Intracranial aneurysm

Introduction to intracranial aneurysms Intracranial aneurysm is a kind of tumor-like protrusion of the arterial wall caused by the abnormal enlargement of the cerebral artery lumen. The intracranial aneurysm is caused by the congenital defect of the cerebral artery wall and the increase of intraluminal pressure. Sexual bulging is the first cause of subarachnoid hemorrhage. In the past, people called congenital cerebral aneurysms. In fact, congenital cerebral aneurysms accounted for 70% to 80% of cerebral aneurysms. basic knowledge The proportion of illness: 0.03%--0.05% Susceptible people: no special people Mode of infection: non-infectious Complications: subarachnoid hemorrhage, subarachnoid hemorrhage

Causes of intracranial aneurysms

Congenital factors (35%):

The thickness of the cerebral arterial wall is 2/3 of that of other parts of the body and the diameter of the artery. There is no tissue support around it, but the blood flow is large, especially in the bifurcation of the artery. The middle layer of the wall lacks elastic fibers, and the smooth muscle is less. For hemodynamic reasons, the bifurcation is most susceptible to impact. This is the most common finding in the bifurcation aneurysm, which is consistent with the direction of blood flow impact. There are cracks in the middle layer of the wall and residual embryonic blood vessels. Congenital arterial dysplasia or defects (such as internal elastic plate and middle dysplasia) are important factors in the formation of aneurysms. Congenital dysplasia can not only develop into cystic aneurysms, but also evolve into fusiform aneurysms, patients with aneurysms There is more variation in the Willis ring than in normal people. There is a positive relationship between the development of the proximal anterior cerebral artery and the occurrence of anterior communicating artery aneurysm. The aneurysm is supplied by the developing side of the anterior artery. Aneurysm, also supplying blood to the bilateral anterior arteries, aneurysms often associated with some congenital disorders such as intracranial arteriovenous malformations, aortic arch stenosis, polycystic kidney disease, recessive spina bifida, vasospasm Deposit, the literature there have familial intracranial aneurysm is reported that this is evidence of a congenital causes.

Arteriosclerosis (27%):

Atherosclerosis occurs in the arterial wall, causing the elastic fiber to break and disappear, weakening the arterial wall and not being able to withstand tremendous pressure. The hardening causes arterial vascular occlusion and degeneration of the vessel wall. 40 to 60 years old is a distinct stage in the development of arteriosclerosis, and is also an artery. The age of tumor is good enough to explain the relationship between the two, especially the fusiform aneurysm is related to arteriosclerosis, but also due to congenital arterial dysplasia, late detection of pituitary adenoma patients easier to co-ordinate with intracranial artery Tumor, but whether it is caused by long-term high levels of growth hormone induced arteriosclerosis is still inconclusive.

Infection (15%):

Infections in all parts of the body can be spread in the form of small embolism through the blood to stay in the cerebral artery of the weekend branch, a small number of emboli stay in the arterial bifurcation, skull base bone infection, intracranial abscess, meningitis, etc. will also be outside The square erodes the arterial wall, causing an infectious or fungal aneurysm, and the shape of the infectious aneurysm is irregular.

Trauma (10%):

Closed or open injury to the brain, surgical trauma, direct injury to the arterial wall due to foreign bodies, instruments, bone fragments, etc., or weakening of the wall caused by pulling the blood vessels, forming a true or pseudoaneurysm, a traumatic artery in peacetime The tumor is located in the cavernous sinus of the internal carotid artery. Due to the skull fracture in this part, the intracranial aneurysm caused by the war shrap is 2.5% of the war wound patients; most of it is due to the shrapnel from the wing point (front, top, tibia) Penetrating into the boundary of the sphenoid wing, causing the main branch of the middle cerebral artery, the periorbital artery of the anterior cerebral artery and the ophthalmic artery aneurysm.

Other factors (5%):

In addition, there are some rare reasons such as tumors can also cause aneurysms, abnormal vascular network of the skull base, cerebral arteriovenous malformations, abnormal intracranial vascular development and cerebral artery occlusion can also be associated with aneurysms.

In addition to the above reasons, a common factor is the hemodynamic impact factor. Hashimoto ligates one side of the common carotid artery of the hypertensive rat in the neck, and the aneurysm appears in the anterior communicating artery and the posterior communicating artery on the ligature side. When both common carotid arteries are ligated, aneurysms appear in the posterior cerebral artery and basilar artery. The site of these aneurysms is the site of increased blood flow impact. Clinically, the cerebral artery malformation is removed, and the relevant cranial The internal aneurysm also becomes smaller or disappears. One side of the internal carotid artery supplying the anterior communicating artery aneurysm also supplies both anterior cerebral arteries, while the contralateral anterior cerebral artery is poorly developed at the proximal end, which supports hemodynamics. Factors, young patients with polycystic kidneys to raise blood pressure can also cause aneurysms, and even multiple aneurysms.

