RU2294696C1 - Method for evaluating the areas of cerebral epileptic activity - Google Patents

Abstract

FIELD: medicine, neurosurgery, neurology, epileptology.

SUBSTANCE: it is necessary to carry out dopplerographic inspection of cerebral vessels to detect the index of peripheral resistance (IPR), vasoconstrictor reserve (R(-)) upon hypocapnic loading and vasodilation reserve (R(+)) upon hypercapnic loading. Moreover, for each artery one should calculate the cerebral autonomic index (CAI) by the following formula: CAI = R(-)) : R(+)) : IPR, the value of which should be determined as epileptogenic or boundary or nonepileptogenic. If one should apply pulsation index as IPR, as R(-) - the coefficient of reactivity upon hypocapnic loading, and as R(+) - the coefficient of reactivity upon hypercapnic loading it is possible to detect CAI value as: epileptogenic at 0.3≤CAI≤0.5; boundary at 0.27≤CAI<0.3 or 0.5<CAI≤0.53; nonepileptogenic at CAI<0.27 or CAI>0.53. Then it is necessary to compare every epileptogenic or boundary CAI value against IPR value of corresponding arteries: at epileptogenic CAI and IPR within the norm - one should evaluate the area of epileptic activity (AEA) as primary; at epileptogenic CAI and IPR being below or above the norm - as secondary; at boundary CAI and IPR of any values - as boundary; and epileptogenesis-dominating hemisphere should be detected according to quantitative majority of AEA at the highest value. The innovation enables to obtain quantitative criteria that favor to conduct comparative evaluation of disorders in every vascular basin.

EFFECT: higher accuracy of evaluation.

3 ex, 4 tbl

Description

The invention relates to medicine, namely to neurosurgery, neurology and epileptology, and can be used to identify primary areas of epileptic activity (OEA) for assessing the brain epileptic system and predicting further epileptogenesis, as well as for dynamic observation and correction of treatment tactics.

Various processes in the brain change its bioelectric activity, which can lead to the appearance of OEA, epileptic foci and manifest itself as epileptic seizures. In the early stages of epileptogenesis, primary OEA (focus) is formed, later on, under the influence of various neurophysiological processes, epileptic activity is projected into other structures of the brain [4]. A necessary condition for the success of treatment, especially surgical, is the removal of the primary epileptic focus and the separation of the epileptic system formed in the brain, however, these structures are often not found [5]. According to the modern concept, cerebral blood flow disorders are preceded by paroxysmal changes in electroencephalography (EEG) [9], and ischemia is the trigger of an epileptic seizure [1].

A known method for assessing OEA clinically by the structure of the attack [5]. However, this method has only indicative value, since epileptic seizures can be polymorphic, change their structure during epileptogenesis, and, moreover, they can have a conversion nature rather than an epileptic one. Needs objectification.

There is a method of assessing OEA by EEG by fluctuations in the electrical potentials of the brain with an amplitude of about 50 μV, recorded in a visual form with the help of encephalographs with powerful amplifiers. The vibrations are recorded on paper ("paper" EEG) or on a computer (computer EEG). Assess background recording and, if necessary, recording with various methods of provoking epileptic activity (photostimulation, hyperventilation, sleep deprivation) [2]. However, the evaluation of the research result depends on the “human factor”, since it is either completely performed by visual analysis of the oscillations and has a descriptive character (“paper” EEG), or a visual selection of the oscillations is made for subsequent computer-aided quantitative analysis and topographic mapping (computerized EEG). The results of computerized EEGs have no equivalents in clinical practice [3]. Only areas of the brain that already have epileptic activity and do not reveal areas that will be involved in the epileptic process in the further course of the disease are determined by EEG. The primary focus is not always determined, and sometimes in the interictal period the epi-activity of the brain is not detected.

