Secondary Headache: Current Update.

PURPOSE: The purpose of this paper is to review some of the causes of secondary headache particularly focusing on the subcategories of secondary headache in the International Classification of Headache Disorders, 3rd edition, the clinical features of these headaches, and their associated features and management. OVERVIEW: Headache attributed to trauma or injury to the head and/or neck, headache attributed to cranial or cervical vascular disorder, headache attributed to non-vascular intracranial disorder, headache attributed to a substance or its withdrawal, headache attributed to infection, headache attributed to disorder of homeostasis, and headache or facial pain attributed to disorder of the cranium, neck, eye, ears, nose, sinuses, teeth, mouth, or other facial or cervical structure are discussed in this paper. DISCUSSION: Headache is a common symptom of multiple medical conditions. Although a minority of headache patients have a secondary basis for their headaches, it is important to identify clinical features of secondary headache disorders including both the headache and non-headache features of the condition, diagnose the secondary etiology correctly, and treat them appropriately.

Migraine Aura: Updates in Pathophysiology and Management.

PURPOSE OF REVIEW: To provide an updated review of the pathophysiology, diagnosis, and management of migraine with aura. RECENT FINDINGS: Thalamic and other subcortical regions may play a role in the pathophysiology of migraine. There is inter-patient and intra-patient attack variability in the characteristics of typical aura especially visual aura symptoms. Migraine with brainstem aura may originate cortically. Migraine with retinal aura may be associated with structural and functional changes in the retina. Although cortical spreading depression (CSD) continues to be the predominant theory surrounding the pathophysiology of migraine with aura, the exact mechanism of action of CSD and its role in relation of all phases of migraine including features of aura are not fully understood. Novel experimental models and newer diagnostic tools including neuroimaging are currently being used to enhance of understanding of migraine with and without aura. Transient ischemia attacks, stroke, and epilepsy should be considered in your differential diagnosis of migraine with aura. There are no specific therapies for migraine with aura.

Cold Stimulus Headache.

PURPOSE OF REVIEW: To provide an updated review on cold stimulus headache. RECENT FINDINGS: Age, type of stimulus, comorbidities, and study design but not necessarily gender appear to influence the reported prevalence of cold stimulus headache (CSH). Different cold stimuli appear to provoke different types of CSH. Ice water appears to provoke more frequent and higher pain intensity with a shorter latency compared to CSH provoked by ice cubes. Cold stimulus headache is very common unusual headache with limited literature. The severity, frequency, and latency appear to be influenced by the speed and size of the exposed area.

Primary Stabbing Headache.

PURPOSE OF REVIEW: To provide a comprehensive and updated review of the literature on primary stabbing headache. RECENT FINDINGS: Changes to the ICHD-3 criteria have resulted in increased sensitivity to capture primary stabbing headache (PSH). According to the ICHD-3, the sharp stabbing pain is no longer restricted to the first division of the trigeminal nerve. Age, gender, and co-morbidities such as migraine seem to influence the prevalence of PSH. Subclassification into monophasic, intermittent, and chronic forms have been proposed in a recent prospective study and may be helpful from a prognostication perspective; however, further studies are required. Secondary etiologies for stabbing headaches are part of the differential diagnosis of primary stabbing headache; therefore, it is reasonable to perform neuroimaging. For severe frequent attacks, indomethacin continues to be considered first line. Other treatment options include COX2 inhibitors and melatonin.

Photophobia: When Light Hurts, a Review.

PURPOSE OF REVIEW: To provide an updated overview of Photophobia with a particular focus on photophobia related to migraine. RECENT FINDINGS: Melanopsin-containing photoreceptors called intrinsically photosensitive retinal ganglion cells (ipRGCs) have been identified in the retina and explain the rational for photophobia in individuals who are blind. Photophobia, a sensory disturbance provoked by light, is a common neurological and ophthalmological symptom. Migraine, a common neurological condition, is pathognomonic of photophobia; however, other primary headache conditions, traumatic brain injury, and impairment of the optic pathway can cause photophobia. In addition, anterior and posterior segment ocular pathology, medications, and psychiatric conditions can result in photophobia. At least 2 (possibly three) distinct neural pathways are involved in photophobia. Some of the basic science regarding these pathways is discussed in this review including the role of calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating polypeptide. Management of photophobia includes treatment of the underlying etiology and conservative strategies such as wearing sunglasses.

