B Csd And Migraine Genetics
The genetics of migraine are clearly complex and are addressed in section X. It is however clear from a number of studies that alterations in CSD properties are a common phenotype. Initial studies characterizing the transgenic FHM mice which represent rare monogenic forms of migraine with aura highlighted an increased susceptibility to CSD, likely via increased cortical excitability. This increased propensity for cortical spreading depression was initially highlighted in FHM 1 mice and later in FHM 2 mice . Despite early suggestions , the lack of a clear link with more common forms of migraine , the above models of genetic susceptibility for migraine with aura have advanced our understanding of possible links between the two related conditions . Recently a mutation in the casein kinase 1 enzyme was found to be associated with increased prevalence of migraine with aura; interestingly, a common phenotype of the newly developed transgenic mouse is also an increased susceptibility to CSD .
The question of the role CSD has in migraine remains, that is, does CSD predispose individuals to migraine without aura or is it simply an additive phenotype which transforms migraine without aura, to that with aura? Regardless of the ongoing debate which will only be answered by detailed translational research, the impact of CSD on the trigeminovascular system is giving up its secrets.
C Photophobia And Phonophobia
Proposed mechanisms for the neural basis of photophobia in migraine. A: it is proposed that there is convergence of photic signals from the retina, via an intact optic nerve, onto posterior thalamic neurons that also receive nociceptive inputs from the dura mater, via the trigeminothalamic tract. These inputs subsequently project to nociceptive areas of the cortex resulting in the exacerbation of migraine headache by light, and areas of the visual cortex that cause hypersensitivity to light itself. B: PET imaging during the interictal phase of migraine demonstrates that 600-1,800 Cd/m2 light causes activation in the visual cortex in migraineurs, whereas in controls there is no activation . During pain in the trigeminal distribution, light does cause activation in the visual cortex of control subjects, and a hypersensitive response in the visual cortex of migraineurs. C: during migraine, low-intensity light also causes activation in the visual cortex which is significantly greater compared with that after headache relief with sumatriptan and headache-free interval. Also, activation of the visual cortex to the low level light after headache relief is still greater than that during headache-free interval. These data indicate that further physiological mechanisms may contribute to the hypersensitivity to light as it appears to be not dependent on a trigeminovascular nociceptive input.
1. CGRP and photophobia
Exploring Different Types Of Migraine And Headaches Compare Your Symptoms
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There are many different types of migraine or headache disorders.; The list of different types of migraine and headache disorders is below with their typical symptoms as well. Because many of them overlap, or for the overachievers who have multiple different types of headache, its best to get diagnosed by a headache specialist. This is usually a neurologist that has spent an additional year of training, called a fellowship, studying headache medicine. The best way to get a proper diagnosis of the type of migraine you have is to see a certified specialist. You can find them using this link from the American Migraine Foundation.
I have been seeing a headache specialist for years and the difference is marked. These doctors have a special interest in treating different types of migraine and headache disorders. Just like other neurologists might have a special interest in stroke or multiple sclerosis. Its best to see a doctor that understands, on a higher level,;different types of migraine and headache and all that accompanies them. Especially if you have a chronic form of migraine which can occur with any of the types listed below.
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Viii Neural Basis For Headache Pain Quality And Associated Symptoms
As indicated by the ICHD-III and outlined in section 2 specific criteria are laid out for the headache quality in migraine, and migrainous symptoms are not just restricted to headache pain, but it is also accompanied by many other symptoms of the sensory system and homeostatic function that occur throughout the duration of the migraine attack. These can include hypersensitivity to sensory inputs such as light , sound , and touch , but also symptoms caused by disruption to normal homeostatic functions such as altered sleep, feeding, and even mobility. Most patients consistently experience a subset rather than all symptoms, but each seems to be driven by similar pathophysiological mechanisms. Below we outline the likely neural basis for the headache quality and some of the most well-known associated symptoms that accompany migraine.
Common Headaches And Migraines
Pinpointing the cause of a headache can be difficult because headaches are a symptom of a multitude of conditions, rather than a disease itself. What many dont know is that headaches can actually be rooted in visual dysfunction, especially following a traumatic brain injury or stroke. And while migraines are a more severe form of headache, they too can be related to visual dysfunction. If you suffer from sporadic headaches or migraines, make an appointment with Dr. Cameron McCrodan or Dr. Scott Irvine to rule out visual dysfunction as the cause or contributing factor.
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What Are The Possible Complications Of Migraine Headaches
Although migraine headaches are a benign condition, it can result in further complications like prompting other diseases. The most common complication is status migrainosus.
This happens when a migraine headache lasts more than 72 hours, and the patient needs hospital care. Most of the time, status migrainosus results from a rebound headache after youve taken too many medications. Instead of making the migraine better, it gets worse.
Status migrainosus may cause sleeplessness and dehydration because of vomiting.;
Another complication is the migrainosus stroke or migrainosus infarction. One cause for migraines is the contraction or narrowing of the blood vessels in the brain.
