Symptoms of aneurysm rupture

All aneurysms of cerebral vessels are anatomically located in subarachnoid cisterns and are washed by cerebrospinal fluid. Therefore, when the aneurysm ruptures, the blood first flows into the subarachnoid space, which is a distinctive feature of aneurysmal hemorrhage. Parenchymal hemorrhages with the formation of intracerebral hematomas are less common, in 15-18% of cases. In 5-8% of patients, blood can break into the ventricular system, usually through the third ventricle, sometimes causing a tamponade of the ventricles of the brain. As a rule, this leads to a lethal outcome. However, in the overwhelming majority of cases, the symptoms of aneurysm rupture are accompanied only by subarachnoid hemorrhage (SAH). It is established that within 20 seconds after the rupture of the aneurysm, the blood spreads throughout the subarachnoid space of the brain. In the spinal subarachnoid space, blood penetrates after a few minutes. This explains the fact that when carrying out lumbar puncture in the first minutes after rupture of the aneurysm, the cerebrospinal fluid may not contain the uniform elements of the blood. But after an hour, the blood already spreads evenly over all the liquor spaces.

How does the aneurysm rupture?

The bleeding from the ruptured aneurysm lasts for a few seconds in most cases. The relatively rapid stopping of bleeding is due to a number of factors: 

1. Reflex spasm of the resulting artery due to the depressurization of the arterial bed and the tension of the arachnoid filaments in which the mechanoreceptors are located. 
2. Hypercoagulation, as a general biological defense response in response to any bleeding. 
3. Equalization of intra-arterial pressure and pressure in the subarachnoid cistern in which the aneurysm is located.

The last factor is explained by the fact that, despite the interconnectedness of all cerebrospinal spaces, the blood, having a greater viscosity than the cerebrospinal fluid, does not spread instantaneously over all the tanks, but at some point it mainly accumulates in the tank where the aneurysm is located, increasing the pressure in it to the level of the arterial. This leads to the cessation of bleeding and subsequent thrombus formation both outside the aneurysmal sac, and inside it. Those cases where bleeding in a few seconds does not stop, end up lethal. In a more favorable course, after the cessation of bleeding, a number of pathogenetic mechanisms are activated to restore cerebral circulation and brain functions, but simultaneously they can have a negative effect on the patient's condition and prognosis.

The first and most important of them is angiospasm.

According to clinical symptoms, there are three stages of arterial vasospasm:

1. Acute (1 day after rupture of aneurysm).
2. Subacute (the next two weeks after the hemorrhage).
3. Chronic (more than two weeks).

The first stage has a reflex-protective character and is realized by myogenic mechanisms (contraction of the smooth muscle fibers of the arterial wall in response to mechanical and dopaminergic stimulation caused by the fact of blood entering beyond the vessel). Thus, the pressure in the feeding artery decreases, which creates optimal conditions for intra- and extravasal thrombus formation with closure of an aneurysmal wall defect.

The second stage - is formed gradually, under the influence of the substances released by lysis streamed into the subarachnoid blood space (oxyhemoglobin, hematin, serotonin, histamine, decomposition products of arachidonic acid) and is characterized by the addition of myogenic vasoconstriction formirova-niem folds internal elastic membrane, destruction of the circular bundles of collagen fibers , damage to the endothelium with activation of the external hemocoagulation pathway.

In its prevalence, it can be divided into: local (segmental) - involving only the segment of the artery carrying the aneurysm; multisegmentary - seizure of adjacent arterial segments within a single basin; diffuse - spread to several arterial basins. The duration of this stage is 2-3 weeks (from 3-4 days, with a maximum of symptoms on the 5th-7th day).

Third stage (chronic) - formation of large longitudinal creases due to intimal myocytes cramps projecting into the lumen of the vessel and form a relatively autonomous muscle bundles in the inner layer tunica forming the developed muscular - intimal elastic pads at the mouths perforator artery narrowing exit from the main vessel. In the future, necrosis of medial smooth muscle cells with a gradual expansion of the lumen of the vessel. This stage takes a time period from the third week after SAC.

Given the above morphological features of the flow of narrowing the lumen of the arteries after hemorrhage into the subarachnoid space, the most adequately reflecting the essence of the process at present is the term constrictive-stenotic arteriopathy (CSA).

At the height of the narrowing of the vessel, there is a deficit of regional cerebral blood flow leading to transient or persistent ischemia in the corresponding basin, in some cases fatal. The origin and severity of ischemic damage directly depend on the effectiveness of the collateral blood supply of the affected area, the depth of disorders of autoregulation of cerebral blood flow.

Thus, the narrowing of the arteries, in the initial stages of playing a protective role in the end is a pathological condition, exacerbating the prognosis of the disease. And in those cases when patients do not die directly from the hemorrhage itself, the severity of the condition and the prognosis are directly related to the severity and prevalence of angiospasm.

The second important pathogenetic mechanism of aneurysmal SAK is arterial hypertension. Its cause is irritation with the blood flowing diencephalic region. In the future, the developing processes of ischemia of different regions of the brain with disruption of local autoregulation stimulate systemic vasoconstriction and an increase in the shock volume of the blood in order to maintain the maximum possible time of adequate perfusion of the affected areas. The phenomenon of Ostroumov-Beiliss, which determines the volume cerebral blood flow in the intact brain under conditions of ischemia and altered morphology of the vascular wall, is not realized.

Along with these compensatory features of increasing systemic arterial pressure, this condition is pathological, contributing to the development of repeated hemorrhages in the phase of incomplete organization of the arterial thrombus.

As evidenced by the data of many studies, arterial hypertension, as a rule, accompanies the aneurysmal SAK and its severity and duration are unfavorable prognostic factors.

In addition to increasing blood pressure, as a result of dysfunction of diencephalic stem structures, there is tachycardia, respiratory disorders, hyperglycemia, hyperazotemia, hyperthermia and other vegetative disorders. The nature of changes in the function of the cardiovascular system depends on the degree of irritation of the hypothalamo-diencephalic structures and, if relatively easily flowing and medium-heavy forms of the disease, a compensatory-adaptive reaction occurs in the form of an increase in cardiac output and intensification of the blood supply to the brain - i.e. Hyperkinetic type of central hemodynamics (according to AA Savitsky), then in severe cases the cardiac output drops sharply, the vascular resistance increases and cardiovascular insufficiency increases-the hypokinetic type of central hemodynamics.

The third pathogenetic mechanism is rapidly occurring and progressive cerebrospinal hypertension. In the first minutes and hours after the rupture of the aneurysm, the pressure in the cerebrospinal fluid increases as a result of a one-stage increase in the volume of the cerebrospinal fluid due to the outflow of blood. Subsequently, irritation of the vascular plexuses of the brain's ventricles with blood leads to an increase in the number of liquor products. This is the usual reaction of wreaths to the change in the composition of the CSF. At the same time, the resorption of the cerebrospinal fluid decreases sharply, because access to the pachyon granulations is hampered by the accumulation of large amounts of blood in the convectional tanks. This leads to a progressive increase in cerebrospinal pressure (often above 400 mm H2O), internal and external hydrocephalus. In turn, cerebrospinal hypertension causes compression of the brain, which undoubtedly adversely affects cerebral hemodynamics, since compression is primarily affected by the smallest vessels forming the hemocirculatory circulation, at the level of which the blood and brain tissue are directly exchanged. Consequently, developing cerebrospinal hypertension aggravates the hypoxia of brain cells.

The most catastrophic consequences of the accumulation of massive blood clots on the basis of the brain is tamponade IV of the ventricle or separation of cerebral and spinal liquor spaces with the subsequent development of acute occlusive hydrocephalus.

There is also a delayed hydrocephalus (normal pressure), which develops as a result of a decrease in liquoroadsorption and leads to a decrease in the perfusion of brain tissue with the development of dementic, atactic syndromes and pelvic disorders due to the predominant defeat of the practical (anterior) parts of the brain.

The fourth mechanism of the pathogenesis of aneurysmal SAK is due to the toxic effect of the decomposition products of the blood cells. It has been established that practically all blood decay products are toxic for neurocytes and neuroglia cells (oxyhemoglobin, serotonin, histamine, prostaglandin E2a, thromboxane A2, bradykinin, oxygen radicals, etc.). Process potentiated release of excitotoxic amino acids - glutamate and aspartate, firing IMEA, AMPA, kainate receptors, providing a massive entry of Ca ²⁺ into the cell blocking ATP synthesis, formation of secondary mediators that promote avalanche increase the concentration of Ca ²⁺ in the cell due to the extra- and intracellular reserves, destruction of intracellular membrane structures and further avalanche-like spread of the process to nearby neurocytes and gliocytes. Changes in the pH of the extracellular medium in the damage zones lead to additional extravasation of the liquid part of the blood due to a significant increase in the permeability of the vascular wall.

