What Is Ischemic Vascular Disease?

Ischemic cerebrovascular disease, also known as ischemic cerebral diseases, is a general term for different degrees of ischemic cerebrovascular disease.

Basic Information

nickname: Cerebral ischemic disease
English name: ischemic cerebrovascular disease
English alias: ischemic cerebral diseases

Visiting department: neurosurgery
Common causes: Vascular wall disease, changes in blood composition, and hemodynamic changes
Common symptoms: Monocular vision loss, contralateral hemiplegia, numbness, and blindness

Classification of ischemic cerebrovascular disease

Its clinical types include:

1. Transient ischemic attack (transientischemicattack, TIA)

It is a transient loss of nerve function caused by ischemia and completely recovered within 24 hours.

2. Reversible ischemic neurological deficit (reversible ischemicneurologicdeficit, RIND)

It is a type of local neurological deficit that lasts for more than 24 hours (the boundary with TIA), but fully recovers within 3 weeks; neurological examination can reveal positive signs of focal neurological deficit, and there may be a small range of cerebral infarction.

3. Progressive stroke (PS)

Cerebral ischemia symptoms gradually develop and worsen, reaching a peak after more than 6 hours, and infarcts appear in the brain, which mostly occur in the vertebral-basal artery system.

4. Complete stroke (CS)

Peak within minutes to 1 hour after onset, no later than 6 hours (limit with PS).

5. Marginal zone (watershed area) infarction (watershedinfarction, WI)

It accounts for about 10% of cerebral infarction. It is mostly adjacent to the peripheral areas where blood vessels are distributed. The most obvious is between MCA and PCA subdivisions. It can also be seen between the main blood vessels of the cerebellum (such as PICA and AICA). Between branches of the same aorta.

6. Lacunarinfarction (LI)

It is a cerebral infarction with a diameter ranging from 3 to 20 mm caused by a single terminal perforating artery occlusion in the brain parenchyma, accounting for 12% to 25% of all cerebral infarctions. It is mostly located in the basal ganglia, and is rare in the thalamus, inner capsule and deep white matter. No symptoms or stroke-like symptoms.

Causes of ischemic cerebrovascular disease

Ischemic cerebrovascular disease (ICVD) has a variety of etiologies and complex pathological mechanisms, but different etiologies may involve three basic pathological processes: vascular wall lesions, changes in blood components, and hemodynamic changes. All factors that affect the structure and function of blood vessel walls, blood composition, and hemodynamics may be the cause of ICVD. The main diseases are: hypertension atherosclerosis; atherosclerosis; arteritis; dysplasia of arterial muscle fibers; vasospasm; other: vascular abnormalities (arteriovenous malformations, abnormal cerebral basal vascular network disease, subclavian Arterial stealing syndrome), heart disease (valvular disease, endocarditis, cardiac myxoma), hematological diseases (malignant lymphoma vascular lesions, erythrocytosis), etc. can cause cerebral ischemic diseases.

Clinical manifestations of ischemic cerebrovascular disease

Intracranial internal carotid artery system

(1) Proximal occlusion of the ophthalmic artery does not cause blindness, but occlusion of the distal branch of the middle retinal artery can cause monocular vision loss or blindness.

(2) The posterior communication artery (PComA), the larger branch of which is the distribution area of the premammary artery, is characterized by repeated speech, indifference, lack of initiative, loss of orientation, and mild to moderate sensory and motor disorders, which can also occur in half. Lateral neglect and spatial disorientation syndrome.

(3) Anterior choroidal arteries (AChA) are mainly manifested as contralateral hemiplegia, numbness and blindness.

(4) Anterior cerebral artery (ACA) ACA is occluded proximally and AComA blood supply is limited. Cortical and subcortical infarcts may occur (motor aphasia in dominant hemispheres, contralateral neglect in non-dominant hemispheres), and deep perforator supplies Deep brain tissue damage (difficulty in articulation and behavioral disorders); ACA involving the distal segment of AComA may have contralateral sensory and motor disorders, lower limbs are heavier than upper limbs, eyes and head turn to the diseased side, and those with dominant hemispheres may have speech failure Non-dominant hemispheres may have apraxia and loss of spatial sensation syndrome. Contralateral hypertonia is common and signs of primitive reflexes or frontal lobe release appear. Bilateral frontal lobe lesions can cause urinary incontinence and cognitive changes.

(5) There are 2 to 5 perforating branches of the anterior communicating artery (AComA) , which can cause some memory disorders after occlusion.

(6) Contralateral hemiplegia, hemiplegia, and isotropic hemianopia occur in the main embolism of the middle cerebral artery (MCA) . Aphasia occurs in dominant hemispheres, and body disturbances, spatial apraxia and neglect may occur in non-dominant hemispheres. May have head and eye turning to contralateral, contralateral staring paralysis.

(7) When the internal carotid artery (ICA) collateral circulation (such as AComA, etc.) is poor, ICA occlusion can cause cerebral infarction in MCA and ACA blood supply areas, and those with contralateral A1 dysplasia may have bifrontal cerebral infarction with constant Occipital lobe infarction may occur in those with embryonic posterior cerebral arteries. Patients often have hemiplegia, hemiplegia, and blindness, often have a coma and have a poor prognosis.

2. Intracranial vertebrobasilar system

(1) Anterior spinal artery occlusion causes anterior spinal cord syndrome, with contralateral hemiplegia and ipsilateral tongue weakness, with loss of contralateral proprioception and vibration.

