Abdominal migraine | |
---|---|
Specialty | Neurology |
Symptoms | episodes of abdominal pain |
Usual onset | variable |
Causes | migraine triggers |
Risk factors | cyclic vomiting syndrome, PTSD, functional gastrointestinal disorder |
Diagnostic method | symptoms |
Differential diagnosis | irritable bowel syndrome, peptic ulcer disease, gastroesophageal reflux disease, mast cell activation syndrome, celiac artery compression syndrome |
Prevention | avoiding triggers (different for each patient) |
Treatment | a range of experimental medications, including TCAs and anticonvulsants |
Prognosis | good in pediatrics, variable in adults |
Frequency | between 1% and 9% of children |
Deaths | poorly studied |
Abdominal migraine(AM) is a functional disorder that usually manifests in childhood and adolescence, without a clear pathologic mechanism or biochemical irregularity. Children frequently experience sporadic episodes of excruciating central abdominal pain accompanied by migrainous symptoms like nausea, vomiting, severe headaches, and general pallor. [1] Abdominal migraine can be diagnosed based on clinical criteria and the exclusion of other disorders. [2]
The US Food and Drug Administration has not approved any drugs for the treatment of abdominal migraine. The goal of treatment is usually to prevent attacks, and this is often achieved through nonpharmacologic intervention. [3]
Research has indicated that the incidence of abdominal migraine in children falls within the range of 0.4% [4] to 4%. [2] The condition primarily affects children aged 3 to 10 years, with a higher prevalence in females. [5]
Midline abdominal pain with paroxysmal, recurrent, acute onset attacks that last an average of 17 hours are the hallmarks of abdominal migraine. [6] There have been reports that these attacks can last anywhere from two to seventy-two hours. [5] Although it has also been reported to be diffuse and colicky, the pain is usually described as dull and periumbilical. 91% of patients have anorexia, 73% to 91% have nausea, 35% to 50% vomit, and 93% to 100% of patients have associated pallor. [7] The attack usually comes to an abrupt end. [5] The average annual frequency of abdominal migraine attacks in patients is 14. [6]
Although nonspecific prodromes can occur before attacks, abdominal migraine attacks are usually sporadic. This can include behavioral and mood swings, anorexia, flushing, diarrhea, and auras that include numbness, slurred speech, tingling in the distal extremities, and flashing lights. [5] Weeks to months may pass between episodes, and during this time patients usually experience no symptoms. [8]
Abdominal migraine has been linked to specific alterations in the gut-brain axis, vascular dysregulation, modifications in the central nervous system, and genetic factors. [9]
Abdominal migraine pathophysiology may involve psychological factors. Abuse and stressful events are two risk factors for recurrent abdominal pain, for instance. Furthermore, it has been demonstrated that kids with functional gastrointestinal disorders experience mental health conditions like anxiety and depression more frequently than kids without these conditions. [10]
There are several typical causes of attacks of abdominal migraines. Stressors related to work and family life, irregular sleep patterns, extended fasts and food deprivation, dehydration, exercise, travel, high-amine foods, foods containing flavoring, coloring, and monosodium glutamate (MSG), and flashing lights are a few common triggers. [5] [8]
A significant hereditary component may be involved in abdominal and other migraines due to their strong familial incidence, [11] especially in the case of mutations affecting cell membrane transport (channelopathies). [12] [13]
While the pathophysiology of functional gastrointestinal disorders (FGIDs) has many potential contributors, the etiology of abdominal migraine is still unknown. [14]
It is thought that abnormal electrical discharge from the hypothalamus that travels to the cortex and autonomic nervous system [15] or variations in the cerebral artery's blood flow velocity cause attacks. [16] In patients with FGIDs, there appears to be a disruption in the complex brain-gut axis. [17] Many episodic functional gastrointestinal disorders in childhood have been linked to mitochondrial disease, [18] hypothalamic-pituitary-axis dysfunction, and gene mutations; these associations have not, however, been studied in patients diagnosed with abdominal migraine. [19]
This article contains instructions, advice, or how-to content .(August 2024) |
It's critical to rule out organic diseases as the source of a child's symptoms while also taking the patient's functional state into account. When diagnosing abdominal migraine, a patient's complete medical history and physical examination are crucial. Additionally, any potential alarm signs and symptoms should be carefully examined. The presence of visible or occult blood in the stool, dysphagia, hematemesis, bilious vomiting, fever, changes in growth pattern, and weight loss are a few examples of alarm symptoms. [20] Further imaging and testing should be carried out if these alarm signs or symptoms are apparent. [21]
