What medications to take for a concussion. Consequences of traumatic brain injury - treatment General principles of management of patients with head injury

The development of a complex pathogenetic treatment of patients with traumatic brain injury is based on the study of some of the mechanisms of its pathogenesis and the results of conservative therapy.

The impact of a traumatic agent is a starting point for a complex of pathogenetic mechanisms, which are mainly reduced to disturbances in neurodynamic processes, disorders of tissue respiration and energy metabolism, changes in cerebral circulation in combination with a restructuring of hemodynamics, homeostatic reactions of the immune system with the subsequent development of an autoimmune syndrome. The complexity and variety of resulting TBIs pathological processes, which are closely intertwined with the processes of adaptation and compensation of impaired functions, make it necessary to carry out conservative therapy for TBI in a differentiated way, taking into account the clinical form of the lesion, age and individual characteristics of each victim.

With a concussion pathogenesis is based on temporary functional disorders of the activity of the central nervous system, in particular its vegetative centers, which leads to the development of astheno-vegetative syndrome.

Victims with concussion are placed on bed rest for 6-7 days.

Medical therapy for concussion does not have to be aggressive. Basically, therapy is aimed at normalizing the functional state of the brain, relieving headaches, dizziness, anxiety, insomnia and other complaints. Typically, the spectrum of drugs prescribed at admission includes analgesics, sedatives and hypnotics. With dizziness, betaserc, belloid, bellaspon are prescribed.

Along with symptomatic treatment with a concussion, it is advisable to conduct a course of vascular and metabolic therapy for a faster and more complete recovery of brain function disorders and the prevention of various post-concussion symptoms. A combination of vasoactive (cavinton, stugeroni, etc.) and nootropic (nootropil eniefabol, aminolone, picamilon) drugs is preferable. In CSF hypertension, lasix (furosemide) is prescribed orally at a dose of 40 mg once a day.

To overcome asthenic phenomena after a concussion, it is orally prescribed: pantogam 0.5 three times a day, cogitum 20 ml 1 time a day, vasobral 2 ml 2 times a day, multivitamins 1 table. 1 per day. Of the tonic preparations, ginseng root, eleutherococcus extract, lemongrass fruits are used.

There is no need to prescribe anticonvulsants.

The criteria for expanding the regimen and discharge should be considered the stabilization of autonomic reactions, the disappearance of headaches, normalization of sleep and appetite.

Brain injuries.

The volume, intensity and duration of pharmacotherapy and other components of conservative treatment are determined by the severity of the injury, the severity of cerebral edema, and intracranial hypertension. disorders of microcirculation and liquor flow, peculiarities of the premorbid state and age of the victims.

Brain contusion, unlike concussion, is accompanied by morphological damage to the vessels and brain substance. Cerebral symptoms are more intense and last longer than with concussion, which determines the timing of drug therapy. Therapeutic effects for mild to moderate brain contusions include the following main areas:

improvement of cerebral blood flow;

improvement of energy supply of the brain;

3) elimination of pathological shifts of water sectors in the cranial cavity;

metabolic therapy;

anti-inflammatory therapy.

Restoration of cerebral microcirculation is the most important factor determining the effectiveness of other therapeutic measures. The main technique here is to improve the rheological properties of blood - increasing its fluidity, reducing the aggregation ability of formed elements, which is achieved by intravenous drip infusions of cavinton, xanthine derivatives (eufillin, theonikol). Improving microcirculation helps to increase the energy supply of the brain and prevent its hypoxia.

To relieve vascular spasm, which in mild traumatic brain injury causes transient neurological focal symptoms, stugeron (cinnarizine), papaverine, eufillin are used in therapeutic doses along with hemostatic agents (dicynone 250-500 mg every 6 hours parenterally or orally). The rapid elimination of vascular spasm and the removal of outflowing blood reduce the exposure of brain antigens to immunocompetent blood cells, which reduces the effect of the antigenic stimulus and reduces the intensity of the immune response. Due to the fact that a mechanical "breakthrough" of the blood-brain barrier in the area of ​​damage occurs during a brain injury, and the nervous tissue is alien to the immunocompetent system, with the development of an autoimmune aggression reaction in some cases, it is advisable to include hyposensitizing drugs (dimedrol, pipolfen, suprastin injections, tavegil, calcium preparations) in therapeutic dosages for 1-1.5 weeks.

Stabilization of membrane structures normalizes the volume ratios of intracellular, intercellular and intravascular water sectors, which is necessary for the correction of intracranial hypertension. Glucose is used as an energy substrate in the form of a polarizing mixture. The presence of insulin in it contributes not only to the transfer of glucose into cells, but also to its utilization according to the energetically favorable pentose cycle.

Eufillin, papaverine, which contribute to the accumulation of cyclic adenosine monophosphate, which stabilizes cell membranes, have a specific effect on the function of the blood-brain barrier. Given the multifactorial effect of aminophylline on cerebral blood flow, cell membrane function, airway patency, that is, those processes and structures that are especially vulnerable in acute TBI, the use of this drug for any type of brain damage is justified.

