Posts Tagged "headache treatment"

Last updated on July 13th, 2021 at 07:16 am

SUMMER HEADACHES AND SUMMER MIGRAINES.

@Neuralgroover

The likelihood of a headache increases during the summer months. According to a recent study which surveyed ER visits for headaches, every 9°F rise in temperature increased a person’s short-term risk of a headache by about 7.5% before their emergency room visit. Heat, dehydration, weather changes and barometric pressure changes are the primary drivers of headaches during the summer months, but some lifestyle factors, such as the foods we eat during the summer, can also increase the risk of headaches.

Heat, Headaches, and the Weather

During the summer months, heat can be a contributor to both headaches and migraines. In certain areas of the country where barometric pressures can change suddenly during a storm, people frequently report headaches. This is a common and classic migraine trigger. Sometimes a headache may be caused by heat exhaustion, which has the following associated symptoms:

  • Dizziness
  • Muscle cramps or tightness
  • Numbness in the face and neck
  • Fainting
  • Nausea or vomiting
  • Cold, clammy, pale skin
  • Fast and weak pulse
  • Weakness or tiredness
  • Drenching sweat
  • Extreme thirst

For a summer headache that is not related to heat exhaustion, your symptoms may only include a throbbing or dull achy sensation in your head, fatigue, sensitivity to light, and dehydration. If you do have heat exhaustion, it is best to seek medical help because heat exhaustion can lead to heat stroke.

 

Relief for Heat and Weather-Related Headaches

For people prone to headaches and migraines triggered by heat, there are some ways to mitigate them. It might be wise to limit outdoor times on hotter days. Sunglasses, a hat, and sunscreen can also help. If you need to exercise, try to stay indoors in an air-conditioned environment. Sports drinks that contain electrolytes and plenty of water will also help you stay hydrated. If you already are suffering from a heat-related headache, certain essential oils, cold compresses, iced herbal teas (without caffeine), and NSAIDs can help reduce the intensity of the headache.

 

Exercise and Summer Headaches

Heat and exercise are often a combination of conditions for a headache, but if you choose to exercise, there are certain things that you can do to avoid getting a headache. Generally speaking, it is understood that when a person exercises, the blood vessels within their skull dilate. If you participate in strenuous activities, like rowing, running, weight lifting, or team sports (like baseball, softball, or volleyball), these can contribute to a headache.

Avoiding activities like these in high heat is advisable. However, another way to avoid headaches related to exercise is to develop a set of warm up exercises, which can help prevent headaches. Some good warmup exercises include stretches, followed by some light jogging and walking.

 

The Importance of Staying hydrated To Prevent Headaches

As a rule of thumb, people have generally learned that you should drink at least eight 8-ounce glasses of water each day. That is about two liters. However, during hot summer days when you are active, you might need to increase that to about 2-½ liters. When you are dehydrated, the brain can shrink and this causes the brain to pull away from the skull, causing a headache. When you relieve your dehydration, the brain returns to a normal state, relieving the headache.

 

Pollution, Allergens, and Summer Headaches

During the summer months, there are also other factors, like pollution and allergens, that can lead to headaches. Various air pollutants tend to increase during the summer months due to more people traveling and there being vehicles on the road. Lead, carbon monoxide, nitrogen dioxide, sulfur dioxide, and particulate matters all increase during the summer months and can cause headaches. Headaches that are related to pollution are often intense, sometimes leading to the point of being disabling, because they are often migraine. Pollution irritates the lungs, eyes, and triggers what is sometimes a very intense headache.

Allergy headaches have unique symptoms. Sometimes a person may experience pain localized over the sinus area and some other facial pain. More intense headaches can be throbbing and one-sided and sometimes are accompanied by nausea, and these are more likely to represent migraine.

Foods and Headaches During the Summer

More people typically barbecue and picnic during the summer months. Certain “summer foods” can trigger headaches. For example, hot dogs can potentially trigger headaches because of nitrites. Nitrites are generally present in some foods in very small quantities, but sensitivity will vary depending upon the person to this chemical. Processed meats like salami and bacon also can contain varying levels of nitrites. In this situation, it is best to substitute processed meats for something like a salad. Even the condiments that you put on your food can trigger headaches. Instead of pickles, you might want to consider swapping them for fresh vegetables on your burger. Avoid aged cheeses and try fresh herbs instead of soy-based condiments. More detailed discussion of migraine triggers can be found here.

 

Sunburn and Headaches

Generally, when we get sunburn, we think nothing of it and it goes away within a few days. However, sunburn can be more severe in certain types of situations. When swimming, sunburn is often more intense if you don’t use sunscreen. Sunburn can happen relatively quickly, within just 10 to 15 minutes of sun exposure. Some of the symptoms that you can get with severe sunburn include:

  • Tenderness and blistering of the skin
  • Pain and tingling sensations in the burned area
  • Headaches, fevers and chills
  • Nausea, dizziness, and dehydration.

The type of headache that accompanies a severe sunburn can sometimes feel like exhaustion and will often cover the entire head. To relieve a sunburn headache, cool/cold treatments can often help alleviate the intensity, including cold compresses, a cold shower, and drinking water.

 

Taking Care of Headaches During the Summer

Headaches are more frequent during the late spring and summer months. By drinking plenty of water, staying hydrated, regulating our exposure to sunshine, paying attention to food triggers, and not overexerting ourselves, we can reduce the potential for frequent and intense headaches. However, even with taking these precautions, headaches and migraines will still periodically happen. Thus, it is important to have a good abortive headache treatment such as the gepants (Ubrelvy, Nurtec ODT), Ditans (Reyvow)triptans, or regular over the counter (OTC) pain medicines such as acetaminophen, aspirin, ibuprofen, or naproxen if they work for you and if you can use them safely. If the headache frequency is high enough (generally more than 4 per month), a preventive headache or migraine treatment should be considered until your high frequency headache cycle subsides.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

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Last updated on July 13th, 2021 at 07:10 am

TMJ DISORDER AND TMJ ASSOCIATED HEADACHE AND FACIAL PAIN.

