I. Blood supply to the brain
Blood to the brain is supplied by the carotid artery system and the vertebrobasilar artery system. The aortic arch divides into the cephalic trunk, the left common carotid artery, and the left subclavian artery. The cephalothoracic trunk is further divided into the right common carotid artery and the right subclavian artery. The internal carotid artery emanates from the common carotid artery and the vertebral artery from the subclavian artery.
1.Internal carotid artery starts from the common carotid artery, goes up through the neck to the base of the skull, and then divides into the ophthalmic artery, posterior communicating artery, anterior choroidal artery, anterior cerebral artery, and middle cerebral artery after entering the skull. It supplies blood to the eye and the frontal lobe, temporal lobe, parietal lobe and basal ganglia of the cerebral hemisphere.
The anterior cerebral artery supplies the entire anterior frontal lobe, the frontal lobe, the medial aspect of the parietal lobe, and a narrow area of the superior lateral convexity of the frontoparietal lobe, i.e., the motor and sensory cortices of the lower legs and feet. Its deep penetrating branch, the anteromedial thalamic artery, supplies the head of the caudate nucleus, the anterior part of the shell nucleus, the anterior part of the thalamus, the lateral nucleus of the pallidum, and the anterior branch of the internal capsule. Therefore, when the cortical branch of the anterior cerebral artery is blocked, the paralysis of the contralateral limb is more severe than that of the lower limb.
Cerebral middle artery is the direct continuation of internal carotid artery and is the thickest of all cerebral arteries. Its cortical branches supply the entire lateral aspect of the cerebral hemisphere except the frontal pole and occipital lobe, including the motor and sensory cortical areas that innervate the facial cloth, hands and upper extremities, the optic radiations, and the speech cortical areas of the main cerebral hemisphere. Its deep penetrating branches supply the internal capsule and basal ganglia.
Therefore, when its cortical branch is obstructed, it causes paralysis of the contralateral limb, and the upper limb is more important than the lower limb. The deep penetrating branch obstruction causes contralateral trigeminal symptoms. Among them, the striated artery of the nucleus pulposus, which runs along the lateral side of the nucleus pulposus up to the internal capsule, is thicker and is prone to rupture and cause cerebral hemorrhage during atherosclerosis and hypertension, so it is also known as the hemorrhagic artery.
2.Vertebral-basilar artery system (Vertebral-basilar artery) The vertebral artery starts from the subclavian artery, penetrates the transverse convex foramen of the 6th to 1st cervical vertebrae, and enters the cranial cavity through the foramen magnum of the occipital bone. At the junction of the cerebral bridge and medulla oblongata, the right and left vertebral arteries merge to form a basilar artery, which travels up the basilar sulcus on the ventral side of the cerebral bridge to the midbrain where it divides into two major terminal branches, the right and left posterior cerebral arteries. The vertebral-basilar artery emanates intracranially from the posterior inferior cerebellar artery, anterior inferior cerebellar artery, pontine branch, internal auditory artery, and superior cerebellar artery, supplying the cerebellum and brainstem in turn.
The Cerebral posterior artery supplies the posterior part of the cerebral hemispheres including the visual center of the occipital talar fissure and the base of the temporal lobe. Its deep penetrating branches supply the thalamus and the superior brainstem. Therefore, obstruction of the posterior cerebral artery causes cortical blindness, which is manifested as homonymous partial blindness, but macular vision is preserved and light reflex exists.
3. The ring of the fundic artery (Willis ring) is connected by the anterior communicating artery between the two anterior cerebral arteries and the posterior communicating artery between the two internal carotid arteries and the posterior cerebral artery, forming the ring of the fundic artery. It is extremely important for regulating and balancing the blood supply between the carotid artery and vertebrobasilar artery and between the two hemispheres of the brain, as well as forming the collateral circulation when this ring is narrowed or occluded somewhere.
Second, the etiology of cerebrovascular disease
Most of them are the brain manifestations of systemic vascular and hematologic diseases, and only a small proportion is caused by localized lesions of cerebral vessels such as congenital malformations, trauma or tumors.
1, atherosclerosis (atherosclerotic): is the most important cause.
2, arterial embolism (embolism)
3.Arteritis
4.Developmental abnormalities
5.Vascular injury
6.Heart disease
7.Hematological diseases and blood rheology abnormalities
8.Metabolic disease
9.Drug reactions
10.Tumor
Risk factors.
1, Age: The incidence, prevalence and mortality of stroke increase with age, especially more significantly from 55 to 75 years old.
