Anomalies and normal variants of intracranial arteries: an approach to...

Translation of the presentation “Anomalies and normal variants of the intracranial arteries: proposed workflow for classification and significance.”

Congress:	ECR 2016
Poster No.:	C-0199
Authors:	A. Hakim1, J. Gralla1, C. Rozeik2, P. Mordasini1, F. Pult1, L. Leidolt1, E. Piechowiak1, K. Hsieh1, M. El-Koussy1; 1Bern/CH, 2Loerrach/DE
DOI:	10.1594/ecr2016/C-0199
DOI-Link:	https://dx.doi.org/10.1594/ecr2016/C-0199

Translation into Russian: Simanov V.A.

1.1. Variants of origin (discharge) of vessels

1.1.1. Common origin : two different vessels can have the same origin (discharge)

SCA/PCA: 2-22% Fig.3 :

The common trunk arises from the basilar artery, then branches into the posterior cerebral artery (PCA) and the superior cerebellar artery (SCA) [1].

Variations in the development of cerebral arteries and epilepsy

The prevailing ideas about the mechanisms of development of cerebral ischemia imply the occurrence of a discrepancy between the available blood supply and the needs of brain tissue. The most important achievements in the field of clinical angioneurology include the modern concept of heterogeneity of ischemic stroke, which is based on the idea of the diversity of causes and mechanisms of development of acute focal ischemic brain damage. The amount of reversible and irreversible brain damage largely depends on the state of the hemodynamic, collateral, perfusion and metabolic reserves of the brain. Pathological tortuosity of the main arteries of the head - a hereditarily determined functional inferiority of connective tissue - occurs in at least 10% of the population. Among the main forms of lesions of intracranial arteries, kinks and loop formations, aneurysmal dilatations of arteries, and arteriovenous aneurysms are distinguished. Excessive tortuosity of blood vessels contributes to the formation of blood clots in them. In 71% of patients with arterial occlusion, a tortuous course of vessels was noted. Underdevelopment of the cerebral arteries in the form of hypoplasia or stenosis of the posterior inferior cerebellar artery and/or basilar artery, rarely the inferior anterior cerebellar artery and tortuosity of the vertebral artery are causes of hearing loss and deafness. Weak cerebral artery anastomoses cause cerebral ischemia after cervical discectomy. In Parkinson's and Alzheimer's diseases, neuroimaging and pathological studies have detected cerebrovascular lesions in 20-30% of cases, and vascular disease of the brain may be the basis of dementia. Structural changes in cerebral vessels, a decrease in blood flow velocity and the presence of 30% stenosis in the middle cerebral artery can be prerequisites for the development of stroke in patients with sleep apnea syndrome.

In case of Kimmerle anomaly, it is necessary to take into account the presence of congenital changes in the vertebral arteries. Dysplastic disorders in the area of the craniovertebral junction are 2 times more often noted with pathological tortuosity of the vertebral arteries, to a lesser extent due to hypoplasia of the vertebral arteries. Up to 51.9% of patients with Chiari malformation and syringomyelia have structural features of the cerebral arterial circle. Tortuosity, asymmetry and hypoplasia of the vertebral arteries with signs of impaired blood flow are characteristic of vertebrobasilar insufficiency due to cervical dorsopathy and were noted in 76.6% of cases with central vestibulocochlear syndrome.

The arterial bed of the brain is also affected in such systemic diseases of the body as rheumatoid arthritis, polyarteritis nodosa, Takayasu's disease, Henoch-Schönlein disease. When performing dental procedures in patients with Sturge-Weber disease or Recklinghausen disease, as typical neurofibromatosis, the development of threatening bleeding is possible. Primary damage to the cerebral arteries in the form of vasculitis and endarteritis underlies the development of neurosyphilis and leads to secondary damage to the nervous tissue and the occurrence of infarctions in the brain. Cerebral vasculitis and herpetic cerebral vasculitis can develop against the background of herpetic infection. With ischemic strokes, in 70% of cases in the brain tissue, along with changes caused by acute cerebrovascular accident, focal lesions are observed, similar to changes in meningoencephalitis caused by herpes zoster and herpes simplex.

Changes in the structure of the cerebral arteries must be taken into account when assessing cancer metastases, as well as in 40% of patients with severe traumatic brain injury when identifying traumatic subarachnoid hemorrhages and concomitant angiographic vasospasm.

In the course of carrying out research to study the relationship between variants of human cerebral arteries and cerebrovascular disorders within the framework of acute cerebrovascular accidents and chronic cerebral ischemia, we have developed observations about the relationship between variants of the structure and topography of human cerebral arteries with a number of other nosological units. In this regard, we present the results of our own research on the development of cerebral arteries in humans with various types of epilepsy.

We analyzed the state of the arterial bed of the brain in 748 outpatient and inpatient patients from 22 years to 81 years old, who were examined and treated in the neurological and neurosurgical departments of OKB No. 2 named after. Professor I.N. Alamdarov, Astrakhan in the period 1983-1998, the neurological departments of City Hospital No. 3 and City Hospital No. 4 of Tambov, the neurosurgical department of the Tambov Regional Hospital, the rehabilitation and health complex of the family “B. Lipovitsa", neurological offices and in day hospitals of City Hospital No. 4, Nodal Clinic at the station. Tambov JSC "Russian Railways" and the Central House of Children's Hospital "Tambovmedservice" LLC, as well as in the outpatient clinic "Home Doctor" (Tambov) during 1998-2009.

All patients underwent a comprehensive clinical and instrumental study, including data from a clinical examination by a neurologist, therapist and ophthalmologist, standard laboratory data, electrocardiography, fluorography or plain radiography of the chest organs. According to indications, consultations and examinations were carried out with a neurosurgeon, gynecologist, otolaryngologist, cardiologist, endocrinologist and psychotherapist; a study of the cognitive sphere using a brief mental status assessment scale or a mini-mental status study, transcranial Doppler sonography, electroencephalography. All patients underwent magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA).

According to the data obtained, variants of the structure and topography of the arterial circle of the cerebrum were verified in only 27 cases (61.4% of observations) out of 44 patients with epilepsy or encephalopathies with leading epileptiform syndromes. Among the analyzed group of patients with various types of epilepsy, the following variants of the structure and topography of the arterial circle of the cerebrum were identified: 1) bending of both anterior cerebral arteries in 1 (3.7%) patient; 2) hypoplasia of the left vertebral artery in 2 (7.4%) patients; 3) posterior trifurcation of both internal carotid arteries and anterior trifurcation of the left internal carotid artery, hypoplasia of the basilar artery in 3 (11.1%) patients; 4) anterior trifurcation of the left internal carotid artery, hypoplasia of the basilar artery in 6 (22.2%) patients (Fig. 1); 5) hypoplasia of the right vertebral artery, aplasia of the posterior communicating artery on the right in 4 (14.8%) patients; 6) hypoplasia of the right vertebral artery, hypoplasia of the basilar artery in 5 (18.5%) patients (Fig. 2); 7) anterior trifurcation of the left internal carotid artery, hypoplasia of the posterior communicating artery, hypoplasia of the right posterior cerebral artery in 3 (11.1%) patients; tortuosity of both vertebral arteries in 2 (7.4%) patients; 9) hypoplasia and tortuosity of both vertebral arteries in 1 (3.7%) patient. Below are quite indicative clinical observations from the totality of our own studies.

Example 1. Patient N., 54 years old, is observed in the Nodal clinic at the station. Tambov JSC "Russian Railways" with a diagnosis of encephalopathy as unspecified (epileptic and dyscirculatory) with polymorphic paroxysms (like Todd's palsy) against the background of abnormalities in the structure of the cerebral arteries. Complaints of noise in the head, unsteadiness when walking, attacks of weakness in the right limbs and loss of consciousness. Neurologically: there are no meningeal signs in consciousness, cognitive functions are reduced, emotionally labile, pupils d = s, convergence is weakened, slight weakness of the facial muscles on the right, paresis of the right hand up to 4 points, no sensory disorders, tendon reflexes are increased d > s, staggering in the Romberg position , coordination tests are performed with DetS missing, eyelid tremor. Ophthalmologist: hypertensive angiosclerosis of the retinal vessels of both eyes. Therapist: stage II hypertension, severity of arterial hypertension II, risk category 3. BAC: cholesterol - 4.5 mmol/l, β-lipoproteins - 3.5 g/l, creatinine - 69 µmol/l, urea - 7, 9 mmol/l. Prothrombin - 88%, fibrinogen - 4.25 g/l. ECG: syn, rhythm 80 per minute, normal position of the EOS. MRI and MRA: shown in Figure 1. Outpatient treatment: piracetam, glycine, Cavinton, cinnarizine, aminalon, Enap, Prestarium, indopamine. She underwent a course of treatment in a day hospital: Mexidol, magnesium sulfate, Prestarium, indopamide, mildronate, enalapril. The complaints remain the same. Neurologically - there are no meningeal signs in consciousness, cognitive functions are reduced, cranial nerves without dynamics, paresis of the right hand up to 4.5 points, staggering in the Romberg test, coordination tests with intention on both sides. Consulted at the Tambov psychiatric hospital, where a diagnosis was made: consequences of organic damage to the central nervous system of complex origin with polymorphic paroxysms. EEG: pronounced cerebral changes in biological and bioelectrical activity, practically no α-activity. In all regions the polyri is less than 5 μm. There is no regionality, no activation reaction, no assimilation. Persistent disorganization of the activities of central structures. Interest in the left temporal region, where a focus of slow-wave irritation was identified. Low functional state of the cortex with high sensitivity to hypoxia, with a decrease in the threshold of excitability of the trunk. Single discharges of the posterior trunk sections. Vascular influences are pronounced. Follow-up: while taking Depakine-Chrono, complaints decreased significantly, no attacks were noted.

