My husband drinks after a traumatic brain injury. Relevance of the problem and the relationship between traumatic brain injury and alcoholism. Treatment for concussion

Combination traumatic brain injury (TBI) and alcohol intoxication is determined by the continuing growth of neurotraumatism in the world and a significant number of patients injured while intoxicated.

Currently, alcoholism has become another of the socio-demographic problems of our time. Although, as evidenced by archaeological finds, humanity has been familiar with intoxicating and intoxicating substances since ancient times.

So the Peruvians, back in the 6th century BC, buried their dead with coca leaves so that they would not get bored in the other world. However, only in the 2nd half of the twentieth century did alcoholism reach epidemic proportions. The 90s of the twentieth century went down in history as a period of unprecedented destructive consequences of the demographic crisis in Russia. Over the last 5 years of this century alone, the country’s population decreased by 1 million 600 thousand.

Today in Russia over 700 thousand people die annually from alcoholism alone.

Alcohol is an absolute risk factor for TBI. In European countries, alcohol is named the second risk factor for disease, injury and mortality. The level of alcohol consumption per person per year characterizes the alcohol situation in the country.

In recent years, in European countries including Russia and Belarus, this figure ranges from 13.4 to 20.0 liters per capita per year. This is one of the highest rates in the world.

Today the United States has 12 million alcoholics, and the beginning of the 21st century is marked by an increase in alcoholism in Latvia, Estonia, Lithuania, Slovenia, Finland, and Poland. In Russia, 2% of the population suffers from alcoholism, and 76% drink alcohol regularly.

In the Republic of Belarus, 1/1 of one million people abused alcohol and were dependent on it in 2007. According to official statistics in Belarus, from 1970 to 2005, the mortality rate as a result of injuries and accidents increased by 2-3 times, and as a result of alcohol poisoning by 6-8 times.

According to A. Edwards et al. Every 2nd case of TBI is associated with alcohol intake. Russia, Belarus and the Baltic countries are ahead of most European countries in this regard. Murders while intoxicated occur in 72%, road traffic accidents from 67.7 to 90%. The percentage of offenses committed by teenagers under the influence of alcohol or drugs is growing catastrophically. In Russia in 2007 it reached 63.6%.

On the one hand, alcohol intoxication, due to the similarity of clinical manifestations, easily masks TBI, and on the other hand, along with infections, arterial hypertension, and cerebral vasculitis, it is a predisposing factor in the formation of intracranial hemorrhages.

Pathogenetic mechanisms of alcohol intoxication in traumatic brain injury

The pathogenetic mechanisms underlying TBI and alcoholic damage to the central nervous system are close to each other and represent a chain of adaptive reactions in response to damage to brain tissue. This can be microstructural only functional in nature in mild traumatic brain injury, and in severe forms of injury it causes macrostructural changes.

There is a mismatch between the chemical control systems of cellular and tissue homeostasis.

Ethyl alcohol, due to its physicochemical properties, biological and toxic effects, stands out sharply from the circle of psychoactive substances. Ethanol, having a membranotopic (impairs the excitability of the heart muscle) and conformational effect, reduces the direct toxic effect on all human organs and systems.

The first blow naturally falls on the nervous, endocrine and immune systems, which carry out coordination functions in the body. The mechanisms of disruption of the functioning of homeostatic systems in alcoholism are associated both with the direct effects of ethanol and its oxidation products on cells, and with a violation of the central regulation of function. Plays an important role in alcohol adduction lipid peroxidation (LPO). LPO plays an important role in regulating the permeability of cell membranes and the state of oxidative phosphorylation of the cell. In normal tissue, the process of lipid peroxidation constantly occurs, the intensity of which is inversely related to the activity of natural antioxidant systems.

The degree of severity of cerebral edema depends on the relationship of these systems in the clinic of TBI during alcohol intoxication. In turn, an increase in the permeability of the cerebral vascular endothelium contributes to intracranial hemorrhages. Excessive formation of reactive oxygen species can cause damage and death of the cell itself.

Antioxidant systems are necessary to preserve LPO. The action of external pro-oxidants, lack of supply of obligate oxidants and activation of endogenous generation of reactive oxygen species lead to tension in the antioxidant defense mechanisms. This can ultimately lead to the development of oxidative stress, which can manifest itself at the cellular, tissue and organismal levels.

Under conditions of alcohol intoxication, the products of ethanol metabolism can damage any organs and tissues due to their membranotropic properties. Changes in the metabolism of the latter lead to the death of immunocompetent cells. Severe alcohol intoxication is characterized by a shift in hormonal balance and a prolonged increase in glucocorticoid levels, which can be equated to severe long-term stress.

Recently, much attention has been paid to neurosteroids, in particular dehydroepiandrosterone. The latter has neuroprotective and stress-protective effects. Together with cortisone, it regulates the process of apoptosis and the level of oxidative stress in the body.

As a result of the interaction of ethanol oxidation products with monoamines in the liver, compounds with morphine-like characteristics arise. In terms of its pharmacological properties, ethyl alcohol in this case is close to ether, although its therapeutic effect is weaker. The mechanism of direct and indirect effects of alcohol provokes the development of multiple disorders, primarily on certain brain structures and almost all visceral organs (pancreas, etc.). The released neurotransmitters of catecholamine nature - norepinephrine and dopamine from presynaptic structures into the limbic parts of the brain and cause that phase of mental, vegetative and motor excitation that are observed during alcohol intoxication.

Initially, the cerebral cortex, hypocate, limbic system, and then the reticular formation of the brain stem are affected. Inhibition of inhibitory processes in the cerebral cortex leads to the release of subcortical centers.

In large doses, alcohol inhibits the activity of subcortical centers, which leads to coma. These same structures are also affected in TBI.

Ethanol is easily absorbed and perfectly penetrates the blood-brain barrier. Its action depends on its concentration in the body, and clinically this is manifested by general cerebral and focal symptoms of the central nervous system.

The same symptoms are observed with TBI. Thus, the condition of patients and the clinical course of TBI is determined on the one hand by the severity of traumatic brain injury, and on the other hand by the severity of intoxication.

Clinical features of the course of traumatic brain injury during alcohol intoxication

Since the clinical manifestations of alcohol intoxication and TBI are in many ways similar, sometimes difficult to resolve diagnostic and expert-legal problems arise, especially when mild TBI. MTBI is accompanied only by axonal damage to the brain without gross local changes in brain tissue and blood vessels. FMS, as one of the forms of MTBI, is manifested by rapidly growing functional disorders with polymorphic “variegated” unstable symptoms of central nervous system damage with a predominance of autonomic disorders. Often, autonomic disorders can be almost the only sound of MTBI; it is not for nothing that in the past TBI was called “vegetative shock.” With UGM, macrostructural destruction of the brain substance with a slight hemorrhagic component is observed.

Clinical picture In both forms, MTBI is similar and differs only in the severity and duration of symptoms. Autonomic disorders, being one of the leading symptoms of MTBI, are manifested by marbling of the skin, hyperhidrosis, low-grade fever, fluctuations in blood pressure, bradycardia, tachycardia, and pulse lability. Focal microsymptoms affect the cranial nerves, cerebellar, and motor spheres during LMBI, and are sometimes accompanied by minor sensory disturbances and a mild meningeal symptom complex. All of the above neurological and autonomic symptoms are observed in persons intoxicated and without TBI.

With small and medium doses of alcohol intoxication (not exceeding the ethanol content in the blood of 2.5‰), pronounced autonomic disturbances appear, often of a sympathoadrenal nature: facial hyperemia, sweating, acrocyanosis of the extremities, tachycardia, increased blood pressure.

Some patients may have vagoinsular disorders: pallor of the skin, bradycardia, decreased blood pressure, lack of air, gastrointestinal discomfort, mild psychomotor agitation.

Sometimes such paroxysms end in chills and polyuria. Often, autonomic disorders are of a mixed nature, but are always accompanied by a feeling of fear. At a dose of ethanol of 2.5-3.0 ‰, focal microsigns from the central nervous system appear in the blood in the form of anisocoria, horizontal nystagmus, mild insufficiency of the VII, XII pairs of cranial nerves of the central type. Reflexes of oral automatism, hyperreflexia from deep reflexes, anisoreflexia, and mild ataxic disorders appear. When the concentration of ethanol in the blood is 3.0-4.0 ‰, the picture changes, although autonomic disorders persist, but the patient’s behavior changes.

He becomes lethargic, drowsy, coordination, both static and dynamic, is grossly impaired, the pupils become narrow, and mydriasis is extremely rare. Against the background of hyperreflexia of the tendon and periosteal reflexes, the Babinski reflex may occur, and nystagmus persists. Sometimes the clinical picture resembles acute Leiden-Westphal ataxia: the patient falls in the Romberg position, walking is grossly impaired, coordination tests are difficult to perform, and muscle tone decreases. All these symptoms completely regress after 5-7 days.

Real examples

Traumatic brain injury alcohol

An example would be the following observation:

Patient Z., born in 1974, a bulldozer driver, was taken to the hospital by ambulance on July 12, 2007 with complaints of headache, pain in the nose, lower back, and general weakness. According to the patient, he celebrated his friend’s birthday. As a result of a conflict in the company, he was punched in the head and face area. He doesn’t remember whether there was a loss of consciousness. There was no vomiting. Two years ago he suffered a concussion, also in a fight while intoxicated.
Objectively: strong constitution, adequate nutrition. General condition is satisfactory. There are bruises in the area of the left temple and bridge of the nose. Abrasions in the area of the right forearm and thigh. The face is hyperemic. Severe sweating. Breath smells like alcohol. Talkative, fussy. Pulse 92 beats. in a minute. Blood pressure 150/90 mmHg. The liver is at the edge of the costal arch, painless. There is no other pathology of the internal organs. Conscious. Adequate. The pupils are slightly dilated, the reaction to light is preserved. Finely sweeping horizontal nystagmus. The face is asymmetrical due to bruises. Speech is slurred and dysarthric. The pharyngeal reflex is alive. Tongue in the midline. There are no paresis of the limbs. Muscle tone is reduced. Tendon and periosteal reflexes are alive S=d. There are no pathological signs. Sensitivity is preserved. In Romberg's pose he falls. Performs coordination tests with difficulty with moderate intentional tremors. The gait is ataxic. There are no meningeal signs. General blood and urine tests without deviations from the norm. Total bilirubin is 32.7 mmol/l (normally 8.5-20.5 mmol/l). Glucose 6.3 mmol/l. Fundus, EchoEG without deviations from the norm. CT scan of the brain shows a slight atrophic process (slight expansion of the subarachnoid space on the convex and slightly dilated ventricular system). An X-ray of the facial bones revealed a non-displaced fracture of the nasal bridge. All subsequent days in the hospital he complained of headache, pain in the nose, and general weakness. Pulse and blood pressure are within normal limits. The atactic syndrome has regressed. By day 8, gait is within normal limits. Stable in the Romberg position. Performs coordination tests satisfactorily. The nystagmus disappeared on the second day. Speech was restored.
Clinical diagnosis: mild closed craniocerebral injury, concussion.
Concomitant diagnosis: non-displaced nasal dorsum fracture. Severe alcohol intoxication (dose of ethanol in the blood 2.59‰).
He was discharged on the 14th day with an open medical certificate to continue treatment in the clinic.
According to the outpatient card, in 2005 he was treated for 5 days for a concussion and alcohol intoxication. In subsequent years, I applied only in connection with medical examinations. After discharge from the hospital, I was on the ENT doctor’s list for 7 days due to a fracture of the nasal bridge.

