RU2317805C2 - Method for treating acute posttraumatic cephalgia cases - Google Patents

Abstract

FIELD: medicine.

SUBSTANCE: method involves administering traditional combined therapy including vasoactive resorbing therapy, introducing nootropic agents, vitamins, biostimulators, therapeutic physical training, physiotherapy and massage. 3-4 procedures of subaponeurotic introduction of 1.5-2.0 ml of are additionally given in mastoid cranial process base region. The procedure is carried out once a day and repeated every other day.

EFFECT: alleviated local inflammatory response manifestations; no adverse side effects observed.

9 tbl

Description

The present invention relates to medicine, namely to neurology, and can be used in the complex treatment of patients with post-traumatic headaches. Traumatic brain injuries (TBI) are the most frequent and severe injuries, the number of which is constantly increasing. Among injuries of all types, TBI accounts for 25 to 40%. TBIs in frequency occupy first place among neurosurgical pathologies, surpassing all others taken together by 5 times, and among causes of death and disability up to 45 years. During the time interval of 45 years - 64 years more die from TBI than from strokes.

The most common clinical manifestation of TBI is headache. The criteria for the connection of headache with trauma are:

1. The presence of documentary data on the subject's injury, its nature, degree of neurological impairment.

2. The presence in the history of the fact of loss of consciousness of various durations.

3. Post-traumatic amnesia for more than 10 minutes.

4. The occurrence of headache no later than 10-14 days after injury.

According to the International Classification of Headache, post-traumatic cephalalgia is divided into acute and chronic. Acute post-traumatic headaches are believed to occur in the first 14 days after head injury and last no more than 8 weeks.

The occurrence of clinical symptoms in TBI is determined by the interaction of vascular, mechanical, cerebrospinal fluid, neurodynamic, humoral, immune, endocrine factors. The combination of these pathogenesis factors causes a mixed type of cephalgic syndrome in TBI. The pathogenetic types of headache that occur during head injury can include vascular, cerebrospinal fluid, sheath, muscle tension, neuralgic, neurotic type of cephalgia.

Inflammatory processes that irritate the receptors of the dura mater, venous sinuses, cerebral arteries can also be the cause of cephalgia in TBI. At the same time, sensitive immunological tests, even with mild head injury in the acute period, reveal the release of neurospecific proteins in the blood and cerebrospinal fluid: an increase in the level of the main myelin protein and S-100 protein, which reflects neuroglia damage, a decrease in the number of CD4 lymphocytes carrying suppressor function, which indicates about the development of autoimmune inflammatory processes.

Autoimmune disorders, the effects of aseptic inflammation play an important role in the formation of post-commotion syndrome after mild traumatic brain injury, accounting for 80% of all cases of head injury. The characteristic features of this syndrome are headache, increased fatigue, anxiety, cognitive impairment, behavioral changes, manifestations of autonomic dysfunction. Usually, a year after a mild TBI, post-commotion syndrome persists only in 10-15% of patients, but the chronic course of the syndrome is also described [DR Stulman, OS Levin, 1999, Mons, 2000].

The traditional method of treatment of acute post-traumatic cephalalgia is complex therapy, which includes: vasoactive, absorbable therapy, nootropics, exercise therapy, massage (if indicated), physiotherapy, vitamins, biostimulants, as well as, if indicated, anticonvulsants, HBO. Wherein:

- vasoactive therapy includes: xanthinol nicotinate, trental, pentoxifylline,

- resolving therapy includes injections of lidase,

- nootropics,

- exercise therapy,

- massage

- physiotherapy,

- vitamins

- biostimulants (aloe).

Traditional complex therapy is accepted as the standards for the provision of inpatient care (see, for example, the standards developed by the Territorial Fund for Compulsory Medical Insurance of the Nizhny Novgorod Region (Approved by order of the Ministry of Health of the Nizhny Novgorod Region dated 05/14/02 No. 379-B). This method was chosen by the authors for the prototype of inventions. However, the prototype method has insufficient efficiency. The results of a detailed study of the effectiveness of the prototype method by the authors of this application are shown in table 1-9, group prototype, which shows insufficient quantitative characteristics of the normalization of the following indicators: headache intensity, psychoemotional and autonomic disorders, disturbances in electrical activity, vasospasm, interhemispheric asymmetry of cerebral blood flow and other indicators.

The objective of the invention is to increase the effectiveness of treatment, namely, a large, compared with the prototype, normalization of headache intensity indicators, psychoemotional and autonomic disorders, rhythms of electrical activity of the brain, reduction of vasospasm, more pronounced regression of interhemispheric asymmetry of cerebral blood flow and a more pronounced recovery of cerebral reactivity vessels. A new technical result of the invention is to achieve the task, which is reflected in detail in tables 1-9 (main group). The task is achieved by the fact that they additionally carry out 3-4 procedures of subaponeurotic administration of xefocam to the base area of the mastoid processes of the skull, with 1.5-2 ml injected into each procedure, the procedure will be repeated every 2 days, 1 procedure per day.

