Cerebral infarction (CI) is a general term for ischemic stroke, including cerebral thrombosis, lacunar infarction and cerebral embolism, which accounts for about 70% of all strokes. Cerebral infarction is caused by a sudden decrease or cessation of blood flow in the local blood supply artery of brain tissue, resulting in ischemia and hypoxia in the area of blood supply, leading to brain tissue necrosis and softening, and accompanied by clinical symptoms and signs in the corresponding area, such as hemiplegia, aphasia and other neurological deficits.
Clinical manifestations
Cerebral infarction is more likely to occur in people aged 50 to 60 years or older, often with atherosclerosis, hypertension, wind heart disease, coronary heart disease or diabetes mellitus, as well as in patients with bad habits such as smoking and alcohol consumption. About 25% of the patients have a history of transient ischemic attack before the disease. Most patients have prodromal symptoms before the onset of the disease, which are headache, dizziness, vertigo, transient limb numbness and weakness. The onset of the disease is usually slow, and patients tend to start in quietness and during sleep. Most patients’ symptoms reach their peak after a few hours or even 1 to 3 days.
Most patients are conscious after the onset of cerebral infarction, and a few may have varying degrees of impaired consciousness, with no significant changes in general vital signs. If the cerebral hemispheres have large infarcts, ischemia and edema, the function of the mesencephalon and brainstem may be affected, and consciousness may be impaired soon after the onset of the disease, and even brain herniation and death may occur. If there is unconsciousness immediately after the onset, consider vertebrobasilar artery system cerebral infarction.
1.Main clinical symptoms: The clinical symptoms of cerebral infarction are complex, which are related to the location of brain damage, the size of cerebral ischemic vessels, the severity of ischemia, the presence of other diseases before the onset of the disease, and the presence of other important organ diseases, etc. The milder cases can be completely asymptomatic, i.e. asymptomatic cerebral infarction; they can also show recurrent episodes of limb paralysis or vertigo, i.e. transient ischemic attack;
In severe cases, there can be not only limb paralysis, but even acute coma and death. If the lesion affects the cerebral cortex, the acute phase of cerebrovascular disease may manifest as the appearance of seizures, with the highest incidence within 1 day after the disease, while cerebrovascular disease with epilepsy as the first seizure is rare. Common symptoms include.
(1) Subjective symptoms: headache, dizziness, lightheadedness, vertigo, nausea and vomiting, motor and/or sensory aphasia, and even coma.
(2) Cerebral neurological symptoms: bilateral eye gaze to the side of the lesion, central facial and tongue palsy, pseudomyelinating palsy such as choking on water and dysphagia.
(3) Somatic symptoms: limb hemiparesis or mild hemiparesis, hemiplegia, gait instability, limb weakness, urinary and fecal incontinence, etc.
2.Clinical classification of cerebral infarction site The infarct area of cerebral infarction is the most lacunar infarction, and the clinical manifestations are: subacute onset, dizziness, dizziness, gait instability, limb weakness, a few of them have choking cough and swallowing difficulty, and they may also have hemiparesis and hemianesthesia, and some patients have no localization signs.
The clinical manifestations include sudden headache, vertigo, frequent nausea and vomiting, mental clarity, hemiplegia, hemiplegia, hemianesthesia, hemianopsia, central facial and tongue palsy, pseudomyelitis, and aphasia.
Patients with large infarcts have an acute onset and critical clinical manifestations, and may have hemiparesis, hemiplegia, or even quadriplegia, cerebral herniation, coma, etc.
(1) Internal carotid artery occlusion: Internal carotid artery occlusion can be asymptomatic. Symptomatic occlusion can cause manifestations similar to middle cerebral artery occlusion such as hemiparesis contralateral to the lesion, hemianesthesia, ipsilateral hemianopsia, and aphasia may result from dominant hemisphere involvement. Intracranial or extracranial internal carotid artery occlusion accounts for 1/5 of ischemic cerebrovascular disease.
