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, 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 of cerebral vessels, disruption of blood flow in them consistently develop, stasis and thrombosis appear, and as a result, areas 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 by deep disturbances of 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). Syndromes of cerebrovascular accidents and psychopathological syndromes are often associated.
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. An early manifestation of the syndrome may be 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, the patency of the respiratory tract is restored, and artificial ventilation of the lungs is carried out.
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 of the possible use of 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 of the 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 predominate) and neurotic (neurotic disorders predominate). 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 in a shorter 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.
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- an unconscious state in which the patient does not react to the environment; Only with difficulty, using harsh painful stimuli (pinches, injections, etc.), is it possible to bring the patient out of the soporotic 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; blood pressure is 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. The smell of poison, interviews with others, and other data indicating poisoning (detection of poison residues, etc.) are of great importance. 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.
What is Central Nervous System Stimulant Poisoning?
The caffeine group and its apologists (theophyllip, theobromine, aminophylline, aminophylline, theophedry, diprophylline, etc.). Of the entire group, caffeine has the greatest stimulating effect, the toxic dose of which is at the level of 1 g, and the mortal dose is about 20 g with large individual differences. With intravenous administration of aminophylline, there are cases of death from a dose of the order of OD g; lethal doses in children when administered in suppositories are 25 mg/kg.
Symptoms of Central Nervous System Stimulant Poisoning
The main signs of toxic effects with long-term use of relatively large doses (for example, in people who abuse coffee and tea) are manifested in irritability, anxiety, excitability, persistent headaches that are difficult to respond to drug therapy, and sleep disorders. The effect on the gastrointestinal tract is manifested by a burning sensation in the epigastric region, nausea, vomiting, a sharp increase in gastric secretion, which is especially dangerous for patients with ulcers, and constipation.
Acute caffeine poisoning is expressed in psychomotor reactions that turn into delirium and hallucinations, there are disturbances in sensory functions (determining time and distance) and movement speed. The initial phase of excitation quickly gives way to a soporous state. The most dangerous complication of caffeine and its analogues is the development of acute cardiovascular failure with symptoms of collapse. Heart paralysis is also possible with rapid injection of aminophylline into a vein.
Treatment of Central Nervous System Stimulant Poisoning
First aid
Gastric lavage with a 1-2% solution of tannin or sodium bicarbonate (baking soda), a suspension of activated carbon. If poisoning is caused by suppositories containing aminophylline, give an enema and take a saline laxative.
To relieve psychomotor agitation and seizures, use chloral hydrate in an enema (1.5-2 g per 50 ml of water), chloral hydrate (2 ml of a 2.5% solution with novocaine), diphenhydramine (1 ml of a 2% solution with novocaine) - intramuscularly.
Correction of cardiovascular failure in case of caffeine poisoning is difficult in the conditions of first aid, since most vasoconstrictors will enhance the toxic effect of caffeine and its analogues. It is advisable to carry out this type of resuscitation in a hospital setting, where an exchange transfusion of blood (plasma) can be performed and forced diuresis with alkalization can be used.
Which doctors should you contact if you have poisoning from central nervous system stimulants?
Toxicologist
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Very common causes of damage to the nervous system are infections and intoxications.
Damage to the nervous system due to infection
Penetration of the pathogen into the body occurs in the following ways: with direct damage to the membranes (dura, vascular and soft) of the brain and spinal cord associated with injuries to the skull or spine, when damage to the dura mater occurs; with complications of diseases of the paranasal sinuses of an inflammatory nature of the nose and ear; through the intervertebral foramina in the spinal cord membrane, the epidural space and the spinal cord.
Bacteria and viruses penetrate the brain and spinal cord through the blood and lymph flow from the source of infectious inflammation, which can be located at different distances from the central nervous system (CNS). More often, infection leads to the development of meningitis (inflammation of the meninges).
Viruses of rabies, polio, and herpes zoster can penetrate the central nervous system through the axial cylinders of the peripheral nerves.
Nervous system damage due to intoxication
In some infectious diseases (diphtheria, tetanus, influenza), damage to the central nervous system can occur under the influence of toxins secreted by microorganisms. In addition, alcohol, some medications, poisonous mushrooms, as well as chemicals used in production, agriculture, and everyday life have a toxic effect on the central nervous system.
Moreover, the degree of the pathological process in the central and peripheral parts of the nervous system is associated with the chemical structure of the toxic substance, the degree of its effect on the nervous tissue, the dose taken and the route of entry into the body. Damage to the nervous system of toxic origin can be either acute or chronic.
The cause of this damage to the nervous system can also be endogenous (associated with internal causes) intoxication, which occurs in diseases of the liver, pancreas, kidneys, and gastrointestinal tract.
In addition, vitamin deficiencies, impaired metabolism due to porphyria, and galactosemia can lead to toxic damage to the nervous system.
The toxic effect is on the cerebral cortex, subcortical structures, and cerebellum, but most often peripheral structures are affected and toxic polyneuropathies develop.
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