I. Concept of ischemic cerebrovascular disease
Ischemic cerebrovascular disease (ICVD) is a disorder of blood supply to the brain that occurs on the basis of lesions or hemodynamic disorders in the vascular walls of the blood vessels supplying the brain, resulting in brain tissue necrosis or softening due to ischemia and hypoxia in the corresponding blood supply area, and causing transient or persistent local or diffuse damage, resulting in a series of neurological deficits. This causes a series of neurological deficit syndromes. Ischemic cerebrovascular disease is one of the three major diseases causing human death, second only to heart disease and cancer, with high morbidity, high disability and high mortality. Once the cerebral arteries are blocked, a series of “ischemic waterfall-like reactions” occur immediately in the ischemic and hypoxic brain tissue cells, leading to cell death. The traditional ischemic cerebrovascular diseases include transient ischemic attack (TIA), cerebral infarction (CT), and cerebral infarction, also known as ischemic stroke, and the most common clinical types are cerebral thrombosis, lacunar infarction, and cerebral embolism. The most common clinical types are cerebral thrombosis, lacunar infarction and cerebral embolism.
Cerebral thrombosis
Cerebral thrombosis is the most common type of cerebral infarction, which is caused by atherosclerosis or thrombosis of cerebral arteries resulting in thickening of the vessel wall, narrowing or occlusion of the lumen, resulting in reduced blood flow or interruption of blood supply to the brain, ischemia, hypoxia, softening and necrosis of brain tissue, and focal neurological deficits with signs and symptoms. Cerebral thrombosis accounts for about 70% of all strokes.
Etiology and pathogenesis
1. Etiology
(1) Basic etiology.
①Vascular wall lesions: A large number of clinical and basic studies have found that cerebrovascular wall lesions are the basis of cerebrovascular disease, and cerebrovascular wall lesions are mainly caused by hypertension and atherosclerosis, so the main causes of cerebrovascular disease are hypertension and atherosclerosis. Other causes are congenital vascular developmental abnormalities, vasculitis, vascular amyloidosis, and vascular wall lesions caused by diseases of the internal medicine system.
② Heart disease: rheumatic heart valve disease, bacterial endocarditis, and atrial fibrillation produce intracardiac emboli dislodgement as the main cause of cerebral embolism.
③Lateral circulation insufficiency is a major factor in the development of ischemic cerebrovascular disease.
④Other etiologies include emboli (air, fat, cancer cells and parasites, etc.), cerebral vasospasm, trauma, entrapment aneurysm, Moyamoya disease, etc.
⑤ Some cerebral infarcts are of unknown cause and may be related to antiphospholipid antibodies, protein C and protein S, etc.
(2) Contributing factors.
① Hemodynamic disorders: abnormal blood pressure, hypertension or hypotension; cardiac insufficiency or arrhythmia; hypovolemia, etc.
(2) Blood component abnormalities: tethering from various sources, mainly cardiogenic and arterial vessel wall detachment; blood hyperviscosity; thrombocytopenia or abnormal function; abnormal function of coagulation system or fibrinolytic system.
2.Pathogenesis
The cerebral vessels are narrowed or occluded due to thrombosis or embolism, and the blood supply to the brain tissue in the blood supply area is insufficient or absent, resulting in a series of clinical manifestations due to ischemia and hypoxia or necrosis of brain tissue. Among them, thrombosis roughly needs to go through the following process: vascular endothelial injury, platelet adhesion, platelet aggregation and release, clotting and thrombus formation. Embolism is a blockage of blood flow in the cerebral vasculature with a diameter comparable to that of the embolus when a plaque detached from the wall of the heart or large arteries enters the cerebral circulation with blood flow. The cerebral perfusion is insufficient when hemodynamics are impaired, especially in the so-called “watershed” area, which is the first to be affected and forms a watershed infarction. Within 6 hours of cerebral artery occlusion, brain tissue changes are not obvious, and within 8-48 hours, softening occurs in the central part of the brain where ischemia is most severe, and a semi-dark band forms around it. In massive cerebral infarction, the brain tissue swells and softens, the boundaries of gray and white matter become indistinct, and in severe cases, cerebral herniation can be formed.
