Numbness in the trigeminal distribution

Introduction Basal artery branch syndrome: It is due to the small branch occlusion of the lower part of the basilar artery or the upper part of the vertebral artery, resulting in infarction of the hypothalamus and brainstem. It is characterized by dizziness, nystagmus, diplopia, side palsy, internuclear ophthalmoplegia, dysphagia, cerebellar ataxia, gait instability, facial muscle weakness, burning of the eyes and numbness in the trigeminal distribution area. . It is one of the symptoms and signs of lacunar infarction. Hypertension, atherosclerosis, diabetes, etc. are the main predisposing factors of the disease.

Cause

1. Hypertension: Hypertension is the most direct cause of this disease, especially when chronic hypertension exceeds 21.3/12.7 kPa (160/95 mmHg). The incidence of hypertension in patients with lacunar infarction is 45% to 90%. And the effect of increased diastolic blood pressure on the disease is more obvious. Hypertension leads to two possible mechanisms for lacunar infarction:

1 persistent hypertension acts on the deep penetrating artery or other tiny arterial wall of the brain, which increases vascular permeability, coagulation function and anticoagulant function, leading to segmental fat hyaline degeneration, fibrin necrosis and micro-arteries Changes in tumors, etc., resulting in obstruction of small arteries and formation of microemboli.

2 persistent hypertension causes the basilar artery of the brain to elongate, the deep perforating artery is displaced, the blood vessel is twisted, and the lateral blood flow is further reduced to cause ischemic microinfarction.

2. Arteriosclerosis: Lacunar infarction is closely related to arteriosclerosis. Fisher used continuous sectioning to confirm that the blood supply artery of the basal ganglia and the sacral cavity has severe cerebral arteriosclerosis, ie, segmental arterial structural destruction, fibrinoid necrosis or vascular necrosis. Other scholars have also found that the obvious changes in the medullary arteries are the transparent thickening of the wall and the narrowing of the lumen of the vessel. The frequency of lacunar infarction in each brain is directly proportional to the degree of arteriosclerosis.

3. Diabetes: It is well known that diabetes can cause small infarct lesions in the distal limbs, kidneys, retina, peripheral nerves, and cranial nerves, but the role of diabetes in small vessel lesions of the brain has not been clearly defined. Epidemiological findings suggest that diabetes is one of the risk factors for stroke, but there is still evidence of a link between diabetes and lacunar infarction. Studies by Mast et al have only confirmed that diabetes is associated with multiple lacunar infarction, but not with single-shot. However, the increase in blood coagulation and viscosity and the increase in platelet adhesion during diabetes may undoubtedly increase the blood supply to the deep perforating artery of the brain and play an important role in the formation of lacunar infarction.

4. Embolism

(1) Cardiac emboli: the attachment of the wall embolus for rheumatic heart disease or non-rheumatic heart disease.

(2) Arterial emboli: including atherosclerosis with or without ulcers, fibromuscular vascular disease, and thrombus detachment of dissecting aneurysms. In particular, the emboli formed by the atherosclerotic plaque in the ascending aorta and carotid artery is one of the important causes of lacunar infarction and has attracted more and more attention.

5. Other factors: factors such as hyperlipidemia, hyperviscosity, smoking, drinking and changes in brain blood flow also have an effect on the occurrence of lacunar infarction.

an examination

Related inspection

Brain CT examination EEG examination

Clinical features: general symptoms include dizziness, headache, limb numbness, dizziness, memory loss, unresponsiveness, convulsions, dementia, unconsciousness, and psychiatric symptoms are rare. The main clinical signs were tongue stiffness, slow speech, altered tone of speech, mild central facial paralysis, paralysis of the limbs or sensory disturbances, partial pyramidal tract signs were positive, and ataxia was rare.

(1) The onset is caused by hypertensive arteriosclerosis, which is acute or subacute.

(2) Many unconscious obstacles.

(3) There is no red blood cell in the cerebrospinal fluid.

(4) The clinical manifestations are not serious, and it is often manifested as pure sensory stroke, pure motor hemiparesis, ataxia hemiparesis, dysplasia-hand clumsy syndrome or sensorimotor stroke.

(5) If necessary, perform a CT examination to confirm the diagnosis.

Differential diagnosis

Multi-infarct dementia is a type of vascular dementia, and lacunar infarction is an important pathological change.

The clinical manifestations are: sudden onset, stepwise deterioration, volatility course, nighttime confusion, relative preservation of personality, emotional vulnerability, strong crying, strong history of hypertension, heart disease and stroke, combined with atherosclerosis Signs, symptoms and signs of focal damage to the nervous system, CT or MRI showed multiple infarcts and/or brain atrophy in the brain. The diagnostic criteria of the Fourth National Conference on Cerebrovascular Diseases of the Chinese Medical Association (in Chengdu in 1995) were:

(1) Meet the criteria for diagnosis of dementia in the Diagnostic and Statistical Manual of Psychiatry.

(2) Neurological symptoms and signs of acute or subacute onset.

(3) There is a history of stroke in the past.

(4) The course of disease fluctuates in a stepwise progression.

(5) often combined with hypertension, diabetes, coronary heart disease, hyperlipidemia and so on.

(6) Hachinski ischemic scale score 7 points.

(7) CT and MRI confirmed multifocal cortical or subcortical ischemic changes in the brain.

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