C Ascending Projections From The Tcc
All nociceptive information from craniovascular structures is relayed through the TCC, and via ascending connections to other areas of the brain stem and diencephalon, involved in the processing of pain and other sensory information. Functional physiological and tracing studies have allowed mapping of these ascending connections. Activation of these structures is thought to contribute to the perception of pain during migraine, and also to autonomic, endocrine, cognitive and affective symptoms that last throughout the entire migrainous episode.
What Are The Types Of Headaches What Type Of Headache Is A Migraine
There are over 150 types of headaches, divided into two categories: primary headaches and secondary headaches. A migraine is a primary headache, meaning that it isnt caused by a different medical condition. Primary headache disorders are clinical diagnoses, meaning theres no blood test or imaging study to diagnose it. A secondary headache is a symptom of another health issue.
Vii Cortical Processing Of Trigeminovascular Pain
In recent years evidence has been growing that migraineurs suffer an alteration in cortical excitability that may act as a susceptibility factor for migraine attacks . While the mechanism of how this might contribute to migraine is not known, it is certainly undeniable that there is endogenous corticofugal modulation of trigeminovascular nociceptive inputs via medullary and midbrain structures. In a recent study in rats, descending projections from the cerebral cortex, specifically from contralateral insular and primary somatosensory cortices, to laminae III and IIIIV, respectively, of the TNC were demonstrated , although ipsilateral functional connections have also been demonstrated . These descending connections have been previously shown in humans . Functionally it has been demonstrated that CSD, the experimental paradigm believed to represent the neural mechanism of migraine aura , is able to inhibit neuronal activity in the NRM. Furthermore, repetitive CSDs were able to reverse the descending inhibitory effects that the NRM has on dural nociceptive trigeminovascular responses , demonstrating a cortico-NRM modulation of trigeminovascular nociceptive inputs.
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A Neurophysiology Of Migraine As A Backdrop To Imaging
The application of neurophysiological methods in migraine patients has offered important insights into the condition. These approaches offer temporal over spatial discrimination and prior to MRI, and still to some extent, better opportunities for repetition. What has emerged very clearly from studies in visual, somatosensory, auditory, and nociceptive domains is activation that differs from controls reliably. A prevailing synthesis of the data is to consider thalamocortical dysrhythmia to be key to migraine pathophysiology . It has been observed for some time that migraine patients fail to habituate normally between attacks, for example, the intensity dependence auditory evoked potentials is augmented between attacks in migraine patients . Remarkably this normalizes in the days before an attack . Interestingly, this measure has a serotonin dependence that can be altered by triptans, serotonin 5-HT1B/1D receptor agonists . Potentiation of the passive oddball auditory event-related potential similarly suggests migraineur’s brains do not habituate as non-migraineurs do , as does an interical habituation deficit as measured by the nociceptive blink reflex in migraineurs . This has led to the concept that the migraine brain over-responds, as distinct from being hyperexcitable .
Don’t Miss Dr Goadsby Busting More Migraine Myths At The Migraine World Summit
Paula Dumas: What symptoms do you see after the headache phase resolves?
Dr. Goadsby: The postdromal phase is the phase that occurs afterwards, as the headache settles down. Almost everyone, certainly we see in clinic, will complain of or mention tiredness, a feeling of washed out like they’ve been run over by a truck.
Cognitive problems sometimes there are thinking and word finding problems that can last for hours, up to a day, and ruin the day afterwards.
So, Migraine is much more than just headache. It has neurological symptoms occurring beforehand has disabling headache when it’s there and then neurological symptoms that are further disabling afterwards.
These are all parts of a big package of the brain disorder that it is.
Paula Dumas: You made a simple yet profound observation about caring for our Migraine brains to help reduce the most common triggers.
Dr. Goadsby: Yes … Migraine brains are susceptible to change. Regularity is important … consistency of behavior. It helps if you get up at the same time and go to sleep at the same time. It helps if your meals are regular.
It helps if you exercise a little bit regularly. It helps if you have a little bit of regular grief.
It’s the highs and lows, the changes, the variation that challenges the very biology that is Migraine.
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What Does An Attack Look Like
There are four distinct phases of a migraine attack: prodrome, aura, headache, postdrome. You dont have to experience all the phases. In fact, only about 20% of people with migraine have an aura. Understanding the phases can help you manage the disease better.
The prodrome and aura phases usually occur before the headache develops. Prodrome may precede the migraine attack by several hours or even days. Typical prodrome symptoms include extreme tiredness and yawning, irritability or moodiness, difficulty concentrating, and food cravings. About 75% of people with migraine experience a prodromebut often they dont recognize it as the beginning of an attack. Aura is rarer and usually begins just before the headache starts. Most people experience changes in their vision, while others notice tingling, numbness or trouble speaking.
These symptoms can serve as a warning sign and allow you to take acute medication before the headache begins. Identifying and treating a migraine early can even help prevent further symptoms in some people.
What Should I Do To Prepare For My First Doctor Visit For My Headaches
If possible, keep a headache diary for as many days as possible before your visit. Whether or not you keep a diary, you should be prepared to answer the following questions:
- When did you get your first headache?
- Do you have family members who get headaches?
- How often do you get headaches?
- How long do they usually last?
- How intense are they on a scale of 1 to 10 ?
- What is the location of your headaches?
- What kind of pain do you usually have?
- Are there triggers that usually bring on your headache?
- What do you do when you get a bad headache? Are there things you avoid doing?
- What medicine, including over-the-counter medicines, do you currently take for the headaches ?
- What medicines have you tried in the past?
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What Is An Aura
An aura is a group of sensory, motor and speech symptoms that usually act like warning signals that a migraine headache is about to begin. Commonly misinterpreted as a seizure or stroke, it typically happens before the headache pain, but can sometimes appear during or even after. An aura can last from 10 to 60 minutes. About 15% to 20% of people who experience migraines have auras.
Aura symptoms are reversible, meaning that they can be stopped/healed. An aura produces symptoms that may include:
- Seeing bright flashing dots, sparkles, or lights.
- Blind spots in your vision.
- Numb or tingling skin.
Possible Shared Mechanisms Between Migraine With Aura And Cvd
First, subjects with migraine with aura may have other traditional cardiovascular risk factors, which increase the risk of vascular diseases, such as higher total cholesterol, lower high-density lipoprotein cholesterol , higher total cholesterol-to-HDL ratios and higher blood pressure . Second, the proinflammatory or vasoactive peptide released during migraine attacks may damage the vascular endothelium and result in stroke or other vascular events . Third, lower levels of endothelial progenitor cells in migraineurs indicated a reduced endothelial repair capacity, particularly in migraine with aura, which may contribute to the association between migraine and vascular diseases . Fourth, the genetic risk factors are possible shared mechanisms between migraine and cardiovascular diseases . The ACE DD genotype was reported to act in combination with the MTHFR T/T genotype to increase migraine susceptibility, with the greatest effect in those with aura .
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A International Classification Of Headache Disorders
The International Classification of Headache Disorders , a valuable tool for the standardized diagnosis of primary and secondary headache disorders, which is now available in its third edition . From its first through second editions, it led to a significant improvement in diagnostic accuracy, and to improved and focused preclinical and clinical research, in particular clinical trials, in an unprecedented way. However, given its aim to define the clinical picture for the use in a clinical setting, it focuses on the headache and aura phases as they are characterized by disabling symptoms that commonly require medical intervention. Its weakness is the over-reliance on a polythetic approach where there are a broad set of criteria without one or the other being necessary or sufficient. This contrasts to a monothetic approach where some or all parts are necessary and sufficient. The conflict comes with face validity for clinicians it remains an unresolved issue. The impact on physiology is where migraine symptoms, such as osmophobia , are not mentioned because they are not usually needed by a polythetic approach, which may leave them less studied. In the review, we aim to capture as much of the pathophysiology as possible, and will be inclusive where possible, symptom-wise, and use the concept of phases, as limited as they be in a disorder that often is marked by a continuum.
D Csd And Trigeminovascular Activation
Thus it is likely that a combination of CSD peripheral trigeminovascular activation and central pain modulatory dysregulation underlie the association of CSD/aura and migraine. Perhaps the field of migraine research has been too focused on if CSD/aura is a trigger for migraine with or without aura, as many triggers are known to exist and should look at the disease as a whole. As presented above, migraine occurs in three stages with a premonitory phase starting 2448 h before the attack long before CSD is known to occur. It is thus conceivable that a central disruption predisposes individuals to specific triggers, of which CSD/aura is one of many which may potentiate an already perturbed system.
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A Csd And Brain Injury
For some time, CSD-like events had not been clearly demonstrated in migraine with aura patients, despite the evidence available from cases of brain injury . In a number of patients who had undergone craniotomies for subarachnoid hemorrhage, stroke, and traumatic brain injury, direct cortical electrocorticography recording demonstrated repetitive CSDs, which were negatively associated with outcome. It is clear from the available clinical data that the occurrence of CSDs may have a severe detrimental outcome, and this has recently been supported using experimental stroke models in familial hemiplegic migraine mice . FHM mice exposed to transient occlusion of the middle cerebral artery experienced increased numbers of CSD, greater brain damage, and poorer outcome than controls. Originally the association between CSD and aura was postulated based on a number of similar features including rate of propagation. More recently, advances in brain imaging have enabled characteristic blood flow changes to be observed in humans, where an initial brief hyperemia is followed by a more prolonged oligemia spreading across the cortex, starting at the occipital lobe . The hypoperfusion correlates with the scotoma experienced by some patients during aura , and it is thought the hyperperfusion correlates with the negative symptoms.
Genetic And Epigenetic Component Of Migraine
Genetic factors may determine susceptibility to migraine, while different environmental factors can contribute to the development of a migraine attack . Mainly through genome-wide association studies , which tested for differences in allele frequencies of single nucleotide polymorphisms over the genome in migraine patients and controls , it is now understood that multigenetic variants, rather than individual genes, influence the susceptibility to migraine. Although GWAS in migraine, similarly to other disorders studied with GWAS , failed to shed light on the molecular changes that are responsible for the evolutive nature of migraine, one can envisage that combined knowledge from many variants will highlight which molecular pathways potentially could be involved in migraine pathophysiology .
Regardless of these outcomes, due to their small effect size no single SNP has any clinical use in predicting the risk of developing migraine. There is still a big challenge in the field of GWAS to link associated SNPs to actual genes and pathways. GWAS in migraine are yet to offer further knowledge on the functional consequences of the associated SNPs and how they influence susceptibility to migraine.
Is there a role for epigenetic mechanisms in migraine susceptibility and chronification?
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 .
The Neurological Nature Of Migraines
It has long been established that migraines are neurological in nature. Researchers have identified possible causes of migraines, and one of the contributors is a problem in the brainstem. Together with the trigeminal nerve, the brainstem is the bodys main road for sensing pain. Brain chemistry also plays a part as serotonin levels and other factors are involved in the central nervous systems function to regulate pain.
The findings in these studies suggest that both neurological and vascular functions must be examined when a patient struggles with migraines. Whether food, weather changes, or inadequate sleep trigger migraine attacks in a patient, the best solution to reduce the frequency and severity of migraines permanently is to address the underlying cause.
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When To See Your Doctor
If youre experiencing migraines for the first time or with increased severity or frequency, talk to your doctor. You can see your general practitioner, who may refer you to a neurologist or headache specialist. If you start experiencing any new symptoms along with a migraine, you should also call your doctor.
A sudden or unusual migraine can be a symptom of a medical emergency. If a sudden, severe headache comes on with the following symptoms, seek emergency medical attention immediately:
- severe vomiting and nausea
Diseases That Commonly Coexist With Migraine
Migraine is a complex brain disorder that is believed to result from a slew of factors including trigeminal nerve fiber activation, serotonin release, structural brain changes, genetics, and a phenomenon called central sensitization, to name a few.
In addition to migraine’s fascinating and tangled biology, this neurological disorder is also believed to coexist with a number of health conditions.
Gaining knowledge about these conditions may provide clues into your migraine and overall health, and potentially even affect your treatment plans.
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A Familial Hemiplegic Migraine
FHM represents a monogenic subtype of migraine with aura that involves at least one limb weakness. It does not, in spite of the name, usually involve plegia, rather weakness the term hemiplegic is retained for historical consistency rather than neurological accuracy. The three responsible genes currently recognized were identified by classical linkage analysis in which genetic markers are compared with a specific disease trait. All three known FHM mutations encode mechanisms that impact ion transporters: the CACNA1A , ATP1A2 , and SCN1A genes their dysfunction ultimately leads to an increase in neuronal excitability .
The CACNA1A gene was the first gene to be identified as causal for FHM1 . It is located on chromosome 19p13 and encodes the 1 subunit of neuronal CaV2.1 voltage-gated calcium channels . All known FHM1 mutations induce gain-of-function effects as they enhance channel open probability, thereby increasing neurotransmission . Two mouse models, R192Q and S218L transgenic mice, have been developed to gain insight into the functional consequences of these mutations through a large amount of preclinical in vivo studies. Findings from these animal studies have substantially enhanced the understanding of migraine aura.
4. Pathophysiology of FHM
5. Triggering and FHM
Want To Find Out More About Migraine
Lifestyle factors in Migraine
I particularly recommend the site Headache Relief Guide . This site made by Dr Jennifer Bickel and Dr Mark Connelly, paediatric neurologists in Kansas was designed for children and teenagers to give advice about modifiable lifestyle factors like exercise, sleep, hydration and diet. I think its really helpful for people with migraine and headache of any age.
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Why Has It Happened
Chronic Daily Headache is a complex phenomenon that probably has lots of different causes. Try thinking of the problem as a volume knob in your head that has been turned up too high.
As we understand more about the way pain works we know that there really are places in the nervous system, both in the nerve endings in the head and in the brain itself where this process of sensitisation and amplification of pain can occur. Try thinking of the problem as a volume knob in your head which has been turned up too high and which you need to turn down
These are some potentially relevant factors: