Disorder of motor and sensitive functions of nervous system

CM 6(2)

DISORDER OF MOTOR AND SENSITIVE FUNCTIONS OF NERVOUS SYSTEM. PAIN.

DISORDER OF  TROPHIC FUNCTION OF NERVOUS SYSTEM

 PATHOPHYSIOLOGY OF EXTREME STATES

DISORDER OF MOTOR AND SENSITIVE FUNCTIONS OF NERVOUS SYSTEM

Etiology of nervous  system disorders

         The nervous system coordinates and organizes the functions of all body systems. This intricate network of interlocking receptors and transmitters is a dynamic system that controls and regulates every mental and physical function. It has three main divisions:

·         Central nervous system (CNS): the brain and spinal cord

·         Peripheral nervous system: the motor and sensory nerves, which carry messages between the CNS and remote parts of the body

·         Autonomic nervous system: actually part of the peripheral nervous system, regulates involuntary functions of the internal organs.

 

Main divisions of nervous system

 

The fundamental unit that participates in all nervous system activity is the neuron, a highly specialized cell that receives and transmits electrochemical nerve impulses through delicate, threadlike fibers that extend from the central cell body. Axons carry impulses away from the cell body; dendrites carry impulses to it. Most neurons have several dendrites but only one axon. Sensory (or afferent) neurons transmit impulses from receptors to the spinal cord or the brain. Motor (or efferent) neurons transmit impulses from the CNS to regulate activity of muscles or glands. Interneurons, also known as connecting or associatioeurons, carry signals through complex pathways between sensory and motor neurons. Interneurons account for 99% of all the neurons in the nervous system.

From birth to death, the nervous system efficiently organizes and controls the smallest action, thought, or feeling; monitors communication and instinct for survival; and allows introspection, wonder, abstract thought, and self-awareness. Together, the CNS and peripheral nervous system keep a person alert, awake, oriented, and able to move about freely without discomfort and with all body systems working to maintain homeostasis.

Thus, any disorder affecting the nervous system can cause signs and symptoms in any and all body systems. Patients with nervous system disorders commonly have signs and symptoms that are elusive, subtle, and sometimes latent.

Nervous system is sensitive to injury influences. Its activity disorders can be caused with:

·        physical factors (mechanical trauma, electricity, high and low temperature, noise and vibration, changed atmospheric pressure),

·        poisons (narcotics, nicotine, carbon dioxide),

·        infectious disease agents (encephalitis, poliomyelitis, rabies), bacterial toxins (botulinic, titanic, diphtheritic),

·        parasites (Echinococcus, Cysticercus, Toxoplasma gondii),

·        сerebral blood circulation functional and organic disorders (arteriosclerosis, thrombosis, embolism, arterial hyperemia, ischemia, hemorrhagy),

·        tumors, 

·        inflammatory processes, which destroy the neural tissue,

·        endocrinic diseases (thyrotoxicosis, myxedema),

·        metabolism violations (starvation, hypoglycemia, hepatic coma),

·        many neural system diseases are genetically based.

         Such phenomena, as insufficient synthesis of energy ieurons, interneuronal and neuro-muscular synaptic contacts get caused with mediators synthesis increase or specific receptors blocked and are of great  importance iervous disorders pathogenesis.

MOTOR DISORDERS

Motions can be divided into intentional and unintentional. The intentional movements are controlled with pyramidal system, which consists of two motoral neurons – the central and peripheral ones. Central neurons corpuses (pyramidal cells) are fixed at locomotoral parts of cerebral hemispheres cortex – precentral gyrus, upper and medial frontal gyruses, parietal lobe, paracentral lobule. Their axons reach locomotory function disorders the anterior horn of the spinal cord, where peripheral motoral  neurons are located. Their long processes give the muscular innervation.

 

Pyramidal system

 

 

            In the pyramidal tract, most impulses from the motor cortex travel through the internal capsule to the medulla, where they cross (decussate) to the opposite side and continue down the spinal cord as the lateral corticospinal tract, ending in the anterior horn of the gray matter at a specific spinal cord level. Some fibers do not cross in the medulla but continue down the anterior corticospinal tract and cross near the level of termination in the anterior horn. The fibers of the pyramidal tract are considered upper motor neurons. In the anterior horn of the spinal cord, upper motor neurons relay impulses to the lower motor neurons, which carry them  the spinal and peripheral nerves to the muscles, producing a motor response. Motor impulses that regulate involuntary muscle tone and muscle control travel along the extrapyramidal tract from the premotor area of the frontal lobe to the pons of the brain stem, where they cross to the opposite side. The impulses then travel down the spinal cord to the anterior horn, where they are relayed to lower motor neurons for ultimate delivery to the muscles.

The motions are also get regulated with extrapyramidal system. It includes nucleus caudatus, the shell, globus pallidus, substantia nigra, red nucleus, subthalamic nucleus.

         The body equilibrium, movements coordination and muscular tonus are provided by cerebellum.

  

The central and peripheral paralyses. The total central or peripheral neuron falling out causes the central or peripheral paralyses appearance. The partial violation of these neurons provokes the conforming paresis. The central paralyses differs the peripheral one with many signs. These differenses matter for the topographical diagnostics of nervous system injuries.

Upper motor neuron dysfunction reflects an interruption in the pyramidal tract and consequent decreased activation of the lower motor neurons innervating one or more areas of the body. Upper motor neuron dysfunction usually affects more than one muscle group, and generally affects distal muscle groups more severely than proximal groups. Onset of spastic muscle tone over several days to weeks commonly accompanies upper motor neuron paresis, unless the dysfunction is acute. In acute dysfunction, flaccid tone and loss of deep tendon reflexes indicates spinal shock, caused by a severe, acute lesion below the foramen magnum. Incoordination associated with upper motor neuron paresis manifests as slow coarse movement with abnormal rhythm.

Lower motor neurons are of two basic types: large (alpha) and small (gamma). Dysfunction of the large motor neurons of the anterior horn of the spinal cord, the motor nuclei of the brainstem, and their axons causes impairment of voluntary and involuntary movement. The extent of paresis is directly correlated to the number of large lower motor neurons affected. If only a small portion of the large motor neurons are involved, paresis occurs; if all motor units are affected, the result is paralysis.

The small motor neurons play two necessary roles in movement: maintaining muscle tone and protecting the muscle from injury. Usually when the large motor neurons are affected, dysfunction of the small motor neurons causes reduced or absent muscle tone, flaccid paresis, and paralysis.

The muscles innervated by motor neurons in the anterior horn of the spinal cord may also be affected. Paresis results from a decrease in the number or force of activated muscle fibers in the motor unit. The action potential of each motor unit decreases so that additional motor units are needed more quickly to produce the power necessary to move the muscle. Dysfunction of the neuromuscular junction causes paresis in a similar fashion; however, the functional capability of the motor units to function is lost, not the actual number of units.

         The central (spastic) paralyses appear in case of cerebrum cortex violation, where the first neurons corpuses are located, or eather, internal capsule and the cerebrum column, where pyramidal tracts are passing. The central paralysis is characterized with the intentional motions loss; tendonal and periostal reflexes (hyperreflexia) activation, pathological reflexes appearance, for example, the extension of the first ringer in case of the external foot-side irritation (Babinsky reflex) or the crus frontal surface (Openhame reflex). All these changes follow the absence of cerebrum hemispheres cortex inhibiting influence upon the spinal cord neurons. Atrophic and degenerative changes in muscles are not presented.

         Peripheral (flabby) paralysis is observed in fact of spinal cord column. anterior horns, anterior radicles, plexuses and nerves. For peripheral paralysis the total movements loss characteristic – intentional and reflectory. Muscular tonus is absent (atonia). Tendonal reflexes disappear (areflexia), following ars breaking up. Denervated muscles get atrophia exposed, connective tissue spreads. Degenerative changes are characterized.

The next kinds of paralyses are differentiated:

·        monoplegia – one extremity is injured;

·        hemiplegia – one half muscles of the body are violated;

·        paraplegia – the upper or the lower extremities are injured,

·        tetraplegia – all of extremities are violated.

 

Myasthenia. Myasthenia gravis is an unusual disorder affecting muscle function. Normally, when a person decides to move, an impulse is sent down a nerve to the muscle. When the impulse reaches the end of the nerve, the nerve releases a substance called acetylcholine. Acetylcholine theormally binds to the muscle and causes the muscle to contract, which creates movement.

In myasthenia gravis, the body produces antibodies which attack the acetylcholine receptors found on muscles. The purpose of these muscle receptors is to bind the acetylcholine that is released from the nerves, which lets the muscle know when to contract. When the antibodies bind to these muscle receptors, the receptors are then blocked or destroyed, making them unable to bind acetylcholine. This causes muscle weakness, because the signals sent by the nerve cannot get to the muscle. So, while the nerves and muscles both technically are okay in myasthenia gravis, they are blocked from interacting because of the antibodies that are produced.

 

Because the antibodies produced in myasthenia gravis attack the persons own body, myasthenia gravis is known as an autoimmune disease. There are many other autoimmune diseases, such as lupus, rheumatoid arthritis and scleroderma. It is not known why a persons body would produce antibodies that attack their own body, but unfortunately, taken as a group, autoimmune diseases are fairly common.

 

Myasthenia gravis tends to affect younger women, however older persons and males can also be affected. The primary symptom is muscle weakness and fatigue. Classically, the weakness gets worse as the day progresses. The eye muscles are almost always affected, which can lead to a drooping of the eyelids and double vision because the eyes fail to move in a coordinated fashion. The more a muscle is used, the weaker it becomes. If the muscle becomes very weak, a period of rest will often improve its strength. This disease signs are connected with fast fatiguability and muscles weakness. Sometimes the typical paresis and paralyses may happened. Patholodical weakness meets at all muscles at the same time (generalized form) more often, and the separate muscles groups more seldom. Disorders of speaking, chewing,swallowing appear in fact of bulbar form; vision (diplopia), eyelid lowering (ptosis), strabismus – in case of ophthalmic form.

Right ptosis due to myasthenia gravis showing fatiguability of the right lid on sustained upgaze

 

 

When suspected, a simple test can be done to make the diagnosis of myasthenia gravis. A short acting medication called an anticholinesterase can be given. This medicine works by increasing the amount of acetylcholine around muscles. If a person has myasthenia, this medication will make their weak muscles stronger. If they dont have myasthenia gravis, their muscles will not get stronger with the medication. A blood test that detects the muscle receptor antibodies is often used to confirm the diagnosis.

         Hyperkineses – are the unintentional forcible motions, pyramidally or extrapyramidally caused.

         Pyramidal hyperkineses get shown with the convulsive state. Long lasting unintentional are called tonic convulsions (cramps). If muscular contractions alternate with relaxations, such cramps are called clonic. The first appear in fact of subcortical nuclei irritation, while the second – in of cortical neurons activation.

            Generalized convulsions attacks are characterized for epilepsy. They include two phases – tonic ant clonic. Tonic phase lasts about one minute and reflects the total muscular spasm – tetanus. Muscles contraction and relaxation in clonic phase lasts longer – up to 2-3 minutes. During this phase biting of tongue and lips, unintentional defecation and uresis are possible. If cramp attacks come one by one in short time periods, that is called epileptic status.In the majority of cases, the cause of epilepsy is unknown.  Known causes of epilepsy include:

·        Head Injury/Trauma

·        Brain Infection, such as meningitis

·        Brain Tumor

·        Stroke

·        Lead Poisoning

·        High Fever

·        Poor Nutrition

·        Maternal Injury (infection or illness during pregnancy which affects fetal brain development)

·        Lack of Oxygen During Birth

·        Heredity

·        For some epileptic individuals, triggers for seizures can include:

§  Stress

§  Sleep Deprivation/Fatigue

§  Not Eating Enough

§  Alcohol

§  Hormone Fluctuations related to menstruation and/or menopause (in women)

Although epilepsy can develop at any age, most cases of epilepsy develop in children or in adults over the age of 65. Epilepsy is not ign of mental illness or low intelligence.

         Extrapyramidal caused hyperkinesis include tremor, myoclonia, chorea, atetosis.

         Tremor can be observed in case of parkinsonism. It usually appear in state of ward and is combined with muscles rigidity, motional limitation and por facial expression. The reason of  parkinsonism is the injury of substantia nigra and globus pallidus.

         Myoclonia – is the fast and short or like a group and are not followed with the motional action. This can be observed in fact of  encephalitis, atherosclerosis, hypertonic disease.

         Chorea – is non-rythmis, fast, wide extremities and the body movements, with the elements of unnaturality. Some patients with hereditary Gentingtone’s chorea are in state of constant motion, ward periods are practically absent. Rheumatic and atherosclerotic chorea etiology is understood out of their names.

         Atetosis – are slow vermicular movements in distal parts of arms and legs, sometimes – of face and neck. Generalized form of atetosis is called the torsional dystonia.

 

 

Types of hyperkinesia

 

Type	Manifestations	Mechanisms
Athetosis	Slow, sinuous, irregular movements in the distal extremities Characteristic hand posture Slow, fluctuating grimaces	Believed to result from injury to the putamen of the basal ganglion
Ballism	Severe, wild, flinging, stereotypical limb movements Present when awake or asleep Usually on one side of the body	Injury to subthalamus nucleus, causing inhibition of the nucleus
Chorea	Random, irregular, involuntary, rapid contractions of muscle groups Nonrepetitive Diminishes with rest, disappears during sleep Increases during emotional stress or attempts at voluntary movement	Excess concentration or heightened sensitivity to dopamine in the basal ganglia
Intentional cerebellar tremor	Tremor secondary to movement Most severe when nearing end of the movement	Errors in the feedback from the periphery and goal-directed movement due to disease of dentate nucleus and superior cerebellar peduncle
Myoclonus	Shock-like contractions Throwing limb movements Random occurrence Triggered by startle Present even during sleep	Irritability of nervous system and spontaneous discharge of neurons in the cerebral cortex, cerebellum, reticular activating system and spinal cord
Parkinsonian tremor	Regular, rhythmic, slow flexion and extension contraction Primarily affects metacarpophalangeal and wrist joints Disappears with voluntary movement	Loss of inhibitory effects of dopamine in basal ganglia

        

In case of cerebellum violations, such motional disorders take place:

·        atonia – muscles tonus lowering,

·        astasia – unability of keeping the position,

·        ataxia – movements coordination disorders,

·        dismetria – motional power and the vector unequilibrium,

·        astenia – the fast fatiguibility.

SENSITIVITY DISORDERS

         The sensitive function of system provides the transmission of four sensitivity kinds form peripheral up to cerebrum – algesic, themperatural, proprioceptive, tactile. Sensitivity disorders are available in case of any sensory tract part violation.

         The peripheral nerve injury (traumatic overcut, inflammatory process) leads to all sensitivity kinds loss at the zone of its innervation. The total loss is called anesthesia, sensitivity increase – hyperesthesia.

         The total spinal cord break out is also followed with all sensitivity kinds disappearing below the injury point. The half-cutting of the spinal cord (Brown-Sekar’s syndrome is characterized with such signs:

·        the total loss of proprioceptive sensitivity on the violated side;

·        the total loss of algesic and temperatural sensitivity on the opposite side;

·        the partial loss of tactile sensitivity on the both sides.

The local injury of cerebrum or spinal cord (neoplasm, traumatic pressing, hemorrhagy) provides the selective disappearing of sensitivity, depending of what’s the upgoing ways are violated. The loss of sensitivity is called anesthesia, the loss of algesic sensitivity – analgesia, the loss of themperatural sensitivity – thermoanesthesia. The loss of proprioceptive (deep located) sensitivity is also available. The sensitivity increase is called hyperesthesia, and the appearance of unusual feelings (tingling, anttickling) – paresthesia.

PAIN

The sensitive function of the nervous system consists of four kinds of sensitivity  realization from periphery to brain – they are painful, temperature, tactile and proprioceptive. This is one of major functions of the nervous system. To the brightest manifestations it the perception of the painful information.

Pain and anaesthetization – ancient a problem of medicine. On data WHO, each day on earth suffers from a pain of 3.5 million persons. The pain acquires from 30 % from them intolerable character. Very acutely there is a problem of removal of  pain in the hopeless patients, for example in the patients with an inoperable cancer. In 50-80 % such sufferers the pain is not possible satisfactory to remove. These and many other facts testify to an extreme urgency of a pain problems.

There isn’t generally accepted definition of notion “pain”. There are many sights on essence of this process. To generalize them it is possible as follows. Pain is the typical process, which was generated during evolution and which arises for want of action on an organism painful irritable or for want of weakening antipainful system. This process consists of the following components:  а) perception, realization and comprehension of  pain; b) creation vegetative, emotional and behavioural of responses; c) mobilization of anti- painful systems.

Classification of  pain

It is selected physiological and pathological pain. The physiological pain arises as adequate response of the nervous system on situations, dangerous to an organism. it is the factor of warning, signal about a potentially dangerous situation. This pain is directed on protection of an organism against damage. The pathological pain arises for want of the nervous system damage  more often. Protective character it has not. On the contrary, it exhausts protective forces of the patient and aggravates current of illness.

It is distinguished also acute and chronic pain. Acute pain short-term. It is subdivided into two varieties – primary and secondary. The primary pain arises at once after effect painful irritant – injection, cut, stroke of current, touch of  hot subject. This pain located, it arises in the center of damage. It is not removed morphine. Significance of a primary acute pain precautionary, signal. The secondary pain occurs later. In reply to damage of tissues the biological active substances – histamine, serotonin, prostaglandins, bradycinin, substance Р, ions K⁺ and Н⁺ are stored. they form smarting the non-located pain, which is removed morphine. Signal significance it has not. The chronic pain lasts longly – hours, days, weeks, sometimes – all life. It appears as chronic painful syndromes.

The nociceptive system

The pain – reflex process, which is carried out for want of availability of three main parts of reflex arc – receptor, conductors and central cerebral of structures.

Perception, realization and comprehension of a pain. The pain is perceived by the nervous terminations. There are two points of view on this process. They are made out as two theories – theory of specificity and theory of intensity.

According to the theory of specificity, the painful irritation is perceived special painful receptors. The most characteristic property these receptors – high threshold of sensitivity. They are excited only in the event that acts painful irritant of the large force, which is capable to damage to a tissues.

 

THEORIES OF PAIN

Over the years numerous theories have attempted to explain the sensation of pain and describe how it occurs. No single theory alone provides a complete explanation. This chart highlights some of the major theories about pain.

 

Painful receptors are distributed in an organism non-uniformly. Most of all them in skin, brain shells, pleura, peritoneum, periosteum, in eye and internal ear, in tissue of outside sexual organs. But they practically are absent in bones and tissue of  brain. It is not enough of them in parenhyma of internal organs. Besides for receptors of internal organs the extremely high threshold of sensitivity is characteristic. It is much higher, than for painful receptors of skin or mucous. Therefore pain in internal organs does not arise for want of injection or cut them. It occurs only for want of expansion them or them capsules, and also for want of narrowing or extension internal organs of vessels.

The supporters of the theory of intensity explain perception of  pain slightly in another way. They consider, that painful the impulse arises for want of irritation anyone receptor – painful, temperature or tactile. It is necessary only, that this irritation was strong, that it has damaged  tissue.

Painful the information from receptors is transmitted to brain. Three are involved in this transfer neuron: first is in cerebrospinal  node, second – dorsal horns  of spinal cord, third – in thalamus.

From receptors up to first neurons in cerebrospinal a node painful impulses are conducted by  somatical nerves. These nerves consist of fibres of two kinds – myelinized and nonmyelinized. Myelinized of  fibre (group A) provide fast realization painful of impulses, nonmyelinized of  fibre (group С) conduct them slowly.

From first neuron through dorsal radices painful impulses act(arrive) in grey substance of dorsal horns of spinal cord (second neuron). Impulses, which enter into  back brain on fibres А, form the acute primary pain. The impulses, which enter on fibres C, form acute secondary pain.

From dorsal horns of spinal cord (second neuron) begins spinothalamic path. The fibres of second neuron are lifted from the same party on 1-2 segments and pass to the opposite side. Then in structure side funiculus they are lifted in medulla oblongata, trunk of  brain and visual tuber. Third neuron  is located here.

Spinothalamic the path terminates in three areas visual tuber – ventropostlateral  nucleus, dorsal group of nucleuses and medial nucleuses. In ventropostlateral  nucleus is neural representation of  trunk. In ventropostmedial  nucleus the fibres terminate which bring painful impulses from  face. Both these nucleuses make so-called ventrobasal  complex.

Spinothalamic the path is divided on two paths – neospinothalamic and paleospinothalamic. Neospinothalamic path phylogenetic younger. It the nervous fibres achieve ventropostlateral of  nucleus thalamus. Here is formed discriminating painful sensitivity, that is the localization of  pain is defined. Paleospinothalamic path older. It is connected to nucleuses thalamus around of the Selvium water-pipe, with back group of nucleuses thalamus, with hypothalamus, limbic by structures, cortex brain. It forms feeling of acute pain including of responses endocrine, cardiovascular also of respiratory systems, emotional and motor responses.

With ventrobasal by a complex closely are connected somatosensory of  zone cortex brain. The part of fibres third neuron goes from visual tuber to dorsal central girus. A sensory zone S1 here is located. Here there is a comprehension of  pain, analysis of its significance for an organism.

 

Creation of vegetative, emotional and behavioural  responses. The fibres spinothalamic of path are connected to many nucleuses subcortex – by vasomotor centre, respiratory centre, centre of satiation. Therefore process of a pain creation  is accompanied expressed by vegetative responses, which has adjust protective character. It is increase of heart beat, increase of output, acceleration bleeding, increase arterial of pressure, increase of breath, increase of  level of sugar in blood etc.

The important significance in formation of  pain belongs to limbic derivations and front department cortex brain. They are responsible for formation emotions and behaviour. Consider, that hypothalamus executes functions of the executive body in formation emotions, and limbic  structure (septum, hypocampus, tonsil) cause modulating influence. The pain is always accompanied emotions – mental excitation, anger, fear, aggression.

Assessment of  biological significance of painful stimulus carry out mainly front department of  brain cortex and hyppocampus. Tonsil defines behaviour on these stimulus. The upper wall side sulcus is involved in this. In it  is located second somatosensory zone S₂.  It regulates the motor  act  on  pain.

All responses accompanying a pain – vegetative, emotional, behavioural – in the beginning have protective significance. In case of  chronic pain these responses become parts pathogenesis chronic painful of syndromes.

In all departments of the nociceptive system the transfer of painful impulses is carried out with the help mediator of  pain. Here belong substation Р, glutaminic acid, cholecystokinin, neurotenzine and other substances. Major mediator of a pain considers substation Р. It is revealed at all stages of transfer painful  impulses – in dorsal horns of  spinal cord, trunk of  brain, hypothalamus, visual tuber, cortex  brain. The action of substation Р is blocked by external (morphine) and internal (encephalins, β–endorphins) opiate.

The following three variables contribute to the wide variety of individual pain experiences:

·         Pain threshold: level of intensity at which a stimulus is perceived as pain

·         Perceptual dominance: existence of pain at another location that is given more attention

·         Pain tolerance: duration or intensity of pain to be endured before a response is initiated.

The antinociceptive system

This system includes two levels of painful information  control: central – at  level of brain and segmented – at level of  spinal cord. The control is carried out with the help of biologically  active substances. Depending on the mechanism analgesia is selected four antinociceptive systems.

The neuronal opiate system. In 1973 the important opening – in some structures of brain the investigators detected congestions of substances similar on opium. These substances extracted from brain, have determined their chemical structure and have named encephalins. Except for  brain, them have found in cerebrospinal of  liquid and blood.

enkephalins are distributed in  nervous tissue non-uniformly. Most of all them is in those structures of brain, on which the information is transmitted painful. It is gelatinous substation of dorsal horns of spinal cord, reticular formation, grey substance around of Sylvian aquaduct, hypothalamus, limbic  structure, cortex. on neurons, which are included into composition of these structures, are located specific receptors. They are capable to bind endogenous opiate of a type encephalins and exogenous opiates of type morphine and it synthetic analogues. These receptors were called opiate. The binding endogenous or exogenous opiates with specific receptors causes antipainful effect. The mechanism of anti-painful action opiates is connected to the large sizes of their molecules. Opiates competitive bind receptors and do not allow mediators of pain (for example substance Р) to contact with same receptors. The stream of painful impulses from periphery in brain weakens. The pain decreases.

The neuronal neoopiate system. Antipainful action of this system will be realized through noradrenaline, serotonin, dofaminum.

noradrenaline oppresses realization painful of impulses at level of spinal cord and at level of trunk brain. Noradrenergic of structure are concentrated in lateral departments of brain trunk and intermediate brain. Especially it is a lot of them in reticular structure. Stimulation of central adrenergic structures causes analgesia. First of all, are oppressed behavioural and hemodynamical  response.

Serotonin causes antipainful action only for want of significant excess. Manu  of serotoninergic neurons is found in gelatinous  substance of dorsal horns of  spinal cord, medulla oblongata, Varolii pons, medial thalamus.  To serotonin the exclusive role in genesis of  headache belongs. before painful attack the contents serotonin sharply increases and develops vasoconstriction. Then there is  increased serotonin by monoaminooxydase, and also excretion it with urine in the not changed kind. Thus, after hyperserotoninemia the falling it monoamine in blood and antinociceptive structures of  brain occurs. At this particular time appeares headache.

The hormonal opiate system. It is represented by products of anterior hypophysis. adenohypophysis synthesizes difficult substance proopiomelanocortin. Farther with  removal peptide of fragments from it will be derivated adrenocorticotropic, melanocytostimulating and β-lipotropic hormones. All these hormones cause anaesthetic action. Besides from β-lipotropic hormone content substance – β-endorphine. In the structure it contains encephalin and has extremely powerful antipainful effect. Farther from other tissues the new substances containing encephalins were selected. All of them were united in one group and have received the name “large endorphines”. To them belong kytorphine, in – kosomorphine, dinorphine.

The hormones of neopiate system. It is represented vasopressin. This hormone is formed in supraoptic and paraventricular nucleuses hypothalamus and is secreted in blood by dorsal part of  hypophysis. The appearance of a pain quite often is combined with of bloodloss. Vasopressin in these cases influence double action – it detains  liquid and reduces  pain.

Consider that antinociceptive  system influences, mainly, realization of painful  impulses on spinal cord. These submissions base on the theory Melzack and Wall, which  received the name of portal   control  theory.

In opinion of the supporters of this theory, the realization painful of impulses in  spinal cord depends, mainly, on activity neurons gelatinous of substation of spinal cord dorsal horns (substantia gelatinosa). These neurons execute the function of  gate, which pass in brain greater or smaller volume of painful information.

Afferent impulsation come in  spinal cord for two types of nervous fibres – thick and thin. Impulses going on thick fibres, arise for want of operation of the not damaging factors (grinding, electrostriction, acupuncture). The impulses, which go on thin fibres, arise for want of the damaging factors action. They purely also are painful. The balance between these two impulse streams determines how many painful information reaches brain. If the stream of impulses on thick fibres dominates, neurons gelatinous of substation are activated. Arises presynaptic braking nervous terminals, which contact with inserted Т-neurons. The transfer painful of impulses on Т-neurons is braked, and the source gate for painful information is closed. If prevails impulsation on fibres of small-sized calibre, neurons gelatinous substation are oppressed. Painful impulsation breaks on Т-neurons and is transmitted above to brain.

Chronic pain

The chronic pain arises for want of durablis damage of  fabric (fracture, inflammation, tumour). The constant pain impulsation causes extraordinary activation hypothalamus, hypophysis, sympaticoadrenal, limbic  structures. Therefore chronic pain is accompanied by complex and long changes of behaviour of  person, it of mentality, emotions, attitude to the serounding world.  For want of chronic pains nociceptive system always dominate above antinociceptive systems. the sensitivity painful receptors is increased. In this connection even unpainful  influence (touch, easy pressing, movement) can cause painful sensation. The chronic pain appears as painful syndromes.

The phantom pain is a pain in amputated extremeties. The majority of the patients approves, that feels phantom extremety almost at once after amputation. The pain in phantom extremeties has a definite form, it reminds present extremety. The phantom pain lasts very longly, sometimes years and decades.

Causalgia is strong poignant pain connected to strong deformation of nerve for want of wound by high-speed shell (by  bullet, splinter). Causalgia is characterized by unabating intensive pain, which amplifies for want of operation even weak irritable, which in healthy person of pain do not cause (touch, unexpected noise, sharp light, emotional effect).

Neuralgia is characterized by a strong pain also connected to damage of peripheral nerve. On the manifestations it is similar to causalgia. The reasons it is a virus infection (herpes zoster), degeneration of nerves for want of  diabetes mellitus, ischemia extremities, beri–beri, poisoning arsenic or lead.

Especially severe it happens neuralgia trigemnius nerve. Paroxysms of pain arise for want of talk, the use of food or spontaneously.

 

Eccentric pain is a pain in the certain sites of a skin for want of internal organs defeat. Occurrence it explain as follows. Afferent impulsation from internal organs and from appropriate dermatom acts in same neuron of dorsal horns of spinal cord, which give beginning to spinothalamic path. If the internal organ is injured, from it is going extremely powerful streams of painful  impulses. They increase sensitivity skin receptors appropriate dermatom. In the total the pain going from an internal organ, is perceived simultaneously and as  pain in the certain site of skin.