@Neuralgroover

The temporomandibular joint (TMJ) is the joint that connects the jawbone and the skull. This is one of the most powerful joints in the human body, as it can apply 162 pounds per square inch when a person bites. It is important to realize that the TMJ is a synovial joint. In other words, it is a joint composed of a capsule filled with synovial fluid. Similar to a knee joint (but on a much smaller scale), the synovial fluid keeps the joint lubricated and healthy. However, this can also be the source of various types of dysfunction. There is a condition called TMJ disorder that can contribute to facial pain and headaches. TMJ disorder is fairly common, impacting about 12% of Americans at any given time. Women get TMJ disorder more often than men; in fact, for every male TMJ sufferer, there are 9 female TMJ sufferers.

TMJ disorder tends to be higher among younger people, while women using estrogen or contraceptives tend to experience TMJ disorder more frequently.

 

What Is TMJ Disorder and What Causes It?

Loosely put, TMJ disorder is any type of pain and restricted movement that impacts the jaw joint and surrounding muscles. There are several different causes of TMJ, including

  • Injury to the tooth or jaw
  • Grinding or clenching of the teeth
  • Poor posture
  • Stress
  • Other issues

In some instances, even chewing gum can aggravate an outbreak of TMJ. TMJ disorder can lead to headaches and facial pain.

 

TMJ Disorder and Headaches

When TMJ sufferers have a headache, they often report a headache that is like a tension headache in nature. TMJ associated headaches often recur in one or more regions of the head and face and are accompanied by several different symptoms:

  • Tight face and jaw muscles
  • Face or jaw pain
  • Clicking noises in the jaw when chewing
  • Overall restricted movement of the jaw
  • Changes in how the teeth fit together when biting down

It is important to keep in mind that TMJ discomfort can also be a manifestation of migraine headache attacks. Migraines can also cause referred pain to the TMJ areas, neck, shoulders, sinus areas, and face. So if the TMJ discomfort happens primarily when someone has a migraine type headache or symptoms, it could also just be a referred pain syndrome rather than a true TMJ disorder.

 

Is There a Positive Outlook for TMJ Headaches?

TMJ headaches are incredibly uncomfortable, but there is generally a very good outlook for TMJ headaches. Your doctor may suggest a wide variety of treatments to alleviate the pain and often lifestyle changes and other treatments may be required to eliminate and address TMJ disorder. Treatments aimed at alleviating TMJ disorder itself are generally very successful in reducing the frequency of these types of headaches. Let’s take a look at some of the treatments that are available for TMJ headaches.

Very rarely are TMJ disorders serious and long lasting. In these rare situations, diagnosis and treatment must be sought quickly to manage and resolve the condition. Chronic, severe TMJ disorder is very rare, however, tendons, muscles, and cartilage over time can become damaged leading to arthritis. The good news is that most cases of TMJ disorder go away within about two weeks if the jaw is given the necessary time to rest and the root cause, such as stress, is removed.

Occasionally, TMJ disorder will go away on its own. Self-limiting cases are common and being aware of grinding and clenching can help alleviate TMJ over time if it’s not a severe case.

 

Lifestyle Changes to Address TMJ Associated Headaches and Facial Pain

Some behaviors may cause and trigger flare ups of TMJ disorder, as well as associated headaches and facial pain. Some people may experience this disorder from the type of food that they eat, the stress in their life, and certain jaw movements that they have learned as habits over the years. Some small lifestyle changes can help with TMJ disorder and associated headaches and pain, including:

  • Avoiding foods that are hard or require a great deal of chewing
  • Reducing the stress factors in one’s life to prevent jaw clenching and teeth grinding, which are coping behaviors aimed at dealing with stress.
  • Learning jaw exercises to strengthen the jaw muscles themselves and avoiding things like gum chewing and wide yawning, which can irritate the jaw joint.

Over-The-Counter Solutions for TMJ Associated Headaches and Facial Pain

For the short-term, certain medications may help alleviate the headaches and facial pain caused by TMJ disorders. These include NSAIDS, such as aspirin, ibuprofen, and naproxen. These can help eliminate a headache as an abortive treatment. Additionally, icing your jaw can also help relieve the pain associated with a TMJ headache. Jaw exercises can help with muscle relaxation and pain symptoms. Muscle relaxers are often prescribed in conjunction with NSAIDs in an attempt to lessen the muscle spasm and clenching of the muscles surrounding the TMJ.

Long-Term Treatments for TMJ Associated Headaches and Facial Pain

There are a wide variety of different treatments for TMJ disorder, which can help relieve headaches and facial pain. These include physical therapy, Botox, surgery, and other types of treatments.

Sometimes, there are certain exercises that may help address TMJ associated headaches and facial pain. Patients can learn various exercises, like chin tucks, upward tongue, forward jaw, and resisted closing movements. These help with TMJ pain relief. Generally speaking, these exercises provide a very good therapeutic outlook for patients.

Some patients may also benefit from alternative treatments like acupuncture and massage. Consulting with a medical professional is advised to make sure that any exercises are learned correctly.

Splints and Mouthguards For TMJ Disorder

Splints and mouthguards are a treatment that may help alleviate TMJ associated pain and headaches. These do not directly treat the pain itself, but can help prevent clenching and grinding of the teeth. Some dentists may fit these for patients after a consultation with a health professional. Seeing a TMJ specialist for these types of treatments is recommended to ensure precision of the device, because if it is off even slightly, the pain can intensify. The idea behind splints and mouthguards are that they prevent the grinding and biting that typically occurs during sleep, allowing the jaw to rest. Sometimes, a dentist will work on a long-term bite placement solution, which is often a frequently successful treatment for TMJ disorder.

Other Treatments for TMJ Disorder and Associated Headaches and Facial Pain

There are other techniques to help with TMJ disorder that are surgical and alternative in nature. A TMJ arthroscopy is a minimally invasive surgery that allows the surgeon to remove inflamed tissue and align the jaw correctly.

Another treatment that may also work is Transcutaneous Electrical Nerve Stimulation. This provides an electrical pulse that creates muscle contractions so that your jaw muscles will massage themselves. This helps relieve pain and stiffness, simultaneously improving your overall jaw mobility.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

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Last updated on April 30th, 2021 at 11:13 pm

MIGRAINE HEADACHES EXPLAINED.

