intracranial artery spasm



Overview of Intracranial Arterial Spasm (IAS)

Intracranial arterial spasm, also known as cerebral vasospasm, refers to atherosclerotic plaques in the internal carotid artery or vertebral basilar artery system that narrow the lumen of the vessel and cause vortexes of blood flow. When the vortex accelerates, the irritation of the vessel wall leads to vasospasm and transient ischemic attack (TIA), and the symptoms disappear when the vortex decelerates. Cerebral arterial spasm can also be induced by persistent hypertension, localized injury, or microparticle stimulation, leading to transient ischemic attacks.

Etiology

1. Mechanical irritants

Including blood clot compression, vascular nutritional disorders, etc., leading to structural damage of the vessel wall; oxidation of oxygenated hemoglobin into methemoglobin and the release of oxygen radicals caused by damage; other vasoactive substances, such as 5-HT, catecholamines, hemoglobin and arachidonic acid metabolite vasoconstriction; increased intracranial pressure, excessive dehydration therapy without timely replacement of blood volume; as well as inflammation of the vascular wall and immune response, etc. Functional factors

2. Functional factors

Cerebral vasospasm alone refers to the abnormal contraction of cerebral arteries over a period of time. It is a functional disease, which means that the disease is caused by various factors of cerebrovascular dysfunction, and there is no substantial damage or lesion of cerebrovascular.

3. Other factors

Emotional fluctuations, anger and excitement, psychological disorders, tension and stress are the most common causes of cerebral vasospasm.

Common diseases

Intracranial aneurysm, pediatric hypoparathyroidism, etc.

Examination

1. Blood and urine routine, blood sedimentation, blood sugar, blood lipid and electrocardiogram should be listed as routine examination items.

2. Cerebrospinal fluid examination.

3. Cerebral angiography.

4. Cranial CT scan.

5. Magnetic resonance imaging (MRI).

6. Positron emission tomography (PET).

Differential diagnosis

1. Focal epilepsy

The manifestations of various types of focal epileptic seizures are similar to TIA, such as epileptic sensory seizures or motor seizures, which are easily confused with TIA.Focal non-infarcted foci in the brain detected by CT or MRI can also be considered as epilepsy.

2. Meniere’s disease

Vertigo attacks are of long duration (up to 2-3 days), accompanied by tinnitus, hearing loss after repeated attacks, and without other neurological localization signs.

3. Syncope

There are black eyes, dizziness and unsteadiness before the disease, accompanied by pale face, cold sweat, thin pulse and drop in blood pressure, and transient impaired consciousness, but recovered soon after falling to the ground, and there is no neurological localization sign. It occurs mostly in the upright position.

4. Migraine

Most of them start in adolescence, often with family history, and the attacks are mainly characterized by phytoneurological symptoms such as migraine, vomiting, etc. Focal neurological loss is less common and the duration of the attacks is also longer.

Treatment principle

Cerebral vasospasm can be treated with vasodilators, sympathetic nerve blockers, endothelin ETAn and ETA/B antagonists. Hypotension or dilatation therapy is ineffective can be used to elevate the pressure of the therapy. In case of ineffective treatment, local injection of opioid and balloon dilatation of spastic vessels can be considered.