The projectional pain arises for want of compression and damage of nerve or spinal cord horns of counterfoils. It is territorial  limited to a site innervation of  sensitive nerve. Occurrence it explain to  that the excitation from  place of nerve damage is distributed not only in the central nervous system, but also in a zone innervation.

Methods of anaesthetization

In modern medical practice the following methods of decrease or complete removal of  pain are used: psychological, physical, pharmacological, surgical, neurosurgical.

The psychological methods are directed on removal of general nervous tension, suppression of fear  feeling and concern by the state. It achieve by conversations, autotraining, relaxation.

Physical methods is acupuncture, electropuncture, transcutaneous electrostimulation, ultrasound, electrophoresis.

Acupuncture

For want of it at the expense of a durablis and weak irritation and realization impulses on thick fibres the formation encephalins amplifies. They block realization of painful  impulses at  level of dorsal horns of  spinal cord.

The pharmacological preparations are capable to oppress formation, transfer and perception painful impulses at different levels of the nervous system – receptor, conducting and central (back horns of  spinal cord, trunk of  brain, cortex of  large hemispheres).

The surgical methods are reduced to removal of the pain reason: opening abscess, reposition of parts, splinting extremities, excision scars, desympathization, ganglioectomia.

Neuro-surgical anaesthization is achieved by two methods – by the termination of transfer painful information to highter departments of  brain and stimulation descending antinociceptive of systems through electrodes, which implant in grey substance around Sylvian aqueduct and iucleuses of  seam.

 

DISORDER OF  TROPHIC FUNCTION OF NERVOUS SYSTEM

Nerve cells are the functional units of the nervous system. The nervous system is believed to have ten thousand million of such cells, called neurons and glia, the glia being present in greater numbers thaeurons.Figure is an idealized diagram of a neuron with its three most important structural features: the cell body, the dendrites and the axon terminal.

The anatomy of the neuron

 

The dendrites are finely branched processes arising near the cell body of a neuron. The dendrites receive excitatory or inhibitory effects via chemical messengers called neurotransmitters. The cytoplasm is the material of the cell body in which the organelles-including the cell nucleus-and other inclusions are found. The nucleus contains the cell’s chromatin, or genetic material.
      

The organelles

The nucleus of the nerve cell is atypical compared with that of other living cells in that, although it contains the genetic material deoxyribonucleic acid (DNA), the DNA is not involved in the process of cell division; that is, after reaching maturity, nerve cells do not divide. (An exception to this rule are the neurons in the nose lining (olfactory epithelium).) The nucleus is rich in ribonucleic acid (RNA), which is necessary for the synthesis of protein. Three types of proteins have been identified: cytosolic proteins, which form the fibrillar elements of the nerve cell; intracondrial proteins, which generate energy for cell activity; and proteins that form membranes and secretory products. Neurons are now conceived of as modified secretory cells. Secretory granules are formed, stored in synaptic vesicles and later released as neurotransmitter substances, the chemical messengers betweeerve cells. The fibrillar elements, which form the skeleton of the neuron, participate in the trophic function of the neuron, acting as vehicles of transmission. Axonal transport can be anterograde (cell body to axon terminal) and retrograde (axon terminal to cell body). From the thickest to the thinnest, three types of fibrillar elements are recognized: microtubules, neurofilaments and microfilaments.

In contrast to neurons, glial cells do not, by themselves, carry electrical messages. There are two types of glial cells: the macroglia and the microglia. The macroglia is a name given to at least three types of cells: astrocytes, oligodendrocytes and ependymal cells. Microglial cells are primarily scavenger cells for removing debris after neural damage or infection has occurred.The glial cells also have distinctive microscopic and ultramicroscopic features. Glial cells physically support neurons, but a number of physiological properties are also now beginning to be understood. Among the most important neuron-glial interactions are the glial cell’s role in providing the neurons with nutrients, removing fragments of neurons after their death and, most importantly, contributing to the process of chemical communication. Glial cells, in sharp contrast to neurons, can divide and thus can reproduce themselves. Tumours of the nervous system, for example, result from an abnormal reproduction of glial cells.

What appears in the macroscopic observation of neural tissue as “grey matter” and “white matter” has a microscopic and biochemical basis. Microscopically, the grey matter contains the neuronal cell bodies, whereas the white matter is where neural fibres or axons are found. The “white” appearance is due to a sheath-composed of a fatty substance called myelin-covering these fibres. Myelin of the peripheral nerves originates from the membrane of the Schwann cell which wraps around the axon. The myelin of fibres in the central nervous system is provided by the membranes of the oligodendrocytes (a variety of glial cells). Oligodendrocytes usually myelinate several axons, whereas the Schwann cell is associated with only one axon. A discontinuity of the myelin sheath-designated as nodes of Ranvier-exists between continuous Schwann cells or oligodendrocytes. It is estimated that in the longest central motor pathway, up to 2,000 Schwann cells form the myelin cover. Myelin, whose role is to facilitate the propagation of the action potential, may be a specific target of neurotoxic agents. A morphological classification of neurotoxic substances describes characteristic neuropathological changes of the myelin as myelinopathies.

Trophic function of the neuron

The normal functions of the neuron include protein synthesis, axonal transport, generation and conduction of the action potential, synaptic transmission, and formation and maintenance of the myelin. Some of the basic trophic functions of the neuron were described as early as the 19th century by sectioning the axons (axotomy). Among the processes uncovered, one of the most important was the Wallerian degeneration-after Waller, the English physiologist who described it.Wallerian degeneration provides a good opportunity to describe well-known changes in organelles as a result of either traumatic or toxic damage. Parenthetically, the terms used to describe Wallerian degeneration produced by traumatic axotomy are the same ones used to describe changes resulting from neurotoxic agents. At the cellular level, neuropathological changes resulting from toxic damage to neural tissue are far more complex than those occurring as a result of traumatic damage. It is only recently that changes ieurons affected by neurotoxic agents have been observed.

Twenty-four hours after cutting of the axon, the most distinctive feature is swelling of both sides of the mechanical trauma. Swelling results from accumulation of fluids and membranous elements on both sides of the site of injury. These changes are not unlike those observed in a rain-flooded two-way road with vehicles stopped on both sides of the flooded area. In this analogy, stalled vehicles are the swelling. After a few days, regeneration of the ensheathed axons-i.e., those covered with myelin-occurs. Sprouts grow from the proximal stump moving at the rate of 1 to 3 mm per day. Under favourable conditions, sprouts reach the distal (farther from the cell body) stump. When renervation-joining of the stumps-is completed, the basic features of normal transmission have been re-established. The cell body of the injured neuron undergoes profound structural changes in protein synthesis and axonal transport.

If molecular neurobiology is said to be a young discipline, the neurobiology of the neurotoxic processes is even younger, and still in its infancy. True, the molecular basis of action of many neurotoxins and pharmacological agents is now well understood. But with some notable exceptions (e.g., lead, methyl mercury, acrylamide) the molecular basis of toxicity of the vast majority of environmental and neurotoxic agents is unknown. That is why, instead of describing the molecular neurobiology of a select group of occupational and environmental neurotoxic agents, we still are forced to refer to the comparatively abundant strategies and examples from classical neuropharmacology or from work in modern drug manufacture.