2, family history: the prevalence of family history of cerebrovascular disease and hypertension is higher than that of the control group.
3, hypertension or hypotension
4, heart disease
5, diabetes mellitus
6, hyperlipidemia
7, smoking and alcohol abuse
8, obesity
9, dietary factors: excessive consumption of salt, meat and animal oils containing saturated fatty acids, etc.
10, other: including oral contraceptives, etc.
Doctors can reduce the occurrence of stroke by controlling blood pressure, blood sugar, blood lipids, heart disease and adjusting dietary habits.
III. Classification
The classification of cerebrovascular diseases published in Stroke in 1990.
(i) Asymptomatic type: including those who do not yet have vascular brain or retinal symptoms.
(II) Focal brain dysfunction
1, transient ischemic attack: further divided into carotid system and vertebral basilar system.
2, Stroke.
(1), cerebral hemorrhage
(2), subarachnoid hemorrhage
(3), intracranial hemorrhage due to AVM
(4), cerebral infarction: atherosclerotic thrombotic, cardiogenic embolic and lacunar. However, 30% to 40% of the infarcted patients are not easily distinguished clinically as which type of infarction and are called difficult to classify. Atherosclerotic plaque enlarges and causes severe narrowing of the arterial lumen or additional thrombus on it, followed by plaque or thrombus fragments forming embolism causing infarction (arterial-arterial embolism); cardiogenic embolism – the conditions that produce embolism are atrial fibrillation or atrial flutter, recent myocardial infarction, congestive heart failure, valvular lesions, etc.; lacunar – a small infarction deep in the brain caused by small penetrating arterial lesions, whose diameter generally does not exceed 1.5 cm.
(iii) vascular dementia
(iv) Hypertensive encephalopathy: diastolic blood pressure is often higher than 17.3 kPa (130 mmHg). Headache, impaired consciousness, and optic papillary edema are often more pronounced than neurological signs.
IV. Transient ischemic attack
(I) Concept
Transient ischemic attack refers to a transient lack of blood supply to the carotid artery or vertebrobasilar system, resulting in focal neurological dysfunction in the blood supply area and corresponding symptoms and signs. It usually peaks within 5 minutes and lasts for 5 to 20 minutes at a time, and most often does not exceed 24 hours. However, recurrent attacks can occur.
(II) Pathogenesis
1, microembolism theory (the most important): microemboli mainly come from the extracranial arteries, especially the atherosclerotic plaque at the beginning of the internal carotid artery and the debris of the attached wall thrombus clot when ulceration occurs. Because the embolus is very small, it is easy to be decomposed by enzymes, or because of the ischemic dilatation of the vessels distal to the embolism, so that the embolus moves to the distal end of the vessel and is not harmful enough, the blood supply is restored and the symptoms disappear.
2, other: hemodynamic changes; carotid artery compression; small artery spasm; cardiac dysfunction, etc.
(C) Clinical manifestations
1. Ischemic episodes of the carotid system.
①episodic light paralysis (hemiparesis) of the lateral limb or single limb (most common).
(2) Transient monocular blindness.
③Aphasia (aphasia) (primary hemisphere)
2. Ischemic attacks of the vertebrobasilar system: paroxysmal vertigo is the most common. Sometimes it is difficult to diagnose because it only shows vague symptoms such as dizziness, blurred vision and unstable walking. If there are symptoms of brainstem (diplopia, dysarthria, dysphagia, crossed paralysis hemiplegia alternate) and cerebellum (ataxia ataxia), the diagnosis is clearer.
(IV) Diagnostic points
1, the age of onset is more than 50 years old, with atherosclerosis ;
2, sudden, transient episodes of focal neurological deficits with complete recovery within 24 hours;
3, recurrent attacks with stereotyped clinical symptoms;
4, no neurological signs in the interval.
(E) Differential diagnosis
It should be distinguished from seizure disorders
1. Limited epilepsy (Epilepsy): It is also a transient seizure disorder. It is often irritating, such as convulsions, tingling, and extension of functional areas of the symptomatic cortex. It can be identified based on previous epilepsy history and EEG changes.
2. Syncope (Syncope): also transient seizures, but mostly with loss of consciousness without focal neurological deficits and low blood pressure during seizures.
Migraine: Its aura phase is easily confused with migraine disorder. However, it usually starts in adolescence and often has a family history. The attacks are often accompanied by vegetative symptoms and may be prolonged, and less often show focal neurological deficits.
4. Inner ear vertigo: There is often vertigo, tinnitus and vomiting. Other than nystagmus and ataxia, there are few other symptoms and positive signs. It usually starts at a younger age, and the attacks last longer than 24 hours, and there is often a lasting hearing loss after repeated attacks.
