Migrane-Now – Migraine Now

June 10, 2020 In

Botox for Chronic Migraines

Botox for Chronic Migraines

Botox is FDA-approved for chronic migraines (headaches on 15 or more days a month), since 2010. Botox is not recommended for patients who experience fewer than 15 headache days a month. Botox is a form of botulinum toxin, a neurotoxin produced by the bacteria that causes botulism. When the botulinum toxin is purified and used in tiny doses in specific areas, it temporarily reduces muscle contractions for approximately 3 months.

Botox is injected around pain fibers that are involved in headaches. Botox enters the nerve endings around where it is injected and blocks the release of chemicals involved in pain transmission. This prevents activation of pain networks in the brain.

Botox prevents migraine headaches before they start, but takes time to work. Patients will see a decrease in headache frequency with an increase in the number of treatment cycles. One treatment lasts for 10-12 weeks.
In general, the FDA-recommended dosage is 155 units. The doctor uses a very small needle that feels like a pinprick and injects small amounts of Botox into shallow muscles in the skin. Each treatment typically involves 31 injections in seven key areas of the head and neck.

The most common side effect from the Botox shots is a sore neck, and we recommend using an ice pack to reduce the discomfort.

Because Botox is FDA approved for chronic migraines, it’s covered by most plans, including Medicare and Medicaid. Before your insurance approves Botox as a treatment for your chronic migraine, you typically must have tried and failed two other preventative treatments (anti-seizure medications, antidepressants, or blood pressure medications).

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June 4, 2020 In

Pulsed Radiofrequency

Pulsed Radiofrequency

The use of high frequency current at 500 kHz called radiofrequency, is well recognized in pain management. When applied close to a sensory nerve, the heat generated in the cells at the electrode tip causes coagulation which is believed to interrupt the pain conduction. The use of radiofrequency heat lesions adjacent to the DRG for the management of nonmalignant pain is becoming more controversial because of its potential neurodestructive nature. For that reason, a nondestructive or minimally destructive technique would be more attractive.

A modiﬁed technique, pulsed radiofrequency (PRF) treatment was developed whereby in 1 s two bursts of 20 ms each of an alternating current are delivered. The oscillating frequency of the alternating current is 500 kHz. During one cycle the “active” phase of 20 ms is followed by a silent period of 480 ms to allow for washout of the generated heat. The output is usually set at 45 volts, but if the electrode tip temperature exceeds 42°C, it is decreased to prevent cell damage. This temperature is selected based on the ﬁndings that necrosis in various soft tissue cell lines could only be induced by heating to greater than 43°C.

The clinical application of pulsed radiofrequency (PRF) by interventional pain physicians for a variety of chronic pain syndromes, including occipital neuralgia and other peripheral nerves around the head is growing. As a minimally invasive percutaneous technique with none to minimal neurodestruction and a favorable side effect profile, use of PRF as an interventional neuromodulatory chronic pain treatment is appealing. At this time, clinical research regarding the efficacy of PRF is limited but gradually accumulating.

Pulsed radiofrequency has opened new possibilities for the treatment of a variety of chronic pain syndromes, including neuropathic pain syndromes. Twenty years after the first report and more than 200 peer reviewed publications, no complications have been reported making it an attractive option.

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June 4, 2020 In

New Daily Persistent Headaches (NDPH)

New Daily Persistent Headaches (NDPH)

New daily persistent headache (NDPH) is unique in that headache is daily from onset, and soon becomes unremitting, typically occurring in individuals without a prior headache history, although patients with previous headache diagnosis also can develop NDPH. Headache lacks characteristic features, and may be migraine-like or tension-type-like, or have elements of both.

Patients very often recall and can accurately describe the onset of the headaches what is an important diagnostic feature.

The cause of NDPH is still unknown. There have been several studies suggesting a link between a preceding flu-like or upper respiratory infection, a stressful life event, or extracranial surgery.