Cytokines and trophic factors (TF) are involved into the nervous system activity regulation that confirms by their secretion and receptors identification withiervous system. Cytokines and TF production increases tremendously in response to CNS alterations or other CNS pathologic events where they are modulated both alterative and protective effects.

Neurotrophins provide trophic and tropic support for different neuronal subpopulations in the developing and adult nervous systems. Expression of the neurotrophins and their receptors can be altered in several different disease or injury states that impact upon the functions in the central and peripheral nervous systems. The intracellular signals used by the neurotrophins are triggered by ligand binding to the cell surface Trk and p75NTR receptors. In general, signals emanating from Trk receptors support survival, growth and synaptic strengthening, while those emanating from p75NTR induce apoptosis, attenuate growth and weaken synaptic signaling. Mature neurotrophins are the preferred ligand for Trk proteins while p75NTR binds preferentially to the proneurotrophins and serves as a signaling component of the receptor complex for growth inhibitory molecules of central nervous system myelin [ie, myelin-associated glycoprotein (MAG), oligodendrocyte-myelin glycoprotein (OMgP) and Nogo]. The functional antagonism between Trk and p75NTR signaling may significantly impact the pathogenesis of humaeurodevelopmental and neurodegenerative diseases and further complicate therapeutic uses of exogenous neurotrophins.

Trophic function disorders

The notion of a trophic ulcer is nosologically indefinite at present. These disorders involve hemocoagulation, angiopathic, and chronic inflammatory processes in the derma, that lead to necrosis and sclerosis of dermal connective tissue. Contribution of the body reactivity characteristics to the formation of trophic ulcers is discussed, as are the role of skin morphofunctional features and of exogenous factors. Diabetic ulcers are one example of neuropathic ulcers. They always occur on the foot. They occur either as perforating ulcers on the sole of the foot beneath the heads of the metatarsals or at other bony prominences (e.g. the toes, the ball of the great toe, the malleoli).Typically a diabetic ulcer is deep, painless, and infected and has a ‘punched out’ appearance. These ulcers are known as ‘perforating ulcers’. Tissue surrounding the ulcer is generally well perfused. Peripheral pulses are often palpable. In the case of neuropathic ulcers, there is generalised sensory impairment. There is often a history of minor trauma that precedes the development of the ulcer. Note that infection may spread quickly and may lead to extensive limb-threatening necrosis and septicaemia.

Skin trophic ulcer

 

EXTREME STATES. SHOCK. COLLAPSE. COMA

Definition of concept. General characteristic. Reasons and mechanisms of development

Extreme states are the conditions of organism described by an excessive straining or an exhaustion of adaptive mechanisms. Extreme conditions may develop primarily by action on an organism of various extreme irritators (for example, traumas, endogenic intoxications, severe fluctuations of air temperature and concentration of oxygen) or to become a result of adverse course of disease (for example, insufficiency of blood circulation, respiratory, renal or hepatic insufficiency, anemia etc.).

When pathogenicity of extreme irritator exceeds maximum possibilities of adaptation of an organism, heavy disorders of the vital functions and direct threat of life appear. In such cases preterminal and terminal conditions may occur. Many forms of extreme conditions are convertible, while terminal conditions without special emergency help lead to death of  an organism. In these cases life of the patient depends directly on condition of breath and blood circulation, and also from time which has passed after their stop. The most important and frequently occuring extreme conditions are collapse, shock and coma.

In development of extreme conditions important meaning belongs to activation of sympathoadrenal and pituitary-adrenal systems typical for stress. In the process of deepening of condition heaviness there are narrowing of adaptive reactions, disintegration of functional systems which provide complex adaptive behavioural acts and delicate regulation of locomotor and vegetative functions. One of mechanisms of organism transition on extreme forms of adaptation is progressing switching-off of  central neurons from various afferentation which provide formation of complex functional systems. The minimum afferent signals necessary for realization of breath, blood circulation and other vital functions are reminded only. Regulation of life processes basicly passes to a metabolic level. In this stage, as a rule, there are expressed infringements of all physiological functions. For pathogenesis of extreme conditions development of chain of pathological reactions which aggravate organism disturbance is characteristic.

At all extreme conditions similar disturbances of metabolism and physiological functions, first of all hypoxia, are observed. In some cases hypoxia is initial ethiologic factor which results in development of extreme condition. However, more often hypoxia appears secondary during development of extreme condition caused by any other influence.

Extreme conditions are usually accompanied by the strengthened liberation and formation of histamine, serotonin, kinins, lysosomal enzymes and other biologically active substances. Therefore to extreme conditions disturbances of microcirculation are peculiar: infringement of perfusion of microvessels, dilatation and decrease of their sensitivity to vasopressing influences, increase of permeability of vascular walls and their structural infringements even to necrobiosis. Pathological aggregation of erythrocytes, ‘sludg-syndrome’, hypercoagulation of blood, disseminated intravascular coagulation of blood and microthrombosis of vessels. Disturbance of microcirculation in lungs (so-called ‘shock lung’) may result in their severe infringements of gas change functions, similar changes in kidneys (‘shock kidney’) may lead to renal insufficiency. Infringements of microcirculation system in liver and brain may cause hepatic insufficiency and severe disturbances of nervous system.

At all extreme conditions infringements of hemodynamic system is observed, described by decrease of volume of circulating blood and speed of blood flow, increase of blood deposition, decrease of venous return of blood to heart, fall of tone of arterioles and veins even to their paresis and decrease of general peripheral resistance of vascular system are observed also. As to the heart, the tachycardia, various forms of arrhythmias, insufficiency of coronary circulation, decrease of cardiac output and other attributes, characteristic for heart insufficiency are frequently observed.

Infringements of external breath during the extreme conditions are shown by various changes of its depth and frequency, rhythm of respiratory movements, periodic breath.

Infringements of functions of nervous system at early stages of development of an extreme condition are various. So, at the majority kinds of shock after the period of the general excitation in erectile phase original combination of the kept consciousness with the general deep block in torpid phase is typical. Consciousness is lost only at the end of this phase at transition to a terminal condition.

Shock.  Classification. Ethiology, pathogenesis, consequences

Shock is grave pathological process accompanying with an exhaustion of the vital functions of an organism and resulting it on a side of life and death because of critical decrease of capillary blood circulation in lesion organs.

Depending on the reasons of occurrence there are following kinds of shock:

·        traumatic;

·        hemorrhagic;

·        burn;

·        turnicate (develops after removal of jute after four hours and more after imposing);

·        anhydremic (dehydrative);

·        cardiogenic;

·        pancreatic;

·        septic;

·        infectional-toxic;

·        anaphylactic.  

 

Depending on the initial mechanisms underlying in pathogenesis of shock there are:

·        hypovolemic shock (hemorrhagic, anhydremic);

·        shock connected with disturbances of pump function of heart (cardiogenic);

·        vascular forms of shock (anaphylactic, pancreatic);

·        pain shock at which the central regulation of blood circulation (traumatic, after burning) is damaged.

 

Mechanisms of general hemodynamics infringements and microcirculation during shock

Irrespective of the reasons of occurrence the shock is shown by a complex of infringements of hemodynamics for which are characteristic:

·        reduction of arterial pressure;

·        reduction of circulating blood volume ;

·        decrease of volumetric speed of organ circulation;

·        infringement of reologic properties of blood (aggregation of form elements, increase of blood viscosity).

The complex of the specified infringements is designated as acute insufficiency of blood circulation. Initial infringement of its parameters at any version of shock leads again to infringements of all others. In basis of development of blood circulation disorders  at shock the following mechanisms may lay.

I. Reduction of volume of circulating blood:

1) blood loss (hemorrhagic shock);

2) loss of blood plasma at massive exudative inflammation (burn shock);

3) an exit of fluid from blood vessels (anaphylactic shock);

4) dehydration (anhydremic shock);

5) redistribution of blood in vascular system (thrombosis and embolism of main veins).

II. Reduction of minute volume of heart:

1) infringement of contractive functions of heart (heart attack of myocardium);

2) tamponade of heart (heart break, exudative pericarditis);

3) arrhythmias (fibrillation of ventricles).

III. Reduction of the general peripheral resistance in result of generalized dilation of vessels:

1) fall of neurogenic tone of arterioles (pain forms of shock);        

2) reduction of basal tone of vessels under action of biologicaly active substances (anaphylactic, pancreatic shock) or toxic products (traumatic, turnicate, infection-toxic shock).

IV. Infringements of reologic properties of blood:

1) syndrome of intravascular disseminated coagulation of blood (pancreatic shock);

2) aggregation of form elements of blood (septic, infection-toxic shock);

3) concentration of blood – hemoconcentration (anhydremic shock).

Correlation and expressiveness of pathogenetic mechanisms of each kind of shock are various. At the same time in mechanisms of development of all kinds of shock it is possible to allocate the common part. It is submitted by consecutive inclusion of two types of compensatory-adaptive mechanisms.

The first (vasocontractive) type – activation of sympathoadrenal and pituitary-adrenal systems. They are activated by main pathogenetic parts. Absolute hypovolemia (loss of blood) or relative (decrease of minute volume of blood and venous return to heart) results in decrease of arterial pressure of blood and decrease of baroreceptors  activity , which through the central nervous system activates some adaptive mechanism. The pain irritation, sepsis stimulate its switching. As a result of activation sympathoadrenal and pituitary-adrenal systems there is an emission adrenaline and corticosteroids. Epinephrines would cause consrtiction  of vessels through a-adrenoreceptors of skin, kidneys, organs of abdominal cavity). Circulation in these organs is sharply limited. Coronary and brain vessels do not have  a-adrenoreceptors and do not constrict. Centralization of blood circulation, that is presented by remaining of blood circulation in vital organs and pressure in large arterial vessels takes place.

However, acute restriction of blood circulation in skin, kidneys, organs of abdominal cavity causes their ischemia. Hypoxia appears. It switches the second (vasodilating) type of the mechanisms directed on elimination of ischemia. Vasoactive amines are formed, causing dilation of vessels, increase of their permeability and infringement of reologic properties of blood. Besides there is a disintegration of corpulent cells, activation of proteolytic enzymes, output from cells potassium ions. There is an inadequate dilatation of vessels, change of microcirculation in tissues, decrease of capillary and strengthening of shunt blood flow, change of reaction of precapillary sphincters on epinephrines and increase of permeability of capillary vessels. Thus, the fluid goes out from the vessels into tissues and venous return decreases. Vice circle appears at level of cardiovascular system, leading to reduction of cardiac output and decrease of arterial pressure. There are disorders of lungs’ function (shock lung), kidneys, coagulation of blood. Development of shock depends also on condition of an organism. All factors causing its weakening, promote development of shock.

Pathogenesis of shock

 

Heaviness of consequences of shock depends first all on infringement of blood circulation of: a) brain, b) coronary vessels, c) kidneys. As a result of these disorders the central regulation of vital functions is damaged, even to development of coma, acute cardiovascular and renal insufficiency. Occurrence of hypoxia, acidosis and intoxication leads to generalized and irreversible damage of cells.

Each kind of  shock has its features of development.

Traumatic shock develops owing to large damages of tissues.

In its clinic two stages are distinguished: 1) excitation (erectile); 2) inhibition (torpid). The stage of excitation is short-term, is characterized by excitation of the central nervous system owing to reception of pain impulses from the injured tissues. Thus, pain stress which is shown by strengthening of functions of blood circulation  system , breath, some endocrine glands (adenohypophysis, brain and cortex substances of adrenal glands, neurosecretory nucleus of hypothalamus) with liberation in blood of superfluous quantity of corticotropin, adrenaline, noradrenaline, vasopressin develops.

The stage of inhibition is more  long (from several hours to about day) and is characterized by development inhibition processes in the central nervous system. General inhibition seizes also the centres of the vital functions (blood circulation, breath), they are broken, owing to what oxygen starvation develops. Hypoxia, in turn, aggravates infringements in cardiovascular and respiratory centres. Disorders  of haemodynamic and external breath progress vice circle becomes isolated.

Except nervous – reflex mechanisms in occurrence and development of  traumatic shock the certain role plays also toxaemia, caused by absorbcion in blood of products of impractical tissues disintegration. Recently special value is  given to so-called ischemic toxin. Participation of toxic products in pathogenesis  traumatic shock is proved by experiments with crossed  blood circulation.

       Hemorrhagic shock appears during external (knife, bullet wound, erosion bleedings of stomach at stomach ulcer, tumors, from lung at  tuberculosis etc.) or internal (hemothorax, hemoperitonium) bleedings in conditions of tissues traumation.

Anhydremic shock appears owing to significant dehydratation at  loss of  liquid and electrolytes. During the exudative pleurities, intestinal obturation, peritonitis liquid comes from  vascular system into cavities. During the unrestrained vomitting and strong diarrhea the liquid is lost outside. Develops hypovolemia which plays a role of main pathogenetic link.

Burn shock appears at extensive and deep burns. Thus in the first day permeability of capillaries is sharply increased, especially in  zone of  burn that leads to  significant exit of  liquid from vessels into tissues. A large amount of edematic liquid, mainly in  place of damage, evaporates. Main pathogenetic factors are hypovolemia, pain irritation, expressed increase  of vessels permeability .

Septic (endotoxin) shock appears as complication of sepsis. Main damaging (injuring) factor are endotoxins of microorganisms. The most often reason of  sepsis are grammnegative microorganisms, and also streptococci, staphylococci, pneumococci and many others.

Main pathogenetic parts of  septic shock:

1) Increase of requirement of an organism in oxygen owing to amplification of exchange processes, tachypnoe,  tachycardia,  fever. Then decrease of the general peripheral resistance of vessels is observed;

2) Decrease of  blood oxygenation in lungs and insufficient extraction of oxygen from blood by tissues. Oxygenation  is decreased in connection due to circulation infringements in a small circle, aggregation of trombocytes on walls of vessels;

3) Activation by endotoxins of proteolytic systems in biological liquids (kallikrein-kinin’s, complement, fibrinolytic).

Cardiogenic shock is observed at decrease of pump function of cardiac muscle (heart infarction, myocarditis), at heard disorders of  heart rhythm (paroxysmal tachycardia), at tamponade heart (thrombosis of cavities, exudation or  bleeding in pericardium), at massive embolia of lungs arteries (tromboembolia of lungs). Main mechanism cardiogenic a shock is reduction of stroke and minute volume of blood, arterial pressure and increase of heart filling pressure. As well as at anhydremic  shock, owing to sympathoadrenergic reactions, the tachycardia, increase of peripheral resistance of vessels is observed.

Anaphylactic shock develops owing to increased sensitivity of an organism  to substances of an antigenic nature and accumulation histamine and others vasoactive substances (kinins, serotonin).

Thus there is strong reduction of venous return to heart. The reason of it is dilatation of capillary and capacitor vessels. The congestion of blood in capillary vessels and veins results in reduction of circulating blood  volume. Infringement of contractive activity of heart is observed also. Sympathoadrenergic reaction thus is not expressed because of a vascular tone  infringement.

