Causes of an aneurysm

Arterial brain aneurysms are one of the most common causes of non-traumatic intracranial hemorrhages. According to V.V. Lebedeva et al. (1996), the incidence of spontaneous subarachnoid hemorrhage ranges from 12 to 19 cases per 100 000 population per year. Of these, 55% are due to rupture of arterial aneurysms. It is known that about 60% of patients with ruptured arterial aneurysms of the brain die on the 1-7th day after bleeding, i.e. In the acute period of subarachnoid hemorrhage. With repeated aneurysmal bleeding, which can occur at any time, but most often on the 7-14th and 20-25th days, lethality reaches 80% or more.

Arterial aneurysms are more often ruptured in people aged 20 to 40 years. The ratio of the frequency of subarachnoid hemorrhage in women and men is 6: 4 (WU Weitbrecht 1992).

Aneurysms of the arteries of the brain were known in ancient times. In the XIV century. BC. E. Ancient Egyptians met with diseases, currently treated as "systemic aneurysms" (Stehbens W. E.1958). According to R. Heidrich (1952, 1972) the first reports of an aneurysm made Rufus from Ephesus about 117 BC. E., R. Wiseman (1696) and T. Bonet (1679) suggested that the cause of subarachnoid hemorrhage could be an intracranial aneurysm. In 1725, JDMorgagni at the autopsy discovered a dilatation of both posterior cerebral arteries, which was interpreted as an aneurysm. The first description of an unexploded aneurysm was given by F. Biumi in 1765, and in 1814, J. Blackall first described the case of an exploded aneurysm of the terminal section of the basilar artery.

Diagnosis of arterial cerebral aneurysms received qualitatively new opportunities after the introduction in 1927 of Egaz Moniz of cerebral angiography. In 1935, W. Tonnis first reported carotid angiography of the anterior aneurysm of the anterior connective artery. Despite the long history of studying this issue, active surgery of arterial aneurysms began to develop only in the 30's. In 1931, W. Dott produced the first successful operation for the ruptured aneurysm of the segment. In 1973, Geoffrey Hounsfield developed and implemented a computed tomography technique that greatly facilitated the diagnosis and treatment of subarachnoid hemorrhages of any etiology.

Over more than sixty years, the doctrine of aneurysms has changed many times and has now reached a certain perfection. Aneurysm surgery is so developed that it has made it possible to reduce the lethality in surgical treatment from 40-55% to 0.2-2%. Thus, the main task at the present time is the timely diagnosis of this pathology, the provision of urgent specialized examination and treatment of patients.

[1], [2], [3], [4], [5], [6]

Theories explaining the causes of an aneurysm

The most recognized theory explaining the causes of an aneurysm is the Dandy-Paget theory, according to which aneurysms develop due to an irregular formation of the arterial wall in the embryonic period. Characteristic for the morphological structure of aneurysms is the lack of a normal three-layered structure of the wall of the altered portion of the vessel - the absence of the muscle layer and the elastic membrane (or its underdevelopment). In most cases, an aneurysm is formed by 15-18 years and is a sac communicating with the lumen of the artery, in which it is possible to identify the neck (the narrowest part), the body (the most widened part) and the bottom (the thinnest part). The bag is always guided by the blood current taking on the main pulse of the pulse wave. Due to this, arterial aneurysms are constantly stretched, increase in size, and its wall is thinned and, as a result, torn. There are other factors that lead to the development of aneurysms - degenerative diseases of the person, arterial hypertension, congenital malformations, atherosclerotic damage to the arterial wall, systemic vasculitis, mycoses, craniocerebral trauma, which in total make up 5-10%. In 10-12% of cases, the cause of the disease can not be established.

W. Forbus in 1930 described the so-called defects of media. In his interpretation, they represent congenital malformations of the muscular membrane in the form of its absence on a small segment of the artery, just in the branching region. However, it soon turned out that media defects can be found in almost all people and almost in any arterial fork, while aneurysms are encountered immeasurably less.

In recent years, the team of scientists of the Russian Neurosurgical Institute. A. Polenova (Yu.A. Medvedev et al.) Proved that the segmental (metameric) structure of the muscular apparatus of the arterial circle of the large brain plays a decisive role in the occurrence of the aneurysmal sac. The segments are connected by means of a specialized ligament apparatus represented by a fibrous elastic ring. An aneurysm is formed on the basis of stretching of the articulation of segments due to hemodynamic causes, which indicates their acquired nature. The rate of aneurysm formation is unknown.

The number of aneurysms is divided into single and multiple (9-11%). In size - miliary (2-3 mm), medium (4-20 mm), large (2-2.5 cm) and giant (more than 2.5 cm). According to the form of aneurysms, they are prosovid, saccular, in the form of a fusiform extension of the artery wall, spindle-shaped. The primary localization of arterial aneurysms is the anterior parts of the Vilisian circle (up to 87%).