Headaches: a Review of the Role of Dietary Factors.

Dietary triggers are commonly reported by patients with a variety of headaches, particularly those with migraines. The presence of any specific dietary trigger in migraine patients varies from 10 to 64 % depending on study population and methodology. Some foods trigger headache within an hour while others develop within 12 h post ingestion. Alcohol (especially red wine and beer), chocolate, caffeine, dairy products such as aged cheese, food preservatives with nitrates and nitrites, monosodium glutamate (MSG), and artificial sweeteners such as aspartame have all been studied as migraine triggers in the past. This review focuses the evidence linking these compounds to headache and examines the prevalence of these triggers from prior population-based studies. Recent literature surrounding headache related to fasting and weight loss as well as elimination diets based on serum food antibody testing will also be summarized to help physicians recommend low-risk, non-pharmacological adjunctive therapies for patients with debilitating headaches.

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).

Canadian Headache Society systematic review and recommendations on the treatment of migraine pain in emergency settings.

BACKGROUND: There is a considerable amount of practice variation in managing migraines in emergency settings, and evidence-based therapies are often not used first line. METHODS: A peer-reviewed search of databases (MEDLINE, Embase, CENTRAL) was carried out to identify randomized and quasi-randomized controlled trials of interventions for acute pain relief in adults presenting with migraine to emergency settings. Where possible, data were pooled into meta-analyses. RESULTS: Two independent reviewers screened 831 titles and abstracts for eligibility. Three independent reviewers subsequently evaluated 120 full text articles for inclusion, of which 44 were included. Individual studies were then assigned a US Preventive Services Task Force quality rating. The GRADE scheme was used to assign a level of evidence and recommendation strength for each intervention. INTERPRETATION: We strongly recommend the use of prochlorperazine based on a high level of evidence, lysine acetylsalicylic acid, metoclopramide and sumatriptan, based on a moderate level of evidence, and ketorolac, based on a low level of evidence. We weakly recommend the use of chlorpromazine based on a moderate level of evidence, and ergotamine, dihydroergotamine, lidocaine intranasal and meperidine, based on a low level of evidence. We found evidence to recommend strongly against the use of dexamethasone, based on a moderate level of evidence, and granisetron, haloperidol and trimethobenzamide based on a low level of evidence. Based on moderate-quality evidence, we recommend weakly against the use of acetaminophen and magnesium sulfate. Based on low-quality evidence, we recommend weakly against the use of diclofenac, droperidol, lidocaine intravenous, lysine clonixinate, morphine, propofol, sodium valproate and tramadol.

Medication overuse headache.

Medication overuse headache (MOH) is a common and disabling headache disorder. It has a prevalence of about 1-2 % in the general population. The International Classification of Headache Disorders 3rd edition (beta version) has defined MOH as a chronic headache disorder in which the headache occurs on 15 or more days per month due to regular overuse of medication. These headaches must have been present for more than 3 months. The pathophysiology is complex and not completely known. It involves genetic and behavioural factors. There is evidence that cortical spreading depression, trigeminovascular system and neurotransmitters contribute to the pain pathway of MOH. The treatment of MOH includes patient education, stopping the offending drug(s), rescue therapy for withdrawal symptoms and preventative therapy. Relapse rates for MOH are high at 41 %. MOH can severely impact quality of life, so it is important to identify patients who are at risk of analgesic overuse.

Thunderclap headache.

