Basic concepts and classifications:

◆It is the clinical symptoms of brain tissue necrosis and softening caused by local brain blood supply disorders, resulting in corresponding brain function defects.

◆ According to the law of evolution over time after onset, it is divided into three types:

◇Complete stroke: The symptoms and signs reach peak within 6 hours, and the symptoms continue for a period of time;

◇Progressive stroke: The symptoms and signs gradually progress or worsen in a step-by-step manner within 48 hours;

◇Reversible ischemic neurological deficit: Symptoms and signs last for more than 24 hours and can recover within 3 weeks;

◆Clinical classification:

◇Trombotic cerebral infarction: accounts for 40% of ischemic stroke.

◇Embolizing cerebral infarction: accounts for 20-30% of ischemic stroke.

◇Lacial cerebral infarction: accounts for 15-30% of ischemic stroke.

◇Watershed infarction: accounts for 10% of ischemic stroke.

◇Other causes of cerebral infarction: those that account for ischemic stroke include coagulation disorders, chain cell disease, poor muscle fiber structure, and vasoconstriction caused by drug abuse.

◇Unknown cerebral infarction.

Cause mechanism:

◆Trombotic cerebral infarction:

Arterial wall damage, changes in blood composition lead to increased blood viscosity, abnormal hemodynamics → stenosis of the cerebral artery official cavity → slow blood flow, increased viscosity, platelet aggregation, and thrombosis.

◆Embolizing cerebral infarction: Various emboli fall off → enter blood vessels → block blood flow and stimulate blood vessel walls and cause cerebral artery spasm → brain ischemia, symptoms of functional deficiency.

◆Lacral cerebral infarction: hypertension, vasculitis, atherosclerosis, glass-like transformation, amyloid angiopathy degeneration → microartherosclerosis, lipid clear degeneration, cellulose-like necrosis → clinical symptoms.

◆Watershed infarction: It is more common in clinical manifestations of severe stenosis or occlusion of the internal carotid artery, embolism → ischemia in the watershed area or marginal zone between adjacent blood vessel blood supply areas → mild symptoms.

Pathological and pathophysiological changes:

1 Ultra-early stage - cell swelling, mitochondria swelling and vacuolation; ischemic necrosis in the center of the lesion, and ischemia penumbra is formed around it; 2 Acute stage - cell swelling, ischemia changes; 3 Necrosis stage - cell degeneration necrosis, brain

Tissue swelling; 4 softening stage - liquefaction and softening; 5 recovery stage - forming glial scars and stroke capsules.

Clinical manifestations:

1. Clinical manifestations of different subtypes of cerebral infarction:

Thrombotic cerebral infarction:

◆Clinical features: There are many history of hypertension, diabetes, heart disease, TIA or stroke, and it is often acute onset and develops to peak within a few hours. People with more deaths in large areas may experience the opposite side.

Total hemiplegia, sensation disorders of body sway, eyes staring to the opposite side, headaches, consciousness disorders, etc., and progressively worsen.

◆Diagnostic clues: 1. Most of the onset age is higher; 2. Most of the atherosclerosis and hypertension are common; 3. Most of the TIA are common before the onset; 4. More often the disease occurs when resting quietly, and symptoms often appear after waking up;

5 Symptoms tend to gradually worsen within a few hours or longer; 6 patients are more aware of the situation, and have obvious symptoms of neurological focal symptoms such as hemiplegia and aphasia; 7 cerebrospinal fluid is more normal. 8 CT test

It is normal in the early stages, and low-density lesions may appear at 24-48 hours.

Infarct cerebral infarction:

◆It often starts suddenly and the symptoms reach a peak quickly;

◆Have a history of related medical treatment such as rheumatoid heart disease or acute myocardial infarction;

◆Electronic gram examination mostly contains atrial fibrillation;

◆Ultrasound examination of carotid artery or aorta can reveal unstable plates, etc.;

Caval cerebral infarction:

◆Simple motility: mostly new faces involving one side, weak upper and lower limbs, dysarthria, no sensory and ataxia.

◆Simple sensory: Mostly, the newly emerging sensory loss on more than two parts of one side is involved, and there is no movement or abnormal cerebellar manifestation.

◆Sensory movement: Sensory and movement abnormalities occur at least 2 of the three parts of the body at the same time. Tongue sticking out or dysarthria may occur.

◆Ataxia mild hemiplegia: ipsilateral cerebellar ataxia and mild hemiplegia.

◆ Poor athletic hand clumsy: severe dysarthritis, clumsy hands and ataxia, facial weakness, skewed tongue. Hyperreflexia on the ipsilateral and Babinski signs positive.

Watershed Infarction:

◆Site: Ischemia in the watershed or marginal zone between adjacent blood vessel blood supply areas.

◆Clinical features: mild symptoms, quick recovery, unconscious disorder. 1 Cortical type: Watershed infarction between the anterior cerebral and middle artery blood supply area. Central hemiplegia and sensory mainly in the upper limbs

Disorders, faceless and tongue paralysis, may have emotional disorders, strong grip reflexes and focal epilepsy, aphasia on the main side, quadriplegia on both sides, etc.; 2 posterior cortical type: in the cerebral, posterior artery dividing

Areas, located in the parietal, occipital, and temporal junction, hemiopia is common, hemiplegia is mild or absent, emotional indifference, and memory is reduced. 3 Subcortical type: anterior, middle, posterior arteries and middle brain

Infarction in the watershed area between the bean-shaped arteries between the arteries. The lesions are in the white matter, shell, and caudate nucleus. Pure motor hemiplegia or sensory disorders, involuntary movement, etc.

◆Diagnostic clues: including: 1. There is evidence of systemic blood pressure drop in the medical history; 2. Most of them start when they change from sitting or lying position to upright position; 3. Transient blackness repeatedly appears in the medical history;

4 Carotid artery examination found that there was a high degree of stenosis; 5 Imaging examination found that it was consistent with the monetization of infarction in the watershed area.

2. Symptoms of cerebral infarction in different vascular distribution areas:

Internal carotid artery occlusion syndrome:

◆Transparent blackness or Horner syndrome on the lesion side;

◆Three partial symptoms: contralateral hemiplegia, partial sensory disorder and hemiopia.

The main hemisphere involvement may cause aphasia.

Middle artery occlusion syndrome:

Main trunk occlusion: three partial symptoms; may have conscious disorders; main side involvement has aphasia.

Cortical branches: 1. The upper branch is obstructed with hemiplegia on the opposite side, sensory loss, and the facial and upper limbs are heavier than the lower limbs; 2. The lower branch is obstructed with aphasia, behavioral disorders, and no hemiplegia.

Deep penetration: Contralateral central upper and lower limb equal hemiplegia and aphasia.

Anterior cerebral artery occlusion syndrome:

Main trunk occlusion: 1. Contralateral central surface, tongue paralysis and hemiplegia, light upper limbs; 2. Urinary retention or urgency; 3. Mental disorders, strong grip and sucking reflex; 4. Aphasia;

Cortical branches: 1. Countermeasures: central paralysis mainly in the distal lower limbs with sensory disorders; 2. Transient ataxia in the contralateral limbs, symptoms of strong grip reversal myopia, etc.

Deep perforation: contralateral central surface, lingual paralysis and proximal upper limb paralysis;

Posterior cerebral artery occlusion syndrome:

Main trunk occlusion: three partial symptoms, anatomy and thalamic syndrome.

Cortical branch: homogeneous hemiopia or quadrant blindness.

Deep penetration:

red nucleus thalamic syndrome or thalamic syndrome;

Weber syndrome;

Benedikt syndrome.

Vertebral artery occlusion syndrome:

Main trunk occlusion: extensive brainstem infarction, brain nerves, pyramidal tract signs, and cerebellar symptoms.

Basilar artery apical syndrome: 1. Syndromes mainly manifested in midbrain damage such as abnormal pupils of ocular motor machines; 2. Disabling consciousness; 3. Contralateral hemiopia or cortical blindness; 4. Severe memory disorders, etc.

Midbrain occlusion:

Midbrain ventral syndrome or Benediklt syndrome.

Medial ponsor syndrome: ipsilateral gaze paralysis, peripheral facial paralysis, and contralateral hemiplegia.

lateral ponsil syndrome: facial nerve paralysis, contralateral limb paralysis,

Ponchial branch occlusion: expansion, facial nerve paralysis, contralateral limb paralysis.

Obstructive syndrome of posterior inferior cerebellar artery or vertebral artery:

lateral medulla oblong syndrome: manifested as: 1 dizziness, vomiting, nystagmus; 2 sensory disorders on the ipsilateral and contralateral hemibody; 3 ataxia

4. Hoarseness, dysphagia, pharyngeal reflex disappears; 5. Horner's sign on the ipsilateral side.

◆Atlantic syndrome: clear consciousness, quadriplegia change, unable to speak or swallow, and can indicate with eyes.

Cerebellar infarction:

Due to occlusion of the upper and lower cerebellar arteries, dizziness, nausea, vomiting, nystagmus, ataxia, instability in standing, decreased muscle tone, etc. Brain stem compression and increased intracranial pressure may also occur.

symptom.

Auxiliary inspection:

Blood biochemical examination: abnormalities such as blood sugar, blood lipids, etc. can be found.

Electrocardiogram, echocardiography: Check the heart condition for embolics and their lesions.

Brain CT or MRI: It can clarify the nature and location of stroke and other related conditions.
To be continued...