Stroke in children?

Cerebral infarction is mostly a disease that only the elderly will suffer from, but children can also suffer from cerebral infarction. Most cerebral infarctions in children are caused by acute cerebral artery disease, but it may also be caused by cerebral aneurysm. If you want to treat it, it is best to go to the hospital for examination, and then cooperate with acupuncture to improve blood circulation in the brain. In daily life, give your baby more nutrition and maintain adequate sleep.

What are the symptoms of cerebral infarction?

People who are more likely to suffer from cerebral infarction are people over 50 to 60 years old, often those with atherosclerosis, hypertension, rheumatic heart disease, coronary heart disease or diabetes, as well as those with bad habits such as smoking and drinking. About 25% of patients have a history of transient ischemic attack before the onset of the disease. There are often prodromal symptoms before the onset of the disease, such as headache, dizziness, vertigo, transient limb numbness and weakness. The onset is generally slow, and patients often develop the disease when they are quiet or sleeping. For most patients, symptoms reach their peak after a few hours or even 1 to 3 days.

After a cerebral infarction, most patients are conscious, while a few may have varying degrees of consciousness disorders. Generally, there are no obvious changes in vital signs. If a large area of ​​cerebral hemisphere is infarcted, ischemic, or edematous, the function of the diencephalon and brainstem may be affected, resulting in impaired consciousness and even brain herniation and death soon after the onset of the disease. If the patient becomes unconscious immediately after the onset of the disease, vertebral-basilar artery system cerebral infarction should be considered.

1. Main clinical symptoms The clinical symptoms of cerebral infarction are complex, which are related to the site of brain damage, the size of ischemic blood vessels, the severity of ischemia, the presence or absence of other diseases before the onset of the disease, and the presence or absence of other important organ diseases. In mild cases, there may be no symptoms at all, that is, asymptomatic cerebral infarction; it may also manifest as recurrent limb paralysis or dizziness, that is, transient ischemic attack; severe cases may not only have limb paralysis, but may even lead to acute coma and death. If the lesion affects the cerebral cortex, epileptic seizures may occur in the acute phase of cerebrovascular disease, with the highest incidence rate within 1 day after the onset of the disease. Cerebrovascular disease with epilepsy as the first onset is rare.

Common symptoms include:

(1) Subjective symptoms: headache, dizziness, vertigo, nausea and vomiting, motor and/or sensory aphasia, and even coma.

(2) Cranial nerve symptoms: both eyes staring toward the side of the lesion, central facial paralysis and tongue paralysis, pseudobulbar palsy such as choking on water and difficulty swallowing.

(3) Physical symptoms: hemiplegia or mild hemiplegia, hemisesthesia, unstable gait, limb weakness, incontinence, etc.

2. Clinical classification of cerebral infarction site: Lacunar infarction has the largest infarction area in cerebral infarction, and its clinical manifestations are: subacute onset, dizziness, unsteady gait, limb weakness, a few have choking when drinking water, difficulty swallowing, hemiplegia, hemisensory loss, and some patients have no localizing signs.

Medium-sized infarction is more common in the basal ganglia, paralateral ventricle, thalamus, bilateral frontal lobe, and temporal lobe areas. The clinical manifestations are: sudden headache, dizziness, frequent nausea and vomiting, clear consciousness, hemiplegia, or hemisensory disturbance, hemianopsia, central facial paralysis and tongue paralysis, pseudobulbar palsy, aphasia, etc.

Patients with large-area infarction have an acute onset and severe clinical manifestations, and may suffer from hemiplegia, hemisesthesia, or even quadriplegia, cerebral hernia, and coma.

(1) Internal carotid artery occlusion: Internal carotid artery occlusion may be asymptomatic. Symptomatic occlusion can cause manifestations similar to those of middle cerebral artery occlusion, such as hemiparesis on the side contralateral to the lesion, hemiesthesia, homonymous hemianopsia, and aphasia if the dominant hemisphere is involved. Intracranial or extracranial internal carotid artery occlusion accounts for 1/5 of ischemic cerebrovascular disease.

In cases of internal carotid artery atherosclerotic occlusion, nearly 15% of cases have precursors, including TIA and monocular blindness caused by ipsilateral retinal artery ischemia. Due to the effect of the skull base artery ring, the symptoms of internal carotid artery occlusion are complicated. Sometimes internal carotid artery occlusion may not cause focal symptoms, which depends on the compensatory function of collateral circulation such as the anterior and posterior communicating arteries, ophthalmic artery, and superficial cerebral arteries. It may also be accompanied by transient blindness and Horner's syndrome.

(2) Middle cerebral artery occlusion: Since the middle cerebral artery supply area is the most commonly affected area by ischemic cerebrovascular disease, the clinical signs that occur depend on the affected area.

① Occlusion of the main trunk of the middle cerebral artery: occurs at the proximal end of the lenticulostriate artery that gives off the middle cerebral artery. Because the entire area supplied by the middle cerebral artery is affected, this is the most serious type of cerebrovascular disease caused by occlusion of this artery. The clinical manifestations of main trunk occlusion are hemiplegia, hemisensory disturbance and hemianopsia on the side opposite to the lesion. Occlusion of the main trunk of the dominant hemisphere artery may cause aphasia, agraphia and alexia. If the infarction area is large, severe cases may cause increased intracranial pressure, coma, brain herniation, and even death.

② Occlusion of the deep branches of the middle cerebral artery or the lenticulostriate artery: It can cause hemiplegia on the side opposite the lesion, generally without sensory impairment or homonymous hemianopsia. The dominant hemisphere is damaged and may cause aphasia.

③ Occlusion of the cortical branches of the middle cerebral artery: It can cause hemiplegia on the side contralateral to the lesion, mainly on the face and upper limbs. The dominant hemisphere can cause motor aphasia, sensory aphasia, alexia, agraphia, and apraxia, while the non-dominant hemisphere can cause body image disorders such as contralateral hemi-neglect.

(3) Anterior cerebral artery occlusion: Anterior cerebral artery occlusion is uncommon, probably because emboli from outside the skull or the heart tend to enter the middle cerebral artery with a larger diameter and greater blood flow. When the proximal end of the anterior cerebral artery on one side is occluded, there may be no symptoms if the anterior communicating artery circulation is good. Posterior occlusion of the anterior communicating artery may result in:

① Cortical branch occlusion: causes sensory and motor disorders in the lower limb contralateral to the lesion, accompanied by urinary retention.

② Deep perforating branch occlusion: It can cause central facial paralysis, tongue paralysis and upper limb paralysis on the opposite side of the lesion, and may also cause mental disorders such as emotional apathy, euphoria and strong grip reflex.

(4) Posterior cerebral artery occlusion: Occlusion of the posterior cerebral artery causes homonymous hemianopsia that affects the contralateral visual field, but macular vision is preserved because two arteries (the middle and posterior cerebral arteries) supply the cortex that innervates the macula. Unlike the visual impairment caused by infarction in the middle cerebral artery area, the one caused by the posterior cerebral artery is more severe.

① Cortical branch occlusion: mainly visual impairment caused by ischemia of the visual pathway, homonymous hemianopsia or upper quadrantanopia on the opposite side of the lesion.

② Deep perforating branch occlusion: Typical thalamic syndrome occurs, with decreased sensation in the contralateral half of the body accompanied by thalamic pain, choreoathetosis in the contralateral limbs, etc.

In addition, occlusion of the posterior cerebral artery at the midbrain level can cause visual disturbances, including vertical gaze palsy, oculomotor nerve palsy, internuclear ophthalmoplegia, and vertical eye diastasis. When posterior cerebral artery occlusion involves the occipital cortex of the dominant hemisphere, the patient presents with anomia.

(5) Basilar artery occlusion: Since the basilar artery mainly supplies blood to the brainstem, cerebellum, occipital lobe, etc., the clinical symptoms of occlusion of this artery are more complicated.

Common symptoms include dizziness, nystagmus, diplopia, crossed paralysis or crossed sensory disturbances, and limb ataxia. If the main trunk of the basilar artery is occluded, quadriplegia, eye muscle paralysis, pupil constriction, often accompanied by paralysis of the facial nerve, abducens nerve, trigeminal nerve, vagus nerve and hypoglossal nerve, and cerebellar symptoms, etc. In severe cases, the patient may quickly fall into a coma, suffer from central fever, decerebrate rigidity, gastrointestinal bleeding, and even death. Partial obstruction of the vertebral basilar artery causes extensive softening of the ventral pons, which can produce locked-in syndrome clinically. The patient is paralyzed in all four limbs, expressionless, silent, and unable to speak, but is conscious and can understand what people say and use eye movements to indicate his understanding.