(F) Treatment
1, anti-platelet aggregation drugs: enteric aspirin, Pansentin, Ticlid, etc.
2, cerebral vasodilators: low-molecular dextrose, Nimoton, etc.
3, calcium antagonists: blocking the inward flow of calcium ions, preventing cerebral artery spasm, dilation of blood vessels, maintaining the deformability of red blood cells and other effects. Commonly used: Nimodipine, Cipro, etc.
4.Anticoagulation therapy: At present, this treatment can eliminate or reduce the number of transient cerebral ischemic attacks and has positive significance in preventing possible cerebral infarction. If the attacks are frequent, serious and the symptoms are gradually aggravated, and there are no obvious contraindications, anticoagulation therapy can be carried out early.
5.Surgical treatment: If it is determined that the artery is obviously narrowed or occluded due to carotid atherosclerotic plaque, endarterectomy-repair, extracranial-intracranial vascular anastomosis, etc. are feasible.
(VII) Prognosis
1/3 later develop into cerebral infarction, 1/ 3 continue to have TIA episodes, and the other 1/ 3 can resolve on their own.
V. Cerebral infarction
Here we mainly talk about cerebral thrombosis.
(I) Preferred sites: middle cerebral artery, siphon and beginning of internal carotid artery, vertebral artery and middle and lower part of basilar artery.
(ii) Clinical manifestations.
Tracing the medical history, about a small percentage of patients with cerebral infarction have a history of transient ischemic attack. After the occurrence of cerebral infarction, some of them show deteriorating stroke, some of them recover completely within 1 to 3 weeks, which is called reversible ischemic neurological deficit (RIND), and part of them show stable stroke.
1. Internal carotid artery: The main manifestation is hemiparesis or hemianesthesia of the limb contralateral to the lesion; the main hemisphere is often hemianopsia. Both eyes of the patient often gaze at the side of the lesion. If the semi-lesion side is blinded in one eye, the localization is more clear.
2. Middle cerebral artery: hemiparesis, hemianesthesia and hemianopsia on the contralateral side of the lesion may occur. If the cortical branch is involved, the hemiparesis and hemianesthesia are more severe in the face and upper extremities.
3. Anterior cerebral artery: If the cortical branch is involved, motor and sensory impairment of the contralateral lower extremity may occur, but this paresis may not occur due to the lateral circulation supply of the anterior communicating artery.
4.Posterior cerebral artery: supplying the posterior part of the brain, thalamus and upper brainstem, may appear contralateral isotropic hemianopia, (with macular evasion) and transient blackness, etc.
5. Vertebrobasilar artery: Brainstem and cerebellar symptoms and signs are often seen. Locked-in syndrome can occur in the infarction of the base of the cerebral bridge. The patient is conscious, but cannot eat, speak, or make various movements due to tetraplegia, bilateral lateral palsy, and ball palsy, and can only express his will by up and down eye movements.
6. Inferior posterior cerebellar artery: dorsolateral medullary syndrome.
(II) Auxiliary examination
CT examination shows hypodense foci in the infarct area after 24-48 hours. However, CT shows poorly for brainstem and cerebellar infarction. MRI examination can be done when available.
(C) Diagnosis
1.Higher age of onset.
2. There is often cerebral atherosclerosis and atherosclerosis of other organs.
3.Often accompanied by hypertension, diabetes mellitus, etc.
4. There may be a history of antecedent transient cerebral ischemic attack.
5.The onset is more frequent at quiet rest, and the symptoms are often found in the morning after waking up from sleep.
6. Symptoms often worsen gradually over a few hours or over a longer period of time, showing a worsening stroke.
7. Consciousness often remains clear, with relatively obvious focal symptoms.
8. Cerebrospinal fluid is mostly normal, and hypodense foci appear 24 to 48 hours after CT examination.
(IV) Treatment
General treatment in the acute phase of stroke.
① Keep quiet and avoid moving.
② Keep the airway unobstructed. For those with impaired consciousness and poor breathing, tracheal intubation and tracheotomy should be performed early.
③ Observe the condition, vital signs and consciousness closely.
④Anti-brain edema.
1. Low right + Salvia: It can reduce blood viscosity and improve blood circulation. It should be used with caution in patients with bleeding tendency or left heart failure.