Thus, the patient’s clinical picture was characteristic of acute ataxic syndrome, which arose in a state of severe alcohol intoxication. The rapid and complete regression of neurological symptoms as alcohol intoxication is removed is well known in the literature as “benign acute cerebellar ataxia of Leiden-Westphal.” Mild autonomic disorders noted upon admission in the form of tachycardia, a slight increase in blood pressure, and hyperhidrosis were also associated with alcohol intoxication. Apparently, both of these syndromes (atactic and vegetative) were regarded by hospital doctors as manifestations of MTBI.

The isolation of the cerebellar syndrome, in the absence of other microorganisms from the central nervous system, normal fundus data, and echo-EG indicated that he did not have LMBI.

In some cases, with a strong and severe degree of alcoholic intoxication (the dose of ethanol in the blood is from 2.5 to 5.02 ‰), and in depleted people with alcoholic hepatitis and cirrhosis of the liver, with lower doses of ethanol, acute alcoholism may occur.

Clinically, this pathology is manifested by a syndrome of increased intracranial pressure and cerebral edema or acute hemorrhagic encephalopathy by Gaye-Wernicke. These clinical forms of alcoholic injury may resemble a brain contusion with predominant damage to the brainstem. In the neurological status in these cases, a meningeal symptom complex (stiff neck, Kernig, Brudzinski symptoms) also develops in combination with brainstem disorders, depending on the level of the lesion.

When the upper and middle parts of the brainstem (the cerebral peduncle and the pons) are affected, oculomotor disorders, gaze paresis, ataxia, and mental disorders occur. The face may become hyperemic, miosis gives way to mydriasis, and pronounced autonomic disorders appear. When the medulla oblongata is damaged, bulbar syndrome develops, accompanied by severe disturbances in cardiac activity and respiration.

In large doses, alcohol inhibits the activity of subcortical centers, which leads to coma. In an alcoholic coma, the skin is pale, vomiting is observed, cardiac activity decreases, blood pressure decreases, the pulse is weak, breathing slows down to 6-8 per minute. Coming out of a coma or stupor is most often accompanied by delusions and hallucinations.

The observation below demonstrates this trend.

Patient I., born in 1969, unemployed. On September 21, 2008, she was taken to the hospital after a generalized convulsive attack. The accompanying person could only report that on September 18, she was beaten by her roommate at home.
Objectively: grave condition, deep stupor. Not available to contact. There are multiple “fresh” and “old” bruises on the face, head, torso, and limbs. Pulse 112 beats. in a minute. Blood pressure is 175/115 mmHg, heart sounds are muffled. There are no features from the internal organs.
The face is hyperemic. Severe hyperhidrosis. The pupils are wide, the reaction to light is sluggish. The face is asymmetrical due to bruising on the right side. There are no paresis of the limbs. Tendon and periosteal reflexes are animated S=d. Achilles reflexes are sharply reduced. There are no pathological signs. Hyperesthesia of the feet in the shape of a “sock”. Meningeal symptoms. In the intensive care unit, the patient’s condition remains serious for 2.5 days. Constant tachycardia 100-120 beats. per minute Arterial hypertension 160/100 - 180/120 mmHg. Breathing is rapid 22-24 per minute.
Low-grade fever. On the 3rd day, the general condition improved, temperature, pulse, and breathing returned to normal. However, the patient’s behavior changed dramatically. Severe motor agitation, auditory and visual hallucinations, and disorientation appeared. Examined by a psychiatrist. Additionally, it became known that he was registered with a narcologist for alcoholism. Alcohol delirium was removed. Due to the patient's memory impairment, details of the injury could not be revealed. The patient only reported that an attack with loss of consciousness occurred for the first time. The fundus and the composition of the cerebrospinal fluid were without deviations from the norm. The content of bilirubin in the blood is 36.9 mmol/l (normal 8.55-20.5 mmol/l), a sharp increase in indirect bilirubin (11.2 mmol/l), high levels of transaminases.
CT scan of the brain shows a moderately pronounced atrophic process. On the 9th day she was discharged home.
Clinical diagnosis: Mild closed head injury, concussion.
Concomitant diagnosis: Alcoholism, alcoholic epilepsy (first identified), alcoholic polyneuropathy, sensory-areflex form. Alcohol delirium. The entire clinical picture of the patient fit into the framework of acute alcoholic encephalopathy, when during the period of abstinence a generalized convulsive seizure initially occurred, then a mixed type vegetative paroxysm (sympatho-adrenal and vago-insular), at the end of which hallucinations and full-blown alcoholic delirium arose. Thus, the diagnosis made at the clinic as “TBI” was removed.

Differential diagnosis is especially difficult in cases of severe traumatic brain injuries in persons with stage II-III alcoholism if they have so-called “late” syndromes of central nervous system damage. The clinical picture in these cases is manifested by gross focal symptoms: spastic paralysis, depending on the location of the lesion; disorders of higher nervous activity, cognitive disorders, apraxia, astasia-abasia, pseudobulbar syndrome, etc.

A similar clinical picture can be found in a patient with UGM. Diagnosis in these cases is based on clinical data. With UGM, focal symptoms increase, as a rule, against the background of a general cerebral symptom complex and the presence of red blood cells in the CSF.

Alcohol disorders manifest as isolated disorders without a cerebral syndrome, but against the background of visceral disorders and corresponding changes in biochemical tests (bilirubin, transaminases, etc.). A CT scan of the brain is of great help in diagnosis. In this case, UHM manifests itself as a zone of reduced density with a hemorrhagic focus within the zone of cerebral edema. In type IV bruises, single or multiple foci of hemorrhage are defined as intracerebral hematomas. Regression of the lesions occurs according to the type of resorption, or instead of resorption, progression occurs, up to the formation of gross dislocations of the brain and the formation of intracerebral hematomas. With alcohol impairment

CT scan of the brain reveals degeneralized processes, foci of demyelination in individual brain structures against the background of a pronounced atrophic process of the brain. As an example, we give the following observation.

Patient R., 47 years old, homeless, was taken by ambulance to the hospital on June 7, 2007. He was found in the entrance of a residential building with traces of bruises on the head and face. Contact with the patient is almost impossible, speech is slurred, disoriented in place, time, and self. Based on the documents found in the clothes, full name and age became known; he is registered in the Bryansk region and has a class II disability.
Objectively: severe condition of low nutrition, unkempt.
Looks older than his age. There are traces of bruises on the head, face, and torso. Tattoos on arms and back. Pulse 68 beats. per minute Blood pressure 105/60 mmHg. Heart sounds are muffled. The liver protrudes beyond the edge of the costal arch and is painful. Conscious, but due to speech impairment and severe cognitive impairment, contact is not possible. The pupils are of medium size, the reaction to light is preserved. Exotropia. Partial contracture of the right facial nerve with pathological synkinesis. Dysarthria, dysphagia, dysphonia.
The pharyngeal reflex is increased. Rough reflexes of oral automatism. Moderate central tetraparesis. Muscle tone is increased according to the spastic type. Babinski reflex on both sides. Abdominal reflexes are absent. No clear sensitivity disorders could be identified. Stiff neck. Kernig's sign is not pronounced. Pelvic disorders. In the fundus there is partial atrophy of the optic nerves. Echo-EG-hypertension. In the general blood test, leukocytosis 8600-109 formula was not changed. ESR - 27 mmHg. Biochemical blood tests: total bilirubin – 52.1 mmol/l; indirect – 14.3 mmol/l; urea 9.5 mmol/l; sugar – 8.6 mmol/l, high level of transaminases.
CT scan of the brain shows a linear fracture of the calvarium, a small accumulation of blood in the basal parts of the frontal lobes. The subarachnoid space and ventricles of the brain are sharply dilated. In the area of the pons and the lower parts of the cerebral peduncles there is a focus of demyelination.
Conclusion: linear fracture of the calvarium. Minor subarachnoid hemorrhage. Communicating hydrocele of the brain. Pontine myelinolysis.
During lumbar puncture, cerebrospinal fluid flowed out under pressure and was bloody. Protein 0.65 g/l. Cytosis 265×106 cells. The sediment contains fresh red blood cells. Under the influence of treatment, the general condition improved slightly. Pseudobulbar disorders decreased, speech improved, spasticity of the limbs became pronounced, and meningeal symptoms regressed.
I started walking. The gait is spastic-atactic. However, in general, the neurological status remains the same. He was discharged on the 20th day.
Clinical diagnosis: open traumatic brain injury of moderate severity. Traumatic subarachnoid hemorrhage.
Concomitant diagnosis: alcoholism. Central pontine myelinolysis. Moderate tetraparesis, pseudobulbar syndrome. Dysfunction of the pelvic organs. Alcoholic dementia.

Thus, in this case, the attending physicians initially had the impression of a severe traumatic brain injury, a contusion of the brain stem. However, the entire symptom complex of neurological disorders with data from computed tomography and laboratory tests convincingly showed that the severity of the patient was not due to TBI, but to alcoholism. The leading clinic was a rare “late” syndrome of damage to the nervous system due to alcoholism - central pontine myelinolysis.