A known method for assessing OEA by EEG-video monitoring. It allows you to evaluate in detail the ratio of the various phases of a clinical seizure with the dynamics of epileptiform discharges by EEG. Digital video monitoring allows you to track the sequence of events in steps of 40 milliseconds, which gives an accurate definition of the onset of the epileptic discharge and, therefore, the localization of the primary epileptic focus [5]. But significant information can be obtained only at the time of the attack and only from those areas of the brain that are directly involved in the recorded seizure. It does not determine the area where the spread of the epileptic process is possible in future. It does not provide information in the interictal period. The method is not acceptable for rare epileptic seizures.

A known method for assessing OEA by invasive intracranial and intraoperative EEG registration: with invasive electrodes (oval hole electrode, long-term intracranial electrodes), with electrical stimulation through intracranial electrodes. Allows you to accurately identify the primary epileptic focus. But the method is traumatic, serious complications are possible both at the time of the manipulation, and delayed. High qualification and coordination of the work of various specialists is required [5].

There is a method of assessing OEA by intraoperatively performing the Wada test under the control of EEG and neuropsychological testing [5]. Allows you to determine the lateralization of epileptic activity. However, in many cases it does not reveal the exact localization of the primary focus; traumatic because it requires catheterization of the carotid arteries and the introduction of a pharmacological drug (sodium amital); Highly qualified staff needed.

A known method for assessing OEA by magnetic resonance imaging (MRI) and MRI angiography to visualize pathological areas of the brain and cerebral vessels. The aim of the study is to identify volume formations of various genesis, degeneration of cellular neuronal elements, hippocampal sclerosis and hyalinosis, and manifestations of cortical dysgenesis [5]. However, the organic pathology of the brain is not necessarily manifested by epileptic activity, and, conversely, the failure to identify organic pathology does not exclude the epileptic activity of the brain.

A known method for assessing OEA by positron emission tomography (PET). After the introduction of a natural metabolite - glucose labeled with a positron-emitting radionuclide into the body, OEA (focus) is detected by a significant decrease in metabolism in the interictal period and an increase - at the time of the attack. It is possible to obtain a quantitative assessment, as well as a serial tomographic image, which allows you to connect mediator processes with anatomical structures [7]. But there may be difficulties in interpreting data obtained in the pre-crime and post-crime periods, which reduces the value of the results. To conduct the study, the patient is administered a radioactive pharmaceutical product. Sometimes an additional anesthetic benefit is necessary, which can negatively affect the detection of OEA. The equipment is complex, you need a special room and specially trained personnel.

A known method for assessing OEA by single-photon emission computed tomography (SPECT) with the intravenous administration of a radiopharmaceutical (labeled with radioactive technetium hexamethyl-propylene-oxime-lipophilic amine). The drug passes through the blood-brain barrier and is distributed in the brain tissue in proportion to the regional cerebral blood flow, which is displayed in the form of tomographic sections. In the interictal period, a decreased volumetric blood flow is determined in the area of the primary focus. With a reduction in blood circulation, the amount of accumulation of the drug in the corresponding region of the brain drops significantly and thus a pool of damage to one of the main arteries is detected [8]. However, the area of the brain with reduced perfusion is not pathognomonic for epilepsy, but may be with various pathological processes. There is the possibility of obtaining erroneous results in the pre- and post-attack periods. For research, a patient is administered a radioactive drug. Sometimes an additional anesthetic benefit is necessary, which can negatively affect the detection of OEA. The equipment is complex, it requires specially trained personnel and a special room.

Closest to the claimed method is a method for assessing OEA by dopplerography of cerebral vessels with test effects that change the gas composition of the blood (hypocapnia and hypercapnia), adopted as a prototype. According to calculated indicators, showing separately: the initial vascular wall tone, determined by the peripheral resistance index (IPA), vasoconstriction reserve (for hypocapnic load) and vasodilation reserve (for hypercapnic load) and by logical reasoning, arteries with impaired cerebrovascular reactivity are detected (CV) . In case of a disturbed CVR, the “state change” of the vascular wall against the background of the load with respect to its “initial state” (tone) does not correspond to adaptive expediency and orientation. OEA are topically determined by their correspondence to the pool of blood supply to arteries with impaired CVR. Accordingly, these OEA are evaluated by the severity of violations of CVR [6]. The method is not invasive, not traumatic, it is possible to conduct a study at the patient's bedside, as well as dynamic observation.

