Unilateral headache

Introduction A unilateral headache is characterized by a headache on one side. The headache begins with a frontal frontal area, around the eyelids, behind the eyeball, or on one side of the head, which can be accompanied by other symptoms. Migraine is the most common type of primary headache in clinical practice. The clinical manifestations of episodic moderate-to-severe, pulsatile headache are mostly unilateral, usually lasting 4 to 72 hours, may be accompanied by nausea and vomiting. Light, sonic stimulation or daily activities can aggravate headaches, and a quiet environment and rest can alleviate headaches. Migraine is a common chronic neurovascular disease, which occurs in children and adolescence. It reaches the peak incidence in middle and young age, and is more common in women. The ratio of male to female patients is about 1:2 to 3, and the prevalence rate in the population is 5. % ~ 10%, often have a genetic background.

Cause

Causes:

The cause of migraine is not clear and may be related to the following factors:

genetic factors:

About 60% of migraine patients have a family history, and their relatives have a risk of migraine 3 to 6 times that of the general population. Familial migraine patients have not found a consistent Mendelian inheritance, reflecting different penetrance and multiple genes. The interaction between genetic characteristics and environmental factors. Familial hemiplegic migraine is a well-defined autosomal dominant inheritance with a high degree of abnormal penetrance, which has been localized at 19p13 (related to the voltage gate P/Q calcium channel gene mistranslation mutation expressed in the brain), 1q21 and 1q31, etc. Three disease gene loci.

Endocrine and metabolic factors:

More women than men, more common in adolescence, menstrual period is prone to attack, pregnancy or postmenopausal seizures reduce or stop. This suggests that endocrine and metabolic factors are involved in the onset of migraine. In addition, metabolic abnormalities such as serotonin (5-HT), norepinephrine, substance P, and arachidonic acid may also affect migraine development.

Diet and spiritual factors:

Migraine attacks can be induced by certain foods and drugs, including tyramine-containing cheeses, nitrite-containing preservatives and preserved foods, phenylethylamine-containing chocolates, and food additives such as sodium glutamate (MSG). , wine and wine, etc. Drugs include oral contraceptives and vasodilators such as nitroglycerin. Other environmental and mental factors such as stress, overwork, emotional excitement, excessive or too little sleep, menstruation, and glare can also be induced.

Pathogenesis:

The pathogenesis of migraine is still not very clear. At present, there are mainly the following theories:

Angiography:

Traditional vascular theory considers migraine to be a primary vascular disease. Intracranial vasoconstriction causes aura symptoms of migraine, followed by extracranial and intracranial vasodilatation, and the production of vasoactive polypeptides in perivascular tissue results in aseptic inflammation leading to pulsating headaches. Local compression of the carotid and superficial temporal artery, vasoconstrictor ergot alkaloids such as ergotamine can alleviate the theory of headache support during the attack. Neuroimaging develops clinical applications such as TCD and PET, and further develops the angiogenic theory, suggesting that both aura and aura-free migraine are the same disease with different degrees of vasospasm. The sensitivity of various neurons to ischemia is different. The appearance of aura symptoms is due to vasoconstriction. After the blood flow is reduced, the neurons in the visual cortex are most sensitive to ischemia. Therefore, visual aura is the first to appear, and then more and more Neuronal function is affected, and other neurological symptoms such as finger numbness gradually appear.

Neurology:

Neurology believes that changes in neurological function during migraine attacks are paramount, and changes in blood flow are secondary. The migraine aura is caused by cortical spreading depressing (CSD). CSD refers to the nerve electrical activity inhibition zone originating from the posterior cortex (occipital lobe) of various brains caused by various noxious stimuli. This inhibition zone spreads to the adjacent cortex at a rate of 2 to 5 mm/min, accompanied by a prolonged blood loss. (spreading oligemia). Both do not expand according to the distribution of cerebral arteries, but according to the cerebral cortical cell construction model, and the forward expansion generally does not exceed the central groove. CSD can explain the symptoms of migraine aura. In addition, 5-hydroxytryptamine (5-HT) is involved in headaches. At the beginning of the headache attack, 5-HT is released from the platelets, directly acting on the intracranial small blood vessels to contract, and attached to the blood vessel wall. When the plasma 5-HT concentration decreases, it acts on the aortic tonic contractility and the blood vessel wall expands to cause headache. 5-HT is both a neurotransmitter and a humoral medium that affects both nerves and blood vessels. The triptans used to treat migraine are central 5-HT receptor agonists or partial agonists. This confirms that neurological disorders are involved in the onset of migraine.