The toxic effect of these products of blood decay is also explained by meningeal syndrome. It does not appear immediately after aneurysm rupture, and after 6-12 hours and disappears as the liquor is sanitized - after 12-16 days. This syndrome correlates with the severity and prevalence of constrictive-stenotic arteriopathy. This is indicated by the fact that his disappearance in terms of time corresponds to the regression of the CSA. For more than three weeks, the persisting meningeal syndrome is due to the retention of spasm of small pial and meningeal arteries and is a poor prognostic sign in terms of surgical treatment.

The fifth inherent pathogenetic factor of all aneurysmal hemorrhages is cerebral edema. Its development and progression is caused, first of all, by circulatory hypoxia, which develops as a result of arteriopathy, hemoconcentration, hypercoagulation, sluggish syndrome, capillarostasis, cerebrospinal fluid and cerebral blood flow autoregulation disorders.

Another cause of brain edema is the toxic effect on brain cells of blood decay products. Promotes edema and increased blood levels of vasoactive substances (histamine, serotonin, bradykinin), proteolytic enzymes, ketone bodies, arachidonic acid, kallikrein and other chemical compounds that increase the permeability of the vascular wall and facilitate the release of fluid beyond the vascular bed.

By itself hypoxia of brain cells leads to inhibition of aerobic processes and activation of anaerobic glycolysis with final products - lactic and pyruvic acid. Forming acidosis causes the progression of edema. In mild cases, edematous reaction is compensatory in character with regress of edema to 12-14th day in parallel with normalization of the lumen of the vessels. But in severe cases, this compensatory reaction acquires a pathological character, leading to a fatal outcome. The direct cause of death in such a situation is a dislocation syndrome with a temporal lobe in the incision of the cerebellum nerve (the legs of the brain and quadruplemia are subjected to compression) and / or the tonsils of the cerebellum to the large occipital foramen (the medulla oblongata is squeezed).

Thus, the pathological process of an aneurysmal SAK begins with constrictive-stenotic arteriopathy and a complex of other factors causing cerebral ischemia, and ends with a heart attack, edema and a dislocation of the brain with compression of its vital structures and death of the patient.

A similar course occurs in 28-35% of patients. In other cases, after a regular worsening of the patient's condition on the 4th-6th day, arteriopathy, ischemia and cerebral edema regress to the 12th-16th day.

This period is favorable for a delayed operation aimed at shutting down the aneurysm from the blood stream in order to prevent repeated bleeding. Undoubtedly, postponement of surgical treatment for a longer period improves the postoperative outcome, but at the same time, one should not forget about repeated ruptures of aneurysms, most often occurring in the 3-4th week, which in most cases are fatal. In view of this, delayed surgical intervention should be performed immediately after regress of arteriopathy and cerebral edema. The emergence of nimodipine derivatives (nimotop, nemotan, diltzer) in the arms of doctors makes it possible to combat CSA more efficiently and to perform operative interventions at an earlier time.

Pathophysiology of arteriovenous malformations

Since most AVM have arteriovenous shunting, resistance to blood flow in them is reduced several times, and consequently, the velocity of blood flow in the leading arteries and diverting veins increases by the same amount. The larger the size of the malformation and the more arteriovenous fistulas in it, the higher these indices, and therefore the greater the amount of blood passes through it in a unit of time. However, in the aneurysm itself, because of the large total volume of dilated vessels, the blood flow slows down. This can not but affect brain hemodynamics. And if these disorders are insignificant and are easily compensated for in single anastomoses or small malformations, then cerebral hemodynamics is grossly violated for multiple malformations and large sizes of malformation. AVM, working as a pump, attracting the bulk of blood, "stealing" other vascular pools, causes ischemic brain. Depending on how strongly this is expressed, there may be different variations in the manifestation of this ischemia. In case of compensation or subcompensation of the missing volumetric blood flow, a clinic for ischemia of the brain may be absent for a long time. In conditions of moderate decompensation, ischemia exhibits transient disorders of cerebral circulation or progressive discirculatory encephalopathy. If a rough decompensation of cerebral circulation develops, this usually ends with an ischaemic stroke. Along with this, general hemodynamics is also violated. Chronic severe arteriovenous discharge permanently increases the load on the heart, leading first to hypertrophy of its right divisions, and then to right ventricular failure. These features should be taken into account, first of all, during anesthesia.