Increased intracranial pressure and insidious infectious processes have to be ruled out to establish an NDPH diagnosis.

Treatment of NDPH is difficult and symptoms (unremitting headaches) can last years and subside one day without explanation.

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June 4, 2020 In

Cluster Headaches

Cluster headache (CH) is a primary headache disorder classified alongside with trigeminal autonomic cephalalgias. CH still is commonly misdiagnosed and patients can wait many years before receiving proper diagnosis and adequate care.

Typically CH consists of recurrent attacks of unilateral pain, which are very severe and usually involve the orbital or periorbital region innervated by the first (ophthalmic) division of the trigeminal nerve.

The activation of the cranial autonomic pathways causes ipsilateral lacrimation, conjunctival injection, nasal congestion or rhinorrhea (or both), ptosis or miosis (or both), and periorbital edema. Only a few, if any, medical disorders are more painful than CH.

The term cluster headache originates from the tendency of attacks to cluster together into stretches lasting several weeks. In the episodic form the attacks can occur at certain times of year, often with a seasonal predilection separated by periods of remission, which last at least a month. Ten percent of patients have the chronic form and have continuous attacks with no interval.

Imaging studies with functional MRI (FMRI) have detected activation ipsilateral to the pain in the region of the posterior hypothalamus which may have a critical role in integrating the pain, cranial autonomic features, and unique timing of cluster headache.

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June 4, 2020 In

Tension Type Headaches (TTH)

Tension-Type Headaches

Tension-type headaches (TTH) are the most common primary headache disorder, with a lifetime prevalence of 78%. Its prevalence varies by age, sex, and continent. In the United States, the 1- year prevalence is estimated to be around 38.3% in adults. In both sexes, the prevalence peaks between the ages of 30 and 39 years (42.3% in men and 46.9% in women) and declines with increasing age. The prevalence of TTH is slightly higher in women in all age, race, and education groups. TTH is much more common in Europe, with various studies reporting a 1-year prevalence of up to 80%, than in Asia or the Americas, where prevalence ranges from 20% to 30%.

The global prevalence of current headache in all ages was found to be 47% for all headache, 38% for TTH, and 10% for migraine. Although migraine is by far the most common diagnosis at the doctor’s offices.

TTH is divided into three subtypes based on attack frequency: an infrequent episodic form, in which headaches occur 1 day or less per month on average; a frequent episodic form, in which headaches occur between 1 to 14 days per month for at least 3 months; and a chronic form with 15 or more headache days per month.

Diagnostic criteria for all three subtypes include at least two of the following pain characteristics: bilateral location, non-pulsating quality, mild or moderate intensity, and lack of aggravation with routine physical activity.

TTH has a greater socioeconomic impact due to its higher prevalence. While

the absenteeism among migraine sufferers is higher than in patients with TTH, those with TTH account for a greater total loss of workdays per year and a higher percentage of decreased work effectiveness

TTH is prevalent in children, adults, and elderly adults across the globe. Psychiatric and physical comorbidities may contribute to the burden, conferring a worse prognosis. Treatment needs to address both headache and associated diagnoses to be effective.

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June 4, 2020 In

Cervicogenic Headaches

Cervicogenic Headaches.

Cervicogenic headache is a well-recognized syndrome that can be differentiated from migraines and tension-type headaches clinically for being a side-locked unilateral pain, radiating from the back of the neck with evidence of neck involvement—attacks may be precipitated by digital pressure over trigger spots in the cervical/nuchal areas or sustained awkward neck positions.

Migrainous features may be present in some cases and lesions of the cervical spine are not necessarily seen on the imaging methods currently available.

Whiplash and head trauma (any kind of head trauma is transmitted to the cervical spine) may induce headaches. This is suspected when the pain onset and the whiplash and/or concussion are close in time.

Whiplash-related headaches tend to be short-lasting.

Whiplash and concussed patients must undergo cervical imaging to rule out structural lesions of the cervical spine.