The timely and rational use of many of the above remedies for mild brain injuries often prevents or eliminates disturbances in the distribution of water in various intracranial sectors. If they do develop, then we are usually talking about extracellular fluid accumulation or moderate internal hydrocephalus. At the same time, traditional dehydration therapy gives a quick effect. Dehydration is carried out depending on the magnitude of intracranial pressure and consists in the use of lasix (0.5-0.75 mg / kg) parenterally or orally. When carrying out dehydration, it must be remembered that in elderly patients in 20-30% of cases in the acute period, cerebrospinal fluid hypotension is noted. This point emphasizes the importance of lumbar puncture for determining treatment tactics. Significant fluctuations in intracranial pressure are associated primarily with edema-swelling of the brain, necessitating the use of osmodiuretics (mannitol) along with saluretics. Mannitol is used in the form of a 5-10% solution intravenously at a rate of at least 40 drops per minute.

In the presence of massive subarachnoid hemorrhage, verified by CT, the treatment complex includes hemostatic antienzymatic therapy: contrykal, trasylol, Gordox. The last three drugs have a more powerful antihydrolase effect, and their use blocks many pathological reactions caused by the release of enzymes and other biologically active substances from the foci of brain destruction. The drugs are administered intravenously at 25-30 thousand units 2-3 times a day. Dicynon and ascorutin are also used.

Pathogenetic therapy for CT-verified subarachnoid hemorrhage includes the obligatory prescription of neuroprotectors from the group of slow Ca ++ channel blockers - Nimotop. Nimotop is prescribed from the first hours after injury as a continuous intravenous infusion at a dose of 2 mg/(kg h). Infusion therapy is carried out during the first two weeks after the injury. Subsequently, they switch to a tablet form (360 mg / day).

If there are wounds on the head, subarachnoid hemorrhage and, especially, liquorrhea in case of brain bruises, there are indications for antibiotic therapy, including preventive therapy.

The treatment and recovery complex usually includes metabolic therapy (nootropics, cerebrolysin, actovegin).

With mild to moderate brain contusions, analgesics and sedatives, hypnotics and hyposensitizing drugs are widely used. With convulsive syndromes, there are indications for the appointment of anticonvulsants (depakin, phenobarbital, clonazepam, carbamazepine).

Duration inpatient treatment with an uncomplicated course of mild bruises up to 10-14 days, with moderate bruises up to 14-21 days.

Clinical picturesevere brain contusion, brain compression and diffuse axonal injury due to the involvement of subcortical formations and the brain stem in the pathological process, which is manifested by the predominance of diencephalic and mesencephalobulbar syndrome. In this regard, the volume of therapeutic measures is expanding significantly and should be directed primarily to the elimination of pathological factors that are of decisive importance in the chain of pathogenesis. In this case, pathogenetic therapy should be carried out simultaneously with symptomatic correction of systemic hemodynamics and respiration. With severe bruises of the mortuary (crushing of its substance), compression and diffuse axonal damage, conservative treatment is carried out in intensive care units under the control of monitoring of cerebral, focal and stem symptoms, the activity of the cardiovascular and respiratory systems, body temperature, the most important criteria for the state of homeostasis, CT data, direct measurement of intracranial pressure.

The main groups of drugs used in the intensive care of severe brain injury.

1. Dehydrants;

a) saluretics (lasix - 0.5-1 mg per 1 kg of body weight per day intravenously);

b) osmotic diuretics (mannitol - intravenous drip in a single dose of 1 - 1.5 g per 1 kg of body weight);

c) albumin, 10% solution (intravenous drip 0.2-0.3 g per 1 kg of body weight per day).

An indication for the appointment of corticosteroid hormones is a picture of acute adrenal insufficiency observed in victims with severe trauma.

2. proteolysis inhibitors: counterkal (gordox, trasylol) - intravenous drip 100,000-150,000 IU per day.

3. Antioxidants: alpha-tocopherol acetate - up to 300-400 mg per day orally for 15 days.

4. Antihypoxants- activators of the mitochondrial electron transport system: riboxin up to 400 mg per day intravenously drip for 10 days.

Hyperbaric oxygenation is an effective method of treatment and prevention of hypoxic conditions in case of severe brain contusion with foci of crushing of the cerebral hemispheres. It is most effective in patients with lesions of the diencephalic and mesencephalic parts of the brain stem of secondary origin. The optimal mode is a pressure of 1.5-1.8 atm for 25-60 minutes (with mesencephalic lesions 1.1-1.5 atm for 25-40 minutes). Contraindications to hyperbaric oxygen therapy in case of severe brain contusion are: unremoved intracranial hematoma, unresolved upper respiratory tract obstruction, bilateral pneumonia, severe epileptic syndrome, primary brainstem suffering at the bulbar level and other individual contraindications established by a specialist.

