An Overview of Migraine in Case Studies
Migraine (UK: /ˈmiːˡreɪn/, US: /ˈmaɪ-/) is a complicated neurological illness that is impacted by heredity and is typified by episodes of moderate-to-severe headache, usually occurring in one side of the body and typically accompanied by nausea and sensitivity to light and sound. Allodynia, dizziness, nausea, vomiting, and cognitive impairment are possible additional defining symptoms.
The aggravation of headaches while engaging in physical activity is an additional characteristic. Aura, a premonitory phase of sensory disruption often believed to be generated by cortical spreading depression at the outset of a migraine episode, affects up to one-third of migraine sufferers.
Although migraine is mainly thought of as a headache problem, it is actually more appropriate to think of migraine as a spectrum disease rather than a single clinical entity due to its widely variable clinical presentation.
The burden of sickness can vary from chronic illness to episodic discrete bouts, which might occur as little as few times in a lifetime.
It is thought that a combination of hereditary and environmental variables affects how nerve cells in the brain are excited and inhibited, which is why migraines occur. An earlier “vascular hypothesis” suggested that vasoconstriction causes the aura and vasodilation causes the headache in migraineurs, but this process has been shown to be false.
According to the widely recognized theory, a number of fundamental neuronal deficits cause a cascade of intracranial and extracranial modifications, which in turn set off a physiological process that results in the symptomatology of migraines.
Over-the-counter analgesics (pain medicine) such ibuprofen and paracetamol (acetaminophen) for headache, antiemetics (anti-nausea medication) for nausea, and avoiding triggers are the first recommended treatments for acute episodes.
Patients with headaches that don’t respond to over-the-counter painkillers may be prescribed certain drugs like triptans, ergotamines, or CGRP inhibitors. Prophylactic medication is advised for people who have four or more attacks per month or who might otherwise benefit from prevention.
Prophylactic prescriptions are often written for antidepressants like amitriptyline, beta blockers like propranolol, anticonvulsants such sodium valproate, and other off-label classes of drugs.
Preventive drugs work by decreasing the pathophysiology of migraines through a variety of mechanisms, including matrix metalloproteinases, gap junctions, and the blockage of calcium and sodium channels. Aerobic exercise, dietary modifications, nutritional supplements, and better sleep are examples of nonpharmacological preventative therapy.
About 15% of people worldwide suffer from migraines. According to the 2010 Global Burden of Disease Study, migraines were the third most common condition worldwide. It usually begins at adolescence and peaks in middle age.
It is among the most prevalent causes of disability as of 2016. The Ebers Papyrus, written in ancient Egypt circa 1500 BCE, contains an early account that is compatible with migraines. The Greek term “migraine” (ϼμικρᾱvίᾱ (hēmikrāníā) means “pain in half of the head,” and it is derived from the words “half” (ϼμι-) and “skull” (κρᾱνίον) (krāníon).
Explains the Symptoms and Signs in Case Book Work
A severe headache that is self-limited, recurrent, and accompanied by autonomic symptoms is the usual presentation of migraine. Aura-producing migraineurs account for about 15–30% of all migraineurs, however they also commonly undergo aura-free episodes. There is variation in the headache’s duration, intensity, and frequency of bouts. Status migrainosus refers to a migraine attack that lasts more than 72 hours. A migraine attack can occur in four different phases, albeit not every phase is felt at the same time:
- The prodrome, which manifests itself days or hours before a headache
- The aura, which appears just before a headache
- The headache- or pain-related phase
- The aftermath, or the period of time after a migraine attack ends
Major depressive disorder, bipolar disorder, anxiety disorders, and obsessive-compulsive disorder are all linked to migraines. In those without aura, these psychiatric problems are roughly 2.5–5 times more common; in those with aura, they are 3–10 times more common.
Phase of prodrome
About 60% of migraine sufferers experience prodromal or premonitory symptoms, which can start two hours to two days before pain or aura begins. Numerous phenomena might accompany these symptoms, such as mood swings, agitation, euphoria or despair, exhaustion, cravings for particular foods, tense muscles, particularly in the neck, constipation or diarrhea, and sensitivity to sounds or odors.
People who have migraine without aura or migraine with aura may experience this. Neuroimaging suggests that prodromal symptoms in migraine are originating in the limbic system and hypothalamus.
Phase of Aura
Aura is a pre- or during-headache transient focused neurological phenomena. Aura often lasts less than sixty minutes and manifests gradually over a period of time, usually spanning five to sixty minutes. There are many other types of symptoms that many people suffer, including visual, sensory, and motor ones.
The most common type of effects are visual ones, which can happen in as many as 99% of cases and over 50% of them don’t have any accompanying sensory or motor effects. Persistent aura is the term for a state in which any symptom lasts longer than sixty minutes.