Trigeminal vascular theory:

The anatomical and physiological basis of this theory is the trigeminovascular complex. Intracranial pain sensitive tissues such as cerebrovascular, meningeal vasculature, venous sinus, the perivascular nerve fibers enter the trigeminal ganglion with the trigeminal ocular branch, or enter the posterior root of the 1 and 2 cervical nerves (C1, C2) from the posterior fossa; After the trigeminal ganglion and the C1 and C2 spinal ganglia, the nerve fibers are sent to the trigeminocervical complex, which consists of the caudal nucleus of the trigeminal nucleus and the posterior horn of C1 and C2. The complex emits nerve fibers that are projected through the brainstem to the thalamus. The peripheral pain mechanism of the theory suggests that trigeminal ganglion damage may be the neural basis for migraine production. When the trigeminal ganglion and its fibers are stimulated, it can cause an increase in the release of substance P (SP), calcitonin gene-related peptide (CGRP) and other neuropeptides. These active substances act on the adjacent cerebral vascular wall, which can cause vasodilatation and pulsating headache. It can also increase vascular permeability, bleed out of plasma proteins, produce aseptic inflammation, and stimulate the afferent fibers into the center, forming malignant cycle.

an examination

Related inspection

EEG cerebral angiography

EEG examination

The incidence of abnormal EEG in patients with migraine is higher than that in the normal control group, whether in the attack or intermittent period. However, the EEG changes in migraine patients are not specific because they can have normal waveforms. Common slow waves, spike discharges, focal spikes, waves, and various waveforms that respond abnormally to hyperventilation and flash stimulation. The abnormal rate of electroencephalogram in children with migraine is high, and spikes, paroxysmal slow waves, fast wave activity and diffuse slow waves can occur.

2. Cerebral blood flow chart examination

The main changes in the cerebral blood flow map during the onset and intermittent periods are asymmetry on both sides, with one side being high or one side being low.

3. Cerebral angiography

In principle, patients with migraine do not need cerebral angiography. Only in patients with severe headache episodes, cerebral angiography is highly suspected for patients with subarachnoid hemorrhage, in addition to diseases such as intracranial aneurysms and arteriovenous malformations.

4. Cerebrospinal fluid examination

Routine examination of cerebrospinal fluid in patients with migraine is usually normal, and lymphocytes in cerebrospinal fluid can generally be increased.

5. Immunological examination

The number and percentage of immunoglobulin IgG, IgA, C3 and E rosette formation tests in migraine patients are generally considered to be higher than normal.

6. Platelet function check

Platelet aggregation can be elevated in migraine patients.

Differential diagnosis

Differential diagnosis of unilateral headache:

1. Total headache: Total headache includes tension headache, low intracranial headache, infectious headache, hypertensive headache and headache caused by brain tumor.

2, deep headache: deep headache is more common in brain abscess, encephalitis, brain tumors, and radiate to the same side external.

3, vascular headache: vascular headache refers to the head vasomotor dysfunction and cerebral cortex dysfunction, or the clinical syndrome caused by temporary changes in certain body fluids. It is characterized by paroxysmal pulsating jump, pain or drilling in one or both sides of the ankle. It may be accompanied by symptoms of vascular autonomic dysfunction such as visual hallucinations, photophobia, hemianopia, nausea and vomiting. It includes headaches caused by migraine, cluster headache, hypertensive headache, cerebrovascular disease (such as subarachnoid hemorrhage, cerebral hemorrhage, arteriovenous malformation, temporal arteritis, etc.).

4, neurological headache: neurological headache mainly refers to tension headache, functional headache and vascular nerve headache, mostly caused by mental stress, angry, Chinese medicine belongs to the category of headache, brain wind, head wind, is a blood loss Caused by deficiency, liver yang, sputum, etc.

5, fixed in one eye and eyelids around the night headache: headache is fixed in one eye and around the eyelids, the attack is mostly in the evening, more common in cluster headaches. A cluster headache is one of the more serious headaches and is one of the vascular headaches. Named for the onset of headaches over a period of time. Previous textbooks have used this disease as a subtype of migraine. In recent years, it has been identified as an independent disease entity because of its different pathogenesis, clinical appearance and migraine.

6, local headache: local headache This is an vascular nerve headache, is a functional disease. The typical headache of migraine is characterized by pulsation. The degree of headache is moderate or severe. It will increase when walking or climbing stairs, coughing, often accompanied by nausea or photophobia, and fear of noisy. About 60% to 80% of headaches manifest as unilateral headaches.

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