What Is a Cerebral Infarction?

Cerebral infarction, formerly known as cerebral infarction, is also known as cerebral ischemic stroke, which refers to ischemic necrosis or softening of localized brain tissue caused by impaired blood supply to the brain, ischemia and hypoxia. The common clinical types of cerebral infarction include cerebral thrombosis, lacunar infarction and cerebral embolism. Cerebral infarction accounts for 80% of all strokes. The diseases closely related to it are: diabetes, obesity, hypertension, rheumatic heart disease, arrhythmia, dehydration for various reasons, various arteritis, shock, blood pressure falling too quickly and too much. Clinical manifestations are characterized by sudden fainting, unconsciousness, paraplegia, speech impairment, and mental retardation. Cerebral infarction not only poses a great threat to human health and life, but also brings great pain and heavy burden on patients, families and society.

Basic Information

nickname

Ischemic stroke

Visiting department

Neurology

Multiple groups

45 to 70 years old

Common locations

Cerebrovascular

Common causes

Cerebral arteriosclerosis, embolism, etc.

Common symptoms

Sudden fainting, paraplegia, speech and mental impairment

Causes of cerebral infarction

Clinically, there are cerebral thrombosis and cerebral embolism. The former is due to arterial stenosis, which gradually forms thrombus in the lumen and eventually blocks the artery. The latter is caused by an abnormal substance called emboli in the bloodstream that blocks the arteries, such as emboli that have fallen off the thrombus in the heart cavity of some heart diseases.

Clinical manifestations of cerebral infarction

Main clinical symptoms

The clinical symptoms of cerebral infarction are complicated. It is related to the location of brain damage, the size of cerebral ischemic blood vessels, the severity of ischemia, whether there are other diseases before the onset, and whether they are combined with other important organ diseases. Symptoms, that is, asymptomatic cerebral infarction; can also be manifested as recurrent limb paralysis or dizziness, that is, transient ischemic attack; severe cases can not only have limb paralysis, but even acute coma, death, such as lesions affecting the cerebral cortex, In the acute phase of cerebrovascular disease, seizures can occur, with the highest incidence within 1 day after the disease, and cerebrovascular disease with epilepsy as the first occurrence is rare. Common symptoms are:

(1) Subjective symptoms: headache, dizziness, dizziness, dizziness, nausea, vomiting, exercise and / or sensory aphasia or even coma.

(2) Cerebral nerve symptoms Gaze to the lesion side, central facial paralysis and tongue paralysis, pseudobulbar paralysis, such as coughing with drinking water and difficulty swallowing.

(3) Physical symptoms Hemiplegia or mild hemiplegia of limbs, loss of sensation of leaning, gait instability, limb weakness, incontinence, etc.

2. Clinical classification of cerebral infarction site

(1) The infarct area of lacunar infarction cerebral infarction is less than 1.5 cm, which is manifested as: subacute onset, dizziness, dizziness, unstable gait, weak limbs, a few have drinking water, cough, and have difficulty swallowing; they may also have hemiplegia 2. Leaning sensation decreases, and some patients have no positioning signs.

(2) Medium-area infarcts are more common in the basal nucleus, lateral ventricle, parathalamic thalamus, bilateral frontal lobe, and temporal lobe. Presented as: sudden headache, dizziness, frequent nausea, vomiting, consciousness, paralysis or paraplegia, hemianopia, central facial paralysis and tongue paralysis, pseudobulbar palsy, aphasia, etc.

(3) Patients with large-scale infarcts have a rapid onset of illness and are critically ill. They may have hemiplegia, hemiplegia, decreased sensation, or even quadriplegia, cerebral hernia, and coma.

Cerebral infarction

1.CT examination

Brain CT showed that the accuracy of the size and location of the focal cerebral infarction was 66.5% to 89.2%, and the accuracy of the initial cerebral hemorrhage was 100%. Therefore, early CT examination is helpful for differential diagnosis and can rule out cerebral hemorrhage. When the cerebral infarction occurs within 24 hours, or the infarct is smaller than 8 mm, or the lesion is in the brainstem and cerebellum, brain CT examination often does not provide a correct diagnosis. It should be reviewed shortly if necessary to avoid delay in treatment.

CT showed that the infarcts were low-density, and the location, shape, and size of the lesions could be clarified. Larger infarcts could compress the ventricle, deform and shift the midline structure. However, only 4 to 6 hours after the onset of cerebral infarction, only some cases Slightly low-density lesions with unclear boundaries can be seen, and most cases can only display low-density lesions with clearer boundaries and infarcts smaller than 5 mm after 24 hours. Posterior fossa infarcts are not easily visualized by CT, and infarcts on the cortical surface are often not detected by CT. Enhanced scanning can increase the rate of detection and qualitative diagnosis of lesions. The CT manifestation of hemorrhagic infarction is irregular patchy high-density areas in a large area of low-density area. The difference from cerebral hematoma is that the low-density area is broad and the hemorrhages are scattered in small pieces.