(2) Proximal inferior cerebellar artery (PICA) occlusion or vertebral artery occlusion can produce dorsal lateral medulla oblongata syndrome (Wallenberg syndrome): ipsilateral Horner syndrome involving the descending sympathetic fibers, involving the spinal tract and the ascending trigeminal system Pain and temperature changes in the ipsilateral and contralateral torso, nausea, vomiting, dizziness, and nystagmus involving the vestibular nucleus, hoarseness and difficulty in swallowing the nucleus of the suspected nucleus or nerves XI and X, rare facial muscle weakness and hearing Loss or eye movement disorders.

(3) Involvement of the level of the central perforating branch beside the vertebral artery (VA) may lead to medial medullary syndrome, which is manifested by weakness of the contralateral limbs and ipsilateral tongue, with decreased contralateral proprioception and vibration.

(4) Similar to lateral lateral medullary syndrome during ischemia of the anterior inferior cerebellum (AICA) , with nausea, vomiting, dizziness, nystagmus, loss of pain and temperature sensation on the ipsilateral and contralateral sides of the trunk, and ataxia on the ipsilateral side. Rare; peripheral facial paralysis, deafness, tinnitus, and lateral gaze paralysis can be distinguished from PICA (Wallenberg) syndrome.

(5) Occlusion of the superior cerebellar artery (SCA) can cause contralateral detached sensory sensation, affecting the face, arms, trunk, and legs, and may have Horner syndrome and epicondylotic myoclonus, ipsilateral or contralateral hearing loss, and May have gaze disorders, dizziness, nausea, vomiting, nystagmus, ipsilateral ataxia, and ipsilateral upper limb tremor.

(6) The most common signs of bilateral basilar artery (BA) VA infarction at the junction of the bridge extension are bilateral and often develop in steps over a period of hours or days. The patient appears lethargic or has a significant decrease in consciousness, more laterally. Lesions in the midbrain area can appear "locked up", and progressive infarction of BA often causes patient death.

(7) Occlusion of the posterior cerebral artery (PCA) cerebral foot branch may cause BA apex syndrome (abnormal visual and eye movements and altered consciousness); vertical girth artery occlusion with limited vertical gaze.

Ischemic cerebrovascular disease examination

Medical history

(1) Onset of sudden neurological dysfunction is most common in cerebral ischemic stroke, and a small number of patients are accompanied by sudden disturbances of consciousness.

(2) Duration and frequency of symptoms TIA is a recurrent, transient, reversible local cerebral blood circulation disorder, which generally does not exceed 24 hours.

(3) Accompanying symptoms and causes include history of heart valve disease, no seizures and infections.

(4) Previous history of hypertension heart disease, hematological diseases, diabetes, etc., smoking, obesity, oral contraceptives and alcohol abuse.

2. Physical examination

(1) Examination of vital signs such as bilateral blood pressure, respiratory rhythm and amplitude, heart rate, heart rhythm and presence or absence of murmurs, and monitoring of intracranial pressure.

(2) Fundus examinations such as thinning of fundus arteries, enhanced reflection or arteriovenous notches, and cholesterol emboli.

(3) Nervous system examination

3. Special inspection

(1) CT (electronic computed tomography), MRI (magnetic resonance imaging), PET (positron emission computed tomography) and (TCD transcranial Doppler) can be used to detect cerebral ischemic damage, such as infarcted Site, range, hemodynamic changes, and changes in brain metabolism.

(2) DSA (digital subtraction angiography), MRA (magnetic resonance angiography) and CTA (CT angiography) can be used to identify the cause of cerebral ischemia, such as intracranial and extracranial arterial stenosis, thrombus or embolism, cerebral arterioles Sclerosis, etc .; Because the most common cause of cerebral ischemic stroke is atherosclerosis of the internal carotid artery, DSA is the best test method.

Diagnosis of ischemic cerebrovascular disease

Assessment and diagnosis include: medical history and signs, imaging studies, laboratory tests, disease diagnosis, and etiology typing.

Ischemic cerebrovascular disease treatment

Medical treatment

(1) The most common cause of TIA is the loss of emboli in the heart. Early anticoagulation therapy should be performed. Warfarin is orally administered for 2 to 6 mg for the first time, and the maintenance amount is 2 to 8 mg. The treatment can be stopped for at least six months. After treatment with aspirin.

(2) Control of hypertension.

(3) Treatment of abnormal blood components, such as hyperglycemia and hyperlipidemia.

2. Surgical treatment

(1) Alternative surgery for external carotid artery stenosis : Carotid artery thrombectomy (CEA). Angioplasty, or autogenous saphenous vein bypass, or artificial blood vessel transplantation. Carotid artery bypass is only applicable to those with complete occlusion of extracranial arteries. Fogarty catheter method is an alternative method that can not be used in the arterial bypass surgery.

(2) Alternative surgery for occlusive stenosis of intracranial arteries : Extracranial-intracranial arterial anastomosis is commonly used with superficial temporal artery and middle cerebral artery (STA-MCA) anastomosis, occipital artery-inferior cerebellar artery (OA- PICA) anastomosis. (pedicled or free) Omentum intracranial transplantation (IOT) is suitable for those who have ligated or occluded the external carotid artery, or the intracranial artery is too small for arterial anastomosis. Temporal muscle brain attachment is suitable for those who are unable to undergo intracranial transplantation of the omentum. Intracranial arterial thrombectomy is suitable for cases of intracranial internal carotid artery or MCA main embolism, and the onset time is less than 24 hours.