Cerebral thrombosis in the elderly
Introduction
Introduction to cerebral thrombosis in the elderly Cerebral thrombosis (cerebralthrombosis), referred to as cerebral thrombosis, refers to the formation of blood vessels due to cerebral arterial wall lesions, especially on the basis of atherosclerosis, blood components change or blood viscosity increases, resulting in arterial lumen An acute ischemic cerebrovascular disease that is markedly narrowed or occluded, causing cerebral infarction in the corresponding site. It is the most common type of acute cerebrovascular disease with the highest incidence. basic knowledge The proportion of illness: 0.1% - 0.3% Susceptible people: the elderly Mode of infection: non-infectious Complications: pneumonia, acne, arrhythmia, brain edema, cerebral palsy
Cause
Causes of cerebral thrombosis in the elderly
(1) Causes of the disease
The most common pathological atherosclerosis of the cerebral arterial wall is the primary cause of thrombosis. Hypertension, hyperlipidemia and diabetes can accelerate the development of cerebral arteriosclerosis; followed by various cerebral arteritis, including leptospirosis Inflammation, arteritis, syphilitic cerebral arteritis, nodular polyarteritis, thromboangiitis obliterans, tuberculous cerebral arteritis, giant cell arteritis, lupus erythematosus, collagen system diseases, etc. In addition, rare causes are Direct trauma of the neck artery, congenital artery stenosis, malformation; changes in blood components (such as polycythemia vera, thrombocytopenia, sickle cell anemia, macroglobulinemia), increased blood coagulation (eg, after childbirth, Tumors, oral contraceptives, postoperative, dehydration), lower blood pressure (hypertension with antihypertensive drugs, shock) and bradycardia, cardiac insufficiency, etc. are all factors of thrombosis.
Based on current knowledge, known risk factors for cerebral thrombosis include:
1 atherosclerosis: it can make the cerebral artery diameter thinner, can promote the formation of cerebral infarction when encountering changes in blood rheology.
2 Hypertension: Japanese scholars believe that cerebral hemorrhage is the most dangerous with elevated diastolic blood pressure, and cerebral infarction is most dangerous with elevated systolic blood pressure.
3 Diabetes: easy to complicated with cerebrovascular damage, is a common risk factor for arterial cerebral infarction and lacunar infarction.
4 blood rheology disorder: increased hematocrit and increased fibrinogen levels, is a dangerous indicator of cerebral thrombosis.
5 Others: age, genetic factors, smoking and alcoholism, obesity, oral contraceptives, etc. have an impact on cerebral thrombosis.
Among the many risk factors mentioned above, only a few are hereditary or difficult to intervene (such as age), and most of them are personal habits (such as smoking, drinking) or multi-factor synthesis (such as high blood pressure, obesity), through prevention and treatment. change.
(two) 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.
Prevention
Prevention of cerebral thrombosis in the elderly
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.
Complication
Cerebral thrombosis complications in the elderly Complications pneumonia acne arrhythmia cerebral edema cerebral palsy
Can be complicated by hemiplegia, aphasia, pneumonia, hemorrhoids, arrhythmia, heart failure, cerebral edema or cerebral palsy.
Symptom
Symptoms of cerebral thrombosis in the elderly Common symptoms Intracranial hypertension coma, nausea, dizziness, weakness, quadriplegia, vertigo, palsy, deafness, sensory disturbance
Cerebral thrombosis is generally more common in middle-aged and older people, cerebral arteriosclerosis over 60 years old, hyperlipidemia and diabetes patients are most likely to occur, some patients have prodromal symptoms before the onset, such as dizziness, transient limb numbness, etc. TLA symptoms, slow onset, mostly in the nighttime sleep, only wake up in the morning to find limbs paralysis; some patients in the daytime, often have a short-term ischemic attack, and later progress to hemiplegia, most patients with cerebral thrombosis Unconsciousness, headache, vomiting and other symptoms, the slow progress of focal signs in many hours or 2 to 3 days to reach the peak, a small number of cases of cerebral infarction, or involving the brain stem network structure, there may be varying degrees of disturbance of consciousness If combined with severe brain edema, it may also be accompanied by symptoms of intracranial hypertension.
Clinical classification
(1) Reversible ischemic attack: also known as reversible cerebral ischemic neurological dysfunction, which is different from transient ischemic attack, in which the clinical symptoms have not fully recovered after 24 hours, often accompanied by large or small infarcts. However, it has not caused irreversible neurological damage, or because of collateral circulation compensation, thrombolysis, cerebral edema subsided, etc., the symptoms and signs of the patient completely relieved within 3 weeks without leaving sequelae.
(2) Progressive stroke: cerebral thrombosis mostly belongs to this type. As the thrombus develops gradually, the scope of cerebral ischemia and edema continues to expand, and the symptoms gradually progress from light to heavy until complete stroke is called, which is called progressive stroke. It usually lasts for days or even weeks.
(3) fulminant: a small number of cerebral thrombosis, rapid onset, involving the main carotid artery trunk, patients often quickly coma, accompanied by cerebral edema, intracranial hypertension symptoms, complete hemiplegia, aphasia, etc., symptoms and signs are very similar to cerebral hemorrhage However, CT scans often help identify, called fulminant or cerebral hemorrhage.