5. Means that contribute to the regulation of the aggregate state of the blood:

a) direct-acting anticoagulants - heparin (intramuscularly or subcutaneously up to 20,000 IU per day for 3-5 days), low molecular weight heparin (10,000 IU per day), after the abolition of which they switch to antiplatelet agents;

b) antiplatelet agents (trental intravenous drip 400 mg/day, reopoliglyukin intravenous drip 400-500 ml

5-10 days, reogluman intravenously drip for 4-5 days at the rate of 10 ml per 1 kg of body weight per day) with the transition to tablet forms;

d) native plasma (250 ml per day).

6. Antipyretics - aspirin, paracetamol, lytic mixtures.

Vasoactive drugs - eufillin, cavinton, sermion.

Neurotransmitter metabolism normalizers and repair stimulantsactive processes:

a) nootropics (nootropil, piracetam) - parenterally orally in a daily dose of up to 12 g;

c) gliatilin - parenterally up to 3 g per day;

d) cerobrolysin - up to 60 ml intravenously per day.

9. Vitamin complexes.

10. Means that reduce the immune reactivity of the body in relation to the antigens of the nervous tissue: suprastin (0.02 g 2-3 times a day), diphenhydramine (0.01 g 2-3 times a day).

11. Anticonvulsants: depakine, phenobarbital, etc.

The period of inpatient treatment depends on the intensity of the recovery processes, the activity of rehabilitation measures and averages 1.5-2 months. Those who have undergone brain contusions are subject to long-term dispensary observation and, according to indications, rehabilitation treatment. Along with the methods of physical therapy, physiotherapy and occupational therapy, metabolic (nootropil, gliatilin, piracetam, aminalon, pyriditol, etc.), vasoactive (cavinton. sermion, cinnarizine, geonicol, etc.), vitamin (B, B6, B12, C , E, etc.), general tonic drugs and biogenic stimulants (aloe, actovegin, apilac, ginseng, etc.).

In order to prevent epileptic seizures after brain contusions, in cases where the risk of their development is justified, valproic acid preparations (Depakine-Chrono 500) are prescribed. Under EEG control, their long-term use is indicated. When epileptic seizures occur, therapy is selected individually, taking into account the nature and frequency of paroxysms, their dynamics, age, premorbid and general condition of the patient. Use various anticonvulsants and sedatives, as well as tranquilizers. In recent years, along with barbiturates, carbamazepine, tegretol, finlepsin and valproates (convulex, depakine) are often used.

Basic therapy includes a combination of nootropic and vasoactive drugs. It is preferable to conduct it in 2-month courses at intervals of 1-2 months for 1-2 years, taking into account the dynamics of the clinical condition.

For the prevention and treatment of post-traumatic and post-operative adhesive processes, it is advisable to additionally use agents that affect tissue metabolism: amino acids (cerebrolysin, glutamic acid), biogenic stimulants (aloe), enzymes (lidase, lecozyme).

According to indications, on an outpatient basis, various syndromes of the postoperative period are also treated - cerebral (intracranial hypertension or hypotension, cephalgic, vestibular, asthenic, hypothalamic) and focal (pyramidal, cerebellar, subcortical, aphasia).

Severe brain contusions or foci of crushing of the brain are a substrate that can be the subject of surgical intervention. However, the concept of expanding indications for conservative treatment of severe brain contusions has also been substantiated. The body's own mechanisms, with adequate medical support, are better able than surgical aggression to cope with severe damage to the medulla.

Indications for conservative treatment of severe brain contusions are:

stay of the victim in the phase of subcompensation or moderate clinical decompensation;

state of consciousness within moderate or deep stunning (at least 10 GCS points);

lack of expressed clinical signs dislocations of the brain stem (hypertensive-discirculatory or hypertensive-dislocation stem syndrome);

the volume of the crush focus according to CT or MRI is less than 30 cm 3 for localization in the temporal lobe and less than 50 cm 3 for the frontal lobe;

the absence of pronounced CT or MRI signs of lateral (displacement of the median structures no more than 10 mm) and axial (preservation or slight deformation of the surrounding cisterna) dislocation of the brain.

Indications for surgical intervention with foci of crushing of the brain are:

persistent stay of the victim in the phase of gross clinical decompensation;

a state of consciousness within the sopor or coma (on the Glasgow coma scale below 10 points);

3) pronounced clinical signs of stem dislocation;

the volume of the crush focus according to CT or MRI data is more than 30 cm 3 (with temporal localization) and more than 50 cm 3 (with frontal localization) with a homogeneity of its structure;

pronounced CT or MRI signs of lateral (displacement of the median structures over 7 mm) and axial (gross deformity of the surrounding cisterna) dislocation of the brain.

Treatment of victims should begin immediately, often at the scene, and the fate of the patient, especially with a severe closed craniocerebral injury, often depends on the measures taken in the first minutes and hours. All patients who have received a head injury with loss of consciousness or the presence of antero- or retrograde amnesia should be hospitalized for observation, examination and treatment. This is due to the fact that the course of CTBI is dynamic and its formidable complications may not appear immediately.

Principles of conservative treatment of traumatic brain injury

Conservative treatment of the acute period of CTBI is pathogenetic. There are two stages in the treatment of a closed craniocerebral injury.

