Cerebral vasospasm

Introduction Cerebral vasospasm: Arteriosclerotic plaque of the internal carotid artery or vertebral-basal artery system narrows the vascular lumen and presents eddy currents. When the eddy current accelerates, the blood vessel wall is stimulated to cause vasospasm and a transient ischemic attack occurs, and the symptoms disappear when the vortex decelerates. However, some scholars believe that due to the special nature of the cerebral vascular structure, it is not easy to occur. However, most scholars believe that vasospasm can undoubtedly occur in the internal carotid artery and the cerebral artery ring, cerebral angiography can be seen in the aortic stenosis; subarachnoid hemorrhage can cause extensive and focal cerebral vasospasm; brain surgery on the brain When the aorta is operated, the diameter of the artery is significantly thinned. Therefore, cerebral arterial spasm can also be caused by persistent hypertension, local injury or microparticle stimulation, and cause transient ischemic attack.

Cause

Emotional fluctuations, angry excitement, psychological disorders, stress is the most common cause of cerebral vasospasm. Most of the patients are students, especially high school entrance examination students, intense study life, lack of sleep time, no chance to relax, most likely to occur Cerebrovascular spasm, insomnia can also cause cerebral vasospasm. For young women, the incidence of mental workers is relatively high.

The mechanical stimulation of the blood vessel wall; the compression of blood clots, vascular dystrophy and other damage caused by the destruction of the vascular wall structure, the oxidation of oxyhemoglobin into methemoglobin and the release of oxygen free radicals, and other various vasoactive substances, such as 5-HT The vasoconstriction of catecholamines, hemoglobin and arachidonic acid metabolites, increased intracranial pressure and excessive dehydration without timely supplementation of blood volume, as well as vascular wall inflammation and immune response. In addition, the balance of sympathetic and parasympathetic, and the self-regulation mechanism of cerebral blood flow are also hot topics of research.

May be due to hematoma or blood clots, mechanical traction and compression of the skull base artery, the neurotransmitter released by the hypothalamus changes the sympathetic tone, and cerebral vasospasm is caused by nerve reflex. Increased vasoconstrictor substances in body fluids, such as thromboxane A2, catecholamines, angiotensin and other serotonin increase are the main causes of delayed cerebral vasospasm. Cerebral vasospasm is the main cause of disability and death of subarachnoid hemorrhage. Therefore, rescue treatment should be actively carried out.

Simple cerebral vasospasm refers to the abnormal contraction state of the cerebral artery over a period of time. It is a functional disease, that is to say, the disease is caused by various factors, cerebrovascular dysfunction, and there is no substantial damage or pathological damage to the cerebral blood vessels. Most of the patients are young people, and the self-regulation ability is better, so the prognosis is good, most of them. After treatment and relaxation, the patient can recover completely. The disease does not occur with hemiplegia and psychotic abnormalities.

However, if combined with intracranial aneurysms, or cerebral arteriosclerosis, high blood pressure and other diseases, it is easy to cause cerebral hemorrhage, if not treated in time, there may be paralysis or other nervous system symptoms or even life-threatening.

an examination

Common diagnostic methods for cerebral vasospasm include CT, digital subtraction angiography (DSA), and transcranial Doppler flow analysis (TCD).

CT diagnosis found that SAH accuracy rate of more than 99%, but the detection rate of aneurysm and cerebrovascular malformation is only 34%, so it can not be the only means of etiological diagnosis.

Clinically, the severity of cerebral vasospasm can be estimated based on the amount of bleeding displayed by CT, ie Fischer grading. According to the standard, grade 0 is no bleeding, the incidence of cerebral vasospasm is about 3%, grade 1 is only see basal cell hemorrhage, vasospasm incidence is 14%, grade 2 is peripheral cerebral pool or lateral fissure pool hemorrhage, vasospasm The incidence rate was 38%. Grade 3 was extensive SAH with intracerebral hematoma. Grade 4 was thicker in the basal and peripheral cerebral pools and lateral fissure pools. The corresponding incidence of vasospasm was more than 50%.

Whole cerebral angiography has a high positive rate of aneurysm and cerebral vascular malformation, which can clearly show the branches of the cerebral vessels, the size of the aneurysm or the shape distribution of the deformed blood vessels, providing a reliable and objective basis for treatment. It is used as a gold standard for judging cerebral vasospa However, there are certain disadvantages, such as being an invasive examination, and the price is relatively expensive, the operation is complicated, and sometimes it is not accepted by the patient.

TCD is also a good method to monitor cerebral vasospasm after SAH. In particular, it can be monitored multiple times in one day. Dynamic observation of cerebral hemodynamic changes after SAH is of great value in the diagnosis and prognosis of cerebral vasospasm. The basic principle is to estimate the degree of lumen stenosis by changes in blood flow velocity. The most important detection site is usually bilateral MCA, and the blood flow of the internal carotid artery of the extracranial segment can also be monitored.

The normal MCA blood flow velocity is 30~80 cm/s. The diagnostic criteria for general cerebral vasospasm is blood flow velocity over 120 cm/s. The advantages of TCD are simple operation, low price, no trauma to patients, but indirect diagnosis of cerebral vasospasm by blood flow velocity, high specificity and relatively low sensitivity. Therefore, it has been proposed that the standard for diagnosis of vasospasm from TCD is 120. The cm/s is reduced to 80 cm/s. If vasospasm is suspected, TCD is continuously performed during the entire treatment period. For microvascular spasm, a new detection method, orthogonal polarization spectrum imaging, has emerged. This method can qualitatively and quantitatively analyze the microcirculation of the cerebral cortex. The related literature reports that the capillary density can be significantly reduced in the early stage of SAH, and vasospasm occurs in the cerebral cortex arterioles and arterioles.

In the early stage of SAH, 55% of patients develop segmental microvascular spasm, and the diameter of the blood vessels can be reduced by up to 75%, which can cause clinical symptoms and ultimately affect clinical outcomes. Based on the above findings, the authors believe that early SAH, even if cerebral angiography or TCD has not found vasospasm, should start treatment as soon as possible.

Differential diagnosis

Differential diagnosis

First, focal epileptic seizures of various types of focal seizures have similarities with TIA, such as epileptic seizures or motor seizures are easily confused with TIA. Tension-free seizures are similar to those of a trip. It is more convenient to perform 24-hour EEG Holter monitoring. If there is focal epileptic discharge, it can be diagnosed as epilepsy. If there is no abnormality, it is considered as TIA. CT or MRI findings have focal non-infarct lesions in the brain and may also be considered epilepsy.

Second, Meniere's disease has a long duration of vertigo (up to 2-3 days), accompanied by tinnitus, hearing loss after multiple episodes, and no other signs of nervous system localization.

Third, before the syncope, there are many eyes black, dizziness and unstable standing, accompanied by pale, cold sweat, fine pulse and blood pressure drop, and transient disturbance of consciousness but quickly recovered after falling to the ground, and no nerve positioning Signs. More than an upright position occurs.

Fourth, migraine attacks in adolescence, often family history, episodes of unilateral headache, vomiting and other autonomic symptoms, less focal neurological loss, seizure time is also longer. Regardless of the factors, TIA should be considered as an important risk factor for complete stroke, especially in the short-term repeated authors. The disease can be relieved by itself, and treatment focuses on preventing recurrence.

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