The causes of development of arteriovenous malformations

Peculiarities of the pathomorphology of arteriovenous malformations are explained by the violation of cerebral vascular embryogenesis at the earliest stages of fetal development (4 weeks). Initially, only a capillary system is formed. Then part of the capillaries dissolves, and the rest under the influence of hemodynamic and genetic factors are transformed into arteries and veins. Vessel development occurs capillary-fugally, i.e. In one direction, the arteries grow from the capillary, and in the opposite direction, the veins. It is at this stage that AVMs are formed. Some of them arise from capillaries to be resorbed, but for whatever reason preserved. Of these, a tangle of pathological vessels that only remotely resembles arteries and veins develops. Other arteriovenous malformations are formed due to agenesis of the capillary system or delay of the directly premodial connections between arteries and veins. They are represented mainly by arteriovenous fistulas, which can be single or multiple. Both described processes can be combined, giving a wide variety of AVM.

Thus, three variants of morphogenesis are possible:

1. preservation of embryonic capillaries, from which the intertwining of pathological vessels develops (plexiform AVM);
2. complete destruction of the capillaries with preservation of the connection between the artery and the vein gives the formation of fistular AVM;
3. partial destruction of capillaries leads to the formation of mixed AVM (plexiform with the presence of arteriovenous fistulas).

The latter species occurs most often. Proceeding from the above, all AVM can be characterized as local sets of numerous metamorphotic vessels, anomalous in number, structure and functions.

The following morphological variants of malformations are distinguished:

1. Actually AVM - a tangle of pathological vessels with a lot of fistulas, having a spider or wedge shape. Between the loops of the vessels and around them is located the gliazed brain tissue. They are localized in any layer of the brain and anywhere. Wedge-shaped or conical AVMs always point to the ventricles of the brain with their apex. They are also called spongy. In 10% of cases, they are combined with arterial aneurysms. Separately, fistular AVM or racemose isolates are isolated. They have the form of vascular loops piercing the brain substance.
2. Venous malformations arise from agenesis of the connective venous segment. They look like an umbrella, jellyfish or mushroom. The veins are surrounded by a normal brain tissue. More often such malformations are localized in the cortex of the cerebral hemispheres or the cerebellum.
3. Cavernous malformations (cavernomas) arise as a result of sinusoidal changes in the capillary-venous system. Externally reminiscent of honeycomb, mulberry or raspberry. In the enlarged cavities blood can circulate, and can practically stand still. There is no inside cerebral cavernous substance, but the surrounding brain tissue undergoes gliosis and can contain hemosiderin due to diapedesis of the formed blood elements.
4. Teleangiectasias arise due to the expansion of capillaries. Localized most often in the varioly bridge, macroscopically reminiscent of petechiae.

In addition, as a variant of arterial malformation, some authors consider Moya-Moya's disease (in the translation from Japanese - "cigarette smoke"). This pathology is a congenital multiple stenoses of the main arteries of the base of the skull and brain with the development of a variety of pathological collateral vessels that have the form of spirals of various diameters on the angiogram.

Actually AVM macroscopically represent vascular coils of different sizes. They are formed due to a disorderly interlacing of vessels of different diameter (from 0.1 cm to 1-1.5 cm). The thickness of the walls of these vessels also varies widely. Some of them are varicose, they form lacunas. All vessels of AVM have a similarity with arteries and veins, but can not be attributed to either, or to others.

AVM is classified by location, size and hemodynamic activity.

By localization AVM are classified according to the anatomical divisions of the brain in which they are located. In this case, all of them can be divided into two groups: superficial and deep. The first group includes malformations located in the cerebral cortex and the white matter before it. The second group - AVM, located in the depths of the brain's gyri, in the cortical ganglia, in the ventricles and trunk.

According to the size, micro-computers (up to 0.5 cm), small (1-2 cm in diameter), medium (2-4 cm), large (4-6 cm) and giant (more than 6 cm in diameter) are distinguished. It is possible to calculate AVM as the volume of an ellipsoid (v = (4/3) 7i * a * b * c, where a, b, c are the semiaxes of the ellipse). Then small AVMs have a volume - up to 5 cm ³, medium - up to 20 cm ³, large - up to 100 cm ³ and giant or widespread - over 100 cm ³.

There are AVM in hemodynamic activity. Active MMAs are mixed and fistulous. Inactive - capillary, capillary, venous and individual types of cavern.

Hemodynamically active AVMs are well contrasted on angiograms, and inactive during normal angiography may not be detected.

From the point of view of the possibility of radical surgical removal, AVM can be divided into silent zones of the brain, functionally important areas of the brain and the middle line, which include the AVM of the subcortical ganglia, the scab of the brain, the variolium bridge and the medulla oblongata. In relation to the brain, its shells and skull bones, AVM intracerebral, extracerebral (AVM of the dura mater and AVM of the soft covers of the skull) are isolated and extra-intracerebral.