Sometimes, these blood vessels can contract so much that blood flood to the brain is interrupted. When this happens, the brain doesnt receive enough oxygen, and the stroke occurs.
The patients who are most likely to suffer a migrainosus stroke are women on birth control pills, especially if they smoke. Migrainosus infarction is an emergency and needs medical assistance.
Persistent aura without infarction is another form of migraine complication. Sometimes, a migraines aura symptoms can stick way longer than usual, even if the headache is not there anymore.
You can have aura almost for as most as a week after the headache attack. The sufferer can also experience other symptoms like weakness or numbness in some parts of the body.;
Treating Different Types Of Migraine
The treatment for different types of migraine and headache disorders varies but has similar underlying features. We frequently recommend minimizing the effects of different triggers through lifestyle changes and medication intervention. Ensuring that we have good sleep, regular movement , a migraine friendly diet, eliminating caffeine, limiting acute medications and use of preventive medications can help us reduce our overall frequency and severity of attacks. We call all of this the Treatment Pie.;
The topic I wish we heard more about is ways to avoid progressing from episodic to chronic migraine. If you are currently episodic, please read this article to help minimize your chances of progressing to chronic. Avoiding the overuse of medications can go a long way to stopping this progression.;
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Data Management And Analysis
The neurologists diagnoses were confirmed with responses from the headache questionnaire. Headaches were classified under categories of migraine, tension-type headache, cervicogenic headache or mixed headache.
Participant data were assessed for extreme influence on the diagnostic model when Cooks distance values were over D=0.13 . Inclusion of data from participant #19 led to a model that was unstable. Furthermore, the participants predictor data did not match that of other participants and therefore was removed from further analysis. Complete data sets were available for all other participants.
Explained variance, calibration and discrimination were used to assess diagnostic model performance. Explained variance was calculated from the apparent prediction error of the model . Calibration was assessed with a calibration plot that incorporated a locally weighted smoothing technique for binary outcomes. Discrimination was to be assessed with the area under a receiver operating characteristic curve . However, a zero cell in the contingency table for C2/C3C3/C4 joint dysfunction and relief with diagnostic blocks prevented reporting a true AUC with a valid CI. Discrimination was therefore quantified by calculating the standardised mean difference between predicted probabilities for participants who did and did not experience relief with blocks. Data were analysed using SPSS statistical package V.25.
Causes & Risk Factors
Migraine can be caused by a number of different biological mechanisms and environmental factors. The biology behind migraine is complex and not fully understood. It involves the activation of trigeminovascular pathways and central parts of the brain including the brain stem . The trigeminovascular system controls sensation in your face and jaw which is why trigeminal disorders cause head pain. The brain is thought to be in an altered state of excitability, which can also lead to disruptive symptoms like nausea, light sensitivity and aura .;
Neurotransmitters are chemical messengers that communicate between neurons. These play a very important role in brain function . When the brain is more sensitive, neurotransmitters can become overactive and trigger pain signals.;
Neurotransmitters also control things like hunger, wakefulness, anxiety and focus. This causes many of the prodromal symptoms , and also causes nausea, photophobia, and phonophobia during an attack. The difficulty in migraine treatment arises because there are often many different neurotransmitters active during an attack. Some patients may be more responsive to treatment that addresses their serotonin neurotransmitters, while others might find treatment more effective if it inhibits calcitonin gene-related peptides .;
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Common Types Of Migraine In Children And Youth
Children can also suffer from chronic or episodic headaches, and it is important to recognize the symptoms
According to the National Headache Foundation,;20% of school-aged children from 5 to 17 are prone to headaches. Of that population, 15% will suffer from tension-type headaches, while the other 5% will be prone to migraine .
Headaches and migraine can happen to anyone, at any age, including young children. Not only that, but the intricacies and symptoms of the disorder are different in children than in adults; common migraine symptoms such as nausea, vomiting, and sensitivity to light and sound are not always prevalent in child sufferers. Children, in addition, cannot always vocalize or describe in detail what they are feeling, which makes diagnosis even more difficult. These patients may go undiagnosed for years, leading into adulthood, which can take a toll on their emotional and mental well being.
The American Migraine Foundation;outlines a few key differences between childrens migraine and those of adults:
- migraines in children are typically shorter in duration and occur less frequently
- the pain children experience tends to be more bilateral, such as across the forehead, rather than unilateral
- while common symptoms may not be reported, a lot can be deferred from a childs behavior, such as wanting to sleep or lay down in a dark, quiet room.
Common Migraine Without Aura
Classic Migraine With Aura
What Tests Are Done For People With Migraine Headaches
A;doctor doesnt actually need any tests to make the diagnosis of common or classic migraine . Only with an exhaustive interrogatory of your symptoms and medical history can a doctor determine you have this condition.
Most migraine sufferers have normal findings on the physical examination. However, many conditions can cause headaches. Sinus headaches caused by sinus infections, strokes, tension headache, meningitis, and brain tumors are common causes.