@Neuralgroover

Migraines are a very intense type of headache that are often accompanied by other symptoms, including nausea, vomiting, sensitivity to light and sound, as well as neurological symptoms such as visual disturbances, numbness or tingling, speech disturbances (slurred speech, difficulty getting words out), weakness, vertigo, cognitive dysfunction or “cognitive fog”, among other things. Migraines tend to be more prevalent in women than in men, with a 3:1 ratio. A common risk factor for migraines often involves family history, but not for everyone.  People who suffer from migraines report intense feelings of pain, including a pulsating/throbbing sensation. This often occurs on 1 side of the head, but can also involve both sides. Exercise and activity during a migraine will often make it worse. Migraine is usually associated with nausea, and/or sensitivity to light (photophobia) and sound (phonophobia)  Migraines often come in different phases, which are called prodrome, aura, the headache phase, and postodome, but not everyone gets all 4 phases:

  • The prodromal phase of a migraine often marks the beginning of a migraine attack and can happen over a period of a few hours ranging to a few days. Some of the symptoms include irritability and depression; food cravings; yawning and tiredness; and fatigue or muscle stiffness. Some patients report their prodrome as just a difficult to describe feeling that they recognize as an early warning sign of an impending migraine. Not every migraine attack includes the prodromal phase.
  • The aura phase of a migraine doesn’t necessarily always happen in every migraine attack, and only about 25% of patients with migraine get aura. Historically, those that get aura are called “classical migraine”, whereas “common migraine” refers to the more common variety of migraine which isn’t associated with aura. A large number of people who have migraines report that during the aura phase, they experience loss of sight, numbness, and other symptoms. Visual aura (loss of vision, jagged lines, flashing, colors, shapes, wavy lines, kaleidoscope, shimmering, expanding blind spot, etc.) are the most common aura. This is followed by numbness and tingling on 1 side (especially face and arm), and then dysphasia (trouble speaking; slurred speech, getting words out). There are also less common types of aura such as hemiplegic migraine aura (1-sided weakness), and brainstem aura (previously called “basilar migraine”; slurred speech, vertigo, tinnitus, double vision, hearing impairment, decreased level of consciousness, ataxia/imbalance). The aura phase should last between 5-60 minutes per ICHD3 criteria. Hemiplegic migraine can be associated with 1-sided weakness which can last up to 3 days. If the other types of aura last longer than 60 minutes, it is called prolonged or atypical aura, and usually warrants a brain CT or MRI, although it is not too uncommon to see. .
  • The headache phase of a migraine is often the longest and most intense period of a migraine. Symptoms include intensive throbbing, nausea, giddiness, irritability, stiffness, and soreness. According to ICHD3 criteria, an untreated or unsuccessfully treated migraine attack should last 4-72 hours. A headache lasting longer than 72 hours (3 days) is called status migrainosus. It is not uncommon for a refractory migraine to last days and sometimes weeks for some patients.
  • The postdrome phase is the drawing down of a migraine attack. It can last for up to 48 hours and some of the lingering symptoms remain from the other phases of a migraine attack. Patients often report feeling wiped out, fatigued, and sore as if they were “hit by a bus”.

 

According to the American Migraine Foundation, more than 36 million people suffer from migraines (although now estimated to be closer to 39 million), but only one out of three people actually talk to their doctors about their pain.

Statistics About Migraines and Their Prevalence

According to several different sources, migraines are one of the most common types of illness in the world. More specifically, it is ranked as the 3rd most prevalent illness in the world. It is estimated that migraine affects about 39 million Americans, and 1 billion worldwide. For example, 1 in 4 households in the United States have an individual that suffers from migraine attacks. Migraines impact 18-20% of women (1 in 5) and 6% of men (1 in 16) in the United States and they are also fairly common in children.

Migraines are also a common cause for an emergency room visit. In fact, there are more than 1.2 million emergency room visits each year in the United States for someone who is suffering from an acute migraine attack. Patients with migraine have a greater than 1.5 fold increase in office visits, and a greater than 2 fold increase in ER visits and hospital admissions. Migraines can also diminish the quality of life for the people who suffer from them. More than 4 million adults suffer from chronic migraine pain, which is an individual who is experiencing more than 15 days of migraine pain each month. Approximately 3% of patients will transform from episodic migraine to chronic migraine each year. Overall, it is estimated that 3-5% of patients in the United States have chronic migraine. Also, 20% of people who suffer from chronic migraines are disabled. Disability due to migraine peaks between the ages of 15-49 years old, which are peak employment years. Thus, migraine now accounts for the 2nd leading cause of years lived with disability following low back pain! Migraine also accounts for 50% of all neurologic disability. All of this puts a very high price tag on migraine, with an estimated 36 billion dollars spent in migraine costs in the United States each year.

 

Migraines in Children

Migraines are commonly undiagnosed in children. They are more commonplace in adolescent children, but 10% of school-age children suffer from migraines. Half of all migraine sufferers have their first migraine attack before they turn twelve and if a child has one parent who suffers from migraines, they have a 50% chance of developing migraines during their lifetime. Also, boys under the age of twelve tend to have migraines more often than girls, but that trend reverses in adolescence, typically with onset of menarche (which also highlights the hormonal influence on migraine).

 

What Causes Migraines?

There are a number of reasons that people suffer from migraines, but the true cause of them is not fully understood. Genetics and environmental factors play a role. In fact, around ⅔ of migraine cases run in families. Migraines also tend to happen in people who are prone to stress, bipolar disorder, and depression. There are also some common triggers for migraines, including:

  • Drinks, such as alcohol and caffeinated beverages.
  • Work stress or stress at home.
  • Bright lights or strong smells.
  • Drastic changes in one’s sleep cycle.
  • Bouts of overexertion.
  • Changes in the weather or other barometric pressure changes
  • Certain foods and food additives such as MSG, nitrates, aspartame, and other substances such as artificial sweeteners.

