Posts Tagged "stroke"

Last updated on November 16th, 2021 at 08:32 am

THUNDERCLAP HEADACHES EXPLAINED.

@Neuralgroover

Thunderclap headaches are not common in individuals in developed countries, such as the United States. In fact, they happen to about 43 out of 100,000 adults. This is a very severe (“first or worst”) headache of an abrupt onset, reaching maximum intensity in less than 1 minute and lasting for 5 or more minutes. This headache requires emergent evaluation at the nearest emergency department for testing and evaluation, especially the first time that it occurs. One of the main diagnoses that needs to be evaluated for is a blood vessel related headache such as subarachnoid hemorrhage from aneurysm rupture (brain bleed).

 

One of the more notable characteristics of a thunderclap headache is that there is not an obvious trigger. Thunderclap headaches are sometimes indicative of a sudden, serious medical condition that requires immediate treatment. Let’s take a look at some of the causes of thunderclap headaches, headaches that are typically secondary in nature. Before we do that, keep in mind that thunderclap headache is a medical emergency requiring an emergency evaluation by a physician, preferably by calling 911 and having an ambulance take you to the emergency department.




What Does a Thunderclap Headache Feel Like?

Imagine a thunderclap headache as a thunderbolt lightning strike to the head with immediate and maximum pain. Thunderclap headaches have a rapid onset that happens rather quickly. Some people who get thunderclap headaches will notice the pain reaches its greatest intensity within 1 to 5 minutes of the onset of the headache. Sometimes, thunderclap headaches are accompanied by other symptoms. These can include a fever, blurred vision, complete loss of vision, nausea, dizziness, difficulty standing, numbness, weakness, loss of speech, or other neurological symptoms, all of which require emergent evaluation by a physician.Some symptoms that may be associated with a thunderclap headache could also be related to the primary cause of the headache itself.

 

What Causes Thunderclap Headaches?

 

Subarachnoid hemorrhage

A common cause of thunderclap headaches is a condition known as subarachnoid hemorrhage. This is always the #1 condition that requires emergent evaluation to rule out because the death rate is so high if it is not evaluated and treated quickly. This is a condition where bleeding occurs in the membranes that are surrounding the brain. The bleeding happens between the arachnoid membrane, just above the pia mater (the innermost membrane of the brain). Subarachnoid hemorrhages are responsible for about 5% of strokes but cause twenty-five percent of deaths related to strokes. Ruptured aneurysms are a major cause of subarachnoid hemorrhages.

 

Ischemic or Hemorrhagic Stroke

Ischemic strokes can also cause thunderclap headaches. Strokes are the fifth leading cause of death in the United States and ischemic strokes are the most common type of stroke. Ischemic strokes happen when arteries become blocked in the brain. When plaque builds up in the arteries, it can block blood flow to the brain. Another common type of ischemic stroke happens when a blood clot forms in blood vessels in the brain, depriving it of oxygen. People with diabetes, high blood pressure, high cholesterol, smokers and carotid artery disease are at extreme risk for developing an ischemic stroke.

Hemorrhagic stroke is when there is a bleed into the tissues of the brain, rather than a blockage of an artery. Between ischemic and hemorrhagic strokes, hemorrhagic strokes are more commonly associated with a bad headache, although it is certainly possible with both.

 

Vasculitis

Vasculitis occurs when there is inflammation and narrowing of various arteries in the brain. It is often associated with thunderclap headache. It can be caused by a number of things including medications (over the counter decongestants are sometimes culprits, along with many other medicine types), infections, or autoimmune disorders. Reversible Cerebral Vasoconstrictive Syndrome (RCVS) is a common cause of this, and is often medicine induced.

 

Cerebral Venous Thrombosis

Cerebral venous thrombosis occurs when a large blood clot forms and blocks blood flow in the brain. The large cerebral venous sinuses drain the brain of blood after the blood has delivered oxygen to the brain. From the venous sinuses, they drain into the jugular veins, and back into the normal circulation. Sometimes a blood clot can be formed in one of these venous sinuses causing blood flow to back up. This leads to headache (sometimes can be thunderclap) and can cause a variety of other neurological symptoms as well.

 

Arterial Dissection

This can occur when there is a tearing of one of the arteries in the neck or brain such as the carotid or vertebral arteries.

 

Bacterial and Viral Meningitis

Meningitis is another condition that can cause a thunderclap headache. This is usually associated with fevers, chills, bad neck pain, and often confusion. Caused by either bacteria or viruses, meningitis is an inflammation of the brain and spinal cord lining that puts pressure on the brain. Infections of the brain are responsible for about 7% of thunderclap headaches, according to the National Institute of Health. 

 

Head Injury Or Trauma

A severe head injury can also bring about a thunderclap headache. By and far, the most common cause of a head injury are falls and motor vehicle accidents. Sports and other physical activities can often result in a head injury. Depending upon the severity of the injury, one may experience a thunderclap headache. Head injuries often result in a concussion, which may include some additional symptoms, such as confusion, a dislike of noise or light, memory problems, difficulty with balance, and an inability to concentrate.

 

Migraine

For some patients, their migraines can come on abruptly and wake them up, or they can come on during the day as well with fast onset. This cause is established after proper testing has been completed for thunderclap headaches, and after a recurring pattern has been observed.




What Should I Do If I Have a Thunderclap Headache?

You have very limited time to act if you notice the onset of a thunderclap headache. If you have a subarachnoid hemorrhage, it can start causing permanent brain damage in as little as three to four minutes. If a patient is able to secure treatment quickly, the odds of survival and recovery are better. Generally speaking, about 33% of patients who receive treatment for this type of hemorrhage have a favorable outlook of recovery, meaning that they experience no disability after the fact. This type of headache requires emergency evaluation in the emergency department.