Symptoms of rupture of arterial aneurysm

There are three variants of aneurysm flow: asymptomatic, pseudotumorous and apoplectic (hemorrhagic). Asymptomatic aneurysms are identified as a "finding" during the course of cerebral angiography in order to identify any other neurosurgical pathology. They are rare (9.6%). In a number of cases, large aneurysms (gigantic aneurysms more than 2.5 cm in diameter) manifest themselves as a pseudotumorous clinical picture (volume effect on the adjacent cranial nerves and brain structures, which causes a clear progressively growing focal symptom complex.

The most frequent and the most dangerous are the aneurysms that exhibit a rupture and intracranial hemorrhage (90.4%).

Symptoms of aneurysmal subarachnoid hemorrhage

Symptoms of rupture of an aneurysm depend on the localization of an aneurysm, the size of the hole formed in its wall, the amount of blood flow, the severity and prevalence of arteriopathy, which largely determines the severity of the condition and the severity of the focal deficit, because the aneurysm-bearing artery, as a rule, spasms more than others, with ischemic disorders corresponding to localization. In the presence of the parenchymal component of hemorrhage, the initially identified focal neurological deficit is mainly due to this factor. A similar situation is observed in the data of various researchers in 17-40% of cases. With the breakthrough of blood into the ventricular system of the brain (17-20% of cases), the severity of the condition deteriorates significantly, and the more unfavorable factor is the presence of blood in the lateral ventricles. Massive ventricular hemorrhages with a tamponade of the ventricular system in most cases cause a dubious vital prognosis.

Symptoms of rupture of an aneurysm are quite stereotyped and the formation of a corresponding diagnostic hypothesis occurs with a rare exception in the collection of an anamnesis before carrying out special diagnostic measures. Usually this happens suddenly against the background of the full well-being of the patient without prodromal phenomena. 10-15% of patients report quite nonspecific complaints 1-5 days before the development of hemorrhage (diffuse headache, transient focal neurologic symptoms, respectively, localization of aneurysm, convulsive seizures). To provoke an aneurysm rupture, any stressful situation, physical overstrain, a viral infection, often a rupture happens during the act of defecation, after taking large doses of alcohol. At the same time, often enough hemorrhage develops without any provoking factors in a state of complete rest, and even during sleep. Epidemiological studies have shown that temporary peaks occur in the morning (around 9:00), evening (21:00) hours, at night - around 3:00. There are also seasonal patterns of development of pathology with two major peaks in March and September. This rhythm is not performed for smokers.

In cases where patients do not lose consciousness or lose it for a short time, they describe the following complaints: a sharp blow to the head, more often to the occipital region, or a sensation of a rupture in the head accompanied by a rapidly increasing intense headache like "pouring hot liquid." It lasts a few seconds, then dizziness, nausea, vomiting, and loss of consciousness may occur; Sometimes there is psychomotor agitation, hyperthermia, tachycardia, an increase in blood pressure. Upon the return of consciousness, patients feel a headache, general weakness, dizziness. With prolonged finding in a coma, there is retrograde amnesia.

Along with similar complaints in a number of cases, the symptomatology is very scarce, minimally affects the activity of the patient and regresses independently for several days. This is characteristic of the so-called mini leak - small hemorrhages, consisting in an aneurism wall rupture with the allocation of a minimal amount of blood into the subarachnoid space. The presence of such episodes in an anamnesis determines a less favorable prognosis for this patient and must necessarily be taken into account in the complex of clinical symptoms.

Worldwide, the classification scale of the severity of HAAC by Hunt & Hess (H-H), proposed in 1968, is universally accepted and widely used in clinical practice. It is optimal for all physicians involved in assisting patients with subarachnoid hemorrhages in order to unify the approach to assessing the condition and the correct choice of treatment tactics.