Several concepts need to be understood here: ischemic time window, blood flow threshold for ischemia, semidark zone (electrical failure, membrane failure), and reperfusion injury. The mechanism of cerebral infarction injury: excitatory amino acid theory, oxygen free radical theory, calcium overload theory, acidosis theory, NO theory, endothelin theory, genetic theory, etc.
Clinical type
1. According to the evolution of symptoms and signs, they are classified as
(1) Complete stroke: The clinical manifestations of stroke are more severe and progress faster, often reaching a peak within a few hours (<6h).
(2) Progressive stroke: The clinical symptoms are mild after stroke, but progressively worsen and continue to progress within 48 hours until more severe neurological deficits occur.
(3) Reversible ischemic neurological defict (RIND): clinical symptoms are milder after stroke onset, but can persist and recover within 3 weeks.
2. Classified according to clinical manifestations combined with imaging evidence.
(1) Massive cerebral infarction: usually complete stroke of the main trunk of the internal carotid artery and its branch trunks, and the main trunk of the vertebrobasilar artery, with heavy clinical symptoms, progressive aggravation, prone to cerebral edema and signs of high cranial pressure, which can develop into brain herniation.
(2) Watershed cerebral infarction: localized ischemia at the boundary of adjacent vascular supply area or watershed area, also called marginal zone cerebral infarction, mostly due to hemodynamic disorders, which can be divided into cortical and subcortical types. The symptoms are mild and recovery is rapid.
(3) Hemorrhagic cerebral infarction: vascular structure dysfunction at the distal end of the lesioned vessel after cerebral infarction, causing blood leakage or secondary hemorrhage, mostly seen in large cerebral infarction, which is more likely to occur when the vessel is recanalized, and can be used to determine whether there is recanalization.
(4) Multiple cerebral infarcts: cerebral infarcts caused by vascular lesions of different blood supply systems, mostly due to recurrent attacks.
3. Classified according to different blood supply systems.
(1) Internal carotid artery system thrombosis.
(2) Vertebrobasilar artery system thrombosis.
[Clinical manifestations
This disease is mostly seen in middle-aged and elderly people, arteritis and cerebrovascular developmental abnormalities are mostly seen in young people. The onset of the disease is often acute or subacute in quiet or sleep, and some patients may have one or more transient ischemic attacks before the disease. Symptoms tend to peak gradually within 1 to 3 days, with general awareness and no increase in intracranial pressure. Approximately 10-30% of patients have a slow onset or no clinical symptoms. The clinical symptoms of cerebral thrombosis depend on the infarct site, volume size and the degree of collateral circulation compensation.
1.Internal carotid artery system
(1) Internal carotid artery thrombosis: accounting for 20% of ischemic strokes, the most common sites of lesions are the beginning of the internal carotid artery and the siphon. Clinical manifestations vary widely, depending on the presence or absence of good collateral circulation, which may be asymptomatic if present, or clinically symptomatic if not. The area supplied by the middle cerebral artery is the most prone, with hemiparesis, hemianesthesia, hemianopsia, and hemianopsia as the most common three signs. There may also be varying degrees of aphasia, dysarthria, and dyscalculia in the main hemisphere. Loss of vision on the side of the lesion, Horner’s sign, arterial nerve palsy, and decreased retinal arterial pressure may also occur. In cases of extracranial segmental artery occlusion, the carotid artery may be tender, striated, with decreased or absent pulsation, and an abnormal vascular murmur may be heard in the neck. In a few patients with lack of collateral circulation, occlusion or severe stenosis of the internal carotid artery can lead to hemispheric ischemic edema and brain herniation formation, which can lead to death in a short time.