The disadvantage of the method chosen for the prototype is its lack of accuracy and information. It does not provide quantitative assessment criteria that allow assessing severity in a single numerical format and conducting a comparative assessment of CVR disorders in each vascular pool. In this regard, it does not allow to reliably and in a single numerical format evaluate each OEA by its significance in epileptogenesis. The result depends on the “human factor”, since the researcher needs to make speculative logical comparisons of three indicators (tonus, vasodilation reserve and vasoconstriction reserve) to determine the state of CVR in each cerebral artery, and then conduct a comparative assessment between them to identify the vessel with the most severely impaired CVR . With greater reliability, the method allows to determine and evaluate those OEA that are supplied with blood vessels with increased tone and increased vasoconstrictor reserve. But in this case, the reliability of the conclusion will be doubtful, since the assessment of the vasodilatory reserve can change the "speculative" interpretation of the direction of the reactions. In cases with normal or low vascular tone, as well as with multiple OEA, the method is uninformative. Confirmation by other means of determining and evaluating the OEA is required.

The objective of the proposed method is to increase the accuracy and information content of the OEA assessment. The problem is achieved in that quantitative criteria are added to the prototype method, which allow one to evaluate OEA by significance in epileptogenesis in a single numerical format.

The method is as follows.

The patient is examined for cerebral great vessels by Dopplerography according to the generally accepted method, determining the linear blood flow velocity (LSC) and its calculated indicator - IPA - in all examined arteries from two sides: the middle cerebral artery (SMA), the anterior cerebral artery (PMA), and the posterior cerebral arteries (ZMA), vertebral artery, internal carotid artery and main artery (OA).

Test effects on hypocapnia and hypercapnia are carried out. For each artery, the vasoconstrictor reserve indicator P (-), determined during hypocapnic loading, and the vasodilation reserve indicator P (+), determined during hypercapnic loading, are calculated.

Then, the calculation is made according to the formula of cerebral autonomic index (CVI) for each artery:

CVI = P (-): P (+): IPS, where

P (-) - an indicator of a vasoconstrictor reserve,

P (+) - indicator of vasodilation reserve,

IPS is an index of peripheral resistance.

The numerical value of CVI determines the value of the indicator: epileptogenic, or borderline, or non-epileptogenic.

Then, each epileptogenic or borderline CVI value is compared with the IPS of the corresponding arteries and the corresponding OEA basins of blood supply are evaluated for their importance in epileptogenesis.

Allocate:

- primary OEA, if CVI is within the limits of epileptogenic values and IPA is within the normal range,

- secondary OEA, if CVI within the limits of epileptogenic values and IPA is less or more than the norm,

- border OEA, if CVI is within the border values, IPA is not significant.

In multiple OEA in both hemispheres, the hemisphere dominating in epileptogenesis is determined by the numerical majority of OEA with the greatest significance.

For example, the Gosling pulsation index (PI), which is considered the most informative and, as a rule, is calculated automatically during the study (PI = Vsyst.-V diast .: Vred., Where Vsyst. - systolic LSC, Vdiast. - diastolic, is used as IPS. LSK, Vred. - average LSK). Normal values are 0.7≤PI≤0.9.