Your doctor may want to run some tests to make sure your headache is just a migraine. Some blood tests, X-rays, and CT scans of the head to look for tumors or bleeding may be useful in the differential diagnosis of a headache.;
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Which Condition Commonly Accompanies Migraine Headaches
Do you always feel pulsing or throbbing on one side of the head? Is your headache accompanied by nausea, vomiting, sensitivity to sound, and light? Do you often see flashes of light across your field of vision? Then, you probably suffer from migraines.
Xiii Theories Of Migraine
However, over the last two decades, an overwhelming volume of data has been generated which make this theory seem implausible, and in some respects impossible. First, only CGRP has been shown to be released during migraine, with no evidence of substance P or neurokinin A release . Furthermore, of all the inflammatory molecules shown to induce dural and retinal plasma protein extravasation, only CGRP, a marker of a migraine attack, failed to produce a response . It has proven very difficult to induce plasma protein extravasation in human skin, a process that is readily induced in guinea pigs, implying there may be a clear species difference that negates these preclinical studies . Also retinal plasma protein extravasation is not present during migraine , and there is little evidence of inflammatory pathology in migraineurs. Furthermore, a plethora of molecules developed to block extravasation without the vasoconstrictive effects of triptans, including neurokinin 1 receptor antagonists and extravasation inhibitors , failed as both acute and preventive treatments of migraine. These data indicate that it is unlikely that neurogenic dural inflammation plays a significant role in the pathophysiology of migraine, and the fact migraine can be so frequent and debilitating, and occur over many years, such an inflammatory insult would likely leave a pathology that is picked up on imaging, but nothing has been found .
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Common Triggers For Different Types Of Migraines
Many of us with migraine can point to at least a couple of variables that can trigger an attack for us. These include, but are not limited to, certain foods, caffeine, weather, hormones, lack of sleep, stress or stress let down, smells/odors and bright lights. Flickering candles will trigger me most of the time if they are in my sight line and centerpieces that obscure part of another persons face is also a trigger. Imagine trying to explain why you have to move the centerpiece at a dinner party, not to mention the food triggers you are trying to avoid. And heaven forbid someone has those cinnamon pine cones that are so popular around the holiday seasons. That is an instant trigger for me and I cant be around them at all. Navigating life with migraine can be tricky and irritating for all those involved.;
Panic Attacks And Panic Disorders
Panic disorder is characterized by repeated, unexpected panic attacks episodes of sudden fear and feelings of danger or impending doom, along with physical symptoms. The illness may be accompanied by depression or other serious conditions because the effects on peoples lives are not just limited to the attack itself. Some people avoid everyday activities such as driving or shopping, for fear of experiencing a panic attack in a potentially dangerous setting. Others avoid any other environment where they had such an attack in the past.
Panic disorders symptoms include:;Repeated, unexpected panic attacks episodes of sudden fear and feelings of danger or impending doom, along with physical symptoms such as heart palpitations, chest pain, lightheadedness or dizziness, nausea, shortness of breath, feelings of imminent danger, shaking or trembling, choking, fear of dying, sweating, feelings of unreality, numbness or tingling, hot flashes or chills, and a feeling of going crazy.;Panic attacks strike without warning and usually last 15-30 minutes. Since many panic disorder symptoms mimic those found in illnesses such as;heart disease, thyroid problems and breathing disorders, people with panic disorder often make multiple visits to emergency rooms or doctors’ offices, convinced they have a life-threatening illness.
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Iv Anatomy Of Trigeminovascular Pain Pathways
The previous section has described what we have learned from imaging the brain in migraineurs. Distinct areas of the brain are activated, suggesting a role for them in migraine pathophysiology, whether this is triggering the attack, generating the pain, or an involvement in some of the associated neurological symptoms that occur in the duration of an attack. Much has been learned from preclinical anatomical and physiological studies about the association of these different brain regions to each other, defining the involvement of specific brain stem and diencephalic nuclei and cortical areas in this network. These studies have also been able to determine how nociceptive information from craniovascular structures is processed resulting in the perception of headache during migraine, as well as associated neurological sensory symptoms.
A Peripheral Afferent Projections
Anatomy of the trigeminovascular systemascending projections. The trigeminal ganglion gives rise to pseudo-unipolar trigeminal primary afferents which synapse on intra- and extracranial structures as well as the spinal cord trigeminocervical complex . Second-order neurons from the TCC ascend in the quintothalamic tract synapsing on third-order thalamocortical neurons. Direct and indirect ascending projections also exist to the locus coeruleus , periaqueductal grey , and hypothalamus. The third-order thalamocortical neurons in turn synapse on a diffuse network of cortical regions including the primary and secondary motor , somatosensory , and visual cortices. A reflex connection from the TCC to the superior salivatory nucleus exists, which projects via the sphenopalantine ganglion providing parasympathetic innervation to the extra- and intracranial structures. Ins, insula; PtA, parietal association; RS, retrosplenial; Au, auditory; Ect, ectorhinal; RVM, rostral ventromedial medulla.
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