 

Collapse.  Classification. Ethiology, pathogenesis and consequences.

Collapse is an acute vascular insufficiency  which is characterized by fall of a vascular tone, and also acute reduction of circulating blood  volume .

At the collapse there is a reduction of venous blood  inflow to heart, decrease of heart output, fall of arterial and venous pressure, infringement of tissues perfussion and  metabolism, comes hypoxia of brain appears, the vital functions of an organism are oppressed. It is shown in clinics by short-term loss of consciousness,  general weakness, features of acute vascular insufficiency with infringements hemodynamics practically in all organs and  tissues.

In a basis of development of collapse discrepancy between volume of circulating blood and capacity of a vascular system lays. The reasons may be  sudden reduction of blood volume (blood loss, dehydratation), and sudden  dilatation of vessels. Collapse develops as complication at heard diseases and pathological conditions.

The infectious collapse develops as complication of acute infectious diseases: meningoencephalitis, and typhoid fever typhus fever, acute dysentery,  pneumonia, botulism, the Siberian ulcer,  virus hepatites,  toxic influenza. The reason of such complication is the intoxication by endo- and exotoxins of microorganisms, mainly that influence on central nervous system, or receptors of pre- and postcapillaries.

Hypoxic collapse may appear in conditions of reduced partial pressure of oxygen in air. The direct reason of circulation infringements thus is insufficiency of adaptive reactions of an organism to hypoxia. To development of  collapse in these conditions may promote also hypocapnia owing to hyperventilation which leads to expansion of capillaries and vessels, and from here to deposition and decrease   of circulating blood volume.

Ortostatic collapse appears at fast transition from horizontal position in vertical, and also at long time of standing. Thus there is a redistribution of blood with increase of total amount of a venous system and decrease of inflow to heart. In a basis of this condition insufficiency of a venous tone lays. Ortostatic collapse may be observed at recovers after heard diseases of endocrine and nervous system, in the postoperative period, at fast removal of ascitic liquids or as a result of spinal and peridural anesthesias. Iatrogenic ortostatic collapse sometimes appears during wrong use of neuroleptics, ganglioblockers, adrenoblockers, sympatolytics. Among pilots and cosmonauts ortostatic collapse may be caused by redistribution of blood at action of acceleration when blood from vessels of the upper half of body and a head moves into vessels of organs of  abdominal cavity and inferior extremitus, causing hypoxia of brain. Also it may be observed at practically healthy children and teenagers.

Hemorrhagic collapse develops at massive blood loss as a result of fast reduction of circulating blood.

Collapse also may be observed at acute diseases of internal organs ( peritonitis, acute pancreatitis, duodenitis, erosive gastritis), at diseases of heart which are accompanied by acute and fast reduction of strike volume (heart  infarction, infringements of  heart rhythm, acute myocarditis or pericarditis with accumulation  of exudation in  cavity of  pericardium).

It is  possible to mark  two basic mechanisms in pathogenesis: 1) fall of  veinis and arteriols tone  as a result of action of infectious, toxic, physical, allergic and other factors directly on a vascular wall, vasomotoric  centre and on vascular receptors (sinocarotid zones, arches of an aorta); 2) fast reduction of circulating blood volume (blood loss,plasma loss). Reduction of circulating blood  volume  results in decrease of return of blood to heart by veins of the big circle of blood circulation and heart output. Thus the system of microcirculation is damaged, blood accumulates in capillaries, the blood pressure falls, develops circulatory hypoxia, metabolic acidosis, permeability of vessels increases. It promotes transition of water and elctrolytes from blood in intercellular space, are damaged reologic properties of blood, there is a hypercoagulation of blood and pathological aggregation  of erythrocytes and trombocytes, that creates conditions for formation of microblood clots. At a long lasting collapse as a result of hypoxia and disturbances of  metabolism are released vasoactive substances (histamine, kinins, prostaglandins) and formed tissue metabolites – lactic acid,adenosine and its derivatives which cause  hypotonia.

Progressing changes lead to infringement of functions of a brain,  deepening of regulatory and hemodynamic disorders. The death at a collapse comes owing to an exhaustion of power resources of brain,  intoxication and disturbances of  metabolism.

 

Cоmа. Classification. Ethiology, pathogenesis, consequences

Cоmа is a pathological condition which is characterized by deep oppression of functions of the central nervous system and it is shown by loss of consciousness, absence of reflexes on external irritators and disorders of the vital functions  regulation  of an organism.

By origin distinguish:

1. Cоmas at initial injury and diseases of the central nervous system (insult, craniocerebral trauma).

2. Cоmas during the endocrine diseases which apper as at insufficiency of some glands of internal secretion (diabetic, hypocorticoid, hypopituitary, hypothyreoid), and at their hyperfunction (thyreotoxic, hypoglycemic).

3. Toxic cоmas are observed at endogenic ( uraemia, hepatic insufficiency, toxicoinfections, pancreatitis) and exogenic intoxications (alcoholic poisonings, barbiturate poisoning, phosphororganic poisoning and by other substances).

4. Cоmas, caused by infringements of gas exchange at various kinds of hypoxias.

5. Cоmas, caused by loss of electrolytes, water and energetic substances.

Cоmа is a stage of development of some diseases. Conducting in their pathogenesis is  defeat of the central nervous system with infringement of function of  cortex brain, subcortex formations and  trunk brain that results in loss of consciousness. A special role in development of coma plays infringement of reticular formations function  with loss of its activating influences on  cortex brain and oppression  of subcortex formations function and  centres of vegetative nervous system.

Main pathogenetic parts in development of coma are:

1. Infringement of cellular breath and an exchange of energy in  brain. A basis of them is hypoxia, anemia, disorders of brain blood circulation, blockade of respiratory enzymes by cytotoxic poisons, acidosis (at diabetic and uraemic cоma), deficiency of power substances or blockade of their recycling (starvation hypoglycemis coma). In development of brain  hypoxia disorders of microcirculation play role. Owing to hypoxia it is broken oxidizing phosphorelation, the content and use АТP and creatinphosphate decreases.

2. Infringement of synaptic transmission to the central nervous system. They may be connected with:

·        infringement of synthesis, transport, deposition and secretion of neuromediators;

·        replacement of neuromediators by pseudomediators;

·        excessive activation of inhibition postsynaptic receptors;

·        blockade stimulating postsynaptic receptors. This mechanism has the great value in development of hepatic, uremic and toxic comas.

3. Infringement of electrolyte balance with changes of cellular potentials and process of polarization of neurons membranes, and also infringement of osmotic pressure. Disorders of metabolism of K, Ná, Mg, Са in a combination with infringements of the acid-base balance (diabetic, uraemic, chlorinehydropenie, hepatic etc. comas) have the greatest value.

4. Changes of physical properties and structures of  brain and intracranial formations. Pathogenetic value has swelling and edema of brain and brain membrane, increase of intracranial pressure which strengthen infringement of haemodinamics and liquordynamic, make hypoxia of nervous cells heavier and oppress their physiological activity. Mechanical damage  of brain matters cells  at a craniocerebral trauma, tumours,  hemorrhage in brain. At separate kinds of comas whom each of the listed factors may have leading mean, however they act together more often. At deep coma disorders of regulation of vegetative functions result in addition in heavy infringements of  metabolism in an organism, including brain, and create vise circle in pathogenesis of coma.