The Rome IV criteria state that paroxysmal bouts of intense, acute periumbilical, midline, or diffuse abdominal pain lasting at least an hour, exhibiting a recurrent pattern, being incapacitating, and interfering with regular activities can be used to diagnose abdominal migraine if at least two of these episodes take place over a six-month period. There should be weeks or months without any symptoms in between attacks. The following symptoms must be present in at least two instances: pallor, photophobia, headache, nausea, vomiting, and anorexia. Lastly, there is no other medical diagnosis that can account for the symptoms. [22]
Abdominal migraine is defined by the International Classification of Headache Disorders III criteria as five or more episodes of abdominal pain lasting two to seventy-two hours. A minimum of two out of three of the following criteria must also be met by the pain: dull or "just sore" quality; midline location, periumbilical, or poorly localized; and moderate to severe intensity. Pallor, nausea, vomiting, and anorexia are associated symptoms that the patient should have at least two of. [7]
Abdominal migraine must be distinguished from other causes of chronic or recurrent abdominal pain. These include irritable bowel syndrome, peptic ulcer disease, and gastroesophageal reflux disease. [3] It must also be distinguished from causes of acute abdominal pain, such as appendicitis, as wrong diagnosis may lead to unnecessary appendectomy. [23]
Because there are so few studies in the literature, there are no firm recommendations for the treatment of abdominal migraines. [24] The majority of treatment options are predicated on anecdotal evidence, a small number of studies conducted on a relatively small number of children, and a close correlation between abdominal migraines and both migraine headaches and FGIDs. [25]
When treating patients with abdominal migraines, doctors may find the STRESS mnemonic useful. It stands for stress management, travel advice, rest, emergency symptoms, sparkling lights, and snacks to avoid. [26]
Certain triggers, like bright light, restless nights, travel, and extended fasting, should probably be minimized or avoided once they have been identified. [19] Emotional stressors from family or school activities can be a trigger for certain kids, so it's best to minimize or stay away from them. [3] Although there are no particular randomized trials evaluating the efficacy of biofeedback and counselling in treating abdominal migraines, it is believed that these interventions may be helpful if emotional stress is a trigger factor in the development of migraine in children. [27]
It's unclear what function elimination diets serve. Nonetheless, in patients experiencing both migraine and IBS symptoms, an immunoglobulin G (IgG)-based elimination diet shows promise in lowering migraine episodes. [28] There isn't much more proof that a child's diet has a significant impact on when migraines begin. [29]
In one study, 14 children with abdominal migraine were administered pizotifen syrup, a serotonin and histamine antagonist. After four months, 70% of the patients said their symptoms had improved. Their symptoms were noticeably milder and less frequent. [30] Propranolol and cyproheptadine syrup were found to alleviate symptoms in a retrospective review. [25] Flunarizine use was found to reduce the frequency and duration of abdominal migraine attacks in another retrospective review. [31]
Analgesics, triptans, and antiemetics may be helpful for sudden attacks of abdominal migraines. It has been suggested that patients with nausea, vomiting, or anorexia might benefit more from nasal sprays or suppositories. [5] Acute attacks have been reported to be resolved by acetaminophen and ibuprofen. [32] Intranasal sumatriptan alleviated the symptoms of abdominal migraine in two children, according to a case report. [33] In refractory cases, intravenous sodium valproate has been reported to resolve abdominal migraine episodes. [34] According to a case series, intravenous dihydroergotamine treatment prevented abdominal migraine attacks in five out of six pediatric patients. [35]
Abdominal migraine can have a significant impact on day-to-day life. [36] Children may miss school or other activities. [36] It resolves in many patients. [23] [37]
Abdominal migraine primarily affects children, for whom it is a common cause of chronic abdominal pain. It may be as high as 9% or as low as 1% among children. [23] It is rare in adults. [3] However, children diagnosed with abdominal migraines may have migraine headaches as adults. [38] The mean age of diagnosis is 7 years. [39] [40] It appears to be slightly more common in women. [23]
This condition was first described in 1921 by Buchanan. [41] It was once considered a controversial diagnosis. [42] However, it is now accepted as a common cause of chronic abdominal pain in children. [43]
Migraine is a genetically influenced complex neurological disorder characterized by episodes of moderate-to-severe headache, most often unilateral and generally associated with nausea and light and sound sensitivity. Other characterizing symptoms may include vomiting, cognitive dysfunction, allodynia, and dizziness. Exacerbation of headache symptoms during physical activity is another distinguishing feature. Up to one-third of migraine sufferers experience aura, a premonitory period of sensory disturbance widely accepted to be caused by cortical spreading depression at the onset of a migraine attack. Although primarily considered to be a headache disorder, migraine is highly heterogenous in its clinical presentation and is better thought of as a spectrum disease rather than a distinct clinical entity. Disease burden can range from episodic discrete attacks to chronic disease.