At the first stage, with impaired consciousness, especially for persons who are intoxicated, it is necessary to administer analeptic mixtures: 2 ml of 20% caffeine and 25% cordiamine subcutaneously or 10% sulfocamphocaine 2 ml subcutaneously (intramuscularly or intravenously slowly).

In cases of intracranial hypotension, manifested by an increase in stupor, severity of neurological focal symptoms, tachycardia, a decrease in arterial and cerebrospinal pressure, 500-1000 ml of 5% glucose, distilled water at a dose of 10 ml 2 times a day should be administered intravenously , hydrocortisone 100 mg per 500 ml of physiological solution 2-3 times a day intravenously. Up to 40 ml of polyglucin or rheopolyglucin can be administered intravenously. Additionally, 1 ml of 1% mezaton, 1% fetanol or subcutaneously 5% ephedrine is used. It is also advisable to inject a mixture of 40% glucose (100 ml), 10 units of insulin, 100 mg of cocarboxylase, 0.06% corglucone (0.5 ml), 5% ascorbic acid (6 ml).

At high blood pressure ganglionic blockers are used: 5% penta-min or 2.5% benzohexonium is administered intravenously, 0.5-1 ml per 50 ml of physiological saline, until blood pressure drops by 20-30%. This can be supplemented intravenous administration 5-10 ml of 2.4% aminofillin.

In the fight against increasing cerebral edema, diuretics and glucocorticoid hormones are administered. Already on prehospital stage apply 2 ml of 1% lasix in 20 ml of 40% glucose intravenously or 50 mg of uregit in 100 ml of 5% glucose. It is recommended to use 15% mannitol (mannitol) at a dose of 1-1.5 g per 1 kg of the patient's body weight. In severe cases, intravenous drip of glucocorticoid hormones should be administered: 8-12 mg of dexazone or 40-80 mg of methylprednisolone in 200 ml of 5% glucose. After 6-8 hours, they switch to intramuscular administration of one of the drugs in smaller doses (4 mg of dexazone or 40 mg of methylprednisolone).

If there is psychomotor agitation, convulsive syndrome, it is necessary to inject 2-4 ml of Seduxen intravenously, if there is no effect, repeat the injection after 20 minutes. For the same purpose, an intramuscular mixture is used. 2 ml of 2.5% chlorpromazine, 1% dimedrol, 0.5% seduxen and 50% analgin or 2 ml of dropidol with fentacyl. In the case of a convulsive syndrome during a traumatic illness or registration of epileptic activity, the EEG shows a longer anticonvulsant therapy. Depending on the form and frequency of paroxysms, phenobarbital, difenin, benzonal, finlepsin, chloracone, etc. are used. A control EEG is performed after 6 months. treatment.

Treatment of mild MCT

The basis of therapy for mild CTBI is desensitizing (diphenhydramine, tavegil, pipolfen, calcium preparations) and vasoconstrictor drugs. Of the vasodilators, Cavinton 2 ml (10 mg) intravenously 1-2 times a day for 200 ml of saline has a good therapeutic effect. You can also use eufillin, halidor, papaverine. Means that improve microcirculation are used (Curantyl 0.05 mg, 1 tab. 3 times a day, Trental OD mg, 1 tab. 3 times a day, Prodectin 0.25 mg, 1 tab. 3 times a day day), venotonic agents (anavenol 20 drops 3 times a day, escusan 15 drops 3 times a day orally), as well as diuretics (diacarb, triampur, veroshpiron) in medium therapeutic doses. According to the relevant indications, symptomatic therapy is carried out with analgesics (acetylsalicylic acid, amidopyrine, baralgin, analgin, pentalgin, etc.), tranquilizers (seduxen, tazepam, mebicar, elenium, eunoctin). Increased excitability of the autonomic nervous system is reduced by bellataminal, belloid, phenibut, butyroxane. Vitamin therapy, glutamic acid, nootropil, aminalon, encephabol are prescribed.

Treatment for mild brain injury

Treatment of severe brain contusion is aimed at correcting vascular and metabolic disorders, combating increasing hypoxia, cerebral edema, hemorrhagic syndrome, and preventing complications. At the very early stage, brain protection against hypoxia is used. Enter 20% sodium oxybutyrate - 20 ml in 200 ml of 5% glucose, for the prevention of hypokalemia also 10% potassium chloride - 10 ml or panangin (asparkam) 10 ml intravenously drip. In parallel, a neurovegetative blockade is carried out, which includes: 2.5% chlorpromazine, 0.5% seduxen solution, 1 ml intramuscularly after 4 hours. In the case of arterial hypertension, ganglionic blockers are included in the mixture or 100 ml of 0.25% novocaine is injected intravenously. The initial period of treatment can also be carried out under light barbiturate anesthesia (sodium thiopental, hexenal, etc.). This increases the resistance of the brain to hypoxia, reduces its energy needs and delays the processes of lipolysis, preventing metabolic disorders. Against the background of dehydrating therapy, 400 ml of a glucose-insulin-potassium mixture from rheopolyglucin, rheogluman or hemodez can be administered.