 

Migraine Theories:

1) Vascular theory; “vascular headache” (outdated):

a) Lack of blood flow (ischemia) caused by vasoconstriction (narrowing) of the intracranial arteries (arteries inside the brain) caused migraine aura.

b) The vasoconstriction was then followed by rebound vasodilation (dilation) of the arteries. This dilation activated pain receptors on the arteries, and this was the cause of the pulsating headache.

c) This theory has since been disproven and outdated. Studies have also shown that the physical pulsations of the arteries did not correlate to the pulsating sensations of the headache pain.

2) Neurovascular theory (current):

a) Migraine is a neurogenic process with secondary changes in cerebral perfusion (related to neuronal dysfunction and hypometabolism during an attack). In other words, migraine is an electrical neurological event in the brain, not an event triggered by blood flow changes. This electrical event influences changes in brain metabolism such as hypometabolism and hypermetabolism. When the neurons are in a hypometabolism state, they have less oxygen and glucose requirement since they are not as active, and thus there is a lack of blood flow (not due to vasoconstriction of the brain arteries). This can be followed by hypermetabolism in which there is an increase in oxygen and glucose requirements and thus, increase in blood flow (so not necessarily simply rebound vasodilation).

 

b) Migraine aura is a good illustration of this phenomenon. Migraine aura is caused by an electrical wave spreading across the cortex of the brain moving at about 3 mm per minute (not by vasoconstriction as per the older vascular theory). At the front of this spreading electrical wave it causes hypermetabolism and an increase in blood flow. This hypermetabolism causes the “positive” migraine aura features (colors, flashing lights, kaleidoscope, shapes, zig-zags, tingling sensory changes, etc.). Following this electrical wave there is “neuronal depression” and hypometabolism, associated with a decrease in blood flow. This hypometabolism causes the “negative” migraine aura features (loss of vision, black spots, numbness, etc.). Depending on where this wave spreads, you may get different aura symptoms; visual aura as it spreads across the occipital (visual) cortex, sensory/numbness/tingling as it spreads across the parietal (sensory) cortex, dysphasia (trouble speaking, slurred speech) as it spreads across the frontotemporal (speech) cortex, one sided weakness in hemiplegic migraine as it spreads across the frontal (motor) cortex, brainstem symptoms such as vertigo, tinnitus, double vision, hearing loss, imbalance, decreased level of consciousness, slurred speech (previously called basilar migraine, now called migraine with brainstem aura) as it spreads across the brainstem.

 

c) The electrical event of migraine not only causes the changes in metabolism as described above, but the trigeminal nerves are also activated. Think of migraine as an electrical switch that gets turned on in the brainstem. It then turns on and activates the trigeminal nerves. The trigeminal nerves innervate all of the arteries in the brain and through the meninges surrounding the brain. When activated, the trigeminal nerves release a variety of inflammatory proteins (such as CGRP) and neuropeptides. The result of this is 3-fold:

1st, these inflammatory peptides cause neurogenic inflammation around the brain. Think of it like a sterile (non-infectious) meningitis. So, when you’re having a migraine, exercise and activity, moving around, bouncing in a car, etc. often worsen the pain.

2nd, it causes cerebral vasodilation in the brain and meninges. The dilation itself does not cause the pain, but rather it triggers the trigeminal nerves which innervate the arteries, and this sends signals back to the brain that something is going on, which in turn causes more release of inflammatory proteins and causes the migraine to worsen. This is the basis of why it is called the neurovascular theory of migraine.

3rd, it enhances and exaggerates the transmission of pain from the trigeminal nerves, into the brainstem, and into the cortex of the brain where the pain is recognized.

 

At baseline, a patient with migraine who is not having a headache always has a state of neuronal hyperexcitability in the cerebral cortex, especially in the occipital cortex (which is why the majority of aura symptoms tend to be visual aura). So, they have a much lower threshold to a migraine being activated and triggered as compared to someone without migraine. In other words, the neurological system in a patient with migraine can be thought of as always being in a hyperactive, hypersensitive, overdrive state with the “volume turned way up” compared to a person without migraine. Thus, I tell my patients the goal of preventive treatment is to “turn the volume down” and increase the threshold of migraine being triggered so easily.

 

What Are Some Common Treatments for Migraines?

There are two categories of treatment for any type of headache, including migraines. Migraines can be treated through abortive or preventive means. Abortive treatment for any type of headache includes medications such as aspirin, which treats the headache while it’s happening. Preventative treatments are intended to keep a headache or migraine from happening so frequently. Here are some of the different types of treatments for migraines.

 

Abortive Treatment for Migraines

The goal of migraine abortive treatments is to stop individual migraine attacks at onset so the migraine does not reach full severity, ends quickly, and your function is restored and maintained rather than having to go lay down and miss the whole day in bed.  Over-the-counter pain relievers for migraines, such as aspirin or ibuprofen, are fairly commonplace. Some more aggressive abortive treatments include prescription medications like triptans (such as Maxalt) that block pain pathways within the brain. Some people may also receive anti-nausea drugs and opioid prescriptions to deal with more intense migraine symptoms. The migraine specific abortive/acute (as needed) treatments include triptansgepants (Ubrelvy, Nurtec), ditans (Reyvow) or neuromodulatory devices.

Preventative Treatments for Migraines

Medications that lower blood pressure, antidepressants, anti-seizure drugs, CGRP monoclonal antibodies, and even botox are some of the common preventative treatments for migraines. The classification of the preventive medicine typically has nothing to do with its purpose when it is used for migraine. For example, there are specific anti-blood pressure medicines that are good for migraine prevention. However, they do not work for migraine because of blood pressure changes, but rather they affect the electrical pathways of migraine. The same scenario goes for the antidepressant/anti-anxiety and anti-seizure categories. The medicines selected within each of these preventive categories are very specific and based on clinical trials and evidence. In other words, not all medicines within a specific medication class (such as all antidepressants) have evidence for migraine prevention, but rather very specific ones within that class. Medications that are designed to lower blood pressure can sometimes prevent migraines with aura and without aura. Certain types of antidepressants can help prevent migraines, but have some undesirable side effects in some individuals. Anti-seizure drugs, such as Topamax, can reduce the frequency of migraines in some individuals. The preventive migraine treatments should be used until the migraine and headache frequency is significantly improved consistently for several months. As mentioned above, this can be done with a variety of medications which may also include the CGRP monoclonal antibody (mAb) treatments (Aimovig, Ajovy, Emgality, Vyepti), Botox, natural supplements, herbals and vitamins, or neuromodulatory devices.