Headache, also known as cephalalgia, is the symptom of pain in the face, head, or neck. It can occur as a migraine, tension-type headache, or cluster headache. There is an increased risk of depression in those with severe headaches.
A medication overuse headache (MOH), also known as a rebound headache, usually occurs when painkillers are taken frequently to relieve headaches. These cases are often referred to as painkiller headaches. Rebound headaches frequently occur daily, can be very painful and are a common cause of chronic daily headache. They typically occur in patients with an underlying headache disorder such as migraine or tension-type headache that "transforms" over time from an episodic condition to chronic daily headache due to excessive intake of acute headache relief medications. MOH is a serious, disabling and well-characterized disorder, which represents a worldwide problem and is now considered the third-most prevalent type of headache. The proportion of patients in the population with Chronic Daily Headache (CDH) who overuse acute medications ranges from 18% to 33%. The prevalence of medication overuse headache (MOH) varies depending on the population studied and diagnostic criteria used. However, it is estimated that MOH affects approximately 1-2% of the general population, but its relative frequency is much higher in secondary and tertiary care.
Functional gastrointestinal disorders (FGID), also known as disorders of gut–brain interaction, include a number of separate idiopathic disorders which affect different parts of the gastrointestinal tract and involve visceral hypersensitivity and motility disturbances.
Cyclic vomiting syndrome (CVS) is a chronic functional condition of unknown pathogenesis. CVS is characterized as recurring episodes lasting a single day to multiple weeks. Each episode is divided into four phases: inter-episodic, prodrome, vomiting, and recovery. Inter-episodic phase, is characterized as no discernible symptoms, normal everyday activities can occur, and this phase typically lasts one week to one month. The prodrome phase is known as the pre-emetic phase, characterized by the initial feeling of an approaching episode, still able to keep down oral medication. Emetic or vomiting phase is characterized as intense persistent nausea, and repeated vomiting typically lasting hours to days. Recovery phase is typically the phase where vomiting ceases, nausea diminishes or is absent, and appetite returns. "Cyclic vomiting syndrome (CVS) is a rare abnormality of the neuroendocrine system that affects 2% of children." This disorder is thought to be closely related to migraines and family history of migraines.
Intestinal malrotation is a congenital anomaly of rotation of the midgut. It occurs during the first trimester as the fetal gut undergoes a complex series of growth and development. Malrotation can lead to a dangerous complication called volvulus, in which cases emergency surgery is indicated. Malrotation can refer to a spectrum of abnormal intestinal positioning, often including:
Chronic paroxysmal hemicrania (CPH) is a severe debilitating unilateral headache usually affecting the area around the eye. It normally consists of multiple severe, yet short, headache attacks affecting only one side of the cranium. Retrospective surveys indicated that paroxysmal hemicrania was more common in women. However, subsequent prospective research showed an equal prevalence between females and males, with a ratio close to 1:1. Unlike in migraine, it has no neurological symptoms associated with it. CPH headaches are treated through the use of non-steroidal anti-inflammatory drugs, with indomethacin found to be especially effective in eliminating symptoms.
An aura is a perceptual disturbance experienced by some with epilepsy or migraine. An epileptic aura is actually a minor seizure.
Intestinal pseudo-obstruction (IPO) is a clinical syndrome caused by severe impairment in the ability of the intestines to push food through. It is characterized by the signs and symptoms of intestinal obstruction without any lesion in the intestinal lumen. Clinical features mimic those seen with mechanical intestinal obstructions and can include abdominal pain, nausea, abdominal distension, vomiting, dysphagia and constipation depending upon the part of the gastrointestinal tract involved.
Abdominal epilepsy is a rare condition most frequently found in children, consisting of gastrointestinal disturbances caused by epileptiform seizure activity. Though a few cases of it have been reported in adults too. It has been described as a type of temporal lobe epilepsy. Responsiveness to anticonvulsants can aid in the diagnosis. Distinguishing features of abdominal epilepsy include (1) Abnormal laboratory, radiographic, and endoscopic findings revealing paroxysmal GI manifestations of unknown origin (2) CNS symptoms (3) Abnormal EEG. Most published medical literature dealing with abdominal epilepsy is in the form of individual case reports. A 2005 review article found a total of 36 cases described in the medical literature.