The pathophysiology revolves around the anatomy and physiology of upper cervical segment nociceptive afferents, and their projections to second order neurons. In experimental animals, the cervical and ophthalmic divisions of trigeminal neurons clearly synapse on common second-order neurons in the trigeminocervical complex. The basic data are supported by clinical observations, such as referred pain from cervical muscles and the C2–3 zygapophysial joint.

Clinical data suggest that the caudal limit of cranial referral in the neck is at the level of the C3 afferents.

Caudal pressure on the head with lateral rotation is a very sensitive marker of upper cervical pathology.

Treatment consists basically on anticonvulsants (Pregabalin or Gabapentin), muscle relaxants, physical therapy, occipital nerve blocks and in refractory cases cervical medial branch block followed by Radiofrequency ablation of the medial branches.

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June 4, 2020 In

Medication Overuse Headaches (MOH)

Medication Overuse Headaches (MOH)

Medication overuse headache (MOH), previously called rebound headache, drug-induced headache, and medication misuse headache, is a subset of chronic daily headache (CDH), occurring on 15 days or more per month, 4 or more hours per day, for 3 or more months with the added feature of overuse of at least 1 class of abortive drug. In clinical practice, the common scenario is a patient with episodic migraine (EM) that transforms to chronic migraine (CM) in the setting of overusing 1 or more classes of abortive drugs. The main classes of drugs that cause MOH are: opioids, butalbital-containing mixed analgesics, triptans, simple analgesics, except for plain aspirin, and perhaps NSAIDs. There is an increase in frequency and intensity of headache attacks and enhanced sensitivity to stimuli that would trigger these attacks.

MOH prevalence is estimated in about 1-2% of the general population and is overwhelmingly more prevalent in women than in men. In specialized headache centers, the prevalence of MOH can be as high as 70% among referred patients, and if its high socioeconomic impact is taken into account (work absenteeism, recurrent emergency room visits, hospital admissions, and unnecessary diagnostic tests), MOH is likely to be one of the most if not the most costly neurological disorder known.

The general quality of life of MOH patients is worse than patients with episodic headaches

The most frequent headache diagnoses at onset are the following: migraine in 65%, tension-type headaches in 27%, and mixed or other headaches in 8%.

It also appears that migraine starts earlier in the life of patients with MOH than in those with EM. Cluster headache with coexisting migraine disorder can also be susceptible to developing MOH, and triptans along with opioids are the most common offending drugs.

The treatment of MOH consists of discontinuation of the offending drug(s), acute treatment of the withdrawal symptoms and escalating pain, establishing a preventive treatment when necessary, and the implementation of educational and behavioral programs to prevent recidivism.

In most patients MOH can be treated in the outpatient setting but for the most difficult cases including those with opioid or butalbital overuse, or in patients with serious medical or behavioral disturbances, effective treatment requires a multidisciplinary, comprehensive headache program, either day-hospital with infusion or inpatient hospital setting.

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June 4, 2020 In

Triggers, co-morbidities and premonitory symptoms of migraines

Triggers, co-morbidities and premonitory symptoms of migraines.

Migraine triggers and premonitory symptoms are reported by the vast majority of patients with migraine. The interaction of environmental triggers and a susceptible brain is what is thought to initiate migraines.

Kelman (Cephalalgia 2007;27:394-402), studying a sample of 1750 patients with migraines found that 76% of migraineurs reported triggered attacks of migraine and that triggers were very frequent in 9%, frequent in 27%, and occasional in 40%. The most common trigger factors (occurring at least occasionally) included stress (80%), hormones (65% of women), missed meals (57%), weather (53%), sleep disturbance (50%), odors (44%), alcohol (38%), heat (30%), and foods (27%). Subjects reported an average of 7 triggers.

Patients with migraine and triggers seem to have more severe headache profiles (longer attacks, more pronounced symptoms, higher recurrence rates, and more associated sleep and mood disturbances), longer lifetime duration of migraine, and more family members with migraine. Migraine with aura (MA) and chronic migraine were more frequently associated with triggers than migraine without aura (MO) and episodic migraine.