Example 2. Patient VN., 21 years old, is observed in the Nodal clinic at the station. Tambov JSC Russian Railways with a diagnosis of epilepsy with polymorphic cerebral paroxysms and cognitive impairment. Observed since childhood - complaints of attacks with loss of consciousness. After starting treatment at the age of 14 in the neurological department of the Tambov Regional Children's Hospital, he was registered with a diagnosis of epilepsy, partial seizures with secondary generalization. EEG (Psychiatry and Narcology, 04/17/02): no paroxysmal activity was detected, unstable α-rhythm. Dysfunction of the diencephalic region. Vascular influences with increased autonomic excitability (06/15/04): AMI is moderate, but persistent, with low-amplitude dysrhythmia. Regionality is unclear. The activation reaction is reduced, there is no assimilation. No gross slow-wave or paroxysmal activity was detected. Reduced reactivity of the cortex. High vegetative excitability. Vascular influences 02.22.05: compared to 06.15.04, positive dynamics. General cerebral changes are moderate and of a regulatory nature. Moderate dysfunction of the diencephalic region with increased activity. An unstable α-rhythm appeared, fragmented. The reactivity of the cortex has improved. The sensitivity of the cortex to RFS has increased somewhat, which leads to a decrease in the threshold of excitability of the posterior brainstem structures. There are no paroxysmal tendencies of the cortex. Increased autonomic excitability. MRI and MRA: shown in Figure 2. Neurologically: there are no meningeal signs in consciousness, cognitive functions are slightly reduced, emotionally labile, distal hyperhidrosis, tremor of the eyelids and outstretched fingers, pupils d = s, converges, weakness of facial muscles on the right, in the Romberg position lung staggering, performs coordination tests, paresis, no sensory disorders, tendon reflexes d = s, Babinski's symptom is weakly positive on both sides, Epileptologist: cognitive disorders due to epilepsy. He constantly receives finlepsin (attacks are associated with irregular use of the drug).

Thus, we consider it necessary to draw the following conclusions. 1. Variations in the structure and topography of the arterial circle of the cerebrum can be considered as predictors of epileptiform phenomena in brain structures. 2. For various cerebral paroxysms, it is obviously advisable to study the arterial circle of the cerebrum. 3. Variants of the structure and topography of the arterial circle of the cerebrum in each specific case should be considered from the point of view of minor developmental anomalies.

1.2. Change in the number of vessels

1.2.1. Reducing the number of vessels

ICA agenesis: 0.01% Fig.11 , Fig.47 :

Around day 24 of embryogenesis, the ICA develops from the dorsal aorta and third arch. Subsequently, at approximately the 5th - 6th week, the base of the skull begins to take its shape. Thus, absence of ICA will result in absence of the carotid canal, identification of which is the most practical method in identifying this anomaly in a clinical setting. Typically, patients with ICA agenesis are asymptomatic due to well-developed collateral circulation through the ECA and vertebrobasilar system [2].

Aplasia of the A1 segment: 1-2%. Fig.12 and Fig.15 :

In this situation, both A2 segments are supplied by the existing A1 segment [2].

Azygos ACA: less than 1% Fig. 13 :

Both A1 segments form a common A2 segment, which supplies blood to both hemispheres[2].

Lack of Acom: 5% Fig.14 [2]:

Typically, the absence of the anterior communicating artery (Acom) is not easy to detect on time-of-flight MR angiography because the artery may be present but the flow signal is too weak to be visualized.

Lack of Pcom: 0.6% Fig.15 :

The posterior communicating artery (Pcom) is usually smaller than the P1 segment. Complete absence is rare [2].

Artery of Percheron: 4-11.5% Fig. 16 :

The thalamo-mesencephalic arterial supply can be divided into 3 types: type 1 is the most common, with perforating arteries on both sides arising from the P1 segments; type 2 , known as the artery of Percheron, arising from one of the P1 segments, supplying both sides; type 3 is an arch that connects both P1 segments and from which the perforating arteries arise [5].

1.2.2. Increase in the number of vessels

Incremental MCA: 2.7% Fig. 17 :

Literary definitions of accessory middle cerebral artery (MCA) and MCA duplication are quite dichotomous. In this paper, we use the definition of Teal et al., who limited the term “accessory MCA” to the branch arising from the anterior cerebral artery (ACA) and the term “duplicate MCA” to the artery arising from the distal segment of the ICA [6]. To distinguish an accessory MCA from a duplex one, the dominant vessel must be identified by carefully searching for the MCA bifurcation. Comparison with the contralateral side is also useful to find the level of ICA bifurcation [1].

Duplication: refers to two separate arteries that do not exhibit distal fusion. For example:

MCA duplication: 0.2-2.9% Fig. 18 : MCA duplication is an artery that arises from the ICA and runs parallel to the main trunk of the MCA. This variant should not be confused with early branching of the MCA, in which a short single M1 segment is present. It should also not be confused with the anterior temporal branch, which often arises from the M1 segment.
Acom doubling: 18% Fig. 19 [1].
SCA doubling: 14% Fig. 12 [2].

Trifurcation:

ACA trifurcation: 2-13% Fig. 20 : trifurcation refers to the presence of three A2 segments and is described by various names such as pericallosal triplex, arteria mediana corporis callosi and persistent primitive median artery of the corpus callosum [2]. Early origin of a frontopolar branch, for example from Acom, may appear as a third A2 segment.

MCA trifurcation: 12% Fig. 21 : The horizontal segment of the MCA is divided into superior and inferior trunks in approximately 78%. In 12% there is an additional (middle) trunk, this situation is called trifurcation, and the presence of more than 3 trunks, for example, quadrifurcation, is observed in approximately 10% Fig. 22 [2].

Fig. 11 Agenesis of the left ICA. TOF MRA (a), no signal from the flow in the left ICA. MIP CTA (c), CCA continues as ECA with no ICA. Bone window CT (b), absence of bony carotid canal on the left side. The normal carotid duct on the right side is marked with a red arrow for comparison.

Fig. 12 3D MRA, absence of A1 segment of ACA, both A2 segments extend from the contralateral side. Note the partial fetal PCA (white arrow), duplication of the superior cerebellar artery (blue arrow), and hypoplastic vertebral artery (red arrow) that terminates as the PICA.

Fig. 13 3D MRA, fusion of both A1 segments to form a single A2 segment (azygos ACA) (arrow).

Fig.14 3D TOF MRA, no Acom.

Fig. 15 3D TOF, absence of Pcom and A1 segment on one side. The significance of this option is that if the ICA is occluded on that side, there will be no possibility of collateralization through the circle of Willis. Incidental finding: aneurysm of the terminal portion of the contralateral ICA (arrow).

Fig. 16 MIP (a) and 3D TOF (b), type 2 thalamo-mesencephalic arterial supply (artery of Percheron) with a single arterial trunk (arrow) arising from the P1 segment, the branches of which supply blood to both sides.

Fig. 17 3D TOF, additional MCA (arrow) extending from the A1 segment.

Fig. 18 3D TOF of a duplicated MCA (red arrow) extending from the distal ICA. This artery should not be confused with the anterior temporal branch (white arrow), which is a common finding.

Fig. 19 3D TOF, Acom duplication (white arrows), proximal A2 segment fenestration (red arrow), A1 segment aplasia and complete fetal PCA (blue arrow).

Fig. 20 3D TOF, ACA trifurcation with three A2 segments (arrows), the third branch arises from Acom

Fig.21 3D TOF, MCA trifurcation with additional middle trunk.

Fig.22 3D TOF, MCA quadrifurcation.

Everything about the treatment of hypoplasia of the vertebral arteries

Most diseases affecting the brain are vascular in nature. Hypoplasia is no exception. This is a congenital pathology affecting the intracranial blood supply. The essence of the disease, its symptoms, diagnosis and treatment - this is the subject of research in this article.

