The OD’s Role in Diagnosing and Managing Headaches

Optometrists are often the first health care professionals that patients consult when they have various types of head pain. Whether the cause is a primary headache syndrome such as a tension-type headache or migraine or a more pathologic condition such as sinusitis or idiopathic intracranial hypertension, many times patients are concerned that their symptoms are at least in part related to their vision or visual system. This article provides insights from a panel of esteemed clinicians on the differential diagnosis and management of the headache conditions that optometrists are likely to encounter in clinical practice.

IS IT SINUSITIS?

What would you advise for a colleague confronted with a suspected case of sinusitis?

James Fanelli, OD, FAAO: Sinus disease often manifests itself as ocular or periocular pain and discomfort. Eye care specialists often see patients with similar symptoms that are truly eye-related, be they binocular vision problems such as convergence insufficiency or disease processes such as anterior segment inflammation. The challenge for us is to differentiate those periocular aches and pains that are truly ocular in origin from those that have the same symptoms but are not of direct ophthalmic origin. For example, many times the source of the discomfort is sinus-related.

Optometrists should be able to assess patients’ paranasal air sinuses in clinic, in a reasonable amount of time and with good certainty. Many instances of periocular pain originate in the paranasal air sinuses. From a simply anatomic perspective, the orbits are for the most part surrounded by the sinuses. The large maxillary sinus lies below the orbital floor, the ethmoidal sinuses lie medial to the nasal orbital wall, the frontal sinus lies above the orbit, and the sphenoidal sinus lies behind the orbits. So it makes sense that, as part and parcel of a clinical ophthalmic examination of a patient presenting with signs and symptoms of sinus disease, we should be able to efficiently evaluate the sinuses in the orbit.

The next issue would be how to manage sinusitis. Some of these folks need imaging, but, with a quick in-office evaluation that points to active sinus disease, many patients can be treated empirically. The clinical information provided by an evaluation of the sinuses is often enough to make an accurate diagnosis. From there, the focus turns to managing the sinusitis. The mainstay of therapy is oral antibiotics, as well as a short course of oral decongestants and nasal steroids, but which antibiotic is used will depend on whether the patient has acute or chronic disease, as the pathogens implicated tend to be different.

In acute sinusitis, more often than not, the offending pathogens are Haemophilus influenzae and/or Streptococcus pneumoniae. Consequently, antibiotics that are effective against such pathogens would be selected. Compare that with chronic sinusitis, which often has a preponderance of gram-negative pathogens as the underlying pathogens, so of course antibiotics effective against gram-negative flora in the sinuses would be chosen.

What is one of the biggest challenges our colleagues face when making decisions about sinusitis?

Dr. Fanelli: No question, the biggest challenge our colleagues face is in evaluating the sinuses. As far as I know, it’s not taught in optometry school. Although it’s simple to do, we go through our educational system so focused on the eye, we sometimes pay little or no attention to relevant adjacent structures such as the sinuses. Once a practitioner knows how to evaluate the paranasal air sinuses, diagnosis and management is easy.

MIGRAINE MATTERS

A number of treatment options for patients with chronic migraine, both pharmacologic and nonpharmacologic, have recently been introduced. Do any of these new options stand out to you?

Leonid Skorin Jr, OD, DO, MS, FAAO, FAOCO: The first specific therapy for acute migraine was available in the 1990s. These drugs, known as triptans, have become the first-line treatment of choice, and they are more efficacious when used in the early stage of a migraine. They are available in generic formulations and can be administered as oral tablet, sublingual troche, intranasal spray, or subcutaneous injection. The various triptan tablets may be combined with simple nonsteroidal antiinflammatory drugs for added efficacy.

It is important to note that triptans can have serious adverse effects in patients with vascular disease. They have to be avoided in patients with familial hemiplegic migraine, basilar migraine, ischemic stroke history, ischemic heart disease history, Prinzmetal angina, uncontrollable hypertension, and those who are pregnant.

In 2018, several members of a new category of medication, calcitonin gene-related peptide receptor antagonists, or CGRP antagonists, received FDA approval for migraine prevention. These medications are also specifically tailored therapies geared to known pathophysiologic mechanisms. These monoclonal antibodies have a long half-life and are administered once a month as a subcutaneous injection. They are also useful in patients with refractory migraine headaches. What makes them distinctive and potentially much safer than the triptans is that they can be used in medically complicated patients and seem to have no significant cardiovascular effects.