Thunderclap headache (TCH) is a sudden severe headache that peaks to maximum intensity within 1 minute. Subarachnoid hemorrhage is the most commonly identified etiology for this headache, however, other secondary etiologies should be considered. Sentinel headache, reversible cerebral vasoconstriction syndrome, arterial dissection, cerebral venous sinus thrombosis, pituitary apoplexy, intracranial hemorrhage, ischemic stroke, reversible posterior leukoencephalopathy, spontaneous intracranial hypotension, colloid cyst, and intracranial infections are other possible causes of TCH. Investigations for the etiology of TCH begin with noncontrast CT head and lumbar puncture. MR brain, CT angiogram, MR angiogram, or CT/MR venogram may need to be performed if the initial investigations are negative. Treatment and prognosis depend on the etiology of the TCH.

Canadian Headache Society Guideline: acute drug therapy for migraine headache.

OBJECTIVES: The primary objective of this guideline is to assist the practitioner in choosing an appropriate acute medication for an individual with migraine, based on current evidence in the medical literature and expert consensus. It is focused on patients with episodic migraine ( headache on ≤ 14 days a month). METHODS: A detailed search strategy was used to find a relevant meta-analyses, systematic reviews and randomized double-blind controlled trials. Recommendations were graded with the Grading of Recommendations Assessment, Development and Evaluation (GRADE) Working Group, using a consensus group. In addition, a general literature review and expert consensus were used for aspects of acute therapy for which randomized controlled trials were not available. RESULTS: Twelve acute medications received a strong recommendation for use in acute migraine therapy (almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan, zomitriptan, ASA, ibuprofen, naproxen sodium, diclofenac potassium, and acetaminophen). Four received a weak recommendation for use (dihydroergotamine, ergotamine, codeine-containing combination analgesics, and tramadol- containing medications). Three of these were NOT recommended for routine use (ergotamine and codeine- and tramadol- containing medications). Strong recommendations were made to avoid use of butorphanol and butalbital- containing medications. Metoclopramide and domperidone were strongly recommended for use when necessary. Our analysis also resulted in the formulation of eight general acute migraine management strategies. These were grouped into: 1) two mild-moderate attack strategies, 2) two moderate-severe attack or NSAID failure strategies, 3) three refractory migraine strategies, and 4) a vasoconstrictor unresponsive-contraindicated strategy. Additional were developed for menstrual migraine during pregnancy, and migraine during lactation. CONCLUSION: This guideline provides evidence-based advice on acute pharmacological migraine therapy, and should be helpful to both health professionals and patients, The available medications have been organized into a series of strategies based on patient clinical features. These strategies may help practitioners make appropriate acute medication choices for patients with migraine.

The effect of prophylactic medications on TMS for migraine aura.

PURPOSE: Low frequency transcranial magnetic stimulation (TMS) has recently been shown to be effective for the acute treatment of migraine with aura. TMS has recently been shown to inhibit cortical spreading depression (CSD). Prophylactic medications (PM) may reduce the frequency of migraine attacks by elevating CSD threshold. The interaction between PM and TMS is unknown. METHODS: Subgroup analysis was performed on a double-blind, Sham-controlled study that evaluated the efficacy and safety of TMS for the acute treatment of migraine with aura. Analysis of the primary efficacy endpoint pain-free at 2 hours (pain-free rate [PFR]) between TMS and Sham groups was performed based on the non-randomized use of PM. RESULTS: A total of 164 subjects eligibly treated at least 1 migraine with aura attack with TMS (n = 82) or Sham stimulation (n=82). Baseline pain intensity at the time of treatment for the first attack was no pain (31%), mild (40%), moderate (23%), or severe pain (6%). PM were used by 37% (31/82) and 41.5% (34/82) in the Sham- and TMS-treated patients, respectively. Sham patients on no PM (Sham without) had significantly higher PFR than Sham-treated patients on PM (Sham with) (P = .0014). There was no difference in PFR between TMS-treated patients on (TMS with) or off (TMS without) PM (P = .5513). However, TMS with had significantly higher PFR than Sham with patients (P= .002). There was no difference in PFR between TMS without and Sham without patients (P = .4061). CONCLUSION: Prophylactic medications do not appear to influence the treatment response to TMS. The better response in Sham-treated patients not on PM may indicate a more responsive subgroup or different patient phenotype than those currently using PM. These findings will need to be verified in a larger patient sample randomized by presence or absence of PM.