Migraine and tension-type headache (TTH) are common primary disorders that carry significant morbidity and socioeconomic effect. In this article, we will review the epidemiology, presentation, and diagnosis of these disorders. First-line acute treatment for migraine consists of analgesics, triptans, and antiemetics, while nonsteroidal anti-inflammatory drugs are the mainstay treatment for TTH. Patients with frequent or chronic headaches warrant prophylactic therapy. For migraine, various classes of preventives can be used (β-blockers, tricyclics, antiepileptics, botulinum toxin), with the choice of therapy tailored to the patient's risk factors and symptoms. For TTH, tricyclics have the most evidence as prophylactic therapy. A new class of medication, monoclonal antibodies to calcitonin gene receptor peptide or its receptor, became available in 2018, and is the first class of medication specifically designed to treat migraine. In addition to pharmacotherapy, we will also review nonpharmacologic interventions as well as neuromodulation for migraine.

Genetic variations and gender contribute significantly to the large interpatient variations in opioid-related serious adverse effects and differences in pain relief with other analgesics. Opioids are the most commonly used analgesics to relieve moderate-to-severe postoperative pain. Narrow therapeutic index and unexplained large interpatient variations in opioid-related serious adverse effects and analgesia negatively affect optimal perioperative outcomes. In surgical, experimental, chronic, and neuropathic pain models, females have been reported to have more pain than males. This review focuses on literature evidence of differences in pain relief due to multiple genetic variations and gender of the patient.

Chronic pain is a major contributor to the global burden of disability. Prior studies on the association between serum 25-hydroxyvitamin D (25(OH)D) levels and chronic pain have yielded mixed results. The Vitamin D Assessment study, a large randomized controlled trial from New Zealand, offered the opportunity to examine this association in data collected at baseline in all participants, and among those with arthritis or depression. A total of 5110 participants aged 50-84 years were recruited from community general practices. Chronic pain (lasting ≥6 months) and other baseline characteristics were collected at baseline interview. Serum 25(OH)D concentration was measured by liquid chromatography-tandem mass spectrometry. Associations between 25(OH)D levels and chronic pain were explored using multivariable log-binomial regression to estimate relative risks (RRs). Out of 5,049 participants with complete data, 871 (17%) reported having this clinical outcome, and 1254 (25%) had a 25(OH)D concentration <50 nmol/L. There was no significant association between 25(OH)D and chronic pain, with vitamin D status categorized in four groups: <25.0, 25.0-49.9, 50.0-74.9, and ≥75.0 nmol/L (the highest group as reference). The unadjusted RRs were 1.09, 1.10, and 1.08, respectively (Ptrend = 0.24). Adjustment for demographics, lifestyle, BMI, medical history, prescription of analgesics and vitamin D supplements did not change this finding. Similar non-significant results were observed in participants with arthritis (n = 1732) or depression (n = 528). In this multi-ethnic, community-selected sample of older adults in New Zealand, serum 25(OH)D levels were not associated with chronic pain. These results do not support a role for low vitamin D status in the prevalence of chronic pain in older adults.