2. Positioning diagnosis
The clinical manifestations of cerebral thrombosis are often directly related to the blood supply status of infarcted blood vessels, and localization diagnosis can be made according to its symptoms.
(1) The common feature of cerebral thrombosis in the internal carotid artery system is that one side of the cerebral hemisphere is involved, and the symptoms of the contralateral side of the lesion appear: central hemiplegia, partial sensory disturbance, hemianopia, such as dominant hemisphere damage, aphasia can still occur. among them:
1 middle cerebral artery: the outer side of the cerebral hemisphere includes the frontal lobes, parietal lobe, temporal lobe, cerebral cortex and subcortical white matter of the insula, and the deep perforating branch dominates the basal ganglia and the inner capsular knee and the first 1/3 of the brain. Arteries and their branches are the most prone to occlusion of the cerebral blood vessels. When the main occlusion and deep artery occlusion, they can often cause contralateral hemiplegia, partial sensory disturbance, hemianopia and aphasia (dominant hemisphere); cortical branch occlusion can cause aphasia , disuse, contralateral hemiplegia (upper limb is heavier than lower limbs), sensory disturbances, etc.
2 anterior cerebral artery: 3/4 in front of the inner side of the cerebral hemisphere including the central lobule, the first 4/5 and the frontal corpus of the corpus callosum, and the deep perforator supports the forelimb and caudate nucleus of the sac, and the anterior cerebral artery occlusion is often Causes contralateral lower limb sensation and movement disorder, accompanied by dysuria (paracentral lobule), strong grip, sucking reflex, mental and behavioral changes (frontal lobe), deep perforation due to involvement of the medial striatum artery - Heubner artery, Contralateral upper extremities and facial central spasms often appear, but clinical occlusion of the anterior cerebral artery is less common.
(2) The vertebral-basal artery system mainly supplies the brainstem and cerebellum and the posterior cerebral artery blood supply area, among which:
1 posterior cerebral artery: mainly supply occipital lobe, temporal lobe, thalamus and midbrain, etc., main occlusion often causes contralateral hemianism and thalamic syndrome, deep perforator including thalamic penetrating artery, thalamic geniculate artery, once occluded Causes thalamic syndrome, including partial paralysis, partial sensory disturbance, thalamic pain, dance hand and foot hyperactivity disorder, hemiplegia, vertical gaze and other symptoms.
2 vertebral artery: mainly supply medulla, posterior cerebellum and upper part of the cervical spinal cord, more branches, vertebral artery occlusion, often cause medullary dorsolateral syndrome, also known as Wallenberg syndrome, contralateral pain temperature and ipsilateral facial pain Decreased temperature, Horner's sign, vestibular nerve and IX, X-brain neurological disorder, and cerebellar ataxia, such as involvement of the medial branch of the vertebral artery, can cause the medial medullary syndrome, contralateral upper and lower extremities and ipsilateral tongue, accompanied by There is a loss of deep lateral sensation, but sometimes one side of the vertebral artery occlusion can not appear symptoms due to compensation, only the bilateral vertebral artery blood supply is insufficient, the symptoms appear.
3 basilar artery: more branches of the basilar artery, the main branches include: anterior inferior cerebellar artery, internal auditory artery, para-median artery, upper cerebellar artery, etc., clinical manifestations are also more complex, often constitute various syndromes, basilar artery occlusion can be Causes the softening of the pons, rapid death of the patient, or the generation of atresia syndrome, the patient's quadriplegia (including face), can not speak, but conscious, and can use blinking, closed eye activity to express meaning, caused by clinical common basilar artery branches Syndrome, such as Weber syndrome: ipsilateral oculomotor palsy, contralateral hemiplegia; Millard-Gubler syndrome: ipsilateral and axillary palsy, contralateral hemiplegia and sensory disturbance; Foville syndrome, ill side gaze, internal Auditory arterial lesions often cause dizziness, accompanied by nausea, vomiting, deafness and other symptoms.
Examine
Examination of cerebral thrombosis in the elderly
Blood, blood lipids, blood sugar, blood flow abnormalities.
Brain CT or MRI showed a change in low-density infarcted area after 24 to 48 hours.
Diagnosis
Diagnosis and diagnosis of cerebral thrombosis in the elderly
Diagnostic criteria
1. There may be a history of transient cerebral ischemic attacks.
2. When there is a quiet rest, there is more morbidity, and it usually occurs when you wake up in the morning.
3. Symptoms often worsen over a period of hours or longer, showing a progressive stroke type.
4. Consciousness is often kept clear, while partial neurological deficits such as hemiplegia and aphasia are more obvious.
5. The age of onset is higher, and the incidence rate is significantly higher than 60 years old.
6. Often cerebral arteriosclerosis and arteriosclerosis of other organs, often accompanied by hypertension, diabetes and so on.
7. The cerebrospinal fluid is clear and the pressure is normal.
8. Diagnosis can be made according to the above auxiliary examination.
In addition to the identification of hemorrhagic cerebrovascular disease, cerebral thrombosis needs to be differentiated from cerebral embolism and transient ischemic attack. In addition, it should be associated with other craniocerebral diseases such as intracranial space-occupying lesions, brain tumors, and subdural. Hematoma, brain abscess, encephalitis, brain parasitic diseases, etc., but rely on medical history and examination (including auxiliary examination), often difficult to identify.