Several nonpharmacologic treatments for migraine have been developed in recent years. These modalities include transcutaneous magnetic stimulation and transcutaneous direct current stimulation. Their main advantage is that they are noninvasive, painless, and can be used quickly. Cefaly (Cefaly) is a device that is applied to the forehead to stimulate the trigeminal nerve via the supraorbital nerve. A handheld device applied to the neck, known as gammaCore Sapphire (electroCore), is a noninvasive vagus nerve stimulator. The sTMS mini (eNeura) is applied to the back of the head and works through central neuromodulation. The newest FDA-approved noninvasive device, Nerivio (Theranica Bio-Electronics) is a remote-controlled stimulator that is applied to the patient’s arm at the onset of a migraine headache or aura and is controlled by a smartphone app. A prescription is required for all these devices.

What has been the biggest barrier to effectively managing patients with chronic migraine?

Dr. Skorin: I have found that the biggest barriers in prescribing any of the new medications and noninvasive devices are their cost and getting health insurance companies to approve reimbursement for the patient. You have to document a previous patient history of drug intolerance or lack of efficacy from multiple other categories of less costly but potentially less efficacious medications. Any other conservative nonpharmacologic therapies that have been tried and failed must also be documented.

MANAGING ARTERITIS

Giant cell arteritis (GCA), or temporal arteritis, is a potentially sight- and life-threatening condition that often has a presenting feature of new onset localized temporal headache. What advice can you provide to colleagues confronted with this chief complaint, especially when the patient appears to have no other findings consistent with GCA?

Richard Mangan, OD: My first response to that practitioner would be: Are you sure there are no other findings consistent with GCA? Although GCA sequelae such as acute vision loss (arteritic ischemic optic neuropathy), jaw claudication, and new onset temporal headache make the clinical diagnosis relatively straightforward, it is important to remember that sometimes signs and/or symptoms of GCA can be quite subtle. A published example of this was a case of temporal artery biopsy-proven GCA with the only clinical finding being unexplained fever.¹

Any patient 50 years of age or older who presents with new onset localized temporal headache, especially unilateral, should raise suspicion for GCA, with or without a report of transient vision loss. Evaluation of such a patient should include a thorough case history for both GCA (ie, constitutional symptoms, fever, weight loss, jaw claudication, and scalp tenderness) and polymyalgia rheumatica (ie, proximal joint pain or stiffness), as there is a high association between these two disease entities (Table).² The next step is to do a physical examination of the temporal artery and surrounding tissue (see Exam Tips).

Why is this important? According to the American College of Rheumatology, the presence of three or more of the following five criteria is sufficient to make a diagnosis of temporal arteritis with a sensitivity of 93.5% and specificity of 91.2%³:

1. Age 50 years or older;

2. New onset of localized headache;

3. Abnormality of the temporal artery (tenderness, pulselessness, nodularity);

4. Raised erythrocyte sedimentation rate: >50 mm/1st hour;

5. Positive temporal artery biopsy.

This means that a patient who has a negative sedimentation rate and a negative temporal artery biopsy could still have GCA if he or she has extracranial temporal tenderness and/or pulselessness. A negative sedimentation rate does not always rule out temporal arteritis. Of patients with positive temporal artery biopsies in one study, 15% to 30% had a normal erythrocyte sedimentation rate.⁴ A negative temporal artery biopsy does not always rule out temporal arteritis. Due to the potential for “skip lesions” within the temporal artery, histology may provide a false negative interpretation.⁵

Therefore, in answer to the question, if the patient truly has no other signs or symptoms consistent with GCA, then other causes of temporal head pain must be ruled out. However, if you cannot rule out the possibility of GCA, then timely blood work (stat-ordered erythrocyte sedimentation rate, C-reactive protein, complete blood count with differential, and platelets) is still warranted.

What have you found to be the biggest barrier to managing these patients?

Dr. Mangan: The most frustrating thing to me is how cavalier some patients are about their symptoms, especially those who have experienced prodromal symptoms (ie, fever, temporal head pain, and transient vision loss) for weeks, only to finally see me after they have developed arteritic anterior ischemic optic neuropathy in one eye. Timely diagnosis and treatment could have prevented this.