As a test effect on hypocapnia and hypercapnia, for example: hypocapnia is tested with hyperventilation (the patient breathes deeply and often over time until the blood flow decreases to the formation of a “plateau”, this indicator of BFV (V (-)) is fixed) and for hypercapnia - a test with a breath hold (the patient is asked to hold his breath, without a previous deep breath, for as long as he can; the maximum value of BFV (V (+)) observed immediately after the first breath is fixed). As indicators P (-) and P (+), the most used in practice are used: reactivity coefficient for hypocapnic load (Cp (-)) and reactivity coefficient for hypercapnic load (Cp (+)). (Кр (-) = 1-V (-): V (0); Кр (+) = V (+): V (0), where V (-) is the LFV value for the sample with hyperventilation, V (+) - LSC in the sample with a breath-holding, V (0) - LSC initial, obtained before the load tests). Normal values are: 1.3≤Kr (+) ≤1.6 and 0.3≤Kr (-) ≤0.5.

CVI for each studied artery is calculated by the formula

CVI = Kr (-): Kr (+): PI, where

PI - Gosling pulsation index,

Кр (-) - coefficient of reactivity to hypocapnic load,

Cr (+) is the coefficient of reactivity to hypercapnic load.

The numerical value of CVI determines the value of the indicator:

- epileptogenic, if 0.3≤CVI≤0.5,

- borderline, if 0.27≤ CVI <0.3 or 0.5 <CVI≤0.53,

- non-epileptogenic if CVI <0.27 or CVI> 0.53.

Then, each epileptogenic or borderline CVI value is compared with the IPS of the corresponding arteries and the corresponding OEA basins of blood supply are evaluated for their importance in epileptogenesis.

Allocate:

- primary OEA, if 0.3≤CVI≤0.5 and 0.7≤PI≤0.9,

- secondary OEA, if 0.3≤CVI≤0.5 and PI <0.7 or PI> 0.9,

- border OEA, if 0.27≤ CVI <0.3 or 0.5 <CVI≤0.53 and PI is not significant.

The inventive method has passed clinical trials on the basis of the Russian National Scientific Research Institute named after prof. A.L. Polenova during the examination of 4 healthy volunteers, 23 patients with epilepsy, 5 - brain tumors with epileptic syndrome, aged 5 to 46 years, without bad habits. When examining patients, a complex of neurosurgical methods was used, including EEG, PET, SPECT, MRI and MRI angiography.

During clinical trials, the quality of diagnosis and treatment of patients with epileptic diseases and syndromes was improved, since diagnostic errors and inaccuracies in identifying and differentiating the primary epileptic focus and secondary structures in the epileptic system were excluded, a forecast was made for the development of new foci of epileptic activity in the further course diseases, which allowed to adequately and accurately adjust the treatment of patients.

Example 1. Healthy volunteer, 17 years old, m.

EEG - without pathology. MRI of the brain - without pathology.

Table 1 presents the data of the Doppler study.

Table 1 SMA right SMA left PMA right PMA left ZMA right ZMA left OA LSK 76 74 58 60 46 40 38 PI 0.86 0.84 0.82 0.84 0.88 0.64 0.62 K + 1.45 1.49 1.44 1.49 1.44 1.31 1.30 TO- 0.32 0.33 0.31 0.33 0.32 0.49 0.46 tsvi 0.26 0.26 0.26 0.26 0.25 0.58 0.57

According to table 1, according to the prototype method, in the right SMA, right PMA, right ZMA, left SMA and left PMA, the values of PI, Kp (+) and Kp (-) are within the normal range (0.7≤PI≤0.9, 1.3≤Kr (+) ≤1.6, 0.3≤Kr (-) ≤ (0.5), which indicates the safety of CVR. In OA and left ZMA, PI (PI <0.7) is lowered, against which Kr (+) is less and Kr (- ) - more than in the other vessels and within the normal range, which has an adaptive orientation and indicates the preservation of the CVR, since the CVR has been preserved in all the vessels, there is no OEA.

According to the study conducted according to the claimed method, in all the studied vessels CVI has non-epileptogenic values (CVI <0.27, or CVI> 0.53). Therefore, there is no OEA.

Example 2. Patient G., 44 years old, female, and / b No. 936-04. Diagnosis: temporal lobe epilepsy.

According to EEG - epileptic activity in the mediobasal departments of both temporal lobes, according to SPECT - hypoperfusion of the frontal and temporal lobes on the right, the decrease in perfusion of the hippocampal nuclei on the right is greater than on the left. Doppler data are presented in table.2.

table 2 SMA right SMA left PMA right PMA left ZMA right ZMA left OA LSK 67 53 61 58 31 35 43 PI 0.73 0.74 0.76 0.56 0.66 0.69 0.66 Cr + 1.40 1.58 1.46 1.40 1.32 1.4 1.51 Cr 0.40 0.34 0.38 0.40 0.39 0.37 0.35 CVI 0.39 0.29 0.34 0.51 0.45 0.38 0.35

According to table 2, according to the prototype method, in the left PMA, left ZMA and right ZMA and OA, the PI values are reduced (PI <0.7), in the remaining PI vessels within the normal range (0.7≤PI≤0.9). In all vessels, Кр (+) and Кр (-) are within the normal range (1.3≤Kr (+) ≤1.6 and 0.3≤Kr (-) ≤0.5). In this case, significant differences in the values of Kp (-) between the vessels with normal and reduced PI are not determined. This may indicate a violation of CVR in vessels with a low tone, but unconvincing. Thus, the prototype method is not informative.

According to a study conducted according to the claimed method:

primary OEA (0.3≤CVI≤0.5 and 0.7≤PI≤0.9) corresponds to the vasotope of the right SMA (CVI - 0.39, PI - 0.73) and the right PMA (CVI - 0.34, PI - 0.76); secondary OEA (0.3 ≤ CVI≤0.5 and PI <0.7) - the right ZMA (CVI - 0.45, PI - 0.66), the left ZMA (CVI - 0.38, PI - 0.69) and OA (CVI - 0.35, PI - 0.66); border OEA (0.27≤ CVI <0.3 or 0.5 <CVI≤0.53 and PI is not significant) - left SMA (CVI - 0.29), left PMA (CVI - 0.51).

Thus, the prototype method was not informative. The inventive method allowed to evaluate the data of a comprehensive study. So, to the right frontal and temporal lobes (according to OEFT) there is a primary OEA (pool of the right PMA and right SMA), and the rest of the brain, determined by EEG and OEFT, to the secondary OEA. Border OEA (pools of left MCA and left PMA) without adequate treatment, with certain provoking factors, will exhibit epileptic activity in the future.

Subsequently, the patient underwent surgical treatment with removal of the primary epileptic focus (respectively, primary OEA). This led to a regression of epileptic activity in general.

Example 3. Patient 3., 26 years old, female, and / b No. 2591-04. Diagnosis: epilepsy with polymorphic seizures.

The examination did not reveal the side of the primary lesion location: localization on the left was indicated: EEG-epileptic activity is recorded in both temporal leads, more on the left and OEFT is the focus of hypoperfusion in the left temporal lobe. Localization on the right was indicated: MRI - hypoplasia of the right hippocampus, and PET - the focus in the right temporal lobe. Table 3 presents the data of the Doppler study.

Table 3 SMA right SMA left PMA right PMA left ZMA right ZMA left OA LSK 80 78 64 61 52 38 58 PI 0.73 0.95 0.76 1.25 0.75 0.68 0.67 Cr + 1.41 1.23 1.41 1.46 1.19 1.45 1.28 Cr 0.29 0.4 0.29 0.3 0.38 0.34 0.33 tsvi 0.28 0.34 0.27 0.16 0.43 0.34 0.38

According to table 3, according to the prototype method, in the left SMA, PI is increased (PI> 0.9), while Kr (-) is within the normal range (0.3≤Kr (-) ≤0.5), but its value is maximum (0.4) among of all other vessels, and Кр (+) is reduced to 1.23 (Кр (+) <(. 3), which indicates a disturbed CVR. In the right ZMA, PI is within normal limits, Cr (-) is within normal limits, but one of the maximum according to the value of (0.38) and Кр (+), it is significantly reduced - to 1.19 (Кр (+) <1.3), which indicates a disturbed CVR. Since the tone of the left SMA is increased, and the right ZMA remains normal, the violation of CVR in the left is more pronounced SMA by comparison CVI is assessed as moderately impaired in all other vessels, and it is not possible to make a comparative assessment: in the left PMA, PI is maximally increased (1.25), Kr (-) is at the lower limit of the norm, and Kr (+) is closer to upper boundary; in the left ZMA, PI is moderately reduced to 0.68 (PI <0.7), Kr (+) is the norm, Kr (-) is at the lower boundary of normal values; in the right SMA and right PMA, PI is within the norm, Kr (+) - normal, but Cr (-) is moderately reduced; in OA, PI is reduced and Cr (+) is moderately reduced, while Cr (+) is normal. Thus, the pool of the left MCA (vasotopically - the left temporal lobe) has the maximum epileptogenicity (primary focus), the pool of the right ZMA is less pronounced, all other brain areas are involved in the epileptic process, but less significantly.

According to a study conducted according to the claimed method (table 3): primary OEA (0.3≤CVI≤0.5 and 0.7≤PI≤0.9) corresponds to indicators of the right ZMA (CVI - 0.43, PI - 0.75); secondary OEA (0.3≤CVI≤0.5 and PI <0.7 or PI> 0.9) - left SMA (CVI - 0.34, PI - 0.95), left ZMA (CVI - 0.34, PI - 0.68) and OA (CVI - 0.38, PI - 0.67); border OEA (0.27≤ CVI <0.3 and PI is not significant) corresponds to the right SMA (CVI - 0.29) and the right PMA (CVI - 0.27). The pool of blood supply to the left PMA is not an OEA. The right hemisphere dominates in epileptogenesis (the numerical majority of primary OEA).

When planning surgical treatment, the results of OEFT, EEG and the prototype method were chosen as the basis, and the results of the proposed method, which coincided with MRI and PET, were not taken into account. Therefore, the patient underwent a partial resection of the left temporal lobe under the control of electrocortography, in which the paroxysmal activity of the pole of the left temple was recorded. This served as additional confirmation of the correct choice of the primary epileptic focus already during the operation.

However, after the operation, a significant deterioration was observed: seizures became more frequent, including frequent generalized seizures, and diffuse epileptic activity on EEG. Doppler data after surgery are presented in table 4.

Table 4 SMA right SMA left PMA right PMA left ZMA right ZMA left OA LSK 78 137 132 70 56 64 54 PI 0.78 0.93 0.73 0.91 0.77 0.75 0.65 Cr + 1.35 1.24 1.23 1.53 1.18 1.32 1.41 Cr 0.4 0.45 0.33 0.37 0.39 0.43 0.33 CVI 0.38 0.39 0.37 0.27 0.43 0.43 0.36

According to table 4, according to the prototype method, after the operation, the CVR remains violated: in the left SMA (in the operation zone), as well as in the right ZMA, since PI, Kr (-) and Kr (+) did not significantly change. In the remaining vessels, the CVR remains moderately disturbed, taking into account the dynamics of the indicators: in the right SMA - with a tendency to increase the PI, Cr (-) increased (from 0.29 to 0.4) and Cr (+) decreased (from 1.41 to 1.35); in the right PMA - with a PI decreasing tendency, Cr (+) decreased below the norm (from 1.41 to 1.23), Cr (-) increased to the norm (from 0.29 to 0.33); in the left ZMA - PI increased to normal (from 0.68 to 0.75), but Cr (+) decreased, and Cr (-) increased; in the left PMA, the initially high PI decreased (from 1.25 to 0.91), but at the same time, Kr (+) increased above normal values to 1.53 (Kr (+)> 1.5); in OA - against the background of unchanged decreased PI and normal Cr (-), Cr (+) increased (from 1.28 to 1.41).