The additional effect of the present invention with a modern non-steroidal anti-inflammatory drug by the original method of its subaponeurotic administration can significantly reduce the intensity of post-traumatic headache by reducing the severity of local inflammatory reactions, and the method of subaponeurotic administration by directly bringing the drug to the substrate of its activity can significantly reduce the necessary for clinical effect dose of the drug and to minimize the side effects of xefocam. In addition, the technique is easy to use and does not require any additional technical means to complete the usual procedural tool kit.

During the development of the proposed method, the authors, by conducting a special comparative study, proved the effectiveness of 3-4 procedures of subaponeurotic administration of xefocam in comparison with 14-24 procedures (7-12 days 2 times a day) with intramuscular administration of xefocam.

The results obtained during treatment using intramuscular injection are shown in tables 1-9 as a control group.

The results obtained during treatment using subaponeurotic administration are shown in tables 1-7 as the main group.

The results of this comparative treatment are described below, in addition, the results of treatment using the prototype method (prototype group) are given in tables 1-7.

A clinical examination was conducted of 45 patients aged 17 to 54 years (average age was 30 years) of which were treated: men - 24 people, women - 21 with a diagnosis of acute traumatic brain injury (concussion, mild brain injury). The control group and the prototype group included 20 people with acute head injury of the same severity, in the control xefocam was used for intramuscular injection of 2 ml 2 times a day for at least 7 days (up to 10-12 days), and the traditional prototype was repeated in the group therapy.

All patients of the main group received subaponeurotically 2 ml of xefocam 1 time per day with a course of 3-4 procedures, 1 procedure per day with a break of 2 days between procedures) on the background of basic therapy, which was carried out in both groups in accordance with the standards of in-patient medical care for adults Nizhny Novgorod Region, developed by the Territorial Fund for Mandatory Medical Insurance of the Nizhny Novgorod Region (Approved by order of the Ministry of Health of the Nizhny Novgorod Region dated 05/14/02 No. 379-В). Basic therapy included: vasoactive, absorbable therapy, nootropics, exercise therapy, massage (if indicated), physiotherapy, vitamins, biostimulants. According to indications: anticonvulsants, HBO.

Subponeurotic administration of xefocam in the base of the mastoid processes of the skull was used for headaches with the aim of influencing pain receptors and areas of possible post-traumatic autoimmune inflammation in the dura mater and venous sinuses. The principle of subaloneurotic administration of medicinal substances is to bring them to the meninges by "soaking" through the emissaries of the skull. Normally, part of the venous blood from the soft tissues of the cranial vault under the aponeurosis and border regions of the face flows into the sinuses of the dura mater. In this direction of blood flow, it can be assumed that, together with venous blood, a drug substance also leaves the solid membrane, which, washing the sheath nerves, reduces the flow of pain impulses from the zone of its irritation, and provides anti-inflammatory and analgesic effects.

Scheme of subaponeurotic administration of xefocam. After processing the skin with an antiseptic, a needle is inserted in the horizontal direction at the base of the mastoid process at the border of the hairline The introduction of xefocam is carried out in three stages. First, intradermally - until a dense lemon peel infiltrate is obtained, which serves as a kind of “cork” after removing the needle. Then the needle is slowly advanced under the aponeurosis, previously exfoliating with the introduction of xefocam, to a distance of 5-6 cm in the same direction. The procedure is completed by the slow administration of 1.5-2 ml of xefocam. Repeating the procedure after 2 days, only 3-4 procedures per course, the procedure is performed once a day. In the control group, intramuscular administration of xefocam was used in accordance with the recommendations for use of 2 ml 2 times a day for a period of persistent headache, usually at least 7 days, up to a maximum course time of 10-12 days.

In all patients, a dominant complaint in the clinical picture was a headache of varying intensity, within 4–9 points according to the visual analogue scale. For a clinical integrative assessment of treatment effectiveness, we used the headache index indicator, which was calculated by the formula: HHB = (number of days with GB / 7 + number of hours of GB per day / 24 + intensity of GB / 10 + number of tablets per week / 7) × 25 /one hundred. At the same time, treatment was considered highly effective if the headache index indicator changed by 50-80%. The average treatment efficiency corresponded to a change in the headache index by 20-49%. Low efficiency corresponded to a change in the headache index of less than 20%.

