and a new proposal. Annals of Indian Academy of Neurology. 2012;15(Suppl 1):S2-S6. 
7. Biousse V, Trobe JD. Transient monocular visual loss. Am J Ophthalmol. 2005;140(4):717-e1.
8. Estemalik E, Tepper S. Preventive treatment in migraine and the new US guidelines. Neuropsychiatr Dis Treat. 2013;9:709-20.
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10. Lipton RB, Göbel H, Einhäupl KM, et al. Petasites hybridus root (butterbur) is an effective preventive treatment for migraine. Neurology. 2004;63(12):2240-4. 
11. Schoenen J, Jacquy J, Lenaerts M. Effectiveness of high-dose riboflavin in migraine prophylaxis. A randomized controlled trial. Neurology. 1998;50(2):466-70. 
12. Sándor PS, Di Clemente L, Coppola G, et al. Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial. Neurology. 2005;64(4):713-5. 
13. Ferrari MD, Odink J, Tapparelli C, et al. Serotonin metabolism in migraine. Neurology. 1989;39(9):1239-42.