2, control blood pressure: some patients with high blood pressure is due to cerebral edema and not hypertension, can be used appropriately with dehydrating agents, blood pressure can be restored to normal. If the blood pressure is too high, the appropriate use of antihypertensive drugs, should be maintained at the usual or patient age should be slightly higher. Avoid lowering blood pressure too quickly or too low, so as not to affect cerebral blood flow.
3.Thrombolytic therapy: urokinase, rt-PA (recombinant tissue-type fibrinogen activator).
4.Lowering embolism therapy: Dongling, Longjin.
5.Anticoagulation therapy: applicable to progressive cerebral infarction.
6.Vasodilators: Currently, it is thought that they can only be used for small infarcts without edema, or for those whose cerebral edema has subsided after 3 weeks of onset. For example, Nimoton.
7.Anti-platelet aggregation agents: slightly.
8.Calcium antagonists: omitted.
VI. Cerebral hemorrhage
Bleeding in the brain parenchyma is called cerebral hemorrhage. Including injury and non-injury. Non-injurious cerebral hemorrhage is mentioned here. Also known as primary or spontaneous cerebral hemorrhage, refers to bleeding caused by vascular lesions, necrosis and rupture in the brain, the vast majority of which are caused by small cerebral artery lesions associated with hypertension and rupture when blood pressure rises suddenly, called hypertensive cerebral hemorrhage.
(I) Clinical manifestations
1, internal capsule hemorrhage: the basal ganglia of the brain is the most common site of hemorrhage, because of the damage to the internal capsule, so called internal capsule hemorrhage. The symptoms are “focal gaze” and “three deviations”, hemiparesis, hemianesthesia and hemianopsia.
2.Lobar hemorrhage: the most common is in the parietal lobe.
3.Pontocerebral hemorrhage: If the hemorrhage is large, the condition is critical and often starts with dizziness, vomiting, double vision, severe headache, etc. Except for the onset of the disease, consciousness can be partially preserved, but often enters deep coma within minutes. The first manifestation is “crossed paresis”, a paralysis of the bleeding side and a paralysis of the contralateral limb. The head and eyes are turned to the non-hemorrhagic side in the form of a “staring limb”.
When the hemorrhage spreads to both sides, the head and eyes return to a neutral position, with “pinpoint” pupils (due to damage to sympathetic fibers on both sides), central hyperthermia (damage to the subthalamic thermoregulatory center), and limb paresis (damage to the pyramidal bundles bilaterally). At the same time, breathing is irregular, and death mostly occurs within 24 to 48 hours.
4, cerebellar hemorrhage: sudden onset of vertigo, vomiting, posterior occipital headache, physical examination with ataxia of the diseased limb, nystagmus, cranial nerve symptoms, cervical resistance, etc. It is easily misdiagnosed as spider blood. Any hypertensive patient with sudden onset of severe pain on one side of the posterior occipital region, frequent vomiting, severe vertigo, pupil narrowing, gaze paralysis, gradually worsening impaired consciousness, without obvious paralysis must be alert to the possibility of cerebellar hemorrhage.
5. Ventricular hemorrhage: there are two kinds: primary and secondary. Caudate nucleus hemorrhage breaks into the lateral ventricle, cerebellar hemorrhage and pontocerebellar hemorrhage may break into the fourth ventricle. This condition and its seriousness. Consciousness often falls into a deep coma within 1 to 2 hours after the onset of the disease, and tetanic seizures or tetraplegia occur. The symptoms of primary ventricular hemorrhage are similar to spider blood.
(II) Ancillary examinations
CT examination is preferred. The hematoma is a high-density foci. CT can show the location and size of the hematoma, whether there is ventricular translocation, and whether there is breakthrough into the ventricles, which can help in treatment.
(III) Diagnosis
1. The age is mostly above 50 years old.
2. Most of them have previous history of hypertension.
3.More often occurs during emotional excitement and physical activity.
4.Sudden onset and rapid progression.
5, There are focal signs with different degrees of consciousness disorder and cranial hypertension symptoms.
6.CT shows high-density foci, and lumbar puncture cerebrospinal fluid pressure is often increased, mostly bloody. (Lumbar puncture is prohibited for those with brain herniation and cerebellar hemorrhage).
(IV) Treatment
1.Keep quiet to prevent continued bleeding.
2.Control blood pressure: lower it to the original level before bleeding or about 20/12 (150/90mmHg).
3.Lower cranial pressure and control cerebral edema: mannitol (pay attention to cardiac and renal function), glycerol fructose, sodium hesperidin, adrenocorticotropic hormone (short-term use).
4, hemostatic drugs: PAMBA, hemostatic min, etc. It plays a certain role in punctate bleeding and oozing blood, especially when combined with gastrointestinal bleeding.