(2) Middle cerebral artery thrombosis: the most common. When the main trunk is occluded, there is a triple deviation syndrome, and the main hemisphere is involved in the fashion of aphasia, aphasia, aphasia, aphasia of reading and aphasia of writing. In the case of middle artery cortical branch occlusion, hemiparesis and hemianesthesia are more severe in the head and upper extremities, and there may be aphasia, aphasia, aphasia, aphasia, aphasia, etc. in the case of main hemisphere involvement; the clinical manifestations of different cortical branch occlusions vary: ① Posterior parietal artery: superior parietal artery.
①Posterior parietal artery: involvement of the superior parietal lobule and superior marginal gyrus, with loss of use, cortical sensory impairment, disorientation, or hemianopia.
(ii) Central artery: Occlusion may present with monoplegia or incomplete hemiplegia and mild sensory impairment of the contralateral upper extremity.
③Angular gyrus artery: Named aphasia, aphasia, aphasia, Gersmann syndrome, somatosensory disorders and sensory neglect signs may occur in the non-dominant hemisphere.
(4) Posterior temporal artery: sensory aphasia or isotropic hemianopia after involvement of the posterior part of the superior, middle and inferior temporal gyri.
(3) Anterior cerebral artery thrombosis: it is relatively rare. Because the anterior communicating artery provides collateral circulation, proximal occlusion may be asymptomatic; when the anterior communicating artery is absent and the main trunk is occluded, sensory impairment is mainly cortical and deep sensation, paralysis is more severe in the lower extremities, and may be accompanied by ataxia, dysuria and mental abnormalities, etc. Motor aphasia may be present in the dominant hemisphere. The cortical branch occlusion often invades the medial frontal lobe and varies according to the extent. Deep penetrating branch occlusion, affecting the anterior branch of the internal capsule or the knee, often presents with contralateral central facial and tongue palsy and mild paralysis of the upper extremities, with proximal heaviness, and may have ataxia and involuntary movements.
2.Vertebral-basilar artery system
(1) Vertebral artery thrombosis: thrombosis of the vertebral artery and its branches may have the following manifestations.
(1) Wallenberg syndrome: posterior inferior cerebellar artery thrombosis, a common type of brainstem infarction, causes infarction of the dorsolateral part of the medulla oblongata and cerebellum, vertigo, vomiting, nystagmus, crossed sensory impairment, linguopharyngeal and vagal nerve palsy on the side of the lesion, cerebellar ataxia and Hroner’s sign, generally without symptoms of damage to the pyramidal bundle.
(ii) Medial medullary syndrome: thrombosis of the vertebral artery, anterior spinal artery, and lower branches of the basilar artery, involving the pyramidal bundle, medial thalamus, and hypoglossal nerve, with paralysis on the contralateral side of the lesion, upper body tactile, vibratory, and positional sensory deficits, and isometric peripheral hypoglossal nerve palsy.
(3) Medullary hemi-lateral syndrome: caused by occlusion of the vertebral artery, manifesting as some or all of the symptoms of the two syndromes mentioned above.
(2) Basilar artery thrombosis: the clinical manifestations are complex. Bilateral vertebral artery or basilar artery trunk occlusion is a life-threatening cerebrovascular event with deep coma, tetraplegia, pinpoint pupils, central hyperthermia, central respiratory distress, medullary paralysis, and most deaths soon after. Thrombosis of the basilar artery branches leads to brainstem infarction with multiple syndromes.
(i) Middle cerebral branch occlusion: Weber syndrome, crossed arteriovenous palsy; Benedit syndrome, ipsilateral arteriovenous palsy with contralateral involuntary movements.
② Pontocerebellar branch occlusion: Millard-Gubler syndrome, adductor and facial nerve cross paresis; Fovill syndrome, ipsilateral gaze palsy and peripheral facial paresis, contralateral hemiparesis. Pontocerebellar periportal syndrome (Raymond-Cestan syndrome), involuntary movements and cerebellar signs on the side of the lesion, contralateral limb and mild paresis and sensory disturbances, and inability to gaze toward the side of the lesion.
(3) Occlusion of superior cerebellar artery, posterior inferior cerebellar artery or anterior inferior cerebellar artery: mainly cerebellar infarction may cause vertigo, ataxia, nystagmus, gaze of both eyes to the contralateral side of the lesion, tinnitus and deafness on the side of the lesion, Horner’s sign and cerebellar ataxia, loss of sensation or loss of sensation on the side of the lesion and the contralateral limb, decreased muscle tone, etc. In severe cases, brain herniation may occur. In more severe cases, vertigo, limb flaccidity and medullary paralysis, ataxia, coma and hyperthermia may occur. The pupils of the affected midbrain become large and fixed, and the pontocerebellar lesions show pinpoint pupils, and some patients show atresia syndrome.
(3) Posterior cerebral artery thrombosis: it is relatively rare, accounting for about 3% of all cerebral infarcts. Deep penetrating branch occlusion manifests as the following syndromes.
(① Thalamic syndrome: thalamic geniculate artery involvement, manifested by spontaneous pain in the thalamus, contralateral profound and superficial sensory impairment, mild hemiparesis, contralateral ataxia, chorea-like or tardive dyskinesia signs.
(ii) Bilateral parietal median thalamic syndrome: occlusion of the anterior hypothalamic parietal median artery, which originates between the posterior cerebral artery and the posterior communicating artery, presents with acute onset, transient coma, followed by drowsiness, unresponsiveness, impaired perception of the environment, Korsakoff’s amnesia syndrome and vertical gaze palsy.
③ Weber syndrome.
④ Claud’s syndrome: manifested by homoeopathic motoneural palsy and contralateral cerebellar ataxia.
⑤ Parinaud syndrome: bilateral supraocular inability, convergence inability, and loss of pupillary dilatation in response to light. Cortical branch occlusion: acute onset of memory deficits and visual field deficits. Medial temporal lobe hippocampal infarction may present with confusion, recent memory loss, and distant preservation. Occipital lobe infarction may present with visual field deficits, causing contralateral ipsilateral hemianopsia and macular avoidance. Cortical blindness is a bilateral posterior cerebral artery occlusion, with loss of vision and preserved pupillary response to light, and may present with Anton syndrome. Occipital parietal syndrome, with hemianopia and transient visual impairment such as black haze, etc., in addition to body image disorder, loss of recognition, loss of use, etc.
Auxiliary tests
1, laboratory tests: blood, urine, fecal routine, blood sedimentation, blood glucose, lipids, liver and kidney function, blood rheology, coagulation and fibrinolytic system examination, electrocardiogram, some patients can check C-reactive protein, antiphospholipid antibodies, leptospira coagulation test, etc., if necessary, to help the diagnosis of the cause of the disease.
2.Cerebrospinal fluid examination: cerebrospinal fluid examination in cerebral infarction is mostly normal, which is important for the differentiation of cerebral hemorrhage, but has no significance for the differentiation of hemorrhagic infarction. Cerebrospinal fluid changes usually appear 24 hours after the onset of the disease. The pressure may increase in extensive infarction, and the cell count and protein may be higher than normal several days after the onset.
3.Neuroimaging examination.
(1) CT scan of the head should be a routine examination, which is more popular and economical than MRI, with a short scanning time, and is important for the diagnosis of early excluded cerebral hemorrhage. Most patients can be normal within 24 hours of onset and gradually show hypointense infarct foci after 24 hours, which evolve into uniform lamellar or wedge-shaped distinct hypointense foci in 2-14 days. Indirect signs such as small or absent sulci or lateral fissures and poorly defined cortical and medullary boundaries can be seen within 24 hours in large cerebral infarcts, and cerebral edema and occupational effects tend to become apparent after 24 hours. Hemorrhagic infarcts may show mixed density foci, with dotted high-density shadows within the low-density foci. In the resorption phase of cerebral infarction, due to edema absorption and inflammatory cell infiltration, CT is difficult to distinguish, which is called “blurring effect”, and enhanced scan has a differentiating significance. In the chronic phase, CT shows clear and sharp edges of infarct lesions, which can form cystic cavities of different sizes, and can be accompanied by focal brain atrophy without enhancement effect; the shortcoming of CT is that it is not easy to show small infarct lesions in the brainstem and cerebellum, and lesions below 1 cm are often missed; CTA can reconstruct intracranial arteries in three dimensions, which is meaningful for the diagnosis of vascular lesions.
(2) Cranial MRI: The detection rate of cerebral infarction reaches 95%, which is better than CT scan. Conventional MRI includes T1-weighted imaging, T2-weighted imaging, and proton-weighted imaging. For acute cerebral infarction, the advantage is that T2-weighted imaging can detect abnormal manifestations as early as 5-6 hours of ischemia: T1 low signal and T2 high signal, but it usually shows better at 18-24 hours, which is not significant for diagnosis and treatment in the time window, but has greater value for excluding tumors and inflammation. Functional MRI diffusion-weighted imaging (DWI) can be used for early diagnosis of ischemic stroke, and can show ischemic lesions within 2 hours of onset, which is significant for early diagnosis and treatment. Advantages: high resolution, lesions smaller than 1 cm can be detected; more sensitive and reliable than CT for the diagnosis of infarct lesions under the curtain. Disadvantages: long imaging time; patients cannot have iron implants, pacemakers, etc. in their bodies; MRI is not easy to distinguish between cerebral hemorrhage and cerebral infarction in the ultra early stage; relatively expensive.
4.Vascular ultrasound examination: extracranial vessels can be examined by double work ultrasound or color ultrasound imaging system, which can find vascular lesions such as stenosis and occlusion, and determine the degree and location. Intracranial vessels can be examined by transcranial ultrasound Doppler, which can determine the location and nature of intracranial vascular lesions through the examination of blood flow velocity, spectrum, impedance, etc.
5, cerebral angiography (DSA): invasive angiography, is the gold standard for the diagnosis of cerebrovascular lesions, the site, nature and collateral circulation of vascular lesions can be found through angiography, with the popularity of interventional techniques, this method has been widely used in the diagnosis and treatment of cerebrovascular disease, but because it is an invasive test, there are certain risks, need to be carefully selected.
6.ECT and EEG: they have certain significance for some cerebral infarcts. ECT can show the site and extent of cerebral tissue ischemia; EEG may appear abnormal in large cerebral infarcts, with low wave amplitude, slow rhythm and no specificity, mostly used for differential diagnosis, and is not commonly used now.
PET is the only quantitative technique that can directly provide the main physiological parameters related to cerebral blood flow and cerebral metabolism, which can measure not only cerebral blood flow but also local glucose metabolism and oxygen metabolism, and if it is reduced or stopped, it indicates the presence of infarction. It is currently used to predict the occurrence and size of cerebral infarction, to study reperfusion injury and hemidesmosomal zone, and to explore the molecular mechanism of cerebral infarction.
Diagnosis and differential diagnosis
1, diagnosis: elderly patients with hypertension and atherosclerosis, the onset of the disease in sleep or quiet state, some patients may have TIA before the disease, symptoms gradually worsen in a few hours or more, most conscious but focal signs of the nervous system is obvious, and can be explained by an intracranial arterial occlusion syndrome, clinical consideration can be given to acute cerebral thrombosis, combined with cranial CT appears low-density foci, MRI shows that the lesion The diagnosis is not difficult when combined with the presence of hypointense foci on cranial CT and foci with T1 low signal and T2 high signal on MRI. For young patients, we should consider the presence of arteritis, abnormal vascular development, etc., and need to further clarify the diagnosis.
2.Differential diagnosis
(1) Cerebral hemorrhage: cerebral infarction is sometimes not easily distinguished from a small cerebral hemorrhage cluster clinically, CT examination can confirm the diagnosis, and the distinction is as follows.
Table 1 Differentiation points of cerebral infarction and cerebral hemorrhage
Cerebral infarction
Cerebral hemorrhage
Age of onset
Mostly above 60 years of age
Mostly under 60 years old
State of onset
Quiet or during sleep
During activity or excitement
Speed of onset
Peak symptoms in more than 10 hours or 1-2 days
Peak symptoms within minutes to hours
Headache
None
Most common
History of hypertension
Mostly absent
Mostly
Whole brain symptoms
Mild or absent
High cranial pressure symptoms such as headache, vomiting, drowsiness
Disorders of consciousness
Usually mild or absent
More severe
Neurological signs
Mostly non-homogeneous hemiparesis (trunk or branches)
Mostly homogeneous hemiparesis (basal ganglia region)
CT examination
Low-density foci in the brain parenchyma
High-density foci in the brain parenchyma
Cerebrospinal fluid
Colorless and transparent
hematogenous
(2) cerebral embolism: the onset is acute, clinical symptoms mostly peak within seconds or minutes, there may be headache, nausea, vomiting and other high cranial pressure manifestations, often with a history of heart disease such as atrial fibrillation, bacterial endocarditis, myocardial infarction, etc. Some patients have emboli originating from the walls of large arteries.
(3) Subarachnoid hemorrhage: It occurs in all age groups, mostly acute onset during activity, severe headache, vomiting, mostly without focal localization signs such as hemiparesis, significant neck resistance, history of intracranial vascular anomalies, hemorrhagic CSF, high pressure, and cranial CT showing high density shadow of subarachnoid space.
(4) Intracranial occupying lesions: intracranial tumors, subdural hematomas, brain abscesses, etc., have a slow onset, some may present with stroke-like episodes, appear hemiparesis, intracranial pressure increase signs easily confused with cerebral infarction, cranial CT, MRI shows obvious edema around the lesion, with occupying effect, can be distinguished.
(5) Coma must be differentiated from other systemic or intracranial diseases: hepatic coma: no hemiparesis, abnormal liver function, high blood ammonia, liver cirrhosis, peritoneal effusion, swelling, etc. can be differentiated. Pulmonary encephalopathy: history of pulmonary disease, no hemiparesis, obvious cyanosis, decreased oxygen saturation, and can be awake after treatment such as oxygenation. Intracranial infection, hydrocephalus, demyelinating lesions, etc.: history, clinical manifestations, imaging examinations and cerebrospinal fluid laboratory tests can be identified.
(6) Other diseases: some patients need to be differentiated from spinal cord lesions, tumors, myopathies, endocrine diseases, etc.
Treatment】
The treatment for cerebral thrombosis can be divided into three stages: ultra-early stage (within 1-6 hours of onset), acute stage (within 24 hours of onset), and recovery stage. Treatment principles.
①Pay attention to the treatment of ultra-early stage and acute stage, and combine the comprehensive, targeted and individualized treatment;
②Take various treatment programs to restore the blood supply to the ischemic area as soon as possible, improve microcirculation, and block the pathological process of cerebral infarction;
③Pay attention to neuroprotective treatment of ischemic cells;
④Strengthen monitoring and nursing care, prevent and treat complications and cerebral edema, etc;
⑤ Early systematic and individualized rehabilitation treatment;
⑥Treatment for etiology and risk factors to prevent recurrence. Domestic and foreign research on the treatment of ischemic cerebrovascular disease believes that ischemic cerebrovascular disease will eventually make a breakthrough in gene therapy and cell therapy and become the most effective method for the treatment of cerebrovascular disease.
(1) General treatment: bed rest, overall care, functional position of the affected limbs, prevention of dislocation, keeping the airway open, prevention of decubitus ulcers and venous thrombosis; reasonable use of antihypertensive drugs to stabilize blood pressure; maintaining nutrition and water-electrolyte balance; controlling blood sugar; preventing and controlling infection; controlling fever, etc.
(2) Acute treatment treatment principles: adjust blood pressure, expand volume, improve microcirculation; prevent thrombus progression and reduce the scope of infarction; large cerebral infarction should control cerebral edema and intracranial pressure elevation (ICP) and prevent brain herniation; prevent and control complications; deal with cerebral infarction hemorrhage transformation.
(3) Special treatment of cerebral infarction