cerebral ischemic disease
Introduction
Introduction to cerebral ischemic diseases Cerebral ischemia is seen in the pathological processes of various neurosurgical diseases, such as cerebrovascular diseases and brain tumors. It can also be seen in systemic pathological processes such as cardiac arrest and shock. Cerebral ischemia can be manifested in different forms and focally. And diffuse cerebral ischemia, permanent and transient cerebral ischemia, but in any way, the pathophysiological and biochemical changes of cerebral ischemia are basically similar, and related to the degree and duration of cerebral ischemia . basic knowledge The proportion of sickness: 0.002%-0.003% Susceptible people: no special people Mode of infection: non-infectious Complications: cerebral infarction cerebral hemorrhage myocardial infarction
Cause
Causes of cerebral ischemic diseases
(1) Causes of the disease
The causes of cerebral ischemia are complex and can be summarized in the following categories:
1 intracranial, external artery stenosis or occlusion;
2 cerebral artery embolization;
3 hemodynamic factors;
4 hematological factors, etc.
1. Cerebral artery stenosis or occlusion
The brain is supplied by the internal carotid artery and the vertebral artery on both sides. The blood supply from the internal carotid artery accounts for 80% to 90% of the total blood supply to the brain, and the vertebral artery accounts for 10% to 20%. When one of the arteries occurs, it can affect the blood flow. In the case of stenosis or occlusion, if the collateral circulation is good, clinical ischemic symptoms may not occur. If the collateral circulation is poor, or if multiple arteries have a stenosis that affects blood flow, it may cause local or whole brain cerebral blood. Flow (CBF) is reduced, and when CBF is reduced to a critical level of cerebral ischemia [18-20 ml/(100 g·min)], cerebral ischemia is produced.
Mild arterial stenosis does not affect the blood flow. It is generally considered that it must be narrowed to more than 80% of the original lumen cross-sectional area to reduce the blood flow. The cross-sectional area cannot be measured from the cerebral angiogram. When measuring the inner diameter and narrowing the inner diameter of the artery beyond 50% of its original diameter, it is equivalent to a 75% narrowing of the lumen area, which is considered to be a degree of stenosis that is sufficient to affect blood flow, that is, a surgically narrow stenosis.
Multiple cerebral artery stenosis or occlusion has a greater impact on cerebral blood flow because it may cause the whole cerebral blood flow to be at the edge of ischemia [CBF is 31ml/(100g·min)], if there is systemic blood pressure fluctuation, It can cause cerebral ischemia, the main cause of cerebral artery stenosis or occlusion is atherosclerosis, and the vast majority (93%) involve the extracranial aorta and intracranial middle arteries, including carotid and vertebral arteries. The greatest chance of involvement at the beginning, and arteriosclerosis is more involved in the small arteries of the brain.
2. Cerebral artery embolization
In addition to atherosclerotic plaque, atherosclerotic plaque often has platelet clots, wall thrombi and cholesterol fragments on the ulcer surface of the plaque. These attachments are washed away by blood flow to form emboli. It is carried into the intracranial artery by the blood flow, and the distal artery is blocked to cause cerebral embolism, which causes ischemia in the blood supply area.
The most common source of emboli is the atherosclerotic plaque at the beginning of the internal carotid artery, which is considered to be the most common cause of TIA in transient ischemic attacks. The embolus can be quickly disintegrated into fragments and dissolved, or The distal arteries move, and most of the embolus in the internal carotid artery (3/4) enters the middle cerebral artery with the mainstream of the blood, causing the corresponding clinical symptoms.
Another main cause of arterial embolization is cardiogenic emboli, rheumatoid heart disease, subacute bacterial endocarditis, congenital heart disease, prosthetic valve and heart surgery. The embolus enters the brain with blood flow. Embolism is caused inside, and rare emboli such as septic emboli, fat embolus, air embolus can also cause cerebral embolism.
3. Hemodynamic factors
Short-term hypotension can cause cerebral ischemia. If there is severe stenosis of the cerebral blood vessels or multiple cerebral artery stenosis, the cerebral blood flow is in a state of less blood, and mild blood pressure can cause cerebral ischemia, such as myocardial infarction. Severe arrhythmia, shock, carotid sinus allergy, orthostatic hypotension, subclavian artery steal syndrome.
4. Hematological factors
Oral contraceptives, hyperglycemia caused by pregnancy, maternal, postoperative and thrombocytopenia; erythrocytosis, sickle cell anemia, increased viscosity due to macroglobulinemia can occur cerebral ischemia.
(two) pathogenesis
1. Normal cerebral blood flow and cerebral ischemia threshold
Since the energy material ATP or ATP metabolic substrate stored by the neurons itself is very limited, the brain needs continuous cerebral blood flow to supply glucose and oxygen. The normal cerebral blood flow value is 45-60 ml per minute per 100 g of brain tissue, when the cerebral blood flow When descending, brain tissue regulates blood flow through an automatic regulation mechanism, minimizing the effects of cerebral ischemia on neurons.
However, when CBF falls to a certain threshold, the brain autoregulation mechanism is decompensated, and the minimum energy requirement of the brain is not satisfied, which may cause functional or organic changes in the brain. When CBF20ml/(100g·min), it causes Neurological dysfunction and electrophysiological changes, this is the threshold of cerebral ischemia. When CBF is 1518ml/(100g·min), neurotransmitter is depleted, synaptic transmission stops, and electrical activity disappears. This is the lack of neuronal activity. The blood threshold, when the cerebral blood flow is quickly restored, the brain function can be restored, but when the CBF is further decreased to 15 ml/(100 g·min), the brain evoked potential can disappear, and when the CBF is <10 to 12 ml/(100 g·min). ATP depletion, ion homeostasis, membrane phospholipid degradation, K+ release from neurons to extracellular, Ca2 enters into neurons in large quantities, causing calcium overload in the latter, with abnormal increase of Na+, Cl- and water in glial cells. Destruction of death, this is the ion homeostasis threshold, usually below this threshold, and brain damage is irreversible.
However, the occurrence of cerebral infarction is not only related to cerebral blood flow, but also related to cerebral ischemia time. In the monkey cerebral ischemia model, such as ischemia time is 1-3 hours, the cerebral blood flow limit level of cerebral infarction is 10 ~ 12ml / (100g · min); if ischemia is permanent, 17 ~ 18ml / (100g · min) cerebral blood flow can cause cerebral infarction.
2. Semi-dark area of cerebral ischemia
Relative to the ischemic core region, blood supply is reduced after ischemia of the brain tissue around it, but relying on the collateral circulation of the brain, the neurons have not undergone irreversible death, and the blood flow is restored within a certain time limit, and the neurons can restore function, although the cells The electrical activity disappears, but the ionic homeostasis of the cells is still maintained. In the anatomical structure, it is more difficult to strictly distinguish the semi-dark regions, mainly referring to brain tissue that can be rescued after drug treatment or recovery of cerebral blood flow, but if cerebral ischemia is further developed The cells in the semi-dark area can be killed, and the semi-dark area is the research focus of pathophysiology after cerebral ischemia, and is also the core part of cerebral ischemia treatment.
3. Pathophysiological changes of cerebral ischemia
(1) Energy disorder: It is the main pathological process after cerebral ischemia. When the brain tissue is completely ischemia for 60s, it can cause the depletion of high-energy substance adenosine triphosphate (ATP), leading to energy and protein synthesis disorders, resulting in cellular structural proteins and Lack of functional protein, due to lack of oxygen, anaerobic glycolysis, increased lactic acid production, resulting in intracellular and extracellular acidosis, ionic membrane pump dysfunction, increased cell membrane permeability, ion gradient inside and outside the cell can not be maintained, K+ outflow, Na+ influx Depolarization of the cell membrane promotes the release of Ca2 influx and glutamate. With the influx of Na+, water begins to accumulate in the cells, causing cell edema and eventually leading to cell death.