A number of authors point to EEG changes both during MTBI and during alcohol intoxication. These changes are manifested by the irregularity of the alpha rhythm, the presence of single low slow theta and acute waves. The asynchrony of beta activity with the absence of the alpha rhythm indicates the active influence of the reticular formation and mesencephalic structures, emphasizing the involvement of the suprasegmental parts of the nervous system in the process both during LMBI and during alcohol intoxication. If during TBI no significant changes are observed in biochemical tests, then with alcoholic damage to the central nervous system, pronounced changes occur in a number of biochemical tests: a decrease in the level of cholinesterase, an increase in total protein, urea, the level of free myoglobulin, bilirubin, a sharp increase in criatinine. The composition of CSF in patients with LMBI, either within normal limits, or in cases of UHM, subarachnoid or intracerebral traumatic hemorrhage, can be xanthochromic, bloody with increased protein and cytosis. In case of alcohol intoxication and neurological manifestations of alcoholism, with the exception of acute hemorrhagic encephalopathy of Gaye-Wernicke, the cerebrospinal fluid is colorless with a low protein content (< 0,2‰).

In the Gaye-Wernicke form, the cerebrospinal fluid is xanthochromic with a slight increase in protein, fresh and leached red blood cells.

In the differential diagnosis of TBI, alcohol intoxication and neurological complications due to alcoholism, anamnesis and the appearance of the victim are of great help. With TBI, you can find a paraorbital hematoma, a symptom of “spectacles” or “raccoon eyes”, a hematoma in the mastoid region (Battle syndrome), hemotympanum (rupture of the eardrum), a fracture of the facial skull bones, and a soft tissue hematoma. A non-invasive diagnostic method such as echoEG can help in differential diagnosis. With LMBI, hypertensive syndrome may occur, and with UGM, a shift in the echo signal can be detected.

In case of mild alcohol intoxication (dosage of ethanol in the blood up to 1.5‰), echo-EG, as a rule, without deviations from the norm. In moderate and severe forms of intoxication (dose of ethanol in the blood 2.0-2.5‰), Echo-EG reveals hypertension syndrome without displacement. We must not forget that alcohol intoxication can mask and simulate TBI.

Differential diagnosis is especially difficult for intracranial hemorrhages, in particular subdural hematomas and alcohol intoxication. For the latter, as E.M. writes. Kondakov and V.V. Krivetsky, a variety of symptoms are characteristic. With this combination, they identify three variants of the leading syndrome of subdural hematomas.

First option– classic course of subdural hematomas with a “light gap” (≈ 12%). Occurs during mild intoxication and occurs after detoxification therapy.

Second option– symptoms of alcohol intoxication are gradually replaced by symptoms of cerebral compression (23%).

Third option– general cerebral and focal symptoms occur immediately after injury and quickly increase and lead to vital disturbances (23%).

The first two options are characterized by cyclical disturbances of consciousness. The appearance of sensorimotor excitation in this case is often caused not by traumatic brain injury, but by the onset of abstinence. Domnality, stupor, stupor and coma with increasing compression of the brain and the appearance of brainstem symptoms can be caused by severe alcohol intoxication (dose of ethanol in the blood 2.5-3‰). With intensive detoxification, these symptoms can quickly regress. The pupils provide significant assistance in diagnosis with this combination (with alcohol intoxication, they are either narrow or dilated, and with a hematoma, anisocoria often occurs).

The state of the motor sphere also plays a major role in diagnosis (in case of injury there is persistent paralysis, but in case of alcohol intoxication there is none). Local seizures occur with hematomas, generalized convulsive syndrome is characteristic of both pathologies, but more often occurs in a state of withdrawal.

Topic of the article: Alcohol consequences after a head injury - we understand the issue, trends for 2019.

Although a concussion is the most mild injury to the brain, it is an injury with potentially far-reaching consequences. How treatment is carried out and whether the necessary regimen is followed will determine whether complications arise after a concussion or not. And problems can arise with it functions such as memory, balance, concentration, thinking and coordination.

According to the World Health Organization (WHO), 70 to 90% of head injuries are concussions, and 6 in 1,000 people are diagnosed with a concussion every year. This is a relatively common brain injury that occurs without or with a brief loss of consciousness, resulting in temporary disturbances in brain function occur.

When treating a concussion, as a rule, there is no need for hospitalization. However, patients must remain in bed. In case of a head injury, concussion or bruise, specialists categorically prohibit drinking coffee, alcoholic beverages, and even smoking. Such products are incompatible with brain injury, because how alcohol poisons the body and destroys brain vessels.

When drinking alcohol simultaneously with treatment for a head injury, damage to brain cellular structures increases many times over. Patients with a similar diagnosis require bed rest, which, if violated, is likely to develop complications such as:

decreased intellectual abilities;
dementia develops;
problems with motor concentration and coordination appear;
chronic headaches;
intense dizziness.

Treatment for concussion

The diagnosis of SHM is established in the case of a mild brain injury. But what to do if there is no specialist nearby. First aid for a concussion does not cause difficulties, so household members or people around the victim are quite capable of providing it on their own.

If there are signs of a concussion, you should go to the emergency room or call an ambulance.
The victim must not be left without attention, because there is a high risk of vomiting and severe convulsions. The general condition may worsen, sometimes the victims lose consciousness.
It is recommended to place the unconscious victim in a lateral position, take the pulse, check the breathing or heartbeat.
The head and upper half of the victim’s body are placed at some elevation.
Cold can be applied to the head, and if there are wounds, they must be treated.

Even if the symptoms of a concussion indicate a mild degree of injury, treatment is still necessary. The specialist prescribes a course of therapy in accordance with the condition of the individual patient, lasting about 10 days, half of which the patient must remain in bed. For a mild concussion, treatment can be done at home, with In this case, you should avoid any work activity and remain at rest. After several days, physical activity is resumed again so that cerebral circulation is restored again and starts working as before.

As already mentioned, on average, treatment for a concussion lasts about 10 days. During these days, the patient is prescribed drugs to normalize blood circulation in the brain, such as Cavinton or Encephabol. If severe vomiting, antiemetic drugs are indicated. For headaches, take painkillers (Sedalgin or Baralgin) or NSAIDs (Nimesulide , Nurofen, Ibuprofen). In some cases, tranquilizers like Elenium, Nozepam, Phenobarbital, etc. are indicated.

Dizziness is eliminated by the use of papaverine drugs like Tanakan or Belloid. Sympathomimetics are often prescribed to stimulate the activity of the autonomic nervous system. If the victims did not abuse alcohol before the injury, then the probability of a complete cure is about 97%.

Effect of alcohol on the brain

Alcohol products have a detrimental effect on all organic structures, the brain is especially severely affected. With alcohol abuse, the brain shrinks, its volumes are catastrophically reduced, the convolutions are smoothed out, the vessels undergo changes, and the membranes swell. Such changes develop gradually, manifesting themselves as dementia. Alcohol intoxication causes irreversible processes in all brain functions, even the most advanced ones such as logical and abstract thinking.

This effect of alcohol on brain cells is determined by its ability to glue erythrocyte cell structures, which is especially dangerous for the smallest vessels, because the resulting blood clots block the vascular lumens, depriving the brain cells of nutrition. With each intake of alcohol, the number of dead cells is replenished, so with prolonged alcohol abuse, tissue and the organs gradually die and die.

Even with moderate alcohol consumption, over 7-12 years, the tissue structures of the brain seriously change, and mental activity noticeably deteriorates. If such a factor is supplemented by a traumatic brain injury, then all pathological and destructive processes increase in intensity, which is why doctors prohibit patients with concussions from drinking alcohol .

With a concussion, its functions deteriorate for about a week or two. The degree of impairment depends on the force of impact, according to which the injury can be mild, moderate or severe. The main signs of injury are:

Dizziness;
Amnestic manifestations;
Nausea;
Brief confusion;
Lethargy;
Visual impairment;
Poor appetite.

To diagnose a concussion, studies such as MRI, CT, electroencephalography, X-ray, Doppler ultrasound, etc. are used.

Contraindications after a concussion

During a concussion, active mental activity, including reading, is not recommended. During the treatment of a concussion, experts prohibit straining the eyesight, so victims are strictly prohibited from watching television, reading for long periods of time, sitting in front of a computer, etc. To speed up recovery, it is recommended:

compliance with the regime;
exclude mental work, reading books, working on a computer, watching TV shows, etc.
ensure sufficient time for sleep;
do not drink coffee, tobacco, or alcohol;
exclude driving, housework that requires stress.
Avoid physical strain and stress, noise and light.

After a month has passed from the date of treatment, the patient is recommended to undergo some diagnostic tests again to exclude the possibility of developing various kinds of complications.

Remember that symptoms of depression can occur even with minor concussions. Therefore, if you want to see a psychologist or psychiatrist to get a prescription for antidepressants, be sure to tell your doctor about any head injuries, as taking antidepressants can lead to complications and longer treatment .

How much should you not drink after a concussion?

There are several opinions regarding the use of alcohol after a concussion. Some are inclined to believe that with a mild concussion it is permissible to take small portions of alcohol after the end of treatment. This is not true. Small doses of alcohol are permissible only after six months from the end of treatment procedures, or even more. Although it will be It is better if, after an injury, the patient gives up alcohol forever, since ethanol can worsen brain processes and activity in general, and against the background of an injury, it can also cause complications after a concussion.

In later life, cheap strong alcohol or wine will have to be excluded. A small consumption of high-quality cognac or a glass of excellent red wine is acceptable.

Consequences and complications after a concussion

Even with a single concussion, there is a possibility of developing consequences that will worry the rest of your life. Even after ten years, a person who has once suffered from a concussion may show signs of increased irritability or excessive impressionability caused by a long-standing injury. Such persons are more likely than others to suffer from excessive tearfulness, chronic fatigue, deep depressive states. Also, after a concussion, a chronic sleep disorder, fear of enclosed spaces, difficulty trying to concentrate, and hypersensitivity to weather conditions may develop.

The consequences of a concussion can be very dangerous. And if the patient begins to drink alcohol during a concussion, then the likelihood of complications increases many times over. Against the background of alcohol abuse during a brain injury, the following occurs:

headache not relieved by analgesics;
hypertensive crisis;
stroke;
sudden mood swings;
cerebral edema;
coma.

To avoid such complications, it is imperative to take the necessary measures to treat brain injury. During the treatment process, it is extremely important to comply with the requirements regarding the regimen, taking medications and quitting alcoholic beverages, as well as smoking. Such brain injury is dangerous due to mental changes and physical disorders, and alcohol greatly increases the likelihood of such consequences.

Negative relationship between alcoholism and traumatic brain injury.

Is alcoholism a disease? developing due to hereditary predisposition and environmental factors, such as: frequent consumption of alcoholic beverages, mental illnesses, consequences of traumatic brain and mental injuries.

