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Is Migraine A Nervous System Disorder

Treatment For Pregnant And Breastfeeding Women

Migraine and Cluster Headaches – Medical-Surgical (Med-Surg) – Nervous System – @Level Up RN

In general, migraine treatment with medicines should be limited as much as possible when you’re pregnant or breastfeeding. Instead, trying to identify and avoid potential migraine triggers is often recommended.

If medication is essential, then your GP may prescribe you a low-dose painkiller, such as paracetamol. In some cases, anti-inflammatory drugs or triptans may be prescribed. Speak to your GP or midwife before taking medication when you are pregnant or breastfeeding.

How Are Migraines Diagnosed

Despite their dramatic symptoms, migraines are almost never due to an underlying problem that will show up on any testing, even on brain MRIs. Many experts do not recommend brain imaging at all, even in severe cases, as long as the patient’s symptoms are typical for migraines and a thorough neurological examination is normal.

There are extremely rare families that have migraines as a result of a single genetic mutation in one of four known genes that can lead to the condition called familial hemiplegic migraine. There are no genetic tests for the vast majority of patients. Because the condition cannot be diagnosed by scan or blood test, the diagnosis is “clinical” made by an experienced physician.

What Are Nervous System Symptoms

We often call symptoms of the nervous system, aura. These symptoms can occur during or before your migraine and can differ in severity and frequency. If you are suffering from symptoms that affect your touch, movement, speech or sight, you are experiencing nervous system symptoms that could last for as long as 60 minutes.

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How Are Headaches Evaluated And Diagnosed

If you have headaches often or if they are very severe, reach out to your healthcare provider. You can usually start with your family physician, where the diagnosis process will begin. Its important to diagnose headaches correctly so that specific therapy can be started to help you feel better. Your healthcare provider will complete a physical examination, discuss your medical history and talk to you about your headache symptoms. This conversation is part of a headache evaluation. During the headache evaluation, your provider will ask you about your headache history, including:

  • A description of your headaches.
  • What the headaches feel like.
  • How often the headaches happen.
  • How long the headaches last each time.
  • How much pain the headaches cause you.
  • What foods, drinks or events trigger your headaches.
  • How much caffeine you drink each day.
  • What your stress level are.
  • What your sleep habits are like.
  • If you have any work issues.

Your headache can be more accurately diagnosed by knowing:

  • When the headache started.
  • How long you have had the headache.
  • Whether there is a single type of headache or multiple types of headaches.
  • How often the headache occurs.
  • What causes the headache, if known .
  • If physical activity aggravates the headache pain.
  • What events are associated with the headache.
  • Who else in your family has headaches.
  • What symptoms, if any, occur between headaches.

Clinical description of headaches

History of headache treatments

A International Classification Of Headache Disorders

Migraine Headaches

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 âneededâ 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.

Table 1. International classification for headache disorders -3β

See Reference 386 for details.

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Migraine Chronification As A Progressive Sensory Dysplasticity

Along with understanding how the migraine attack starts, understanding how episodic migraine becomes chronic is one of the most important challenges in migraine neuroscience. The vast majority of the clinical, financial, and emotional burden of migraine is from chronic migraine. There is also psychophysical and physiological evidence that sensory processing is altered in chronic migraine. For example, cutaneous allodynia is more common as disease duration increases , and indeed is associated with chronification. Visually-evoked magnetoencephalographic potentials show higher amplitudes in chronic migraine, and return to sizes seen in episodic migraine when patients are effectively treated.

From the neuroscientific perspective, understanding how an episodic neurologic disorder becomes chronic could offer deep insights into sensory learning and plasticity as well as pain progression. Animal models of chronic migraine provide foundations for mechanistic understanding. Both inflammatory mediators and NTG, when dosed repeatedly over 1â2 weeks, cause long-lasting reductions in mechanical withdrawal threshold, as well as reduced time spent in the light portion of a light/dark box. Importantly, these changes in sensory response persist after the migraine-relevant stimulus has stopped, suggesting that a persistent sensitization has been entrained.

What To Expect After Your First Visit With A Neurologist

After your first visit with a neurologist, the next steps will vary. If theyre not able to diagnose migraine from your medical history or exam, they may ask you to keep a symptom log.

They may also send you for a variety of imaging tests to rule out any other diagnoses. If they want you to get any other assessments with other specialists, youll need to schedule those as needed.

If you do have a diagnosis of migraine, you may be prescribed medication based on your symptoms. Youll also get instructions for taking any medication they prescribe.