(2) Excitatory neurotoxicity: Abnormal depolarization of cell membrane after ischemia and massive Ca2 influx can cause abnormal release of neurotransmitters, including glutamate, dopamine, gamma-aminobutyric acid (GABA), acetylcholine And aspartic acid, etc., the synthesis and ingestion of these substances require the supply of energy substances, energy supply disorders during cerebral ischemia, can accumulate these substances, produce toxic effects, glutamate is the main excitatory nerve in the brain The transmitter is currently thought to bind to two types of receptors, one of which is a ionic receptor such as N-formaldehyde-D-aspartate (NMDA), amino-3-hydroxy-5-methyl -4-isopyrrolidinic acid (AMPA), etc., activation of such receptors can affect the transmembrane movement of ions; the other is a metabolic receptor that does not affect the function of ion channels, when glutamate and NMDA, AMPA When the receptors bind, the ion channels are open, Ca2 is intensive, and cytotoxicity is exerted by Ca2. Therefore, cells with more glutamate receptors, such as hippocampal CA1 cells and cerebellar Pujinye cells, are susceptible to ischemic damage. Using glutamate receptor antagonists to reduce cerebral ischemia Infarct volume, improving damage in the ischemic penumbra, demonstrating that excitatory neurotoxicity, represented by glutamate, plays a role in the pathophysiology of cerebral ischemia, but also found that glutamate receptor antagonists are diffuse Brain damage in the core region of forebrain ischemia or focal cerebral ischemia is not significantly improved, indicating that the evolution of damage after cerebral ischemia is not only the participation of excitatory amino acids.
(3) Calcium balance disorder: Ca2 is an important second messenger in cells, which plays an important role in cell differentiation, growth, gene expression, enzyme activation, release of synaptic vesicles, and maintenance of membrane channel status. Usually, the intracellular Ca2 concentration is about 10,000 times lower than that outside the cell, that is, 10-5-10-7 mol/L in the cell and 10-3 mol/L extracellular. Maintaining the ion gradient requires energy supply to control the following ion regulation. Process: Ion transmembrane in and out, intracellular calcium pool uptake and release, combined with intracellular proteins to form calcium, extracellular calcium into the cell mainly depends on calcium channels, and discharge depends on Ca2-ATPase, Na+-Ca2 exchange To be realized, the endoplasmic reticulum and mitochondria are intracellular Ca2 storage sites and buffer systems. The release of Ca2 from the endoplasmic reticulum depends on two receptors: one receptor channel is controlled by inositol triphosphate (IP3); the other receptor is The ryanodine receptor (RyR) is controlled by the intracellular Ca2 concentration. In addition, there is a calcium pump ATPase on the endoplasmic reticulum membrane. Therefore, the release or uptake of Ca2 by the endoplasmic reticulum depends on intracytoplasmic Ca2, IP3. And ATP concentration, there is dependence on the mitochondrial inner membrane The electrochemical gradient of phosphorylation controls the entry and exit of calcium ions. When cerebral ischemia, energy metabolism slows or stops, cell membrane depolarization, extracellular Ca2 cis ion concentration inflow, and intracellular calcium pool can not maintain concentration gradient Ca2 is released into the cytoplasm, causing an increase in intracellular Ca2.
Increased intracellular Ca2 is the main pathophysiological change after cerebral ischemia, which can trigger a series of reactions leading to cell death, mainly manifested by activation of Ca2-dependent enzymes such as proteolytic enzymes, phospholipases, protein kinases, and nitric oxide synthesis. Enzymes and endonucleases, etc., which maintain the integrity of the cell structure under normal conditions, thereby maintaining cell function, but during cerebral ischemia, phospholipases such as phospholipase A2 and phospholipase C are overactivated, releasing free fatty acids. Finally, free radicals, vasoactive substances and inflammatory substances are produced. Phospholipase A2 can convert aminoglycol phosphate, phosphorylcholine and other cell membrane phospholipids into a hemolyzed state, and a hemolyzed phospholipid acts as a detergent for cell membranes. Destruction of membrane stability; also promotes the formation of platelet activating factor (PAF), a cytokine that mediates adhesion of inflammatory cells to endothelial cells and platelet formation, inflammation and oxygen after cerebral ischemia Free radical reaction can accelerate cell damage after ischemia, and phosphorylation and dephosphorylation of intracellular proteins are important forms regulating protein function. Protein kinases phosphorylate cellular structural proteins and regulatory proteins, thereby altering protein function, such as elevated intracellular Ca2 during cerebral ischemia, activation of protein kinase C, alteration of membrane protein and channel protein functions, and affecting cellular ions Steady state, intracellular calcium also regulates gene expression, especially in super early genes such as c-fos, c-jun can increase expression during cerebral ischemia.
