Rashmi Halker

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.

Occipital nerve block for the short-term preventive treatment of migraine: A randomized, double-blinded, placebo-controlled study:

Background Occipital nerve (ON) injections with corticosteroids and/or local anesthetics have been employed for the acute and preventive treatment of migraine for decades. However, to date there is no randomized, placebo-controlled evidence to support the use of occipital nerve block (ONB) for the prevention of migraine. Objective The objective of this article is to determine the efficacy of ONB with local anesthetic and corticosteroid for the preventive treatment of migraine. Participants and methods Patients between 18 and 75 years old with ICHD-II-defined episodic (> 1 attack per week) or chronic migraine (modified ICHD-II as patients with > 10 days with consumption of acute medications were permitted into the study) were randomized to receive either 2.5 ml 0.5% bupivacaine plus 0.5 ml (20 mg) methylprednisolone over the ipsilateral (unilateral headache) or bilateral (bilateral headache) ON or 2.75 ml normal saline plus 0.25 ml 1% lidocaine without epinephrine (placebo). Patients completed a one-month headache diary prior to and after the double-blind injection. The primary outcome measure was defined as a 50% or greater reduction in the frequency of days with moderate or severe migraine headache in the four-week post-injection compared to the four-week pre-injection baseline period. Results Thirty-four patients received active and 35 patients received placebo treatment. Because of missing data, the full analysis of 33 patients in the active and 30 patients in the placebo group was analyzed for efficacy. In the active and placebo groups respectively, the mean frequency of at least moderate (mean 9.8 versus 9.5) and severe (3.6 versus 4.3) migraine days and acute medication days (7.9 versus 10.0) were not substantially different at baseline. The percentage of patients with at least a 50% reduction in the frequency of moderate or severe headache days was 30% for both groups (10/30 vs nine of 30, Δ 0.00, 95% CI –0.22 to 0.23). Conclusions Greater ONB does not reduce the frequency of moderate to severe migraine days in patients with episodic or chronic migraine compared to placebo. The study was registered with ClinicalTrial.gov (NCT00915473).

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.

Cluster Headache: Diagnosis and Treatment

Cluster headache is a rare yet exquisitely painful primary headache disorder occurring in either episodic or chronic patterns. The unique feature of cluster headache is the distinctive circadian and circannual periodicity in the episodic forms. The attacks are stereotypic--they are of extreme intensity and short duration, occur unilaterally, and are associated with robust signs and symptoms of autonomic dysfunction. Although the pathophysiology of cluster headache remains to be fully understood, there have been a number of recent seminal observations. To exclude structural mimics, patients presenting with symptoms suggestive of cluster headache warrant at least a brain magnetic resonance imaging (MRI) scan in their work-up. The medical treatment of cluster headache includes acute, transitional, and maintenance prophylaxis. Agents used for acute therapy include inhalation of oxygen, triptans, such as sumatriptan, and dihydroergotamine. Transitional prophylaxis refers to the short-term use of fast-acting agents. This typically involves either corticosteroids or an occipital nerve block. The mainstay of prophylactic therapy is verapamil. Yet, other medications, including lithium, divalproex sodium, topiramate, methysergide, gabapentin, and even indomethacin, may be useful when the headache fails to respond to verapamil. For medically refractory patients, surgical interventions, occipital nerve stimulation, and deep brain stimulation remain an option. As the sophistication of functional neuroimaging increases, better insight into the pathophysiological mechanisms that underlie cluster headache is expected.

Chronic Daily Headache: An Evidence-Based and Systematic Approach to a Challenging Problem

Individuals presenting with chronic daily headache (CDH) are considered among the most difficult and labor-intensive patients in a neurologists practice. However, when treated successfully, they can be the most rewarding. Successful treatment plans can be life-changing for patients. Unfortunately, due to both patient and physician-related factors, many individuals with CDH lapse from medical care and seek alternative therapies, and some continue spiraling downward, fueled by medication misuse and overuse. CDH is not a diagnosis but the presence of headache on at least 15 days/month for at least 3 months. Patients with CDH need secondary etiologies excluded through appropriate investigations before establishing treatment programs. Table 1 lists secondary causes of CDH to which the clinician must be alert. Imaging is frequently necessary to exclude secondary causes, and in the majority of cases, MRI is superior to CT because of causes that are often overlooked or not visible on head CT (table 2). In this article, we review primary CDH and discuss evidence-based treatment strategies. View this table: Table 1 Causes of primary and secondary chronic daily headache View this table: Table 2 Potential etiologies for headache that are often overlooked on head CT ### Short-duration CDH. Determining the usual duration (greater or less than 4 hours) of individual headache episodes will refine the differential diagnosis in patients with primary CDH. The prototypical short-lasting primary CDH (<4 hours) is chronic cluster headache (CCH), a trigeminal autonomic cephalalgia (TAC) characterized by severe orbital or temporal pain with accompanying cranial autonomic features such as nasal congestion or lacrimation. Cluster headache becomes chronic if attacks occur for more than 1 year with remissions lasting less than 1 month. Other TACs that may mimic CCH include chronic paroxysmal hemicrania (CPH), short-lasting unilateral neuralgiform headaches with conjunctival injection and tearing (SUNCT) syndrome, and short-lasting unilateral neuralgiform headaches with autonomic symptoms but without lacrimation and conjunctival injection (SUNA). These differ in …

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.

Sensitivity of MRI of the spine compared with CT myelography in orthostatic headache with CSF leak

Objective: To investigate the sensitivity of MRI of the spine compared with CT myelography (CTM) in detecting CSF leaks. Methods: Between July 1998 and October 2010, 12 patients with orthostatic headache and a CTM-confirmed spinal CSF leak underwent an MRI of the spine with and without contrast. Using CTM as the gold standard, we retrospectively investigated the sensitivity of spinal MRI in detecting a CSF leak. Results: Eleven of 12 patients with a CSF leak documented by CTM also had extradural fluid collections on spinal MRI (sensitivity 91.7%). Six patients with extradural fluid collections on spinal MRI also had spinal dural enhancement. Conclusion: When compared with the gold standard of CTM, MRI of the spine appears to be a sensitive and less invasive imaging modality for detecting a spinal CSF leak, suggesting that MRI of the spine should be the imaging modality of first choice for the detection of spinal CSF leaks.

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.

Identifying the Factors Underlying Discontinuation of Triptans

To identify factors associated with triptan discontinuation among migraine patients.

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.