Nearly 15% of cases of atherosclerotic occlusion of the internal carotid artery have aura, including monocular blindness due to TIA and ipsilateral retinal artery ischemia. The symptoms of internal carotid artery occlusion are complicated by the action of the arterial ring at the base of the skull. Sometimes, internal carotid artery occlusion may not present with focal symptoms, depending on the compensatory function of the collateral circulation of the anterior and posterior communicating arteries, the ophthalmic artery, and the superficial cerebral arteries. It may also be associated with transient blindness and Horner’s sign.
(2) Middle cerebral artery occlusion: Since the middle cerebral artery supply area is the most commonly involved in ischemic cerebrovascular disease, the clinical signs that occur depend on the site of involvement.
(1) Middle cerebral artery trunk occlusion: Occlusion occurs at the proximal end of the middle cerebral artery emanating from the doublestem artery. This is the most serious type of cerebrovascular disease occurring in this arterial occlusion because the entire middle cerebral artery blood supply area is involved. The clinical manifestations of trunk occlusion are hemiparesis, hemianesthesia and hemianopsia on the contralateral side of the lesion, and aphasia, dysarthria, and dyslexia may occur with trunk occlusion of the dominant hemispheric artery. If the infarct area is large, the condition may cause increased intracranial pressure, coma, brain herniation, or even death in severe cases.
(ii) Occlusion of the deep branch of the middle cerebral artery or the doublestem artery: it may cause hemiparesis contralateral to the lesion, generally without sensory impairment or isotropic hemianopia, with damage to the dominant hemisphere, and there may be aphasia.
(3) Occlusion of various cortical branches of middle cerebral artery: it can cause contralateral hemiparesis of the lesion, with the face and upper limbs being the most important. The dominant hemisphere can cause motor aphasia, sensory aphasia, loss of reading, loss of writing, loss of use, and the non-dominant hemisphere can cause contralateral hemianopia and other somatic disorders.
(3) Occlusion of the anterior cerebral artery: Occlusion of the anterior cerebral artery is uncommon, probably because emboli from extracranial or cardiac sources prefer to enter the middle cerebral artery, which has a large diameter and high blood flow. Occlusion of the proximal anterior cerebral artery on one side may be asymptomatic if there is good circulation in the anterior communicating artery. In posterior occlusion of the anterior communicating artery there may be.
①Cortical branch occlusion: produces sensory and motor deficits in the lower extremity contralateral to the lesion, accompanied by urinary retention.
(2) Deep penetrating branch occlusion: it may cause central facial palsy, lingual palsy and upper limb paresis on the contralateral side of the lesion, and mental disorders such as emotional indifference, euphoria and strong grip reflex.
(4) Posterior cerebral artery occlusion: posterior cerebral artery occlusion causes isotropic hemianopia affecting the contralateral visual field, but macular vision is preserved because the dual branch arteries (middle and posterior cerebral arteries) supply the cortex innervating the macula, and unlike the visual deficit caused by infarction in the middle cerebral artery region, that caused by the posterior cerebral artery is more severe.
①Cortical branch occlusion: visual impairment mainly caused by ischemia of the visual pathway, with ipsilateral partial blindness or upper quadrant blindness contralateral to the lesion.
(ii) Deep penetrating branch occlusion: typical thalamic syndrome with hemianesthesia with thalamic pain contralateral to the lesion and chorea-like tachycardia in the contralateral limb.
In addition, occlusion of the posterior cerebral artery at the level of the midbrain can cause visual disturbances including vertical gaze palsy, actinic nerve palsy, internuclear ophthalmoplegia, and vertical ocular separation. When posterior cerebral artery occlusion involves the occipital cortex of the dominant hemisphere, patients present with named aphasia.
(5) Basilar artery occlusion: Since the basilar artery mainly supplies blood to the brainstem, cerebellum and occipital lobe, the clinical symptoms of occlusion of this artery are more complicated.
Common symptoms are vertigo, nystagmus, diplopia, crossed paralysis or crossed sensory disorder, and limb ataxia. If the main trunk of the basilar artery is occluded, tetraplegia, ophthalmic muscle paralysis, pupil narrowing, often accompanied by paralysis of the facial nerve, spreading nerve, trigeminal nerve, vagus nerve and hypoglossal nerve, and cerebellar symptoms, etc. In severe cases, coma, central hyperthermia, denervation, gastrointestinal bleeding, and even death can occur rapidly.
