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14 Articles in Volume 15, Issue #6
Antihistamine for G-CSF–Induced Bone Pain
Book Review: Advanced Headache Therapy
Brain Drain: Lymphatic Drainage System Discovered in the Brain
Case History of Chronic Migraine: Update 2015 Part 2
Disturbed Sleep: Causes and Treatments
Is Topical Ketamine Ready For Prime Time?
Letters to the Editor: Central Sensitization, Microglia Modulators, Supplements
New App Helps Interpret Urine Drug Test Results
Osteoarthritis Update: 2015
Pain Catastrophizing: What Clinicians Need to Know
PPM Editorial Board: Tips for Treating Osteoarthritis
Practical Overview of Osteoarthritis
Status Report on Role of Stimulants in Chronic Pain Management
Treatment of Osteoarthritis

Case History of Chronic Migraine: Update 2015 Part 2

A step-by-step guide to the diagnosis and treatment of patient with refractory complex headache.
Page 1 of 3

This is the second part of our series titled “Case History of Chronic Migraine.” Our previous article followed the diagnosis of a complex patient with the pseudonym “Heather,” who was initially seen when she was 24 years of age.1 To recap, Heather had moderate chronic daily headache, with migraine 6 times per month. She also suffered from anxiety and depression (the mild end of the bipolar spectrum), had irritable bowel syndrome (IBS; primarily diarrhea), and neck pain.

History: Heather was prescribed topiramate (Topamax, others) as a preventive (starting dose, 25 mg at night, increasing to 50 mg) as well as the following abortive medications: sumatriptan (Imitrex, others), naproxen (Naprosyn, Aleve, others), ondansentron (Zofran, others) (for nausea), and occasional hydrocodone-acetaminophen (Vicodin, Norco, others). Heather reported that the topiramate helped her headaches but possibly exacerbated her depression and caused mild memory disturbances—50 mg of topiramate was the most she could tolerate because she experienced memory disturbances at a higher dose. Sumatriptan was only mildly helpful, but over-the-counter naproxen was useful and ondansetron relieved her nausea. She was exercising 20 minutes daily. We added quetiapine (Seroquel, others), slowly increasing to 50 mg at night, and substituted rizatriptan (Maxalt, others) for sumatriptan. Quetiapine helped her moods, but she could not tolerate more than 25 mg qhs. Rizatriptan was not very helpful, so we prescribed zolmitriptan (Zomig) nasal spray. We also encouraged Heather to see a psychotherapist.

Six Months Later

Heather returned 6 months later at age 25. At this point, her menstrual migraines were severe, but zolmitriptan nasal spray (with naproxen) helped at least most of the time. Heather was cycling in and out of depression, alternating with hypomania. She was chronically irritable and somewhat angry, which was interfering with relationships. Heather had had a rough go of it. She had a deadbeat boyfriend, Eric, who somehow neglected to inform her of his wife and two kids. She also had to deal with an alcoholic, abusive mother, although her 2 sisters were fairly supportive. Heather was not ruminating about suicide but occasionally wished she were dead. She had no active suicidal plans. Heather loved her job as a hairdresser, finding solace in the salon, but she bickered with Alan, a new stylist who had been stealing some clients. So, along with headaches and neck pain, Heather was angry and depressed. She found herself looking at every young, married woman with envy.

Q: What Treatment Options Should Be Considered?

Of course, I had a long talk with Heather about psychotherapy. She was reluctant to go, due to money, time, and stigma. I suggested a “sliding scale” therapist or a publicly-funded therapy organization and tried to “de-stigmatize” going to therapy. I often say, ”If it was up to me, everybody in our country would see a therapist.” I have found that it may take many years of pushing and suggesting to convince reluctant patients to seek therapy.

Heather’s headaches were somewhat controlled on topiramate (50 mg qhs) and quetiapine (25 mg), with the following abortives: zolmitriptan nasal spray, naproxen, ondansetron, and occasional hydrocodone. Her moods were more of an issue at this point. Thus, I searched for medication options that could help Heather’s (mild) bipolar moods as well as her headaches.

Possibilities included: lamotrigine (Lamictal, others), oxcarbazepine (Trileptal, Oxtellar XR, others), valproate sodium (Depokene, others), another atypical antipsychotic (such as aripiprazole [Abilify, others]), or lithium (Lithobid, others). I wanted to avoid antidepressants, although some patients with bipolar disorder who are on an adequate mood stabilizer may tolerate antidepressants.

Lamotrigine has minimal side effects (rarely does lamotrigine cause tiredness or weight gain). Oxcarbazepine is a mild (and often overlooked) mood stabilizer that is available in a long-acting form (Oxtellar XR). Although related to carbamazepine (Tegretol, others), oxcarbazepine has markedly fewer adverse effects. Valproate sodium can help stabilize moods as well as headaches, but it tends to cause weight gain and fatigue and has greatly increased risks if the patient becomes pregnant. Adding aripiprazole is an option because it does not tend to cause the weight gain and fatigue that quetiapine may produce. Lithium, in low doses, often is very effective. Lithium is probably underused in the “mild” bipolar population. However, with lithium, particularly in higher doses, weight gain, fatigue, and hypothyroidism somewhat limit its use.

We decide to proceed with lamotrigine—starting at 25 mg and, after 10 days, increasing to 50 mg (Table 1). The risk with lamotrigine is the development of Stevens-Johnson Syndrome (SJS) and toxic epidermal necrolysis (TEN). SJS is an immunologically based form of erythema multiforme—SJS and TEN are probably manifestations of the same disease process, with SJS being milder and TEN more severe. SJS usually involves the mucous membranes and skin. With SJS, the male-to-female ratio is 2:1 in patients with a genetic predisposition. Infectious SJS begins with nonspecific upper respiratory infection symptoms, with a sudden onset of skin lesions. Drug causes are varied—from oxicam-containing NSAIDs to sulfa drugs to anticonvulsants. The more severe TEN implies more skin area involvement than is seen with SJS.

These serious systemic and skin reactions only are observed in approximately 1 in 2,500 to 3,000 patients taking lamotrigine. However, a “regular” drug rash often is seen (at least 10% of patients). TEN carries a mortality rate of 30% to 50%, whereas SJS has a mortality rate of 1% to 5%. With any rash, I stop lamotrigine (or any drug new to the patient).

Lamotrigine Follow-up

Three weeks after we initiated the lamotrigine, Heather called and reported no rash but also no improvement in moods. We increased the lamotrigine to 75 mg for 10 days, then 100 mg per day. I instructed her to discontinue lamotrigine at the first sign of a rash. Six weeks later, Heather came for a visit, and stated that her mood is significantly improved. She had been working out her differences with Alan at work. She had been less irritated and depressed, and her feeling of “mind racing” had lessened. Mind racing may be a result of several conditions, particularly anxiety vs. mania (or hypomania). It is important to inquire as to the “quality” of the rumination and racing. If it is constant worry, anxiety is the likely cause. With hypomania, it may simply be random thoughts racing through the brain and not necessarily connected to worry or anxiety.

Last updated on: June 12, 2017
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Alternative Medicine in Chronic Migraine 2014: What Clinicians Need to Know
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