Alternative Treatments for Migraines

Some other types of treatment for migraines include acupuncture, cognitive behavioral therapy, supplements, essential oils, yoga, meditation, and other techniques designed to enhance relaxation. For some individuals, exercise can decrease the frequency of migraines. In fact, some studies have shown that a routine exercise program can be just as effective as some of the prescription preventive medications used for migraine. Neuromodulatory devices that are FDA cleared for migraine prevention are also available and include sTMS (SAVI, SpringTMS, sTMS mini),  eTNS (CEFALY), and nVNS (GAMMACORE), all of which are discussed in much greater detail here. There are also nutraceuticals and supplements which have good evidence for migraine prevention.

 

Finding Help For Migraines

Migraines remain a poorly understood medical condition, but there are treatments available. Only 4% of people suffering from migraines work with a headache specialist or a pain specialist. It is estimated that preventative treatment could benefit around 25% of people who suffer from severe migraines.

If you suspect that your headaches are migraines, you should see your doctor. Furthermore, any type of headache warrants at least one visit with your doctor to make sure there are no concerns by medical history or examination for any other worrisome causes of your headaches. They may refer you to a neurologist or other type of headache specialist. Oftentimes, a wide variety of tests may be given, including CT scans and MRIs, to see what is contributing to the cause of the migraine. The good news is that migraines can be successfully managed for the majority of patients, and that many people live with them thanks to the treatments that they receive.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

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Last updated on May 13th, 2021 at 01:19 pm

WHEN TO SEE A HEADACHE SPECIALIST AND HOW TO PREPARE TO GET THE MOST FROM THE APPOINTMENT.

@Neuralgroover

Background

I see patients in our headache center from all over the United States and from many other countries. Many patients travel hundreds of miles by car or airplane for these visits, due to the shortage of available headache specialists (about 570 in the US). Many patients are lucky enough to be relatively close to a headache specialist. Whichever scenario you fall into, you want to get the most out of your appointment with a headache specialist in order to get on a better path to less headache or facial pain burden.

 

When to see a headache specialist

So first of all, when should you see a headache specialist? First off, any type of headache, head pain, or facial pain, is reason enough to see a headache specialist. Basically, headache specialists specialize in any type of pain or discomfort involving anywhere in the head or face. They also commonly see patients that may have other neurological symptoms which may not necessarily be associated with headaches, but their doctor wants to rule out a migraine “equivalent” disorder. Some patients can have neurologic symptoms without headache (visual, sensory, speech, vertigo, weakness, nausea/vomiting, abdominal pain), which may actually reflect a painless migraine disorder, such as migraine aura without headache. I have compiled a list below of a few of my thoughts of when your headache or facial pain treatment journey signals that it is time to see a headache specialist.

 

Reasons to see a headache specialist:

-You have a headache, head pain, or facial pain.

-Your doctor tells you, “your headache is all in your head”.

-Your doctor tells you, “there’s nothing else I can do for you”.

-Your doctor says, “I don’t treat much headache, but…”.

-You continue to have frequent headaches despite trying several preventive medications.

-You just don’t feel like you are making any progress despite a couple office visits with your doctor or their NP or PA (or you never even get to see the doctor).

-You don’t feel like your doctor is listening to you or taking your symptoms seriously.

-The doctor spends only a few minutes in the visit, so you feel rushed and unable to discuss all of your concerns.

-Your doctor is googling your symptoms in the office.

-Your doctor recommends that you take opiates/opioids for migraine treatment.

-Your doctor says it is ok to use NSAIDs, OTCs or triptans more than 10 days per month or butalbital/fioricet/fiorinal more than 5 days per month on average for migraine treatment.

-Your doctor says your headache is “because you are depressed”.

-Your doctor does not give you a more specific classification or name for your diagnosis.

 

What information should you gather before the visit?

Unfortunately, we all know how strapped for time most physicians are during office visits due to a variety of factors such as low insurance reimbursement and the need to increase patient volume to compensate for this and break even. So to get the most out of your office visit, making it efficient and helpful, it is important to compile certain information in preparation. Typing out this information and bringing it to your office visit is a great idea. It is also a great idea to keep this as a running file that you can continue adding to in your personal files. This helps to eliminate time wasted in the office that could easily be organized and thought through prior to the visit, allowing more time for the important parts of the office visit; optimizing the diagnosis and treatment plans. Some of this information you may not have available, and that is certainly ok. You may be able to retrieve some of it from records, memory, and your local pharmacist.

Never assume that your local doctor’s office has faxed all of your records ahead of the visit. If that happens, great. However, many times patients are told that the records will be sent, but when we see the patient, we have no records that were sent. So, it is always best to bring all of your records yourself. Furthermore, it is good to have copies of all of your medical records, testing, etc. for your personal files anyway.

 

The following list are items that I have found to be the most useful for patients to have gathered and thought of prior to the visit, allowing the most efficient and useful office visit:

A) Acute/abortive headache or pain treatments (used “as needed”). This information is also needed in order to pursue insurance approvals for various types of treatments such as the newer gepants (Ubrelvy, Nurtec) or ditans (Reyvow).

-All that have been tried (which triptans, NSAIDs, neuromodulation devices, etc.)

-Doses used

-Responses (effectiveness, side effects) of each treatment

 

B) Preventive headache or pain treatments (used daily to lessen headache frequency/severity). This information is also needed in order to pursue insurance approvals for various treatments such as Botox or the CGRP mAb antagonists (Aimovig, Ajovy, Emgality, Vyepti).

-All that have been tried

-Maximum doses used

-Duration that each treatment was used

-Responses (effectiveness, side effects) of each treatment

 

C) Testing

-All CD and radiology reports for all brain MRIs, CTs, and other relevant testing for your headache or pain. Most CDs do not include the radiology report, and you need to request that separately. It is a good idea to have copies of all of these things for your personal files regardless. Bring them all to the office visit for the doctor to review.

