migraine in children

Introduction

Introduction to pediatric migraine Migraine is a recurrent neurovascular headache, mostly on one side. The nature of each episode is similar to the process. The interval is normal. It can be accompanied by nausea, vomiting, visual changes, and excessive sensitivity to light and sound. And other symptoms. basic knowledge The proportion of illness: 0.02% Susceptible people: children Mode of infection: non-infectious Complications: abdominal pain, vomiting in children, vertigo, nystagmus

Cause

Pediatric migraine cause

(1) Causes of the disease

It is currently believed that migraine is a paroxysmal abnormal reaction of local intracranial and extracranial blood vessels on the neuro-humoral regulation mechanism based on genetic quality, tension, fear, agitation, lack of sleep, climate change, noise, flash stimulation, some special foods. Ingestion such as cheese, chocolate and other factors can induce migraine attacks.

(two) pathogenesis

The true etiology and pathogenesis of migraine have not been clarified, and many theories have been proposed, but intracranial and extravascular vasomotor disorders have been confirmed during migraine attacks.

1. Genetic factors: It is believed that migraine is related to heredity, and its positive family history is 50%-80%. Both parents suffer from migraine, and their children suffer from migraine: 70%; single parents with migraine, children The chance of illness is about 50%; the co-occurrence rate of monozygosis is more than 50%, which indicates that genetic factors play an important role in the occurrence of migraine, which is polygenic, but the basilar artery type migraine and familial hemiplegia type The exception is headache, which is autosomal dominant. The pathogenic gene of familial hemiplegic migraine may be located at 19p13.1~13.2. Ducros is equal to the pathogenic gene of familial hemiplegic migraine in 1q21~23. It is suggested that the disease is genetically heterogeneous.

2. Vascular source theory: It is believed that the aura symptoms of migraine are related to the contraction of intracranial blood vessels. Subsequently, due to the expansion of extracranial blood vessels, the perivascular tissue produces vasoactive polypeptides, which leads to aseptic inflammation and induces headaches. Olsen in the 1990s Further developed the angiogenic theory, suggesting that migraine with aura and no aura is the same disease with different degrees of vasospasm.

3. Neurogenic theory: It is considered that the change of neurological function in migraine is the primary, and the change of blood flow is secondary.

(1) Neurotransmitter hypothesis: 5-HT plays an important role in the pathogenesis of migraine, which can cause aseptic inflammation in the blood vessel wall or cause cerebral vasoconstriction through the receptor to cause local cerebral blood flow to cause headache, - Neurotransmitters such as endorphins, methotrexate, substance P, catecholamines, histamine, vasoactive peptides and prostacyclin are also associated with the development of migraine.

(2) Diffusion inhibition hypothesis: refers to the inhibition of cortical electrical activity from the stimulation site to the surrounding tissue after various factors stimulating the cerebral cortex. This inhibition passes through the cortical region very slowly in the form of waves. Diffuse inhibition with significant cerebral blood flow reduction (lasting 2 to 6 hours), this hypothesis can fully explain the neurological dysfunction of migraine attacks, but can not successfully explain headache.

4. Trigeminal vascular reflexology: refers to the release of substance P and other neurotransmitters from the afferent fibers of the trigeminal nerve. After the efferent nerve acts on the intracranial and extracranial vessels, causing headache and vasodilation, migraine as an unstable trigeminal Nerve-vascular reflexes, accompanied by segmental defects in the pain-control pathway, cause excessive impulses from the trigeminal nucleus and respond to excessive afferent impulses from the trigeminal tract or cortical medulla oblongata, ultimately causing the brain stem Interacts with intracranial angiogenesis.

5. Other doctrines: There are low magnesium theory on the pathogenesis of migraine, high potassium induced vasospasm, autonomic dysfunction theory and brain cell current disorder theory.

Prevention

Pediatric migraine prevention

1. Removal of incentives: The first step in the prevention of migraine is to eliminate or reduce the predisposing factors of seizures, such as avoiding emotional stress, fatigue, lack of sleep, sound and light stimulation, and not eating foods containing cheese.