In short, the arterial wall has the above-mentioned congenital factors, arteriosclerosis, infection or trauma, plus the impact of blood flow is the cause of aneurysm formation. In the clinic, the following conditions can sometimes be seen to develop into an aneurysm:

1 residual aneurysm pedicle: that is, a small part of the thin wall remains when the aneurysm is clipped.

2 bulging at the bifurcation of the arteries: such as the bulging at the junction of the internal carotid artery and the posterior communicating branch.

3 A part of the arterial wall protrudes outward, which can evolve into an aneurysm in 2 to 10 years.

Pathogenesis

After the occurrence of an aneurysm, it often develops further, and aneurysm enlarges. Hypertension is an important acquired factor that causes the aneurysm to gradually expand. The size of the aneurysm cavity and the neck of the tumor, the direction of the expansion of the aneurysm, etc. There is a certain relationship. After the aneurysm is formed, due to the turbulent state of the intratumoral pressure and blood flow, the tumor wall is damaged, resulting in enlargement and thickening of the tumor cavity, which enlarges the aneurysm and can also form a tumor cavity. Wall thrombosis, expansion of the tumor wall, enlargement of the aneurysm, and formation of a fibrin protective membrane around the aneurysm after the aneurysm rupture, the membrane gradually thickens after 3 weeks, and there is capillary proliferation, forming a new tumor wall. Newborn capillaries can also rupture and hemorrhage. The bleeding is limited to the wall or the wall, which thickens the tumor wall or forms a new tumor wall. The aneurysm gradually expands. This process is also considered as a new mechanism for the formation of giant aneurysms. .

The rupture of the aneurysm is actually only the oozing of the tumor wall. In the case of rupture and bleeding, although the intracranial hemorrhage is common in the direct craniotomy, the aneurysm remains intact and there is no perforation of the aneurysm wall visible to the naked eye. The rupture is different from the imaginary aneurysm rupture (such as intraoperative aneurysm rupture). In this case, the bleeding is very turbulent. The patient often falls into a coma within a few minutes, and the brain stem is quickly killed and hemorrhages. The resulting increase in intracranial pressure and cerebral vasospasm can be used as a counterforce to stop bleeding in the aneurysm, but this can cause ischemic damage to the brain due to insufficient cerebral perfusion pressure. The rupture is often caused by necrosis of the arterial wall, glassy changes, calcification, and eddy currents in the aneurysm. Under the microscope, there is a small necrotic area in the intima of the bleeding artery wall. The cause of this necrosis may be arteries. Insufficient blood supply on the wall, this necrosis causes oozing, not bleeding from arterial perforation, sometimes intramural hemorrhage and infiltration of inflammatory cells and cellulose in the wall, leading to rupture, blood The impact causes small damage to the intima of the aneurysm, and the blood enters the dissection of the tumor wall into the dissection of the tumor wall, forming a division process of the tumor wall, and finally leading to oozing of the tumor wall. In addition, hypertension can increase the tension and tumor in the aneurysm cavity. The wall load accelerates the arteriosclerosis of the tumor wall and increases the likelihood of rupture. The above changes are most pronounced at the top of the aneurysm. It is estimated that approximately 83% of the ruptured aneurysms are at the top of the sac.

Anxiety, nervousness, excitement, sudden increase in blood pressure, urination, exertion, late pregnancy, childbirth, physical labor, sexual life, etc. are only predisposing factors for aneurysm rupture. Many patients have paroxysmal headaches before the bleeding, eye muscles. Paralytic symptoms such as paralysis, diplopia, dizziness, and neck pain indicate that the aneurysm has a pathological change before the rupture. In the presence of the cause, the wall of the aneurysm that has split has ruptured, and the patient with cerebral aneurysm When doing the lowering motion and exerting the stool, the pressure in the aneurysm cavity suddenly increases, leading to rupture. In more cases, the bleeding suddenly occurs without obvious incentives.

After aneurysm rupture and hemorrhage, the hemorrhage is caused by coagulation of blood clots and contraction of vasospasm to achieve hemostasis. In addition, the cerebrospinal fluid promotes the bleeding, and the rupture stops bleeding. After 1 to 2 weeks of hemorrhage, fibrinolysis is hyperactive and the rupture is caused. The fibrous network is fragile and the blood clot is liquefied. Since the fibrosis of the rupture of the arterial wall is not yet firm, rebleeding is prone to occur. In addition, intracranial pressure also has an effect on the re-rupture of the aneurysm. When the intracranial pressure is lower than 3.8 kPa. When a newly bleeding aneurysm is prone to rupture and bleeding again.