According to the inventive method after the operation (Table 4), as the primary OEA (0.3 ≤ CVI ≤ 0.5 and 0.7 ≤ PI ≤0.9), the right ZMA pool is assessed without changes, and, due to the deterioration, the right SMA basins (CVI - 0.38, PI - 0.78), the right PMA (CVI - 0.37, PI - 0.73) and the left ZMA (CVI - 0.43, PI - 0.75). As the secondary OEA (0.3≤CVI≤0.5 and PI <0.7 or PI> 0.9), the basins of the left SMA (area of operation) and OA are evaluated without changes. As a borderline OEA (0.27≤CVI≤0.3 and PI is not significant), due to deterioration, the pool of the left PMA is evaluated (CVI - 0.27). The right hemisphere dominates in epileptogenesis, as well as before the operation (the numerical majority of primary OEA).

In this example, only the claimed method allowed to identify the primary OEA before surgery and evaluate the remaining OEA by their participation in epileptogenesis. The preservation of the primary focus on the background of surgical trauma during removal of the secondary OEA led to an aggravation of the epileptic process.

Thus, as shown by the examples, the proposed method for assessing epileptogenic foci is accurate, informative. It makes it possible to evaluate OEA in a single digital format, which makes it possible to increase the accuracy of identifying primary OEA and assessing the epileptic system of the brain as a whole, to predict the further course of epileptogenesis, and also to carry out correction of therapeutic tactics under dynamic observation. The method helps to improve the quality of diagnosis and treatment results for epileptic syndrome.

Information sources

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2. Grindel O. M Electroencephalography in TBI / Neurootraumatology Handbook, ed. A.N. Konvalova, L. B. Likhterman, A. A. Potapov. - M .: CPI "Bazar-Ferro", 1994, S. 384-385.

3. Zenkov L.R., Ronkin M.A. Functional diagnosis of nervous diseases. - M .: "MEDpress-inform", 2004, p. 65-71.

4. Zenkov L.R., Prityko A.G. Pharmacoresistant epilepsy. - M .: "MEDpress-inform", 2003, pp. 11-24.

5. Zenkov L.R., Prityko A.G. Pharmacoresistant epilepsy. - M .: "MEDpress-inform", 2003, p. 84-90.

6. Kasumov V.R., Vayshenker Yu.I., Ivanov A.Yu. Changes in cerebrovascular reactivity in patients with temporal paroxysmal syndrome / materials VII international. symp New technologies in neurosurgery. - St. Petersburg, 2004, p.119.

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Claims (1)

A method for assessing areas of cerebral epileptic activity (OEA) by dopplerographic examination of cerebral vessels and determining the peripheral resistance index (IPA), vasoconstrictor reserve (P (-)) for hypocapnic loading and vasodilation reserve (P (+)) for hypercapnic loading, characterized in that for each artery the cerebral autonomic index (CVI) is calculated according to the formula CVI = P (-): P (+): IPA, the value of which is defined as epileptogenic or borderline or non-epileptogenic, and if your IPS uses a pulsation index, as P (-) - coefficient of reactivity to hypocapnic load, as P (+) - coefficient of reactivity to hypercapnic load, CVI value is defined as epileptogenic at 0.3 Ц CVI 0 0.5; borderline at 0.27 ≤ CVI <0.3 or 0.5 <CVI ≤0.53; non-epileptogenic with CVI <0.27 or CVI> 0.53; then each epileptogenic or borderline CVI value is compared with the IPA value of the corresponding arteries in case of epileptogenic CVI and within the IPA norm, the OEA is evaluated as primary; with epileptogenic CVI and less or more than the norm of IPA - as secondary; with border CVI and any values of IPS - as border; and the hemisphere dominating in epileptogenesis is determined by the numerical majority of OEA with the greatest significance.