The Sphenopalatine Ganglion: Anatomy, Pathophysiology, and Therapeutic Targeting in Headache.

The sphenopalatine ganglion (SPG) has attracted the interest of practitioners treating head and face pain for over a century because of its anatomical connections and role in the trigemino-autonomic reflex. In this review, we discuss the anatomy of the SPG, as well as what is known about its role in the pathophysiology of headache disorders, including cluster headache and migraine. We then address various therapies that target the SPG, including intranasal medication delivery, new SPG blocking catheter devices, neurostimulation, chemical neurolysis, and ablation procedures.

Primary exertional headache: updates in the literature.

Primary exertional headache (PEH) has been recognized by the International Headache Society as a primary headache diagnosis since 1994. It is an uncommon, self-limited, and short-lasting disorder that is precipitated by exertion and is frequently comorbid with migraine. PEH shares a number of features with other headache disorders, including thunderclap headache, primary cough headache, and headache associated with sexual activity. Upon its initial occurrence, PEH requires a thorough neurologic evaluation and imaging studies to help eliminate possible underlying secondary causes, including subarachnoid hemorrhage and sentinel bleed. Although PEH is incompletely understood with regard to its epidemiology and pathophysiology, it is generally considered to be a benign disorder that is self-limited and responsive to trigger avoidance and indomethacin.

Establishing a diagnosis of benign paroxysmal positional vertigo through the dix-hallpike and side-lying maneuvers: a critically appraised topic.

BACKGROUND: Many patients consult neurologists because of vertigo. Benign paroxysmal positional vertigo (BBPV) is one of the most common types of vertigo. Although the clinical presentation of this common condition is straightforward, the diagnosis and diagnostic maneuvers can be challenging. OBJECTIVES: How useful is the Dix-Hallpike test in establishing the diagnosis of BPPV? How useful is an alternative positional test, such as the side-lying maneuver, in the diagnosis of BPPV? METHODS: We addressed the question through development of a structured critically appraised topic. Participants included consultant and resident neurologists, clinical epidemiologists, medical librarian, and clinical content expert in the field of otolaryngology. Participants started with a clinical scenario and structured questions, devised search strategies, located and compiled the best evidence, performed critical appraisals, synthesized the results, summarized the evidence, provided commentary, and declared bottom-line conclusions. RESULTS: A single study comparing the Dix-Hallpike and side-lying tests was identified. For the Dix-Hallpike test, the estimated sensitivity was 79% [95% confidence interval (CI) 65-94], specificity was 75% (33-100), positive likelihood ratio (LR) was 3.17 (95% CI 0.58-17.50), negative LR was 0.28 (95% CI 0.11-0.69). For the side-lying test, the estimated sensitivity was 90% (95% CI 79-100), specificity was 75% (33-100), positive LR was 3.59 (95% CI 0.65-19.67), negative LR was 0.14 (95% CI 0.04-0.46). The study employed very weak methodology, and therefore the results had limited validity. CONCLUSIONS: The Dix-Hallpike test is the standard from which the diagnosis of posterior semicircular canal BPPV is made. Hence evaluations of its diagnostic test properties and utility are challenging. For patients unable to move into the Dix-Hallpike test positions, alternative tests such as the side-lying test can be attempted. These modifications, however, are rarely necessary.

Caffeine for the prevention and treatment of postdural puncture headache: debunking the myth.

OBJECTIVE: Is caffeine effective in preventing and treating postdural puncture headache (PDPH)? METHODS: The question was addressed with a structured evidence-based clinical neurologic practice review via videoconferencing between 3 academic institutions. Participants included consultant and resident neurologists, clinical epidemiologists, medical librarians, and clinical content experts. A critically appraised topic format was employed, starting with a clinical scenario and structured question. Participant groups at each of the 3 institutions independently devised search strategies, located and compiled the best evidence, performed critical appraisals, synthesized the results, summarized the evidence, provided commentary, and declared bottom-line conclusions. RESULTS: Three directly relevant randomized controlled trial articles were selected as the best available evidence for the clinical questions. Two investigated caffeine [oral and intravenous (IV)] as PDPH prophylaxis and 1 (oral) as PDPH treatment. One additional quasirandomized trial (IV) and 1 open-label trial (IV) of caffeine for PDPH treatment were located by reviewing bibliographies. Articles describing the pharmacological basis for caffeine therapy were also identified. No valid pharmacological rationale for caffeine as an antinociceptive agent for PDPH exists. The clinical trials are few in number, small in sample size, methodologically weak or flawed, and either demonstrate no effectiveness, contradictory and conflicting results, or invalid answers. CONCLUSIONS: The wide endorsement for caffeine to prevent and treat PDPH found in textbooks and review articles appears to be unwarranted and insufficiently supported by the available pharmacological and clinical evidence.

ACE and ARB Agents in the Prophylactic Therapy of Migraine-How Effective Are They?

OPINION STATEMENT: Angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are antihypertensive agents that can be considered for migraine preventative therapy. Although the exact mechanisms by which ACE inhibitors and ARBs may work for migraine prophylaxis are unknown, there are several plausible hypotheses as to why modulating the activity of the renin angiotensin system could result in migraine prevention. Clinical trials of ACE inhibitors and ARBs provide evidence that they are effective and generally well tolerated when used for migraine prophylaxis. Based upon biologic plausibility, the quality of evidence for efficacy from clinical trials, and recommendations in published guidelines, we consider ACE inhibitors and ARBs as second- or third-line options for migraine prophylaxis.

Risk of development of medication overuse headache with nonsteroidal anti-inflammatory drug therapy for migraine: a critically appraised topic.

BACKGROUND: The development of medication overuse headache (MOH) is associated with frequent use of analgesics, especially opiates, for treatment of primary headache disorders, particularly migraine. Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used to treat migraine. OBJECTIVE: To critically evaluate evidence estimating the risk of MOH associated with NSAID therapy in patients with migraine. METHODS: The objective was addressed through the development of a structured, critically appraised topic. This included a clinical scenario, structured question, literature search strategy, critical appraisal, results, evidence summary, commentary, and bottom line conclusions. Participants included consultant and resident neurologists, a medical librarian, clinical epidemiologists, and headache neurology content experts. RESULTS: The 1-year incidence of MOH was 2.5%. In patients with low (0 to 4 d monthly) to moderate (5 to 9 d monthly) baseline headache frequency, NSAIDs were not associated with progression to MOH and may be protective (odds ratio=0.31; 95% confidence interval, 0.27-0.34). However, in patients with a high baseline headache frequency (10 to 14 d monthly), NSAIDs are associated with progression to MOH (odds ratio=1.93; 95% confidence interval, 1.82-2.06). CONCLUSIONS: Acute NSAID therapy is associated with progression to MOH in migraineurs with a high baseline migraine frequency but may be protective in patients with low baseline headache frequency. However, a causal role for NSAIDs in progression from episodic to chronic headache has not been established.