A number of studies have shown that stress and sleep significantly triggered headaches in patients with MA.

The most common migraine trigger is stress. Migraine sufferers are thought to be highly responsive emotionally. Anxiety, worry, shock, and sadness can all release certain brain chemicals that lead to a migraine headache. Paradoxically, the sense of release after a stressful period can trigger migraines (let-down headaches).

For many women, menstruation is a major trigger. Attacks may occur before or during menstrual period or at ovulation. The abrupt fall in estrogens is believed to be the cause. High levels of estrogens may explain why two thirds of women during pregnancy have less migraine attacks. Fluctuating estrogen levels around menopause may cause an increase in migraines attacks.

Sensory stimuli such as bright lights and sun glare can induce migraines, as can loud sounds. Unusual smells (perfume, paint thinner, secondhand smoke etc) can also be a trigger. Strong perfumes may be an immediate trigger for some patients as well as flickering lights such as TVs and movie screens or sunshine flashing through trees on a road.

A change of weather can prompt a migraine. The relationship between weather and migraines is poorly understood. Variations in barometric pressure, temperature and humidity can be the cause. It also has been hypothesized that changes in the ionic composition of the air that precede storms may also be a factor.

Missing sleep or getting too much sleep may trigger migraines in some people, as can jet lag.

Oral contraceptives and vasodilators, such as nitroglycerin, can aggravate migraines

Intense physical exertion, including sexual activity, may provoke migraines.

Aged cheeses, salty foods and processed foods may trigger migraines. Skipping meals or fasting also can trigger attacks.

Ripened cheeses that contain tyramine (such as cheddar, emmental, stilton, brie, and camembert).
Chocolate
Sugar in excess.
Marinated, pickled, or fermented foods
Foods that contain nitrites or nitrates (bacon, hot dogs) or MSG (soy sauce, meat tenderizers, seasoned salt), sweeteners (aspartame).
Sour cream
Nuts, peanut butter
Sourdough bread
Broad beans, lima beans, fava beans, snow peas
Figs, raisins, papayas, avocados, red plums, bananas, citrus fruits, pineapple etc.
Alcohol (including red wine and beer)
Excessive amounts (more than 300mg) of caffeinated beverages such as tea, coffee, or cola.

Starbucks brewed coffee caffeine content: Short (8 floz) 180mg, Tall (12 floz) 260mg, Grande (16 floz) 330mg and Venti (20 floz) 415mg.

While caffeine can trigger migraine and cause rebound headaches (Medication Overuse Headaches) in some individuals, caffeine may be an effective ally in treating acute migraines. Caffeine can assist in restoring the stomach’s motility that may be reduced during a migraine attack and beyond simply promoting absorption of oral medications caffeine may itself exert a more direct therapeutic effect on the migraine process. For that reason caffeine is a component of many preparations available for acute headache treatment.

Kelman (Headache 2004; 44:865-872), evaluated 893 patients found that nearly one third of the patients fulfilling diagnostic criteria for migraine had premonitory symptoms. The median duration of premonitory symptoms was 2 hours (mean 6.8 hours). The most common premonitory symptoms were fatigue (25.6%), changes in mood (23.4%), and gastrointestinal (GI) symptoms (22%). Less common symptoms included head pain, aching and twitching, eye symptoms, cognitive changes, temperature changes, yawning, food craving, etc.

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June 1, 2020 In

Migraine Epidemiology, Prevalence and Incidence

Migraine Epidemiology, Prevalence and Incidence.

Migraine is a prevalent and disabling brain disorder with strong genetic component. Migraine is ranked 19th by the WHO among the leading causes of years lived with disability. In the US, migraine affects approximately 18% of women and 6% of men (12% of the US population), causing a 50% reduction in productivity at work or school in 51% of affected individuals, and absenteeism at work or school of at least 1 day every 3 months. It is believed that healthcare costs of migraine are $US19.6 billion and €27 billion per year to the US and European economies, respectively.

