Food poisoning and weakening of the nerve system are interconnected. Toxic damage to the nervous system

Impaired consciousness is caused either by the effect of poison on the cerebral cortex (in case of poisoning with sleeping pills, alcohols, opium and its preparations, chlorinated hydrocarbons, ethylene glycol, etc.), or the onset of cerebral hypoxia (in case of poisoning with carbon monoxide, hydrogen sulfide, nitrate, etc.).

Disorder of consciousness is one of the syndromes that often occurs in severe poisoning and serves as one of the criteria for assessing the severity of poisoning. There are several types of consciousness disorders.

State of oblivion which is a slight clouding of consciousness; the patient can be brought out of this state only by persistently addressing him; patients usually complain of headache and general weakness.

Sopor - unconsciousness, in which the patient does not respond to the environment; Only with difficulty, using harsh painful stimuli (pinches, injections, etc.), is it possible to bring the patient out of the soporous state. This condition is observed in case of poisoning with opium, morphine, omnopon, dicaine, anesthesin, sleeping pills, alcohol and a number of industrial poisons.

Toxic coma- an unconscious state in which there is no reaction of the body to painful stimuli (injections, pinches); there is a smell of poison if the cause of poisoning was alcohols or aniline. The face, arms and legs are cyanotic, the body is covered with sticky, cold sweat; pulse is hard to palpate, frequent (more than 120 beats per minute); breathing is rare and noisy; arterial pressure low (less than 110 mm Hg). Involuntary urination and defecation are observed; delirium, hallucinations and periodic agitation, sometimes convulsions. Toxic coma occurs due to the effect of poison on the nervous system during poisoning with carbon monoxide, alcohol, sleeping pills, etc.

A comatose state is always life-threatening, therefore, in case of coma, urgent measures are required. It should be remembered that this condition occurs for various reasons (injury, disease, poisoning). Before providing assistance, it is necessary to exclude various diseases of the internal organs and nervous system. Great importance have the smell of poison, interview others, other data indicating poisoning (detection of poison residues, etc.). It is necessary to clarify when the unconscious state occurred and what preceded it (fall, bruises, illness). In any case, you must urgently call a doctor.

Mental disorders (delirium, psychosis) occur due to poisoning with alcohol, atropine, sleeping pills, drugs (hashish, heroin, opium, etc.), tetraethyl lead. In this case, the leading place is occupied by hallucinations (visual, tactile, auditory), and movement disorders, while at the same time preserving the sense of one’s own personality. The victim's mood is extremely unstable (anxiety, fear, horror); possible motor excitement (state of affect).

Convulsive syndrome manifested by involuntary muscle contractions - paroxysmal or constant. Cramps can affect many muscle groups in the body (generalized cramps) or be limited to one muscle group (localized cramps).

Convulsions can be tonic ( slow contraction), clonic (fast contraction). Causes of convulsive syndrome: poisoning with strychnine, analeptics, penicillin, potassium, etc.

The problem of exogenous damage to the nervous system has become particularly relevant due to the widespread use of chemicals in industry, agriculture, military service and everyday life. Significant “chemicalization” of human life has led to an increase in acute and chronic poisoning by toxic substances. These substances enter the general circulation through the lungs with inhaled air, through the gastrointestinal tract with drinking water and food, or penetrate through the skin and mucous membranes. Most of the poison that enters the bloodstream affects the nervous system, which is sensitive to all kinds of harm.

Chemical compounds Depending on their effect on the nervous system, they are divided into two groups: neurotropic poisons and poisons that do not have pronounced neurotropism. Neurotropic poisons themselves or through metabolic products have a direct effect primarily on nervous tissue, penetrating the blood-brain barrier and accumulating in the nervous system. In case of poisoning with poisons that do not have pronounced neurotropism, the nervous system suffers secondarily due to gross disturbances of homeostasis.

Pathogenesis. Despite the variety of toxic substances that cause damage to the nervous system, some main pathogenetic mechanisms for the formation of neurological disorders can be identified. Of leading importance is hypoxia, caused by disturbances in external respiration and alveolar-capillary oxygen transport (asphyxiants, organophosphorus compounds), a decrease in the oxygen-carrying capacity of the blood (hemoglobin poisons and hemolytic agents), damage to cytochromes, and disorders of general and cerebral hemodynamics. The angiotoxic effect of poisons is characteristic. Atony develops consistently cerebral vessels, disruption of blood flow in them, stasis, thrombosis appear and, as a result, foci of softening of the nervous tissue appear. Due to the release of the liquid part of the blood into the interstitium, liquor circulation is disrupted, edema and swelling of the brain substance develop. An important role in some poisonings is played by autointoxication and dysmetabolic processes as a result of widespread tissue breakdown, loss of the antitoxic function of the liver and excretory ability of the kidneys. A number of poisons also have a direct cytotoxic effect, which causes gross morphological changes in nervous tissue.

Pathomorphology. In acute poisoning with various poisons, a largely similar picture is revealed. The most typical are vascular disorders caused by damage to the vasoconstrictors of the vessels themselves and the vascular endothelium. Vascular dystonia, perivascular edema and hemorrhages, blood clots in small vessels, focal micro- and macronecrosis, and brain swelling are noted. Degeneration of nerve cells is detected, especially the cerebral cortex, cerebellum, and reticular formation of the brain stem. Severe dystrophic changes in nerve cells can lead to the death of the latter and their transformation into “shadow cells”. Axons and dendrites of dead cells disintegrate, undergoing Wallerian degeneration. In some cases, the processes of nerve cells are affected first, which is clinically manifested by conduction disorders or multiple lesions of peripheral nerves.

Chronic intoxication causes more diverse changes in neurons. A decrease in the number and volume of neurons and their deformation are detected, which is combined with degenerative changes in glia. Phenomena of demyelination of conductors and peripheral nerves are detected. In a number of intoxications, there is a predominant selectivity of damage to nervous structures (for example, the predominance of changes in the globus pallidus and substantia nigra during carbon monoxide poisoning, which is clinically expressed in parkinsonism syndrome).

Classification. According to the nature of the course, acute, subacute and chronic poisonings are distinguished.

Acute poisoning is caused by large doses of a toxic substance and is characterized by the rapid development and occurrence of life-threatening respiratory and cardiovascular disorders. Collapse, convulsions, psychomotor agitation, disturbances of consciousness, even coma are possible. Against the general background of acute poisoning, particular symptoms of damage to the nervous system characteristic of this poison appear.

Subacute poisoning occurs when exposed to smaller doses of poison and is characterized by less pronounced changes in the body. These changes develop gradually and are not accompanied deep violations consciousness and pronounced changes in breathing and cardiovascular activity.

Chronic poisoning is a consequence of prolonged exposure to small doses of poison that systematically enters the body. Neurological disorders develop slowly and gradually, and can be persistent and persist for a long time. An exacerbation of the process is possible in cases of infection and other somatic pathology.

According to clinical criteria, there are a number of main neurological syndromes that develop during poisoning, regardless of the type of toxic agent:

1. Toxic encephalopathy.

2. Toxic encephalomyelopathy.

3. Toxic polyneuropathy (mononeuropathy).

4. Toxicathy.

5. Toxic neuromuscular syndrome.

6. Toxic astheno-vegetative syndrome.

1. Toxic encephalopathy. In the clinical picture of acute poisoning, a combination of cerebral and focal symptoms is observed, and the latter are more clearly identified as the cerebral symptoms are eliminated. The same encephalopathic syndrome can be caused by different poisons and, on the contrary, poisoning with the same poison is accompanied by a different symptom complex. The cerebral syndrome can be expressed in depression of consciousness (stunning, stupor, coma) or in the development of psychomotor agitation or intoxication psychosis. The development of convulsive syndrome is possible, caused both by the direct effect of “convulsive” poisons and by the development of deep hypoxia and cerebral edema. Transient symptoms of “meningism” are detected.

Focal symptoms of toxic encephalopathy are diverse and are represented by amyostatic disorders, extrapyramidal hyperkinesis, optic-vestibular and cerebellar symptoms, pathological foot reflexes, and dysfunction of the pelvic organs. Some organic symptoms reflect the selectivity of damage to certain brain structures by poisons. Thus, toxic encephalopathy with parkinsonism syndrome develops due to poisoning with manganese, carbon monoxide, and tetraethyl lead. Vestibular Meniere-like disorders are characteristic of poisoning with gasoline, bromoethyl, chloromethyl. Recovery from acute toxic encephalopathy is accompanied by an astheno-vegetative symptom complex of varying severity.

Chronic toxic encephalopathies are clinically represented by both diffuse organic microsymptoms and focal syndromes(amyostatic, hyperkinetic, cerebellar, epileptic). Disorder syndromes are often associated cerebral circulation and psychopathological syndromes.

2. Toxic encephalomyelopathy. The clinical picture is represented by a combination of general cerebral, focal cerebral and spinal syndromes. The already noted encephalopathic syndromes are accompanied by spinal symptoms in the form of fasciculations in the muscles with anterocorneal lesions, mixed cerebellar-sensitive ataxia, and dysfunction of the pelvic organs. Most often, encephalomyelopathy occurs due to poisoning with carbon monoxide, bromoethyl, lead and carbon disulfide.

3. Toxic polyneuropathy (mononeuropathy). Toxic polyneuropathies occur quite often and are accompanied by symmetrical sensory disturbances of the “polyneuritic” type, distal peripheral paresis and vegetative-trophic disorders. Depending on the toxic agent, polyneuropathy manifests itself either predominantly in sensory disorders, or in motor disorders, or in mixed disorders. Thus, chronic alcohol intoxication leads predominantly to sensory polyneuropathy, in which deep sensitivity fibers (peripheral “pseudotabes”) are primarily affected, and lead intoxication leads to predominantly motor disorders.

Toxic polyneuropathies are divided into acute (as a result of a single exposure to toxic doses of a substance), subacute (with repeated short-term exposure to a toxic agent) and chronic (with systematic exposure to small doses). Pre-existing diseases of the nervous system, poor nutrition and lack of vitamins enhance the effect of toxic substances.

In some cases, toxic mononeuropathies may develop. Thus, with lead intoxication, the radial (dangling hand) and peroneal (dangling foot) nerves are affected, and when using certain antibiotics (streptomycin, kanamycin, neomycin), the auditory nerve suffers.

4. Toxicathy. The toxic factor during acute or prolonged exposure is rarely limited to a pathological effect only on the brain or on peripheral nerves alone. There is often combined damage to the brain, spinal cord and peripheral nerves, which is reflected in the name of the syndrome. However, even with such diffuseness of damage, depending on the specific toxic agent, there is a certain selectivity in the suffering of certain structures of the nervous system.

5. Toxic neuromuscular syndrome. A number of poisons, disrupting neuromuscular conduction, cause the development of myasthenia-like disorders. This syndrome is manifested by symptoms of increasing muscle weakness and pathological muscle fatigue, which intensify with physical activity. Early manifestation syndrome may include diffuse muscle fasciculations. In severe poisoning with organophosphorus compounds, potassium chloride, curare-like drugs, pachycarpine, methyl bromide, muscle weakness can reach the level of paresis and paralysis.

6. Toxic astheno-vegetative syndrome. The subjective characteristics of the complaints of patients with this syndrome resemble those of neurasthenia, however, the complaints are based on an organic basis and are observed during chronic intoxication or upon recovery from acute or subacute poisoning. Weakness, fatigue, rapid mental and physical fatigue, headaches, and sleep disturbances come to the fore. The mood is unstable, mostly anxious and depressed. An objective examination may reveal individual residual organic microsymptoms as a consequence of toxic encephalopathy. Characteristic is the instability of vegetative functions: increased sweating, play of vasomotors of the face and chest, acrocyanosis, marbling of the skin of the extremities, persistent dermographism. Revitalization of deep reflexes, tremor of the fingers of outstretched arms, tongue, and eyelids are detected.

Diagnostics. Diagnosis of poisoning, especially at the prehospital stage, has its own difficulties. In acute poisoning, rapid development of depression of consciousness and respiratory and circulatory disorders is possible. These circumstances force a differential diagnosis with acute cerebral pathology of another origin (stroke, meningoencephalitis, dysmetabolic processes). Delirium that occurs in the early stages of poisoning must be differentiated from acute psychosis.

By interviewing the victim, his relatives and friends, it is necessary to find out the cause of poisoning, the amount of poison taken or the duration of inhalation poisoning (assessment of the “toxicological situation”). The diagnosis can only be confirmed in a hospital through a chemical and toxicological study of biological media (blood, urine, gastric contents).

The diagnosis of chronic intoxication is established by clarifying the medical history (presence of occupational and household hazards), identifying a typical neurological syndrome, and conducting a qualitative and quantitative toxicological study.

Treatment. In case of acute poisoning, therapeutic measures should primarily be aimed at stopping exposure and removing toxic substances from the body. If poisoning occurs through the mouth, it is necessary to lavage the stomach through a tube and introduce an adsorbent - activated carbon - into the stomach. In case of inhalation poisoning, emergency evacuation of the victim from the zone of action of toxic substances is organized. Victims are evacuated to a poison control center or intensive care unit. Powders, tablets, liquids of an unknown nature, as well as gastric lavages found at the first aid site are sent for toxicological testing.

The hospital continues to take measures to stop exposure and remove toxic substances from the body. If a toxic substance is identified, antidote therapy is carried out: administration of atropine sulfate for opiate poisoning, ethyl alcohol for methanol poisoning, oxygen inhalation for carbon monoxide poisoning, etc. Measures are taken to remove toxic substances from the bloodstream: forced diuresis, hemodialysis, detoxification hemosorption, exchange transfusion . With the development of a coma of toxic origin, patency is restored respiratory tract, held artificial ventilation lungs.

Measures are being taken to correct emerging dysfunctions of organs and systems, including neurological disorders. To relieve seizures, benzodiazepine derivatives are used (0.5% seduxen 2-4-6 ml intramuscularly or intravenously), sodium hydroxybutyrate, barbituric acid derivatives (thiopental, hexenal). For developing cerebral edema, hyperoncotic solutions (10-15% albumin solution, 20-40% glucose solution) are used with the simultaneous administration of osmodiuretics (urea solutions, mannitol 1-1.5 g per 1 kg of body weight) or fast-acting saluretics (Lasix 80 -120 mg intravenously). Glycerin is administered orally through a probe in an amount of 50-70 ml. Craniocerebral hypothermia, carried out using special devices or by covering the head with ice packs, helps reduce cerebral edema. Drugs are used that reduce the permeability of cerebral vessels (calcium preparations, ascorbic acid), improve blood supply to the brain (Trental, Cavinton, nicotinic acid), and antihypoxants.