Treatment of hemorrhagic syndrome

Hemorrhagic syndrome is stopped by the following means: 10% calcium chloride - 10 ml intravenously, 1% vikasol - 1 ml intramuscularly, ascorbic acid - 2 ml intravenously or intramuscularly. For the same purpose, proteinase inhibitors are used - trasylol (or contrykal) 25 thousand U drip in saline after 12 hours, or 5% aminocaproic acid - 100 ml intravenously, drip after 6 hours. With massive subarachnoid hemorrhages together with neurosurgeons, repeated lumbar punctures are performed with active washing of the CSF spaces with saline or CSF drainage is established with the removal of 200-300 ml of cerebrospinal fluid during the day. This accelerates its sanitation and serves as a preventive measure for the development of aseptic arachnoiditis.

To improve microcirculation and prevention of thrombosis, in the absence of hemorrhagic syndrome, heparin is administered subcutaneously - 2-3 thousand units every 8 hours. In the acute period (up to 1 month) for the prevention of infectious complications (pneumonia, pyelonephritis) in In medium therapeutic doses, broad-spectrum antibiotics are used: erythromycin, oletethrin, tseporin, etc. If swallowing is impaired in a coma, one should not forget about parenteral nutrition. The loss of protein is compensated by the introduction of hydrolysin or aminopeptide through the probe up to 1.5-2 l / day, anabolic hormones (nerobol, retabolil).

Medical therapy for CTBI

On the 3-5th day of PTBI, drugs are prescribed that stimulate metabolic processes in the brain. These are aminalon (0.25 g, 2 tablets 3 times a day), glutamic acid (0.5 g, 1-2 tablets 3 times a day), cocarboxylase (200 mg intramuscularly), vitamins 5% B 6, B 12 (200-500 mcg), ATP (1 ml intramuscularly). A course of treatment is carried out with nootropic and GABAergic drugs - cerebrolysin, nootropil (piracetam), encephabol (pyriditol), etc. Desensitizing therapy (gluconate and calcium chloride, ascorutin, tavegil, diphenhydramine, diazolin) is also recommended. They use vasodilators (cavinton, halidor, papaverine, eufillin) and drugs that improve the condition of the venous wall (anavenol, aescusan, troxevasin). According to indications, dehydrating therapy is continued (diacarb, veroshpiron, triampur).

Differentiated treatment of the acute period of severe CTBI can be schematically presented in the following form. The first five days of treatment is carried out in the intensive care unit. On the day of admission, an X-ray of the skull and a lumbar puncture are mandatory. This makes it possible to exclude or confirm a skull fracture, pneumocephalus, intracranial hematoma, as well as to clarify the massiveness of subarachnoid hemorrhage and the presence of CSF hyper- or hypotension. Attention should be paid to the displacement of the pineal gland. In cases of an increase or appearance of focal neurological symptoms, the patient's stupor, or the development of a convulsive syndrome, an urgent consultation with a neurosurgeon is necessary. EEG, Echo-EG, carotid angiography or diagnostic burr holes are made to exclude intracranial hematoma.

Surgical treatment for intracranial hematoma of any localization is practically performed without taking into account contraindications. Explorator milling holes overlap even in the final stage.

Examination of working capacity: MSEK after CTBI.

With a mild closed craniocerebral injury (concussion), the period of inpatient treatment is 2-3 weeks. The total duration of temporary disability is 1-1.5 months. In some cases, with ongoing feeling unwell terms of temporary disability can be extended up to 2 months. Employment through MSEK is shown, it is possible to determine the III group of disability.

In the case of a moderate injury (brain bruises of mild and moderate severity), the duration of inpatient treatment is from 3-4 weeks to 1.5 months. The terms of temporary disability are on average 2-4 months and depend on the nearest labor forecast. With a favorable prognosis sick leave through MSEK you can continue up to 6 months. If signs of persistent disability are found, then patients are sent to MSEC after 2-3 months. after injury.

If severe CCI (severe contusion, brain compression), the duration of treatment in the hospital is 2-3 months. The clinical prognosis is often either unclear or unfavorable, therefore, to resolve the issue of temporary disability for up to 4 months. inappropriate, except for operated hematomas. Depending on the severity of the motor defect, psychopathological, convulsive and other syndromes, it is possible to establish (with the participation of a psychiatrist) II or I group of disability. The duration of temporary disability and the group of disability after removal of surgical hematomas are determined individually, taking into account the immediate prognosis and the nature of the work performed.

doctor of medical sciences, Leonovich Antonina Lavrentievna, Minsk, 1990 (as amended by MP website)

After traumatic brain injury, the following are most commonly used: narcotic analgesics (72%), then antidepressants (67%), anticonvulsants (47%), anxiolytics (33%), hypnotics (30%), stimulants (28%), antipsychotics ( 25%), antiparkinsonian drugs (25%) and other psychotropic drugs (18%). In children with autism spectrum disorders, psychotropic drugs are used in 42% of cases.