 

How Do Doctors Investigate Thunderclap Headaches?

Emergency medical personnel and headache specialists have a unique challenge when diagnosing the cause of a thunderclap headache, as the investigation is often a race against time. If evaluated promptly, a physician will often do a CTA of the head and neck blood vessels (CT angiogram, which is a special CT scan with IV contrast to look at the brain and the arteries). An MRI and MRA of the brain and neck blood vessels is another option. They would be looking for an outpouching of blood vessels (indicating an aneurysm), tearing of an artery (dissection), blood vessel inflammation, or a tear. If a cerebral venous thrombosis is suspected, an MRV or CTV of the brain may also be done. The “V” in these tests is for venogram to look at the deep venous blood channels which the blood from the brain drain into, but can become blocked with a blood clot. If there is a high suspicion for an aneurysm rupture (tearing), a lumbar puncture may be done to look for blood in the spinal fluid. A lumbar puncture may also be done if there is concern for meningitis, along with blood tests looking for signs of infection.

 

How Do Doctors Treat Thunderclap Headaches?

Doctors deal with thunderclap headaches by immediately addressing the primary cause. For example, if a person is having a stroke, they may receive blood thinners to help break up a blood clot. Surgery can also attempt to repair brain bleeds by securing blood vessels, repairing aneurysms, and relieving pressure on the brain. Infections, such as meningitis, can be treated with antibiotics (if bacterial) and with antiviral drugs (in very rare instances of viral meningitis). For concussions, doctors can prescribe rest and the concussion will generally resolve itself within about 14 days. Pain relievers and nausea medications are typically prescribed for concussion.

 

What Are the Risk Factors for a Thunderclap Headache?

There are a plethora of risk factors for a thunderclap headache. For strokes and hemorrhage, diabetes, high blood pressure, genetic history, smoking, and age are all risk factors. The risk of a stroke doubles each decade for individuals who are over the age of 45. Over 70% of all strokes happen once a person reaches the age of 65. Smoking, alcohol, and hypertension (stress) are the major risk factors for a subarachnoid hemorrhage.

 

The Seriousness of Thunderclap Headaches

Thunderclap headaches are a medical emergency. In some of the primary causes of thunderclap headaches, a physician will have a matter of minutes to act to prevent brain damage and prevent loss of life. Also, physicians have to use all the diagnostic tools available to them. For example, a CT scan can miss around 25% of subarachnoid hemorrhages. However, the prevalence of thunderclap headaches is quite low. Less than .3% of people will experience a thunderclap headache during their lifetime. Additionally, lifetime prevalence of thunderclap headaches in emergency room patients is less than 6%.

 

There is a benign form of thunderclap headache called primary thunderclap headache, which is not caused by something bad. However, this cannot be diagnosed until examination, further history, testing, and a recurrent pattern of events have been established (never assume this during the first attack). Evaluations to exclude other more dangerous causes of the headache must have been performed with a physician first before considering this.




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 November 23rd, 2021 at 08:53 pm

VISUAL SNOW, MIGRAINE AND STROKE RISK, PERSISTENT MIGRAINE AURA, 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. 

 

What Causes Migraine Aura?

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. In other words, we now look at a migraine as an electrical event, not a vascular (blood vessel) related event. 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.

 

In other words, 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.

 

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 Migraine 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)neuromodulatory devices, and NSAIDs/over the counter analgesics, although triptans and ergots should be avoided.

Migrainous Infarction (Stroke)

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.

 

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.

 

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

 

Treatment of migrainous infarction is the same as with any ischemic stroke acutely and preventively. 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/smoking cessation, and healthy lifestyle changes.

 

Abortive migraine options can include the gepants (Ubrelvy, Nurtec ODT), ditans (Reyvow)neuromodulatory devices, and NSAIDs/over the counter analgesics, although triptans and ergots should be avoided.

 

Does Migraine With Aura Increase Your Risk of Stroke or Heart Attack?

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.

 

One study 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 (CVD). 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

 

A more recent larger follow up study evaluated the association of migraine with aura and other vascular risk factors with major CVD events (stroke, heart attack, death due to cardiovascular disease) in women aged 45 years or older. Women 45 years or older who had migraine with aura had a higher rate of CVD compared to women who had migraine without aura or no migraine. Basically, they looked at the likelihood of having heart attack or stroke if you have migraine with aura and compared the risk with a number of individual vascular risk factors which included diabetes, current smoker systolic blood pressure 160 mm Hg or higher, total cholesterol 280 mg/dL or higher, HDL cholesterol less than 40 mg/dL, triglycerides 194 mg/dL or higher, family history of heart attack prior to age 60 years old, and body mass index (BMI) of 30 or more.

 

Results showed that compared to having migraine with aura, only 2 other individual risk factors led to a higher incidence rate of major CVD; diabetes and current smoking. Women with migraine with aura had a similar risk of major CVD as those with high blood pressure, high total cholesterol, and family history of heart attack. Furthermore, adding migraine with aura to each individual risk factor led to a significantly increased risk of major CVD compared to having the vascular risk factor alone. These significant increases in CVD risk were associated specifically to migraine with aura, not migraine without aura.

 

These studies highlight the importance of optimizing medical treatments for vascular risk factors which lead to heart attack or stroke, especially in the setting of having migraine with aura.

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

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  2. Wolff HG. Headache and Other Head Pain. New York: Oxford University Press, 1963.
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  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.
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  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.
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  20. Chronicle E,  Mulleners W. Might migraine damage the brain? Cephalalgia 1994;14:415-8.
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  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.
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  29. Kurth T. Migraine and ischaemic vascular events. Cephalalgia 2007;27:965-75.
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