Watershed Cerebral Infarction in the Elderly

Introduction to watershed cerebral infarction in the elderly Cerebral watershed infarction (CWSI) refers to the ischemia of the watershed or border zone between adjacent blood supply areas. It can occur on one side or on both sides, accounting for about 10% of all cerebral infarctions. basic knowledge The proportion of sickness: 0.01-0.03% Susceptible people: the elderly Mode of infection: non-infectious Complications: hemiplegia

The cause of watershed cerebral infarction in the elderly

Cerebrovascular disease itself (30%):

Cerebral arteriosclerosis, thrombotic occlusive vasculitis is more common, in addition to itself can cause changes in the blood vessel wall, but also can make the carotid artery stenosis and occlusion, when the extracranial stenosis of the internal carotid artery reaches more than 50% of the normal lumen, the whole body CWSI can occur when there is a drop in blood pressure.

Hypotension or cardiac output reduction (25%):

CWSI can be caused by various reasons, such as systemic hypotension and decreased cardiac output. It is often multiple, common causes are: cardiac surgery; excessive blood loss in various other surgical procedures; vasodilation caused by various drugs; Causes of shock, syncope; cardiac arrest; severe arrhythmia; spontaneous volatility hypotension, etc., these causes lower blood pressure, slower blood flow, resulting in reduced blood flow to the distal blood vessels, causing brain tissue infarction.

Microembolism (25%):

It has been reported that CWSI is accompanied by an embolus in the pial arteries to occlude the blood vessels, and it is speculated that embolism may be another cause of the disease. These microemboli usually enter the distal blood vessels, often on the surface of the blood vessels, with the anterior cerebral artery and brain. The cerebral cortex watershed between the middle arteries is more common, and atherectomy of atherosclerosis is an important source of embolism.

Pathogenesis

Cerebral artery wall disease is the basis of cerebral thrombosis. The atherosclerotic degeneration or inflammatory changes of the wall can make the intima of the artery rough, the lumen is narrow, and the blood forms such as red blood cells, platelets, fibrinogen, etc., especially Platelets tend to adhere to the endometrial lesions; adhering to aggregated platelets, and releasing arachidonic acid, serotonin, ADP, etc., can cause platelet aggregation and vasoconstriction, accelerate platelet re-aggregation, and form arterial wall Thrombosis, thrombosis gradually enlarges, eventually causing complete occlusion of the arteries and causing cerebral infarction. On the basis of arteriosclerosis, such as increased blood viscosity due to changes in blood components, hyperlipidemia due to metabolic disorders, abnormal proteinemia and cardiovascular disease Hemodynamic changes due to dysfunction also contribute to thrombosis.

In the process of thrombosis, such as collateral circulation, blood supply is sufficient, symptoms may occur or only transient cerebral ischemia may occur. If the collateral circulation is poor, the symptoms are serious, and the thrombus can be formed within a few hours. The antegrade or retrograde development causes more branches to occlude, and the thrombus can dissolve itself within a few days. The embolus can break into the distal vessel or block its branches.

1. Cerebral atherosclerotic changes

(1) The site of good hair: in the bifurcation and bending of the arteries, such as the carotid sinus area, the carotid siphon, the cerebral artery, the anterior, middle and posterior arteries, the vertebral artery and the basilar artery.

(2) The arterial wall bulges due to local atherosclerotic lesions, ie, a fusiform aneurysm is formed.

(3) The vascular wall of arteriosclerosis shows irregular plaques of pale yellow lipidoids in the early stage, and gray-white hyperplasia of fibrous tissue plaques in the late stage.

(4) Carotid extracranial atherosclerosis can cause arteries to elongate, distort or even form kinks, or form ulcerative plaques, hemorrhage or necrosis on the inner wall of the artery.

2. Changes after cerebral thrombosis

(1) Because the blood flow is blocked or interrupted after thrombus formation, such as collateral circulation can not compensate for blood supply, the brain tissue of the affected arteries provides ischemia, softening and necrosis. This softening necrosis can also be multiple, such as the lesion Deep white matter, mostly ischemic infarction; in the cortex due to blood vessels more abundant than white matter, often hemorrhagic infarction.

(2) due to local CO2 accumulation, vasodilation, increased permeability of the vessel wall, cerebral edema may occur around the softened necrosis.