During treatment, sociometric and psychometric tests were used. (The level of depression was evaluated according to the Beck scale, the degree of reactive and personal anxiety was assessed according to the test of Ch.D. Spilberger and Yu.Ya. Khanin (1995). As a measure of the state of the autonomic nervous system in the treatment process, a standard questionnaire was used to identify autonomic disorders (Wayne AM, 1991). Additional instrumental research data was studied (EEG, UZDG). Transcranial ultrasound dopplerography (TKUDG) was performed using the Premier and Angiodin devices of BIOSS company, Russia, 2 and 4 MHz sensors. average linear blood flow velocity in the main intracranial vessels (middle cerebral artery - SMA, anterior cerebral artery - PMA, posterior cerebral artery - ZMA, main artery - OA, vertebral artery - PA, siphon of the internal carotid artery - ICA). The asymmetry coefficient (CA) was studied. ) is a value characterizing the degree of difference in the performance of Doppler signals obtained from symmetric sections of the same arteries: KA (%) = XY / Y · 100, where X is the largest value of the indicator, Y is the lowest value of the indicator. Normally, the allowable value of asymmetry does not exceed an average of 15-20%.

A study of cerebrovascular reactivity was carried out, insonation of the middle cerebral artery was carried out from the middle temporal ultrasound window. Hypercapnic and hyperventilation test loads were used.

In the first case, after receiving a steady signal and registering background indicators, the patient was asked to hold his breath for 30 seconds (apneetic or hypercapnic load), which leads to an increase in blood flow velocity.

- reactivity coefficient for apneetic load: Кр + = Va-Vo / (VoTa) · 100%, where

Vo is the average background LSC;

Va is the average BFV against the background of apneetic load;

Ta is the duration of apnea;

Forced breathing at a frequency of 30 times per minute for 30 s (hyperventilation test) causes a decrease in blood flow velocity.

- reactivity coefficient for hypocapnic (hyperventilation) load:

Cr - = 1-V ^- / Vo, where

Vo is the average background LSC;

V ^- - average BFV against the background of hyperventilation load.

Cerebrovascular reactivity was also determined by conducting thirty-second samples with respiratory retention and hyperventilation and was calculated as the ratio of the difference in BFK during breath-holding and BFV when hyperventilating to BFV alone · 100%. The vasomotor reactivity index (IVMR) allows us to judge the severity of adaptive reactions and the degree of compensatory capabilities of the blood supply to the brain. Normally, it should not be lower than 80%.

The state of the tone of the resistive vessels of the brain can be estimated using the carotid compression test by calculating the overshoot coefficient (Ko) (Svistov D.V., 1995). Co characterizes the magnitude of the vasodilator reserve of autoregulation of cerebral circulation and the state of the tone of resistive vessels of the pial-capillary system.

Carotid compression test procedure

1. Registration of Vm in the ipsilateral middle cerebral artery (SMA) before compression (initial data)

2. Compression of ipsilateral common carotid artery (OCA) for 5-10 heart cycles.

3. Termination of OCA compression in diastole.

4. Registration of Vm in ipsilateral MCA immediately after the termination of OCA compression.

5. Calculation of the overshoot coefficient (Ko): Ko = Vm2 / Vm1, where Vm1 is the initial average blood velocity before compression of the ipsilateral common carotid artery, Vm2 is the average speed of the first or second peaks after the termination of OCA compression.

The state of neurodynamics was assessed using an EEG study on the Encephalan-131-01 computer complex version 4.1M (by NPKF Medicom LTD, Taganrog) with topographic mapping and spectral analysis of brain BEA by basic rhythms from the background recording.

Data processing was carried out on an IBM PC using the statistical data analysis software package “Biostatistics” (Primer of Biostatistics, version 4.03 by Stanton A.Glantz) and Excell-2000 in accordance with the objectives of the study. We used the T-test, nonparametric criteria of Wilcoxon, Kruskal-Wallis.

An analysis of the data yielded the following results: in 30% of patients, headache was completely eliminated; in 45% of patients, cephalgic syndrome decreased significantly; 25% of headaches decreased, but did not completely disappear. The dynamics of headache intensity according to the visual analogue scale (YOUR) and headache index (IHB) are presented in table 1.

Table 1. No. Characteristic Control group Main group Prototype Before treatment After Before treatment After Before treatment After one. YOUR (cm) 7.3 ± 1.4 6.2 ± 1.2 7.2 ± 1.5 3.8 ± 1.1 * 7.1 ± 1.3 6.3 ± 1.2 2. Change in HMB (%) 41 ± 4.71 62 ± 5.89 38 ± 4.62 Note: * - significance of differences (p <0.05) in comparison with the initial data

The dynamics of the results of a study of the intensity of cephalgia according to YOUR and IHB data indicates a more pronounced regression of headache when xefocam is included in the treatment complex.

Table 2. Features regression of psychoemotional and autonomic disorders are presented in table 2. No. Test (points) Control group Main group Prototype Before treatment After Before treatment After Before treatment After one. Reactive anxiety 37.9 ± 3.4 33.1 ± 2.9 38.3 ± 2.7 29.2 ± 1.6 * 36.4 ± 2.1 34.5 ± 1.8 2. Personal anxiety 48.5 ± 2.6 46.6 ± 2.1 48.3 ± 2.2 40.1 ± 1.4 * 48.1 ± 2.5 47.1 ± 2.3 3. Depression 28.0 ± 3.5 26.2 ± 2.8 27.8 ± 2.7 17.3 ± 1.5 * 27.4 ± 2.2 25.3 ± 1.5 four. Vegetative status 32.1 ± 1.8 29.5 ± 2.1 31.5 ± 2.7 18.4 ± 1.3 * 31.7 ± 2.9 28.4 ± 1.8 Note: * - significance of differences - (p <0.05) in comparison with the initial data.

According to the Spielberger – Khanin test, increased levels of reactive and personal anxiety were recorded in the main group, with some prevalence of the latter with a decrease during treatment more pronounced compared to the control group. The severity of autonomic disorders according to the vegetative questionnaire by A.M. Wayne and depression according to the Beck scale also decreased more pronounced in the main group.

Table 3. The results of a visual assessment of the EEG of patients with post-traumatic cephalgia are presented in table 3 EEG Characteristics Control group Main group Prototype Before treatment After Before treatment After Before treatment After abs % abs % abs % abs % abs % abs % EEG Type I 0 0 2 10 2 four 13 29th 0 0 one 5 II 6 thirty 7 35 12 thirty fifteen 33 7 35 6 thirty III 10 fifty 8 40 21 47 fourteen 31 9 45 10 fifty IV four twenty 3 fifteen 10 9 3 7 four twenty 3 fifteen Α-rhythm disorganization fourteen 70 eleven 55 32 72 16 36 12 60 10 fifty Decrease or inversion of the α-rhythm gradient 16 81 13 65 35 78 25 56 fifteen 75 12 60 Bilateral synchronous flashes α, β, θ, Δ 17 85 fifteen 75 38 84 37 83 17 85 16 80 Focal discharge activity eighteen 90 fifteen 75 42 93 21 47 fifteen 75 fourteen 70

Features of the visual analysis of the EEG of patients with post-traumatic cephalalgia revealed the prevalence of pathological types of EEG (II, III, IV) and the presence of a number of pathological changes in the EEG presented in the table above. The regression of these changes in the main group significantly exceeded the dynamics of the control group, namely, the appearance of a significant amount of EEG type I mainly due to a decrease in the representation of type III and IV, an improvement in the α-rhythm parameters, and a decrease in discharge activity.

- и Δ-активности - более выраженно по сравнению с контрольной и прототипом. В контрольной группе аналогичная тенденция статистически недостоверна.The data presented in Table 3 indicate a redistribution of the zonal neurodynamic powers in the main group in all three directions - increasing the power of the α-rhythm, reducing the power of the previously pathologically enhanced β-

- and Δ-activity - more pronounced in comparison with the control and prototype. In the control group, a similar trend is statistically unreliable.

The zonal distribution of the specific gravity of the power of electrical activity (in%) in a state of relaxed wakefulness in healthy and patients with post-traumatic cephalalgia is presented in table 4.

The leading pattern of distribution of zonal capacities of patients with post-traumatic cephalalgia included the following main features:

1. Decreased α-rhythm power, more in the occipital leads, slightly higher in the frontal

2. The increase in β-activity is quite uniform with a slight predominance in the frontal leads.

3. A marked increase in power in θ and Δ ranges.

Note: PL is the anterior frontal zone, GL is the posterior frontal zone, PV is the anterior temporal zone, 3B is the posterior temporal zone, C is the central, T is the parietal, 3 is the occipital.

Table 4. Type of electrical activity Healthy group Control group Main group Prototype Before treatment After Before treatment After Before treatment After α- Sub 40.4 ± 2.1 32.7 ± 2.3 34.2 ± 2.3 32.5 ± 2.2 39.1 ± 1.9 31.7 ± 2.1 34.1 ± 2.2 ZL 43.2 ± 2.2 33.5 ± 2.4 33.5 ± 1.4 33.4 ± 2.3 41.8 ± 2.1 ^* 32.4 ± 2.2 33.7 ± 1.5 PV 41.5 ± 2.9 32.3 ± 2.2 35.4 ± 1.9 32.2 ± 2.4 40.6 ± 2.1 ^* 31.3 ± 2.1 32.4 ± 1.9 NE 51.3 ± 2.4 33.8 ± 2.1 36.6 ± 2.8 33.7 ± 2.2 47.3 ± 2.5 ^* 32.8 ± 2.4 33.4 ± 2.1 ST 53.4 ± 2.9 34.6 ± 3.2 35.7 ± 2.5 34.5 ± 3.1 51.2 ± 2.4 35.7 ± 3.1 34.5 ± 2.2 Ts 54.2 ± 3.4 30.6 ± 2.4 32.7 ± 1.7 30.5 ± 2.2 49.3 ± 2.2 ^* 31.8 ± 2.2 31.5 ± 1.6 T 58.7 ± 3.5 42.7 ± 3.1 45.8 ± 2.8 42.6 ± 3.4 52.3 ± 2.3 41.9 ± 3.2 43.8 ± 2.7 3 65.2 ± 4.3 50.1 ± 3.3 51.3 ± 2.6 50.3 ± 3.2 59.8 ± 2.7 50.5 ± 3.2 50.7 ± 2.1 β- Sub 7.1 ± 1.4 11.3 ± 0.7 9.2 ± 0.5 11.2 ± 0.5 8.2 ± 0.8 10.8 ± 0.6 11.2 ± 0.4 ZL 8.2 ± 1.5 13.4 ± 1.1 12.9 ± 1.8 12.7 ± 1.2 7.9 ± 0.9 ^* 12.9 ± 0.9 13.9 ± 1.5 PV 9.1 ± 1.3 13.1 ± 1.2 12.7 ± 1.5 13.2 ± 1.4 9.3 ± 1.3 13.3 ± 1.1 13.7 ± 1.6 NE 8.8 ± 1.4 12.9 ± 1.3 12.5 ± 1.3 13.8 ± 1.3 8.5 ± 1.2 12.8 ± 1.2 12.9 ± 1.1 ST 8.5 ± 0.9 13.9 ± 1.4 13.6 ± 1.5 12.7 ± 1.4 8.8 ± 1.1 13.7 ± 1.5 13.8 ± 1.4 Ts 7.4 ± 0.8 14.7 ± 1.3 14.5 ± 1.1 15.6 ± 1.2 8.1 ± 0.7 ^* 14.5 ± 1.2 14.4 ± 1.8 T 11.7 ± 1.2 16.7 ± 1.4 15.8 ± 1.3 16.6 ± 1.3 10.5 ± 1.4 ^* 16.6 ± 1.3 16.8 ± 1.7 3 14.3 ± 1.3 17.8 ± 1.6 16.1 ± 1.9 15.7 ± 1.5 13.5 ± 1.6 17.5 ± 1.4 17.1 ± 1.2 θ- Sub 24.3 ± 1.2 26.4 ± 1.1 26.1 ± 1.6 27.1 ± 1.8 25.1 ± 1.5 26.5 ± 1.2 26.2 ± 1.2 ZL 24.8 ± 1.1 25.8 ± 1.1 25.1 ± 1.5 25.3 ± 1.2 24.9 ± 1.4 25.7 ± 1.1 25.2 ± 1.1 PV 24.3 ± 0.9 25.3 ± 0.9 25.2 ± 1.3 26.8 ± 1.1 25.7 ± 0.9 25.1 ± 0.8 24.1 ± 1.1 NE 20.5 ± 1.3 22.5 ± 1.3 21.4 ± 1.7 23.3 ± 1.5 20.3 ± 1.1 21.5 ± 1.4 21.3 ± 1.5 ST 18.2 ± 1.4 20.2 ± 1.4 19.6 ± 1.1 21.7 ± 1.4 17.8 ± 1.5 20.3 ± 1.3 19.7 ± 1.3 Ts 15.5 ± 1.2 17.6 ± 1.2 17.3 ± 1.6 18.8 ± 1.4 16.3 ± 1.9 17.5 ± 1.1 16.2 ± 1.5 T 14.6 ± 1.3 16.5 ± 1.3 15.4 ± 1.4 17.4 ± 1.2 14.7 ± 1.2 16.7 ± 1.2 15.2 ± 1.3 3 8.3 ± 1.1 11.3 ± 1.9 10.3 ± 1.9 12.5 ± 1.2 9.8 ± 1.7 11.2 ± 1.7 11.1 ± 1.8 Δ- Sub 25.3 ± 1.4 33.5 ± 2.2 31.5 ± 2.2 34.2 ± 2.1 26.2 ± 1.4 ^* 32.7 ± 2.5 30.5 ± 2.1 ZL 24.4 ± 1.2 32.2 ± 1.7 32.7 ± 1.7 33.5 ± 1.6 25.2 ± 1.8 ^* 31.2 ± 1.6 30.7 ± 1.6 PV 21.3 ± 1.6 32.6 ± 1.8 32.4 ± 1.5 32.8 ± 1.9 23.4 ± 1.7 ^* 31.5 ± 1.8 31.4 ± 1.3 NE 20.7 ± 1.1 31.2 ± 1.6 30.3 ± 1.2 32.6 ± 1.5 22.8 ± 1.9 ^* 32.2 ± 1.9 30.2 ± 1.8 ST 19.4 ± 1.2 28.6 ± 1.4 29.2 ± 1.4 29.3 ± 1.3 20.6 ± 1.2 ^* 27.9 ± 1.4 28.2 ± 1.7 Ts 18.9 ± 1.3 28.4 ± 1.3 27.7 ± 1.3 27.9 ± 1.1 21.3 ± 1.5 28.5 ± 1.2 26.3 ± 1.5 T 15.7 ± 1.2 23.5 ± 1.1 22.3 ± 1.8 23.4 ± 1.4 17.8 ± 1.6 ^* 21.5 ± 1.8 20.1 ± 1.7 3 13.4 ± 0.8 18.9 ± 1.2 17.7 ± 1.3 19.3 ± 1.6 15.2 ± 1.1 ^* 17.7 ± 1.5 16.5 ± 1.2 Note: * - significance of differences - (p <0.05) in comparison with the initial data.

The data presented in table 4 reflect that the degree of regression of these changes in the main group significantly exceeded the tendency to decrease in the control group.

Table 5. The average linear velocity of blood flow in the main cerebral intracranial arteries, cm / s No. Arteries Control group Main group Prototype Before treatment After treatment Before treatment After treatment Before treatment After treatment one. PMA 68.1 ± 3.5 64.1 ± 2.7 67.7 ± 4.1 52.4 ± 3.2 * 67.1 ± 3.3 65.2 ± 2.5 2. SMA 90.4 ± 3.2 87.2 ± 2.6 91.5 ± 3.2 71.2 ± 2.5 * 91.4 ± 3.1 89.1 ± 2.2 3. ZMA 46.3 ± 2.9 43.5 ± 2.5 45.8 ± 3.3 39.9 ± 2.1 46.4 ± 2.9 45.5 ± 2.1 four. OA 47.5 ± 4.8 45.3 ± 4.7 47.7 ± 5.8 39.3 ± 3.6 * 47.9 ± 4.8 46.2 ± 4.1 5. PA 45.9 ± 2.6 42.1 ± 2.8 46.3 ± 2.7 36.5 ± 4.1 * 44.8 ± 2.5 43.2 ± 2.4 6. ICA (siphon) 52.7 ± 3.8 50.7 ± 3.5 51.6 ± 3.6 47.2 ± 3.8 51.9 ± 3.9 51.7 ± 3.1 Note: * - significance of differences - (p <0.05) in comparison with the initial data.

The data obtained during ultrasound dopplerography indicate an increase in the average linear blood flow velocity in the main intracranial arteries, which reflects the presence of cerebral vascular dystonia with the development of vasoconstriction. This trend is most pronounced in the basin of the anterior and middle cerebral artery, and the highest values of blood flow velocity, as a rule, were noted on the side of the headache. The decrease in vasospasm during treatment is more pronounced in the main group compared with the control and prototype.

Table 6. The results of the study of the coefficient of asymmetry (CA) in patients with post-traumatic cephalalgia. No. Asymmetry coefficient,% Control group Main group Prototype Before treatment After Before treatment After Before treatment After one. Front carotid pool 23.8 ± 2.7 21.4 ± 3.1 23.6 ± 3.6 15.5 ± 2.7 ^* 23.5 ± 2.2 22.5 ± 3.2 2. Vertebrobasilar system 18.1 ± 2.4 17.9 ± 1.2 17.9 ± 2.8 12.7 ± 2.2 ^* 17.5 ± 2.5 17.2 ± 1.8 Note: * - significance of differences (p <0.05) in comparison with the initial data

The results obtained in the study of the asymmetry coefficient indicate an increase in interhemispheric asymmetry of cerebral blood flow, mainly in the carotid pool. The degree of CA regression is more pronounced in the main group compared to the control and prototype.