Congenital cerebral aneurysms occur in the bifurcation of the cerebral artery and its main branches. About 85% of congenital aneurysms are located in the inner semicircular internal carotid artery system of the Willis arterial ring, ie the intracranial segment of the internal carotid artery, the anterior cerebral artery The anterior communicating artery, the middle cerebral artery, and the posterior part of the posterior communicating artery, in which the siphon of the internal carotid artery occurs most frequently, the anterior cerebral artery and the anterior communicating artery are second, the middle cerebral artery is again, and the incidence of the left and right hemispheres Similar, the right side is slightly more than the left side, wherein the anterior cerebral artery accounts for 4.3% to 9.0%, the anterior communicating artery accounts for 9.6% to 28%; the vertebral artery accounts for 2.3% to 4.6%, and the basilar artery accounts for 1.7% to 8.9%. In the literature, 6570 cases of aneurysms were distributed as follows: 41.3% of internal carotid artery, 26.1% of anterior communicating artery, 20.4% of middle cerebral artery, 7.6% of anterior cerebral artery, and 4.6% of vertebral artery.

There was no significant difference in the distribution of aneurysms between the autopsy report and the clinical statistics. Some autopsy statistics showed that the internal carotid artery accounted for 26%, the middle cerebral artery accounted for 39%, and the anterior cerebral artery and anterior communicating artery accounted for 24%. The vertebral-based artery Accounted for 8%, other parts accounted for 3%, the aneurysm of the posterior half of the basilar artery ring accounted for 3% to 16%. In the past, because the vertebral-based angiography was not comprehensive, the incidence was low, and now 4 are widely used. In angiographic cases, the incidence of vertebral-based aneurysms accounts for about 15% of all cerebral aneurysms.

If the arterial wall has an asymmetrical cystic dilatation, which is called a saccular aneurysm, a small saccular aneurysm with a neck stenosis is also called a berry aneurysm, and most congenital aneurysms are saclike. Or berry-like, can also be small nodular, called lobulated aneurysm, other forms have gourd-like, globular, sausage-like, etc., the tumor wall is generally smooth as a sac, most of which consist of congenital weak blood vessel wall, Often located in the bifurcation of the larger artery, the aneurysm is narrower than the junction of the artery, called the neck (pedicle) or the base, the width of the neck is very inconsistent; the most prominent part of the far side opposite the neck is the bottom of the tumor (Top), the part between the neck of the tumor and the base of the tumor is called the tumor (capsule), and the small sputum is a small bulge on the tumor sac, often the rupture of the aneurysm or the ruin after rupture.

The thickness and length of the aneurysm neck determine the shape of the aneurysm. The neck of the tumor is sometimes long, causing the aneurysm to hang from the side of the artery in a lantern shape. Sometimes the neck is thick and short, causing the aneurysm to protrude from the artery wall. One side; sometimes the neck is completely absent, that is, when the diameter of the neck and the artery is close to or greatly exceeds its diameter, especially a large aneurysm, part of the wall of the artery is directly involved in the composition of the neck, aneurysm The thickness difference of the wall is also larger. The thicker is similar to the main artery. The thinner can only have one inner membrane. The tumor base is often the weaker aneurysm. The bottom wall is prone to degenerative changes and is directly affected by blood flow. Impact, easy to damage, therefore, the greatest chance of rupture here (64%), lobulated or gourd-like aneurysms are more likely to rupture, a few cases can be in the tumor (10%) or tumor neck (2%) When rupture, the bottom of the tumor is most likely to adhere to the surrounding tissue. The direct operation of the tumor should be contraindicated to prevent the rupture of the aneurysm. The aneurysm often has different degrees of thrombosis. The blood clot is often layered and tight. Adhered to the tumor wall, which is clinically cerebral blood An important cause of aneurysm cannot be found during tube angiography. In rare cases, the aneurysm cavity is completely filled with blood clots, which is called the natural healing of an aneurysm. This is a rare condition.

The size of congenital aneurysms is very large, usually 0.5 ~ 2cm, small must be seen with a magnifying glass, no clinical symptoms before rupture, can be found in autopsy, large to reach the size of oranges, and produce obvious Occupation performance, the literature reported that the aneurysm diameter can reach more than 8cm, the largest diameter is 12cm, most of the aneurysms that can produce symptoms are 0.7-1.0cm in diameter, and the diameter less than 0.3cm rarely produces symptoms, more accidental It is found that the rupture of the aneurysm has a certain relationship with its size. The aneurysm with less than 0.3cm has less chance of rupture. It is generally considered that the ruptured aneurysm is larger, the unruptured aneurysm is smaller, and the critical size of the aneurysm rupture is 0.5. 0.6cm, the diameter of the aneurysm with a diameter of more than 0.5cm gradually increases. After the diameter exceeds 3.0cm, the symptoms of increased intracranial pressure replace the bleeding symptoms. The larger the aneurysm, the more chance of rupture and bleeding. Because there is often a large amount of stratified blood clots in the cavity of the giant aneurysm, the wall of the tumor is reinforced, so the chance of rupture and bleeding is correspondingly reduced. Large aneurysms can be seen at any age, age. The larger the larger the aneurysm, the higher the incidence of large aneurysms. More than 50% of patients with giant aneurysms are over 45 years old.

The multipleity of congenital cerebral aneurysms, due to the different diagnostic methods used by various scholars, the incidence of reports varies greatly. The incidence of multiple aneurysms in the literature is 4.2% to 31%, generally around 20%. Multiple aneurysms found by autopsy were more reliable than those found by cerebral angiography alone. In 1966, the American Collaborative Group reported that the incidence of multiple aneurysms was 22%, and cerebral angiography was 18.5%. Cerebral angiography and autopsy were 19%. The number of multiple aneurysms was the most common. The number of aneurysms was the highest in the literature. In the multiple aneurysms, 2 aneurysms accounted for 15%. Three of them accounted for 3.5%, and four or more were only 1.5%. The distribution of multiple aneurysms was often in the symmetrical part of the cerebral hemisphere, or multiple aneurysms occurred in different parts of the same artery. The chances are different, with the most internal carotid artery, accounting for 48%, followed by the middle cerebral artery, accounting for 30%. Multiple aneurysms in the anterior cerebral artery and vertebral-basal artery are rare.

The cerebral artery belongs to the muscular artery. The wall is composed of three layers: the inner membrane, the middle membrane and the outer membrane. The inner membrane is composed of a layer of endothelial cells and an inner elastic layer. The middle membrane is composed of a thick layer of muscle rings. Thinner, composed of connective tissue, containing collagen, reticular and elastic fibers. Compared with arteries in other parts of the body, the cerebral arteries have no outer elastic layer, and at the bifurcation, especially at the corners thereof, lacking the middle membrane, only It consists of the inner membrane and the inner elastic layer and the outer membrane. In addition, the larger artery at the bottom of the brain runs in the subarachnoid space and lacks the support of the brain parenchyma. This congenital membrane defect of the cerebral artery starts from the formation of the aneurysm. The intrinsic decisive role, under the long-term effect of blood flow and blood pressure, makes the inner elastic layer slightly protruding, which may be the earliest stage of aneurysm formation, and the intima is often excavated through the defect on the media. The elastic layer can have elastic fiber breakage, and the gap of the middle membrane is enlarged, and the degree of sputum is increased, so that a complete aneurysm is formed.

The aneurysm wall is characterized by a lack of the medial muscular layer. The wall of the aneurysm may only be a layer of intima or a fiber in the elastic layer that breaks or disappears, leaving only the inner and outer membranes. Significant hypertrophy, under the microscope visible muscle layer of the tumor-bearing artery, suddenly interrupted and disappeared at the opening of the neck, the inner and outer membranes were connected by collagen fibers of different thickness, and the endometrium of the tumor wall consisted of one or more layers of vascular endothelial cells and a small amount. Connective tissue and granulation tissue, the outer membrane may have fibrosis, inflammatory cell infiltration and a small amount of hemosiderin-containing phagocytic cells can be seen in the tumor wall shortly after hemorrhage, sometimes see the repair process of the tumor wall, under the intima Connective tissue hyperplasia, fibrous tissue proliferation of the tumor wall, often accompanied by atherosclerotic deposition.

Under the electron microscope, there are characteristic thickening of the basement membrane and loosening between the layers of the aneurysm wall. Many cell debris are visible in the tumor wall, and the elastic layer is lacking or completely disappearing. Sometimes, phagocytic cells containing fat are visible.

In the autopsy cases of aneurysm rupture, it can also be found that the brain parenchyma of each part also has lesions. Different parts of the aneurysm cause brain parenchymal damage in different parts. For example, an aneurysm on the internal carotid artery can cause the lenticular nucleus and the lateral ventricle. Anterior horn, forehead and subventricular cerebral tissue damage, anterior cerebral artery aneurysm can cause damage to the medial and lateral frontal lobes, corpus callosum and caudate nucleus, and middle cerebral artery aneurysms can cause lateral fissure and subcortical lesions. Vertebral-based aneurysms can cause damage to the cerebellar hemisphere and brainstem, including brain tissue necrosis, softening, gliosis, etc. Generally, these lesions occur in the distal region of the aneurysm, and the cause of the above-mentioned damage may occur in the aneurysm. It is caused by rupture of the aneurysm and circulatory dysfunction of the distal branch of the artery and cerebral vasospasm after hemorrhage. In addition, the increase of intracranial pressure and secondary cerebral parenchymal edema and cerebral blood circulation after aneurysm rupture are related to the above damage.

Intracranial aneurysm prevention

Primary prevention refers to the promotion of health and the reduction of risk factors. This first line of defense is to promote the healthy lifestyle of the general population and reduce the harmful factors in the contact environment, so as to completely avoid the occurrence of cancer. In addition to preventing air, water, food and workplace carcinogens and suspected carcinogens, lifestyle changes in smoking, drinking and other bad habits are primary prevention. Pay attention to the prevention of atherosclerosis, prevent the damage of blood vessels caused by infectious diseases, and strengthen the treatment of vascular injuries during traumatic brain injury.

Intracranial aneurysm complications Complications, subarachnoid hemorrhage, subarachnoid hemorrhage

Complications such as respiratory tract, urinary tract, skin, limbs, and joint stiffness may occur.

Intracranial aneurysm symptoms Common symptoms Deficiency nausea Cerebrovascular arteriovenous malformation Cranial hyperplasia Mental disorder Drowsiness olfactory disorder Balance dysfunction Intelligent disorder Frontal sensation Decreased

1. Hemorrhagic symptoms: Aneurysm rupture is the most common cause of subarachnoid hemorrhage. The performance is acute, severe headache, nausea and vomiting, disturbance of consciousness and mental disorders. Meningeal irritation is more common. It can also form intracranial hematoma, which produces hemiplegia and disturbance of consciousness.

2. Non-hemorrhagic symptoms: The aneurysm itself is caused by the compression of adjacent nerves and blood vessels, and is mostly related to the volume and location of the aneurysm. (1) Intra-cervical-posterior communicating aneurysms often cause paralysis of the affected arteries, drooping of the eyelids, enlargement of the pupils, exotropia, and even decreased vision. (2) anterior communicating aneurysm: often causes hypothalamic dysfunction, especially in bleeding, conscious disturbance, intelligent disorder, gastrointestinal bleeding and other manifestations. (3) Middle cerebral artery aneurysms sometimes cause epilepsy and hemiparesis. (4) vertebral basal aneurysms may have asymmetry of limbs, pyramidal tract signs, and even symptoms such as difficulty swallowing and hoarseness.

Examination of intracranial aneurysms

Laboratory inspection

1. Blood routine, erythrocyte sedimentation rate and urine routine : generally no specific change, early stage of aneurysm rupture, white blood cells often exceed 10 × 109 / L, erythrocyte sedimentation rate is often mild to moderately increased, the degree of increase and leukocytosis The degree is consistent, proteinuria and diabetes can occur in the early stage, tubular urine can occur in severe cases, proteinuria lasts for a short period of time, and usually returns to normal after several days.

2. Lumbar puncture: When the aneurysm is not ruptured, there is no abnormal change in the lumbar cerebrospinal fluid examination. In the case of rupture and bleeding, lumbar puncture is the direct evidence for diagnosis of subarachnoid hemorrhage after rupture of aneurysm. The waist wear pressure is mostly 1.96~2.84. kPa, but the time of waist wear is also related to the change of pressure. It is found that after the aneurysm rupture, the intracranial pressure can be rapidly increased to 8.8 to 19.6 kPa. After half an hour, the intracranial pressure drops, and the lumbar cerebrospinal fluid is often bloody. It can be seen that the cerebrospinal fluid contains a lot of red blood cells, and repeated lumbar puncture examination can determine whether the bleeding stops according to the number of fresh and old red blood cells in the cerebrospinal fluid. However, when the intracranial pressure is high, the lumbar puncture should be carefully carried out, and the liquid should be slowly discharged to avoid induction. Cerebral palsy, if there is not much bleeding, and simply break into the brain parenchyma or subdural or subarachnoid adhesion, there is no red blood cells in the cerebrospinal fluid, generally 2h after the bleeding can be found in the cerebrospinal fluid with blood or after centrifugation The liquid turns yellow, and the white blood cells in the initial cerebrospinal fluid are proportional to the red blood cells, that is, there is one white blood cell per 10,000 red blood cells; after 12 hours of bleeding, the white blood cells in the cerebrospinal fluid begin to increase, and the early stage is mainly neutral. In the late stage, lymphocytes are mainly used. After the cerebrospinal fluid turns yellow for 2 to 3 weeks, it returns to normal. Sometimes the lymphocytes can persist for up to 48 days. After 1 to 2 weeks, the red blood cells disappear. After 3 weeks, the cerebrospinal fluid turns yellow. Cerebrospinal fluid The cells in the cells can be found to contain iron cells by special staining. The cells increase after 4 to 6 weeks of bleeding and persist for 17 weeks. This method can still be judged after 4 months of subarachnoid hemorrhage. Bleeding.

Cerebrospinal fluid biochemical examination, sugar and chloride are normal, protein is increased, which is due to the release of a large amount of hemoglobin after red blood cell lysis and bleeding after exudation reaction, usually around 1g / L, some people think that every 10,000 red blood cells in the cerebrospinal fluid dissolve It can increase the protein of 150mg/L. Generally, the protein increase is the largest after 8-10 days after hemorrhage, and then gradually decreases. In addition, attention should be paid to distinguish the blood cerebrospinal fluid caused by lumbar puncture injury, generally the lumbar puncture bloody cerebrospinal fluid, after centrifugation There was no red or yellow change in the upper liquid and no positive reaction to the benzidine.

Film degree exam

1.CT: Although CT scan is not as good as cerebral angiography in determining the existence, size or position of aneurysm, it is safe and rapid, the patient has no pain, does not affect the intracranial pressure, can be used at any time, and can be repeated many times. Follow-up observation, high-resolution CT diagnosis of aneurysms has the following advantages:

(1) Intensive scanning: aneurysms with a diameter of more than 5 mm can be displayed, and the diagnosis rate of the skull base aneurysm can reach 50% to 60%; the CT scan of the giant aneurysm or the intensive scan can be found as an aneurysm There is cerebral edema or brain softening around, which is in a low-density area. The wall of the tumor can be highly dense due to calcification. The intratumoral density is high due to layered thrombus, and the blood flow density in the center of the tumor cavity is different. Therefore, the density is different. The concentric annular image, called the "target ring sign," is a CT feature of a giant aneurysm.

(2) In addition to showing aneurysms, it can also show its associated subarachnoid hemorrhage, intraventricular or subdural hematoma, cerebral infarction, hydrocephalus, etc., and can show the size of hemorrhage, infarction The extent, the degree of hydrocephalus, whether there is rebleeding, etc., thus avoiding repeated lumbar puncture and repeated cerebral angiography.

(3) Multiple aneurysms can be found and can show which aneurysm ruptures.

(4) According to the distribution and density of subarachnoid hemorrhage, the source of bleeding can be estimated. For example, the median cleft and the frontal lobe and intraventricular hemorrhage suggest more anterior communicating artery aneurysm hemorrhage; lateral fissure hemorrhage Middle cerebral artery aneurysm rupture and hemorrhage; temporal lobe hemorrhage may be bleeding of internal carotid artery and middle cerebral artery aneurysm.

(5) can understand the limitations of subarachnoid space and diffuse hemorrhage, predict the occurrence of cerebral vasospasm, such as the subarachnoid space, especially the blood clot or diffuse in the cerebral pool above 3mm × 5mm When the blood is up to 1 mm thick, it is often suggested that severe cerebral vasospasm may occur.

(6) CT scan can dynamically observe the aneurysm in order to grasp the timing of surgery and prognosis in time. However, CT scan can not completely replace cerebral angiography, and finally need cerebral angiography to confirm.

2.MRI scan

(1) In the acute phase of aneurysm hemorrhage, CT scan should be performed first. MRI is difficult to detect very early acute intracerebral hematoma and subarachnoid hemorrhage. However, when high field strength and severe T2-weighted images, MRI can also be found very early. Acute bleeding.

(2) For asymptomatic aneurysms with a small amount of oozing but not ruptured, MRI can be detected and valuable for predicting aneurysm rupture.

(3) MRI is the most valuable for cerebral angiography negative for subarachnoid hemorrhage. Because of its small size, it is a thrombotic aneurysm. It is difficult to fully develop cerebral angiography. MRI can accurately display aneurysms. s position.

(4) MRI is very useful in patients with suspected subarachnoid hemorrhage and negative CT scan because of the T1 and T2 weighted images of methemoglobin released after subacute (less bleeding) and chronic subarachnoid hemorrhage (equal density) Both are high signals.

(5) For multiple aneurysm hemorrhage, CT can show hemorrhage but can not point out the specific aneurysm of hemorrhage. Cerebral angiography is not accurate enough to judge hemorrhagic aneurysm, while MRI can show hemorrhagic aneurysm.

(6) For the old subarachnoid hemorrhage caused by aneurysm rupture, MRI can also show that it is characterized by iron surface deposition on the surface of the brain, that is, a line-like "fringe" shadow on the T2-weighted image, while CT It is not clear whether there has been a subarachnoid hemorrhage or an aneurysm with rupture.

(7) MRI can directly display aneurysms and can display blood flow in the arteries. On the T1 and T2 weighted images, the tumor has no signal, and the aneurysm thrombus has a high signal on the T1 and T2 weighted images. It is a ring-shaped low signal.

(8) The giant aneurysm showed a mixed signal on MRI, that is, there was no signal in blood flow and eddy current, no signal in calcification, high signal in thrombus, and low signal in hemosiderin.

3. Somatosensory evoked potential examination: Somatosensory evoked potential can be recorded when stimulating the median nerve, and subarachnoid hemorrhage and clinical symptoms occur in patients with intracranial aneurysms. The somatosensory evoked potential is significantly different from that of normal people, ie, central conduction time (CCT) Prolonged, its significant prolongation indicates poor prognosis. This difference can be detected 48 hours after surgery. The difference in conduction time between the two hemispheres can also be used to judge the prognosis, but this significant difference should be 48-72 h after surgery. It only appeared, it was smaller than the change of CCT.

4. Doppler ultrasonography : blood supply to the common carotid artery, internal carotid artery, external carotid artery and vertebral basilar artery, blood flow direction and blood flow after ligation of these arteries or intracranial and external arteries can be made estimate.