Depending on the leading neurological syndrome that has formed during acute or chronic poisoning, appropriate pathogenetic and symptomatic agents are prescribed. Prescribed remyelinators (retabolil, Keltican, vitamin B 12), absorbents (pyrogenal, solcoseryl), anticholinesterase drugs (do not prescribe in case of poisoning with organophosphorus compounds!), “nootropics” (Cerebrolysin, nootropil, piracetam), herbal adaptogens, vegetotropic agents, general restorative drugs . Physiotherapeutic procedures, balneotherapy, massage, and physical therapy are widely used.

Clinic of neurological disorders in case of damage

combat organophosphorus substances (OPS).

Considering the pronounced neurotropic effect of many toxic agents, one cannot ignore the fact possible application a number of toxic substances as weapons of mass destruction. Therefore, it is no coincidence that the so-called “nerve gases” synthesized on the basis of organic derivatives of phosphoric and phosphinic acids are stored in the arsenal of a number of countries. Such nerve agents include tabun, sarin, soman, VX gases and other compounds. In peacetime, organophosphorus compounds used in everyday life and agriculture (chlorophos, thiophos, karbofos, mercaptophos) and causing a similar clinical picture of poisoning can serve as models of damage to OPA.

OPAs penetrate the body in different ways: in a vapor state with inhaled air, in a droplet-liquid form and in an aerosol state - easily absorbed through the skin, and if they contaminate food and water - through the alimentary route through the gastrointestinal tract.

The pathogenesis of the action of FOV on the nervous system is complex and diverse. The mechanism of intoxication is based on the selective effect of the poison on cholinoreactive structures - suppression of the activity of the enzyme acetylcholinesterase. Due to the inhibition (inhibition) of this enzyme, the mediator acetylcholine accumulates in synaptic formations and overexcitation of cholinergic structures occurs. The toxic effect of FOV on the nervous system is regarded as muscarinic-like, associated with the excitation of M-cholinergic receptors, which is expressed in the appearance of profuse sweating, salivation, bronchorrhea, bronchospasm, and the development of severe miosis. The nicotine-like effect of FOV is due to the stimulation of H-cholinergic receptors located in the muscles, ganglia, and adrenal medulla. An important place is occupied by the effect of poisons on the central nervous system. Due to the excitation of the central M- and N-cholinoreactive structures, cerebral disorders occur in the form of general cerebral, mental and focal symptoms (excitement, disorientation, hyperkinesis of choreic and myoclonic nature, clonic-tonic convulsions, coma).

A number of nonspecific factors play a significant role in the pathogenesis of damage to the nervous system under the influence of FOV: a membrane toxic effect caused by the activation of free radical oxidation of lipids, activation of membrane-bound phospholipases, disturbances in the metabolism of serotonin and catecholamines, a disorder of cerebral microcirculation, the development of metabolic acidosis, histotoxic brain hypoxia.

The clinical picture of the lesion is determined by the amount of poison, the aggregate state of the substance, and the route of entry.

Based on the nature of the clinical manifestations of damage to the relevant organs and systems, the following syndromes are distinguished:

Ophthalmic-vegetative (miosis, spasm of accommodation, decreased visual acuity, decreased or absent reaction of the pupils to light and convergence with accommodation, lacrimation);

Somatovegetative (hyperhidrosis, hypersalivation, bronchorrhea, bronchospasm, respiratory rate disturbance, diarrhea, increased urination);

Vegetative-vascular (arterial hypertension or hypotension, tachycardia, bradycardia, hyperemia or pallor skin, acrocyanosis);

Peripheral neuromuscular (flaccid synaptogenic myoneural paresis and paralysis of the muscles of the limbs and trunk, including the respiratory muscles, muscles of the pharynx and larynx);

Cerebral, manifested by cerebral, meningeal and focal symptoms (nystagmus, symptoms of oral automatism, changes in muscle tone and deep reflexes, pathological foot reflexes, coordination and extrapyramidal disorders);

Mental disorders in the form of neurosis-like symptoms (anxiety, fear, low mood, less often euphoria) or acute psychotic state (visual and auditory hallucinations, delusions).

There are mild, moderate, severe and extremely severe degrees of severity of OPA poisoning.

With a mild degree of intoxication, moderately expressed ophthalmovegetative symptoms are detected. Those affected complain of blurred vision (fog or a grid before the eyes, inability to distinguish small printed text, poor visibility of distant objects, decreased vision in artificial light), tightness and constriction in the chest, nausea, headache, dizziness. Coordinating disorders appear in the form of an ataxic gait and instability in the Romberg position. Restlessness, anxiety, fear, memory, attention and sleep disturbances may occur.

The following clinical forms of mild poisoning are distinguished: miotic (visual disturbances dominate) and neurotic (prevalent neurotic disorders). The prognosis for mild lesions is favorable, recovery occurs in 2-5 days.

The average degree of poisoning is characterized by a more rapid development of intoxication symptoms (minutes, tens of minutes), especially when the poison is inhaled.

The leading clinical signs are somatovegetative disorders against the background of pronounced ophthalmovegetative symptoms and moderately expressed vegetative-vascular and peripheral neuromuscular disorders. The predominant complaints are difficulty breathing, chest compression, chest pain, and cough. A condition occurs that resembles an attack of suffocation during bronchial asthma, accompanied by a feeling of fear, increased blood pressure, and dysuric phenomena. More pronounced cerebral changes are revealed in the form of mild stupor, disorders of motor coordination, increased deep and suppressed superficial reflexes. Mild paresis of the muscles of the limbs, mainly of the proximal parts, develops. Affective disorders become longer lasting, and acute psychotic disorders may occur.

Recovery occurs in 2-3 weeks. Complications and consequences are possible.

In severe cases of poisoning, the leading ones are neuromuscular and cerebral disorders against the background of pronounced ophthalmic-vegetative, somato-vegetative and vegetative-vascular manifestations of intoxication. These symptoms develop over short time. Depression of consciousness occurs (stupor, coma), tonic-clonic convulsions, widespread paresis and paralysis of the limbs and trunk muscles appear. Bulbar myasthenic syndrome and diplopia may occur. Upon recovery from a comatose state, movement coordination disorders and dysarthria are revealed. An acute psychotic state often develops. Recovery occurs in 4-6 weeks. Various complications and consequences are possible.

Depression in chronic hepatitis is quite common and requires drug treatment immediately after diagnosis. In principle, any antidepressant can be used for hCG, but the drugs of choice are still serotonin reuptake inhibitors due to the small number of side effects, convenient dosing and the absence of the danger of overdose.

Antidepressants

Valproic acid preparations

Valproic acid preparations (Depakine, Convulex, etc.) are known as anticonvulsants, mood stabilizers for mania, and a prophylactic for migraines. In chronic hepatitis, they are used in the treatment of muscle spasms. The initial dose for adults is 300 mg/day, a single dose is possible (half-life ranges from 6 to 16 hours depending on the activity of microsomal liver enzymes). The dose is gradually increased, bringing it to 2000 mg/day in 2-3 doses. Contraindications: hypersensitivity, including “familial” (death of close relatives while taking valproic acid); diseases of the liver and pancreas; hemorrhagic diathesis; first trimester of pregnancy; lactation. Side effects: thrombocytopenia and increased VSC (bleeding, subcutaneous hemorrhage); hyperammonemia leading to liver damage (general malaise, fatigue, swelling of the face, decreased appetite, jaundice, nausea, vomiting); increased appetite; stomach pain; drowsiness; tremor; paresthesia; confusion; leukopenia. With long-term use, reversible hair loss is possible. Interactions: the effect is enhanced by other anticonvulsants, sedatives and hypnotics; dyspeptic disorders are less common when taking antispasmodics and enveloping agents; cimetidine, salicylates, felbamate, erythromycin, alcohol increase toxicity. Valproic acid may significantly alter carbamazepine concentrations, increase the toxicity of diazepam and ethosuximide, and increase phenobarbital and diphenine concentrations (while they may decrease valproic acid concentrations).

Paroxetine, a representative of this group of antidepressants, is available in 20 mg tablets. Most patients prefer to take it in the morning due to the development of a stimulating effect. If there is a sedative effect, the drug should be taken in the evening. The initial dose for adults is 10-20 mg/day with meals. If the effect is insufficient, the dose can be increased by 10 mg at intervals of 1 week to a maximum of 40-60 mg/day. It takes 6-8 weeks to assess therapeutic effectiveness. Contraindications: documented hypersensitivity, simultaneous administration of MAO inhibitors and a period of 14 days after their discontinuation. Side effects: dry mouth, nausea, asthenia, drowsiness or insomnia, tremor, sweating, impaired libido, anorgasmia and ejaculatory disorders, increased risk of suicide, hypomanic/manic states. Prescribe with caution in the presence of seizures, manic episodes, or a history of renal or cardiac disease. Interactions: enhances the effects of barbiturates, diphenin, indirect anticoagulants, tricyclic antidepressants, phenothiazine neuroleptics and class 1c antiarrhythmics (propafenone, flecainide). Phenobarbital and diphenine reduce effectiveness. Alcohol, cimetidine, sertraline, phenothiazine antipsychotics and indirect anticoagulants increase toxicity.
Ataxia hereditary cerebellar Pierre-Marie's a chronic progressive disease, the main manifestation of which is cerebellar ataxia. The disease is hereditary and is transmitted in an autosomal dominant manner. Clinical picture. The main symptom of the disease is ataxia, which is of the same nature as in Friedreich's ataxia. The disease usually begins with a gait disorder, which is then joined by ataxia in the hands, speech impairment, and facial expressions. Severe static ataxia, dysmetria, and adiadochokinesis occur. Patients may experience shooting pains in the legs and lumbar region, involuntary muscle twitches. There is a significant decrease in strength in the muscles of the limbs, a spastic increase in muscle tone, mainly in the legs. Tendon reflexes are increased and pathological reflexes may be caused. Oculomotor disorders are often observed - ptosis, abducens nerve paresis, convergence insufficiency; in some cases, optic nerve atrophy, Argyll Robertson's sign, narrowing of visual fields and decreased visual acuity were observed. Sensitive disorders, as a rule, are not detected.
One of the characteristic signs of cerebellar ataxia is mental changes, manifested in a decrease in intelligence, sometimes depressive states. The disease is characterized by great clinical variability, both between different families and within the same family. Rudimentary forms of the disease occur in many families; Extrapyramidal symptoms are sometimes observed. Numerous transitional forms between cerebellar ataxia and Friedreich's ataxia have also been described.
The average age of onset of the disease is 34 years, in some families there is an earlier onset in subsequent generations. The course of the disease is steadily progressive. As with Friedreich's ataxia, various infections and other exogenous hazards have an adverse effect on the manifestation and course of the disease.

The differential diagnosis between cerebellar ataxia and Friedreich's ataxia is very difficult. The main distinguishing features between these diseases are the nature of inheritance (dominant in cerebellar and recessive in Friedreich's ataxia) and the state of tendon reflexes, which are absent or decreased in Friedreich's ataxia and increased in cerebellar ataxia. In addition, with cerebellar ataxia there is a later onset of the disease, bone deformations and sensory disorders characteristic of Friedreich's ataxia are rare, and dementia and oculomotor disorders are much more common.
Treatment is symptomatic.

Multiple sclerosis- a chronic demyelinating disease characterized by signs of multifocal damage to the nervous system, occurring with exacerbations (exacerbations) and remissions, or progressively. It was first described as a nosological form by J. Charcot in 1866. Frequency diseases in the CIS range from 2-7 per 10,000 population. There is a clear geographical dependence: in the equatorial countries of the CIS it is rare, and with distance from the equator to the north, the frequency of the disease increases. For example, in the northern regions of the United States, the prevalence of multiple sclerosis exceeds 10 per 10,000 people, while in the southern regions it is only 2 per 10,000 inhabitants. Women get sick almost 2 times more often.
Causes of development of multiple sclerosis . Multiple sclerosis is considered a polyetiological disease. There are several theories about the etiology of multiple sclerosis. A viral infection (retroviruses, human herpes virus-6, paramyxoviruses, measles, canine distemper; coronaviruses, adenoviruses, etc.) damages oligodendroglia, then an immune reaction is triggered to the myelin breakdown products and to the viruses themselves, which causes an exacerbation of clinical manifestations. Invading the nervous system, the virus exists latently in it, as happens with so-called slow infections (persists), and manifests itself only after a long period of time. incubation period. An increase in the synthesis of antibodies to viral and other antigens is a reflection of the defective immune status of the patient's body. To realize the pathogenic properties of the putative virus, the action of a number of additional factors is necessary, in particular a constitutional genetic predisposition to the disease and allergies.

Bacterial infection has similar antigens; under the influence of high temperature, proteins acquire irreversible changes and trigger a cascade of cytokine reactions that lead to demyelination.
Symptoms of Multiple Sclerosis . The disease occurs mainly between the ages of 15 and 40, less often in childhood and old age.
The onset of clinical manifestations is often imperceptible and monosymptomatic. Sometimes multiple sclerosis occurs acutely and manifests itself with multiple neurological symptoms. Most often, the first symptoms of the disease are signs of damage optic nerve(retrobulbar neuritis): a feeling of blurred vision, transient blindness, decreased visual acuity, scotomas. The disease can begin with oculomotor disorders (diplopia, strabismus), unstable pyramidal symptoms (central mono-, hemi- or paraparesis with high deep reflexes, clonus of the feet, pathological foot and hand signs), cerebellar disorders (unsteadiness when walking, intentional tremors), disorders sensitivity in the limbs (numbness, paresthesia). Much less frequently, the first signs of the disease may be dysfunction of the pelvic organs (urinary retention, urgency), autonomic-vascular dystonia, lesions of the facial, trigeminal and bulbar nerves. In women, the menstrual cycle may be disrupted, and in men, impotence develops.