Table 7. The results of a study of cerebrovascular reactivity in patients with post-traumatic cephalgia. No. Indicators of cerebrovascular reactivity (CMA) Control group Main group Prototype Before treatment After Before treatment After Before treatment After one. Cr + 1.18 ± 0.06 1.21 ± 0.06 1.19 ± 0.07 1.24 ± 0.05 1.17 ± 0.05 1.20 ± 0.06 2. Cr 0.25 ± 0.03 0.26 ± 0.03 0.27 ± 0.04 0.31 ± 0.06 0.24 ± 0.05 0.28 ± 0.02 3. IWMR 69.7 ± 6.2 71.3 ± 7.2 71.2 ± 7.2 77.8 ± 7.5 69.8 ± 6.1 71.1 ± 6.5 four. To 1.24 ± 0.12 1.25 ± 0.12 1.23 ± 0.11 1.29 ± 0.13 1.25 ± 0.11 1.26 ± 0.13 Note: * - significance of differences (p <0.05) in comparison with the original data.

Indicators of cerebrovascular reactivity indicate the presence of moderate vasoconstriction in the carotid pool, which leads to a decrease in reactivity for samples with carbon dioxide. An increase in angiospasm is due to a decrease in IVMR and Co.

The restoration of the reactivity of cerebral vessels is more pronounced in the main group compared with the control and prototype.

Thus, the hemodynamic pattern of post-traumatic cephalalgia is the presence of vascular dystonia with a tendency to vasoconstriction, which is expressed in an increase in blood flow velocity, an increase in hemispheric asymmetry of blood flow, a decrease in overshoot coefficient, and a decrease in IVMR. The decrease in the effects of post-traumatic angioedema under the influence of subaponeurotic administration of xefocam is more pronounced in comparison with traditional therapy.

Computed tomography and magnetic resonance imaging of the brain in the main group compared with the control group also indicated an acceleration of the regression of diffuse changes in the brain and subshell spaces. In the main group, a more pronounced regression of cerebral and focal neurological symptoms was noted.

Table 8. No. Adverse reactions with the use of the drug "Xefocam" (%) Control group Main group one. Reactions at the injection site (pain, redness), 5 2 2. Allergic reactions (skin rashes, shortness of breath, tachycardia) one 0 3. Nausea, vomiting 0 0 four. Flatulence, diarrhea 0 0 5. Abdominal pain and other dyspeptic symptoms 3 0 6. Dry mouth one 0 7. Impaired appetite 2 0 8. Gastritis, esophagitis one 0 9. Peptic ulcer formation 0 0 10. Bleeding from the gastrointestinal tract, including rectal and hemorrhoidal, nosebleeds 0 0 eleven. Impaired liver function and urination 0 0 12. Drowsiness (or sleep disturbance) 2 0 13. Depression (or agitation) 0 0 fourteen. Arterial hypertension one 0 fifteen. Increased palpitations, trembling, increased sweating 0 0 16. Leukopenia or thrombocytopenia one 0 17. Body weight change 0 0

Serious side effects (including from the mucous membranes) during the treatment by means of subaponeurotic use of xefocam were not noted. A greater number of adverse reactions in the traditional use of xefocam compared with the subaponeurotic route of administration, apparently, is associated with a longer treatment course and an effective daily dose of the drug.

Table 9. Assessment of the effectiveness of treatment in dynamics. No. Quantitative parameters for evaluating the effectiveness of treatment Control group Main group Prototype one. Relapses of cephalgia after treatment, (%) After 1 year 48 ± 4 15 ± 2 * 55 ± 3 After 2 years 32 ± 2 9 ± 2 * 35 ± 4 2. The level of social and labor rehabilitation, (%) (2 months after treatment) 75 ± 6 100 ± 8 * 77 ± 5 3. Period of temporary disability (treatment time, days) 21 ± 3 14 ± 3 * 25 ± 2 Note: * - significance of intergroup differences (p <0.05).

According to the follow-up data, relapses in the exacerbation of post-traumatic headache were noted after 48 years after 48% and after 2 years 32% of patients in the control group, while in the main group% of cephalgia relapses were an order of magnitude lower - 15% after a year and 9% after 2 years.

The initial level of social and labor rehabilitation (61.5%) increased after 2 months to 100% in the main group versus 75% in the control group. By the second month of observation, out of the total number of patients treated in the main group, everyone worked according to their previous specialty, and in the control group, four patients were employed in lightened working conditions.

The use of subaponeurotic administration of xefocam in combination with basic therapy allowed to reduce the period of temporary disability, reduce treatment costs and improve outcomes of patient rehabilitation.

Thus, according to clinical and physiological studies, xefocam has a powerful analgesic and anti-inflammatory effect and is indicated for patients in the acute stage of traumatic brain injury in order to eliminate the cephalgic syndrome, and the most effective and safe way to use it is subaponeurotic administration.

An example of a specific performance is given in the form of an extract from the medical history.