5.Cooling therapy: It is beneficial to brain cell recovery and reduce brain edema.
6.Surgical treatment: It is generally believed that 15cm below the curtain and 30cm above the curtain.
Indications.
(1)Surgery can be considered for cerebellar hematoma >10ml and diameter >3cm; hematoma >20ml or with brainstem compression signs should be operated urgently.
(2) If the hematoma of shell nucleus hemorrhage is >50ml, or if the cranial hypertension is significantly increased and brain herniation may be formed.
(3)Thalamic hemorrhage hematoma >10ml, and the condition continues to deteriorate. External ventricular drainage is feasible in severe cases of ventricular hemorrhage.
Contraindications.
(1)Advanced age with other medical diseases.
(2) Unstable vital signs.
(3) Hemorrhage located deep in the internal capsule, thalamus, or brainstem. As for those with small hematoma and stable vital signs, surgery is often not required.
VII. Subarachnoid hemorrhage
(I) Concept
It refers to the inflow of blood into the subarachnoid space from various causes of bleeding. It is divided into injurious and non-injurious forms (spontaneous), and the latter is further divided into primary and secondary. Secondary refers to brain parenchymal hemorrhage that penetrates brain tissue and blood flows into the ventricles and subarachnoid space. Primary is due to lesions and ruptures of blood vessels at the base or surface of the brain that allow blood to flow directly or predominantly into the subarachnoid space.
(II) Etiology
1.Intracranial aneurysm is the most common etiology.
2.Arteriovenous malformation.
3.Arterial rupture caused by hypertension and atherosclerosis.
4, caused by blood diseases.
5.Intracranial tumor.
6.Arteritis.
7.Complications of anticoagulation therapy.
8.Anomalous vascular disease at the base of the brain. etc.
(C) Pathology (Preferred site)
Cerebral aneurysms mostly occur at the bifurcation of arteries, mostly at the anterior part of the arterial ring at the base of the brain, especially at the bifurcation of the internal carotid artery and the posterior communicating artery, and the anterior cerebral artery and the anterior communicating artery are most common. Although the aneurysm is congenital, it develops in youth, and 50% of the patients develop it after 40 years of age.
(IV) Clinical manifestations
1. Symptoms: It is common from 40 to 70 years old, with sudden onset, mostly during activity. The most common symptoms are headache and vomiting. The headache is severe, especially like an explosion. Half of the patients may have varying degrees of impaired consciousness, with more transient confusion and more severe coma. Some start with convulsive seizures or psychotic symptoms. Generally, there is no focal syndrome, but in posterior communicating aneurysm, one side of the arteriovenous nerve paralysis may appear; in vasospasm or a few cases of brain parenchyma, one side of the focal syndrome may appear.
2. Signs: Meningeal irritation often appears within 1 to 2 days. Fundus examination performed 1 hour after onset may reveal subvitreous lamellar hemorrhage.
(E) Complications
1, rebleeding: sudden onset of impaired consciousness is aggravated. Sixty percent of them recur within the 2nd week of onset.
2, vasospasm: early spasm occurs shortly after onset and resolves within minutes or hours. Delayed spasms mostly occur 5 to 15 days after the onset of the disease. It is characterized by impaired consciousness and focal neurological symptoms.
3. Traffic hydrocephalus.
(F) Auxiliary examination
1.CT shows high-density foci in the cerebral sulcus, cerebral pool, and lateral fissure.
2.Lumbar puncture: cerebrospinal fluid pressure is mostly elevated, and the appearance is homogeneous and bloody. The cerebrospinal fluid turns yellow after 1 week and returns to normal after 3 to 4 weeks.
3.DSA: The site of the aneurysm can be clarified. Examination time: within 3 days of onset or 1 month later.
(vii) Treatment.
1.absolute bed rest for 4-6 weeks, avoid constipation and emotional excitement, use laxatives, sedatives such as Valium.
2.Lowering cranial pressure: mannitol.
3.Hemostatic agents: PAMBA, hemostatic min, etc., can prevent the clot around the aneurysm from dissolving and causing bleeding.
4.Anti-vascular spasm: Nimoton.
5.Surgical treatment: The aim is to eradicate the aneurysm and avoid rebleeding.
6.Other: cooling, anti-infection, prevention of emergency ulcers, upper gastrointestinal bleeding.
(H) Prognosis
The death rate of intracranial aneurysm hemorrhage in the acute phase is about 30%, the death rate of the 2nd hemorrhage is 30-60%, and the third is almost 100%.