If the vertebrobasilar artery causes extensive ventral softening of the cerebral bridge due to partial obstruction, it can clinically produce the atresia syndrome, which is manifested by the patient’s tetraplegia, expressionless face, muteness, inability to speak, but clear mind, ability to understand people’s speech, and understanding signified by eye movement.
(6) Posterior inferior cerebellar artery occlusion: The posterior inferior cerebellar artery mainly supplies blood to the dorsolateral part of the medulla oblongata. When occluded, it can cause the lateral part of the medulla oblongata syndrome (Wallenberg syndrome), which manifests as vertigo, nausea, vomiting, nystagmus, ipsilateral lateral sensory deficit, ipsilateral Horner’s sign, swallowing difficulty, hoarseness, ipsilateral limb ataxia, and pain and temperature deficit below the contralateral side. . The clinical symptoms caused by the occlusion of the posterior inferior cerebellar artery are complex and variable, but two basic symptoms must be present, namely: cerebral nerve palsy on one side of the posterior group and loss or loss of pain and warmth on the contralateral side, in order to be diagnosed.
3. Types of clinical manifestations: According to the speed and degree of cerebral infarction, whether the condition is stable or not and the severity, cerebral infarction is divided into the following five types.
(1) Complete cerebral infarction: the condition reaches its peak within 6h of cerebral ischemia, often with complete hemiparesis, and the condition is generally severe.
(2) Progressive cerebral infarction: the condition is still progressively aggravated after 6h of ischemic attack, and such patients account for more than 40%. There are many reasons for progression, such as the expansion of thrombus, obstruction of other vessels or collateral vessels, cerebral edema, hyperglycemia, high temperature, infection, cardiopulmonary insufficiency and electrolyte disorders, most of which are caused by the first two reasons.
(3) Slowly progressive cerebral infarction: symptoms are still progressing within 2 weeks of onset.
(4) Stable cerebral infarction: Those whose condition does not change significantly after onset tend to have stable stroke. It is generally considered that those with ischemic episodes of more than 24h in the internal carotid artery system and more than 72h in the vertebrobasilar artery system have stable condition and can be considered as stable stroke. In this type of stroke, there is a high chance of infarct foci consistent with clinical manifestations seen on brain CT scan, suggesting that there has been irreversible lesion in brain tissue.
(5) Reversible ischemic neurological deficit (RIND): ischemic focal neurokinetic deficits that recover within 24-72 hours, or at the latest within 4 weeks, without sequelae, and without infarct lesions in the corresponding area on CT scan.
Diagnostic tests
Elderly people with previous history of hypertension, diabetes mellitus, heart disease, etc., who develop focal neurological signs such as hemiparesis, aphasia and other focal brain symptoms at quiet rest, or other focal brain symptoms, usually without obvious impairment of consciousness, should consider the possibility of cerebral infarction and need to do brain CT scan or brain MRI examination in time to help confirm the diagnosis.
Cranial CT is the common examination means for the diagnosis of acute cerebral infarction; MRI examination can detect cerebral infarction at an early stage, especially lesions in the brainstem and cerebellum; DSA, CTA, MRA and transcranial Doppler (TCD) are mainly aimed at finding the vascular aspects of cerebrovascular disease, and TCD is inexpensive and convenient, and can detect larger vessels (such as anterior cerebral artery, middle cerebral artery, posterior cerebral artery, and basilar artery) early. and basilar artery).
DSA is the most reliable test for the diagnosis of cerebrovascular disease because it can detect small vascular lesions and can be used for timely interventional treatment.
Treatment methods
1.The treatment principles of acute cerebral infarction are
①Comprehensive treatment and individualized treatment: at different times of disease development, targeted comprehensive treatment and individualized treatment measures are taken for different conditions and causes.
② Actively improve and restore the blood supply to the ischemic area, promote cerebral microcirculation, and block and terminate the pathological process of cerebral infarction.
③Prevent and treat ischemic cerebral edema.