Traumatic brain injuries are divided into open and closed. Closed craniocerebral injuries include concussion, contusion and compression of the brain. Similar conditions arise from various influences, differ in the severity of the condition at the time of injury, as well as the severity of long-term consequences. Of closed craniocerebral injuries The most common injury is a concussion. It can occur due to an unfortunate fall, a blow to the head, car and train accidents, etc.

Depending on the severity, the symptoms of this condition vary. With severe concussions, there is a prolonged loss of consciousness, amnesia, severe headache, nausea, vomiting, and impaired coordination of movements. After restoration of consciousness, symptoms such as nausea, dizziness, headache and weakness may be felt for several weeks. With a mild concussion, loss of consciousness and amnesia do not occur, but weakness, nausea, and dizziness are always present. These phenomena can go away on their own after a few days.

Any head injury can cause long-term consequences in a person, expressed in impaired ability to concentrate, rapid fatigue, and in severe cases, memory impairment and behavioral disorders. This occurs due to disruption of the condition of brain tissue and disruption of blood microcirculation in the vessels. Head injury can have a negative impact both for a person suffering from alcohol addiction and for a practically healthy person.

In patients suffering from alcoholism, after a head injury, the mood changes sharply, severe irritability appears, and criticality decreases. Against this background, the amount of alcohol consumed increases, which further accelerates the onset of harmful consequences. Characterized by severe memory impairment, loss of criticism, impairments of intelligence and behavior, making it difficult adaptation of a person in society.

For people who do not suffer from alcohol addiction, head trauma is a factor leading to emotional instability, mood changes, and apathy. Subsequently, when drinking alcoholic beverages, many people's reaction to alcohol changes. Alcohol intoxication can last a long time, accompanied by behavioral disorders, amnesia, euphoria .Often there is a strong desire to repeat alcohol consumption, which subsequently leads to alcohol dependence. Much less often a negative reaction to alcohol occurs when, when using small dosages, severe headache, vomiting, and general discomfort appear, which prevents further alcoholization. The relationship between alcohol consumption and the consequences of cranial -brain injuries consist of a more rapid progression of alcohol dependence, increased memory and mood disorders, and a more rapid appearance of behavioral disorders.

Concussion and alcohol

Alcohol products have destructive properties for humans. They can completely destroy a healthy biological system. If the body has suffered a concussion, then the question of whether one can drink at the same time disappears by itself.

Dysfunctions of the body due to injury

A concussion is a sudden disruption of the functional activity of the brain, obtained mechanically. The clinical picture of the injury is expressed in the manifestation of the following factors:

damage to the frontal or temporal lobes of the hemispheres;
disruption of nerve cells;
slight displacement of brain tissue;
changes in the properties of the fluid surrounding the brain.

Dysfunctions of brain structures are reversible. However, drinking alcohol during this period contributes to the aggravation of pathological changes. Under the influence of alcohol-containing liquids, blood cells (erythrocytes) stick together. A blood clot appears, which further deforms already damaged vessels. All the prerequisites for the development of a stroke are created. Alcohol and concussion are two mutually exclusive concepts.

Compatibility of alcohol and traumatic brain injury

The symptoms of mechanical brain damage are identical to alcohol intoxication of the body:

nausea;
vomit;
dizziness;
impaired coordination of movements.

In this state, even a minimal dose of alcohol can cause: delirium, hallucinations, delirium tremens (delirium tremens).

Strong drinks provoke dysfunction of the autonomic nervous system. Damage to the subcortical structures of the brain occurs. As a result, liquor hypotension syndrome (low intracranial pressure), involuntary urination, defecation.

If, during a concussion, the blood alcohol content was more than 2.6%, memory impairment manifests itself in the form of retrograde or anterograde amnesia (lack of memories of events that occurred before or following the injury). The pathology is caused by a change in the functioning of the pelvic organs, which contributes to the development of impotence.

Alcohol and recovery

The duration of therapeutic measures after the resulting pathological changes depends on the degree of damage and compliance with the rules necessary for the complete restoration of vital functions.

But, having completed the full course, you should not think that after a concussion you can safely drink alcohol. Drinking people tend to suffer repeated traumatic brain injuries. Periodically recurring concussions provoke the development of parkinsonism in a post-traumatic form.

The disease manifests itself as:

musculoskeletal disorders;
reducing reaction speed;
disorientation in space;
tremors of the limbs;
destructive behavior.

People who have suffered a concussion can drink alcohol after at least a year. It is better to forget about low-grade strong drinks forever. You can pamper yourself with a small glass of aged cognac or a glass of good red wine.

Other contraindications

It is believed that strong coffee is contraindicated in case of head injuries. But if this drink is firmly included in the daily diet, then a positive effect is not expected in its abrupt cancellation. Coffee, in minute quantities and insignificant concentrations, will not cause much harm in case of a concussion.

In addition to alcohol-containing liquids, a categorical ban applies to all types of tobacco products. The action of nicotine affects the constriction of blood vessels in the brain. Products with a high content of cholesterol and carcinogenic substances have a negative effect on an organism weakened by pathology.

Is it possible to drink if you have a head injury?

For any traumatic brain injury, any alcohol is contraindicated. The blood supply to the brain is already impaired, and decay products from the area of injury must be removed. If alcohol toxins are added to these products, serious brain damage can develop. In addition, after a TBI, almost all internal organs suffer , including the liver, which should not be killed by the added hard work of inactivating the alcohol.

In case of traumatic brain injury, alcohol is contraindicated. If this is what you mean by “drinking.” Alcohol affects blood pressure and the condition of blood vessels, which can lead to complications after such an injury.

You can drink, depending on what and how much, and most importantly, why. And if it’s very serious, you should always know moderation in everything.

I want to speak in more detail about the head injury. If the injury is superficial and there was no concussion, why not drink it after it heals. If he is young and healthy, you never know when we were young that we experienced various head injuries.

Another question is if this injury led to serious consequences. Then you should undergo a course of rehabilitation treatment to look at your well-being and if everything is in order, then why not drink. In the case described by you, everything is clear, there is nothing wrong with this neighbor, he would be in the hospital .

Alcohol and concussion: possible consequences

A concussion is an injury that can be received either as a result of a strong blow to the head or with a fairly minor impact. But in any case, if a traumatic brain injury has been sustained, it is necessary to undergo appropriate treatment, even if the symptoms are the same as the the damage seems insignificant to you. Even a mild head injury can have serious consequences if you do not undergo treatment and do not follow medical recommendations. This also applies to drinking alcohol. Can you drink alcohol if you have a concussion? What does this mean? These and other questions require detailed answers, and they really need to be provided - this problem is common, questions about it are asked often, and the answers can save health, or even life.

Alcohol and concussion

The head, or rather the brain, is a receptive organ. Alcohol is extremely harmful to the brain and a healthy person, and of course, it is many times more harmful and dangerous for someone who has experienced a concussion. With a concussion, symptoms similar to intoxication may be observed, Among which it is worth noting:

Dizziness of varying intensity,
Hysterical behavior, hallucinations, increased irritability,
Increased sensitivity to the effects of alcoholic beverages.

Concussions can vary in intensity, and the higher the intensity, the higher the risk of an epileptic seizure when drinking alcohol.

The effects of alcohol on the brain

Is it possible to drink alcohol after a concussion? To understand this, it is necessary to analyze in detail the effect of alcohol on the human brain. Alcohol is highly toxic to this organ, and when taken regularly, the brain changes so much that the doctor can recognize the addiction of its owner unmistakably. Thus, regular consumption of alcohol leads to the fact that a set of typical signs appears - the brain decreases in size, its membranes become swollen, the convolutions become smoothed, serious signs of vascular damage are found. Ethanol glues red blood cells together, they clog the microscopic vessels of the brain, which are numerous, which leads to lesions. Brain cells die , this is an irreversible process that gives results after 5-7 years of abuse, and treatment is not possible here.

The human nervous system is also negatively affected; regular intoxication leads to the appearance of tremors, psychoses, paranoid behavior and other typical abnormalities. If alcohol was taken during a concussion, the consequences become many times more significant, this applies to both the destructive aspect of alcoholism for the brain and the consequences the concussion itself. Thus, this condition excludes the intake of alcohol; you cannot drink.

What happens if you drink alcohol after a concussion?

If a person still takes alcohol after a concussion, despite the warnings, this will be fraught with dangerous consequences. Moreover, severe manifestations are possible even with a small dosage of alcohol, since the sensitivity of the brain to this negative factor increases. Among the consequences that can be observed in such In cases, attacks of hysterical behavior, nervousness and abrupt changes in mood are noted. Also characteristic is the appearance of sharp headaches, photophobia, strong reactions to smells, sounds, and other irritants. Blood pressure may rise sharply, and with hypertension, a crisis is sometimes observed. There are also hallucinations.

Among the dangerous and even fatal manifestations is cerebral edema, followed by coma, and a stroke is also possible. The consequences can be very different, and their specific manifestation depends on the dosage of alcohol taken, on the general state of health, the degree of concussion, and general predisposition. The most severe results are observed in those patients for whom a concussion was not the first, and especially for those who experience it regularly. Among these are athletes, stuntmen. If a person knows that this is not his first concussion, and at the same time does not deny himself drinking alcohol - serious complications will be almost guaranteed.

When wondering whether it is possible to drink alcohol during a concussion, it is necessary to note the range of the most severe consequences that are typical for people who have experienced more than their first concussion. These are paranoia, epilepsy, persistent migraine, sudden manifestations of aggression, attacks of general weakness. A severe concussion is fraught with encephalopathy, and if the patient takes alcohol, the course of the disease intensifies, it develops faster. The brain does not receive sufficient nutrition, it constantly experiences oxygen starvation, and as a result, the vestibular apparatus suffers, severe tremors develop, problems with speech, and other lasting consequences are observed. Often It happens that encephalopathy does not manifest itself initially, and its symptoms begin to be observed only 5-10 years after the injury and alcohol abuse as a result.

When can you drink alcohol after a concussion?

However, when can you return to your normal lifestyle and drink alcohol again without fear of such serious consequences? This is a dangerous injury - a concussion, whether alcohol can be taken, and when it can be taken, you need to check with your attending physician. There is an opinion that this can be done after a couple of weeks, immediately after discharge, if the concussion is not severe. However, it is worth cautioning against such possibilities - even after a mild concussion, you should postpone drinking alcohol for at least six months. Moreover, during this period you will still be prescribed medications that are incompatible with alcohol, which will restore brain activity.