(4) Acidosis: Possible mechanisms of neuronal damage caused by acidosis: cerebral edema formation, inhibition of mitochondrial respiratory chain, inhibition of lactate oxidation and damage of intracellular H+ excretion. In addition, acidosis can increase the blood-cerebrospinal fluid barrier. Permeability, the damage of acidosis depends on the pre-ischemic blood glucose level and the degree of ischemia. Hyperglycemia before ischemia can increase the abnormality of lactic acid produced by anaerobic glycolysis after ischemia. When the lactic acid content in tissues is higher than 25g When /g, brain damage can be produced.
(5) Free radicals: Free radicals also play an important role in the pathophysiological process of cerebral ischemia. Oxygen free radicals increase after cerebral ischemia, especially after cerebral ischemia and reperfusion, oxygen radicals can be more obvious. Hydroxy (0H-), oxygen (O2-) and H2O2 are the main sources. After reperfusion, a large number of inflammatory cells enter the infarct area with blood flow, which becomes another source of oxygen free radicals. One source of oxygen free radicals is arachidene. Acid, produced by Ca2-activated phospholipase A2; another pathway is derived from xanthine oxidase, Ca2 influx can convert xanthine dehydrogenase to xanthine oxidase, act on O2, produce O2-, free radicals may change The structure of phospholipids and proteins causes phospholipid peroxidation, destroys cell membrane integrity and DNA structure, and causes cell death, but the exact mechanism by which free radicals cause brain damage is still unclear.
(6) Nitric oxide (NO): In recent years, the role of nitric oxide in cerebral ischemia/reperfusion injury has been paid attention to, and it acts as a kind of active free radical, which can act as a neural information molecule. It can be a neurotoxic substance. Different parts of nitric oxide have different functions, which can regulate cerebral vascular tone and nerve transmission. Nitric oxide itself has no toxic effect, but after cerebral ischemia, elevated intracellular calcium stimulation Nitrogen synthesis increases, as a reverse neurotransmitter, nitric oxide can mediate the production of oxygen free radicals and arachidonic acid, causing free radical reactions, leading to neuronal death, excessive synthesis can further decompose, produce more, more toxic Oxygen free radicals cause cell damage. Because of the short half-life of nitric oxide, direct research is still difficult. It is mainly judged by the study of nitric oxide synthase (NOS). NOS has different cell sources and different effects. Work type, it is currently believed that the protective or destructive effect of nitric oxide in ischemia depends on the evolution of the ischemic process and the source of cells, excitatory amino acid-mediated cerebral ischemia A chain reaction that activates Ca2-dependent NOS, including neuronal NOS (nNOS) and endothelial NOS (eNOS), selectively inhibits nNOS with neuroprotective effects, and selectively inhibits eNOS with neurotoxic effects, in addition, delayed ischemia or Ischemia-reperfusion can induce the production of inducible NOS (iNOS) independent of Ca2, mainly in glial cells, and selectively inhibit iNOS with neuroprotection. Therefore, activation of nNOS and induction of iNOS can mediate ischemic Brain damage, the mechanism of action may play a role in disrupting mitochondrial function and affecting energy metabolism. Recent studies have found that L-NAME, a non-selective NOS blocker, can significantly reduce brain damage after ischemia/reperfusion, using L-NAME Blocking NOS activity by more than 80% can also significantly reduce the infarct volume after ischemia/reperfusion, indicating that free radical damage caused by nitric oxide plays an important role in reperfusion injury.
(7) Cytokines and inflammatory reactions: inflammatory cell infiltration can be seen in the infarcted area 4 to 6 hours after transient cerebral ischemia or 12 hours after permanent cerebral ischemia. Reperfusion after cerebral ischemia can cause more obvious inflammatory reaction in the brain. Inflammatory response plays an important role in the mechanism of ischemia/reperfusion injury. This type of inflammatory reaction begins with the expression of proinflammatory cytokines in the ischemic area, and the accumulation of inflammatory cells in the ischemic area is the main manifestation. A series of damage reactions leading to neurological destruction, such as tumor necrosis factor alpha, beta (TNF-alpha, TNF-beta), interleukin, macrophage-derived cytokines, growth factors, chemokines As a chemotactic substance of inflammatory cells, mononuclear factors play an important role in the aggregation of inflammatory cells in the ischemic area. Among them, the role of interleukin-1 (IL-1) is the most critical, and IL-1 may pass the following two Pathways cause cell damage:
1 activation of glial cells or other cytokines or endothelial adhesion molecules, stimulate inflammatory response, increased expression of IL-1 after cerebral ischemia can stimulate the expression of other cytokines, produce synergistic effects, cause inflammatory cell infiltration, inflammatory cells are lacking In the blood area, on the one hand, it can mechanically block the microvessels, reduce the local blood supply, and further aggravate the ischemic damage; on the other hand, the infiltrating inflammatory cells release the active substances, destroy the vascular endothelial cells, damage the blood-cerebrospinal fluid barrier, and cause neuronal death.