Typically, psychotropic drugs are prescribed after traumatic brain injury in almost 95% of patients, with 8.% receiving only one drug, and 31%, more than ≥6 (psychotropic polypharmacy). Younger patients are more likely to receive anxiolytics, antidepressants, antiparkinsonian drugs, stimulants, antipsychotics, and narcotic analgesics, while those who are older are more likely to take anticonvulsants and various psychotropic drugs. Men were more likely to receive antipsychotics.

Anticonvulsants are given to patients with seizures, usually during treatment. emergency care or rehabilitation. Narcotic analgesics are given to patients with a history of drug abuse, a history of anxiety and depression (premorbid is usually found out or during emergency care), and severe pain during the rehabilitation period. Lower scores on cognitive function rating scales usually require more medication compared to patients with higher cognitive function when admitted to hospital after injury.

At admission and during the rehabilitation stay, the doctor usually checks the prescribed medications, often constantly reviewing the needs of the patient. This review of therapy involves stopping medications that are no longer needed or that may cause an adverse response (side effects, complications) while adding other medications as needed.

The small volume of published studies on the medical treatment of the consequences of traumatic brain injury is usually limited by the requirements and rigor of research (lack of controlled trials, injury information (injury severity and time of injury), mixed type of brain injury, and small sample size.

A randomized, placebo-controlled study of patients recovering from traumatic brain injury showed that amantadine was more effective than placebo in cases of "minimum state of consciousness" in "accelerating the rate of functional recovery." Usually prescribed antipsychotics often lead to more than 7 days of post-traumatic amnesia. Polypharmacy during the treatment of traumatic brain injury and the use of anticholinergic drugs are associated with increased risk fall.

Researchers have shown that anxiolytics, antidepressants, antipsychotics, sleeping pills and antiparkinsonian drugs are less likely to be used in ethnic minorities, especially those of Asian and Hispanic origin.

Despite the fact that 61% of those patients who took antidepressants after a traumatic brain injury did not have a mention of depression, they were prescribed for symptoms such as: pain, sleep disturbances and / or behavioral disturbances. For example, trazadone (SARI trazodone) is frequently used in this patient population to induce sleep. Similar results were found with antipsychotics (24% of patients had no history of premorbid history of psychosis, bipolar disorder, or schizophrenia). Antipsychotics are prescribed in 25% of patients. Typically, practitioners use this class of medication to help control agitation after a brain injury. This use is somewhat controversial, as blocking dopamine is not always considered to be productive in terms of restoring patients' condition. However, second-generation antipsychotics have less of a dopamine D2 blockade effect and are considered to be preferred over first-generation antipsychotics; although even they have a significant profile side effects.

Of those physicians who administered anticonvulsants, 41% of patients were noted to be seizure-free during emergency care or rehabilitation, indicating use of anticonvulsants for seizure prevention or for other reasons (eg, behavior control or management pain).

Almost 30% of patients who received anxiolytics did not have the anxiety mentioned in their medical history, and doctors assumed that many of the patients could be treated with this class of drugs for other reasons, such as agitation or insomnia.

Antiparkinsonian drugs and the introduction of stimulants into therapy were relatively rare cases compared with other psychotropic drugs (narcotic analgesics, antidepressants, anticonvulsants, anxiolytics and hypnotics). During the rehabilitation period, doctors administer antiparakinson drugs to 25% of patients (most often amantadine and bromocriptine). In clinical practice, these drugs are often used to treat a range of rehabilitation-related problems such as agitation, agitation, disinhibition, lack of initiation, akinetic mutism, and cognitive impairment. Similarly, prescription of stimulants (28%) is also relatively rare given that symptoms of inattention, lack of initiation, agitation, and slow processing speed are cardinal features of moderate to severe traumatic brain injury. The most commonly used stimulants are: methylphenidate, modafanil and atomoxetine. Amantadine can help to minimize the manifestations of many, especially cognitive deficits commonly associated with traumatic brain injury, in particular in cases of altered consciousness, cognitive impairment and behavioral disorders (behavioral dysregulation).

Traumatic brain injury is a collective concept that includes damage to the soft tissues of the head, skull bones, brain, meninges. A distinctive feature is that the whole complex of injuries has a single cause and mechanism of development.

One of the features of brain damage is a high percentage of mortality in moderate and severe injuries. Traumatic brain injuries are the main cause of disability of able-bodied persons among all traumatic injuries. In addition, even after mild injuries, residual effects may form.

Brain damage usually has certain consequences

Classification of the consequences of TBI

Depending on how much time has passed since the traumatic brain injury, the consequences are divided into two groups - early and late. The first ones include:

• coma;
• dizziness;
• hematomas;
• hemorrhages;
• accession of infection.

Among the long-term consequences of craniocerebral injuries, the following are most often diagnosed:

• cerebroasthenic syndrome;
• sleep disturbance;
• chronic headache syndrome;
• depressive disorders;
• memory impairment, problems concentrating;
• violation of certain functions of the brain - speech, vision, motor activity, sensitivity;
• convulsive syndrome;
• intracranial hypertension.