Ideally, it is better to give up alcohol completely and forever, because the effect of ethanol on already damaged brain structures can have an extremely negative effect. Even if a person does not drink alcohol, after a traumatic brain injury he may be haunted for years by increased weather sensitivity, convulsions, depression and increased anxiety, as well as problems with sleep, dystonia of a vegetative nature. The brain and nervous system do not always completely return to their healthy functioning, and alcohol causes them additional and very significant damage.

If you decide to drink alcohol after a concussion

Some people decide to return to a bad habit after a while, and if you make such a choice, you need to follow advice that minimizes the risks. You need to choose high-quality alcohol, surrogates are dangerous even for a healthy person, and after a concussion they can take away the rest of your health. It is necessary to control, no matter how much alcohol you take, you cannot drink too much after a concussion. Get into the healthy habit of drinking alcohol in a specific dose that you assess as safe, and not exceeding it, regardless of the situation.

For drinks, it is advisable to choose high-quality cognacs and red wines from an official manufacturer, sold in trusted stores. Limit alcohol consumption to avoid negative consequences. Also, do not forget about the medical recommendations given by a specialist. If you want to recover completely from a concussion, so as not to experience further unpleasant symptoms, or to reduce this to a minimum, it is necessary to follow the recommendations in detail and exactly. If you need to take medications for a long time that are not compatible with alcohol, you do not need to interrupt the treatment regimen to drink, and you should also not combine drugs with alcohol if this unacceptable according to the instructions.

Having decided to return to a bad habit, carefully monitor your condition, especially at first. If you feel unpleasant symptoms, you begin to feel dizzy, you are faced with an attack of panic, hysterical mood, a surge in blood pressure - refuse to continue the banquet, and in the future be more careful with alcohol. The same can be said about situations associated with a severe hangover, delayed negative effects of alcohol, the appearance of unpleasant symptoms that you had not noticed before. After a concussion, you need to be especially careful in all matters related to alcohol, and I would like to emphasize once again , that ideally you should abandon it completely.

Health is the most expensive currency, the most valuable thing you have. You should not risk it by exchanging it for the dubious joys of drinking alcohol, because it has never brought anyone any good. Carefully follow the doctor’s recommendations and do not abuse it if you have suffered a head injury , and you have a concussion. Be careful and take care of your health.

If you have any health problems after drinking alcohol, please contact our drug treatment clinic immediately!

alcohol (traumatic brain injury)

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Certificate EL No. FS 77 – 74583 dated 12/14/2018

Alcohol after a head injury consequences

Alcoholism

So, back in the 6th century BC, the Peruvians buried their dead with coca leaves so that they would not get bored in the other world. However, only in the 2nd half of the 20th century did alcoholism reach epidemic proportions. The 90s of the 20th century went down in history as a period of unprecedented devastating consequences of the demographic crisis in Russia. In the last 5 years of this century alone, the country’s population decreased by 1 million 600 thousand.

Today in Russia over 700 thousand people die annually from alcoholism alone.

Alcohol is an absolute risk factor for TBI. In European countries, alcohol is named the second risk factor for diseases, injuries and mortality. The level of alcohol consumption per person per year characterizes the alcohol situation in the country.

In recent years, in European countries including Russia and Belarus, this figure ranges from 13.4 to 20.0 liters per capita per year. This is one of the highest rates in the world.

In the Republic of Belarus, 1/1 of 1 million people abused alcohol and were dependent on it in 2007. According to official statistics in Belarus, from 1970 to 2005, the mortality rate as a result of injuries and accidents increased 2-3 times, and in as a result of alcohol poisoning by 6-8 times.

According to A. Edwards et al., every 2nd case of TBI is associated with alcohol intake. Russia, Belarus and the Baltic countries are ahead of most European countries in this regard. Homicides while intoxicated are committed in 72%, road traffic accidents from 67. 7 to 90%. The percentage of offenses committed by teenagers under the influence of alcohol or drugs is growing catastrophically. In Russia in 2007 it reached 63.6%.

On the one hand, alcohol intoxication, due to the similarity of clinical manifestations, easily masks TBI, and on the other hand, along with infections, arterial hypertension, atherosclerosis, and cerebral vasculitis, it is a predisposing factor in the formation of intracranial hemorrhages.

Pathogenetic mechanisms of alcohol intoxication in traumatic brain injury

The pathogenetic mechanisms underlying TBI and alcoholic damage to the central nervous system are close to each other and represent a chain of adaptive reactions in response to damage to brain tissue.This can be microstructural only functional in nature in mild traumatic brain injury, and in severe forms of injury it causes macrostructural changes.

There is a mismatch between the chemical control systems of cellular and tissue homeostasis.

Ethyl alcohol, due to its physicochemical properties, biological and toxic effects, stands out sharply from the range of psychoactive substances. Ethanol, having a membranotopic (impairs the excitability of the heart muscle) and conformational effect, reduces the direct toxic effect on all human organs and systems.

The first blow naturally falls on the nervous, endocrine and immune systems, which carry out coordination functions in the body. The mechanisms of disruption of the functioning of homeostatic systems in alcoholism are associated both with the direct effects of ethanol and its oxidation products on cells, and with a violation of the central regulation of function. With alcohol adduction, an important plays a role lipid peroxidation (LPO) LPO plays an important role in the regulation of the permeability of cell membranes and the state of oxidative phosphorylation of the cell. In normal tissue, the process of lipid peroxidation constantly occurs, the intensity of which is inversely related to the activity of natural antioxidant systems.

The degree of severity of cerebral edema depends on the relationship of these systems in the clinic of TBI during alcohol intoxication. In turn, the increase in the permeability of the endothelium of brain vessels contributes to intracranial hemorrhages. Excessive formation of reactive oxygen species can cause damage and death of the cell itself.

Antioxidant systems are necessary to maintain lipid peroxidation. The action of external pro-oxidants, lack of supply of obligate oxidants and activation of endogenous generation of reactive oxygen species lead to tension in the antioxidant defense mechanisms. This ultimately can lead to the development of oxidative stress, which can manifest itself at the cellular, tissue and organismal level .

Under conditions of alcohol intoxication, the products of ethanol metabolism can, due to membranotropy, damage any organs and tissues. Changes in the metabolism of the latter lead to the death of immunocompetent cells. Severe alcohol intoxication is characterized by a shift in hormonal balance and a prolonged increase in the level of glucocorticoids, which can be equated to severe long-term stress.

Recently, much attention has been paid to neurosteroids, in particular dehydroepiandrosterone. The latter has a neuroprotective and stress-protective effect. Together with cortisone, it regulates the process of apoptosis and the level of oxidative stress in the body.

As a result of the interaction of ethanol oxidation products with monoamines, compounds with morphine-like characteristics arise in the liver. In terms of its pharmacological properties, ethyl alcohol in this case approaches ether, although its therapeutic effect is weaker. The mechanism of direct and indirect action of alcohol provokes the development of multiple disorders and, first of all, on certain structures of the brain and on almost all visceral organs (heart, liver, pancreas, etc.). The released neurotransmitters of catecholamine nature - norepinephrine and dopamine from presynaptic structures into the limbic parts of the brain and cause that phase of mental, vegetative and motor excitation that observed during alcohol intoxication.

Initially, the cerebral cortex, hypocates, limbic system, and then the reticular formation of the brain stem are affected. Inhibition of the inhibitory processes of the cerebral cortex leads to the release of subcortical centers.

In large doses, alcohol inhibits the activity of subcortical centers, which leads to coma. These same structures also suffer in TBI.

Ethanol is easily absorbed and perfectly penetrates the blood-brain barrier. Its effect depends on its concentration in the body, and clinically this is manifested by general cerebral and focal symptoms of the central nervous system.

The same symptoms are observed in TBI. Thus, the condition of patients and the clinical course of TBI is determined on the one hand by the severity of traumatic brain injury, and on the other hand by the severity of alcohol intoxication.

Clinical features of the course of traumatic brain injury during alcohol intoxication

Since the clinical manifestations of alcohol intoxication and TBI are in many ways similar, sometimes difficult to resolve diagnostic and expert-legal problems arise, especially when mild TBI.LMBI is accompanied only by axonal damage to the brain without gross local changes in brain tissue and blood vessels. FBS, as one of the forms of LMBI, is manifested by rapidly growing functional disorders with polymorphic “variegated” unstable symptoms of central nervous system damage with a predominance of autonomic disorders. Often, autonomic disorders can be almost the only sound It is not for nothing that in the past TBI was called “autonomic shock.” With UHM, macrostructural destruction of the brain substance with a slight hemorrhagic component is observed.

Clinical picture in both forms of MTBI is similar and differs only in the degree of severity and duration of symptoms. Autonomic disorders, being one of the leading symptoms of MTBI, are manifested by marbling of the skin, hyperhidrosis, low-grade fever, fluctuations in blood pressure, bradycardia, tachycardia, pulse lability. Focal microsymptoms affect MTBI of the cranial nerves, cerebellar, and motor spheres is sometimes accompanied by minor sensory disturbances and a mild meningeal symptom complex. All of the above neurological and autonomic symptoms are observed in persons intoxicated and without TBI.

Some patients may have vagoinsular disorders: pallor of the skin, bradycardia, decreased blood pressure, lack of air, gastrointestinal discomfort, mild psychomotor agitation.

Sometimes such paroxysms end with chills and polyuria. Often, autonomic disorders are of a mixed nature, but are always accompanied by a feeling of fear. With a dose of ethanol of 2.5-3.0 ‰, focal microsigns from the central nervous system appear in the blood in the form of anisocoria, horizontal nystagmus, mild insufficiency of the VII, XII pairs of cranial nerves according to the central type. Reflexes of oral automatism, hyperreflexia from deep reflexes, anisoreflexia, mild ataxic disorders appear. With an ethanol concentration in the blood of 3.0-4.0 ‰, the picture changes, although autonomic disorders persist, but the patient's behavior changes.

He becomes sluggish, drowsy, coordination, both static and dynamic, is grossly impaired, the pupils become narrow, mydriasis is extremely rare. Against the background of hyperreflexia of the tendon and periosteal reflexes, the Babinski reflex may occur, nystagmus persists. Sometimes the clinical picture resembles acute Leiden-Westphal ataxia: in the Romberg position the patient falls, walking is grossly impaired, coordination tests are difficult to perform, muscle tone drops. All these symptoms completely regress after 5-7 days.