It is speculated that the inflammatory reaction in the brain originates from the expression of proinflammatory cytokines such as IL-1, releases chemotactic factors, and induces the expression of leukocyte adhesion molecules, thereby causing inflammatory cells to aggregate in the ischemic region and adhere to vascular endothelial cells. , release inflammatory mediators.
2 stimulate arachidonic acid metabolism or nitric oxide synthase activity, release free radicals, causing free radical damage.
(8) Apoptosis and necrosis: After cerebral ischemia, the cerebral blood flow in the ischemic core region is basically stopped, protein synthesis is terminated, cell membrane stability is destroyed, cell contents are released, and cell death is called so-called cell necrosis. The main form of cell damage after cerebral ischemia, but recent studies suggest that apoptosis or programmed death is also a form of cell damage after cerebral ischemia, especially in neurons in the ischemic penumbra or transient cerebral ischemia. Reperfusion and other ischemic degrees are relatively light, morphologically, the apoptosis is characterized by chromatin condensation and folding or fragmentation, cell shrinkage, and apoptotic bodies appear in the cytoplasm, after cerebral ischemia, withering The phenomenon of death occurs in sites susceptible to ischemic damage such as CA1 pyramidal cells.
Prevention
Cerebral ischemic disease prevention
Active prevention, treatment of atherosclerotic plaque, prevention of emboli detachment, attention to the prevention and treatment of the cause. Early diagnosis and early treatment before the blood vessels are narrow and there is no irreversible damage. The use of non-invasive methods such as magnetic resonance imaging (MRI), CTA, and ultrasound provides the possibility of early diagnosis and treatment; however, there are also many shortcomings. It is necessary to conduct a comprehensive cerebral angiography as early as possible to comprehensively evaluate the condition of cerebrovascular disease. The prevention and treatment plan is individualized and comprehensive; this can better reduce the incidence of stroke.
Complication
Cerebral ischemic disease complications Complications, cerebral infarction, cerebral hemorrhage
Cervical infarction may be complicated by cerebral infarction and cerebral hemorrhage, myocardial infarction, wound hemorrhage or infection, cranial nerve injury, etc. Carotid restenosis may occur after surgery. Endovascular stenting may be complicated by cerebral embolism, dissection Aneurysm, restenosis, hematoma at the puncture site, and pseudoaneurysm.
The transient ischemic attack is due to the short-term medical "vascularization" of the arteries that supply the blood of the brain, which causes the transient dysfunction of the brain tissue responsible for blood supply. Common complications include frequent weakness of the hands and feet, hemiplegia, sudden blackness or blindness in a single eye, aphasia, etc., often accompanied by hypertension, atherosclerosis or diabetes, heart disease, and cervical spondylosis.
Symptom
Symptoms of cerebral ischemic diseases Common symptoms Tinnitus retrograde amnesia, sensory disturbance, transient cerebral ischemia, carotid atherosclerosis, ataxia, diplopia, black dysphagia, vertigo
Clinical classification and performance:
Temporary cerebral ischemia
Including transient ischemic attack (TIA) and reversible ischemic neurological disorder (RIND), the former refers to temporary cerebral ischemia, causing dysfunction of the brain, retina and cochlea, with less conscious changes, symptoms lasting for a few minutes, and a few lasting hours However, they all recovered completely within 24 hours without leaving sequelae. The latter had the same TIA, but the neurological dysfunction lasted for more than 24 hours, but not more than 3 weeks. If it is more than 3 weeks, it is permanent cerebral ischemia. The extent of lesion involvement is divided into:
(1) Internal carotid artery system TIA: sudden onset of partial hemiplegia, partial sensory disturbance, single side, hand involvement is common, single eye short-term blindness or black Mongolian, primary side hemisphere involvement, speech dysfunction, There was a brief loss of reading, loss of writing and aphasia.
