Faculty Bibliography

The aim of this study was to assess the role of depression as a predictor of new onset of chronic migraine (CM) among persons with episodic migraine (EM). The American Migraine Prevalence and Prevention (AMPP) study followed 24,000 persons with severe headache identified in 2004. Using random-effects logistic regression, we modeled the probability that persons with EM in 2005 or 2006 would develop CM in the subsequent year. Depression was assessed in two ways, using a validated questionnaire (PHQ-9 score >/=15) and based on self-reported medical diagnosis. Analyses were adjusted for multiple covariates including sociodemographics, body mass index, headache pain intensity, headache frequency, migraine symptom severity, cutaneous allodynia, acute medication overuse, anti-depressant use and anxiety. Of 6,657 participants with EM in 2005, 160 (2.4 %) developed CM in 2006. Of 6,852 participants with EM in 2006, 144 (2.2 %) developed CM in 2007. In fully adjusted models, PHQ-9 defined depression was a significant predictor of CM onset [odds ratio (OR) = 1.65, 95 % CI 1.12-2.45]. There was a depression-dose effect; relative to participants with no depression or mild depression, those with moderate (OR = 1.77, 95 % CI 1.25-2.52), moderately severe (OR = 2.35, 95 % CI 1.53-3.62), and severe depression (OR = 2.53, 95 % CI 1.52-4.21) were at increased risk for the onset of CM. Among persons with EM, depression was associated with an increased risk of CM after adjusting for sociodemographic variables and headache characteristics. Depression preceded the onset of CM and risk increased with depression severity suggesting a potentially causal role though reverse causality cannot be excluded.

Postherpetic neuralgia has been variably defined but is generally understood to be pain that persists for longer than a few months after an attack of herpes zoster. Pain persists for years in approximately 10 % of those afflicted with acute herpes zoster. The likelihood of postherpetic neuralgia increases with older age, severity of the zoster, trigeminal location, and other factors. Postherpetic neuralgia is a neuropathic pain and treatment usually involves sequential trials of topical and systemic drugs; a variety of other therapies may be considered in refractory cases. A new topical capsaicin 8 % patch has been approved for this indication based on the positive studies in patients with non-trigeminal postherpetic neuralgia. Experience with the use of the capsaicin 8 % patch for trigeminal distribution neuralgia is lacking. We report a case of trigeminal postherpetic neuralgia which was safely and effectively treated with capsaicin 8 % patch.

Migraine is a common primary headache disorder. A subset of patients may become disabled by frequent, severe, or treatment-refractory headache. Most patients respond adequately to drugs administered by the oral, intramuscular, or subcutaneous route. Intravenous therapy is an option for the treatment of severe headache in a monitored setting. The most common scenario is the treatment of acute refractory headache in the emergency department. Intravenous treatment may be undertaken with common analgesics, such as acetaminophen, ibuprofen, and ketorolac, or an opioid, or with a drug used specifically for migraine. Among the latter drugs are antiemetic dopamine antagonists, dihydroergotamine, magnesium, valproate sodium, and glucocorticoids. Some of the latter agents have been studied in controlled trials but data are too limited to inform clinical guidelines. Larger placebo-controlled trials of these and other agents will be needed to better position the intravenous drugs in the treatment strategies for acute refractory headache, refractory chronic migraine, and withdrawal headache during the management of medication overuse headache

Migraine and tension-type headache are common in general population. Recent progress in basic and clinical research has increased our understanding of pathophysiology of these headaches. New treatment modalities and drugs for the treatment of these headaches are emerging. Migraine is a neurovascular headache with complex pathophysiology, which has not been fully clarified. Genes for both migraines, with and without aura, are being identified. Current research indicates importance of cortical spreading depression and abnormal brain stem activity in the pathophysiology of migraine with aura. The migraine headache most likely originates in the sensory fibers innervating intracranial and extracranial blood vessels. Peripheral and central sensitization of trigeminovascular nociceptive pathways may develop during migraine attacks. Central sensitization of second- and third-order trigeminovascular nociceptive neurons may lead to transformation of episodic migraine to chronic migraine. Pericranial myofascial pain sensitivity is increased in patients with tension-type headache and may be of importance in the pathophysiology of this headache. Sensitization of second-order neurons at the level of the spinal dorsal horn or trigeminal nucleus, sensitization of supraspinal neurons, and decreased descending inhibition from supraspinal structures play a major role in the pathophysiology of chronic tension-type headache

Tension-type headache (TTH) is a disorder with high prevalence and significant impact on society. Understanding of pathophysiology of TTH is paramount for development of effective treatments and prevention of chronification of TTH. Our aim was to review the findings from pain perception studies of pathophysiology of TTH as well as to review the research of pathophysiology of TTH. Pain perception studies such as measurement of muscle tenderness, pain detection thresholds, pain tolerance thresholds, pain response to suprathreshold stimulation, temporal summation and diffuse noxious inhibitory control (DNIC) have played a central role in elucidating the pathophysiology of TTH. It has been demonstrated that continuous nociceptive input from peripheral myofascial structures may induce central sensitization and thereby chronification of the headache. Measurements of pain tolerance thresholds and suprathreshold stimulation have shown presence of generalized hyperalgesia in chronic tension-type headache (CTTH) patients, while DNIC function has been shown to be reduced in CTTH. One imaging study showed loss of gray matter structures involved in pain processing in CTTH patients. Future studies should aim to integrate pain perception and imaging to confirm this finding. Pharmacological studies have shown that drugs like tricyclic anti-depressant amitriptyline and nitric oxide synthase inhibitors can reverse central sensitization and the chronicity of headache. Finally, low frequency electrical stimulation has been shown to rapidly reverse central sensitization and may be a new modality in treatment of CTTH and other chronic pain disorders.