A scintillating scotoma, which is a partial modification in the field of vision that flickers and can make it difficult for a person to read or drive, is a common visual disturbance. These are usually located close to the center of vision, and they zigzag outward in a pattern that has been likened to a castle’s walls or fortifications. Although most people only perceive black and white lines, some people can also see colored ones. Hemianopsia, the loss of part of the field of vision, affects some persons, while blurring affects others.
The second most prevalent kind, sensory auras affect 30–40% of aura sufferers.Often, a pins-and-needles sensation starts in the hand and arm on one side and moves to the side of the nose and mouth. After the tingling has subsided, numbness typically follows with a loss of position sensation. Other signs of the aura phase include, less frequently, motor issues, disorientation in speech or language, and world spinning. A hemiplegic migraine is indicated by motor symptoms, and unlike other auras, weakness frequently lasts for more than an hour. There have also been reports of auditory hallucinations or delusions.
Phase of Pain
Traditionally, the headache is pounding, unilateral, and ranges in intensity from moderate to severe. It normally develops gradually and gets worse when exercising when having a migraine attack. The relationship between physical activity and migraine is complicated, though, and some researchers have shown that although regular exercise might prevent migraine symptoms, it can also make attacks less frequent. The pain is not pulsating in time with the pulse. However, in over 40% of instances, the pain may be bilateral, affecting both sides of the head, and it is frequently accompanied with neck pain. Those with migraine without aura are especially prone to experiencing bilateral discomfort.
Less frequently, the back or top of the head may be the primary location of pain. In adults, the pain often lasts between four and seventy-two hours; in young children, it often lasts less than an hour. Attacks can occur anywhere from a few times in a lifetime to multiple times a week, with an average of roughly one per month.
Frequent side effects of the pain include exhaustion, irritation, light, sound, and smell sensitivity, as well as nausea and vomiting. So many people look for a calm, dark space. Common symptoms of a basilar migraine, which is characterized by neurological symptoms associated to the brain stem or on both sides of the body, include dizziness, lightheadedness, and disorientation. About 90% of persons experience nausea, and roughly one-third vomit. Additional symptoms include be sweating, pallor, frequent urination, diarrhea, nose stuffiness, or blurred vision. Neck stiffness and/or scalp swelling are possible side effects. In older people, associated symptoms are less common.
Migraine Without Sound
Auras can sometimes appear without accompanying headaches. This is referred to as a normal aura without headache in modern classification, or as an acephalgic migraine in earlier classifications, or simply as a silent migraine.
Nonetheless, incapacitating symptoms such as visual disruption, loss of vision in half of the eyes, changes in color perception, and other sensory issues like light, sound, and odor sensitivity can still be caused by silent migraine.
It often lasts no more than 60 minutes, although it can last anywhere from 15 to 30 minutes. It can also occur repeatedly or just once.
Post-drome
The group of symptoms that appear after an intense headache has subsided is known as the migraine postdrome. Many describe pain where the migraine was felt, and some report having trouble thinking for a few days following the headache’s resolution. Along with head discomfort, weakness, gastrointestinal issues, mood swings, and cognitive impairments, the person may feel exhausted or “hung over”. According to a summary, “Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise.”
What is the reason for the migraine in the case study?
It is uncertain what causes migraines in the first place. They are thought to be connected to a combination of hereditary and environmental variables, though. In almost two thirds of instances, they run in families, and they are rarely caused by a single gene abnormality. Although it was formerly thought that those with high IQs were more likely to get migraines, this does not seem to be the case. There are other psychological illnesses linked to this, such as bipolar disorder, anxiety, and sadness.
The successful treatment of migraineurs with surgery that involves decompressing extracranial sensory nerves next to vessels raises the possibility that migraineurs are anatomically predisposed to neurovascular compression, which could be brought on by extracranial and intracranial vasodilation brought on by migraine triggers. This may help to explain the variety of migraine symptoms and the involvement of several cranial nerves, in addition to the existence of multiple cranial neural interconnections.
Molecular Biology
Twin studies show that migraine risk is influenced by genes in 34% to 51% of cases. When it comes to migraines with aura versus migraines without, there is a greater hereditary correlation. A handful of particular gene variations raise the risk in a mild to severe way.
It is uncommon for migraines to be caused by single gene abnormalities. Familial hemiplegic migraine is a kind of aura-producing migraine that is inherited in an autosomal dominant manner. It has been demonstrated that familial hemiplegic migraine is influenced by four genes.
These three genes have anything to do with ion transport. The axonal protein PRRT2, connected to the exocytosis complex, is the fourth.
CADASIL syndrome, also known as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, is another genetic condition linked to migraine. Angiotensin converting enzyme polymorphisms have been found in one meta-analysis to have a protective effect against migraine. Migraines have been associated with the cation channel-coding gene TRPM8.