④The acute stage should be treated with cerebral cytoprotection early, and comprehensive measures can be taken to protect the brain tissue in the ischemic peripheral semidark zone to avoid aggravation of the disease.
⑤ Strengthen care and prevention of complications, eliminate pathogenic factors and prevent recurrence of cerebral infarction.
(6) Actively carry out early standardized rehabilitation treatment to reduce the rate of disability.
⑦Other: It is better not to use glucose liquid within 12h after the onset of the disease, and use hydroxyethyl starch (706 substitute plasma) or Ringer’s liquid with triphosphate adenosine (ATP), coenzyme A and vitamin C. Avoid aggravating acidosis and brain damage with high-sugar liquid in the acute phase.
2. General treatment during the acute period: bed rest should be given as much as possible during the acute period, and care of the skin, mouth, respiratory tract and urine and stool should be strengthened. Prevention and treatment of cerebral edema (mannitol, glycerol fructose, diuretic dehydrating agents, hormones and human albumin, etc.) Pay attention to the balance of water and electrolytes, and if you cannot eat on your own after 48 to 72 hours of illness, you should give nasal feeding liquid diet to ensure nutritional supply. The patient’s life care, diet and management of other comorbidities should be given priority.
3. Thrombolytic therapy in the acute phase.
(1) Indications.
①Early start of thrombolytic therapy can prevent large cerebral infarction at least within 4-6h of symptom onset and save the ischemic hemispheric area and hypoperfusion state.
② Age <75 years.
③No impairment of consciousness, but for basilar artery thrombosis, even coma is not contraindicated due to poor prognosis.
④Brain CT scan excludes cerebral hemorrhage and there is no hypointense area corresponding to neurological deficits.
⑤ Thrombolytic therapy can be performed within 6 hours after onset, or within 12 hours in case of progressive stroke.
(6) The patient’s family should sign the consent.
4. Anticoagulant therapy Anticoagulants have a therapeutic effect on early cerebral infarction and can be used for incomplete ischemic stroke, especially vertebrobasilar thrombosis. Anticoagulation therapy is performed by anticoagulant drugs that interfere with one or some of the coagulation factors in the clotting process.
5. Interventional therapy for cerebral infarction and internal carotid artery stenosis Interventional therapy for cerebrovascular disease is also known as endovascular therapy for neurosurgical diseases. It is performed with the help of digital subtraction angiography (DSA) machine with high definition and high resolution, and small catheters are sent to the lesion in the brain under the guidance of TV for examination, diagnosis and treatment. With the application of this technology, a new way of diagnosis and treatment of cerebrovascular and spinal cord vascular disease has been opened up.
Interventional treatment has the characteristics of no craniotomy, less trauma, less pain, faster recovery, and, for some diseases, can achieve the treatment effect that is difficult to achieve with surgery, therefore, it is increasingly valued by doctors and welcomed by patients. At the same time, with the continuous development of new technologies and materials, the application of interventional medicine is becoming more and more widespread, as well as safer and more reliable.
For occlusive cerebrovascular diseases, such as hemiplegia caused by acute cerebral infarction, transient ischemic attack (TIA) and reversible neurological dysfunction (RIND) caused by carotid artery or vertebrobasilar artery stenosis, vision loss caused by occlusion of the central retinal artery or central vein, and increased intracranial pressure caused by venous sinus thrombosis, etc., all can be improved by intravascular interventions, which are Interventional treatment methods include thrombolysis, angioplasty or stent placement, and different treatment methods are chosen according to the lesion.
6.Other therapeutic measures: including the regulation of blood pressure during the acute period, the use of vasodilators, neuroprotective agents (calcium channel blockers, excitatory amino acid receptor antagonists, γ-aminotyrosine (GABA) receptor agonists, free radical scavengers, neurotrophic factors), and hemodilution therapy, etc.
7. Rehabilitation therapy: early start is desirable. Encourage patients to establish confidence in restoring self-care, cooperate with medical treatment and rehabilitation work, and strive for early recovery, while supplementing with acupuncture, massage, physical therapy, etc., to reduce the disability rate and improve the quality of survival.