(2) vertebral artery system TIA: symptoms are more complicated than the internal carotid artery system, dizziness, unilateral hemianopia is the most common symptoms, in addition, facial paralysis, tinnitus and difficulty in swallowing can also occur, headache, diplopia, ataxia can also For the patient's complaint, the perioral sensory disturbance is the brain stem involvement, and the bilateral ischemic internal ischemia may have sudden memory impairment. The elderly are more common. The anterograde amnesia is more common than retrograde amnesia. It can last for several hours, TIA and Shortly after RIND, the high incidence of cerebral infarction, 9% to 20% of patients with TIA and RIND eventually evolved into cerebral infarction, of which 20% occurred within 1 month and 50% occurred within 1 year.
2. Infarction
Often onset, sudden, according to the condition of stable and progressive type, the former refers to stable and no progress, lasting 24 to 72h, also known as complete stroke, 11% to 13% of patients with onset of concealment, no clinical symptoms and signs Only imaging studies have found ischemic lesions.
3. Marginal infarction
The marginal zone is located in the middle cerebral artery, between the anterior cerebral artery and the junction of the middle cerebral artery and the posterior cerebral artery. In addition, there are similar marginal regions between the cerebellar supply vessels, the basal ganglia, and the subcortex. These regions are mainly composed of large The blood vessels of the distal extremity are most susceptible to ischemic damage, forming a sacral ischemic foci from the frontal lobe to the occipital lobe.
Lacunar infarction
Deep microinfarction caused by small perforating arterial lesions, accounting for 12% to 25% of cerebral infarction, infarction occurs in the basal ganglia and in the thalamus, pons, sac and white matter, can conceal the onset, asymptomatic or performance For neurological dysfunction, conscious state and advanced cortical function are not affected.
Examine
Examination of cerebral ischemic diseases
1.CT and MRI scan
For patients with symptoms of ischemic stroke, the first CT scan is performed. The biggest help is to exclude cerebral hemorrhage. It is difficult to distinguish whether the patient is cerebral infarction or cerebral ischemia based on symptoms alone. There is no positive detection of CT scan in TIA patients. It can be mild brain atrophy or small softening lesions in the basal ganglia. The CT findings of RIND patients can be normal, and there may be small low-density softening lesions. CS patients have obvious brain low-density infarcts on CT films. There may be enlargement of the ventricle, and no abnormalities can be found in the initial CT of the cerebral infarction. Generally, the low-density area appears after 24 to 48 hours.
MRI examination has a certain help for the diagnosis of early cerebral infarction. After 6 hours of cerebral infarction, the water in the infarct has increased by 3% to 5%. At this time, the infarct changes with long T1 and long T2, indicating the presence of cytotoxic cerebral edema. At 24h, the blood-cerebrospinal fluid barrier in the infarct was destroyed. The enhanced signal enhancement was observed by injection of Gd-DTPA for MR enhancement. The infarct still showed long T1 and long T2 after 1 week of onset, but the T1 value was shortened earlier. There was bleeding in the infarct, which showed a shortened T1 value and a prolonged T2 value.
2. Cerebral angiography
Cerebral angiography is an indispensable and important examination in the diagnosis of cerebral ischemic disease. The location, nature, extent and extent of vascular lesions can be found. Whole cerebral angiography should be performed as much as possible, including the arteries of the neck and the subclavian artery. If necessary, the aortic arch should also be examined. For example, the first angiography should be performed for a long time. Before the operation, the angiography should be repeated. The cerebral angiography is dangerous. It is more dangerous for patients with atherosclerosis and can cause plaque. Block detachment causes cerebral infarction. In recent years, transfemoral catheterization has been used. It is safer than direct puncture of common carotid artery angiography and has high vascular selectivity. Two-way continuous angiography, including intracranial and extracranial circulation, is available.
A large number of patients with cerebral ischemic disease are caused by extracranial vascular disease. The stenosis or occlusion caused by arteriosclerosis is multiple, and there may be several arteries involved. It may also show multiple lesions on the same artery. .