Real examples

Traumatic brain injury alcohol

An example would be the following observation:

Patient Z., born in 1974, a bulldozer driver, was taken by ambulance to the hospital on July 12, 2007 with complaints of headache, pain in the nose, lower back, and general weakness. According to the patient, he celebrated a friend’s birthday. As a result of a conflict in company was hit in the head and in the face with a fist. He doesn’t remember whether there was a loss of consciousness. There was no vomiting. Two years ago he suffered a concussion, also in a fight while intoxicated.

Objectively: strong build, adequate nutrition. General condition is satisfactory. There are bruises in the area of the left temple and bridge of the nose. Abrasions in the area of the right forearm and thigh. The face is hyperemic. Severe sweating. The breath smells of alcohol. Verbal, fussy. Pulse 92 beats per minute. Blood pressure 150 /90 mmHg. The liver is at the edge of the costal arch, painless. There is no other pathology of the internal organs. Consciousness. Adequate. The pupils are slightly dilated, the reaction to light is preserved. Small-scale horizontal nystagmus. The face is asymmetrical due to bruises. Speech is slurred, dysarthric. The pharyngeal reflex is alive. The tongue is in the midline. There are no paresis of the limbs. The muscle tone is reduced. The tendon and periosteal reflexes are alive S = d. There are no pathological signs. Sensitivity is preserved. In the Romberg position, it falls. Coordination tests are performed with moderate difficulty intention tremor. Ataxic gait. No meningeal signs. General blood and urine tests without deviations from the norm. Total bilirubin 32.7 mmol/l (normal 8.5-20.5 mmol/l). Glucose 6.3 mmol/l .Fundus, EchoEG without deviations from the norm. CT scan of the brain - a slight atrophic process (slight expansion of the subarachnoid space on the convex and slightly dilated ventricular system). X-ray of the facial bones revealed a fracture of the nasal bridge without displacement. All subsequent days in the hospital he complained of a headache pain, pain in the nose, general weakness. Pulse and blood pressure are within normal limits. Atactic syndrome has regressed. By the 8th day, gait is within normal limits. In the Romberg position, it is stable. Performs coordination tests satisfactorily. Nystagmus disappeared on the second day. Speech was restored.

Clinical diagnosis: mild closed craniocerebral injury, concussion.

Concomitant diagnosis: fracture of the nasal bridge without displacement. Severe alcohol intoxication (dose of ethanol in the blood 2.59‰).

He was discharged on the 14th day with an open medical certificate to continue treatment in the clinic.

According to the outpatient card, in 2005 he was treated for 5 days for a concussion and alcohol intoxication. In subsequent years, he was treated only in connection with medical examinations. After discharge from the hospital, he was on the ENT doctor’s list for 7 days due to a back fracture nose

Thus, the clinical picture of the patient was characteristic of acute ataxic syndrome, which arose in a state of severe alcohol intoxication. Rapid and complete regression of neurological symptoms as alcohol intoxication was removed is well known in the literature as “benign acute cerebellar ataxia of Leiden-Westphal.” Mild autonomic disorders , noted upon admission in the form of tachycardia, a slight increase in blood pressure, and hyperhidrosis were also associated with alcohol intoxication. Apparently, both of these syndromes (atactic and vegetative) were regarded by hospital doctors as manifestations of MTBI.

The isolation of the cerebellar syndrome, in the absence of other microorganisms from the central nervous system, normal fundus data, and echo-EG indicated that he did not have LMBI.

In some cases, with a strong and severe degree of alcoholic intoxication (dose of ethanol in the blood from 2.5 to 5.02 ‰), and in depleted people with alcoholic hepatitis and cirrhosis of the liver, with lower doses of ethanol, acute alcoholic encephalopathy may occur.

Clinically, this pathology is manifested by a syndrome of increased intracranial pressure and cerebral edema or acute hemorrhagic encephalopathy by Gaye-Wernicke. These clinical forms of alcoholic damage may resemble a brain contusion with predominant damage to the brainstem. In the neurological status in these cases, a meningeal symptom complex also develops (stiff neck, symptoms of Kernig, Brudzinsky) in combination with brainstem disorders, depending on the level of damage.

When the upper and middle parts of the brainstem are affected (the cerebral peduncle and the pons), oculomotor disorders, gaze paresis, ataxia, and mental disorders occur. The face may be hyperemic, miosis is replaced by mydriasis, and pronounced autonomic disorders appear. When the medulla oblongata is damaged, bulbar syndrome develops, accompanied by severe disorders of cardiac activity and breathing.

In large doses, alcohol inhibits the activity of subcortical centers, which leads to coma. In alcoholic coma, the skin is pale, vomiting is observed, cardiac activity decreases, blood pressure decreases, the pulse is weak, breathing slows down to 6-8 per minute. Coming out of coma or stupor is more common accompanied by delusions and hallucinations.

The observation below demonstrates this trend.

Patient I., born in 1969, unemployed. 09/21/2008 was taken to the hospital after a generalized convulsive attack. The accompanying person could only report that on 09/18 she was beaten at home by her partner.

Objectively: severe condition, deep stupor. Not available for contact. There are multiple “fresh” and “old” bruises on the face, head, torso, limbs. Pulse 112 beats per minute. Blood pressure 175/115 mmHg, muffled heart sounds .No features from the internal organs.

The face is hyperemic. Severe hyperhidrosis. The pupils are wide, the reaction to light is sluggish. The face is asymmetrical due to bruising on the right half. There are no paresis of the limbs. Tendon and periosteal reflexes are animated S = d. Achilles reflexes are sharply reduced. There are no pathological signs. Hyperesthesia of the feet in the form of " sock." Meningeal symptoms. In the intensive care unit for 2.5 days the condition remains serious. Constant tachycardia 100-120 beats per minute. Arterial hypertension 160/100 - 180/120 mmHg. Rapid breathing 22-24 V minute.

Low-grade fever.On the 3rd day, the general condition improved, the temperature, pulse, and breathing returned to normal. However, the pain’s behavior changed sharply. Severe motor agitation, auditory and visual hallucinations, and disorientation appeared. She was examined by a psychiatrist. Additionally, it became known that she was registered with a narcologist for alcoholism. Alcoholic delirium was removed. Due to the patient’s memory impairment, details of the injury could not be identified. The patient only reported that an attack with loss of consciousness occurred for the first time. The fundus of the eye and the composition of the cerebrospinal fluid were without deviations from the norm. Contents bilirubin in the blood 36.9 mmol/l (normal 8.55-20.5 mmol/l), a sharp increase in indirect bilirubin (11.2 mmol/l), high levels of transaminases.

CT scan of the brain showed a moderately pronounced atrophic process. She was discharged home on the 9th day.

Clinical diagnosis: Mild closed head injury, concussion.

Concomitant diagnosis: Alcoholism, alcoholic epilepsy (first identified), alcoholic polyneuropathy, sensory-areflex form. Alcoholic delirium. The entire clinical picture of the patient fit within the framework of acute alcoholic encephalopathy, when during the abstinence period a generalized convulsive seizure initially appeared, then a mixed-type vegetative paroxysm (sympatho- adrenal and vago-insular), at the exit of which hallucinations and full-blown alcoholic delirium arose. Thus, the diagnosis made at the clinic as “TBI” was withdrawn.

Alco- focus inside the area of cerebral edema. In type IV bruises, single or multiple foci of hemorrhage are defined as intracerebral hematomas. Regression of the foci proceeds according to the type of resorption, or instead of resorption, progression occurs, up to the formation of gross dislocations of the brain and the formation of intracerebral hematomas. With alcohol damage

Patient R., 47 years old, homeless, was taken by ambulance to the hospital on June 7, 2007. Found in the entrance of a residential building with traces of bruises on the head and face. Contact with the patient is almost impossible, speech is slurred, disoriented in place, time, personal identity. Based on documents found in clothes, full name, age became known, registered in the Bryansk region, has a class II disability.

Objectively: severe condition of low nutrition, unkempt.

Looks older than his years. There are traces of bruises on the head, face, torso. There are tattoos on the arms and back. Pulse 68 beats per minute. Blood pressure 105/60 mmHg. Heart sounds are muffled. The liver protrudes beyond the edge of the costal arch, is painful. B consciousness, but due to speech impairment and severe cognitive impairment, contact is not possible. The pupils are of medium size, the reaction to light is intact - on. Divergent strabismus. Partial contracture of the right facial nerve with pathological synkinesis. Dysarthria, dysphagia, dysphonia.

The pharyngeal reflex is increased. Gross reflexes of oral automatism. Moderate central tetraparesis. Muscle tone is increased according to the spastic type. Babinski reflex on both sides. Abdominal reflexes are absent. Clear sensitivity disorders could not be identified. Nuchal rigidity. Kernig's symptom is not sharply expressed. Pelvic disorders. In the fundus there is partial atrophy of the optic nerves. Echo-EG hypertension. In the general blood test, leukocytosis 8600-109 formula is not changed. ESR - 27 mmHg. Biochemical blood tests: total bilirubin - 52.1 mmol/l; indirect – 14.3 mmol/l; urea 9.5 mmol/l; sugar – 8.6 mmol/l, high level of transaminases.

CT scan of the brain shows a linear fracture of the calvarium, a small accumulation of blood in the basal parts of the frontal lobes. The subarachnoid space and ventricles of the brain are sharply expanded. There is a focus of demyelination in the area of the pons and the lower parts of the cerebral peduncles.

Conclusion: linear fracture of the calvarium. Small subarachnoid hemorrhage. Communicating hydrocele of the brain. Pontine myelinolysis.

During lumbar puncture, the cerebrospinal fluid flowed out under pressure, bloody. Protein 0.65 g/l. Cytosis 265 × 106 cells. Fresh red blood cells in the sediment. Under the influence of treatment, the general condition slightly improved. Pseudobulbar disorders decreased, speech improved, spasticity of the limbs became pronounced, regressed meningeal symptoms.

He began to walk. The gait is spastic-atactic. However, in general, the neurological status remains the same. He was discharged on the 20th day.

Clinical diagnosis: open traumatic brain injury of moderate severity. Traumatic subarachnoid hemorrhage.

Concomitant diagnosis: alcoholism. Central pontine myelinolysis. Moderate tetraparesis, pseudobulbar syndrome. Dysfunction of the pelvic organs. Alcoholic dementia.