According to this classification, there are 5 degrees of severity or operational risk:

1. Absence of symptoms or minimal: headache and stiff neck.
2. Moderate or severe: headache, stiff neck, lack of neurological deficit (except paralysis of the cranial nerves).
3. Drowsiness, stunning, or mild focal deficiency.
4. Stupor, moderate or severe hemiparesis, possibly early decerebral rigidity, vegetative disorders.
5. Deep coma, decerebral rigidity, terminal condition.

Serious systemic diseases (arterial hypertension, diabetes mellitus, atherosclerosis, etc.), chronic pulmonary pathology, severe vasospasm lead to the patient's transfer to a more severe degree.

Asymptomatic forms of SAK are rarely detected, since such patients do not apply for help to a doctor and only when collecting an anamnesis with a repeated hemorrhage can we find out that the patient has already had one hemorrhage. However, there may be more severe hemorrhage, but by the time of hospitalizations, the state of Moiset is compensated for the 1st degree by NN. This fact is of great importance in the choice of tactics of examination and treatment.

Patients with grade II severity in HH usually seek help, but not to the neurologist, but to the therapist. Clear consciousness, the development of a headache in a patient with a previous arterial hypertension and the absence or later appearance of meningeal syndrome lead to the diagnosis of the "hypertensive crisis"; verification of SAK is carried out only if the condition worsens due to a repeated hemorrhage, or in a delayed period with a satisfactory condition ("false-hypertensive" variant of the clinical course of SAK - about 9% of patients). Sudden development of headache without disorders of consciousness and vomiting with normal blood pressure and subfebrile temperature lead to erroneous diagnosis of autonomic dystonia syndrome or ARVI with subsequent outpatient treatment from 2 to 14 days; With the resistance of the headache to therapy, patients are hospitalized in therapeutic and infectious hospitals, where the lumbar puncture verifies SAK ("migraine-like" variant - about 7%). With the development of headache, together with vomiting, fever, and sometimes short-term loss of consciousness, the doctor inclines to the diagnosis of "meningitis" with infection in the infectious department, where the correct diagnosis is established ("false-inflammatory" variant of 6%). In a number of cases (2%), the predominant complaint of patients is pain in the neck, back, lumbar region (which, with a detailed history, was preceded by a headache - a consequence of blood displacement through spinal subarachnoid spaces with irritation of radicular nerves), which is the reason for incorrect diagnosis of "radiculitis "(" False-radical "version). At the onset of symptoms with psychomotor agitation, delirious state, disorientation, it is possible to diagnose "acute psychosis" with hospitalization in the psychiatric ward ("false-psychological" variant - about 2%). Sometimes (2%) the disease begins with a headache and indomitable vomiting with the consciousness preserved and arterial normotension, which patients are associated with the use of poor quality food - diagnosed with "toxicoinfection" ("false-toxic" variant).

If all the enumerated stages before admission to a specialized department of the patient have time to pass for 12-24 hours, it can be operated in urgent order with a favorable outcome. If the organizational process is delayed for three days and more surgery can be performed in a delayed manner after regression of arteriopathy and cerebral edema.

Patients with a third degree of severity in HH come to neurological and neurosurgical hospitals more often, but in these cases errors in the diagnosis and treatment tactics are possible.

Victims with IV degree of severity are urgently delivered by ambulance teams to neurological and neurosurgical hospitals, but in this category of patients the choice of optimal medical tactics is strictly individual and complex, in view of the peculiarities of the condition.

Patients with V severity of H-H either die before receiving medical care or are left emergency doctors at home, because of the false idea of their non-transportability. In a number of cases, transportation is carried out to the nearest therapeutic or neurological hospital, where the prognosis may be aggravated by a repeated rupture, development of complications. In rare cases, the patient exits from a severe condition only on conservative therapy, after which he is transferred to a specialized center.

Thus, in the next hours and days after the development of an aneurysmal subshell hemorrhage in specialized neurosurgical departments, patients with grade III III severity are more likely to be delivered, less often from patients with II and IV. Patients with V severity of severity require intensive care and intensive care and they are not eligible for surgery. Paradoxical is the fact of late arrival in the patient hospitals of the patients with the most optimal for a radical and timely solution of the created problem (I to H-H), while the early intervention form.

Symptoms of rupture of arterial aneurysms of different localization

Aneurysms of anterior cerebral - anterior connective arteries (32-35%).

