TOAST etiology classification: large artery atherosclerosis, cardioembolic type, small artery occlusive/lacunar type, other clear etiology types (such as coagulation disorder, blood component changes, vasculitis, vascular malformation, connective tissue disease), Unexplained type

Total anterior circulation infarction (TACI): high-level brain dysfunction, ipsilateral visual field defect, and motor/sensory impairment in at least 2 parts of the ipsilateral face/upper and lower limbs → more common in large infarcts caused by occlusion of the proximal main trunk of the MCA

Partial anterior circulation infarction (PACI): Choose 2 from the above 3, or it may only show high-level brain dysfunction, or it may be more limited than the motor/sensory impairment specified by lacunar infarction → more common in the distal main trunk of MCA, branches at all levels or Small and medium-sized infarcts caused by occlusion of the ACA and its branches

Posterior circulation infarction (POCI): ipsilateral cranial nerve palsy with contralateral motor/sensory impairment, bilateral motor/sensory impairment, eye convergence disorder, cerebral symptoms without ipsilateral long tract symptoms, unilateral homonymous visual field defect (vertebral- basilar artery syndrome)

lacunar cerebral infarction (LACI)

Atherosclerotic cerebral infarction is more common in middle-aged and older people; arteritis cerebral infarction is more common in young and middle-aged people

It often occurs in quiet/sleep conditions, and some may have prodromal symptoms of TIA.

Anterior cerebral artery syndrome: paralysis and loss of sensation in the contralateral calf, urge to urinate

Middle cerebral artery syndrome (most common)

Internal carotid artery syndrome: clinical manifestations vary widely; symptomatic occlusion can cause unilateral amaurosis fugax, contralateral hemiplegia, hemi-sensory impairment, and homonymous hemianopia; aphasia can occur when the dominant hemisphere is involved, and aphasia can occur when the non-dominant hemisphere is involved. It may be accompanied by body image disorder; physical examination may reveal weakened carotid artery pulse and vascular murmur.

posterior cerebral artery syndrome

Vertebrobasilar syndrome: Various manifestations; such as locked-in syndrome, Millard-Gubler syndrome, Foville syndrome, Wallenberg syndrome

Reversible ischemic neurologic deficits (RIND): patients with ischemic symptoms lasting more than 24 hours, often with large or small infarcts, but have not yet caused irreversible neurological damage; or due to collateral circulation compensation Timely and complete, or the thrombus will dissolve immediately due to weak firmness, or the associated vasospasm and cerebral edema will subside; the patient's symptoms and signs will be completely relieved within 3 weeks without leaving any sequelae.

Cerebral watershed infarction (CWSI)/marginal zone infarction: It is a cerebral infarction in the blood supply area or marginal zone between the terminal end of the adjacent main cerebral artery, the cortical branch of the main artery and the deep perforating branch in the brain; symptoms are mild, It can be effectively controlled after correcting the cause; reduced cerebral circulation reserve capacity (hypotension) is the main risk factor; volume expansion treatment is the first choice

Blood tests: blood routine, blood rheology, blood biochemistry → discover risk factors and differential diagnosis

Cerebrospinal fluid examination: Generally unnecessary, only considered when intracranial hemorrhage or intracranial infection is suspected; the results are usually normal, there may be a small amount of RBC, and there may be increased pressure in cerebral edema.

CT examination should be performed as soon as possible after the onset of illness (preferred). Low-density lesions consistent with the occluded vascular supply area can be seen 24 to 48 hours after the onset of illness.

MRI (especially DWI) can clearly show early ischemic infarction and can also identify hemorrhagic infarction and cerebral hemorrhage; the area of ​​diffusion-perfusion mismatch is currently considered to be the ischemic penumbra.

DSA is the gold standard for the examination of cerebrovascular lesions, but it is an unconventional diagnostic method.

Transcranial Doppler ultrasound (TCD): evaluates intracranial and intracranial vascular stenosis, occlusion, spasm, and establishment of collateral circulation, and can also be used to monitor the efficacy of thrombolysis

SPECT, PET: can show the location of cerebral infarction and changes in local cerebral blood flow within a few minutes of onset.

Keep your airway open and get oxygen

control blood pressure

Control blood sugar: It is not advisable to inject glucose solution within 24 hours of onset (to avoid aggravating acidosis); hyperglycemia should be corrected, and insulin treatment should be given immediately when blood sugar is >11.1mmol/L.

Control intracranial pressure: such as 20% mannitol, furosemide, glyceryl fructose

Treat dysphagia: prevent aspiration pneumonia, fluid deprivation and malnutrition and treat fever and infection

Treat upper gastrointestinal bleeding: Antiulcer drugs can be administered routinely intravenously

Prevent and treat water/electrolyte/acid-base balance disorders

Prevent and treat heart damage

antiepileptic treatment

Prevent and treat DVT and pulmonary embolism

intravenous thrombolysis

Arterial thrombolysis: suitable for patients with severe stroke caused by large artery occlusion within 6 hours; it has a high vascular recanalization rate, but the drug dose must be reduced and performed under DSA monitoring

Antiplatelet therapy: For those who do not meet the indications for thrombolysis, a loading dose should be taken orally as soon as possible (change to a preventive dose after the acute phase); for those who have thrombolysis, use should be started 24 hours after thrombolysis.

Anticoagulant therapy: suitable for patients with hypercoagulable state and high risk of developing DVT and pulmonary embolism

Fiber-lowering treatment: especially suitable for patients with hyperfibrinogenemia

Hemodilution treatment: When there is no severe cerebral edema or cardiac insufficiency, volume expansion therapy can be used; dextran 40 is commonly used, and the hematocrit is adjusted to 40~42% (at this time, the oxygen carrying capacity is optimal); this method is preferred for patients with watershed infarction

Brain protective treatments: free radical scavengers, opioid receptor blockers, voltage-gated CCBs, excitatory amino acid receptor blockers, magnesium ions

Traditional Chinese Medicine Treatment

Hemorrhagic transformation: refers to secondary bleeding in brain tissue after infarction, which is a common complication of cerebral infarction; antithrombotic drugs need to be stopped at this time

Surgical or interventional treatment: When a large cerebral infarction is life-threatening, subtemporal decompression and necrotic tissue should be removed actively; it should also be used when the cerebellar infarction is large and there are signs of foramen magnum herniation; the time window for mechanical thrombectomy is 8 hours.

Rehabilitation treatment: It is recommended to carry out early; 1 to 2 weeks after the onset, if there are no serious complications, limb function training and language training can be started

It is more common in young adults; it often occurs suddenly during activities, without prodromal symptoms, and focal neurological signs reach a peak within seconds to minutes; it often presents as a complete stroke; embolism in other parts of the body may be present.

Compared with cerebral thrombosis, it is more likely to relapse and bleed; the condition fluctuates greatly; if it is infectious embolism and is complicated by intracranial infection, the condition will be critical; patients with large embolism may leave varying degrees of sequelae

Other symptoms: Most symptoms or signs of the primary disease may appear, and heart disease and AS are more common.

The principles of treatment for cerebral thrombosis are basically the same, but thrombolytic/anticoagulant/antiplatelet drugs should be suspended when combined with hemorrhagic infarction.

Such as infectious embolism, fat embolism, arrhythmia, air embolism

such as antiepileptic treatment

Anticoagulant therapy: atrial fibrillation/cardiac disease with high risk of re-embolization, arterial dissection/high-grade stenosis

Antiplatelet therapy: in principle not used routinely, except for abnormal embolism

It is more common in middle-aged and elderly men, and more than half have a history of hypertension.

It often starts acutely, with focal symptoms such as hemiplegia/hemisomia sensory impairment; the symptoms are mild, the signs are single, and the prognosis is good, and there are generally no symptoms such as headache, intracranial hypertension, and disturbance of consciousness; it is generally believed that TIA lasts for more than a few hours above, it should be considered as the primary disease

Many patients present with silent infarction

Pure motor type (most common): The lesion is located in the internal capsule/corona radiata/pons; manifests as hemiparesis of approximately the same degree on the contralateral face/upper and lower limbs, without sensory impairment, visual impairment, or cortical movement disorder

Pure sensory type: The lesion is located in the ventroposterolateral nucleus of the thalamus; manifests as hemi-sensory loss, which may be accompanied by paresthesia; little/no movement disorder

Sensorimotor type: The lesion is located in the ventral posterior nucleus of the thalamus and adjacent to the posterior limb of the internal capsule; it initially begins with hemi-sensory disorder and then develops hemiparesis.

Dysarthric-clumsy hand syndrome (DCHS): The lesions are located at the base of the pons, the anterior limb of the internal capsule, and the knees; the onset is sudden; manifested by dysarthria, dysphagia, and contralateral central facial and tongue problems. Paralysis, facial paralysis, side hand weakness/clumsy resting movements, inaccurate finger-nose test, mild balance disorder; but no obvious limb paralysis

Ataxic hemiparesis: The lesions are located at the base of the pons, internal capsule, and corona radiata; the symptoms are contralateral hemiparesis and cerebellar ataxia of the ipsilateral limbs. The hemiparesis is heavier in the lower limbs than in the upper limbs, and least in the face; ataxia cannot be treated with weakness. to explain, may be accompanied by pyramidal tract signs

Lacunar state: refers to multiple lacunar infarcts caused by repeated attacks of the disease, involving bilateral corticospinal tracts and cortical brainstem tracts, severe mental disorders, cognitive decline, pseudobulbar palsy, Bilateral pyramidal signs, parkinsonian syndrome, and fecal incontinence; note that not all lacunar infarctions are lacunar states