A characteristic early (but not obligatory) sign of the disease is a decrease or disappearance of abdominal reflexes. Unlike other diseases of the nervous system, with repeated exacerbations of the disease, new symptoms arise. Impaired cognitive functions appear in the later stages of the disease, often in the form of emotional instability, euphoria or depression, irritability, lethargy, apathy, decreased intelligence of varying degrees, up to dementia.
Epileptic seizures in multiple sclerosis are observed rarely, more often in the form of emotional instability, euphoria or depression, irritability, lethargy, apathy, decreased intelligence of varying degrees, up to dementia.
Depending on the predominant localization of multiple sclerosis plaques, the following clinical forms of the disease are distinguished: cerebral, cerebrospinal, cerebellar, brainstem, spinal, and optical.
Occurs in almost half of all cases cerebrospinal a form characterized by multifocal lesions already in the initial stage of the disease, symptoms of damage to the coordination and pyramidal systems in the brain and spinal cord, as well as visual, oculomotor, vestibular and other systems.
Cerebellar form is more often manifested by symptoms of damage to the brain stem and cerebellum, less often - only by cerebellar symptoms: scanned speech, horizontal, vertical, rotatory large-sweeping nystagmus, adiadochokinesis, dysmetria, ataxia, intentional tremor in the upper and lower limbs, handwriting disorders. In advanced stages, intentional trembling becomes pronounced and takes on the character of hyperkinesis, which is more noticeable in the arms and legs, less so in the torso and head. Severe tremors made it possible to identify these cases as a hyperkinetic form of multiple sclerosis.
Rarely found acute stem form of multiple sclerosis with a rapidly progressing course and even death. The disease develops acutely at normal or elevated body temperature within 1-2 days. Against the background of headache with vomiting, symptoms of dysfunction of the brain stem and cerebellum are revealed.
At optical form The leading clinical symptom is a decrease in visual acuity, which recovers after some time on its own or with treatment. In the future, similar phenomena may develop in the other eye. Less commonly, vision in both eyes decreases at the same time. Ophthalmoscopy reveals signs of retrobulbar neuritis: blanching of the optic disc, especially its temporal side, narrowing of the visual fields (initially to red and green), scotomas.
Spinal shape characterized by symptoms of spinal cord damage at various levels. The leading clinical picture is lower spastic paraparesis, conduction sensitivity disorders, and pelvic disorders of varying severity.
Isolated clinical forms of multiple sclerosis in their pure form are rare. Usually, against the background of the dominant syndrome, other focal symptoms can be found, the severity of which is much weaker.
Diagnosis and differential diagnosis .
The polymorphism of clinical manifestations of multiple sclerosis causes significant difficulties in early diagnosis. Its important criteria are: onset of the disease at an early age; detection of clinical symptoms indicating damage to at least 2-3 systems (for example, cerebellar, pyramidal, oculomotor, etc.); inconsistency, “flickering” of symptoms even throughout the day, as well as a discrepancy between the severity of dysfunction and objective signs of damage to the nervous system (for example, against the background of high deep reflexes and bright pathological pyramidal signs, there is sufficient muscle strength); a wave-like course of the disease, manifested by periods of exacerbations and remissions with varying degrees of organic damage to the nervous system, variability of symptoms and often their complete reversibility at the onset of the disease (even without treatment).

Treat multiple sclerosis we need to start as early as possible. In therapy, there are several groups of drugs that suppress the activity of the immune system and promote the restoration of nerve sheaths. IN last years The list of these drugs is progressively expanding:

• firstly, this is a group of hormonal anti-inflammatory drugs - corticosteroids and corticotropic hormone
• secondly, drugs acting directly on the cells of the immune system - immunosuppressors and interferons
• thirdly, substances that improve the conduction of nerve impulses and the nutrition of neurons - biopolymers, non-steroidal anti-inflammatory drugs.
  The complex of therapeutic measures also includes plasmapheresis, massage, prevention of inflammatory complications of the skin, respiratory and urinary tract.

Parkinson's disease. The disease was first described by J. Parkinson in 1817. The incidence of parkinsonism in Europe is 1% among the population under 60 years of age,
5-10% in the group of 60-80 years, over 20% after 80 years and ranges from 60 to 140 cases per 100,000 population.
The type of inheritance for the main family forms is dominant, for rare juvenile variants it is autosomal recessive. In addition to these familial forms (primary parkinsonism, Parkinson's disease), secondary (symptomatic) parkinsonism is distinguished. Secondary parkinsonism can be caused by inflammatory diseases of the brain, atherosclerosis, intoxication, and taking neuroprotective drugs. The Parkinsonian symptom complex often complements the clinical manifestations of other hereditary diseases: the juvenile form of Huntington's chorea, hepatocerebral dystrophy. According to the Moscow Institute of Neurology, among those examined, primary parkinsonism accounts for 50.2% of cases.
ev, atherosclerotic - 34.1%, postencephalitic - 10%, other forms - 5.7%.

The pathogenesis of the disease is associated with degenerative processes in the substantia nigra, causing a decrease in the production of dopamine H and, accordingly, an imbalance of neurotransmitter metabolism. Importance is given to the relative increase in cholinergic activation.

Clinical picture. Key diagnostic signs of the disease:

1) the presence of two of the three main symptoms during the year: plastic rigidity, hypokinesia (akinesia), tremor.

K. secondary symptoms that usually occur during the disease include a shuffling gait, a mask-like face, monotonous quiet speech, micrographia, etc.;

2) unilateral appearance of these symptoms in the first stages of the disease;

3) availability of information about the family nature of the disorder;

4) absence of signs of other diseases (including instrumental ones) that have akinetic manifestations in their clinical picture;

5) high effect of DOPA-containing drugs (lasting at least a year).

Diagnostics. There are no specific instrumental and laboratory criteria.

Differential diagnosis is carried out with the diseases listed above.

Treatment. There are several groups of drugs that do not change the progression of the disease, but reduce akinetic manifestations.

Central anticholinergics that block M-cholinergic receptors in the central nervous system: cyclodol, parkopan, dynesin, tropacin, norakin, amedine and other drugs are prescribed in gradually increasing doses. Their use in older people is limited. The side effect is manifested by dry mouth, impaired accommodation, constipation, and sometimes urinary retention.

Midantan (amantadine) stimulates the release of dopamine from presynaptic terminals. When changing at a dose of 100-300 mg/day. Combined with anticholinergics.

Tricyclic antidepressants (amitriptyline, imipramine) reduce the reuptake of dopamine from synaptic spaces and have anticholinergic activity. Prescribed in moderate, gradually increasing doses (imipramine- up to 40 mg/day, amitriptyline- up to 100 mg/day).

Monoamine oxidase inhibitors (MAO) - Yumex (selegiline, L-denpeHlIL) a selective MAO inhibitor, can be prescribed, unlike other MAO inhibitors, in combination with L-DOPA preparations.

Of the group of drugs containing L-DOPA, the best are those that, in addition to L-DOPA, contain decarboxylase inhibitors that reduce the peripheral effect and increase the concentration of L-DOPA in the blood plasma - nakom, sinemet, modopar. They are prescribed in slowly increasing doses, the average therapeutic dose is 700-1000 mg/day. Currently there are ana-
logical long-acting drugs: sinimet CR, nakom CR, madopar HB5.

Dopamine receptor agonists are used paryaodel (bromocriptine, pergolide) and non-ergoline derivatives (ropinerol or dostinex)- drugs that can directly stimulate dopamine receptors.
Treatment begins with 1.25 mg after dinner, the average therapeutic dose is 30 mg/day.

Patients are recommended to undergo mandatory physical therapy, massage courses, and restorative therapy. The benefits of neurosurgical treatment have not been proven. On average, after 3-6 years, resistance to drug therapy accompanied by side effects.

Cerebral palsy (CP).
A group of diseases arising in the perinatal period, with different etiology, pathogenesis and a common clinical sign in the form movement disorders.

The cause of the disease can be a wide variety of adverse effects on the fetus during pregnancy: abdominal trauma, toxicosis, fetal asphyxia, viral diseases in a pregnant woman, intracerebral hematoma of the fetus. Symptoms of the disease appear from birth. Depending on their nature, the treatment provided, and the influence of additional harmful factors, they may increase, decrease, or remain at the same level.

There are four main clinical forms: diplegic, hemiplegic, hyperkinetic and cerebellar.

Diplegic form (Little's disease) occurs mainly as a result of birth trauma or asphyxia. The upper parts of the precentral gyri are affected, which entails the development of spastic paresis (para-
liches) legs. This is manifested by the child's inactivity during swaddling and bathing. The child's legs are brought one to the other, crossed, the feet are bent, the tone in them is sharply increased. Children develop poorly physically; they begin to hold their heads up, roll over, sit, and walk late. When trying to walk, the legs are straightened as much as possible, pressed against each other, the foot is placed on the tips
fingers.

Hemiplegic form characterized by unilateral or bilateral (tetraplegic) spastic paralysis. In such children, the motor functions of all limbs or the limbs of one half of the body are impaired.

Hyperkinetic form manifests itself in various types of hyperkinesis: congenital chorea, congenital double athetosis, atypical hyperkinesis, mixed rigid-hyperkinetic and combining hyperkinesis and paresis. Patients are sometimes unable to independently perform any actions due to hyperkinesis and paresis.

Cerebellar form is caused by damage to the cerebellum and is expressed by impaired coordination, muscle hypotonia, and scanned speech.

In all forms of cerebral palsy, damage to the cranial nerves and sensitivity may occur. Intelligence suffers to varying degrees - from mental retardation to idiocy.

Treatment. It should start as early as possible, be systematic, long-term, comprehensive, combine physical therapy, massage, physiotherapy
effects, orthopedic means. Exercise therapy and massage are carried out 1-2 times a day for 40-50 minutes systematically for a number of years. The parents of the sick child should be trained in the technique of performing them.

Drug treatment is aimed at reducing muscle tone (mellictin, mydocalm, baclofen), reduction, hyperkinesis (dynesin, metamyel, iclodol, haloperidol), improvement of intracerebral metabolism (nootropil, ierebrolysin, pyraietam, vitamins). Physiotherapeutic treatment consists of thermal procedures, baths, and electrical stimulation. In the presence of contractures, orthopedic treatment methods, including surgical ones, are used.
Basic principles of physical rehabilitation for cerebral palsy.

1. Ontogenetic approach.

2. Pathophysiological approach.

3. Compliance with the level of functional state.

4. Strict consistency and phasing.

5. Continuity.

6. Complexity.

Rehabilitation (habilitation) program for patients with cerebral palsy:

* Drug therapy.

* Physiotherapeutic treatment: thermal procedures, medicinal electrophoresis, magnetic and magnetic vibration therapy; compression massage; electrical stimulation of affected muscles; D" Arsonval currents; therapeutic swimming, pearl baths, hydromassage.

* Kinesiotherapy: therapeutic exercises (group, individual, passive, active), breathing exercises, sedentary/active games, biofeedback.

* Use of technical means and exercise equipment: wall bars, orthopedic ball, hanging supports to facilitate movements, walkers, parallel bars, special exercise equipment.

* Various types of therapeutic massage.

* Targeted orthopedic-surgical treatment: positional treatment (positioning and stretching), use of orthotic products (static, dynamic and functional), therapeutic prosthetics, staged casting, surgical treatment.

* Various types of reflexology. * Manual therapy. * Logotherapy, * Corrective pedagogy. * Occupational therapy. * Music therapy. * Classes with a psychologist. * Methods of sensory correction.

Spasmodic torticollis, cervical dystonia- dystonic disease, a type of torticollis in which incorrect head position is caused by pathological tension of the neck muscles.

Symptoms The first symptoms of the disease usually appear between 30 and 50 years of age. Over time, the affected muscles hypertrophy, and a stable restriction of movement occurs. The antagonist muscles responsible for movement in the other direction atrophy.

Causes: Most cases of spasmodic torticollis are independent (idiopathic). Symptomatic dystonia is possible as the onset of generalized torsion dystonia (in children), Wilson-Konovalov disease or as a response to the administration of neuroleptics, as well as due to rickets, fusion, fractures and dislocations of the cervical vertebrae, injuries to the neck muscles, neuralgia of the occipital nerves, with tumors, scars in the neck area, as well as in cases of deforming spondylosis and osteochondrosis of the cervical spine.

Treatment: Spastic torticollis is very difficult to treat. A positive, but often only temporary effect can be achieved with the help of anticholinergic drugs. The current standard of treatment is injection of botulinum toxin into the affected muscle. They cause temporary muscle damage over several weeks, returning the head to the correct position and stopping the pain. In extreme cases, surgical treatment is required.

Amyotrophic lateral sclerosis. The disease is caused by systemic damage to central and peripheral motor neurons. Unlike multiple sclerosis, morphological examination does not reveal inflammatory changes (edema, infiltration, hyperemia) in areas of damage to the nervous system. Therefore, the pathomorphological process is defined as degenerative.

The etiology of the disease is not fully understood. It is believed that it is caused by a genetic deficiency of the immune system, neurotropic viruses and other factors that weaken the body. Men get sick 13 3-4 times more often than women, the incidence rate is 1.4-6 cases per 100,000 population.

Clinical picture. Clinical manifestations are caused by a combination of flaccid peripheral and central spastic paralysis of the limbs, bulbar disorders (dysphagia, dysphonia, impaired pharyngeal and palatal reflexes). 1-2 years before the development of paresis in patients can be observed fasciculations(muscle twitching in various parts of the body). There are various clinical forms: with predominantly damage to the anterior horns of the spinal cord, pyramidal tracts, nuclei IX, X, CN of cranial nerve pairs, mixed

The disease progresses slowly, lasting on average 3-1 O years and ending in death.

Diagnostics. Based on clinical signs, laboratory diagnostics are not available. Additional information is provided by myography, which determines the level of damage to the motor system.

Treatment. General strengthening drugs and physiotherapy are prescribed. In the later stages of the disease, patients need care: tube feeding, prevention of bedsores, congestive pneumonia, sepsis.

Syringomyelia. It is a chronic progressive disease characterized by the formation of cavities in the gray matter of the brain (trunk) and spinal cord.

Several etiological and pathogenetic options for the development of the disease are currently being discussed. There are two leading hypotheses. The first (gliotic) hypothesis considers syringomyelia as a consequence of a disrupted process of transformation of the germinal ectodermal cells, from which nervous tissue is formed, into neuroblasts. According to this theory, part of the nucleation
neck tissue remains in its original form (keratinizing epithelium) and, gradually growing, forms foci inside the brain that have a destructive effect on neurons and their processes of the spinal cord and brain stem. If these foci are located in the area of ​​the central spinal canal, then they are gradually filled with cerebrospinal fluid, as the epidermal mass is gradually washed away, and cavities with ectodermal walls are formed. The cells of these walls, 13 in turn, also become keratinized and washed away by the cerebrospinal fluid. the cavity increases
destroying functionally active nervous tissue. With this variant of syringomyelia, MRI studies reveal non-communicating forms, in which the formed cavities do not communicate with the central canal of the spinal cord.

According to the second (hydrodynamic) theory, the main cause of syringomyelia is considered to be a defect in the embryonic development of the liquor channels
spinal cord and ventricles of the brain stem. With these forms of the disease, other malformations and, in particular, developmental anomalies in the area of ​​the foramen magnum (Arnold Chiari malformation) are more common (up to 80% of cases). The resulting difficulties in the outflow of cerebrospinal fluid from IV ventricle into the subarachnoid space leads to an increase in cerebrospinal fluid pressure in the central canal of the spinal cord and its expansion. Rupture of the walls of the central canal leads, in turn, to the appearance of cavities located parallel to the central canal (communicating form). Factors contributing to the occurrence of clinical manifestations of the disease are injuries, infections, and heavy physical labor. As already noted, in addition to defects of the nervous system, malformations of other organs and systems are detected in patients with syringomyelia.

Clinical picture. The clinical picture consists of four groups of symptoms: sensitivity disorders, motor disorders, disorders of autonomic regulation, malformations of other organs and systems.

Sensitivity disorders are determined by the fact that at the locations of the cavities, cerebrospinal fluid and glial formations exert increased pressure on the gray matter of the spinal cord, disrupting metabolic processes and leading to the destruction of neurons. The disorders manifest themselves predominantly as a decrease in pain and temperature sensitivity according to the segmental type. Due to a decrease in temperature sensitivity, patients get burns, which is often the first time they visit a doctor.

Over time, foci of gliosis or enlarging cavities gradually destroy the anterior and then the lateral horns of the spinal cord and the lateral cords, which causes the appearance of motor and trophic disorders.

Movement disorders represented by peripheral and central paresis, with damage to the medulla oblongata - speech and swallowing disorders.

Autonomic disorders caused by destruction of the lateral horns of the spinal cord. For this reason, patients experience trophic ulcers on the skin, destruction of joints (argropathy), pallor, cyanosis of the skin,
intolerance to ultraviolet rays.

As part of the dysraphic status, a wide variety of developmental defects are identified: cleft lip, cleft palate, reduced or increased number of fingers on the limbs, their fusion, malformations of the heart, lungs, etc.

Diagnostics. Based on the specifics of the clinical picture, data computed tomography. On tomograms one can see syringomyelitic cavities, glial foci, foci of keratinizing epithelium inside the spinal cord and medulla oblongata.

Developmental defects also include hydrocephalus, cerebral hernias, anomalies of the skull, etc.

Treatment. Predominantly symptomatic treatment is carried out, aimed at improving metabolic processes in the nervous system (vitamins, nootropic drugs), improving the conductivity of nerve impulses with flaccid paresis (prozerin, dibazol, electrophoresis of these preparations
ratov), ​​hydrogen sulfide, radon baths. In the presence of large cavities and impaired outflow of cerebrospinal fluid (according to computed tomography), attempts are made at reconstructive neurosurgical operations. In gliosis forms proven using neuro-
visualization (M RT), radiotherapy is used. When caring for patients and performing physiotherapeutic procedures, it is necessary to remember the danger of burns and other injuries due to impaired skin temperature and pain sensitivity. Patients with syringomyelia are contraindicated from working near hot springs or heavy physical labor.

When identifying signs of hereditary
diseases, mid-level medical workers are obliged to refer them to a consultation with a general practitioner or neurologist, and subsequently carry out treatment or rehabilitation instructions.

Myasthenia gravis- a group of diseases of the nervous and muscular systems, manifested by weakness and increased fatigue of various muscle groups. This disease affects the motor system in the area of ​​the myoneural synapse. Any muscle in the body can be involved, but there is a tendency for the muscles of the face, lips, eyes, tongue, throat and neck to be predominantly affected. In typical cases, the disease begins at a young age. Women get sick 2 times more often than men.

Etiology and pathogenesis
The disease is autoimmune. There is often a combination of myasthenia gravis with hyperplasia or tumor thymus gland. Myasthenic syndromes are sometimes observed in organic diseases of the nervous system (amyotrophic lateral sclerosis, etc.), poly- and dermatomyositis, as well as cancer of the lung, breast, ovary, and prostate gland.
Clinical picture
It usually presents with muscle fatigue with associated weakness, especially of the eye and muscles innervated by the bulbar nerves. Weakness eye muscles leads to diplopia and strabismus, unilateral or bilateral ptosis of the upper eyelids, most pronounced towards the end of the day. Weakness of the facial and chewing muscles is often noted. Difficulties in speaking and swallowing can be detected after more or less prolonged talking and eating. Possible weakness and fatigue of the tongue muscles, nasal tone of voice. Other striated muscles of the limbs and neck may also be affected, resulting in generalized weakness. The exhaustion of deep reflexes is determined with a decrease in reaction when the tendon is repeatedly struck with a hammer. With repeated electrical stimulation, unusual muscle fatigue and a pronounced ability to recover after a short rest are revealed. Characterized by lability, dynamic symptoms with their intensification when reading, fixating gaze, sometimes general physical activity. Myasthenia gravis can be generalized and local (damage to the muscles of the eyes, pharynx, larynx, facial muscles or trunk muscles). The generalized form may be accompanied by respiratory disorders.
Flow
The disease is progressing. Myasthenic episodes (short-term myasthenic disorders and long-term spontaneous remissions) and myasthenic states (stable manifestations over a significant period) are possible. In patients with myasthenia gravis, a sharp deterioration in the condition may occur in the form of a crisis with generalized muscle weakness, oculomotor and bulbar symptoms (aphonia, dysarthria, dysphagia), respiratory disorders, psychomotor agitation followed by lethargy, as well as autonomic disorders. In this case, acute hypoxia of the brain (disorder of consciousness) develops. Possible death.
Treatment
Aimed at correcting the relative deficiency of acetylcholine and suppressing the autoimmune process. To compensate for disorders of neuromuscular transmission, anticholinesterase drugs are used: proserin, oxazil, kalimin. It is important to choose the optimal individual compensating dose depending on the clinical form, severity of symptoms, concomitant diseases, reactions to the drug. For pharyngeal-facial and ocular forms of myasthenia, pyridostigmine bromide is more effective, for myasthenic weakness of skeletal muscles - prozerin and oxazil. Doses of drugs and dosage intervals are individual. Prescribe potassium chloride or orotate, veroshpirone, ephedrine. In very severe cases, prozerin is administered parenterally (1.5-2 ml of 0.05% solution intramuscularly) 20-30 minutes before meals. Taking large doses of anticholinesterase drugs can lead to a cholinergic crisis. The main treatment for this crisis is the withdrawal of anticholinergic drugs and repeated administration of atropine (0.5 ml of a 0.1% solution intravenously or subcutaneously). In severe cases, a cholinesterase reactivator (1 ml of 15% dipyroxime solution) can be prescribed.
At myasthenic crisis resulting from an insufficient dose of anticholinesterase drugs, proserin is urgently administered intravenously (0.5-1 ml of 0.05% solution) and intramuscularly (2-3 ml every 2-3 hours). Oxazil can be administered in suppositories. A 5% solution of ephedrine is also used subcutaneously and potassium preparations intravenously. Progressive and life-threatening weakness respiratory muscles may be observed despite the administration of large amounts of proserin. Patients are intubated or tracheostomized and transferred to mechanical ventilation using breathing apparatus. Patients are fed through a nasogastric tube. It is necessary to maintain the balance of fluids and electrolytes, vitamins; according to indications (metabolic acidosis), a 1% solution of sodium bicarbonate is administered intravenously.

The main methods of pathogenetic treatment of patients with myasthenia gravis are thymectomy, radiotherapy and hormone therapy. The surgical method (thymectomy) is indicated for all patients under the age of 60 who suffer from myasthenia gravis, but are in satisfactory condition. It is absolutely indicated for tumors of the thymus gland. X-ray therapy to the area of ​​this gland is prescribed for the remainder of its tissue after thymectomy, for the ocular form of myasthenia, and also if there are contraindications to surgery in elderly patients with a generalized form of myasthenia. In severe cases - with generalized myasthenia - treatment with immunosuppressive drugs is indicated. Corticosteroids are prescribed, preferably prednisolone (100 mg every other day). The duration of the maximum dose of corticosteroids is limited to the onset of significant improvement, which allows the dose to be subsequently reduced to a maintenance dose.
Forecast
Spontaneous remissions are possible, but as a rule, exacerbation occurs. Pregnancy usually causes improvement, although there is also an increase in existing disorders. Myasthenic crises may occur with death due to respiratory failure. Overdose of anticholinesterase drugs can cause muscle weakness resembling myasthenic crisis. Early use of intubation or tracheostomy in combination with mechanical ventilation has reduced mortality in myasthenic crisis with acute respiratory failure.
Myopathies (primary progressive muscular dystrophies).
Myopathies is a group of hereditary diseases manifested by muscle weakness and muscle atrophy. Progressive myopathies are called myodystrophies. The most common forms of myopathies are the Duchenne form, the Erb form (pelvis-brachial), and the Landouzy-Dejerine form (scapulohumeral-facial myopathy).

Duchenne myopathy- the disease was described by Duchenne in 1853. The incidence is 3.3 per 100,000 population. Inherited in a recessive manner associated with the X chromosome. In the vast majority of cases, boys are affected.

The first signs of the disease appear for the first time 1-3 years of a child’s life. In the first year of life, children begin to lag behind in motor development. With a delay they begin to sit, walk, and get up. Their movements are awkward, they often stumble and fall. At 2-3 summer age Pathological muscle fatigue is revealed, problems arise when climbing stairs, the gait changes and takes on a “duck” type. Children walk, waddling from side to side. It is typical to get up from a squatting position or from a lying position. Rising occurs gradually with the active use of hands. This is called “climbing the ladder” or “climbing by yourself.” Symmetrical atrophy of the muscles of the proximal limbs appears, first the lower, then the upper. The muscles of the pelvic girdle and hips undergo atrophy; after 1-3 years, atrophy of the muscles of the shoulder girdle and back muscles are added. Symptoms characteristic of myopathies appear: a wasp waist, wing-shaped shoulder blades moving away from the chest, hyperlordosis in the lumbar region spine. The pathognomonic symptom for this disease is pseudohypertrophy calf muscles. The muscles are increased in volume, dense to the touch, painless, but muscle strength is reduced. The increase in muscle volume is due to the deposition of adipose tissue between muscle fibers. Over time, contractures and retractions develop in the affected muscles. Muscle tone in the affected muscle groups is reduced. The knee reflexes disappear first, then the reflexes from the biceps and triceps tendons decrease and disappear. Achilles reflexes remain intact for a long time. In addition, dystrophic changes in the osteoarticular system are characteristic. Characteristic deformities of the feet and spine. Changes in the cardiovascular system are detected: pulse lability, arterial hypertension, dullness of sounds, expansion of the boundaries of the heart, changes in the ECG are possible. Among neuroendocrine disorders, the development of Itsenko-Cushing syndrome is possible. Flow of this disease progressive and malignant. By the age of 7-10 years, significant motor defects arise, and by the age of 14, patients are completely immobilized.
Diagnostics is carried out on the basis of clinical picture data and the study of genealogy, although spontaneous mutation is possible in a third of cases. A biochemical study reveals an increase in the activity of Creatine phosphokinase (CPK) 30-50 times higher than normal. Erb-Roth myopathy (pelvis-brachial form).
The incidence is 1.5 per 100,000 population. Inherited in an autosomal recessive manner.
The disease begins at 14-16 years of age. Occurs with equal frequency in boys and girls. There are cases of onset of the disease at 5-10 years of age. Initially, the muscles of the shoulder or pelvic girdle undergo atrophy. Depending on this, ascending and descending types of disease development are distinguished. Symptoms of a wasp waist, duck gait, winged shoulder blades, and hyperlordosis in the lumbar spine appear. To a lesser extent than with the Duchenne form, the appearance of contractures and pseudohypertrophies is characteristic. Tendon reflexes are reduced.
The course of the disease is most often slowly progressive. However, cases with a malignant course are also described.
Diagnostics based on clinical data, the age of patients is 14-16 years old, the genealogy of patients is studied. CPK is either not increased or moderately increased.
An EMG reveals signs of primary muscle damage.
Treatment myopathies is aimed at preserving and maintaining the motor activity of patients for as long as possible long period time.

Exercise therapy plays a special role in this process. It allows you to delay the immobility of patients. Training begins as early as possible. The patient and his relatives are taught a set of exercises. Exercise therapy classes prevent the development of contractures and deformities. Exercises are performed on range of motion, correction of body position in bed, chair, frequent changes of position and posture. Early use of splints is practiced. It is recommended to monitor the weight of patients. Excess weight impairs motor functions. From medications ATP, B vitamins, vitamin E, anabolic steroids (retabolil, nerobol) are prescribed.
Treatment can slow down the course of the pathological process, but it is currently impossible to cure patients with myopathy.
Myotonia is a disease characterized by impaired muscle tone in the form of slower muscle relaxation after active contraction.
Described by Leiden in 1874. In 1876, Thomsen, using the example of his family, drew attention to the hereditary nature of this disease.
The frequency of occurrence is 0.3-0.7 per 100,000 population. The type of inheritance is autosomal dominant.
The first signs of the disease appear at the age of 8-15 years. Myotonic spasms are localized in various muscle groups, most often in the muscles of the hand, legs, masticatory muscles, circular muscles of the eye. Strong clenching of the hand into a fist, or clenching of the jaw, or tightly closing the eyes, or standing for a long time causes tonic spasms. The muscle relaxation phase is delayed for a long time. Patients cannot quickly open their hands, jaws or open their eyes. Repeated movements reduce myotonic spasms.
There are several typical techniques:
-Tapping the thenar muscles with a hammer causes adduction of the thumb. -----When you hit the tongue, a pit appears in the tongue;
-When a large muscle (biceps) is hit, a roller appears.
The appearance of patients resembles athletes. The muscles are dense, hard, and their strength is at the same time reduced. Tendon reflexes are normal, in some cases reduced.
The course of the disease is slowly progressive.
Treatment. Diphenin is prescribed 0.1-0.2 3 times a day for 2-3 weeks. Diacarb 0.125 2 times a day for 2-3 weeks. It is assumed that diphenine has an inhibitory effect on polysynaptic conduction in the central nervous system, and diacarb changes membrane permeability.

Group toxic damage to the nervous system (neurotoxicosis) very diverse. Neurotoxicoses occur under the influence of many chemical factors at work and at home. If symptoms of damage to the nervous system develop over several hours or days, neurotoxicosis is called acute. With prolonged exposure to a toxic factor and a slow increase in symptoms, neurotoxicosis is assessed as chronic. There are exogenous (the toxic agent comes from outside) and encogenic (the toxic agent occurs in the body itself due to metabolic disorders) toxicoses.

Carbon monoxide poisoning). More often it is acute. In industrial conditions, poisoning can occur in people working in coal burning, in garages, at home - in houses with stove heating, bathhouses,
garages.

Clinical picture. The first stage of poisoning is characterized by headache, dizziness, tinnitus, less often - vomiting, drowsiness, decreased visual acuity and hearing.

At the second stage, weakness increases sharply, the person loses the ability to move. The skin, especially the hands, feet, nose, ears, and then the whole body, suddenly turns pale. In the third stage, pathological drowsiness, stupor, and coma occur. Blood pressure drops against the background of tachycardia, and slow, shallow breathing develops. If help is not provided, death may occur.

Treatment. First aid consists of moving the patient to fresh air. It is necessary to evacuate the patient and administer 100% oxygen. In case of severe poisoning, hyperbaric oxygen therapy is performed. To reduce tissue oxygen requirements, tranquilizers are prescribed, and patients are provided with rest. With hyperthermia, body temperature is reduced. When parkinsonism occurs, dopamine receptor stimulants (bromocriptine, pronoran, mirapex) are prescribed.

Poisoning with methyl alcohol (methanol)). Occurs when ingested or when its vapors are inhaled. In terms of smell and color, methyl alcohol is practically no different from ethyl alcohol, which can be the reason for its erroneous use.

Clinical picture. At the early stage of poisoning, sensations resemble those when drinking ethyl alcohol (vodka): dizziness, unsteady gait, slurred speech, euphoria, drowsiness. With a large dose
collapse may develop, preceded by headache, abdominal pain, vomiting, flies before the eyes, loss of vision, motor agitation, and pale skin. A specific symptom is a decrease in visual acuity, which rapidly progresses and often develops complete blindness. The pupils are dilated. In the fundus, swelling and hemorrhage are initially observed, and then optic nerve atrophy develops.

Treatment. First aid consists of gastric lavage 2% solution of soda (sodium bicarbonate). administered intravenously in a medical facility 100 ml 30% ethyl alcohol, and then at intervals of two hours more
50 ml of ethyl alcohol 4-5 times. 8 large amounts of fluid are administered intravenously or orally (saline solution, hemodez, 5% glucose solution), diuretics, electrolyte balance is monitored and regulated. In case of severe poisoning, hemosorption is carried out.

Prevention. It consists of being careful when working with methyl alcohol and informing workers about the consequences of poisoning. The lethal dose of methanol for an adult is 30-100 ml.

Damage to the nervous system in chronic alcohol intoxication.

Alcoholic cerebellar ataxia (degeneration) considered one of the most common complications. Its development is associated with a lack of thiamine (vitamin B1). It occurs 11 times more often in men than in women. Morphologically
the disease is manifested by severe atrophy of the anterior lobes and the upper part of the cerebellar vermis, almost complete loss of neurons in their granular and molecular layers.

Clinical picture. Clinical criteria are ataxia, mainly in the legs, subacute or chronic development, and alcohol history. A positive effect was obtained from treatment with vitamin IN 1 more often in
combination with other neuroprotective therapy.

Diagnostics. Differential diagnosis is carried out with hereditary ataxias, cerebellar tumors, circulatory disorders in the basilar system, in which neuroimaging methods (CT, MRI) provide significant assistance.

Acute Gaye's encephalopathy - Wernicke has now become a fairly common disorder in people of different ages with varying degrees of alcohol abuse. In addition to or in addition to alcoholism, the disease can develop with fasting, uncontrollable vomiting, intestinal obstruction, intoxication with digitalis preparations, and the administration of large volumes of glucose to debilitated patients without vitamin B 1

Clinical picture. It consists of stupor or coma acutely occurring after or against the background of another binge, memory impairment, attention, orientation, nystagmus, paralysis of the oculomotor muscles, gaze paresis (horizontal and, less often, vertical), gait disturbances, ataxia in the limbs when performing special tests, hypothermia , arterial hypotension.
Neurological symptoms may be supplemented by delirious syndrome.

Diagnostics. Differential diagnosis is carried out with botulism, stroke in the brain stem, tumors in the posterior cranial fossa, intoxication with sedatives.

Treatment. Introduction in progress vitamin B, 50 mg intravenously and 50 mg intramuscularly in the first days, then 50 mg daily intramuscularly until nutrition normalizes. Other vitamins (multivitamins) and neuroprotective drugs are also prescribed, and high-calorie nutrition is adjusted. The prognosis depends on the severity of the disorder, with a mortality rate of 10-20%. 60% of surviving patients remain with neurological and intellectual impairments of varying degrees.

Alcoholic polyneuropathy is clinically identical to other forms of metabolic neuropathies and is diagnosed on the basis of clinical manifestations, anamnestic data indicating that the patient has
alcohol addiction, positive effect on the therapy, absence of signs of other diseases that can cause damage to peripheral nerves.
Treatment: it is necessary to prescribe B vitamins. Especially B1 at a dose of 50-100 mg per day. Ascorbic acid, strychnine, and antipsychotics are prescribed for delusional states. IN recovery period proserin, dibazol, physiotherapy.

Prevention of neurological disorders of alcohol origin consists in the fight against alcoholism.

Poisoning with sleeping pills,

They can occur with an overdose of drugs or deliberately, for the purpose of suicide, taking a large amount of medication.

Clinical picture. Clinical manifestations of poisoning by barbiturate-type hypnotics (luminal, phenobarbital, hexenal Etc.), tranquilizers (seduxen, elenium, phenazepam etc.), neuroleptics (aminazine, tiserin, etaparazine etc.) have a similar picture. At an early stage, increasing drowsiness, muscle weakness, unsteadiness of gait, muscle weakness, and weakened reflexes are noted. With large doses of poison, the development of a coma, liver and kidney damage is possible.
Death occurs due to symptoms of acute cardiac vascular insufficiency.

Treatment.

First aid appears in the same volume and sequence as in case of poisoning with OPV. In a medical institution, after gastric lavage, the victim is given a mixture containing 25 g of tannin, 50 g of activated carbon, 25 g of magnesium oxide (burnt magnesia), and after 10-15 minutes - a saline laxative.

The victim is prescribed: calcium gluconate(10% solution), calcium chloride(10% solution) 10 ML intravenously. For convulsions - diazepam 2-4 ml of 0.5% solution per 10 ml 0.9% sodium chloride intravenously. Forced diuresis is carried out under the control of the electrolyte composition of the blood, treatment of acute cardiovascular and acute renal failure.

Arsenic poisoningand its connections. Calcium arsenate, sodium arsenite, Parisian greens, etc. are used as pesticides for treating seeds and controlling agricultural pests. The lethal dose when taken orally is 0.06-0.2 g. After the poison enters the stomach, vomiting appears 2-8 hours later. green contents, metallic taste in the mouth, severe abdominal pain, loose frequent stools,
reminiscent of rice water. Repeated vomiting and diarrhea cause severe dehydration of the body, accompanied by convulsions. As intoxication progresses, acute renal and liver failure and anemia develop. Death occurs from acute cardiovascular failure and paralysis of the respiratory muscles.

Diagnostics is carried out on the detection of arsenic in urine, hair, and nails.

Treatment. First aid consists of immediate gastric lavage with water with a suspension of laxatives - magnesium oxide or sulfate (20 g per 1 liter of water). Treatment involves eliminating the source of intoxication. BAL preparations or penicillamine are administered at a dose of 250-750 mg per day for 4-6 days. In case of acute poisoning, BAL is administered parenterally at a dose of 2.5 mg per 1 kg of body weight.
Neuropathy caused by the action of FOS.
Contact with FOS occurs when substances are inhaled, i.e. through the lungs or when absorbed through a moistened skin surface. FOS have an inhibitory effect on cholinesterase. As a result, acetylcholine accumulates at the synapses of the CNS and PNS. This leads to overexcitation of the central nervous system and disruption of the conduction of nerve impulses. Most often, poisoning occurs with chlorophos, thiophos, etc.
Clinic: in acute poisoning, after a short incubation period, nausea, vomiting, headache, dizziness, sharp abdominal pain, increased sweating and salivation occur, and the pupils sharply constrict. Twitching of individual muscles, ataxia, arterial dystonia, and dysarthria are observed. In severe cases, fainting, disturbances of consciousness, hallucinations, delirium, angry mood, and aggression are possible. If the condition worsens, coma and death occur. In mild and moderate cases, when the condition improves after 1-2 months, polyneuropathy may develop. It is characterized by movement disorders accompanied by paresthesia. Myofibrillar twitching, atrophy of the hand muscles, and increased knee reflexes are observed. The picture resembles amyotrophic lateral sclerosis.
Treatment acute poisoning is reduced to intravenous administration of atropine 0.1% - 1-2 ml; treatment of polyneuropathy is carried out according to the basic principles of treatment of neuropathies.

()manipulation with mercury.

Clinical picture. Mercury and its compounds have local irritant, nephrotic, enterotoxic and neurotoxic effects. Entry into the body is possible through the lungs, gastrointestinal tract, and skin. Metallic mercury in the stomach and intestines is not entirely
.gvaetsya. When inhaling vapors, more than 75% of mercury is absorbed.

When poisoned by mercury vapor, a runny nose and tracheobronchitis develop, which can develop into severe pneumonia and toxic pulmonary edema within a few hours. At the same time, the victim experiences frequent loose stools and drowsiness. On the 3-4th day, the noted symptoms are accompanied by
signs of kidney damage are combined (oliguria, proteinuria, increased levels of urea and creatinine in the blood serum).

Treatment. In case of mercury vapor poisoning, toxic pneumonia and toxic pulmonary edema are treated. Antibiotics prescribed, 5% unithiol solution 1 O ml intramuscularly 2 times a day, forced diuresis is performed. At toxic edema lungs intravenously
100-150 mg is administered prednisolone, 100-150 ml 30% urea solution or 100 mg lasix. In case of sublimate poisoning, the stomach is washed again and activated charcoal is given. Intramuscularly administered unithiol(as in poisoning
mercury vapor). Intravenously administered 10% solution of thetaine-calcium 20 ml in 300 ml 5% glucose solution, sodium thiosulfate- 100 ml of 30% solution. Assign vitamin B/2 to 1000 mg/day.

Pachycarpine poisoning. It occurs more often in women when trying to use pachycarpine to terminate pregnancy, since it, being a ganglion blocker, can have a stimulating effect on the uterus. Highest therapeutic single dose of the drug
is 0.2 g, daily - 0.6 g.

Clinical picture. The first symptoms of poisoning appear 2-3 hours after taking pachycarpine. Dizziness, weakness, nausea, vomiting, coldness and numbness of the extremities, pallor, acrocyanosis, a feeling of lack of air, dilated pupils, impaired accommodation, pain in the lower abdomen appear. Women may experience bleeding from the vagina. As severity increases, stupor, stupor, and coma may develop. Often there is a short period of clonic-tonic convulsions. Cardiovascular disorders at an early stage are expressed in bradycardia, which is subsequently replaced by tachycardia and a drop in blood pressure. Intestinal paresis, stool and urination retention may develop.

Treatment. Urgent Care, as with other acute poisonings, it involves washing the stomach and intestines. Adjustable if necessary artificial respiration for the period of transportation with subsequent transfer to mechanical ventilation. As an intravenous antidote -
1 ml is injected dropwise 0.05% proserine solution for 500 ml physiological solution. IN inpatient conditions other measures are taken to maintain blood pressure, cardiac activity, and excretory functions.
Lead poisoning.

Neurological signs of volumetric processes in the brain can be reduced to three groups of symptoms: 1) focal symptoms; 2) symptoms of increased intracranial pressure; 3) symptoms of brain displacement.

Focal symptoms depend on the location of the tumor and are manifested by symptoms of irritation and loss. Symptoms of irritation- these are various forms of epileptic paroxysms: psychomotor, sensory
bodily, motor paroxysms, mental equivalents.

Symptoms of hair loss are associated with the destruction of brain centers and are manifested by paresis, paralysis, disturbances of sensitivity, coordination, speech, writing, and intellectual functions. In case of pituitary tumors, focal symptoms can conventionally include signs of hormonal disorders.

Symptoms of increased intracranial pressure(hypertension syndrome) manifested by headaches, nausea, vomiting, stiff neck, Kernig's and Brudzinski's symptoms.

Additional examinations reveal congestive optic discs, changes in craniograms (“finger impressions”, widening of the entrance to the sella turcica, thinning of the internal bone plate of the skull, in children - suture dehiscence), increased cerebrospinal fluid pressure during a spinal puncture.

Symptoms of displacement caused by an increase in the volume of intracranial fluid and tissue. Displacement of the brain may be accompanied by entrapment of the temporal lobe in the tentorium notch, or entrapment of the cerebellum in the foramen magnum. With displacement, meningeal syndrome increases, disorders of consciousness appear and increase, vision and swallowing are impaired, and vital functions are upset.

Some forms of tumors may occur without pronounced focal signs. With them, there is an increase in cerebral symptoms.

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Introduction

1. Alcohol (ethyl alcohol)

2. Methyl alcohol (methanol)

3. Barbiturates

4. Manganese

5. Carbon monoxide

6. Pesticides

8. Narcotic analgesics

9. Pahikarpin

10. Hydrogen sulfide

11. Gasoline

12. Botulism

Conclusion

Introduction

Intoxication of the nervous system is associated with the entry into the body of toxic substances used in industry, agriculture or in everyday life (solvents, insecticides, etc.). In other cases, it is a matter of taking excessive dosages or chronic use of medications or, finally, alcoholic beverages.

Pathological anatomy of nervous system intoxications

Pathological studies of acute poisoning with various poisons reveal a largely similar picture. Vascular dystonia, hyperemia, invagination of vascular walls, minor hemorrhages, and perivascular edema are noted. Blood clots are often found in small vessels, especially veins, focal macro- and micronecrosis, and swelling of the brain. At the same time, degeneration of nerve cells is detected, especially the cerebral cortex and the reticular formation of the brain stem, mainly in the form of acute and severe damage to Nissl bodies.

With chronic intoxication, changes in neurons are more diverse: there is both acute and chronic disease, a decrease in the number and volume of cells, or their deformation. Swelling phenomena are not uncommon. These and other changes in ganglion cells are combined with degenerative changes in glia. In some intoxications, phenomena of demyelination of conductors are detected. At the same time, with certain intoxications there is a predominant selectivity of the lesion, for example, the predominance of changes in the globus pallidus and substantia nigra in case of carbon monoxide poisoning, in the striatum in case of manganese poisoning, etc.