2. Drug prevention: The following drugs may be administered, as appropriate, such as beta blockers (propranolol), histamine receptor blockers (cyproheptadine), serotonin receptor blockers (phenthio) ), calcium channel blockers (flunarizine), other drugs valproic acid, carbamazepine, clonidine, phenelzine, amitrptyline, etc., dosage, method as described in the treatment.

Complication

Pediatric migraine complications Complications abdominal pain, vomiting, dizziness, nystagmus

Often accompanied by vomiting, abdominal pain, with nocturia, night terrors, night snoring, motion sickness and seasickness are more common, special types of migraine headaches, side limbs, convulsions, vertigo, diplopia, diplopia, nystagmus, tinnitus, Dysfunction, ataxia, numbness and weakness of both limbs, short-term loss of consciousness, eye muscle spasm, dilated pupils, fixed eyeballs, loss of photoreaction, paroxysmal torticollis, etc.

Symptom

Migraine symptoms in children Common symptoms Fatigue, lethargy, abdominal pain, ankle pain, nausea, gastrointestinal symptoms, pale, tinnitus, vertigo

The clinical manifestations of pediatric migraine are similar to those of adults, but there are many differences compared with adults. The symptoms of pediatric migraine attacks are not as clear as adults, but the gastrointestinal symptoms are very prominent. The clinical features of pediatric migraine are:

1 The duration of the attack is short, but the number of episodes is relatively frequent;

2 bilateral headaches are more common, and partial headaches are relatively rare;

3 visual symptoms and headaches are less common in pulsation;

4 gastrointestinal symptoms are prominent, often accompanied by nausea, vomiting, abdominal pain;

5 more common in family history;

6 with nocturia, night terrors, night snoring, motion sickness and seasickness are more common.

1. Migraine with aura: formerly known as classic migraine, most of the children had a headache before the headache, a few with the headache, occasionally after the headache, individual cases only aura and no migraine attack, the aura with the most visual symptoms Common, such as the appearance of different shapes of shimmering dark spots, "gold star", city-like flash, blurred vision, eccentricity, black Mongolian, etc., can also appear visual hallucinations and visual distortion or discoloration, lasting for a few minutes to several Hours, headache attacks often start on the frontal frontal, squat or posterior, occasionally on the top or occipital, pulsating (jumping) or pain, extending to the semi-head or the entire head. There are also left and right alternate authors, headaches with accompanying symptoms, such as nausea, vomiting, abdominal pain, pale, etc., headache duration varies, short hours or less, up to 1 to 2 days, generally lasting 2 ~ 3h, fall asleep after the attack, headache disappears after waking up, headache can occur once a day, or several weeks, only a few months to several years.

2. Migraine without aura: The old type of common migraine, the most common, is the most common form of headache attack in prepubertal children. There is no clear aura before headache, but there are often some non-specific symptoms such as lethargy, fatigue, and body. Discomfort, loss of appetite, etc., often bilateral or ankle pain, about half of the children's headache is pulsating, the degree of headache is lighter than the classic migraine, duration 0.5 ~ 2h, 70% have nausea, vomiting or abdominal pain, etc. Gastrointestinal symptoms.

3. Special types of migraine

(1) Hemiplegic migraine: headache or paraplegia soon after the occurrence of headache, paralysis of the limbs, may be accompanied by numbness of the limbs, long-term prolongation can cause paralysis of the limbs, hemiplegia is generally light, lasting for several hours to 1-2 days The severe cases can reach several days, generally can be fully recovered, can be divided into two categories: familial mostly autosomal dominant inheritance; sporadic can be expressed as classic, common and hemiplegic migraine alternate episodes.

(2) Basilar artery type migraine: more common in children (girls than boys) or young women, with a variety of aura symptoms originating from the bilateral occipital lobe or brain stem, visual symptoms such as flash, dark spots, visual Blurring, black Mongolian, etc.; brain stem symptoms such as dizziness, diplopia, nystagmus, tinnitus, dysarthria, ataxia, numbness and weakness of both limbs.