Triggers
Triggers may cause migraines; some indicate that this is the case in a minority of cases, while others report that it is the case in the majority. Numerous items, including food, alcohol, exhaustion, and specific weather conditions, have been classified as triggers; however, it is unclear how strong and significant these associations are. The majority of migraineurs say they have triggers. A trigger may cause symptoms to appear up to 24 hours later.
- Physiological Elements
Stress, hunger, and exhaustion are frequently mentioned triggers (all three of these equally contribute to tension headaches). Fifty to eighty percent of people have indicated psychological stress as a role. Additionally, maltreatment and post-traumatic stress disorder have been linked to migraines. Periods are a prime time for migraine attacks to happen. A number of other hormonal factors also come into play, including menarche, the use of oral contraceptives, pregnancy, perimenopause, and menopause. In cases with migraine without aura, these hormonal factors appear to be more significant. Usually, migraine attacks don’t happen after menopause or in the second and third trimesters of pregnancy.
- Nutritional Elements
Many people have reported that tyramine, which is found naturally in chocolate, wine, most cheeses, processed meats, and other foods, can make some people feel like they have migraines. Although monosodium glutamate (MSG) has been linked to migraines, a systematic review found no evidence of a causal link between MSG and headaches. It would seem premature to conclude that headaches are caused by MSG found in food.
- Environmental Features
According to a 2009 analysis, “migraineurs worldwide consistently report similar environmental triggers,” even though there were not enough research to prove that environmental factors cause migraines. The review focused on putative triggers in both indoor and outdoor environments.
Let’s Examine Pathophysiology. When does a book work?
Some people think that migraines are predominantly neurological disorders, however the evidence does not fully support this theory. Others think that migraines are neurovascular disorders, with blood vessels playing a major role. Others think that both are probably significant. One idea links aberrant regulation of pain neurons in the brainstem’s trigeminal nucleus to elevated excitability of the cerebral cortex.
Trigeminal pathway sensitization is a crucial pathophysiological aspect of migraine. Whether sensitization originates in the brain or in the periphery is up for debate.
Aura
Acute cortical spreading depression, also known as spreading depression according to Leão, is a type of migraine characterized by an abrupt spike in neural activity followed by a quiet interval. There are several theories as to why it happens, one of which is that calcium enters the cell through the activation of NMDA receptors. Following the spike in activity, there is a two- to six-hour drop in blood flow to the affected cerebral cortex. It is thought that pain-sensing nerves in the head and neck are activated when depolarization proceeds along the underside of the brain.
Anguish
Unknown is the precise process underlying the headache discomfort that comes on during a migraine attack. There is conflicting information regarding the major significance of structures within the central nervous system, such as the brainstem and diencephalon, vs the role of peripheral activation, such as through the sensory nerves surrounding the blood vessels in the head and neck. The dural, pial, and extracranial arteries—such as those in the scalp—are among the possible candidate vessels. It is thought that vasodilatation of the extracranial arteries plays a major role in this.
Neuro-Stimulants
One possible neuromodulator involved is adenosine. When adenosine triphosphate (ATP) is gradually broken down, adenosine is released. Adenosine acts on adenosine receptors to dilate blood vessels and slow the heart rate, putting the body and brain in a low activity state. This happens before and throughout the early stages of sleep. It has been discovered that adenosine levels are elevated during migraine episodes. The way that caffeine inhibits adenosine may be the reason behind its ability to lessen migraines. Low concentrations of 5-hydroxytryptamine (5-HT), another name for the neurotransmitter serotonin, are also thought to be implicated.
Because levels of calcitonin gene-related peptides (CGRPs) increase during an attack, it has been discovered that CGRPs may be involved in the pathophysiology of migraine-related pain.
Conclusion | Migraine In Case Book Work
To sum up, examining migraines from the perspective of case book work offers a distinctive viewpoint into the complex nature of this crippling ailment. These case studies provide a patchwork of unique experiences that illuminate the various triggers, symptoms, and reactions to therapy that are seen in clinical settings. It is important to acknowledge, nevertheless, that the case book work we have done on migraines is by no means comprehensive.
We hope to learn more about this intricate neurological condition as we record and examine more cases, which will lead to improvements in patient care, diagnosis, and treatment.
The amount of knowledge and understanding that can be gained about migraines through case book work is vast, and this blog post just scratches the surface.
We can leverage the power of our collective knowledge to better support people who live with migraines and work toward more successful preventative and treatment solutions by encouraging continuous research, collaboration, and communication. Watch this space for additional updates and conversations on this important subject in upcoming posts.
image courtesy
Andrea Piacquadio, Mikhail Nilov, Nathan Cowley, Liza Summer, Martin Lopez, Andrea Piacquadio.