-All bloodwork done in the past 5 years. Labs particularly important for headache evaluations include TSH, CBC, CMP, Vitamin D, Vitamin B12, ESR, CRP, ANA, to name a few, but this may vary and include more or less, depending on the specific clinical scenario.

 

D) Think about the clinical features of your headache or facial pain as listed below. These will be important questions that your headache specialist will ask. So, it is good to answer these questions in your head prior to the visit, so you can provide more accurate and thought out answers. This helps to prevent being put on the spot by questions you never really thought about which may result in forgetting some important details. For a free headache and facial pain self-diagnosis tool which incorporates all of these important questions that a headache specialist asks, look here.

-Location of the headache or facial pain

-Frequency of the headache or facial pain attacks

-Duration of the headache or facial pain attacks

-Description and characterization of the headache or facial pain attacks

-Neurological symptoms associated with the headache or facial pain (visual disturbances, numbness, tingling, weakness, speech disturbances, vertigo, etc.)

-Other associated symptoms with the headache or facial pain (nausea, sensitivity to light or sound, one sided autonomic features (runny eye, red eye, runny or congested nose, droopy or puffiness around eye))

 

Conclusions:

If you are able to gather all or much of the above listed information prior to your headache specialist appointment, you’ll be well on your way to a much more efficient and beneficial office visit. As a result, you and your doctor will be able spend more time in the office discussing the most important things rather than spending it trying to look up records or digging through your memory for various details. As a result, your doctor will have more time to better formulate a list of the most likely diagnoses, and best treatment approaches for minimizing the disruption of your headache or facial pain on your life. Good luck!!

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

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Last updated on June 24th, 2021 at 02:56 am

VISUAL SNOW, PERSISTENT MIGRAINE AURA, MIGRAINOUS STROKE, AND WHAT YOU SHOULD KNOW.

@Neuralgroover

INTRODUCTION

The International Classification of Headache Disorders-3 (ICHD-3) classifies persistent aura without infarction (stroke) and migrainous infarction as two of the four reported complications of migraine, both of which are very rare. The other two reported complications of migraine include status migrainosus and migraine aura-triggered seizure, but these will not be discussed here1. 

 

MIGRAINE PATHOPHYSIOLOGY

In order to discuss persistent migraine aura without infarction or migrainous infarction, it is crucial to understand migraine pathophysiology, which involves a multitude of complex processes throughout the cortex, brainstem, and cerebral vasculature. The pathophysiology of migraine has evolved from the vascular theory to the neurovascular theory of migraine. The older vascular theory proposed by Wolff viewed migraine as beginning with cerebral vasospasm causing focal ischemic (lack of blood flow) symptoms (aura) followed by extra and/or intracranial hyperperfusion (excess blood flow) from vasodilatation leading to the migraine pain. 2 This theory made good sense for how stroke or persistent neurological symptoms could develop, from the period of cerebral vasospasm and constriction. However, in later studies of migraine with aura, regional hypoperfusion developed before and outlasted focal neurologic symptoms, and this dissociation of time, perfusion changes and symptoms indicated that these neurologic symptoms were not caused by truly ischemic blood flow, but rather the apparent hypoperfusion is secondary to a disturbance in brain metabolism. 3-6

Lashley first described his own visual aura and hypothesized that the aura was due to a spreading abnormality migrating over the visual cortex at a rate of 3-5 mm per minute in 1941. 7 In 1944, Leão described spreading depression as a wave beginning with a brief neuronal burst associated with transient increased blood flow followed by a longer lasting neuronal electrical suppression with decreased blood flow in an animal model. 8-10 Subsequent studies confirmed this initial focal hyperemia followed by posteriorly to anteriorly spreading oligaemia (reduced blood flow) and regional cerebral blood flow reduction, which does not reach critical ischemic values, in a wave-like manner at approximately 2-5 mm per minute. This spreading regional cerebral blood flow reduction is independent of arterial territories, and does not cross cytoarchitectural borders or neuronal discontinuity such as the central sulcus or lateral sulcus, confirming impaired neuronal metabolism with subsequent regional cerebral blood flow reduction, rather than true ischemia. 3-6 This remains the basis for the now current neurovascular theory of migraine.

Most studies have been unable to show significant ischemic cerebral blood flow changes during migraine attacks. Results have shown alterations in cerebral blood volume, relative cerebral blood flow, and tissue mean transit time (MTT) in the grey matter of the occipital cortex contralateral (opposite) to the side of aura during an attack, while others have shown global cerebral blood flow increase, and others have shown hypoperfusion of the whole hemisphere, but never true ischemic hypoperfusion. 11-14 Notably, cerebral blood flow changes correlate poorly with migraine pain, and neurogenic inflammation in the trigemino-vascular system is suspected to be the primary cause of migraine pain, rather than arterial vasodilatation. 11,15

 

PERSISTENT AURA WITHOUT INFARCTION

The ICHD-3 defines persistent aura without infarction as aura symptoms persisting for 1 week or more without evidence of infarction on neuroimaging. It should occur in a patient with a history of migraine with aura and typical of previous auras except that one or more aura symptoms persist for 1 week or more. Neuroimaging must show no evidence of infarction, and symptoms are not better accounted for by another ICHD-3 diagnosis. The aura symptoms are often bilateral and may last for months or years. It is important to differentiate persistent aura without infarction from symptomatic aura as a result of cerebral migrainous infarction. Aura symptoms lasting more than 1 hour and less than 1 week are classified as probable migraine with aura.