A feature of aneurysm ruptures of this localization is the absence in most cases of focal neurological symptoms. In the clinical picture, symptoms of intracranial hypertension predominate and, what is especially characteristic, mental disorders (in 30-35% of cases: disorientation, delirium, psychomotor agitation, absence of criticism to the condition). 15% of patients develop a focal neurological deficit caused by ischemia in the basin of the anterior cerebral arteries. When spreading also to the perforating arteries, the development of Norlen's syndrome is possible: lower paraparesis with pelvic disorders of the type of incontinence and rapidly increasing cachexia due to activation of ergotrophic and inhibition of trophotropic central regulatory influences on metabolism.

Often, similar aneurysmal hemorrhages are accompanied by a breakthrough into the ventricular system by disrupting the integrity of the terminal plate or with the formation of an intracerebral hematoma acquiring a ventricular component. Clinically, this is manifested by pronounced diencephalic disorders, persistent hyperthermia, oznobopodobnym tremor, lability of systemic arterial pressure, hyperglycemia, expressed cardiocirculatory disorders. The moment of a breakthrough into the ventricular system, as a rule, is accompanied by a significant depression of consciousness, hormoneotonic convulsions.

When the tamponade of the ventricular system develops blood clots or occlusive hydrocephalus, there is a significant deepening of the disorders of consciousness, grossly expressed oculomotor disorders, which testify to the violation of the function of the posterior longitudinal fascicle, nuclear structures of the trunk, corneal and pharyngeal reflexes with aspiration disappear, pathological respiration appears. Symptomatic appears quickly enough, which requires urgent medical measures.

Thus, in the presence of headache and meningeal syndrome without a clear focal symptomatology it is worthwhile to think about rupture of an aneurysm of anterior cerebral - anterior connective arteries.

Aneurysms of the supraclinoid part of the internal carotid artery (30-32%)

By localization they are divided into: aneurysms of the orbital artery, posterior connective artery, bifurcation of the internal carotid artery.

The first, the so-called ophthalmic, can flow pseudotemorously, compressing the optic nerve and leading to its primary atrophy, as well as irritating the I branch of the trigeminal nerve, causing attacks of ophthalmic migraine (intense pulsating pain in the eyeball accompanied by lacrimation). Giant ophthalmic aneurysms can be located in the Turkish saddle, simulating the pituitary adenoma. Those. Aneurysms of this localization can manifest themselves before the rupture. In case of rupture, focal symptomatology may be absent or manifest as a non-rough hemiparesis. In some cases, an amaurosis on the side of the aneurysm may occur due to spasm or thrombosis of the orbital artery.

Aneurysms of the internal carotid artery - the posterior connective artery - are asymptomatic, and when ruptured, contralateral hemiparesis and homolateral paresis of the oculomotor nerve can be produced, producing the impression of an alternating syndrome, but in most cases not the nucleus of the third pair but the spine is affected. In most cases, with the appearance of ptosis, mydriasis and diverging strabismus, one should think about the rupture of an aneurysm of the internal carotid anterior connective artery.

Hemorrhagia from an aneurysm of bifurcation of the internal carotid artery most often leads to the formation of intracerebral hematomas of the posterior basal parts of the frontal lobe with the development of gross motor, sensitive disorders in the hemitip, and aphasic disorders. Characteristic disorders of consciousness before sopor and coma.

Aneurysms of the middle cerebral artery (25-28%)

The rupture of the aneurysm of this localization is accompanied by a spasm of the bearing artery, which causes a focal symptom complex: hemiparesis, hemihopesia, aphasia (in the defeat of the dominant hemisphere). Hemorrhages in the temporal lobe of the temporal focal symptomatology may be absent or extremely meager. But nevertheless contralateral hemisymptotics is the key for such aneurysms.

Aneurysms of the main and vertebral arteries (11-15%).

This group is combined as an aneurysm of the posterior half circle of the Wilisian circle. Their rupture, as a rule, is difficult, with the primary disorder of the trunk function: depression of consciousness, alternating syndromes, isolated lesions of cranial nerves and their nuclei, pronounced vestibular disorders, etc. The most frequent are nystagmus, diplopia, paresis of vision, systemic dizziness, dysphonia, dysphagia, and other bulbar disorders.

Lethality in the rupture of an aneurysm of similar localization is much higher than when an aneurysm is found in the carotid basin.