3. Determination of cerebral blood flow
The measurement methods include inhalation method, intravenous method and internal carotid artery injection method. The most accurate internal carotid artery injection method is to inject the sputum (131Xe) solution into the internal carotid artery, and put a plurality of scintillation counter probes on the head to measure the local and total. The blood flow of the brain can be used to calculate the blood flow of gray matter, white matter and different regions of the brain, and the ischemic area is determined. The determination of regional cerebral blood flow (rCBF) can help determine whether it is necessary to perform surgical anastomosis. It is confirmed whether the ischemic condition is improved after the anastomosis. Therefore, the patient has local neurological dysfunction. The cerebral blood flow measurement shows that the local blood flow is reduced and the whole brain is normal, or the whole cerebral blood flow is reduced and the local reduction is even worse. It is the extracranial intracranial Indications for arterial anastomosis, such as patients with TIA history without neurological dysfunction, angiography showing cerebral artery obstruction, but good collateral circulation, cerebral blood flow measurement showed mild ischemia in both hemispheres, no need for arteries Anastomosis.
4. Other inspection methods
(1) Doppler ultrasonography: the flow and direction of blood can be measured, thereby judging whether the blood vessel is occluded, the upper common iliac artery is occluded from the bifurcation of the common carotid artery to the end of the carotid artery. And the blood in the upper artery of the trochlear artery flows back to the ophthalmic artery, and then enters the internal carotid artery, the middle cerebral artery and the anterior cerebral artery. The above-mentioned internal carotid artery can be judged by Doppler ultrasound for the percutaneous measurement of the above two scalp arteries. Occlusion and stenosis of the site, as well as changes in the direction of blood flow.
Transcranial color Doppler examination can determine the depth of blood vessels, blood direction, blood flow of the cerebral artery ring, anterior cerebral artery, middle cerebral artery, posterior cerebral artery, intracranial artery intracranial segment and vertebral artery. Speed, pulsation index, etc., according to which can determine which blood vessel has lesions.
(2) EEG: EEG was abnormal when cerebral ischemia was severe. After cerebral infarction, the EEG was abnormal. After a few days, it began to improve. About 8 weeks after the onset, about half of the patients showed The limitations were abnormal, but gradually returned to normal. At the same time, the symptoms of nerve damage persisted, and the brain infarct showed a localized slow wave on the EEG.
(3) Brain nuclide scanning: commonly used (99mTc) intravenous injection method, this method can only scan brain lesions larger than 2cm in diameter, TIA patients and brain stem, cerebellar infarction scans are mostly negative, detected The positive rate is related to the development stage of the disease course and the scan time after the injection of nuclides. 2 to 3 weeks after the onset of cerebral infarction, the edema subsides and there is a collateral circulation, so that the nuclides can enter the infarct area, and the scan positive rate is the highest; after the injection of nuclide The positive rate of scanning was the highest in 2~4h.
(4) Measurement of central arterial pressure of the retina: When the extracranial segment of the internal carotid artery is severely stenotic or occluded, the retinal arterial pressure of the ipsilateral side is lower than that of the contralateral side. The contraction of the central retinal artery is measured by the ophthalmic artery pressure gauge. Pressure and diastolic pressure, if the pressure on both sides differs by more than 20%, it is diagnostic.
Diagnosis
Diagnosis and diagnosis of cerebral ischemic diseases
diagnosis
The diagnosis of cerebral ischemic disease mainly depends on medical history, nervous system experience and necessary auxiliary examination. According to the history and positive findings of nervous system, the location of the diseased blood vessel can be preliminarily determined. It is the internal carotid artery system, or the vertebral basilar artery system, which is a blood clot. It is also a possible source of embolism, emboli, and diagnostic classification of patients according to the classification of TIA, RIND, PS and CS.
Differential diagnosis
The disease needs to be differentiated from hemorrhagic diseases. The main features of hypertensive cerebral hemorrhage are:
1. More common in patients with hypertension and atherosclerosis over 50 years old.
2. Often in the daytime activities when the force suddenly occurs.
3. The course of disease progresses rapidly, and the manifestations of complete strokes such as disturbance of consciousness and hemiplegia appear soon.
4. The cerebrospinal fluid is homogeneously bloody.
CT or MRI scan can further confirm the diagnosis.
