Migraine in children

Introduction About one-third of children with migraine have aura symptoms, the most common are visual symptoms, that is, flashes in front of the eyes, dark spots and dark spots, and symptoms of autonomic nervous system disorders such as nausea, vomiting, and abdominal pain. There are also a small number of children with physical paresthesia and speech disorders. Severe headaches at the onset are the main features of migraine in children. Headaches are mostly an example and can occur on both sides of the ankle or even the entire head. The nature of the pain is pulsation or pain, and the duration is as short as several hours and as long as 1-2 days.

Cause

(1) Causes of the disease

It is currently believed that migraine is a paroxysmal abnormal reaction of local intracranial and extravascular vessels on the neuro-humoral regulation mechanism based on genetic quality. Stress, fear, excitement, lack of sleep, climate change, noise, flash stimuli, and the intake of certain special foods such as cheese, chocolate, etc. 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.

Genetic factor

It is believed that migraine is related to heredity, and its positive family history is 50% to 80%. Parents suffering from migraine, about 70% of their children suffering from migraine; single-parent migraine, children with about 50% of the disease, the incidence of single-oval twins more than 50%. These all indicate the important role of genetic factors in the occurrence of migraine, which is polygenic. However, except for basilar artery type migraine and familial hemiplegic migraine, it is autosomal dominant. The pathogenic genes of familial hemiplegic migraine may be located at 19p13.1 to 13.2. Ducros equalized the pathogenic gene of familial hemiplegic migraine in 1q21~23 in 1997, suggesting 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, perivascular tissue produces vasoactive polypeptides, which leads to aseptic inflammation and induces headaches. In the 1990s, Olsen further developed the angiogenic theory, suggesting that migraine with aura and no aura is the same disease with varying degrees of vasospasm.

3. Neurogenic theory

It is believed that changes in neurological function during migraine are primary, and changes in blood flow are secondary.

(1) Neurotransmitter hypothesis: 5-HT plays an important role in the pathogenesis of migraine. It 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 -endorphin, 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 stimulate the cerebral cortex. This inhibition passes through the cortical area very slowly in the form of waves, and cortical diffuse inhibition is accompanied by a significant reduction in cerebral blood flow (lasting 2-6 h). This hypothesis can fully explain the neurological dysfunction of migraine attacks, but can not successfully explain headaches.

4. Trigeminal vascular reflexology

It refers to the release of substance P and other neurotransmitters from the afferent fibers of the trigeminal nerve, which act on the intracranial and extracranial blood vessels through the efferent nerve, causing headache and vasodilation. Migraine as an unstable trigeminal-vascular reflex with a segmental defect in the pain control pathway, resulting in excessive impulse release from the trigeminal nucleus and excessive transmission of the trigeminal tract or cortical medulla oblongata The impulsive response occurs, eventually causing the brain stem to interact with intracranial angiogenesis.

5. Other doctrines

There are low magnesium theory, high potassium induced vasospasm theory, autonomic dysfunction theory and brain cell current disorder theory.

an examination

Related inspection

EEG examination of brain CT

EEG and cerebral blood flow examinations can be found abnormalities. Gastrointestinal symptoms can be severe to metabolic acidosis, blood sodium, potassium, chlorine, calcium, blood pH should be checked.

Differential diagnosis

Differential diagnosis of migraine in children:

1. Tension headache: also known as muscle contraction headache. Its clinical features are: the headache is more diffuse, and it can be placed on the forehead, eyes, top, pillow and neck. The nature of the headache is often dull, the head is oppressive, and the feeling of tightness is often said to be wearing a hat. Headaches are often persistent and can be light and heavy. There are many scalp and neck tenderness points. Massage the head and neck can relieve headaches, and there are many foreheads and neck muscles. How many are accompanied by nausea and vomiting.

2. Cluster headache: also known as histamine headache, Horton syndrome. It manifests itself as a series of intensive, transient, severe unilateral pains. Unlike migraine, the headache area is limited and fixed on one side of the ankle, behind the ball, and frontal. The onset time is often at night and the patient is awakened. The onset time is fixed, the onset is sudden without aura, and the beginning can be a burning sensation on one side of the nose or a feeling of pressure after the ball, followed by pain in a specific part, often painful, and facial flushing, conjunctival congestion, tearing, flow, stuffy nose. A large number of patients have Horner's sign, and there may be photophobia, without nausea and vomiting. The cause can be caused by alcohol during drinking, excitement, or taking vasodilators. The age of onset is often later than migraine, with an average age of 25 years, and the ratio of male to female is about 4:1. A rare family history.

3. Painful ophthalmoplegia: also known as Tolosa-Hunt syndrome. It is an inflammatory disease characterized by headache and ophthalmoplegia, involving idiopathic eyelids and cavernous sinus. The cause may be non-specific inflammation of the intracranial internal carotid artery, and may also involve the cavernous sinus. Often manifested as intractable pain and tingling after the ball and periorbital, double vision after several days or weeks, and may have neurological involvement in III, IV, VI, recurring after several months. Angiography was performed to rule out internal carotid aneurysms. Corticosteroid treatment is effective.

4. Headache caused by intracranial space occupation: early in the occupation, headache can be heavy for intermittent or morning, but with the development of the disease. More persistent headache, progressive exacerbation, symptoms and signs of intracranial hypertension, such as headache, nausea, vomiting, optic disc edema, and focal symptoms and signs, such as mental changes, hemiplegia, aphasia, partial sensation Obstacle, convulsions, hemianopia, ataxia, nystagmus, etc., typical identification is not difficult. However, it should be noted that there are also migraine manifestations of more than a decade, and finally diagnosed as a giant hemangioma.

5. Vascular headache: such as hypertension or hypotension, unruptured intracranial aneurysm or arteriovenous malformation, chronic subdural hematoma, etc. may have migraine-like headache, some cases have localized neurological signs, seizures or recognition Known dysfunction, brain CT, MRI and DSA can show lesions.

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