Lacunar infarction (lacunarinfarction) is one of the common ischemic cerebrovascular diseases and is a type of cerebral infarction (or cerebral infarction), also referred to as lacunar infarction and multiple lacunar infarction. It is the result of long-term hypertension and small arteriosclerosis. It is named after the pathological diagnosis, and is a general term for fresh or old small deep brain infarcts. The luminal diameter is mostly 2 to 15 mm, and 15 to 20 mm is generally considered to be the maximum of luminal space. Luminal cerebral infarction is not completely pathological, in other words luminal cerebral infarction does not always show case symptoms. Many people are very nervous to find reports on CT or MRI suggesting the presence of multiple lacunar cerebral infarcts in the skull during physical examinations or routine checkups, which is not necessary. Even if people do not have predisposing factors such as hypertension, diabetes, obesity, hyperlipidemia, etc., multiple intracranial lacunar cerebral infarcts can also occur as they age, and generally speaking, women >50 years old and men >48 years old will see lacunar infarcts on head MRI, and less on CT. Symptoms and signs of pathological lacunar infarction 1. Common in middle-aged and elderly people, more men, more often suffering from hypertension. 2. There are mainly four classical clinical lacunar syndromes: (1) Pure motor light hemiparesis: common, usually contralateral to the posterior limb of the internal capsule or cerebral bridge lesions. (1) Pure motor mild hemiparesis: it is common, usually the opposite side of the posterior limb of the internal capsule or the cerebral bridge lesion. The face and the upper and lower limbs show roughly the same degree of mild hemiparesis, not accompanied by sensory, visual and cortical functional deficits such as aphasia. It can be caused by occlusion of the internal carotid artery or middle cerebral artery, subdural hematoma or intracerebral occupying lesion. (2) Pure sensory stroke: It is more common and characterized by loss of hemianesthesia, which may be accompanied by sensory abnormalities such as numbness, burning or heaviness, tingling, and stiffness; it is caused by contralateral thalamic ventral posterior nucleus, posterior limb of the internal capsule, posterior part of the radioulnar cortex, and dorsolateral lesions of the medulla oblongata. Similar manifestations can occur with posterior cerebral artery occlusion and small hemorrhages in the thalamus or midbrain. (3) Ataxic mild hemiparesis: the lesion is contralateral to cerebellar ataxia, and the hemiparesis is heavy in the lower extremities (pronounced in the ankles), light in the upper extremities, and lightest in the face; the finger-nose test and heel-knee-shin test are positive. It is usually caused by lesions at the junction of the superior 1/3 and inferior 2/3 of the base of the contralateral cerebral bridge, the posterior limb of the internal capsule and the superior deviation (affecting the temporal and occipital bridge bundles and the pyramidal bundles) and the radial crown and the hemianopia center (affecting the corticobulbar bundle and part of the pyramidal bundle). (4) Dysarthria-hands clumsiness syndrome: manifests dysarthria, dysphagia, central facial tongue palsy on the contralateral side of the lesion, hand weakness and fine motor clumsiness on the side of the facial palsy, easily detectable writing, inaccurate finger-nose test, and mild balance impairment. The lesion is at the junction of the upper 1/3 and lower 2/3 of the base of the cerebral bridge, which is the occlusion of the midline branch of the parabasal artery; it is also seen in the lesion of the knee of the internal capsule. 3.According to the presence or absence of neurological signs in lacunar cerebral infarction can be summarized into 3 categories (1) with focal neurological localization signs: lacunar cerebral infarction that can be clearly classified, the occurrence rate of which accounts for about 75% of lacunar cerebral infarction. (2) lacunar cerebral infarction with neurological symptoms but no focal signs, which cannot be typed and classified, accounting for about 9% of lacunar cerebral infarction. (3) No neurological symptoms and signs: about 16% of lacunar cerebral infarcts.