(3) ocular migraine type migraine: more than 12 years old before the onset, sometimes seen in infants and young children, eyelid pain accompanied by oculomotor complete or incomplete paralysis, some cases involve both the trochlear and the nerve, and eye movement disorders Eyelid spasm can occur before or after headache or at the same time. The above eyelid valgus is the most common. In severe cases, the extraocular muscles are all paralyzed, the pupils are scattered, the eyeballs are fixed, the photoreaction disappears, and the pain can last for several hours. It can last for days to weeks.

(4) It may be a migraine pioneer or a periodic syndrome related to migraine: the so-called migraine allergy in the past refers to the occurrence of transient neurological dysfunction in the clinic. At that time, the headache is only a secondary symptom, or even does not appear. A group of syndromes of headache, characterized by periodic episodes, similar intermittent periods and the same predisposing factors as migraine attacks, effective in the treatment of migraine, mainly including benign paroxysmal vertigo, periodic vomiting (recurrence) Sexual vomiting), abdominal migraine, alternating hemiplegia in children, paroxysmal torticollis, etc.

Examine

Pediatric migraine examination

Gastrointestinal symptoms can be severe to metabolic acidosis, blood sodium, potassium, chlorine, calcium, blood pH should be checked.

EEG and cerebral blood flow diagram examinations should be performed to detect abnormalities.

Diagnosis

Diagnosis and diagnosis of migraine in children

Regarding the diagnosis of migraine, there is currently no objective biological indicator, which is mainly diagnosed according to clinical symptoms and positive family history. As for the auxiliary examination, the diagnosis of migraine is generally unnecessary, and its value is to exclude non-migraine diseases.

1. Migraine without aura In 1988, IHS developed a diagnostic criteria for migraine without aura. At least 5 episodes met the following conditions:

(1) The onset of headache lasts for 4 to 72 hours.

(2) The headache has at least two of the following four characteristics: unilateral headache; pulsating headache; moderate or severe headache, affecting daily life; headache is aggravated when daily physical activity (such as stairs).

(3) At least one of the following two items is manifested in headache: nausea and/or vomiting; photophobia and phobia.

(4) Medical history, physical examination and various examinations did not reveal systemic or central nervous system organic diseases. If there are other diseases, there is evidence that it has nothing to do with headache attacks.

2. Diagnostic criteria for migraine with aura have at least 2 episodes that meet 3 of the following 4 conditions:

(1) One or more fully reversible aura symptoms suggesting limited local cerebral cortex and/or brainstem dysfunction.

(2) The developmental duration of at least one aura symptom is more than 4 minutes or multiple aura symptoms appear in sequence.

(3) The duration of aura symptoms is less than 60 minutes.

(4) The free interval between aura symptoms and headache is less than 60 minutes (sometimes headaches can also begin before or at the same time as aura).

In addition, medical history, physical examination and various examinations should not reveal systemic or central nervous system organic diseases. If there are other diseases, there is evidence that it is not related to headache attacks.

3. Child Diagnostic Criteria The diagnostic criteria for migraine developed by HIS are too cumbersome and rigorous, and are not suitable for clinical work. The diagnostic criteria are for the entire population. Because of the symptoms of migraines in children, the seizures are different from those of adults. (For example, children have shorter episodes, unilateral sex and phobia are less common in children), so there are many revision opinions for children. The following are the following:

(1) abdominal pain accompanied by abdominal pain, nausea or vomiting.

(2) unilateral headache.

(3) The nature of headache is beating or pulsating, stinging.

(4) Complete relief after a short period of time.

(5) There are signs of sight, feeling or movement.

(6) One or more members of the first-degree relatives have a history of headaches. If the headache features more than three of the above items, the diagnosis of migraine is more supportive.

4. Generally accepted diagnostic criteria so far there is no consistently accepted diagnostic criteria for migraine, but the following points are generally endorsed:

(1) Repeated episodes of headache, the interval is completely normal, and headaches caused by other organic diseases are excluded.

(2) It has 3 of the following 6 articles:

1 headache accompanied by nausea, vomiting, headache or no headache when there is paroxysmal abdominal pain.

2 partial side headache.

3 pulsating headaches.

4 short-term rest or relief after sleep.

5 There are signs such as visual anomalies.

6 family history of migraine.

This is in line with Prensky's diagnostic criteria for pediatric migraine.

Different from epilepsy, family history, EEG changes and seizure characteristics can help identify.

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