1. Alcohol (ethyl alcohol)

When drinking alcohol on an empty stomach, its maximum content in the blood is established after 40-80 minutes. Ethyl alcohol is not digested or neutralized by gastric juice. However, proteins and fats in the stomach delay its absorption. The entry of alcohol into the blood and saturation of organs and tissues with it occurs much faster than oxidation and excretion in unchanged form. The elimination phase lasts 5 - 12 hours. Ethyl alcohol can be determined in any environment of the body (blood, urine, etc.). Ethyl alcohol has a narcotic effect, the severity of which depends not only on the amount and speed of alcohol administration, but also on individual sensitivity. The latter is determined by constitutional factors, the psychophysical state of the body and the experience of previous alcohol consumption. Noticeable intoxication occurs when the blood alcohol content is 150 mg%, severe - 350 mg%, fatal - approximately 550 mg%.

The initial stages of alcohol intoxication are characterized by increased mental activity, but the performance of more subtle thinking processes (operator activity, etc.) is reduced. There is an activation of the muscular system, respiratory organs, and blood circulation with a simultaneous decrease in endurance during exercise.

Clinic for alcohol intoxication of the nervous system

The clinical picture of poisoning is characterized in the initial stage (intoxication stage) by a change in the emotional state in the form high mood simultaneously with a decrease in criticism of one’s condition and assessment of the environment (euphoria). Less commonly, depression or anger occurs. Ataxia, diplopia, and general hypoesthesia occur. As the dose of alcohol in the blood increases, a state of depression develops, turning into stupor, and then coma. Alcoholic coma is characterized by facial and conjunctival hyperemia, decreased body temperature, clammy, cold skin, repeated vomiting, and involuntary release of urine and feces. Neurological symptoms are variable: miosis, sometimes moderate mydriasis, often horizontal nystagmus. Increased muscle tone and trismus are replaced by muscle hypotonia and suppressed reflexes. Breathing is slow, with pauses and the appearance of pronounced cyanosis of the face, tachycardia; Arterial hypertension observed at the beginning gives way to collapse. Sometimes aspiration of vomit is observed with the development of laryngospasm. In some cases, generalized seizures occur.

The main complication of alcohol intoxication is aspiration-obstructive breathing disorders as a result of tongue retraction, trismus of the masticatory muscles, hypersalivation with aspiration of mucus and vomit, and bronchorrhea. Against the background of respiratory disorders, moderate arterial hypertension is observed, followed by hypotension and severe tachycardia. One of the dangerous complications of a coma caused by alcohol poisoning is myoglobinuria, which occurs as a result of prolonged positional pressure from one’s own body weight on certain muscle areas. Patients have pronounced swelling, circularly covering the limb, with a dense elastic, sometimes woody consistency. When one or another peripheral nerve is located within the altered tissue, a picture of sensory and motor loss in the area of ​​the corresponding nerve is possible.

Urine on days 1-2 is bloody or brownish-black. Laboratory testing reveals myoglobin. On the 2-4th day, the daily amount of urine decreases (to 100-400 ml), the level of residual nitrogen and urea increases, hyperkalemia, hemorrhagic syndrome, and hypochromic anemia develop.

Diagnosis of alcohol intoxication of the nervous system

The diagnosis of alcohol intoxication, in addition to its characteristic clinical picture, is confirmed by the alcoholic odor from the mouth and vomit, and the presence of alcohol in the blood. Alcoholic coma is not characterized by focal neurological symptoms, the presence of which suggests a combination of alcohol intoxication with traumatic brain injury or acute cerebrovascular accident. A similar assumption may also arise in the case of prolonged coma with low blood alcohol content. In all these cases, it is necessary, in addition to radiography of the skull, the use of echo-encephalographic examination and spinal puncture.

Treatment of alcohol intoxication of the nervous system

Abundant gastric lavage through a tube, followed by the introduction of saline laxatives: intravenous drip up to 600 ml of a 20% glucose solution with insulin (up to 20 units), 4% sodium bicarbonate solution - up to 1500 ml, furosemide, magnesium sulfate, vitamins. When blood pressure decreases, cardiovascular drugs are prescribed; for the prevention of aspiration pneumonia - antibiotics. Repeated administration of corticosteroid hormones is often necessary. In a comatose state - toilet of the oral cavity, suction of mucus from the upper respiratory tract, insertion of an air duct.

Chronic alcohol intoxication

With chronic alcohol intoxication (alcoholism), patients often experience symptoms of damage to the central and peripheral nervous system, which most often manifest themselves in the form of certain neurological syndromes.

Epileptic syndrome in alcoholism is manifested mainly by convulsive seizures with a predominance of tonic seizures, which usually occur during the withdrawal period and often develop into delirium delirium.

Apoplexy of drinkers, alcoholic hemorrhagic stroke manifests itself in young people in the form of a “brain stroke” with a sudden loss of consciousness, coma and severe course, and in people over 50 years of age, as a rule, in the form of a more gradual development with an increasing course and relatively moderate neurological symptoms. Subarachnoid hemorrhages with symptoms of predominantly convexital localization are possible.

Acute alcoholic encephalopathy Guye-Wernicke occurs after a prodromal period, during which there is a deterioration in the somatic, mental and neurological status of the patient (anorexia, thirst, abdominal pain, vomiting, weight loss, hand tremors, slurred speech, senestopathies, asthenia, fears, disturbances sleep, etc.). The disease is characterized by a symptom complex, which is characterized by a combination of severe neurological symptoms with mental disorders. The neurological status is dominated by ataxia, oculomotor and pupillary disorders (ophthalmoparesis, strabismus, miosis), hyperkinesis (trembling lower jaw, myoclonus, choreoathetosis), changes in muscle tone (dystonia), autonomic disorders (fever, tachycardia, hyperhidrosis, leukocytosis, etc.). Characterized by significant dynamism and instability of symptoms.

The end result of chronic alcoholism is the syndrome of chronic alcoholic encephalopathy, characterized by mild diffuse neurological symptoms, agripnia with anxious, affectively rich dreams, early awakenings, symptoms of autonomic-vascular dysfunction, neuroendocrine disorders (sexual weakness, impaired water-salt metabolism, trophic disorders) and characteristic mental changes , up to alcoholic dementia.

Treatment of chronic alcohol intoxication

Treatment of neurological disorders in alcoholic encephalopathy can only be successful when treating the underlying disease.

At the same time, large doses of vitamin B1 up to 10-20 ml of a 5% solution, vitamin B12 1000 mcg at a time, vitamin B6 2-3 ml intramuscularly, ascorbic and nicotinic acid, anabolic steroids are used. For epileptic syndrome, diazepam (Seduxen) 20 ml intravenously in glucose solution twice a day is effective. For hemorrhagic stroke - therapy according to the usual rules.

poisoning intoxication alcohol pesticide

2. Methyl alcohol (methanol)

Methyl alcohol is used in industry as a solvent. Poisoning occurs when inhaling vapors, absorption from the surface of the skin and ingestion instead of ethyl alcohol. The toxic effect is caused mainly by the oxidation products of methyl alcohol - formaldehyde and formic acid. Formaldehyde also selectively damages the cells of the retina of the eyes. The lethal dose when taken orally ranges from 40 to 250 ml, but taking even 5-10 ml can cause blindness.

Clinic: as a rule, symptoms begin a few hours after taking methanol after a period of satisfactory health and gradually increase. In case of mild poisoning, fatigue, headache, and nausea are noted. Moderate poisoning is accompanied by severe headache, dizziness, nausea, vomiting, ataxia, paresthesia in the limbs, pain in muscles, bones, joints, and blurred eyes. Facial hyperemia, acrocyanosis, dry skin and mucous membranes, scleral icterus, febrile temperature, leukocytosis in the blood with low ESR are noted. In case of severe poisoning, after the initial symptoms, psychomotor agitation, severe pain in the abdomen and limbs, progressive deterioration of vision, up to blindness, coma, mydriasis, and often external ophthalmoplegia occur; convulsions, muscle hypertension, toxic hepatitis are possible.

In this case, breathing is shallow, cyanosis is noted. Death occurs from respiratory paralysis and weakened cardiovascular activity against the background of decompensated metabolic acidosis.

The diagnosis of methyl alcohol poisoning is based on a characteristic clinical picture, confirmed by a combination of visual disturbances with changes in the fundus (hyperemia and swelling of the optic nerve nipple), and the presence of methanol in the blood.

Treatment of intoxication with methanol

Urgent gastric lavage with water or 1-2% sodium bicarbonate solution; saline laxative. Ethyl alcohol is used orally as an antidote - every 2 hours, 50 ml of a 30% solution, and in a comatose state, a 5-10% solution intravenously (up to 1 ml per 1 kg of body weight per day). Forced diuresis is required, osmotic diuresis - 150-300 ml of 40% glucose solution intravenously, alkalization of plasma (200-300 ml of 4% sodium bicarbonate solution). In the early period - hemodialysis and peritoneal dialysis. Intravenous administration of prednisolone, 160-200 ml of 0.25% novocaine solution, as well as ATP, cocarboxylase, and B vitamins is indicated.

3. Barbiturates

Barbiturate poisoning occurs due to drug intoxication or suicide attempts.

The following barbiturates are used for oral use in our country:

a) long-acting - barbital, sodium barbital, phenobarbital;

b) medium duration of action - barbamyl (amytal sodium), etaminal sodium (Nembutal), cyclobarbital;

c) short-acting - hexobarbital.

In the clinical picture of the disease, 4 leading syndromes are identified: coma and other neurological disorders; external respiration disorders; dysfunction of internal organs, mainly the cardiovascular system and kidneys; trophic disorders.

For comatose states caused by the inhibitory effect of these drugs on the functions of the central nervous system, a certain stage is characteristic, when falling asleep sequentially develops (stage I of poisoning), superficial coma (stage II of poisoning) and, finally, deep coma with areflexia and lack of reactions to painful stimuli (III stage of poisoning), which occurs most severely with severe impairment of respiratory and circulatory function.

Neurological symptoms characteristic of stage I poisoning include blurred speech, periodically occurring miosis (“play of the pupils”), ataxia, and hypersalivation. Subsequently, persistent miosis occurs, depression of reflexes, muscle hypotonia, and often hypothermia. If patients do not die, then the period of recovery from a comatose state (stage IV) often occurs with psychomotor agitation. Subsequently, depression, insomnia, asthenia, and trophic disorders (dermatoses, hair loss, etc.) are observed.

Aspiration-obstruction and central respiratory disorders are the most common and serious complications of comatose states in barbiturate poisoning. Pneumonia and tracheobronchitis are common. Various forms of external respiration impairment are accompanied by distinct disorders of the acid-base balance of the blood: respiratory or respiratory and metabolic acidosis. Changes in the cardiovascular system are characterized by tachycardia, hypotension, pulmonary edema, collapse, muffled heart sounds, and diffuse changes on the ECG. Renal dysfunction is associated with the development of acute cardiovascular failure (collapse), causing oliguria due to decreased renal circulation. Trophic disorders are not uncommon and are characterized by bullous dermatitis, necrotizing dermatomyositis, which occurs like rapidly developing bedsores.

The diagnosis of barbiturate poisoning is made on the basis of anamnesis, a characteristic clinical picture and can be confirmed by the detection of barbiturates in the blood and pathognomonic changes in the EEG - the presence of oscillations of 14-16/with an amplitude of up to 100-140 μV in the superficial stage (“barbiturate spindles”) and high-amplitude polyrhythmia with periods of bioelectrical silence in the deep stage of coma.

Treatment of barbiturate intoxication

Tracheal intubation or tracheostomy, gastric lavage, drainage of the upper respiratory tract, artificial ventilation, saline laxative, high siphon enemas, cardiovascular drugs, forced diuresis (reopolyglucin, hemodez, mannitol, etc.), antibiotics for the prevention of pneumonia. In severe cases, hemo- and peritoneal dialysis. To eliminate metabolic acidosis (in case of poisoning with long-acting barbiturates), up to 1500 ml of 4% sodium bicarbonate solution is administered intravenously. The use of 1-2 ml of 0.1% atropine sulfate solution, 100 mg of cocarboxylase, ascorbic acid, vitamin B1 is indicated.

4. Manganese

Manganese is used in steel production, in dry batteries, and in medicine. When ingested and when dust is inhaled, manganese compounds become poisoned with the development of degeneration of brain tissue, especially pronounced in the subcortical structures.

Clinic: inhalation of manganese compounds causes acute bronchitis, nasopharyngitis, pneumonia, headache, sleep disorders, liver enlargement. Later, the symptom complex of parkinsonism gradually develops. If drinking water contaminated with manganese is consumed, drowsiness first develops, and then parkinsonism syndrome develops - hypokinesia, amymia, muscle rigidity, tremor.

Treatment of manganese toxicity

First of all, it is necessary to stop further intake of manganese into the body. Special therapy consists of administering thetacine-calcium 0.5 g 4 times a day for a week. If necessary, the course of treatment is repeated after 2 weeks. You can administer 20 ml of a 10% solution of thetacine-calcium intravenously in 500 ml of isotonic solution. Calcium gluconate, vitamins B1, B6 and B12 are also prescribed. When parkinsonism develops, the latter is treated.

5. Carbon monoxide

Carbon monoxide is formed by incomplete combustion of carbon and organic compounds. The source can be any hearth or engine where incomplete combustion of carbon occurs. Carbon monoxide, entering the body, binds to hemoglobin, forming carboxyhemoglobin, which is unable to transport oxygen. When the inhaled air contains 0.1% carbon monoxide, up to 50% of hemoglobin turns into carboxyhemoglobin. There is evidence that carbon monoxide blocks cytochrome oxidase. The result is tissue hypoxia. Poisoning occurs unnoticed, since carbon monoxide is a colorless, odorless gas.

Carbon Monoxide Toxicity Clinic

Clinically, the picture is characterized by headache, dizziness, muscle weakness, especially in the legs, and fainting. There is a scarlet coloration of the skin, tachycardia, and increased blood pressure. In the future, agitation, chest pain, lacrimation, nausea, and vomiting may occur. Adynamia, drowsiness, loss of consciousness, coma, convulsions, respiratory failure, and cerebral edema develop. The development of myocardial infarction and trophic skin disorders is possible.

Treatment of carbon monoxide toxicity

First aid - take the victim to fresh air, use reflex agents ( ammonia), cardiac, oxygen inhalation. The most effective modern method of treatment: oxybarotherapy - breathing oxygen under a pressure of 2-3 atm for 0.5-2 hours in a compression chamber. Injections of 20% glucose solution, 50% ascorbic acid solution, vitamin B1, and corticosteroids are prescribed. In case of prolonged coma, hypothermia of the head and osmotic diuretics are indicated.

6. Pesticides

POISONING BY TOXIC CHEMICALS

The following pesticides are distinguished: insecticides (insecticides), weed killers (herbicides), drugs used against aphids (aficides), etc. Pesticides that can cause the death of insects, microorganisms, and plants are not harmless to humans. They exhibit their toxic effects regardless of the route of entry into the body (through the mouth, skin or respiratory organs). Organic phosphorus compounds (OP) - chlorophos, thiophos, karbofos, dichlorvos, etc. are used as insecticides.

Clinical picture of poisoning. Stage 1: psychomotor agitation, miosis (contraction of the pupil to the size of a point), tightness in the chest, shortness of breath, moist rales in the lungs, sweating, increased blood pressure. Stage II: muscle twitching, convulsions, difficulty breathing, involuntary stool, and frequent urination predominate. Coma. Stage III: respiratory failure increases until breathing stops completely, paralysis of the muscles of the limbs, and a drop in blood pressure. Violation of heart rhythm and cardiac conduction.

Diagnosis is made by clinical picture

Treatment. The victim must be immediately removed or removed from the poisoned atmosphere. Remove contaminated clothing. Wash the skin generously with warm water and soap. Rinse eyes with a 2% warm solution of baking soda. In case of poisoning through the mouth, the sufferer is given several glasses of water, preferably with baking soda (1 teaspoon per glass of water), then vomiting is induced by irritating the root of the tongue. This manipulation is repeated 2-3 times, after which another half glass of 2% soda solution is given to drink with the addition of 1 tablespoon of activated carbon. Vomiting can be induced by injection of a 1% apomorphine solution. Specific therapy is also carried out immediately; it consists of intensive atropinization. In stage 1 poisoning, atropine (2-3 ml 0.1%) is injected under the skin during the day until the mucous membranes are dry. In stage II, atropine is injected into a vein (3 ml in 15-20 ml of glucose solution) repeatedly until bronchorrhea and dry mucous membranes are relieved. In a coma, intubation, suction of mucus from the upper respiratory tract, atropinization for 2-3 days. In stage III, life support is possible only with the help of artificial respiration, atropine drip into a vein (30-50 ml). cholinesterase reactivators. In case of collapse, norepinephrine and other measures. In addition, early administration of antibiotics and oxygen therapy are indicated in the first two stages. For bronchospastic phenomena, use an aerosol of penicillin with atropine. metacin and novocaine. Organochlorine compounds (OCCs) - hexachlorane, hexabenzene, DDT, etc. are also used as insecticides. All COS are highly soluble in fats and lipids, so they accumulate in nerve cells and block respiratory enzymes in the cells. Lethal dose of DDT: 10-15 g. Symptoms. When poison gets on the skin, dermatitis occurs. When inhaled, it causes irritation of the mucous membrane of the nasopharynx, trachea, and bronchi. Nosebleeds, sore throat, cough, wheezing in the lungs, redness and pain in the eyes occur. Upon admission, dyspeptic disorders, abdominal pain, after a few hours, cramps of the calf muscles, unsteadiness of gait, muscle weakness, weakened reflexes. With large doses of poison, a coma may develop. There may be damage to the liver and kidneys. Death occurs due to symptoms of acute cardiovascular failure. First aid is the same for FOS poisoning (see above). After gastric lavage, it is recommended to take the mixture "GUM" inside: 25 g of tannin, 50 g of activated carbon, 25 g of magnesium oxide (burnt magnesia), stir to a paste consistency. After 10-15 minutes, take a saline laxative. Treatment. Calcium gluconate (10% solution), calcium chloride (10% solution) 10 ml intravenously. Nicotinic acid (3 ml of 1% solution) under the skin again. Vitamin therapy. For convulsions - barbamyl (5 ml of 10% solution) intramuscularly. Forced diuresis (alkalinization and water load). Treatment of acute cardiovascular and acute renal failure. Therapy for hypochloremia: 10-30 ml of 10% sodium chloride solution into a vein. Arsenic and its compounds. Calcium arsenate, sodium arsenite, Parisian green and other arsenic-containing compounds are used as pesticides for treating seeds and controlling agricultural pests; they are physiologically active and poisonous. Lethal dose when taken orally 0.06-0.2 g. Symptoms. After the poison enters the stomach, a gastrointestinal form of poisoning usually develops. After 2-8 hours, vomiting, a metallic taste in the mouth, and severe abdominal pain appear. Vomit is greenish in color, loose, frequent stools resembling rice water. Severe dehydration occurs, accompanied by convulsions. Blood in the urine, jaundice, anemia, acute renal failure. Collapse, coma. Respiratory paralysis. Death can occur within a few hours. First aid. If it enters the stomach, immediately rinse vigorously with water with a suspension of laxatives - magnesium oxide or sulfate (20 g per 1 liter of water), emetics: support vomiting with warm milk or a mixture of milk with beaten egg whites. After rinsing, inside - freshly prepared “arsenic antidote” (every 10 minutes, 1 teaspoon until vomiting subsides) or 2-3 tablespoons of the antidote mixture “GUM: dilute 25 g of tannin, 50 g of activated carbon, 25 in 400 ml of water to the consistency of a paste. g magnesium oxide - burnt magnesia. early dates intramuscular administration of unithiol or dicaptol, replacement blood transfusion. For severe pain in the intestines - platiphylline, subcutaneous atropine, perinephric blockade with novocaine. Cardiovascular drugs according to indications. Treatment of collapse. Hemodialysis on the first day after poisoning, peritoneal dialysis, forced diuresis. Symptomatic treatment.

7. Anticholinesterase drugs

Anticholinesterase drugs are used in agriculture and in everyday life as insecticides, namely: chlorophos, thiophos, karbofos, mercaptophos; and as drugs - reversible cholinesterase inhibitors - galantamine hydrobromide (nivalin), physostigmine salicylate (eserine), proserine (neostigmine, prostigmine), pyridostigmine bromide (kalimin, istinone), oxazil (ambenonium chloride) and irreversible cholinesterase inhibitors (organophosphorus compounds) : armies, npbufin, pyrofos, phosphakol.

Anticholinesterase substances, inhibiting the enzyme acetylcholinesterase, lead to the accumulation of endogenous acetylcholine in cholinergic synapses, resulting in excitation of cholinoreactive systems. From a pharmacological point of view, the toxic effect of these compounds on the nervous system is regarded as muscarinic and nicotine-like. The muscarinic-like effect is expressed in the appearance of profuse sweating, salivation, bronchorrhea, bronchospasm, and severe miosis; nicotine-like and central action - in the development of agitation, disorientation, hyperkinesis of choreic and myoclonic types, general clonic-tonic convulsions and deep coma.

Clinic of intoxication with anticholinesterase drugs

There are 3 stages of poisoning.

Stage 1 - stage of excitation (mild form of intoxication). 15-20 minutes after poisoning, patients notice dizziness, headache, decreased visual acuity, nausea, a feeling of fear, psychomotor agitation and aggression often develop. Moderate miosis, sweating, salivation, bronchorrhea, vomiting, and cramping abdominal pain are observed. Blood pressure is increased. Moderate tachycardia is observed in the very initial period of poisoning.

Stage 2 - the stage of hyperkinesis and convulsions (moderate and severe intoxication). Psychomotor agitation persists or is gradually replaced by lethargy, development of stupor, and in some cases coma. Characterized by severe miosis with lack of pupillary response to light. Sweating, hypersalivation, bronchorrhea, and bradycardia are most pronounced. Hyperkinesis of the choreoid and myoclonic types, myofibrillation in the eyelids, chest muscles, and legs appear. Periodically, general muscle hypertonicity, tonic convulsions, and chest rigidity occur with a decrease in its excursion. Blood pressure reaches its maximum level, followed by a drop in cardiovascular activity. Characterized by painful tenesmus, involuntary loose stools, and frequent urination.

Stage 3 - stage of paralysis (extremely severe forms of poisoning). In the vast majority of cases, patients are in a deep comatose state, often with complete areflexia. Despite severe hypoxia, miosis is pronounced, and hyperhidrosis persists. Muscle atony is pronounced. Severe breathing disorders are associated with paralysis of the respiratory muscles and depression of the respiratory center - shallow, irregular breathing. Bradycardia reaches 40-20 per 1 minute or, on the contrary, pronounced tachycardia appears up to 120 per 1 minute. Blood pressure tends to decrease to the point of deep collapse. In 7-8% of patients admitted in the 2nd and 3rd stages of poisoning, from the 2nd to the 8th day after poisoning, a relapse of intoxication symptoms is noted.

In some cases, patients with stage 2 and 3 poisoning experience a convulsive syndrome, the development of which is extremely unfavorable prognostically.

Respiratory and hemodynamic disorders, as well as neurological disorders, manifested by the development of deep coma, depression of the respiratory and vasomotor centers, are leading and responsible for the development of a terminal condition in case of OP poisoning.

Diagnosis of intoxication with anticholinesterase drugs

The diagnosis is made on the basis of a characteristic clinical picture, including symptoms of muscarinic and nicotinic effects and can be confirmed by inhibition of blood cholinesterase.

Treatment of intoxication with anticholinesterase drugs

Treatment depends on the severity of poisoning and consists of removing the poison from the body (gastric lavage, forced diuresis, peritoneal dialysis), active specific therapy and, if necessary, intensive resuscitation measures. Specific therapy consists of the use of anticholinergics - usually atropine. Depending on the severity of poisoning, in the 1st stage of poisoning, 2-3 ml of a 0.1% solution is injected subcutaneously at intervals of several hours, in the 2nd stage - 3 ml of a 0.1% solution in glucose solution with the same intervals, in the 3rd stage of poisoning - 20-30 ml intravenously. The effect of atropine is enhanced by the peripheral M-anticholinergic metacin, 1-2 ml of a 0.1% solution intramuscularly or intravenously.

At the same time, peripherally acting cholinesterase reactivators are used - oximes, for example dipyroxime, 1 ml of a 15% solution subcutaneously or intravenously again up to 10 ml per day. Cholinesterase reactivators may be used central action: 2-3 ml of 40% isonitrosine solution intramuscularly, if necessary, again every 30-40 minutes up to 10 ml.

Specific therapy is carried out under constant monitoring of the activity of the blood cholinesterase enzyme. Magnesium sulfate, sodium hydroxybutyrate, Viadryl, aminazine, promedol, vascular agents, and corticosteroids are also used. Antibiotics are prescribed to prevent pneumonia.

8. Narcotic analgesics

Morphine hydrochloride, promedol, omnopon, codeine, codeine phosphate and others are used as narcotic analgesics. The lethal dose of morphine when taken orally is 0.1-0.5 g [Shvaikova M.D., 1975], codeine - 0.5-1 g [Loktionov S.P., 1977]. The toxicity of narcotic analgesics increases if they are joint use with MAO inhibitors. Morphine enters the brain and spinal cord in the form of oxymorphine, where it selectively binds to CNS lipids, causing so-called functional disorders. Biotransformation of codeine occurs due to demethylation to norcodeine.

Clinic of intoxication with narcotic analgesics

In case of poisoning with narcotic analgesics, 4 leading clinical syndromes are distinguished: coma and other neurological disorders, respiratory failure syndrome, hemodynamic disorder syndrome, trophic disorders [Sukhinin P. L. et al., 1970, Luzhnikov E. A., 1977]. Drowsiness, hyperemia of the skin, dizziness, tinnitus, hyperhidrosis, disorientation of patients, miosis are usually observed, and sometimes muscle twitching and abdominal pain occur. When taking large doses, a coma develops with suppressed reflexes, muscle hypotension and hypothermia. Tonic-clonic seizures are possible.

Respiratory disorders manifest themselves in the form of slow breathing, shortness of breath, and Cheyne-Stokes breathing. In a comatose state, aspiration-obstruction disturbances in external respiration and pulmonary edema may occur.

Hemodynamic disorders are characterized by the development of bradycardia, hypotension, and collapse.

Diagnosis of intoxication with narcotic analgesics

The diagnosis is made based on the medical history and the above clinical picture. A combination of the phenomena of depression of central nervous system functions with miosis and bradycardia is characteristic. However, in the atonal state, miosis is often replaced by mydriasis, and bradycardia by tachycardia.

Codeine poisoning is characterized by respiratory distress while maintaining consciousness.

Treatment of intoxication with narcotic analgesics

Repeated gastric lavage with 0.1% potassium permanganate solution or 0.2% tannin solution, saline laxative. A specific antidote is nalorphine (anthorphine). The most effective are repeated intravenous injections of the drug, 1-2 ml of 0.5% solution at intervals of 15 minutes, no more than 8 ml in total. In severe cases, forced diuresis and peritoneal dialysis.

In the absence of nalorphine, repeated administration of 1 ml of 0.1% atropine solution is used. Warming of patients, administration of caffeine and cordiamine are indicated.

9. Ganglion blocking agents

Ganglioblocking drugs include arfonade, benzohexonium, gangleron, dikolin, dimekolnn, isoprine, quaterone, pachycarpine hydroiodide, pentamine, pyrylene, etc. Pachycarpine, used by women to terminate pregnancy in doses significantly higher than therapeutic ones, deserves special attention.

Clinical poisoning with pachycarpine is characterized by dizziness, decreased vision, nausea, vomiting, abdominal pain, headaches, tinnitus, palpitations, and difficulty breathing. Mydriasis, hypotension, and muscle fibrillation are also observed. Severe poisoning leads to collapse and respiratory paralysis.

The diagnosis is made on the basis of anamnesis and a characteristic clinical picture. Unlike atropine poisoning, which is also accompanied by mydriasis, there are no hallucinations, manic state, high tachycardia.

Treatment of intoxication with ganglion blocking agents

Abundant gastric lavage through a tube, cleansing enemas, saline laxative, forced diuresis, hemodialysis. As an antidote, repeated subcutaneous injections of 1 ml of 0.05% proserine solution are used (up to 30 ml per day); 1% ATP solution is also prescribed intramuscularly, up to 10 ml per day, 6% vitamin B1 solution, up to 50 ml per day. Shown sedatives, when excited hexenal; during collapse.

10. Hydrogen sulfide

Hydrogen sulfide is a colorless, volatile liquid used in the textile and rubber industries.

Acute and subacute poisoning occurs during industrial accidents. In this case, loss of consciousness with psychomotor agitation quickly develops, which in some cases can be fatal. Moderate intoxication is characterized by agitation, euphoria, dizziness, ataxia, headache, nausea, and vomiting. Mild poisoning is similar in clinical manifestations to alcohol intoxication (euphoria, nausea, apathy, adynamia). In some cases, after severe intoxication, toxic encephalopathy develops with significant neurological and intellectual defects.

Chronic hydrogen sulfide intoxication is represented by individual clinical forms, depending on the severity of the process.

1. Toxic neurasthenia (asthenovegetative syndrome). The dominant phenomena are irritable weakness (increased exhaustion, emotional instability), bright red dermographism, hyperhidrosis of the palms with sweating drops. There is a decrease in the excitability of the skin, visual and olfactory analyzers (hyperesthesia followed by hypoesthesia of a symmetrical distal nature). There are frequent cases of enlarged thyroid gland and dysmenorrhea. Timely treatment leads to a reversal of symptoms.

2. Encephalomyelopolyneuropathy (headache, dizziness, optic-vestibular disorders, hallucinations). Characterized by tactile hallucinations with the sensation of someone else’s hand touching the shoulder, nightmares, severe apathy, hypochondria. Symptoms of parkinsonism are often observed, reflexes from the skin and mucous membranes are inhibited, anosmia and severe retrobulbar neuritis with transition to optic nerve atrophy often occur.

3. Polyneuropathic syndrome. It begins with sensitivity disorders, which intensify to complete anesthesia, pain in the limbs, along the nerve trunks during palpation, and tension symptoms. Among movement disorders, suppression of the Achilles reflexes occurs first, followed by weakness in the distal sections limbs. Subsequently, tendon and periosteal reflexes are inhibited. Amyotrophy is unsharp and diffuse. Significant distal autonomic disorders are observed (sweating, cyanosis of the extremities). Sometimes toxic myositis with pain syndrome occurs.

Diagnostics, differential diagnosis consists of summarizing the features of the clinical picture, anamnestic data regarding contact with poison. Detection of hydrogen sulfide in blood and urine is important; urine with a radish odor, dark brown in color due to the presence of hematin. An increase in copper levels in the urine may also be a sign of poisoning.

Treatment. In acute cases, it is necessary to evacuate the victim from the contaminated area, ensure the supply of fresh air, oxygen inhalation, and, if indicated, artificial ventilation, respiratory analeptics. Antidote therapy consists of using sulfhydryl group donors, glutamic acid, glucosamine, and copper acetate. Nonspecific detoxification therapy, vitamin therapy, cardio- and psychotropic drugs are prescribed. Physiotherapeutic procedures and sanatorium-resort treatment are desirable.

11. Gasoline

Gasoline poisoning

Tetraethyl lead TES is a colorless, oily liquid with unpleasant smell, it is soluble in fats, lipids and organic solvents, and practically insoluble in water.

POISON CLINIC

TES can cause both acute and chronic intoxication.

Acute poisoning can be mild, moderate or severe.

In cases of mild poisoning, mild bradycardia, hypotension, hypothermia, increased sweating, salivation (excessive salivation) are noted. Subjective sensations are expressed in headaches, sleep disturbances, and unpleasant dreams. Sometimes subjective complaints may be absent. All these symptoms are usually reversible and do not cause disability.

In cases of acute poisoning of moderate severity, autonomic disorders become more pronounced (temperature drops to 35-36.2 0 C, blood pressure to 90/50 mm Hg, pulse to 45-60 per minute). Patients complain of difficulty falling asleep and insomnia. Tremors of the eyelids, tongue, fingers, and persistent red dermographism are noted. Sometimes there is a decrease in intelligence - decreased memory, difficulty thinking, greater exhaustion due to mental stress, asthenia. With this degree of intoxication, euphoria with an uncritical attitude towards one’s condition, ataxia, and sensation may be observed. foreign body(hair) in the mouth. The sensation of a hair in the mouth is specific symptom in case of TES poisoning and indicates an unfavorable prognosis for the development of intoxication.

When the poison enters the gastroenteric route, the described symptoms are accompanied by dyspeptic symptoms - nausea, vomiting, pain in the epigastric region. The course of intoxication in these cases is more severe.

In case of moderate poisoning, no significant changes in the internal organs are observed; the results of laboratory tests have no diagnostic value.

Cases of severe acute TES poisoning are characterized by confusion, anxiety, agitation, disorientation, general tremor with visual, auditory, olfactory hallucinations, and intellectual impairment. At the height of psychomotor agitation, death can occur. Severe poisonings with a favorable outcome usually take a protracted course (up to 12 months or more) and end in a regressing defective state. Mental disorders often occur unexpectedly, despite the apparent well-being of the patient.

Chronic poisoning can develop as a result of both prolonged intake of small amounts of TES into the body, and repeated, not timely recognized and untreated mild acute poisoning.

According to the severity, chronic TES intoxication is divided into 2 groups. Chronic intoxication of the 1st degree is characterized by persistent vegetative disorders and asthenia phenomena. In case of chronic intoxication of the second degree, vegetative disorders and symptoms of asthenia are accompanied by phenomena of impaired intellectual activity and the emotional-volitional sphere.

Basic pathological symptoms, occurring during chronic intoxication of TES - hypotension (blood pressure below 100 mm Hg), bradycardia (pulse less than 60 per minute), hypothermia (body temperature below 36 ° C), increased salivation, sweating, fatigue, weakness , tremors of hands, eyelids, tongue, headaches, sleep disturbances. These symptoms are characterized by persistence over a number of years.

Chronic intoxication of TES usually proceeds sluggishly, however, under the influence of a wide variety of exogenous influences, exacerbations can occur. Sometimes exacerbations turn into severe intoxication psychosis.

The development of chronic intoxication is usually preceded by a period of illness, which is characterized by labile symptoms with a predominance of autonomic disorders. These disorders may appear suddenly and disappear quickly. This condition may continue for a number of years. The appearance of vegetative symptoms can be facilitated by unfavorable exogenous factors (infection, overwork, alcohol intake, etc.) under unchanged sanitary and hygienic working conditions.

The subjects, as a rule, do not make any complaints in these cases. However, over time, these phenomena become persistent, they are joined by symptoms of an asthenic state, and the picture of TES intoxication becomes pronounced;

Painful conditions with quickly reversible symptoms should be regarded as the initial stage of chronic intoxication of TES.

DIAGNOSIS OF POISONING.

Based on medical history, characteristic clinical picture, and laboratory test results. The maximum permissible content of lead in human blood is 30 µg% (1.4 µmol/l). The most informative tests are the determination of ALA-D activity in erythrocytes and lead in urine. At higher concentrations, many biochemical parameters change - ALT, AST, alkaline phosphatase, cholesterol, uric acid, blood and urine creatinine, bilirubin, etc.

1. Agents that stimulate the elimination of toxins (the drug “IV”, thetacine-calcium, D-penicillamine, etc.)

2.Means of pathogenetic therapy (Vitamin C, nicotinic acid)

3.Symptomatic therapy.

4.Sedative therapy.

5. Vegetotropic drugs (Belloid)

6.Myotropic antispasmodics (papaverine)

7. General strengthening therapy, adaptogens.

8. Physiotherapy (massage, medicinal electrophoresis, phonophoresis)

9.Sanatorium-resort treatment.

12. Botulism

Botulism is a disease resulting from poisoning by toxins of botulism bacteria and characterized by severe damage to the nervous system.

Botulism Clinic

The incubation period for botulism is from several hours to 2-5 days; the more severe the disease, the shorter the incubation period. At severe forms illness it usually lasts about 24 hours. In the vast majority of cases, the disease begins with the following symptoms:

the development of symptoms is very rapid,

vomiting, sometimes up to cramping pain in a stomach,

liquid stool without impurities

These manifestations last about a day. Then a feeling of fullness in the stomach, flatulence, and constipation develop. Lesions of the nervous system appear either simultaneously with the gastrointestinal ones, or after they disappear by the end of the first - beginning of the second day.

TO early signs Botulism is a visual disorder. Patients complain of “fog”, “grid” before the eyes, double vision of objects, difficulty reading.

At the same time, thirst, dry mucous membranes occur due to impaired salivation, as well as a swallowing disorder, and the timbre of the voice changes. In this case, patients are bothered by the feeling of a “lump” in the throat, pain when swallowing, choking caused by damage to the muscles of the larynx and pharynx.

Damage to the nervous system is accompanied by a general toxic syndrome - headache, dizziness, insomnia, weakness, fatigue. However, fever is usually absent, and only some patients experience a slight increase in temperature.

A serious sign indicating an unfavorable course of the disease is respiratory failure. Patients feel a lack of air, heaviness in the chest, sometimes pain in the chest, breathing becomes shallow. The cause of death in botulism is respiratory failure.

Diagnostics

The diagnosis is made based on laboratory data. Important role In the diagnosis of botulism, the fact of a group disease in people who ate the same product (canned food, dried fish, smoked meats, homemade juices, canned vegetables, mushrooms and meat) plays a role.

Laboratory diagnostics: blood, vomit and gastric lavage, feces, and food residues are taken for examination. The presence of botulinum toxin in the test material is determined using a biological method.

Treatment of botulism

All patients with suspected botulism are subject to mandatory hospitalization due to the need for timely specific therapy in order to prevent possible severe complications.

Main tasks emergency care are neutralization, binding and removal of toxins from the body, ensuring the functions of the respiratory and cardiovascular systems of the body.

At the prehospital stage, the following emergency measures must be taken: rinse the stomach first boiled water, then with a 2% soda solution; drinking plenty of water frequently; inject intramuscularly or subcutaneously 2 ml of 0.05 percent proserine, and in case of acute respiratory failure, perform artificial respiration.

To neutralize botulinum toxin, therapeutic anti-botulinum serums are used.

If the type of toxin that caused the disease is unknown, three types of serum are administered - A, B, E. Serotherapy is preceded by an intradermal test and desensitization. In severe forms of the disease, the first doses of serum are administered intravenously, in other cases - intramuscularly. Initially, 10-15 thousand IU of type A and E serum and 5-7.5 thousand IU of type B serum are administered. Subsequent doses and frequency of administration are determined by the severity of the disease and the dynamics of clinical symptoms.

In severe forms of botulism, the administration of the serum is repeated after 6-8 hours until the effect appears. The full course of treatment requires up to 50,000-60,000 IU of serum type A, E and 25,000-30,000 IU of type B, doses can be increased, but the course of serotherapy should not exceed three to four days. Considering that spores can turn into vegetative forms in the gastrointestinal tract, antibacterial therapy (chloramphenicol) or tetracycline drugs are prescribed. At the same time, detoxification therapy is carried out. For respiratory disorders due to paralysis of the respiratory muscles, artificial ventilation is indicated. To combat hypoxia, hyperbaric oxygenation is used.

In recovering patients, residual effects after paralysis (more than 1-2 months) and asthenic syndrome persist for a long time. Botulism can be complicated by pneumonia, sepsis, and myocarditis. Those recovering after discharge from the hospital are observed in the absence of complications - 14 days; in case of complicated course:

in case of myocarditis - a period of incapacity for work of at least 10 days. Treatment by a cardiologist followed by follow-up visits every 6 months for a year with blood tests and ECG;

in case of residual effects of neurological symptoms - a period of incapacity for work of at least 2 weeks, followed by clinical observation by an infectious disease specialist and a neurologist for a year with examination every 3 months (ECG, clinical blood test)

Conclusion

After exposure to poisons, dysfunction of the central nervous system is often observed for a long time. In relatively mild cases, they manifest themselves in the form of a protracted asthenic state (or astheno-vegetative syndrome), in more severe cases - in the form of encephalopathy. When the nervous system is affected by poison, one must keep in mind the possibility of rapid progression of the pathological process and disruption of the vital functions of the body. Intoxication accompanied by a coma poses a particularly great danger to life. In this case, it is necessary, first of all, to ensure the normal functioning of the vital systems of the body and only then look for the cause of the development of coma. If it is based on intoxication, then the nature of the poison, the route of its penetration into the body, the time elapsed from the moment of poisoning, etc. are specified. In each individual case, it is necessary to exclude the possibility of coma developing for other reasons. Thus, it should be borne in mind that coma can be a consequence of acute cerebrovascular accident, meningoencephalitis, arachnoiditis, brain tumor, renal or liver failure, endocrine disorders, blood diseases, nutritional dystrophy, when exposed to physical factors (sun and heat stroke, electrical trauma and etc.), closed skull injury, etc.

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After exposure to poisons Often, dysfunction of the central nervous system is observed for a long time. In relatively mild cases, they manifest themselves in the form of a protracted asthenic state (or astheno-vegetative syndrome), in more severe cases - in the form of encephalopathy.

When the nervous system is damaged by poison one must keep in mind the possibility of rapid progression of the pathological process and disruption of the vital functions of the body. Intoxication accompanied by a coma poses a particularly great danger to life. In this case, it is necessary, first of all, to ensure the normal functioning of the vital systems of the body and only then look for the cause of the development of coma. If it is based on intoxication, then the nature of the poison, the route of its penetration into the body, the time that has passed since the moment of poisoning, etc. are specified.

In each individual case necessary exclude the possibility of developing coma for other reasons. Thus, it should be borne in mind that coma can be a consequence of acute cerebrovascular accident, meningoencephalitis, arachnoiditis, brain tumor, renal or liver failure, endocrine disorders, blood diseases, nutritional dystrophy, when exposed to physical factors (sun and heat stroke, electrical trauma and etc.), closed skull injury, etc.

To clarify the diagnosis necessary consultations with a neurologist, ophthalmologist and other doctors, as well as conducting some biochemical studies (sugar content and residual nitrogen in the blood, sugar in the urine, etc.).

Treatment of acute intoxication of the nervous system

Patients who are in a comatose state, it is advisable to place them in intensive care wards. It is necessary from the very beginning to maintain good patency of the airways (prevention and elimination of tongue retraction, suction of mucus from the nasopharynx, trachea, bronchi, elimination of laryngo- and bronchospasm, laryngeal edema, etc.). If indicated, intubation or tracheostomy is performed; in case of sudden weakening or cessation of breathing - artificial ventilation.

For cardiovascular failure the main pathogenetic mechanism of the hemodynamic disorder is clarified and treatment is prescribed accordingly.

In the presence of seizures their cause is determined and anticonvulsant measures are taken, including pathogenetic and symptomatic therapy. So, if the basis of seizures is cerebral edema or hypoxia, then to eliminate them it is quite sufficient to carry out decongestant measures, prescribe oxygen therapy, etc. If the cause of seizures is unknown, then predominantly symptomatic therapy is carried out: fast-acting barbiturates are prescribed (2-5 ml 2 .5% solution of sodium thiopental intravenously, 5-10 ml of 5% solution of barbamyl intramuscularly), 2-4 ml of 0.5% solution of diazepam (seduxene) intramuscularly, 5-10 ml of 25% solution of magnesium sulfate intramuscularly, etc.

Motor restlessness can be eliminated or reduced by introducing phenothiazine substances (1-2 ml of 2.5% chlorpromazine solution) or muscle relaxants. The latter are used only if an anesthesiologist provides assistance with transferring the patient to mechanical ventilation.