2.MRI examination

MRI is extremely sensitive to the detection of cerebral infarction. It is better than CT for the detection of cerebral ischemic damage. It can detect earlier cerebral ischemic damage and can be seen within 1 hour of ischemia. Six months after the onset of the infarction, almost all of the major infarctions can be shown by MRI, with T1-weighted low signals and T2-weighted high signals.

3. Routine inspection

Blood, urine, stool routine and liver function, renal function, coagulation function, blood glucose, blood lipid, electrocardiogram, etc. are used as routine tests, and those with conditions can perform ambulatory blood pressure monitoring. Chest radiographs should be used as a routine to rule out cancer thrombus and to diagnose whether aspiration pneumonia occurs.

4. Special inspection

Transcranial Doppler ultrasound (TCD), carotid color B-ultrasound, magnetic resonance, angiography (MRA), digital subtraction whole brain angiography (DSA), carotid angiography, can confirm the presence or absence of stenosis or occlusion of intracranial and extracranial arteries .

Cerebral infarction treatment

1. General treatment in the acute phase

The principle of treatment is to improve the blood circulation in the cerebral ischemic area and promote the recovery of neural function as soon as possible. In the acute phase, you should stay in bed as much as possible, strengthen the care of skin, mouth, respiratory tract and urine, prevent pressure ulcers, and pay attention to the balance of water and electrolyte. Nutrition supply. The life care, diet, and management of other comorbidities should be given top priority. Because some patients with cerebral infarction cannot take care of themselves or even have difficulty swallowing in the acute phase, if proper nutrition is not given, there will be problems with energy metabolism. At this time, it is difficult to receive good treatment results even if the treatment is good.

2. Treatment of cerebral edema

(1) Mannitol 20% mannitol hypertonic solution is commonly used in clinical practice. Mannitol is one of the most commonly used effective dehydrating agents.

(2) 10% fructose (glycerol fructose) can undergo pharmacological effects through hypertonic dehydration, and can also use the energy generated by glycerol metabolism into the brain metabolic process to improve local metabolism, which can reduce intracranial pressure and Intraocular pressure, eliminate cerebral edema, increase cerebral blood volume and cerebral oxygen consumption, and improve brain metabolism.

(3) Diuretic dehydrating agents such as furosemide (fast urine) and sodium diureate can be injected intramuscularly or intravenously.

(4) Adrenocortical hormones are mainly glucocorticoids such as hydrocortisone, cortisone, etc., whose secretion and production are regulated by corticosteroids, which have anti-inflammatory effects, immunosuppressive effects, and anti-shock effects, but are generally not used routinely .

(5) Human blood albumin (albumin) Human blood albumin is a medium-molecular-weight colloid that plays an important role in generating colloid osmotic pressure, which is conducive to the retention of fluid in the blood vessel cavity, and is generally not used routinely.

3. Acute Thrombolytic Therapy

Thrombosis and embolism are the basis of the onset of cerebral infarction, so the ideal method is to restore normal blood flow to the ischemic brain tissue before necrosis occurs. Early reperfusion of cerebral blood flow to brain tissue can reduce the degree of ischemia and limit the damage to nerve cells and their functions. Thrombolytic therapy can use streptokinase and urokinase. Anticoagulants can use heparin and dicoumarin to prevent the spread of thrombus and new thrombus.

(1) Ultra-early thrombolytic therapy may restore blood flow perfusion in the infarcted area and reduce neuronal damage. Drug thrombolysis Commonly used urokinase (UK): alteplase (recombinant tissue-type plasminogen activator); intravenous thrombolysis with streptokinase (SK) is not recommended because it may cause bleeding. Arterial thrombolytic therapy As an emergency treatment of stroke, superselective interventional arterial thrombolysis can be performed under DSA direct vision. Urokinase arterial thrombolysis combined with intravenous infusion of low-dose heparin may be beneficial to stroke patients with symptoms in the middle cerebral artery distribution area with symptoms of 3-6 / h.

(2) Cerebral protection therapy The medication before the initiation of ischemic waterfall can reduce cerebral metabolism, interfere with the cytotoxic mechanism caused by ischemia, and reduce ischemic brain injury. Including free radical scavengers (oxide dismutase, barbiturate, vitamin E and vitamin C, 21-aminosteroids, etc.), as well as opioid receptor blockers naloxone, voltage-gated calcium channel blockers , Excitatory amino acid receptor blocking drugs and magnesium ions.

(3) Anticoagulation therapy To prevent thrombus expansion, progressive stroke, and occlusion after thrombolytic therapy, it can be applied for a short period of time. Commonly used drugs include heparin, heparin calcium (low molecular weight heparin) and warfarin. The coagulation time and prothrombin time should be monitored during treatment. Antagonists such as vitamin K and protamine sulfate must be prepared to deal with possible bleeding complications.

(4) Fibrillation therapy By degrading lyophilized human fibrinogen in blood and enhancing fibrinolytic system activity to inhibit thrombosis. The drugs of choice include Batroxobin, defibrase (defibrotase), Ancrod and lumbrokinase.