Early consequences are those that develop in the first 7-14 days after injury - in the so-called early post-traumatic period. With brain contusions, diffuse axonal damage, hemorrhages, it increases up to ten weeks. The interim period is from two months to six months from the moment of receiving a traumatic brain injury. After it, a remote period begins, which lasts up to two years. Central nervous system disorders diagnosed later than two years later are not regarded as residual effects of traumatic brain injury.

Treatment

Timely diagnosis and the beginning of treatment of traumatic brain injuries - key moment which minimizes the risk of developing residual effects.

Consequently, the rehabilitation treatment of a patient with a traumatic brain injury begins in a neurological hospital and continues on an outpatient basis. Full recovery is possible only with an integrated approach to the treatment process, which should include the following areas:

• drug treatment;
• physiotherapeutic procedures and physiotherapy exercises;
• treatment with folk remedies;
• psychological help.

A concussion is treated with a complex of measures, starting with medications and ending with psychological help.

Treatment tactics vary depending on how much time has passed since the brain injury and on the individual characteristics of the patient.

Early post-traumatic period

The patient spends the early post-traumatic period in a specialized department under the supervision of specialists. Volume pharmacological preparations determined strictly individually. This takes into account the degree of brain damage, the type of residual phenomenon, the general condition of the patient, his age, the presence of concomitant pathology. Treatment is aimed at maintaining the functioning of vital organs and systems, normalizing the acid-base and water-salt balance, and correcting blood clotting parameters. In parallel, drugs are prescribed, the task of which is to help the surviving neurons integrate into the activity of the central nervous system. Basically, doctors use the following groups of drugs:

• drugs that reduce intracranial pressure;
• vascular drugs;
• neuropeptides.

Painkillers, antibiotics, hemostatic agents are used according to indications.

Drugs that reduce intracranial pressure

After an injury, intracranial pressure may increase, in which case, the doctor prescribes drugs that lower it

In a hospital setting, osmotic diuretics, most often mannitol, are used to reduce intracranial pressure. It increases the osmotic pressure in the capillaries, resulting in a redistribution of fluid from the tissues into the vessels. Loop diuretics like furosemide are prescribed once to reduce the likelihood of side effects from the use. Diakarb - activates the secretion of sodium by the kidneys, which also leads to a decrease in the volume of circulating fluid. If intracranial hypertension is difficult to treat, in addition to diuretics, glucocorticosteroids are prescribed - dexamethasone, prednisolone, methylprednisolone.

On an outpatient basis, the patient is prescribed diacarb and glucocorticoids. Dosage and duration of treatment are determined individually, depending on the severity of symptoms.

Vascular drugs

Their main task is to normalize blood flow in the capillary bed and improve the blood supply to the lesion. Most often, cavinton, bravinton, vinpocetine, ceraxon are prescribed. With their help, it is possible to reduce the affected area, eliminate or reduce the severity of residual effects.

Neuropeptides

The group of neuropeptides includes cerebrolysin, actovegin, cortexin. These are animal products. Their active substance- protein molecules, the mass of which does not exceed 10 thousand daltons and short amino acid chains. They are able to act as antioxidants, reduce the activity of the inflammatory process, enhance the regeneration of neuronal processes and form new synaptic connections. Outwardly, this is manifested by a significant improvement in the functioning of the central nervous system. Of the nootropics, piracetam is most often prescribed.

Interim period

The vast majority of victims of brain damage spend this period at home. Planned hospitalization require only patients with severe symptoms, requiring the appointment of new groups of drugs or adjustment of doses of drugs already taken. As a rule, the same funds are prescribed as in the early period. According to the indications, in the presence of a convulsive syndrome, sleep disorders and mental disorders, appoint:

• anticonvulsants;
• sleeping pills;
• antidepressants;
• remedies for mood disorders.

In addition, a complex of restorative vitamins and minerals, good nutrition are prescribed. As soon as the patient's condition allows, physical therapy, massage, physiotherapy, exercises aimed at improving cognitive functions are added. These measures are especially effective in patients with focal symptoms brain damage. At the same time, a sufficient level of physical activity of the patient is monitored.

Late period

Treatment in the late post-traumatic period is carried out on an outpatient basis. If necessary, the patient consults with the attending physician. The drugs are prescribed in tablet form, which greatly simplifies the treatment process. Treatment in a hospital is planned and carried out in courses. Their necessity is determined general condition the patient and the severity of the symptoms that remained after brain damage.

The victim must continue to engage in physiotherapy exercises, undergo physiotherapy, massage. To stimulate intellectual activity, reading, learning foreign languages, solving crossword puzzles, and solving logic puzzles are recommended.

Psychological assistance, auto-training sessions and other non-specific treatment are actively used, the main task of which is to help the patient adapt in everyday life and society, increase his independence and sociability.

Folk remedies

Treatment with folk remedies can significantly increase the effectiveness of traditional drugs in patients with residual effects after traumatic brain injury.

With cerebroasthenic syndrome, which is accompanied by weakness, fatigue, irritability, alcohol tinctures of tonic plants are prescribed - ginseng, Chinese magnolia vine, eleutherococcus. Very good effect give morning rubbing with a damp towel, which after two or three weeks should be replaced by a douche.

Also used to treat concussion folk remedies in particular the sedative fee

To eliminate vegetative-vascular manifestations, a sedative collection is used. It includes valerian, hop cones, elecampane, licorice, thyme and lemon balm in equal proportions. A tablespoon of raw materials is poured with a glass of boiling water, insisted in a thermos throughout the night. As a result, get daily dose medication that is taken in two doses.

An infusion of lavender flowers, rosemary, thyme, rue, hop cones, Ivan tea has a sedative and tonic effect. Prepare and take it, as in the previous recipe.

Finally

Traumatic brain injury, especially moderate and severe, is difficult to treat. The likelihood of negative consequences increases with untimely initiation of therapy or with the appointment of drugs in an incomplete volume. At the same time, adequate therapy and careful implementation of all doctor's prescriptions significantly increase the chances of a full recovery. If you have any doubts or questions about the treatment process, discuss them with your doctor. This will give you the opportunity to get a good result in the shortest possible time.

»

the duration and severity of which depends on the degree of mechanical impact on the brain tissue.

Long-term consequences

Long-term consequences of TBI can be manifested by neurological disorders:

• sensitivity disorders (numbness of the hands, feet, burning sensations, tingling in various parts of the body, etc.),
• movement disorders (trembling, coordination disorders, convulsions, blurred speech, stiffness of movements, etc.),
• vision changes (double vision, blurred focus)
• mental disorders.

Mental disorders and behavioral disorders due to brain injuries can be expressed in different conditions: from a state of fatigue to a pronounced decrease in memory and intelligence, from sleep disturbances to incontinence of emotions (attacks of crying, aggression, inadequate euphoria), from headaches to psychoses with delusions and hallucinations.

The most common disorder in the picture of the consequences of brain injuries is asthenic syndrome.

The main symptoms of asthenia after traumatic brain injury are complaints of fatigue and rapid exhaustion, the inability to endure additional stress, unstable mood.

Characterized by headaches, aggravated by exertion.

An important symptom of an asthenic condition that has arisen after a traumatic brain injury is increased sensitivity to external stimuli (bright light, loud sound, strong smell).
It is very important to know that a lot depends on whether the concussion or brain contusion happened for the first time, or whether the patient has repeatedly been able to endure such injuries at home. This directly affects the outcome and duration of treatment.

If the patient has more than 3 concussions in the anamnesis, the period of treatment and rehabilitation is significantly lengthened and the likelihood of complications also increases.

Diagnosis of traumatic brain injury

For traumatic brain injury diagnostic procedures needed urgently.

It is also important to be examined and observed by specialists every month after injury.
As a rule, in the diagnosis of TBI, methods of magnetic resonance imaging are used, computed tomography, radiography.

Treatment of TBI and consequences of brain injuries

In the acute period, anti-edematous, neurometabolic, neuroprotective, symptomatic therapy is carried out, which consists in the selection of several medicines offered both in the form of tablet preparations and in the form of injections (drip and intramuscular).

This treatment is carried out for about a month. After that, the patient remains under the supervision of his attending physician, depending on the severity of TBI, from six months to several years.

For at least three months after a TBI, it is strictly forbidden to take alcoholic beverages and heavy physical activity.

In addition to traditional methods of treating TBI, there are no less effective methods:

In combination with drug therapy and physiotherapy, these techniques can have a more pronounced and faster effect. However, in some cases they are contraindicated for use.

Everyone knows the fact that treatment should be complex, and the more techniques will be used during treatment, the better.

After the end of the course of treatment, the patient must be under the supervision of a doctor, and in the future he may need repeated courses, as a rule, once every half a year.

Possible Complications

If left untreated, brain injury often leads to complications. Most dangerous consequences are considered remote, which are initially formed hidden. When, against the background of general well-being, without visible symptoms, a complex pathology is formed. And only after a few months, or even years, an old brain injury can make itself felt.

The most common among them are:

• headaches, often with nausea and vomiting,
• dizziness,
• memory impairment,
• the formation of mental pathology, etc.

Traumatic brain injuries are a danger that the patient may not be aware of.

Various types of problems can occur after a blow to the head, even when there are no visible symptoms of a concussion ( headache, dizziness, vomiting, pressure on the eyes, feeling of overwork, drowsiness, veil before the eyes).

In many cases, the consequences of a brain injury can be accompanied by a displacement of the cervical vertebrae, which can also lead to:

• headaches,
• pain in the neck
• memory impairment,
• increased fatigue afterwards.

Brain injury is often the "trigger" of diseases such as:

• facial neuritis,
• pathology of the trigeminal and other facial nerves.

this may be accompanied by pain on one side of the face or muscle weakness on one side of the face.

The clinic "Brain Clinic" conducts all types of research and complex treatment of the consequences of brain injuries.