CLINICAL EXAMPLES

- и Δ-активности происходило выравнивание удельного веса электрической активности дельта- и тетта-диапазонов по лобно-затылочному градиенту. По данным допплерографии отмечалось снижение ранее повышенной линейной скорости кровотока в каротидном и вертебральном бассейнах, что говорит об уменьшении вазоспазма, имело место снижение межполушарной асимметрии и нормализация цереброваскулярной реактивности. В результате проведенной терапии отмечалось снижение интенсивности головных болей после второй процедуры, после четвертой процедуры приступы не возникали. После выписки из стационара на протяжении 3,5 месяцев приступы головной боли не повторялись.Example No. 1. Patient K., 35 years old, was admitted to the clinic of nervous diseases with a diagnosis of Acute closed traumatic brain injury, concussion with cephalgic syndrome, vestibulopathy. The patient complained of paroxysmal headaches in the region of the left temple, dull aching pains in the occipital region, the beginning of which is associated with a fall on the ice and head injury with a short-term loss of consciousness about 2 weeks ago. According to the patient, during seizures, severity appears in the left orbital-temporal region, which turns into a high-intensity pulsating headache in the left temporal-parietal region. After several hours of headache, nausea occurs, sometimes vomiting, after which the pain goes away, but a feeling of heaviness in the head remains. Between attacks almost always wakes up in the morning with a feeling of heaviness in the head and aching pain in the occipital region. Deterioration during the last week. Blood pressure 110/70 mm Hg, pulse 67 per minute. In neurological status: the patient is emotionally labile, anxious. Tendon reflexes d = s, animated. There is tremor of fingers of outstretched hands, a positive symptom of Tremner. A bright red dermographism, tachycardia is revealed. Performs dynamic coordinating tests satisfactorily, in the Romberg position staggered without a clear side. Meningeal signs are not detected. On a radiograph of the skull in 2 projections - without bone-destructive changes. ESR - no M-echo displacement, moderate signs of intracranial hypertension. Neuroophthalmologist - NO discs are pale pink, clear borders. The patient received subaponeurotically 2 ml of xefocam 1 time per day for 4 procedures, against the background of basic therapy, which was carried out in accordance with the standards for in-patient medical care for the adult population of the Nizhny Novgorod Region developed by the Territorial Fund for Mandatory Medical Insurance of the Nizhny Novgorod Region (Approved by order of the Ministry of Health of the Nizhny Novgorod Region from 05/14/02 No. 379-B). Simultaneously with the administration of xefocam, the patient received treatment that included taking novopassit, piracetam, intravenous administration of nicotinic acid from 1 to 10 ml according to the scheme on physiological saline, intramuscular administration of B vitamins, she underwent exercise therapy, massage of the neck collar, aeroionization, coniferous baths. As a result of the treatment, the intensity of headache in points decreased from 7.3 to 3.6, reactive anxiety in points decreased from 39.3 to 28.1, personal anxiety - from 49.4 to 41.2 points, the level of depression decreased from 28 to 18 points. The severity of autonomic disorders in points decreased during treatment from 31.6 to 19.1. The dynamics of the EEG was expressed in the evolution of the EEG type from II to I, there was also an increase in bioelectric activity, the total power of the EEG, a decrease in the power of the previously pathologically enhanced β-

- and Δ-activity, the specific gravity of the electrical activity of the delta and theta ranges was aligned according to the fronto-occipital gradient. According to Dopplerography, a decrease in the previously increased linear velocity of blood flow in the carotid and vertebral pools was noted, which indicates a decrease in vasospasm, there was a decrease in interhemispheric asymmetry and normalization of cerebrovascular reactivity. As a result of the therapy, a decrease in the intensity of headaches after the second procedure was noted, after the fourth procedure, no attacks occurred. After discharge from the hospital for 3.5 months, headache attacks did not recur.

Bibliography

1. Post-traumatic headaches. O.V. Vorobiev, A.M. Wayne. Consilium medicum 1999, T1. No2.

2. Pain syndromes in neurological practice. A.M. Wayne. - M: MEDpress, 1999.

3. Pain and anesthesia. A.M. Wayne, M.Ya. Avrutsky. - M: Medicine 1997

4. Pharmacotherapy in neurology. V.N.Shtok. - M: Medical News Agency, 2000

5. Guide "Fundamentals of Neurology." E.M. Burtsev, V.D. Troshin, O.V. Troshin. - Nizhny Novgorod, 1998

Claims (1)

A method of treating acute post-traumatic cephalalgia by traditional complex therapy, including vasoactive, absorbable therapy, the introduction of nootropics, vitamins, biostimulants, physiotherapy, physiotherapy and massage, characterized in that they additionally carry out 3-4 procedures of subaponeurotic administration of 1.5-2.0 ml xefocama in the base of the mastoid process of the skull, while the procedure is performed 1 time per day and repeated every 2 days.