There are two primary types of persistent migraine aura that are described. One is persistent primary visual disturbance in which the patients describe “visual snow” or “television static” in both visual fields in both eyes, and some report additional intermittent scotoma or oscillating lights. 16 The other is persistent migraine aura with typical aura, in which patients describe scotoma, fortification, or oscillation in one hemifield (one side of vision), and does not go away (sometimes also called status aura). 16

The specific pathophysiology of persistent migraine aura without infarction remains unknown, although several theories exist. Some of these theories include low cerebral magnesium levels, abnormal cerebral energy metabolism, greater cerebral reactivity of NMDA receptors to glutamate, lower threshold for triggering cortical spreading depression, low cortical preactivation due to thalamocortical hypoactivity, sustained hyperexcitability of the visual cortex without significant dynamic modulation, sustained cortical neuronal dysfunction, intracortical disinhibition, loss of inhibitory GABA-ergic interneurons resulting in a network imbalance leading to a reverberating cycle of cortical spreading depression (small cortical infarctions below MRI sensitivity in the occipital cortex has been one proposed mechanism), or a combination of any of these possibilities. 16-21

The evaluation for persistent migraine aura without infarction should focus on excluding intracranial pathology, primarily stroke, although other intracranial etiologies need to be excluded. Brain MRI scan is preferable with MRA of the brain and neck (to also assess the arteries), but if medically contraindicated, brain CT scan with CTA of the brain and neck (to assess the arteries) can be pursued. Contrast administration for either type of scan is suggested, although not mandatory. A detailed neuro-ophthalmologic examination is also required. Studies investigating other imaging modalities for persistent migraine aura without infarction, including FDG-PET, MR-PWI, and Tc99m-HMPAO-SPECT, have shown conflicting and inconsistent results.

Treatment for persistent aura without infarction is undefined, and generally based on medication trial and error. The literature reveals an extensive list of medications tried and failed, with most attempting to target neuronal hyperexcitability. Treatments and medications which have been assessed have included anticonvulsants (lamotrigine, topiramate, valproic acid, gabapentin, phenobarbital, phenytoin, carbamazepine), benzodiazepines (clonazepam, diazepam), antidepressants (amitriptyline, cymbalta, buspirone, fluoxetine, nortriptyline, sertraline, dothiepin), anti-hypertensive (atenolol, acetazolamide, flunarazine, metoprolol, propranolol, verapamil, nifedipine, nimodipine, furosemide), NSAIDs (acetylsalicylic acid, ibuprofen, flurbiprofen, diclofenac, indomethacin, naproxen) analgesics (acetaminophen, butalbital, codeine), and a variety of other medications (baclofen, citicholine, ergotamine, ketamine, cyproheptadine, methylphenidate, methylprednisolone, pizotifen, prochlorperazine, promethazine, sumatriptan, memantine). The vast majority of these medications have shown no evidence of benefit. 16 Of them, lamotrigine has shown the most evidence of benefit, while divalproex sodium, baclofen, sertraline, nifedipine, nimodipine, acetylsalicylic acid, and furosemide have reported varying degrees of benefit from complete to partial resolution of symptoms. 16   

Abortive migraine options can include the gepants (Ubrelvy, Nurtec ODT), ditans (Reyvow), NSAIDs and other conventional abortives, although triptans and ergots should be avoided.

MIGRAINOUS INFARCTION

The ICHD-3 defines migrainous infarction as one or more migraine aura symptoms associated with an ischemic brain lesion in a correlating anatomical clinical territory demonstrated by neuroimaging. It should occur in a patient with a history of migraine with aura and typical of previous attacks except that one or more aura symptoms persists for more than 60 minutes, and it should not be better accounted for by another diagnosis. Clearly associating an ischemic stroke and a migraine attack in a migraine sufferer can be difficult. Cerebral infarction of other etiologies can coexist with migraine, can present with symptoms resembling migraine with aura, or cerebral infarction can occur during an attack of migraine with aura, and this is the only scenario that would be consistent with migrainous infarction.

Migrainous infarction occurs predominantly in the posterior circulation and in younger women. In the Cerebral Abnormalities in Migraine, an Epidemiological Risk Analysis (CAMERA) study, these infarct-like white matter lesions found in migraineurs (primarily in migraine with aura) were predominantly located in the posterior circulation, especially in the cerebellum. 22,23 However, these infarctions are not necessarily considered migrainous infarctions and the mechanisms are unclear.

Multiple studies have confirmed the association with increased stroke risk in women with migraine with aura. Women younger than age 45 who have migraine with aura, have a 2 fold increased risk of stroke. Notably, migraine without aura does not appear to have the same increased risk. This risk increases to 6 fold in the setting of oral contraceptive use containing estrogen, and more than 9 fold with combined smoking and oral contraceptive use. 24 Menstrual migraine and the use of hormonal therapy and birth control is discussed in more detail here. Women who are smokers and have migraine with aura should consider estrogen containing oral contraception a contraindication. Oral contraceptive use in non-smoking women with migraine with aura is more controversial. The World Health Organization (WHO) and American College of Obstetrics and Gynecology (ACOG) suggest that in non-smoking women under age 35 with migraine with aura, there is an acceptable lower risk of oral contraceptive use. However, if they are over age 35, the risk is unacceptably higher and oral contraceptive use is contraindicated. According to the International Headache Society (IHS), in non-smoking women with migraine with aura who are either younger or older than age 35, taking into account other risk factors should individualize the decision for oral contraceptives. 24 These would include ischemic heart disease, family history of early heart disease at a young age of less than 45 years old, heart disease with concern for emboli such as atrial fibrillation, uncontrolled hypertension, hyperlipidemia, diabetes, obesity, systemic disease associated with increased stroke (connective tissue disease, sickle cell, hypercoagulability), etc. In women with an increased risk of stroke, and especially with multiple vascular risk factors, non-estrogen methods of birth control such as progesterone-only forms of contraception should be recommended.

Research has also reported that after high blood pressure, migraine with aura was the second strongest single predictor of heart attack and strokes, ahead of diabetes, smoking, obesity, and family history of early heart disease. 25 This increased risk was not seen in migraine without aura. It is not necessarily thought that migraine with aura causes the stroke, but rather it is a marker for young women at a greater risk for cardiovascular disease. However, the reasons for these associations are unclear, likely multifactorial, and clearly need to be further defined. Traditional vascular risk factors such as hypertension, smoking, diabetes and hyperlipidemia still show the strongest contribution to cardiovascular disease, so these should be optimized, especially in those with migraine with aura to reduce risk of both heart disease and stroke. 25

Some theorized mechanisms of migrainous infarction include vasospasm, endothelial dysfunction, vascular endothelium-related hypercoagulability during cortical spreading depression and the aura phase, or genetic alterations of the wall of the small cerebral arterial vessel walls. 26-31

The evaluation for migrainous infarction is similar to that of persistent migraine aura without infarction. By definition, an ischemic infarct in a correlating anatomic area to symptoms should be seen on MRI or CT of the brain. This warrants a further standard stroke evaluation, including imaging of the intra and extracranial vasculature (including carotid arteries), as well as cardiac evaluations beginning with transthoracic echocardiography. Electrocardiogram and telemetry should also be pursued to evaluate for paroxysmal arrhythmias such as atrial fibrillation.