If you find that a medication doesnt work for you, the neurologist will work with you to find medication thats more effective. Theyll also talk with you about lifestyle changes that may help reduce symptoms and offer advice on how to identify any potential migraine triggers.

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How Can I Prevent Headaches

The key to preventing headaches is figuring out what triggers them. Triggers are very specific to each person what gives you a headache may not be a problem for others. Once you determine your triggers, you can avoid or minimize them.

For example, you may find that strong scents set you off. Avoiding perfumes and scented products can make a big difference in how many headaches you have. The same goes for other common triggers like troublesome foods, lack of sleep and poor posture.

Many people, however, are not able to avoid triggers or are unable to identify triggers. In that case, a more personalized multidisciplinary approach with a headache specialist is often necessary.

Altered Behavior And Network Gain In Models Of Allodynia And Photophobia

Migraines, headaches and your nervous system.

Trigeminovascular models have been used to explore allodynia, one of the sensory amplifications of migraine .2). Cutaneous allodynia is seen in approximately two thirds of migraine attacks in humans: it is most prominent on the side of the head where pain is most severe however spread of allodynia to the contralateral head, to ipsilateral and contralateral arms, and even to the legs can occur. These sensory findings have been replicated in animal models, and are used as evidence for central sensitization. The rationale is that while hyperalgesia in the same territory as the head pain could be caused by peripheral sensitization , allodynia cannot be explained without central nervous system modulation . Both peripheral and central sensitization are phenotypes that, in non-headache pain models, are associated with synaptic plasticity . However the underlying mechanisms have not been investigated in migraine models.

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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.

Brain Differences Seen In People With Migraines

MRI study suggests changes occur in areas associated with pain

HealthDay Reporter

TUESDAY, March 26 — People who suffer migraines may have certain structural differences in pain-related areas of the brain, a new study suggests.

Using MRI scans, researchers found that in specific brain regions related to pain processing, migraine sufferers showed a thinner and smaller cortex compared to headache-free adults. The cortex refers to the outer layer of the brain.

It’s not clear what it all means. But the researchers suspect that certain aspects of brain development may make some people more vulnerable to developing migraines — and that migraine attacks create further changes in the brain.

The surface area of the brain “increases dramatically” during fetal development, while the thickness of the cortex changes throughout life, explained senior researcher Dr. Massimo Filippi.

“We speculate that migraine patients might have a sort of cortical ‘signature’ — abnormal cortical surface area — which could make them more susceptible to pain and abnormal processing of painful stimuli,” said Filippi, a professor of neurology at the University Vita-Salute’s San Raffaele Scientific Institute in Milan.

Once migraines develop, they may alter the thickness of the brain’s cortex, Filippi explained.

No one knows precisely what causes migraines, but they do seem to involve abnormal brain activity and — like the new study suggests — abnormal brain structure.

Radiology

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V Modulation Of Trigeminovascular Pain Pathways

Ascending connections from the TCC to many areas of the brain are involved in processing nociceptive somatosensory information from the head and face, and determine how it is perceived. However, there are also many endogenous mechanisms that modulate trigeminovascular nociceptive traffic, which can further determine the perception of this information. As indicated in section III, there is clear evidence of activation in areas of the brain stem and diencephalic nuclei before, during, and after the cessation of migraine with treatment that cannot be explained as solely a consequence of the pain response. Certainly descending modulation of somatosensory processing is not unique to migraine and has previously been described with respect to spinal responses. Brain stem modulation can have both a facilitatory effect, contributing to chronic pain and an inhibitory influence, through supraspinal and spinal stimulation, on spinal nociceptive processing . There is still much debate surrounding the role of brain stem and diencephalic activation during migraine. Does this activation signal an area of the brain where migraine may be triggered, or is it a consequence of activation of the trigeminovascular system, which drives other symptoms in migraine?

B) FUNCTIONAL CONSEQUENCES OF BRAIN STEM MODULATORY DYSFUNCTION.

Alzheimers Disease And Dementia

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Memory loss is a common complaint, especially in older adults. A certain degree of memory loss is a normal part of aging. For example, walking into a room and forgetting why may be totally normal.

However, there are signs that may indicate something more serious, such as dementia or Alzheimers disease. These symptoms may include getting lost, having difficulty managing finances, difficulties with activities of daily living, leaving the stove on, forgetting the names of close family and friends or problems with language. Behavioral changes along with these memory changes could also raise concerns.

Dementia is a slowly progressive condition and should be evaluated by a neurologist. While there is no cure, there are medications and therapies that can help manage symptoms.

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Complex Neurovascular Interactions In Primary Headaches: Migraineas A Pathophysiological Model

Primary headaches share many similarities, primarily trigeminovascular activation. While migraine is the most studied of all primary headaches, from both a clinical and a preclinical perspective, there have been advances in our understanding of the pathophysiology of tensiontype headache and the trigeminal autonomic cephalalgias, through a combination of clinical studies and preclinical animal models.

The meningeal vessels have a motor and sensitive innervation by the trigeminal terminations , which, in the end, establish connections with the secondary trigeminal neurons from the caudal trigeminal nucleus. Trigeminal nucleus is made up of the spinal portion in the converging information about pain and temperature and the pontine region with tactile information. The dendrites of the bipolar neurons from Gasser ganglia receive input from the pain receptors of dura mater and craniofacial structures, but also from the vascular wall and they direct it to trigeminal nucleus, thalamus, and contralateral parietal cortex , including the dorsal reticular nucleus , the rostral ventral medulla , and the midbrain periaqueductal gray .

The motor component of the cerebrovascular system implies an extrinsic innervation of the meningeal vessels, from the cervical , otic, sphenopalatin, and trigeminal ganglia and an intrinsic innervation for the small intraparenchimatous vessels, derived from brain stem nuclei such as locus coeruleus .

How Persistent Migraines Can Affect The Nervous System

Do you suffer from frequent migraines? If you do, you are probably familiar with the symptoms that can accompany your head and neck pain. Did you know that many of these symptoms affect the nervous system and bodily functions such as vision, speech and hearing?

When untreated, migraines usually last anything from 4 to 72 hours and their frequency can differ from person to person. Some people have migraines a number of times every month, while other people may only experience it once or twice a year.

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Personal History Of Other Diseases Of The Nervous System And Sense Organs

    2016201720182019202020212022Billable/Specific CodePOA Exempt
  • Z86.69 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes.
  • Short description: Personal history of dis of the nervous sys and sense organs
  • The 2022 edition of ICD-10-CM Z86.69 became effective on October 1, 2021.
  • This is the American ICD-10-CM version of Z86.69 – other international versions of ICD-10 Z86.69 may differ.
  • Applicable To annotations, or

A Familial Hemiplegic Migraine

Migraine relief with CNSR, Central Nervous System Restoration

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 .

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The Trigeminal Vascular System And Brainstem Nuclei

The trigeminovascular system is one of the key actors in the expression of migraine headache. It consists of peripheral axons from the trigeminal ganglion that reach the meninges and intracranial arteries and converge centrally in the trigeminocervical complex releasing, among other transmitters, calcitonin gene-related peptide . The trigeminocervical complex consists of the trigeminal nucleus caudalis along with the dorsal horn of C1C2 segments of the spinal cord . Its activation is thought to lead to the cascade of events resulting in the migraine pain due to its direct connection with key brain centres such as diencephalic and brainstem nuclei .

How Is Migraine Treated

Theres no cure for migraine, but there are a variety of treatments available.

Treatment can depend on a variety of things, including your age, how often you have migraine attacks, the kind of migraine you have, the severity, any associated symptoms, and any other medical conditions you might have.

Treatment plans can include:

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Viii Neural Basis For Headache Pain Quality And Associated Symptoms

As indicated by the ICHD-IIIβ 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.

Vi Thalamic Processing Of Trigeminovascular Pain

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Evidence of thalamic activation during migraine is clear , but the role it plays is thought to go beyond that of merely a relay in processing sensory nociceptive information to the somatosensory cortices. It has also been demonstrated that activation in thalamic nuclei can also contribute to the modulation of trigeminovascular and other spinal nociceptive inputs. Below we describe in detail how cutaneous allodynia, the perception of pain in response to normally innocuous stimuli, in the cephalic and extracephalic regions, is likely the consequence of sensitization of central trigeminal and thalamic neurons . The particular contribution of the thalamus is the spread of cutaneous allodynia beyond the site of pain to contralateral cephalic and extracephalic regions via sensitization of thalamic neurons, particularly in the posterior, VPM, and lateral regions. Hence, the perception of somatosensory trigeminovascular and spinal inputs are altered as a result of sensitization of thalamic neurons. The authors of these studies propose that the mechanism of sensitization may be the result of a sequential sensitization of first-, second-, and third-order trigeminovascular neurons through incoming signals coming from the peripheral dural trigeminal innervations . Although activation and sensitization of thalamic neurons via mechanisms directly through medullary, midbrain, and hypothalamic nuclei, as described above, could potentially also drive this response .

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