5. Cerebral angiography

The final diagnosis depends on cerebral angiography (Fig. 2, 3). Any patient with subarachnoid hemorrhage, spontaneous III-IV cranial nerve palsy or posterior group cranial nerve disorder should have cerebral angiography, angiography Show the location, size, shape, number of aneurysms, whether there is thrombus in the capsule, the extent of arteriosclerosis and arterial spasm, the extent, whether there is intracranial hematoma or hydrocephalus, the size of the tumor pedicle and whether it is suitable for clipping, etc. Can also understand the normal and variability of blood vessels, collateral circulation, compression of the contralateral neck carotid artery during one-sided carotid angiography, or compression of the carotid artery during vertebral angiography, can observe the blood supply of the former traffic branch or the posterior traffic branch As a reference for the temporary or permanent blockage of the carotid or vertebral artery during surgery, about 16% of the aneurysms have thrombosis, the aneurysm overlaps with the arterial image, or the aneurysm does not develop the aneurysm, the first blood vessel The angiography is not developed. About 20% of the aneurysms can be redeveloped after re-contrast in a few days or weeks. Therefore, repeated angiography, multiple imaging is sometimes necessary, and should be performed four times (both bilateral carotid and bilateral Vertebral artery In order to avoid missing aneurysm or missing multiple aneurysms, the anterior communicating branch aneurysm is mostly supplied by one side of the anterior cerebral artery. When the contralateral carotid artery angiography is used to compress the side of the carotid artery, the anterior cerebral arteries may be developed. The aneurysm is not developed, so only contralateral carotid artery angiography is performed in this case, and the aneurysm may be missed.

Regarding angiography time, patients with grade III can be angiographically as early as possible. It is generally considered that angiography complications are the least within 3 days after hemorrhage, and increase on the fourth day, the highest in 2 to 3 weeks. The clinical symptoms are grade III to IV and there is suspected intracranial hematoma. Patients should also have angiography as early as possible. Patients with grade V can perform CT or MRI examination to exclude hematoma and hydrocephalus, so as to avoid symptoms of angiography. Others advocate that angiography should be performed as early as possible in order to facilitate early surgery to prevent early surgery. Rebleeding, but angiography within 5h, it is easy to cause rebleeding.

The carotid artery aneurysm is applied to the internal carotid artery aneurysm by direct percutaneous puncture. The success rate of the vertebral artery system due to direct puncture is only 50%, and it is easy to cause arterial spasm. Therefore, percutaneous puncture femoral artery cannulation or Puncture of the brachial artery high pressure injection of drugs is better, in order to avoid the omission of multiple aneurysms, the use of transfemoral cannulation four angiography method, the use of different types of catheters in the perspective of swaying, swaying and other methods Drugs were injected into the common carotid artery, internal carotid artery, external carotid artery and vertebral artery.

In the anterior half of the Willis arterial aneurysm, the conventional arterial angiography is positive, the lateral position, the posterior half of the aneurysm and the Tang's position. In addition, depending on the situation, different oblique positions, skull base and three-dimensional film may be added according to the situation. Etc. to show small aneurysms and tumor pedicles, magnification, subtraction devices and tomographic techniques are also helpful in obtaining a clearer aneurysm radiograph, clearly showing the design of the aneurysm pedicle for the surgical incision, aneurysm The selection of clips and the correct estimation of prognosis are very helpful.

MRA can display the entire cerebrovascular system without the need to inject contrast agents, so there is no risk of injection of contrast agents, nor is it allergic to contrast agents.

Multiple aneurysms are mostly distributed on both sides or in the neck. In the two systems of vertebral arteries, some are distributed on one side, even on one main artery. How to determine which hemorrhage in multiple aneurysms is important in angiography, arteries Irregularities in the shape of the tumor are the most likely to be bleeding, the tumor-bearing arteries or the intracranial hematoma compression, and the aneurysms with adjacent neurological damage should be considered bleeding, MRA plus MRI, or MRA plus CT will be here Provide important help in terms of aspects.

The incidence of angiographic complications is about 1, including hemiplegia, aphasia, vision loss, etc., angiography caused aneurysmal hemorrhage accounted for 0.02% to 0.11%, to 1984 has reported 31 cases, of which 23 cases (68%) died 5 cases of residual neurological disorder (4 cases of hemiplegia, 1 case of oculomotor nerve palsy); 3 cases of normal nervous system, the cause of aneurysm hemorrhage during angiography is the strong push of contrast agent to cause sudden increase of pressure in the cerebral artery, thus the artery Tumor rupture and hemorrhage, as for short-term neck measurement of blood pressure and systemic blood pressure may be due to chemical stimulation of contrast agents, may also be caused by paralysis induced intra-arterial pressure, or may be spontaneous bleeding of the aneurysm and coincidence time.

An angiogram can be performed after the aneurysm is clamped or at the end of the operation. It can be understood whether the tumor pedicle is completely clipped. If the clip is not well, the incision is re-clamped. Only the patient who has the blood supply artery is angiographically observed. To understand whether it is effective or not, the aneurysm can not completely clamp the tumor pedicle due to technical reasons. It can be followed up by angiography. If an aneurysm is formed, it can be embolized in time or surgery. These angiograms can also be replaced by MRA.

Diagnosis and diagnosis of intracranial aneurysms

Unruptured aneurysms with local symptoms or increased intracranial pressure, as well as ruptured bleeding caused by subarachnoid hemorrhage are still required with intracranial tumors, cerebral vascular malformations, hypertensive cerebral hemorrhage, moyamoya disease, craniocerebral injury, blood Disease, spinal cord vascular malformation and other diseases are identified.

diagnosis

1. Acute onset, typical symptoms and signs of subarachnoid hemorrhage.

2. There may be local symptoms such as oculomotor nerve paralysis.

3. Head CT can show hematoma, subarachnoid hemorrhage, CT and magnetic resonance angiography can show aneurysms.

4. Cerebral angiography can confirm the location and morphology of aneurysms.

Intracranial tumor

Aneurysms in the saddle area are often misdiagnosed as saddle area tumors, but the aneurysms in the saddle area do not have spherical enlargement of the sella, lacking the performance of hypopituitarism. Intracranial tumor stroke bleeding is more common in various gliomas, metastases, meningioma. Pituitary tumors, choroid plexus papilloma, etc., increased intracranial pressure and lesion localization signs before hemorrhage, no rebleeding phenomenon, according to CT scan and cerebral angiography can be easily identified.

(1) Astrocytoma: Hypothalamus or optic chiasm astrocytoma also occupy the saddle, but the shape is not like the aneurysm rule, and the enhancement is not as obvious as the aneurysm.

(2) pituitary tumors: growth on the saddle, often in the shape of gourd, aneurysms can have similar performance, but the aneurysm generally no saddle bottom subsidence, the normal pituitary structure is also preserved.

(3) craniopharyngioma: more common in adolescents, when it is a solid mass, and aneurysms may have similar changes, but its calcification is more common, and the intensification is often less obvious than aneurysms.

2. Cerebrovascular malformation : The general patient is younger, the lesion is mostly in the lateral cerebral palsy, the middle cerebral artery distribution area, headache (66%), epilepsy (more than 50%) and progressive limb weakness, intelligence Decreased, intracranial vascular murmur and increased intracranial pressure, more than the performance of cerebral palsy.

3. Hypertensive cerebral hemorrhage: more than 40 years old, with a history of hypertension, sudden onset, severe disturbance of consciousness, may have hemiplegia, aphasia is characteristic, and the bleeding site is mostly in the basal ganglia.

4. Moyamoya disease : the age is mostly under 10 years old and 20 to 40 years old. Children often show cerebral ischemic symptoms with progressive intelligence, adults are mostly cerebral hemorrhagic symptoms, but the disturbance of consciousness is relatively light, cerebral angiography An abnormal vascular network characteristic of the skull base can be seen for identification.

5. Traumatic subarachnoid hemorrhage : can be seen at any age, has a history of head trauma, no abnormalities before injury, may be associated with other craniocerebral trauma, such as scalp laceration and skull fracture.

6. Hematological diseases : leukemia, hemophilia, aplastic anemia, thrombocytopenic purpura, polycythemia caused by subarachnoid hemorrhage, often have clinical manifestations of blood disease before the onset, through blood tests and bone marrow Checking is not difficult to distinguish.

7. Spinal vascular malformation : more than 20 to 30 years old, often with numbness of lower limbs or limbs before hemorrhage, weakness and sphincter dysfunction, multiple unconscious disturbances at the time of onset, severe back pain with acute spinal cord compression, not difficult to identify.

8. Cerebral ischemic diseases: more common in the elderly, often have high blood pressure, high blood lipid history, more in the quiet, the incidence is relatively slow, the clinical symptoms are relatively light, no red blood cells in the cerebrospinal fluid, CT scan shows low brain The density area is enough to distinguish.

9. iatrogenic subarachnoid hemorrhage : anticoagulant therapy, insulin shock and electroconvulsive therapy can cause subarachnoid hemorrhage, identification by treatment history is not difficult.

10. Other diseases: various connective tissue diseases such as multiple nodular arteritis, lupus erythematosus, various inflammations such as encephalitis, meningitis, leptospirosis, tuberculous meningitis, fungal meningitis, Brucella Disease, flu, whooping cough, etc., acute rheumatic fever, severe liver disease, hemorrhagic nephritis, allergic nephritis, depression, etc., can cause subarachnoid hemorrhage, but these causes of subarachnoid hemorrhage are clinically rare, according to these The clinical features of the disease and related tests are not difficult to identify.

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