Migraine is the most frequent diagnosis that compels patients with episodic headaches to seek medical care.

Before puberty, migraine prevalence is higher in boys than in girls. When adolescence approaches, the incidence and prevalence of migraines increases more rapidly in girls than in boys. The prevalence of migraines increases throughout childhood and early adult life until around age 40, declining after that. Overall prevalence is highest from 25 to 55 years of age, usually the most economically productive years.

Migraine prevalence is low in Africa and Asia, high in Central and South America and even higher in North America.

Migraine prevalence seems to be inversely related to household income and education.

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June 22, 2017 In

Migraine Physiopathology

Migraine Physiopathology

Migraine can be viewed as the interaction of environmental triggers and a susceptible brain.

Migraine is an abnormal state of the brain but it was once thought to be primarily a disorder of blood vessels. Vascular changes occur, but they are not primary, and while some now prefer to call migraine a neurovascular disorder, there is ample evidence that patients with migraines have an abnormal central nervous system, resulting in various well-recognized clinical symptoms.

Migraine triggers include physical activity, dietary factors, sleep disturbances, head trauma, hormonal influences, and medications.

Several medical conditions have been shown to be comorbid with migraine (they occur with migraine more frequently than in the general population). These conditions include mitral valve prolapse, patent foramen ovale (migraine with aura), Raynaud phenomenon, stroke, epilepsy, depression, anxiety, bipolar disorder, and social phobias.

Migraine is generally hereditary with polygenic inheritance. Trauma can also precipitate headache with migrainous features, and the pathophysiologic consequences of head trauma have many similarities to migraine.

The understanding of migraine pathophysiology has advanced significantly in the past 20 years.

There is compelling evidence that diencephalic and brainstem nuclei can modulate activation of the trigeminovascular system. The trigeminovascular system consists of efferent projections to the craniovascular structures of the dura mater and cranial blood vessels, and afferent projections from these structures back to the trigeminal nucleus caudalis (TNC) that runs from the medulla down into the region of the third cervical segment where it blends gradually into the cervical dorsal horns.

Fibers from upper cervical roots enter the TNC, which sends fibers rostrally to the thalamus and collaterals to the autonomic nuclei in the brainstem and the hypothalamus. Thalamic neurons project to the somatosensory cortex but also to areas of the limbic system.

Pain from the face and head may be referred to the neck, and pain from the neck can be referred to the face, especially in the distribution of the first division of the trigeminal nerve (V1). The greater occipital nerve (formed by C2), is often tender during an attack of migraine or cluster headaches and an occipital nerve blockade can terminate an attack.

Cortical Spread Depression (CSD) may also play an important role in the genesis of a migraine attack.

CSD is a wave of neuronal depolarization followed by a suppression of neuronal activity with blood flow changes that starts at the occipital lobe and moves across the cerebral cortex at rate of about 3 mm/min. Meningeal nociceptors are activated, mast cells are activated and degranulate. The trigeminovascular reflex is activated. Trigeminal neurons supplying the dural vessels release calcitonin gene-related peptide (CGRP), substance P, and neurokinin A.

The vessels dilate and become inflamed, and plasma protein extravasation occurs (also known as sterile neurogenic inflammation) in addition to central sensitization, and is perceived as head pain.

Increased CGRP is found in the jugular veins of patients with migraines during an attack.

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Author archives: Migrane-Now

Botox for Chronic Migraines

Pulsed Radiofrequency

New Daily Persistent Headaches (NDPH)

Cluster Headaches

Tension Type Headaches (TTH)

Cervicogenic Headaches

Medication Overuse Headaches (MOH)

Triggers, co-morbidities and premonitory symptoms of migraines

Migraine Epidemiology, Prevalence and Incidence

Migraine Physiopathology