Diagnostics

It is extremely difficult to identify hypoplasia in the early stages of its development due to the lack of characteristic symptoms and manifestations. There are three main methods for diagnosing narrowing of the lumen of the vertebral arteries, which include:

Ultrasound examination of the vessels of the head and neck . During the procedure, the image of the artery is recorded using an ultrasound machine, after which the type, intensity and diameter of blood flow is analyzed (a narrowing of the diameter of the vessels to 2 mm or less is considered a serious defect).
Tomography of the head and neck . Using computer and magnetic resonance imaging, the condition of the vessels filled with a special contrast agent is assessed.
Angiography . X-ray examination, which reveals abnormalities in the structure of blood vessels and vertebral arteries.

In addition, to diagnose concomitant diseases that may affect the course of hypoplasia (for example, pathology of the cervical vertebrae), the doctor may prescribe additional studies.

Hypoplasia of the left vertebral artery: what is it, causes and treatment features

At the stage of pronounced clinical symptoms of hypoplasia of the right or left vertebral artery, conservative treatment with vasodilators - they eliminate unpleasant phenomena and improve the patient’s quality of life. In cases where there is a risk of blood clots, taking anticoagulants (blood thinning medications) is indicated.

When is vertebral artery hypoplasia diagnosed?

It is in the intracranial segment that pathological narrowing of the vertebral arteries is most often observed. The diameter of these great vessels is uneven along the entire length and ranges from the smallest value - 2 mm, to a lumen of 4.5 mm. The normal diameter of the PA usually ranges from 3.5 to 4 mm.

Hypoplasia of the vertebral artery is considered to be its critical narrowing of up to two millimeters. Congenital breakage or complete absence of one of the branches is also possible - this pathology is called aplasia.

Incorrect position of the fetus in the womb, due to which it is exposed to unwanted mechanical stress.
Carrying a pregnancy to term under negative conditions that negatively affect the development of the embryo: maternal use of alcohol, drugs, smoking;
finding the future woman in labor in a hazardous environment (working in a chemical production facility, living in a gas-polluted or radioactive area);
infectious pathologies, injuries, medication, intoxication, poisoning during pregnancy.

Hereditary mutations.

Barre-Lieu syndrome

A classic sign of a malnutrition of the occipital lobe of the brain. Gives headache, nausea, and rarely vomiting.

Orientation in space also decreases, pathological fatigue and fatigue are detected.

Insomnia, depressive mood, constant depression, apathy and reluctance to do anything.

Hypoplasia of the vertebral artery: what is it?

One of the most common pathologies of the vertebral arteries is their hypoplasia, that is, underdevelopment. This anomaly manifests itself as a significant narrowing of the lumen of the vessel (it becomes less than 2 mm). The left vertebral artery is affected more often than the right. Hypoplasia occurs in utero - this is a congenital pathology. Various factors can provoke the appearance of the disease in question:

Bad habits of the expectant mother.
A woman's use of dangerous drugs in early pregnancy.
Intrauterine infection of the embryo.
Effect of radiation on pregnant women.

It is also worth noting that quite often hypoplasia is found in children who do not have a history of any of the listed factors.

Treatment methods

To treat hypoplasia of the vertebral arteries, methods of conservative therapy and surgical treatment are used.

What is hypoplasia of the right or left vertebral arteries, how to treat this disease?

Diagnosis of hypoplasia of the vertebral artery of the brain

With hypoplasia of the vertebral artery of the brain, typical clinical symptoms are present, which are a direct indication for a number of clinical studies. Typically diagnosis includes:

X-ray of the cervical spine;
MRI of brain structures;
duplex scanning of cerebral blood vessels;
angiography with the introduction of a contrast agent.

It is worth paying attention to the following negative manifestations of the disease:

1.3. Change in morphology

1.3.1. Hypoplasia

ICA hypoplasia: 0.079% Fig. 23 :

In contrast to agenesis, the thin vessel is identifiable. Again, skull base tomography is useful in visualizing the bony carotid canal, which is thinner than normal in hypoplasia [2].

Hypoplasia A1: 10% Fig.24 :

Asymmetry of A1 segments is observed in 80% of cases. Hypoplasia is defined when the vessel diameter is less than 1.5 mm [2].

Hypoplasia A2 (bihemispheric ACA): 7% Fig. 24 :

One of the A2 segments is hypoplastic. In this variant, the blood supply to the ipsilateral hemisphere occurs mainly from the contralateral (dominant) A2 segment [2].

Hypoplasia Pcom: 34% Fig.25 :

but complete absence is a rare finding [2].

Hypoplasia of the vertebral artery:

50% on the right side (left dominant), 25% on the left side (right dominant), 25% codominant. In approximately 0.2%, the vertebral artery ends in the PICA Fig. 12 and Fig. 26 [7] [2]

1.3.2. Hyperplasia

Hyperplasia of the anterior choroidal artery: 2.3% Fig. 27 :

The anterior choriodal artery arises from the posterior surface of the terminal segment of the ICA, distal to the origin of the Pcom. This is usually a small branch. If it is enlarged (hyperplastic), then it supplies blood to part of the territory of the posterior cerebral artery (occipitotemporal branch) [1, 2].

1.3.3. Early bifurcation (early division):

Early MCA bifurcation: This is a common finding Fig.28 :

The horizontal segment of the MCA is usually 12 mm long, but may be shorter, with early branching (bi- or trifurcation) [1].

1.3.4. Fenestration: 0.7% including all intracranial vessels Fig. 6 , Fig. 19 and Fig. 29 . Fenestration is the division of the lumen of an artery into two separate channels. Each canal has its own endothelium and muscle layer and can separate the adventitia. These two canals merge distally. Fenestration is most often observed in the posterior circulation [1, 2].

Fenestration A1: 0-4% [1]
Fenestration A2: 2% Fig. 19 [1]
Acom fenestration: 12-21% [1]
Fenestration of the vertebral artery Fig. 29 : 0.3-2% [1].

Fenestration of the basilar artery Fig. 29 : 0.12-1.33%: the basilar artery is formed by the fusion of two longitudinal neural arteries. Incomplete fusion results in segmental fenestration, which is usually present in the proximal segment of the basilar artery [2].

Fig. 23 CTA (a), hypoplastic ICA (arrows). CT bone window (b) asymmetrical bony carotid canal

Fig. 24 3D TOF, hypoplasia of the A2 segment (white arrow) and the contralateral dominant A2 segment “bihemispheric ACA”. Note hypoplasia of the A1 segment (red arrow).

Fig. 25 MIP CTA, right Pcom hypoplasia (arrow). Note the pathological occlusion of the contralateral ICA.

Fig. 26 3D TOF, hypoplasia of the vertebral artery (white arrow) that ends as a PICA (green arrow).

Fig. 27 3D TOF, hyperplasia of the anterior choroidal artery (white arrow). The contralateral anterior choroidal artery is of normal caliber (green arrow). Red arrow points to fetal PCA, blue arrow to Pcom.

Fig. 28 3D MRA, early bifurcation with short prebifurcation segment M1 (arrow).

Fig. 29 Fenestration of the A1 segment (a), Acom (b), M1 segment (c), V4 segment (d) and the proximal part of the basilar artery (e).

Symptoms

Symptoms of chronic cerebral circulatory disorders depend on the vascular pool in which ischemia of brain tissue develops. All patients may be concerned about:

headache;
dizziness;
noise in the head;
memory impairment;
sleep disorders.

Hypoplasia of the carotid arteries is also characterized by weakness and/or numbness in the limbs and speech impairment. For ischemia in the vertebral artery basin - impaired coordination, gait instability.

To diagnose hypoplasia of cerebral arteries and determine treatment tactics, the following are carried out:

cerebral angiography - X-ray examination of the arteries of the brain with a contrast agent injected into them;
CT angiography;
MR angiography;
ultrasound examination (duplex scanning) of the vessels of the neck and head;
PAT;
single photon emission computed tomography.

Conservative therapy with drugs that improve blood supply and metabolism of the brain is carried out if the examination data suggests that it can prevent further worsening of cerebral ischemia and ischemic stroke.

1.4. Changing the course

1.4.1. Aberrant lateral pharyngeal ICA, tortuous ICA, and kissing carotid arteries:

During embryonic development, the ICA is thought to begin to unwind as the dorsal aortic root descends into the thorax, providing a direct pathway for the ICA. Failure in unwinding results in tortuosity of the ICA, which runs close to the midline of the posterior pharyngeal wall, called the aberrant lateral pharyngeal artery [6].

This morphology is more commonly seen in older patients or those with hypertension, but should not be confused with the fetal variant, although both have the same meaning (see below). The incidence of aberrant lateral pharyngeal ICA is approximately 5%, but the exact prevalence of the anomaly is unknown as it cannot be differentiated morphologically from tortuosity. Studies conducted by Ekici et al. showed that the least affected age group with ICA tortuosity was the younger age group [8].

The term "kissing carotid arteries" describes the elongated carotid arteries that meet at the midline; can be observed retropharyngeal or intrasphenoidal / intrasellar Fig. 30 [2].

1.4.2. Persistent primitive olfactory artery: 0,14%

The ACA is derived from the primitive olfactory artery, which regresses to form the recurrent artery of Heubner. Violation of regression leads to preservation of the primitive olfactory artery. This artery has an extreme anterior-inferior course in the A1 segment, which moves along the olfactory tract before the posterosuperior transition to the A2 segment, forming a hairpin-shaped configuration [9].

1.4.3. Persistent embryological anastomosis

+ persistent carotid-vertebrobasilar anastomosis:

During embryonic development, the anterior circulation supplies the hindbrain through several anastomoses, since the posterior circulation is not yet sufficiently developed. After the development of the vertebral arteries, these anastomoses regress. Impaired regression results in abnormal communication between the anterior and posterior circulation in the postnatal period. The most common form of these anastomoses is the fetal type PCA (see variants of origin/origin of vessels). Recognizing the course of these abnormal vessels, as well as the level of entry into the skull, is critical for their differentiation Table 1

persistent trigeminal artery (PTA): 0.1-0.2% Fig. 31 Fig. 48 : PTA originates from the cavernous segment of the ICA and communicates with the basilar artery. Proximal to the level of the anastomosis, the basilar artery is usually hypoplastic. On the angiogram, when viewed from the side, it has a characteristic “Trident of Neptune” or Tau sign configuration, reminiscent of the Greek letter “Tau” [1] [2]. There are two different classifications Table 2 Fig. 32 and Fig. 33 [10].

PTA variants (Saltzman III): 0.18-0.76%: Arteries that supply the posterior fossa, arising from the precavernous segment of the ICA and not communicating with the basilar artery [1].

Persistent auricular artery (otic artery): the rarest carotid-vertebrobasilar anastomosis. The existence of the auricular artery is controversial because it has not been identified in lower animals. It passes from the petrosal segment of the ICA to the basilar system through the internal auditory canal [2].

Persistent primitive hypoglossal artery (PPHA): 0.03-0.26% Fig. 34 Fig. 49 : This artery runs from the cervical segment of the ICA to the basilar artery through the hypoglossal canal. The vertebral artery is hypoplastic. CT scan of the skull base shows an enlarged bony hypoglossal canal [1, 2].

Proatlantal intersegmental artery: very rare. Connects the cervical segment of the ICA or external carotid artery (ECA) to the vertebrobasilar system. The artery enters the base of the skull through the foramen magnum, which allows it to be differentiated from the hypoglossal artery. There are two types:

Type I: joins the vertebral artery above the atlas.
Type II: enters the vertebral artery through the atlas [1, 2].

+ persistent internal-external carotid anastomosis

Aberrant intratympanic ICA: very rare. This variant is an anastomosis between the ICA and the ECA, as it is believed to arise from agenesis of the cervical segment of the ICA and the development of an anastomosis between the horizontal (petrosal) segment of the ICA and the enlarged inferior tympanic artery, which is a branch of the ECA. The ICA (or rather the enlarged inferior tympanic artery) in this case has a smaller diameter than the usual ICA, with the absence of the ascending part of the carotid canal as it enters the base of the skull, posterior and parallel to the jugular bulb, which resembles a mass in the hypotympanum; there is also no bone plate between the carotid canal and the tympanic cavity [1].

Persistent stapedial artery: 0.48%. This anomaly occurs due to the persistence of the anastomosis through the stapedial artery, which is usually present during development between the ECA and ICA. The artery arises from the petrosal segment of the ICA, passes through the obturator foramen, and ends as the MCA in the epidural space of the middle cranial fossa. A CT scan of the skull base may show a small canal near the carotid canal. Foramen spinosum, which contains MMA, will be absent. a persistent stapedial artery may be associated with an aberrant ICA [1, 2].

Table 3 shows the frequency of variants discussed, however, there are other rare variants that cannot be included in a single document. Finally, having a fully developed Circle of Willis can be considered an option since it is present in less than 50% of the population [2]

*NB: Frequency varies between authors depending on the type of study performed (CT, MRI, surgical or post-mortem). Frequency may also vary depending on geographic distribution; Published data may not always be applicable to other populations.

Table 1: Types of persistent carotid-vertebrobasilar anastomoses

Table 3: occurrence of anatomical variants

Fig. 30 Coronal MIP CTA of a patient with a history of hypertension shows elongated carotid arteries reaching the midline (“kissing” carotid arteries).

Fig. 31 3D TOF, lateral view (a) and dorsal view (b), persistent primitive trigeminal artery (red arrow) arising from the cavernous segment of the ICA and communicating with the basilar artery, which is hypoplastic to the level of the anastomosis (white arrow). In lateral view, the anomalous artery with ICA resembles Neptune's trident and the Greek letter "tau".

Fig. 32 MIP CTA of persistent primitive trigeminal artery (red arrow) in two different cases. According to Salas there are 2 types: medial sphenoidal or intrasellar (a), which extends into the sella turcica and perforates the dura mater or dorsum sella (green arrow), as in this case, and lateral petrosal or parasellar (b), in which the vessel goes with the sensory roots of the trigeminal nerve, on the side of the sella turcica.

Fig. 33 3D TOF showing two different cases of persistent primitive trigeminal artery (red arrow). Classification according to Saltzman: Type I (a), in which the PCA supplies the superior part of the basilar artery, including the posterior territory, and type II (b) with the fetal PCA (white arrow).

Fig. 34 3D CE MRA oblique (a) and posterior (b) views showing the persistent primitive hypoglossal artery (red arrow) which arises from the cervical segment of the ICA (green arrow) and continues as the vertebrobasilar artery (blue arrow). ECA is marked with a white arrow.

Meaning

The list in Fig. 35 shows the values of the anatomical options.

2.1. Recognition of anatomical patterns and the ability to distinguish them from pathological changes:

2.1.1. Knowledge of normal variations is part of the anatomical knowledge that is important for every radiologist and surgeon. Knowledge of normal variants and their proximity to other structures facilitates the understanding and diagnosis of various diseases, such as:

Trigeminal neuralgia, which can be caused by the presence of a variant of PTA (less commonly PTA), due to the proximity of the vessel to the trigeminal nerve [11].
Glossopharyngeal neuralgia or hypoglossal nerve palsy, which can be caused by a persistent hypoglossal artery [1].
Pulsatile tinnitus in cases of persistent stapedial artery [1].

2.1.2. Option against pathology:

Infundibulum: The Pcom infundibulum should not be confused with an aneurysm Fig. 36 .
ICA hypoplasia may be confused with dissection or fibromuscular dysplasia, while ICA agenesis may be confused with occlusion. Visualization of the skull base aids differentiation, as the bony carotid canal will be narrow in cases of hypoplasia and absent in cases of agenesis, but will appear normal in other acquired diseases Fig. 11 and Fig. 23 .
Different patterns of perfusion abnormalities may occur with normal variations that can cause confusion, especially in the context of stroke:

Asymmetry of CT or MR perfusion in the occipital lobes, in the case of unilateral fetal PCA. The contralateral side may show delayed perfusion because it is supplied by the posterior circulation Fig. 37 .
Bilateral perfusion delay in the occipital lobes compared with the frontal and parietal lobes may be observed in the absence of bilateral Pcom Fig. 38 .
Relative hypoperfusion in the PICA territory in cases of vertebral artery hypoplasia. Hypoperfusion may present as prolonged time-to-peak, prolonged main transit time, or decreased cerebral blood flow, but it never affects cerebral blood volume ) Fig.39 [12].

2.2. Hemodynamic effect of normal variants and abnormalities:

2.2.1. Understanding collateral function: The presence of hypoplasia or aplasia of segment(s) in the circle of Willis can affect collateral function when one or more arteries are occluded Fig. 15 .

2.2.2. Explains unclear cases of stroke:

Vascular conditions that cause changes in unexpected vascular territories can be explained by normal variations such as:

Ischemia in the posterior territory may accompany ICA pathology due to the presence of fetal PCA Fig. 40 .
Bilateral ischemia and ischemia in certain areas may draw attention to the presence of pathology in one of the options, such as:

Bilateral anterior infarction in case of thromboembolism of azygos ACA or dominant bihemispheric ACA Fig. 41 .
Bilateral mesencephalothalamic infarction with Percheron's artery Fig. 42 .

2.3. Association with vascular and nonvascular congenital anomalies and other diseases:

2.3.1. Association with aneurysms: Changes in vascular anatomy may be a sign of lack of vascular maturity and vulnerability to aneurysm formation. In the work of Lazzaro et al., normal variants of the circle of Willis were more common in cases with ruptured aneurysms than in cases of unruptured aneurysms [13]. Based on a review of the literature, the following variants and abnormalities were associated with aneurysms: Table 4 Fig. 43

Fenestrations: The incidence of aneurysms (IoA) is approximately 7% of all fenestrations. A defect in the media of the fenestrated segment and turbulent flow at both ends of the fenestration can lead to aneurysm formation. Additionally, in the work of Hudák et al., fenestration was a common finding in patients with unexplained subarachnoid hemorrhage due to a weak arterial wall [1] [2] [14]
ICA agenesis and hypoplasia: IoA 67% [2].
A1 segment aplasia: IoA14% [15].
Azygos ACA: IoA 41%. Due to increased flow from both segments of A1 [2].
Persistent dorsal ophthalmic artery: IoA 45% [4].
Persistent primitive olfactory artery: In the work of Uchino et al, 2 intracranial artery aneurysms were found in 14 patients with PPOA (IoA about 14%); one of them is in the hairpin bend (7%) [9].
PTA: IoA 14% [1].
Persistent hypoglossal artery: IoA 26% [16].
Proatlantal intersegmental artery: IoA 10% [1, 2]
Other variants and anomalies associated with aneurysms whose cases have been reported but not available include infraoptic ACA, superior anterior communicating artery, accessory MCA, MCA aplasia, variant PTA, and asymmetry of the circle of Willis [1, 2].

2.3.2. Association with other vascular anomalies and diseases:

Fenestration of the vertebral artery is associated with arteriovenous malformation in 7% [6].
PTA is observed in vascular anomalies such as AVM, carotid-cavernous fistula, and Moyamoya disease in 25% of cases [17].
Proatlantal intersegmental artery: The incidence of cerebrovascular disorders such as AVM, vein of Galen malformation and aortic arch variants is 59% [18].
Spontaneous vertebral artery dissection was slightly more common in subjects with hypoplastic vertebral artery than in controls (30.4% vs. 17.4%). It was also found that spontaneous vertebral artery dissection occurs more often with hypoplastic vertebral arteries than with dominant vertebral arteries (68% versus 32%) [19].

2.3.3. Association with other congenital anomalies:

Azygos ACA may be associated with holoprosencephaly and migration abnormalities Fig. 44 [1].
ICA hypoplasia is associated with anencephaly and basal telangiectasia [2].
Fenestration of the vertebral artery may be associated with vertebral fusion [6].

2.3.4. Association with other disorders:

Pituitary dysfunction and acromegaly in intrasellar “kissing” carotid arteries[2].
It was found that migraine with aura is more common in patients with an open circle of Willis [20].

2.4. Preoperative planning for cranial surgery, head and neck surgery, and neurointerventional procedures:

The description of normal variations is very important for surgeons and interventional radiologists, as some of these variations must be considered to avoid catastrophic consequences during intervention.

2.4.1. The risk of catastrophic hemorrhage exists in the following cases:

Transsphenoidal pituitary surgery in cases of PTA or intrasellar “kissing” carotid arteries.
Middle ear surgery in cases of persistent stapedial artery and aberrant intratympanic ICA.
Pharyngeal surgeries such as otopharyngeal tumor resection, tonsillectomy, adenoidectomy and palatopharyngoplasty in cases of aberrant lateral pharyngeal artery.

2.4.2. Knowledge of normal variations is important in interventional procedures. This knowledge may help to gain vascular access, such as dominant versus hypoplastic vertebral or variant access, or avoid complications during procedures such as tumor embolization through ECA catheterization in cases of MMA arising from the ophthalmic artery, which can lead to blindness . Fig.45 Fig.50

2.4.3. The presence of persistent carotid-basilar anastomoses should be excluded before certain procedures, such as the Wada test: in this case, injection of amytal can lead to loss of consciousness and apnea [2]

Fig.35 Meaning of normal options

Table 4: Variants associated with aneurysms and their occurrence

Fig. 36 3D TOF MRA, funnel-shaped dilatation with origin of Pcom (white arrow), which should not be confused with an aneurysm. Note the small aneurysm at the origin of the contralateral Pcom (red arrow). Also note the trifurcation of the ACA.

Fig. 37 MR perfusion, TTP map (a) shows slow perfusion in the left occipital lobe; no abnormalities were found in other perfusion parameters. 3D TOF (b), showing fetal PCA on the contralateral side (arrow).

Fig. 38 TTP perfusion map (a) shows a symmetrical delay in the occipital lobes, no deviations in other perfusion parameters were noted. 3D TOF shows no Pcom on both sides.

Fig. 39 (same patient as in Fig. 12) with hypoplasia of the right vertebral artery, which ends as the PICA. TTP map shows perfusion delay in the territory of the right PICA. An examination performed 6 weeks later for other reasons (not shown) showed no pathology in this area.

Fig. 40 MRI of a 56-year-old patient complaining of headache shows dissection of the left ICA (red arrows) with intramural hematoma on T2 (a) and T1FS (b). DWI (c) and ADC (d) show subacute infarction in the territory of the left PCA, which is due to the presence of fetal PCA (TOF not shown).

Fig.41 72-year-old patient with hemiplegia, epilepsy and impaired consciousness. DWI (a) and ADC (b) show bilateral infarcts in the ACA territory. DSA (c), shows proximal occlusion of the azygos ACA (arrow).

Fig. 42 Bilateral acute thalamic infarctions on DWI (a). DSA shows occlusion of the P1 segment of the left PCA (b). Minimal recanalization after intra-arterial thrombolysis (c), with mild opacification of the artery of Percheron (arrows) arising from the left PCA.

Fig. 43 Aneurysms (arrows) associated with abnormalities; a) A1 aplasia with Acom aneurysm. b) Azygos ACA with pericallosal aneurysm. c) fenestration of the basilar artery with proximal basilar aneurysm after coiling.

Fig. 44 Axial (a) and sagittal (b) MRI images of a child with holoprosencephaly, anterior cingulate fusion, and abnormal beak and genu corpus callosum. Note the empty flow of the anterior cerebral artery (arrow), which is single (azygos) and displaced anteriorly.

Fig. 45 55-year-old patient involved in an accident. Initial CT scan (a) shows a fracture of the left temporal bone. She later complained of pulsating tinnitus. DSA (c) with flat panel CT angiography (b and d) was performed. Reconstructed images showed the middle meningeal artery (yellow arrows) arising from the ophthalmic artery (blue arrow) and the traumatic AVM (red arrows) draining into the external jugular vein to form an aneurysm (orange arrow). Knowledge of this option is important when planning therapy.

Ischemic stroke in the posterior cerebral arteries: problems of diagnosis and treatment

I.A. KHASANOV, E.I. BOGDANOV

Republican Clinical Hospital of the Ministry of Health of the Republic of Tatarstan, Kazan

Kazan State Medical University

Khasanov Ildar Akramovich

doctor of the neurological department for patients with acute cerebrovascular accidents

420064, Kazan, st. Orenburgsky Trakt, 138, tel. (843) 237-35-47, e-mail

In the light of modern data, the article examines the problems of diagnosis and treatment of ischemic strokes in the posterior cerebral arteries (PCA), taking into account the characteristics of their etiology, clinical picture and neuroimaging data. The paired posterior cerebral arteries, formed by the bifurcation of the basilar artery and being its terminal branches, serve as the main sources of blood supply to the upper part of the midbrain, the thalami and the posteroinferior parts of the cerebral hemispheres, including the occipital lobes, the mediobasal parts of the temporal lobes and the inferomedial parts of the vertex. Ischemic strokes in the posterior cerebral artery basin account, according to various sources, from 5-10 to 25% of cases of all ischemic strokes. The most common cause of isolated infarctions in the PCA territory is embolic occlusion of the PCA and its branches, which occurs in approximately 82% of cases. In 9% of cases, thrombosis in situ is detected in the PCA; in another 9% of cases, the cause of stroke is vasoconstriction associated with migraine and coagulopathy. A very rare cause of infarction in this region can also be arterial dissection affecting the PCA. The most common and characteristic signs of infarctions in the PCA region are visual disturbances (homonymous hemianopsia), central paresis of the facial nerve, headache, sensory disturbances, aphasic disorders, hemiparesis and nigility.

Key words:
ischemic stroke, cerebral infarction, posterior cerebral artery, neuroimaging, thrombolytic therapy
I.A. KHASANOV, EI BOGDANOV

Kazan State Medical University

Republican Clinical Hospital of the Ministry of Health of the Republic of Tatarstan, Kazan

Ischemic stroke in a system of posterior cerebral arteries: problems of diagnosis and treatment

In the article on the basis of present knowledge are considered the problems of diagnosis and treatment of ischemic strokes in a system of posterior cerebral arteries (PCA) taking into account their causation, clinical presentation and neuroimaging data. Paired posterior cerebral arteries, which are shaped by basilar artery bifurcation and are its terminal branches, are the main sources of blood supply of the upside of midbrain, thalamus and back and bottom parts of cerebral hemispheres, including occipital lobes, mediobasal branches of temporal lobes and lower medial crown branches. Ischemic strokes in a system of posterior cerebral arteries amount to 5-10% or up to 25% of all ischemic strokes. The most common cause of isolated heart attacks
in a system of PCA is the embolic occlusion of PCA and its branches, which occurs in about 82% of cases. In 9% of cases in PCA is revealed thrombosis, in other 9% of cases the cause of stroke are vasoconstriction associated with migraine, and coagulopathy. A very rarely reason for a heart attack in this system can be artery dissection which affects the PCA. The most frequent and characteristic features of heart attacks in a system of PCA are visual impairments (equilateral hemianopsia), central paresis of facial nerve, headache, sensation disorders, aphatic disorders, hemiparesis and neglect.
Key words:
ischemic stroke, cerebrovascular accident, posterior cerebral artery, neuroimaging, thrombolytic therapy.
Ischemic strokes in the posterior cerebral arteries (PCA) account, according to various sources, from 5-10 to 25% of cases of all ischemic strokes [1-4]. They can be the cause of a number of clinical symptoms, which are not always promptly and adequately recognized by the patients themselves, their relatives and doctors, because an acute gross motor deficit, which is usually associated with a stroke, in this case may be unexpressed or completely absent. A delay in timely diagnosis or incorrect diagnosis casts doubt on the possibility of providing the patient with adequate therapy (primarily thrombolysis), which in turn cannot but affect the outcome of the disease [5]. An important role in making a diagnosis is played by the possibility of using neuroimaging, the correct choice of method and competent interpretation of the results [2]. It seems important to present and analyze the features of the clinical picture, neuroimaging and treatment of ischemic strokes in the posterior cerebral arteries in the light of modern data.

The most common cause of isolated infarctions in the PCA territory is embolic occlusion of the PCA and its branches, which occurs in 82% of cases. At the same time, cardiogenic genesis is observed in 41% of cases, while arterio-arterial embolism from the vertebral and basilar arteries is observed in only 32% of cases. In 10% of patients, the source of the embolism cannot be determined. In 9% of cases, thrombosis in situ is detected in the PCA. Vasoconstriction associated with migraine and coagulopathies are the causes of cerebral infarction in 9% of cases [6]. If isolated infarctions in the PCA territory in most cases are of a cardioembolic nature, then involvement of the brainstem and/or cerebellum in combination with an infarction in the PCA territory is most often associated with atherosclerotic lesions of the vessels of the vertebrobasilar system [7, 8]. A very rare cause of infarction in this region can also be arterial dissection affecting the PCA [9]. Regardless of the cause of the infarction, it usually only partially involves the PCA territory [10, 11].

Paired posterior cerebral arteries, formed by the bifurcation of the basilar artery and being its terminal branches, serve as the main sources of blood supply to the upper part of the midbrain, thalamus and posteroinferior parts of the cerebral hemispheres, including the occipital lobes, mediobasal parts of the temporal lobes and inferomedial parts of the vertex [10, 12, 13].

In the early stages of development of the human body, the posterior cerebral artery is a branch of the internal carotid artery (ICA) and is supplied with blood from the carotid system, while the posterior communicating artery (PCA) plays the role of its proximal segment. Subsequently, blood begins to flow into the posterior cerebral arteries from the main artery, and the PCA, being a branch of the internal carotid artery, becomes the most significant anastomosis between the carotid and vertebrobasilar areas. According to various sources, from 17 to 30% of adults have a fetal (embryonic) type of PCA structure, in which the ICA remains the main source of blood supply to the PCA throughout life. The fetal type of PCA structure is in most cases observed unilaterally, with the opposite PCA usually starting from an asymmetrically located, curved basilar artery. In cases where both posterior cerebral arteries are branches of the internal carotid arteries, as a rule, well-developed large posterior communicating arteries are observed, and the superior segment of the basilar artery is shorter than usual (the basilar artery ends with the two superior cerebellar arteries arising from it). In approximately 8% of cases, both PCAs originate from the same ICA [7, 8, 12, 14, 15].

The PCA joins the PCA approximately 10 mm distal to the bifurcation of the basilar artery. Each PCA can be conditionally divided into 3 parts: the precommunication part, or P1 segment according to Fisher, - the section of the PCA proximal to the place where the PCA flows into it, the postcommunication part, or P2 segment, located distal to the place where the PCA flows into the PCA, and the final (cortical) the part that gives off branches to the corresponding areas of the cerebral cortex [12, 16]. The paramedian mesencephalic, posterior thalamoperforating and medial posterior choroidal arteries depart from the precommunicative part, participating primarily in the blood supply to the ventrolateral nuclei of the thalamus and the medial geniculate body. The left and right posterior thalamoperforating arteries may arise from a common trunk called the artery of Percheron; a similar variant of the structure usually occurs in combination with unilateral hypoplasia of the P1 segment and the fetal structure of the PCA. The branches of the postcommunication part are the peduncular perforator, thalamogeniculate and lateral posterior choroidal arteries, supplying the lateral geniculate body, dorsomedial nuclei and thalamic cushion, part of the midbrain and the lateral wall of the lateral ventricle [2, 12, 17]. The main cortical branches of the PCA are the anterior and posterior temporal, parietotemporal and calcarine arteries [10]. The boundaries of the watershed of the middle and posterior cerebral arteries basins fluctuate significantly. Usually the border of the PCA basin is the Sylvian fissure, but sometimes the middle cerebral artery supplies blood to the outer parts of the occipital lobe up to the occipital pole. At the same time, the PCA always supplies blood to areas of the cerebral cortex in the area of the calcarine sulcus, and the optic radiation in some cases receives blood from the middle cerebral artery; accordingly, homonymous hemianopsia does not always imply a heart attack in the PCA territory [12].

With ischemic strokes in the PCA region, depending on the location of the vessel occlusion, as well as on the state of collateral blood supply, the clinical picture may reveal symptoms of damage to the midbrain, thalamus and cerebral hemispheres. In general, up to 2/3 of all infarctions in the PCA territory are cortical, the thalamus is involved only in 20-30% of cases, and the midbrain in less than 10% of cases [7, 18, 19]. Accordingly, the most common variant of ischemic stroke in the PCA basin is an isolated infarction of the cerebral hemispheres, primarily the occipital lobes; combined damage to the thalamus and cerebral hemispheres is less common, in a small percentage of cases - an isolated infarction of the thalamus and, finally, a combination of damage to the midbrain, thalamus and /or hemispheres is the rarest option [2].

Sometimes there is bilateral damage to areas of the brain supplied by blood from the PCA. This occurs primarily in top of the basilar syndrome, which is an embolic occlusion of the distal basilar artery and is characterized by depression of consciousness, visual disturbances, oculomotor and behavioral disorders, often without motor dysfunction [2].

According to a number of authors, the most common and characteristic signs of infarctions in the PCA are visual disturbances (up to 95% of cases), homonymous hemianopia (66.7% of cases), central paresis of the facial nerve (52% of cases), headache, mainly in the occipital region. areas (50 cases), sensory disorders (40% of cases), aphasic disorders (38% of cases), hemiparesis (18% of cases) and niglect (10% of cases). Patients usually have a combination of symptoms [2, 7, 8, 11].

Homonymous hemianopia occurs on the contralateral side with infarctions in the areas of blood supply to the hemispheric branches of the PCA due to damage to the striate cortex, optic radiation or lateral geniculate body. In the absence of occipital pole involvement, macular vision remains intact. The visual field defect may be limited to only one quadrant. Superior quadrant hemianopsia occurs when there is an infarction of the striate cortex below the calcarine sulcus or inferior part of the optic radiation in the temporo-occipital region. Inferoquadrant hemianopsia is a consequence of damage to the striate cortex above the calcarine sulcus or the superior part of the optic radiation in the parieto-occipital region. Occlusion of the calcarine sulcus may also be associated with pain in the ipsilateral eye. Visual disturbances may also be more complex, especially with bilateral occipital lobe lesions, including visual hallucinations, visual and color agnosia, prosopagnosia (agnosia for familiar faces), blindness denial syndrome (Anton syndrome), visual attention deficits, and optomotor agnosia ( Balint's syndrome). Often, visual impairment is accompanied by afferent disorders in the form of paresthesia, disorders of deep, pain and temperature sensitivity. The latter indicate involvement of the thalamus, parietal lobe or brainstem (due to occlusion of the proximal vertebrobasilar region) [2, 8, 10, 20].

Neuropsychological abnormalities associated with PCA infarctions vary significantly and are present in more than 30% of cases. A stroke in the basin of the callosal branches of the left PCA in right-handed people, affecting the occipital lobe and splenium of the corpus callosum, is manifested by alexia without agraphia, sometimes color, object or photographic anomia. Right hemisphere infarctions in the PCA territory often cause contralateral hemiglect. With extensive infarctions involving the medial parts of the left temporal lobe or bilateral mesotemporal infarctions, amnesia develops. Also, with mono- or bilateral mesotemporal infarction, agitated delirium may develop. Extensive infarcts in the territory of the left posterior temporal artery may clinically manifest as anomia and/or sensory aphasia. Thalamic infarctions in the areas of blood supply to the penetrating branches of the PCA can cause aphasia (if the left pillow is involved), akinetic mutism, global amnesia and Dejerine-Roussy syndrome (disorders of all types of sensitivity, severe dysesthesia and/or thalamic pain and vasomotor disturbances in the contralateral half of the body, combined with usually transient hemiparesis, choreoathetosis and/or ballism). Also, infarctions in the PCA region may be associated with dyscalculia, spatial and temporal disorientation. [6, 12, 21, 22].

Bilateral thalamic infarcts are often associated with deep coma. Thus, occlusion of the Percheron artery causes the development of bilateral infarcts in the intralaminar nuclei of the thalamus, which leads to severe impairment of consciousness [2, 12].

Hemiparesis during infarctions in the PCA region occurs in only 1/5 of patients, is often mild and transient and is usually associated with involvement of the cerebral peduncles in the pathological process [23, 24]. Cases of infarctions in the PCA region have been described, when patients exhibited hemiparesis without involvement of the cerebral peduncles. These patients had damage to the distal parts of the PCA, primarily involving the thalamogeniculate, lateral and medial posterior choroidal arteries [23, 25]. It is assumed that hemiparesis during infarctions in the posterior choroidal arteries may be associated with damage to the corticobulbar and corticospinal tracts, even in the absence of visible damage to the internal capsule or midbrain according to neuroimaging data [23]. There are opinions that the development of hemiparesis is associated with compression of the internal capsule by edematous tissue of the thalamus [12].

Infarctions in the PCA territory mimic infarctions in the carotid system in 17.8% of patients [24], especially with combined lesions of the superficial and deep branches of the PCA, which is observed in approximately 38% of cases [7, 19, 26]. Differential diagnosis can be difficult due to the presence of aphasic disorders, nigella, sensory deficits, and usually mild and transient hemiparesis resulting from the involvement of the pyramidal tracts. In addition, memory impairment and other acute neuropsychological disorders can significantly complicate the examination of such patients [2, 18, 19].

Among other conditions that often clinically mimic infarctions in the PCA, we should highlight some infectious diseases (primarily toxoplasmosis), posterior reversible leukoencephalopathy syndrome, neoplastic lesions, both primary and metastatic, and thalamic infarctions caused by deep cerebral vein thrombosis [2 , 27]. Neuroimaging methods often play a decisive role in making a diagnosis.

The main requirements for neuroimaging in the acute period of ischemic stroke are the speed of the study and the information content of the data obtained. The main tasks facing the doctor when using these methods are to exclude a non-ischemic cause of the patient’s symptoms, determine the location and size of ischemic foci and the presence of viable brain tissue, determine the condition of the cerebral vessels, identify cerebral edema and displacement of the midline structures, as well as the presence of hemorrhagic impregnation of ischemic foci. These data should help in quickly determining the patient’s treatment tactics—the possibility of intravenous or intra-arterial thrombolysis, mechanical plaque removal, and brain decompression surgery [28, 29].

Computed tomography (CT) usually does not detect ischemic changes in the brain parenchyma during the first few hours after the onset of stroke, the time most important for initiating therapy, and sometimes even later in the disease. Visualization of the posterior regions of the brain is especially difficult due to artifacts caused by the bones of the skull. However, with strokes in the territory of the PCA, as well as with strokes in the territory of the middle cerebral artery, in some cases, CT may show a hyperintense signal from the PCA itself, which is the earliest sign of a stroke in its territory and is detected in 70% of cases within the first 90 minutes from onset of the disease and in 15% of cases within 12 to 24 hours. This sign appears due to visualization of a calcified embolus or atherothrombosis in situ. On a standard CT scan, the slice plane is parallel to the orbitomeatal line (the line connecting the outer corner of the eye with the external auditory canal and then going to the first cervical vertebra). Based on the course of the SMA, its lumen is usually visualized in one section, which makes it easy to identify hyperdense SMA, especially in the presence of atrophic changes in the brain. The course of the PCA is more complex. Typically, its proximal segment ascends laterally around the cerebral peduncles and, reaching the bypass cistern, goes horizontally inward to the temporal lobe, in close proximity to the tentorium cerebellum. The circular part (P1 and P2 segments) ends in the quadrigeminal cistern, where the cortical part of the PCA begins. Only the P2 segment runs parallel to the cut inside the bypass tank and, accordingly, hyperdensity, if present, can most likely be detected in this area. Subsequently, CT signs of ischemic changes appear as areas of hypointensity in the brain parenchyma [2, 3, 30].

Magnetic resonance imaging (MRI) makes it possible to more accurately determine the presence and nature of ischemic changes in the brain during stroke. Diffusion-weighted imaging (DWI) can detect early ischemic changes, often within an hour of symptom onset, and localize and extend lesions more accurately than CT [2]. The combined use of DWI, ADC and FLAIR modes makes it possible to differentiate acute, subacute and chronic ischemic changes in the brain parenchyma, as well as to distinguish cytotoxic brain edema observed in ischemic stroke from vasogenic edema in the syndrome of posterior reversible leukoencephalopathy and hypertensive encephalopathy [2, 27, 31 , 32].

CT angiography (CTA) plays a significant role in the non-invasive diagnosis of steno-occlusive lesions of large extra- and intracranial arteries. This technique makes it possible to identify the degree of stenosis, plaque morphology, as well as the presence of arterial dissection in both vertebrobasilar and carotid vessels. In addition, the anatomical features of collaterals and circulation options of the PCA are assessed [2, 33, 34]. Additional information about vascular anatomy can be obtained using contrast-enhanced MR angiography, which, in combination with CTA, allows for data that previously could only be obtained using classical angiography. In addition, these methods are important in assessing the effectiveness of thrombolytic therapy in the case of arterial recanalization [2].

Currently, thrombolytic therapy for ischemic stroke can be used for damage to the arteries of both the carotid and vertebrobasilar areas. Nevertheless, all currently existing guidelines for thrombolysis are focused primarily on vascular catastrophe in the carotid region, primarily the middle cerebral artery; this is primarily due to the presence in such patients of obvious neurological deficits in the form of severe paresis and sensory disturbances. A typical functional deficit in a patient with a heart attack in the PCA region in the acute period is not always regarded by the doctor as disabling. The assessment of neurological deficit according to the National Institutes of Health Stroke Scale (NIHSS), which is one of the criteria for selecting patients for thrombolytic therapy, usually is not able to fully reflect the severity of the condition of a patient with a vertebrobasilar infarction [7]. There are no recommendations at all regarding an isolated visual field defect in acute infarction in the PCA territory [2]. Therefore, thrombolytic therapy in patients with infarctions in the PCA is not widely used. However, given that hemiparesis in some cases is a significant clinical component of infarctions in the PCA territory, such patients, in the absence of contraindications, are justifiably treated with systemic and/or intra-arterial thrombolysis [35].

When comparing the efficacy and safety profiles of intravenous thrombolysis administered within the first three hours from the onset of symptoms in patients with carotid infarctions and PCA infarctions, no significant difference in safety and treatment outcome was found [7]. At the same time, according to a number of authors, when conducting intravenous thrombolytic therapy for ischemic lesions in the vertebrobasilar region, and in particular the PCA, it is possible to expand the therapeutic window to 6.5-7 hours and even more compared to 4.5 hours for infarctions in the carotid pool [36, 37].

Intra-arterial thrombolysis for occlusion of the middle cerebral artery is recommended within 6 hours from the onset of symptoms, and for occlusion of the basilar artery - no later than 12 hours [28]. However, to date there are no clear recommendations on the time limits for intra-arterial thrombolysis in patients with PCA lesions [15]. N. Meier et al. (2011) described 9 cases of intra-arterial thrombolysis in patients with PCA occlusion within the first 6 hours from the onset of the disease. 3 months after treatment, functional independence (modified Rankin scale 0-2 points) was detected in 67% of patients, which correlates with similar data for the carotid system [15].

An early diagnosis of ischemic stroke in the PCA allows the doctor to promptly determine the patient’s treatment tactics and, in the absence of contraindications, consider the possibility of thrombolytic therapy, which undoubtedly makes the prognosis for the patient more favorable.

LITERATURE

1. Brandt T., Steinke W., Thie A., Pessin MS, Caplan LR Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome. Multicenter results and a review of the literature // Cerebrovasc. Dis. - 2000. - Vol. 10. - P. 170–182.

2. Finelli P. Neuroimaging in acute Posterior Cerebral Artery Infarction // The Neurologist. - 2008. - Vol. 14. - P. 170-180.

3. Krings T., Noelchen D., Mull M. et al. The hyperdense posterior cerebral artery sign // Stroke. - 2006. - Vol. 37. - P. 399-403.

4. Hill MD Posterior cerebral artery stroke // e-medicine, 2005.

5. Khasanov I.A. Features of infarctions in the basin of the posterior cerebral arteries // Neurological Bulletin. - 2012. - T. XLIV, issue. 3. - pp. 69-74.

6. Caplan L. Posterior Circulation Ischemia: Then, Now, and Tomorrow: The Thomas Willis Lecture-2000 // Stroke. - 2000. - Vol. 31. - P. 2011-2023.

7. Breuer L., Huttner H. B., Jentsch K. et al. Intravenous Thrombolysis in Posterior Cerebral Artery Infarctions // Cerebrovasc Dis. - 2011. - Vol. 31. - P. 448-454.

8. Caplan L., Bogousslavsky J. Posterior cerebral artery syndromes // Cerebrovascular Disease: Pathology, Diagnosis and Management. - 1998. - P. 1028.

9. Caplan L., Estol C., Massaro A. Dissection of the posterior cerebral arteries // Arch Neurol. - 2005. - Vol. 62. - P. 1138-1143.

10. Brazis P. Topical diagnostics in clinical neurology / P. Brazis, D. Masdew, H. Biller - M.: MEDpress-inform, 2009. - 736 p.

11. Caplan L. Posterior Circulation disease: Clinical Findings, Diagnosis and Management / Boston, MA: Butterworth-Heinemann, 1996. - 533 p.

12. Beer M. Topical diagnosis in neurology according to Peter Duus / M. Beer, M. Frotscher. - M.: Practical Medicine, 2009. - 468 p.

13. Tatu L., Moulin T., Bogousslavsky J. et al. Arterial territories of the human brain // Neurology. - 1998. - Vol. 50 - P. 1699-1708.

14. de Monye C, Dippel DW, Siepman TA et al. Is a fetal origin of the posterior cerebral artery a risk factor for TIA or ischemic stroke? A study with 16-multidetector-row CT angiography // J. Neurol. - 2008. - Vol. 255 - P. 239-245.

15. Meier N., Fischer U., Schroth G. Outcome after thrombolysis for acute isolated posterior cerebral artery occlusion // Cerebrovasc. Dis. - 2011. - Vol. 328. - P. 79-88.

16. Phan T., Fong A., Donnan G. et al. Digital map of posterior cerebral artery infarcts associated with posterior cerebral artery trunk and branch occlusion // Stroke. - 2007. - Vol. 38. - P.1805-1811.

17. Chaves CJ Posterior cerebral artery. Stroke syndromes. 2nd edition / Chaves CJ, Caplan LR Cambridge, New York: Cambridge University Press. — 2001. — 747 p.

18. Cals N., Devuyst G., Afsar N. et al. Pure superficial posterior cerebral artery territory infarction in the Lausanne Stroke Registry // J. Neurol. - 2002. - Vol. 249. - P. 855-861.

19. Kumral E., Bayulkem G., Atac C., Alper Y. Spectrum of superficial posterior cerebral artery territory infarcts // Eur. J. Neurol. - 2004. - Vol. 11. - P. 237-246.

20. Ng YS, Stein J, Salles SS et al. Clinical characteristics and rehabilitation outcomes of patients with posterior cerebral artery stroke // Arch. Phys. Med. Rahabil. - 2005. - Vol. 86. - P. 2138-43.

21. Brandt T., Thie A., Caplan L. et al. Infarkte in Versorgungsgebiet der A. cerebri Posterior // Nervenarzt. - 1995. - Vol. 66. - P. 267-274.

22. Savitz SI, Caplan LR Vertebrobasilar disease // N. Engl. J. Med. - 2005. - Vol. 352. - P. 2618-26.

23. Finelli P. Magnetic Resonance Correlate of Hemiparesis in Posterior Cerebral Artery Infarction // Journal of Stroke and Cerebrovascular Disease. - 2008. - Vol. 17. - P. 378-381.

24. Maulaz AB, Bezerra DC, Bogousslavsky J. Posterior cerebral artery infarction from middle cerebral artery infarction // Arch. Neurol. - 2005. - Vol. 62. - P. 938-941.

25. Neau J.-P., Bogousslavsky J. The syndrome of posterior choroidal artery territory infarction // Ann. Neurol. - 1996. - Vol. 39. - P. 779-788.

26. Lee E., Kang DW, Kwon SU, Kim JS Posterior cerebral artery infarction: diffusion-weighted MRI analysis of 205 patients. Cerebrovasc. Dis. - 2009. - Vol. 28. - P. 298-305.

27. Bogdanov E.I., Khasanov I.A., Mamedov Kh.I. and others. Posterior reversible leukoencephalopathy syndrome in patients with preeclampsia and eclampsia // Neurological Journal. - 2011. - No. 5. - P. 35-40.

28. Adams H., Del Zoppo G., Alberts M. et al. Guidelines for the early management of adults with ischemic stroke // Stroke. - 2007. - Vol. 38. - P. 1655-1711.

29. Wahlgren N., Ahmed N., Davalos A. et al. Thrombolysis with alteplase for acute ischemic stroke & the Safe implementation of thrombolysis in stroke - monitoring study (SITS-MOST): an observational study // Lancet. - 2007. - Vol. 369. - P. 275-282.

30. Berge E., Nakstad PH, Sandset PM Large middle cerebral artery infarctions and the hyperdense middle cerebral artery sign in patients with atrial fibrillation // Acta Radiol. - 2001. - Vol. 42. - P. 261-268.

31. Covarrubias DJ, Leutmer PH, Caumpeau NG Posterior reversible leukoencephalopathy syndrome: prognostic utility of quantitative diffusion-weighted MR image // AJNR Am J. Neuroradiol. - 2002. - Vol. 23, N 6. - P. 1038-1048.

32. Garg R. Posterior leukoencephalopathy syndrome // Postgrad. Med. J. - 2001. - Vol. 77, N 903. - P. 24-28.

33. Choi C., Lee D., Lee J. et al. Detection of intracranial atherosclerotic steno-occlusive disease with 3D time-of-flight magnetic resonance angiography with sensitivity encoding at 3T // AJNR Am J. Neuroradiol. - 2007. - Vol. 28. - P. 439-446.

34. Lev M., Farkas J., Rodrigues V. et al. CT angiography in the rapid triage of patients with hyperacute stroke to intraarterial thrombolysis: accuracy in the detection of large vessel thrombus // J Comput Assist Tomogr. - 2001. - Vol. 25. - P. 520-528.

35. Ntaios G., Spengos K., Vemmou AM et al. Long-term outcome in posterior cerebral artery stroke // European Journal of Neurology. - 2011. - P. 156-162.

36. Forster A., Gass A., Kern R. et al. MR Imaging-Guided Intravenous Thrombolysis in Posterior Cerebral Artery Stroke // AJNR Am J. Neuroradiol. - 2011. - Vol. 32. - P. 419-421.

37. Montavont A., Nighoghossian N., Derex. L et al. Intravenous r-TPA in vertebrobasilar acute infarcts // Neurology. - 2004. - Vol. 62. - P. 1854-1856.

Abbreviations:

A1: Horizontal segment of ACA
A2: Vertical segment of ACA
ACA: Anterior cerebral artery
Acom: Anterior communicating artery
AICA: Anterior inferior cerebellar artery
AVM: Arteriovenous malformation
BA: Basilar artery
CBF: Cerebral blood flow
CBV: Cerebral blood volume
CoW: Circle of Willis
DSA: Digital subtraction angiograph
ECA: External carotid artery
ICA: Internal carotid artery
IoA: Incidence of aneurysms
M1: Sphenoidal segment of MCA
MCA: Middle cerebral artery
MMA: Middle meningeal artery
MTT: Mean transit time
PCA: Posterior cerebral artery
Pcom: Posterior communicating artery
PDOA: Persistent dorsal ophthalmic artery
PICA: Posterior inferior cerebellar artery
PPHA: Persistent primitive hypoglossal artery
PPOA: Persistent primitive olfactory artery
PTA: Persistent trigeminal artery
SCA: Superior cerebellar artery
sVAD: Spontaneous vertebral artery dissection