Treatment of migrainous infarction is the same as with any ischemic stroke. The initial goal is to evaluate for potentially treatable etiologies (such as cardioembolic source) and treat accordingly. Otherwise, secondary stroke risk factor modifications are the goal and include antiplatelet therapy in combination with optimal control of blood pressure, hypertension, hyperlipidemia, diabetes, tobacco cessation, and healthy lifestyle changes.

Abortive migraine options can include the gepants (Ubrelvy, Nurtec ODT), ditans (Reyvow), NSAIDs and other conventional abortives, although triptans and ergots should be avoided.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

REFERENCES

  1. Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2013;33:629-808.
  2. Wolff HG. Headache and Other Head Pain. New York: Oxford University Press, 1963.
  3. Olesen J, Larsen B, Lauritzen M. Focal hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine. Ann Neurol 1981;9:344-52.
  4. Lauritzen M. Pathophysiology of the migraine aura. The spreading depression theory. Brain 1994;117 ( Pt 1):199-210.
  5. Lauritzen M, Skyhoj Olsen T, Lassen NA, Paulson OB. Changes in regional cerebral blood flow during the course of classic migraine attacks. Ann Neurol 1983;13:633-41.
  6. Lauritzen M,  Olesen J. Regional cerebral blood flow during migraine attacks by Xenon-133 inhalation and emission tomography. Brain 1984;107 ( Pt 2):447-61.
  7. Lashley KS. Patterns of cerebral integration indicated by the scotomas of migraine. Arch Neurol Psych. 1941;46:331-339.
  8. Leao AAP. Spreading depression of activity in cerebral cortex. Journal of Neurophysiology 1944;7:359-390.
  9. Leao AAP,  Morrison RS. Propagation of spreading cortical depression. Journal of Neurophysiology 1945;8:33-45.
  10. Leao AAP. Pial circulation and spreading depression of activity in the cerebral cortex. Journal of Neurophysiology 1944;7:391-396.
  11. Thomsen LL, Iversen HK, Olesen J. Cerebral blood flow velocities are reduced during attacks of unilateral migraine without aura. Cephalalgia 1995;15:109-16.
  12. Kobari M, Meyer JS, Ichijo M, Kawamura J. Cortical and subcortical hyperperfusion during migraine and cluster headache measured by Xe CT-CBF. Neuroradiology 1990;32:4-11.
  13. Sakai F,  Meyer JS. Regional cerebral hemodynamics during migraine and cluster headaches measured by the 133Xe inhalation method. Headache 1978;18:122-32.
  14. Tfelt-Hansen PC,  Koehler PJ. One hundred years of migraine research: major clinical and scientific observations from 1910 to 2010. Headache 2011;51:752-78.
  15. Moskowitz MA. Neurogenic inflammation in the pathophysiology and treatment of migraine. Neurology 1993;43:S16-20.
  16. Thissen S, Vos IG, Schreuder TH, Schreurs WM, Postma LA, Koehler PJ. Persistent migraine aura: new cases, a literature review, and ideas about pathophysiology. Headache 2014;54:1290-309.
  17. Relja G, Granato A, Ukmar M, Ferretti G, Antonello RM, Zorzon M. Persistent aura without infarction: decription of the first case studied with both brain SPECT and perfusion MRI. Cephalalgia 2005;25:56-9.
  18. Chen WT, Lin YY, Fuh JL, Hamalainen MS, Ko YC, Wang SJ. Sustained visual cortex hyperexcitability in migraine with persistent visual aura. Brain 2011;134:2387-95.
  19. Wang YF, Fuh JL, Chen WT, Wang SJ. The visual aura rating scale as an outcome predictor for persistent visual aura without infarction. Cephalalgia 2008;28:1298-304.
  20. Chronicle E,  Mulleners W. Might migraine damage the brain? Cephalalgia 1994;14:415-8.
  21. Coppola G, Parisi V, Di Lorenzo C, et al. Lateral inhibition in visual cortex of migraine patients between attacks. J Headache Pain 2013;14:20,2377-14-20.
  22. Kruit MC, van Buchem MA, Launer LJ, Terwindt GM, Ferrari MD. Migraine is associated with an increased risk of deep white matter lesions, subclinical posterior circulation infarcts and brain iron accumulation: the population-based MRI CAMERA study. Cephalalgia 2010;30:129-36.
  23. Kruit MC, Launer LJ, Ferrari MD, van Buchem MA. Infarcts in the posterior circulation territory in migraine. The population-based MRI CAMERA study. Brain 2005;128:2068-77.
  24. Tepper SJ, Tepper DE. The Cleveland Clinic Manual of Headache Therapy, 2nd ed. . Switzerland: Springer International Publishing, 2014.
  25. Kurth T, Bubes V, Buring J. Relative Contribution of Migraine with Aura to Cardiovascular Disease Occurrence in Women. Neurology 2013;80.
  26. Pezzini A, Del Zotto E, Giossi A, et al. The migraine-ischemic stroke relation in young adults. Stroke Res Treat 2010;2011:304921.
  27. Pezzini A, Del Zotto E, Giossi A, Volonghi I, Grassi M, Padovani A. The migraine-ischemic stroke connection: potential pathogenic mechanisms. Curr Mol Med 2009;9:215-26.
  28. Kurth T, Chabriat H, Bousser MG. Migraine and stroke: a complex association with clinical implications. Lancet Neurol 2012;11:92-100.
  29. Kurth T. Migraine and ischaemic vascular events. Cephalalgia 2007;27:965-75.
  30. Tietjen EG. Migraine and ischaemic heart disease and stroke: potential mechanisms and treatment implications. Cephalalgia 2007;27:981-7.
  31. Bousser MG,  Welch KM. Relation between migraine and stroke. Lancet Neurol 2005;4:533-42.

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