Lacunar cerebral infarction occurs in ischemic microinfarcts (or softening foci) in deep penetrating cerebral arteries (or other tiny arteries), and irregular lacunae formed after chronic healing, and is a common disease in the elderly, with a high incidence in the 60-70 age group. It is more common in males than females and is two to six times more common in females. The onset of the disease is mostly daytime, most of them have no obvious cause, and it is common to have subacute and chronic onset. General symptoms include dizziness and headache, numbness of limbs, vertigo, memory loss, unresponsiveness, convulsions, dementia, and no impairment of consciousness.
Disease Etiology
Hypertension
Hypertension is the most important direct cause of the disease, especially when chronic hypertension exceeds 21.3/12.7 kP (160/95 mmHg). The incidence of hypertension in patients with lacunar cerebral infarction is 45% to 90%. The effect of elevated diastolic blood pressure on this disease is more pronounced. There are 2 possible mechanisms by which hypertension causes lacunar cerebral infarction.
(1) Persistent hypertension acts on the wall of deep penetrating arteries or other small arteries in the brain, causing increased vascular permeability, hypercoagulability and reduced anticoagulation, resulting in segmental fatty hyaline degeneration, fibrin necrosis and microaneurysms in the microvascular wall, leading to small artery obstruction and microembolism formation.
(2) Persistent hypertension elongates the basilar arteries of the brain, displaces the deep penetrating arteries, distorts the vessels, and further reduces the lateral blood flow, resulting in ischemic microinfarction.
Arteriosclerosis
Lacunar cerebral infarction is closely associated with atherosclerosis, and Fisher’s observation by serial sectioning confirmed severe cerebral atherosclerotic changes in the arteries supplying the lacunar lesions in the basal ganglia and internal capsule regions, i.e., segmental arterial structural destruction, fibrinoid necrosis, or avascular necrosis. Other scholars have also found that the obvious changes in medullary arteries are hyaline-like thickening of the walls and narrowing of the vascular lumen, and that the frequency of lacunar infarction in various brain regions is proportional to the degree of atherosclerosis.
Diabetes mellitus
Diabetes is known to cause small arterial infarct lesions in the distal limbs, kidneys, retina, peripheral nerves and cerebral nerves, but the role of diabetes in small vascular lesions of the brain has not been clearly localized. Epidemiological findings suggest that diabetes mellitus is a risk factor for stroke, but evidence for an association between diabetes mellitus and lacunar cerebral infarction is lacking, and the study by Mast et al. only confirmed the association of diabetes mellitus with multiple lacunar cerebral infarctions, but not with single ones. However, the increased coagulability and viscosity of blood and enhanced platelet adhesion in diabetes mellitus can undoubtedly exacerbate the blood supply to the deep penetrating branch arteries of the brain playing an important role in the formation of lacunar cerebral infarction.
Emboli
(1) Cardiogenic emboli: dislodged emboli attached to the wall in rheumatic heart disease or non-rheumatic heart disease.
(2) Emboli of arterial origin: including thrombus shedding from atherosclerosis, fibromuscular vascular disease, and entrapment aneurysms with or without ulceration. In particular, emboli formed by dislodged atherosclerotic plaques in the ascending aorta and carotid artery are one of the important causes of lacunar cerebral infarction and have attracted increasing attention.
Other factors Hyperlipidemia, hyperviscosity, smoking, alcohol consumption and altered local blood flow in the brain also have an impact on the occurrence of lacunar cerebral infarction.
Clinical features
General symptoms include dizziness and headache, numbness of limbs, vertigo, memory loss, unresponsiveness, convulsions, dementia, no impairment of consciousness, and rare psychiatric symptoms. The main clinical signs are tongue rigidity, slowed speech, phonological changes in intonation, mild central facial palsy, mild paralysis or sensory disturbances in the lateral limbs, some positive cone fasciculation signs, and ataxia is rare.
Clinical types
Simple motor mild hemiparesis
It is the most common, accounting for 40% to 60% of cases. The main features are no sensory impairment, visual field loss, aphasia, dysarthria or dyscognition on objective examination; instead, there is only weakness or incomplete paralysis of one side of the face and upper and lower extremities. The lesions may occur in the internal capsule, pons, peduncle, basal ganglia, cerebral cortex, and radiating crown. Recovery often occurs within 2 weeks, but is prone to recurrence.
Pure sensory stroke
There is no muscle weakness, vertigo, diplopia, aphasia, or visual field loss, but only partial sensory deficits on one side of the face and upper and lower extremities. The lesion is located in the posterior ventral nucleus of the thalamus and is usually due to infarction of the thalamic penetrating branch of the posterior cerebral artery. In a few cases, it can be caused by lesions in the thalamic tracts of the spinal cord, the cortical tracts of the thalamus, or by lesions invading the entire lateral thalamus and the radiating crown of the posterior limb of the internal capsule. Recovery often occurs within a few weeks.
Sensorimotor stroke (SMS)
It presents with sensory disturbance of one side of the head, face, trunk and upper and lower extremities and mild paralysis of the face, tongue muscles and upper and lower extremities. There is no impairment of consciousness, memory impairment, aphasia, loss of recognition, or loss of use. This type was previously thought to be rare and is second only to PMH in the national and international literature, with lesions located in the ventral posterior lateral nucleus of the thalamus and the posterior limb of the internal capsule, usually caused by occlusion of the thalamic penetrating branch of the posterior cerebral artery or the posterior choroidal artery. The prognosis is good.
Ataxic mild hemiparesis
It is characterized by mild hemiparesis and cerebellar ataxia on the contralateral side of the lesion, with the lower limb being more important than the upper limb, sometimes accompanied by sensory disturbances, nystagmus, poor distance discrimination, dysarthria, and tilting to one side. The lesions occur at the base of the pons or in the internal capsule, and can also occur in the corona and cerebellum. Recovery often occurs within a few weeks.
Hand clumsiness syndrome
This syndrome is characterized by ataxia with marked dysarthria, nagging, swallowing difficulties, mild weakness of one hand and fine motor deficits, and may be accompanied by ipsilateral central facial and tongue palsy, hyperreflexia and positive pathological signs, and unsteady gait during walking without sensory deficits. There is no TLA before the onset of the disease, and the onset of symptoms is rapid and peaks. The lesion is located at the intersection of the upper 1/3 and 2/3 of the base of the cerebral bridge or at the knee of the uppermost part of the internal capsule.
Cerebral infarction belongs to the category of stroke in Chinese medicine, and stroke is classified according to the severity of the disease and the depth of the disease location according to the classification method of “Jin Kui Yao” to identify whether it is in the meridians or in the internal organs. In the process of cerebral infarction, there is usually no change in the mind, but the sudden occurrence of boiling in the mouth and eyes without fainting (15) americium circle huanhuan reclamation and glistening of grits and grits, and the Ministry of Health issued the guideline for clinical research of new Chinese medicine in 1993, which is divided into the identification method of meridians in stroke, including hyperactivity of liver and yang, wind and fire; wind, phlegm and blood stasis, paralysis of veins and ligaments; phlegm, heat and internal organs, wind and phlegm; qi deficiency, wind and phlegm The five types of cerebral infarction are The first three types are more common in the acute phase of cerebral infarction.