Thus, in this case, the attending physicians initially had the impression of a severe traumatic brain injury, a contusion of the brain stem. However, the entire symptom complex of neurological disorders with the data of computed tomography and laboratory tests convincingly showed that the severity of the patient was not caused by a head injury, but by alcoholism. Leading in The clinic had a rare “late” syndrome of damage to the nervous system due to alcoholism - central pontine myelinolysis.

A number of authors point to EEG changes both during LMBI and during alcohol intoxication. These changes are manifested by the irregularity of the alpha rhythm, the presence of single low slow theta and sharp waves. The asynchrony of beta activity with the absence of the alpha rhythm indicates the active influence of the reticular formation and mesencephalic structures, emphasizing the involvement of the suprasegmental parts of the nervous system in the process both during LMBI and during alcohol intoxication. If during TBI no significant changes are observed in biochemical analyzes, then with alcoholic damage to the central nervous system, pronounced changes occur in a number of biochemical tests: a decrease in the level of cholinesterase, an increase total protein, urea, the level of free myoglobulin, bilirubin, a sharp increase in criatinin. The composition of the CSF in case of LMBI is either within normal limits, or in case of UHM, subarachnoid or intracerebral traumatic hemorrhage, it can be xanthochromic, bloody with an increase in protein and cytosis. With alcohol intoxication and neurological manifestations alcoholism, with the exception of acute hemorrhagic encephalopathy of Gaye-Wernicke, the cerebrospinal fluid is colorless with a low protein content (

Although a concussion is the most mild type of brain injury, it is an injury with potentially far-reaching consequences. Whether complications arise after a concussion or not depends on how the treatment is carried out and whether the necessary regimen is followed. And problems may arise with its functions such as memory, balance, concentration, thinking and coordination.

According to the World Health Organization (WHO), 70 to 90% of head injuries are concussions, with 6 in 1,000 people diagnosed with a concussion every year. This is a relatively common brain injury that occurs without or with a brief loss of consciousness, resulting in temporary impairment of brain function.

When treating a concussion, there is usually no need for hospitalization. However, patients should remain in bed. In case of a head injury, concussion or brain contusion, experts categorically prohibit drinking coffee, alcoholic beverages, and even smoking. Such products are incompatible with brain injury, because alcohol poisons the body and destroys brain vessels.

decreased intellectual abilities;
dementia develops;
problems with motor concentration and coordination appear;
chronic headaches;
intense dizziness.

Treatment for concussion

The diagnosis of FBS is made in cases of mild brain injury. But what to do if there is no specialist nearby? First aid for a concussion does not cause difficulties, so household members or people around the victim are quite capable of providing it on their own.

If there are signs of a concussion, you should go to the emergency room or call an ambulance.
The victim must not be left without attention, because there is a high risk of vomiting and severe convulsions. The general condition may worsen, and sometimes victims lose consciousness.
It is recommended to place the unconscious victim in a lateral position, take the pulse, check the breathing or heartbeat.
The head and upper half of the victim’s body are placed at some elevation.
Cold can be applied to the head, and if there are wounds, they must be treated.

Even if concussion symptoms indicate a mild injury, treatment is still necessary. The specialist prescribes a course of therapy in accordance with the condition of a particular patient, lasting about 10 days, half of which the patient must remain in bed. For mild concussions, treatment can be done at home, but you should avoid any work activity and remain at rest. After several days, physical activity is resumed again so that cerebral circulation is restored and starts working as before.

As already mentioned, on average, treatment for a concussion lasts about 10 days. These days, the patient is prescribed drugs to normalize blood circulation in the brain, such as Cavinton or Encephabol. For severe vomiting, antiemetic medications are indicated. For headaches, take painkillers (Sedalgin or Baralgin) or NSAIDs (Nimesulide, Nurofen, Ibuprofen). In some cases, tranquilizers like Elenium, Nozepam, Phenobarbital, etc. are indicated.

Dizziness is eliminated by using papaverine drugs like Tanakan or Belloid. Sympathomimetics are often prescribed to stimulate the activity of the autonomic nervous system. If the victims did not abuse alcohol before the injury, then the probability of a complete recovery is about 97%.

Effect of alcohol on the brain

Alcohol products have a detrimental effect on all organic structures, the brain is especially affected. With alcohol abuse, the brain shrinks, its volume is catastrophically reduced, the convolutions are smoothed out, the vessels undergo changes, and the membranes swell. Such changes develop gradually, manifesting themselves as dementia. Alcohol intoxication causes irreversible processes in all brain functions, even the most advanced ones such as logical and abstract thinking.

Even with moderate alcohol consumption, over 7-12 years, the tissue structures of the brain are seriously changed, and mental activity noticeably deteriorates. If such a factor is supplemented by a traumatic brain injury, then all pathological and destructive processes increase in intensity, which is why doctors prohibit patients with concussions from drinking alcohol.

With a concussion, brain function deteriorates for about a week or two. The degree of impairment depends on the strength of the impact, according to which the injury can be mild, moderate or severe. The main signs of injury are:

Dizziness;
Amnestic manifestations;
Nausea;
Brief confusion;
Lethargy;
Visual impairment;
Poor appetite.

To diagnose a concussion, studies such as MRI, CT, electroencephalography, X-ray, Doppler ultrasound, etc. are used.

Contraindications after a concussion

During a concussion, active mental activity, including reading, is not recommended. During the treatment of a concussion, specialists prohibit straining their eyesight, so victims are strictly prohibited from watching television, reading for long periods of time, sitting in front of a computer, etc. To speed up recovery, it is recommended:

compliance with the regime;
exclude mental work, reading books, working on a computer, watching TV shows, etc.
ensure sufficient time for sleep;
do not drink coffee, tobacco, or alcohol;
exclude driving, housework that requires stress.
Avoid physical strain and stress, noise and light.

After a month has passed from the date of treatment, the patient is recommended to undergo some diagnostic tests again to exclude the possibility of developing various kinds of complications.

How much should you not drink after a concussion?

There are several opinions regarding drinking alcohol after a concussion. Some people tend to believe that for mild concussions it is acceptable to take small amounts of alcohol after treatment. This is not true. Small doses of alcohol are permissible only after six months have passed from the end of treatment procedures, or even more. Although it would be better if, after an injury, the patient gives up alcohol forever, since ethanol can worsen brain processes and activity in general, and against the background of an injury, it can also cause complications after a concussion.

In later life, cheap strong alcohol or wine will have to be excluded. A small amount of high-quality cognac or a glass of excellent red wine is acceptable.

Consequences and complications after a concussion

Even with a single concussion, there is a possibility of developing consequences that will affect the rest of your life. Even after ten years, a person who has once suffered from a concussion may show signs of increased irritability or excessive impressionability due to long-standing trauma. Such people more often than others suffer from excessive tearfulness, chronic fatigue, and deep depressive states. Also, after a concussion, a chronic sleep disorder, fear of enclosed spaces, difficulty trying to concentrate, and hypersensitivity to weather conditions may develop.

headache not relieved by analgesics;
hypertensive crisis;
stroke;
sudden mood swings;
cerebral edema;
coma.

To avoid such complications, it is imperative to take the necessary measures to treat brain injury. During the treatment process, it is extremely important to comply with the requirements regarding the regimen, taking medications and quitting alcoholic beverages, as well as smoking. Such a brain injury is dangerous due to mental changes and physical disorders, and alcohol consumption greatly increases the likelihood of such consequences.

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A concussion is a mild form of traumatic brain injury, accompanied by a short-term loss of consciousness (up to 5 minutes). The manifestation of pathology is based on the principle of disruption of functional connections between nerve cells.

A concussion, as a rule, occurs as a result of traumatic effects of a domestic, industrial or sports nature, as well as as a result of road accidents and criminal circumstances. In any case, after a severe blow to the head, you should go to the hospital, take an x-ray to rule out the presence of hemorrhages, skull cracks, and go for a consultation with a neurologist.

Is it possible to drink alcohol if you have a concussion? What are the manifestations of injury, how to provide first aid? Let's take a closer look.

Manifestations of concussions

A strong blow to the head is usually accompanied by a short-term loss of consciousness at the time of injury. This symptom signals the possible occurrence of a concussion and is associated with stress factors. Immediately after a bruise, an increase/slowdown of the pulse, single vomiting, memory impairment (partial amnesia for previous/current events), an increase in the frequency of inhalations and exhalations, twitching of the eyeballs, and disorientation in space may be observed. Soon after the incident, these indicators return to normal.

After regaining consciousness, the victim complains of tinnitus, discomfort, headache, nausea, sleep disturbance, flushing of the face, dizziness, weakness, and sweating. At the same time, body temperature remains normal.

The general condition of the victims improves within 7-14 days. However, subjective symptoms and headaches can last much longer.

Remember, there are currently no laboratory tests to diagnose a concussion. Computed tomography, magnetic resonance imaging, and ultrasound do not reveal any lesions. Often, a concussion can mask severe traumatic injuries that require emergency hospitalization.

First aid

After the concussion, when the victim has come to his senses, he should be placed in a horizontal position with his head slightly raised. If a person continues to be in an unconscious state, he must be turned on his right side, his head thrown back, his face oriented towards the ground, his left arm and leg bent at the joints at a right angle (provided there are no fractures of the limbs or spine). While the victim is in a safe position, which ensures the unimpeded flow of liquid (vomit, saliva, blood) from the oral cavity to the outside, free passage of air into the respiratory system, eliminating the possibility of tongue retraction, you need to quickly call an ambulance.

All people suspected of having a concussion must be transported to a hospital to clarify the diagnosis and prescribe treatment. The victims are placed on bed rest, the duration of which depends on complications, characteristics of the course of the disease and starts from 1 day to 2 weeks.

As a rule, drug treatment is not required. Pharmacotherapy is used to alleviate the patient’s condition if headaches, anxiety and insomnia are severe and cause considerable discomfort. In this case, the range of prescribed medications consists of sleeping pills (Donarmil, Relaxon), sedatives (Corvalol, Valocardin, Phenazepam, Nozepam, Valerian, Motherwort), painkillers (Analgin ", "Maxigan", "Sedalgin", "Dexalgin") tablets.

In order to prevent possible abnormalities in the functioning of the brain after a concussion, it is recommended to be observed by a neurologist for a year. In the absence of factors aggravating the injury and proper adherence to the regimen, the prognosis will be positive.

Clinical picture

What doctors say about alcoholism

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Alcohol for concussion

Alcohol products have a negative effect on the organic structures of the body. With alcohol abuse, the brain is especially affected, which catastrophically decreases in volume, the vessels undergo changes, the convolutions are smoothed out, and the membranes swell. Against the background of such phenomena, dementia gradually progresses.