(3) After the necrotic soft tissue is cleared by the phagocytic cells, the glial scar can be left behind, and the large softening lesion can form the cystic cavity.

Elderly watershed cerebral infarction prevention

The main measures to prevent this disease are to actively control various risk factors of stroke, especially those with high risk factors, such as transient ischemic attack, and more active treatment to prevent the development of cerebral infarction.

Elderly watershed cerebral infarction complications Complications, hemiplegia, epilepsy

Can be complicated by hemiplegia, focal epilepsy, aphasia and so on.

Older watershed cerebral infarction symptoms Common symptoms Sensory disorder Intelligent disorder Involuntary motion dementia Body image disorder Angle back damage Strong grip reflex Movement aphasia hemianopia

The watershed cerebral infarction is mostly over 60 years old, accounting for 55.6%. There is no gender difference. There are many diseases that cause blood pressure reduction and cardiac output reduction. Especially the elderly, they have arteriosclerosis, and there is chronic blood supply. Once the blood pressure is lowered, Prone to this disease, the common site is the marginal zone between the middle cerebral artery and the anterior cerebral artery, the middle cerebral artery and the posterior artery or the marginal zone between the anterior, middle and posterior cerebral arteries, the middle cerebral artery cortex and deep perforator The marginal zone between the two, clinically often stroke-like onset, multiple unconscious disorders, mild symptoms, rapid recovery, combined with CT can be divided into the following common types:

Precortical type

It is a watershed cerebral infarction in the blood supply area of the cerebral artery and middle cerebral artery. It has central hemiplegia and partial sensory disturbance mainly in the upper limbs. It generally has no facial palsy, and may have affective disorder, strong grip reflex and focal epilepsy. Lateral lesions may have percutaneous motility aphasia; bilateral lesions appear quadriplegia, mental retardation or dementia; lesions are located in the mid-media, and can be moved along the anterior and posterior anterior and posterior anterior and posterior cerebral lobes.

2. Cortical type

The lesion is located at the junction of the apex, occipital and temporal iliac crests. It is the watershed zone between the brain and the posterior cerebral artery, or the anterior, middle and posterior arterial cortex. The most common hemianopia, more than the following quadrants are blind; may have cortical sensation Obstacles, partial or slight hemiplegia; about 1/2 cases have emotional apathy, may have memory loss and Gerstmann syndrome (angular injury), dysplasia of the main side lesions and percutaneous sensory aphasia; non-primary side occasional Physical obstacles.

3. Subcortical type

It is a watershed infarction between the anterior, middle, posterior arterial cortex and deep perforator or anterior cerebral artery recurrent branch (Heubner artery) and the middle cerebral artery. The lesion is located in the deep white matter of the brain, the nucleus, and the caudate nucleus. In other places, pure motor hemiparesis or (and) sensory disturbances, involuntary movements, etc. may occur.

Examination of watershed cerebral infarction in the elderly

General examinations should include blood glucose, blood lipids, hemorheology, plasma prothrombin time, and thromboplastin time.

Other: CSF, cranial CT, cerebral angiography, and magnetic resonance imaging are all associated with cerebral thrombosis.

Head CT

The watershed cerebral infarction is a low-density area in the brain parenchyma. The CT plane of the cerebrovascular watershed area is pointed toward the lateral ventricle, and the bottom is facing the wedge-shaped band in front of the soft membrane. The basal ganglia can be irregularly formed into a sheet-like low-density shadow.

Angiography

After angiography, it can be clearly shown that the two adjacent blood vessels are occluded or significantly narrow at the end, and no embolus is found.

Diagnosis and diagnosis of schizont cerebral infarction in the elderly

diagnosis

According to the history and clinical manifestations of stroke-like onset, more unconscious disorders, the symptoms are more serious refer to the auxiliary examination, you can confirm the diagnosis.

Differential diagnosis

In addition to the identification of hemorrhagic cerebrovascular disease, watershed cerebral infarction needs to be differentiated from cerebral embolism, transient ischemic attack, and other brain diseases such as intracranial space-occupying lesions, brain tumors, subdural Hematoma, brain abscess, encephalitis, brain parasitic diseases, etc., but rely on medical history and examination (including auxiliary examination), often difficult to identify.

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