Mitochondrial neurogastrointestinal encephalopathy syndrome (MNGIE) is a rare autosomal recessive mitochondrial disease. It has been previously referred to as polyneuropathy, ophthalmoplegia, leukoencephalopathy, and intestinal pseudoobstruction. The disease presents in childhood, but often goes unnoticed for decades. Unlike typical mitochondrial diseases caused by mitochondrial DNA (mtDNA) mutations, MNGIE is caused by mutations in the TYMP gene, which encodes the enzyme thymidine phosphorylase. Mutations in this gene result in impaired mitochondrial function, leading to intestinal symptoms as well as neuro-ophthalmologic abnormalities. A secondary form of MNGIE, called MNGIE without leukoencephalopathy, can be caused by mutations in the POLG gene.
Antimigraine drugs are medications intended to reduce the effects or intensity of migraine headache. They include drugs for the treatment of acute migraine symptoms as well as drugs for the prevention of migraine attacks.
New daily persistent headache (NDPH) is a primary headache syndrome which can mimic chronic migraine and chronic tension-type headache. The headache is daily and unremitting from very soon after onset, usually in a person who does not have a history of a primary headache disorder. The pain can be intermittent, but lasts more than 3 months. Headache onset is abrupt and people often remember the date, circumstance and, occasionally, the time of headache onset. One retrospective study stated that over 80% of patients could state the exact date their headache began.
Vestibular migraine (VM) is vertigo with migraine, either as a symptom of migraine or as a related neurological disorder.
The classification of all headaches, including migraines, is organized by the International Headache Society, and published in the International Classification of Headache Disorders (ICHD). The current version, the ICHD-3 beta, was published in 2013.
Preventive treatment of migraine can be an important component of migraine management. The goals of preventive therapy are to reduce the frequency, painfulness, and/or duration of migraine attacks, and to increase the effectiveness of abortive therapy. Another reason to pursue prevention is to avoid medication overuse headache (MOH), otherwise known as rebound headache, which can arise from overuse of pain medications, and can result in chronic daily headache. Preventive treatments of migraine include medications, nutritional supplements, lifestyle alterations, and surgery. Prevention is recommended in those who have headaches more than two days a week, cannot tolerate the medications used to treat acute attacks, or those with severe attacks that are not easily controlled.
Abdominal aura, also known as visceral aura and epigastric aura, is a type of somatosensory aura that typically manifests as abdominal discomfort in the form of nausea, malaise, hunger, or pain. Abdominal aura is typically associated with epilepsy, especially temporal lobe epilepsy, and it can also be used in the context of migraine. The term is used to distinguish it from other types of somatosensory aura, notably visual disturbances and paraesthesia. The abdominal aura can be classified as a somatic hallucination. Pathophysiologically, the abdominal aura is associated with aberrant neuronal discharges in sensory cortical areas representing the abdominal viscera.
Migraine may be treated either prophylactically (preventive) or abortively (rescue) for acute attacks. Migraine is an complex condition; there are various preventive treatments which disrupt different links in the chain of events that occur during a migraine attack. Rescue treatments also target and disrupt different processes occurring during migraine.
Neck-tongue syndrome (NTS), which was first recorded in 1980, is a rare disorder characterized by neck pain with or without tingling and numbness of the tongue on the same side as the neck pain. Sharp lateral movement of the head triggers the pain, usually lasting from a few seconds to a few minutes. Headaches may occur with the onset of NTS. The typical age of onset is around adolescence and may occur as early as 8–15 years old. However, it is worth noting that clinical onset can occur earlier or later and NTS onset related to trauma can occur at any age, beginning after the incident.
Recurrent painful ophthalmoplegic neuropathy (RPON), previously known as ophthalmoplegic migraine (OM), is a rare neurological disorder that is characterized by repeated headache attacks and reversible ipsilateral paresis of one or more ocular cranial nerves (CN). Oculomotor nerve (CNIII) is by far the most common cranial nerve involves in RPON, while abducens nerve (CNVI) and trochlear nerve (CNIV) involvements are also reported. Globally, RPON was estimated to have an annual incidence rate of 0.7 per million as of 1990, no further epidemiological studies have been conducted. It occurs more often in children and females.
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