Alcohol glues red blood cell structures together, which leads to the formation of blood clots in small vessels, blocking the lumens and depriving brain cells of nutrition. As a result, tissue structures change, and mental activity deteriorates greatly. Pathological, destructive processes progress more intensively in the presence of traumatic brain injury. Therefore, concussion and alcohol are incompatible concepts.

After a head injury, it is not recommended to engage in active mental activity; experts prohibit reading, sitting in front of a computer, or watching TV. To speed up recovery, you should not strain your eyesight, but rather, rest and sleep more. Do not drink coffee, alcoholic beverages, stop smoking, avoid stress, noise, light, and physical strain.

Remember, depression can occur after a concussion. In this case, it is useful to contact a psychologist to prescribe treatment and take sedatives.

How long should you not drink alcohol after a head injury?

It is permissible to take alcoholic drinks 6 months after the end of treatment. However, it is better to permanently eliminate alcohol from your diet. The fact is that ethanol worsens brain processes and its functioning in general, which can lead to complications against the background of injury. An exception is high-quality cognac or red wine, which can be consumed several times a week, 30 ml and 100 ml, respectively.

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Conclusion

A concussion is a head injury when layers of brain tissue are displaced relative to each other, which disrupts communication between centers and deteriorates the nutrition of nerve cells, which leads to their improper functioning. Fortunately, these troubles are temporary.

For mild concussions, the best treatment is rest and sleep. If the injury hides a serious pathology - a brain contusion, the patient requires urgent hospitalization because blood begins to accumulate in the affected area, a hematoma is formed, compressing the structures of the brain, which poses a danger to human life.

Is it possible to independently distinguish a concussion from a bruise?

Recognizing these conditions is quite problematic; it is better to entrust the diagnosis to a specialist in order to eliminate the possibility of an error or the development of consequences of injury (excessive impressionability, deep depression, increased irritability, chronic fatigue, hypersensitivity to weather conditions, fear of confined spaces, sleep disorders).

Remember, alcohol greatly increases the effects of brain injury. The patient may experience sudden mood swings, migraines, dizziness, stroke, hypertensive crisis, cerebral edema, and even develop a coma. In order to avoid mental and physical changes, it is recommended to refrain from drinking alcohol during the course of treatment and the next six months after its completion.

Drawing conclusions

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Navigation

Traumatic brain injuries and alcohol use pose serious threats to brain health. The negative consequences that arise against their background reduce the functionality of the central nervous system. The complex impact of these factors can lead to a decrease in intelligence, personality changes, and the development of psycho-emotional and organic disorders. Drinking alcohol during a concussion can reduce a person’s quality of life and reduce its duration. Even with a mild degree of the disease and drinking alcohol in minimal quantities, the level of danger remains critically high.

The consequences of brain trauma combined with alcoholic beverages pose a serious threat to brain health.

What happens during a concussion

A concussion is a form of mild blunt head trauma. After it, the victim remains conscious until the consequences of the damage appear. They arise against the background of a disruption in the process of interaction between nerve cells at the functional level. At the same time, the structure of the medulla is preserved, and no visible disruptions in the functioning of blood vessels are observed. Despite the fact that doctors know a lot about this type of injury, it is not completely known what happens with a concussion on an organic level. There is a theory about the occurrence of microscopic effusions in tissues that cannot be detected using modern equipment.

Functional disruptions caused by a concussion are sufficient to develop a clinical picture characteristic of the condition. Some time after the blow, the patient loses consciousness for a short time, and he experiences amnesia associated with the moment of injury. Almost always, the victim experiences nausea and vomiting, so the patient must be turned on his right side to prevent asphyxia. Symptoms are supplemented by dizziness, headache, apathy or irritability, and sleep disturbance.

Many people try to cope with such manifestations on their own, without consulting a doctor. Some people hope to relieve discomfort with the help of alcoholic beverages, not realizing that alcohol during a concussion only aggravates the problems.

The effect of alcohol on the brain during a concussion

The euphoria that occurs during alcohol intoxication lasts only a few minutes. This is followed by inhibition of the central nervous system, poisoning of brain tissue with toxins, and massive death of neurons.

The effect of ethanol on the body is considered extremely harmful even without the parallel effect of negative factors.

Systematic intake of alcohol leads to a decrease in the volume of the brain, smoothing of its convolutions, swelling of the gray matter, and changes in the structure of blood vessels.

Euphoria after drinking alcohol lasts only a few minutes, followed by inhibition of the central nervous system.

If you drink alcohol during a concussion, the influence of negative factors will increase many times:

the autonomic nervous system suffers, which leads to the appearance of persistent neurological symptoms. The patient experiences anxiety, apathy, asthenia, fatigue, irritability, and sleep problems;
there is a risk of developing seizures of unknown etiology;
the likelihood of a decrease in mental abilities and the appearance of signs of senile dementia in middle age increases;
persistent swelling of the medulla, decreased functionality of cerebral vessels cause malfunctions in the functioning of internal organs;
there is a suppression of a person’s ability to think abstractly and logically against the background of preservation of instincts, reflexes, and primitive functions of the central nervous system;
there is an increase in blood pressure, which is accompanied by severe headaches and a deterioration in general well-being;
the ability of ethyl alcohol to “glue” red blood cells is enhanced. This leads to the formation of microscopic blood clots that clog small vessels. The result is ischemia of individual areas of the brain, which is complemented by disruption of connections between neurons and leads to tissue atrophy;
A concussion provokes an increase in the susceptibility of the central nervous system. The influence of ethanol begins to be perceived especially acutely; even small volumes of weak alcoholic drinks become a cause of intoxication. Habitual foods and their quantities threaten to cause hysteria, hallucinations, aggressiveness, and delirium.

Alcohol increases persistent swelling of the brain.

The consequences and complications of drinking alcohol due to a concussion are often irreversible. Even a single combination of exposure to these negative factors on the body can cause a decrease in the functionality of parts of the central nervous system. Many of them are not amenable to conservative or surgical correction.

Can you drink alcohol if you have a concussion?

Any head injuries and alcoholic drinks inevitably negatively affect the state of the central nervous system. Under the influence of organic or functional damage, the harmful effect of ethanol on the body increases many times over. The consequences of such a combination are difficult to predict; they may appear immediately or after several years, but in any case they will pose a danger.

Doctors warn that concussions and alcohol intake should not be combined.

To prevent possible serious violations, it is recommended to completely abstain from alcohol if you have a history of TBI, or at least strictly follow the instructions of a neurologist.

When can you start drinking after a concussion?

A concussion is considered one of the mildest forms of TBI. Nevertheless, doctors remind that the consequences of the injury may not appear immediately, but several months or years after the accident. Changes in the state of nervous tissue as a result of external influences are difficult to assess, so the possibility of complications cannot be predicted. After the signs of a concussion have completely disappeared, it is recommended to wait at least six months before returning to drinking alcohol. The condition of the victim and the speed of recovery cannot shorten the duration of this period; they can only increase it.

The consequences of the injury may not appear immediately.

In situations where the cause of injury was alcohol consumption, not only a neurologist, but also a narcologist should work with the patient. The latter specialist will help the victim’s body get rid of the toxic breakdown products of ethyl alcohol. If necessary, the doctor will perform manipulations aimed at treating alcoholism.

Possible consequences and complications of drinking alcohol after a concussion

Depending on the individual characteristics of the body and the severity of the injury, the nervous system may react to a concussion in different ways. In some situations, the accident passes without visible consequences, in others it causes failures in the functioning of systems and organs.

After a severe blow to the head, you need to consult a neurologist so that a specialist can rule out a serious pathology or select a treatment regimen. Any of the approaches involves complete abstinence from alcohol for a period of 6 months from the moment of diagnosis or the disappearance of characteristic symptoms.

Drinking alcohol during a concussion can lead to the following complications and consequences:

chronic severe headaches that do not respond well to conservative treatment;
persistent increase in blood pressure, threat of hypertensive crisis;
increased likelihood of developing ischemic or hemorrhagic stroke;
cerebral edema;
confusion, coma;
sudden mood swings, decreased intelligence, mental changes;
chronic insomnia;
exacerbation of reaction to loud sounds, bright light, strong odors.

Drinking alcohol can lead to sudden mood swings.

A person’s history of traumatic brain injury automatically places him or her at risk for a number of diseases and functional disorders. Such patients are shown to be especially careful about brain health. The basis of the approach is a healthy lifestyle.

You can find information on the Internet that drinking red wine or cognac after a head injury helps improve vascular function and speed up recovery. In fact, drinking alcohol during a concussion can only have a negative effect on the affected organ. Such experiments are unjustified and dangerous to health.

My husband drinks after a traumatic brain injury. Relevance of the problem and the relationship between traumatic brain injury and alcoholism. Treatment for concussion

Pathogenetic mechanisms of alcohol intoxication in traumatic brain injury

Clinical features of the course of traumatic brain injury during alcohol intoxication

Real examples

Traumatic brain injury alcohol

Treatment for concussion

Effect of alcohol on the brain

Contraindications after a concussion

How much should you not drink after a concussion?

Consequences and complications after a concussion

Negative relationship between alcoholism and traumatic brain injury.

Concussion and alcohol

Dysfunctions of the body due to injury

Compatibility of alcohol and traumatic brain injury

Alcohol and recovery

Other contraindications

Is it possible to drink if you have a head injury?

Alcohol and concussion: possible consequences

Alcohol and concussion

The effects of alcohol on the brain

What happens if you drink alcohol after a concussion?

When can you drink alcohol after a concussion?

If you decide to drink alcohol after a concussion

alcohol (traumatic brain injury)

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Alcohol after a head injury consequences

Alcoholism

Pathogenetic mechanisms of alcohol intoxication in traumatic brain injury

Clinical features of the course of traumatic brain injury during alcohol intoxication

Real examples

Traumatic brain injury alcohol

Treatment for concussion

Effect of alcohol on the brain

Contraindications after a concussion

How much should you not drink after a concussion?

Consequences and complications after a concussion

Manifestations of concussions

First aid

Alcohol for concussion

How long should you not drink alcohol after a head injury?

Our readers write

Conclusion

Is it possible to independently distinguish a concussion from a bruise?

Drawing conclusions

What happens during a concussion

The effect of alcohol on the brain during a concussion

Can you drink alcohol if you have a concussion?

When can you start drinking after a concussion?

Possible consequences and complications of drinking alcohol after a concussion

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so that you get the most interesting: