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Functionally neurons spinal cord are divided into

1. motor neurons,
2. Interneurons,
3. Neurons sympathetic system,
4. Neurons of the parasympathetic system.

1. Spinal cord motor neurons taking into account their functions, they are divided into

• alpha motor neurons
• gamma motor neurons.

Motor neuron axons divide into terminals and innervate up to hundreds of muscle fibers, forming motor unit. The more differentiated, precise movements a muscle performs, the fewer fibers innervate one nerve, i.e. the motoneuron unit is quantitatively smaller.

Several motor neurons can innervate one muscle, in which case they form the so-called motoneuron pool. The excitability of motor neurons of one pool is different, therefore, at different intensities of stimulation, different numbers of fibers of one muscle are involved in contraction. With optimal strength of stimulation, all fibers of a given muscle contract, in this case maximum muscle contraction develops (Fig. 15.4).

Alpha motor neurons have direct connections from sensory pathways coming from extrafusal muscle fibers, these neurons have up to 20 thousand synapses on their dendrites, and have a low impulse frequency (10-20 per second).

Gamma motor neurons innervate the intrafusal muscle fibers of the muscle spindle. Contraction of the intrafusal fiber does not lead to muscle contraction, but increases the frequency of discharges coming from the fiber receptors to the spinal cord. These neurons have a high firing rate (up to 200 per second). They receive information about the state of the muscle spindle through interneurons.

2. Interneurons - intermediate neurons - generate impulses with a frequency of up to 1000 per second; these are background active neurons with up to 500 synapses on their dendrites. The function of interneurons is to organize connections between the structures of the spinal cord, to ensure the influence of ascending and descending pathways on the cells of individual segments of the spinal cord. The function of interneurons is to inhibit the activity of neurons while maintaining the direction of the excitation path. Excitation of interneurons of motor cells has an inhibitory effect on antagonist muscles.

Fig. 15.4. Some descending systems influencing the activity of the “common terminal pathway”, i.e. on motor neuron activity. The circuit is identical for the right and left hemispheres of the brain.

3. Neurons of the sympathetic system located in the lateral horns thoracic spinal cord. These neurons are background active, but have a rare firing frequency (3-5 sec.). The discharges of sympathetic neurons are synchronized with fluctuations in blood pressure. An increase in discharge frequency precedes a decrease in blood pressure, and a decrease in discharge frequency usually precedes an increase blood pressure.

4. Neurons of the parasympathetic system localized in the sacral part of the spinal cord. These are background active neurons. Increasing the frequency of their discharges increases the contraction of the muscles of the walls Bladder. These neurons are activated by stimulation of the pelvic nerves, the sensory nerves of the limbs.

Spinal cord pathways

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Axons of the spinal ganglia and gray matter of the spinal cord go into its white matter, and then into other structures of the central nervous system, thereby creating the so-called pathways functionally divided into

1. Propriospinal,
2. Spinocerebral,
3. Cerebrospinal.

1. Propriospinal tract connect neurons of the same or different segments of the spinal cord. They start from the neurons of the gray matter of the intermediate zone, go to the white matter of the lateral or ventral funiculi of the spinal cord and end in the gray matter of the intermediate zone or on the motor neurons of the anterior horns of other segments. The function of such connections is associative and consists in coordinating posture, muscle tone, and movements of different metameres of the body. The propriospinal tracts also include commissural fibers that connect functionally homogeneous symmetrical and asymmetrical sections of the spinal cord.

2. Spinocerebral tracts connect segments of the spinal cord with brain structures.

They are presented

• proprioceptive,
• spinothalamic,
• spinocerebellar,
• spinoreticular pathways.

Proprioceptive pathway begins from the receptors of deep sensitivity of the muscles of the tendons, periosteum, and joint membranes. Through spinal ganglion it goes to the dorsal roots of the spinal cord, into the white matter of the posterior cords, and rises to the Gaulle and Burdach nuclei of the medulla oblongata. Here the first switch to a new neuron occurs, then the path goes to the lateral nuclei of the thalamus of the opposite hemisphere of the brain, switches to a new neuron - the second switch. From the thalamus, the pathway ascends to the neurons of the somatosensory cortex. Along the way, the fibers of these tracts give off collaterals in each segment of the spinal cord, which creates the possibility of correcting the posture of the entire body. The speed of excitation along the fibers of this tract reaches 60-100 m/sec.

Spinothalamic tract starts from pain, temperature,... tactile, skin baroreceptors. The signal from the skin receptors goes to the spinal ganglion, then through the dorsal root to the dorsal horn of the spinal cord (first switching). Sensitive neurons of the dorsal horns send axons to the opposite side of the spinal cord and ascend along the lateral cord to the thalamus (the speed of excitation through them is 1-30 m/s) (second switching), then to the sensory cortex. Some of the fibers of the skin receptors go to the thalamus along the anterior cord of the spinal cord. Somatovisceral afferents also travel along the spinoreticular pathway.

Spinocerebellar tracts start from the receptors of muscles, ligaments, internal organs and are represented by the non-crossing Govers' bundle and the double-crossing Flexig's bundle. Consequently, all spinocerebellar pathways, starting on the left side of the body, end in the left cerebellum, just as the right cerebellum receives information only from its side of the body. This information comes from Golgi tendon receptors, proprioceptors, pressure and touch receptors. The speed of excitation along these paths reaches 110-120 m/s.

3. Cerebrospinal tracts start from the neurons of the brain structures and end on the neurons of the spinal cord segments.

These include paths:

• corticospinal(from pyramidal neurons of the pyramidal and extrapyramidal cortex), which provides regulation voluntary movements;
• rubrospinal,
• vestibulospicash,
• reticulospinal tract - regulating muscle tone.

What unites all of these paths is that their final destination is motor neurons of the anterior horns.

Peripheral motor neurons

Neurons are functionally divided into large alpha motor neurons, small alpha motor neurons and gamma motor neurons. All these motor neurons are located in the anterior horns of the spinal cord. Alpha motor neurons innervate white muscle fibers, causing rapid physical contractions. Small alpha motor neurons innervate red muscle fibers and provide the tonic component. Gamma motor neurons send axons to the intrafusal muscle fibers of the neuromuscular spindle. Large alpha cells are associated with giant cells of the cerebral cortex. Small alpha cells have connections with the extrapyramidal system. The state of muscle proprioceptors is regulated through gamma cells.

The structure of the muscle spindle

Each striated muscle contains muscle spindles. Muscle spindles, as their name suggests, have the shape of a spindle several millimeters long and a few tenths of a millimeter in diameter. The spindles are located in the thickness of the muscle parallel to normal muscle fibers. The muscle spindle has a connective tissue capsule. The capsule provides mechanical protection for the spindle elements located in the capsule cavity, regulates the chemical liquid environment of these elements and thereby ensures their interaction. In the cavity of the muscle spindle capsule there are several special muscle fibers that are capable of contraction, but differ from ordinary muscle fibers in both structure and function.

These muscle fibers located inside the capsule were called intrafusal muscle fibers (Latin: intra - inside; fusus - spindle); ordinary muscle fibers are called extrafusal muscle fibers (Latin: extra - outside, outside; fusus - spindle). Intrafusal muscle fibers are thinner and shorter than extrafusal muscle fibers.

- This two-neuron pathway (2 neurons central and peripheral) , connecting the cerebral cortex with the skeletal (striated) muscles (corticomuscular path). The pyramidal path is a pyramidal system, the system that provides voluntary movements.

Central neuron

Central the neuron is located in the Y layer (layer of large Betz pyramidal cells) of the anterior central gyrus, in the posterior sections of the superior and middle frontal gyri and in the paracentral lobule. There is a clear somatic distribution of these cells. The cells located in the upper part of the precentral gyrus and in the paracentral lobule innervate the lower limb and trunk, located in its middle part - the upper limb. In the lower part of this gyrus there are neurons that send impulses to the face, tongue, pharynx, larynx, and masticatory muscles.

The axons of these cells are in the form of two conductors:

1) corticospinal tract (otherwise called the pyramidal tract) - from the upper two-thirds of the anterior central gyrus

2) corticobulbar tract - from the lower part of the anterior central gyrus) go from the cortex deep into the hemispheres, pass through the internal capsule (the corticobulbar tract - in the knee area, and the corticospinal tract through the anterior two-thirds of the posterior thigh of the internal capsule).

Then the cerebral peduncles, pons, and medulla oblongata pass through, and at the border of the medulla oblongata and spinal cord, the corticospinal tract undergoes an incomplete decussation. The large, crossed part of the tract passes into the lateral column of the spinal cord and is called the main, or lateral, pyramidal fasciculus. The smaller uncrossed part passes into the anterior column of the spinal cord and is called the direct uncrossed fasciculus.

The fibers of the corticobulbar tract end in motor nuclei cranial nerves (Y, YII, IX, X, XI, XII ), and the fibers of the corticospinal tract - in anterior horns of the spinal cord . Moreover, the fibers of the corticobulbar tract undergo decussation sequentially as they approach the corresponding nuclei of the cranial nerves (“supranuclear” decussation). For the oculomotor, masticatory muscles, muscles of the pharynx, larynx, neck, trunk and perineum, there is bilateral cortical innervation, i.e. fibers of central motor neurons approach part of the motor nuclei of the cranial nerves and some levels of the anterior horns of the spinal cord not only from the opposite side, but also to some levels of the anterior horns of the spinal cord. but also with one’s own, thus ensuring the approach of impulses from the cortex not only of the opposite, but also of one’s hemisphere. The limbs, tongue, and lower part of the facial muscles have unilateral (only from the opposite hemisphere) innervation. The axons of the spinal cord motor neurons are directed to the corresponding muscles as part of the anterior roots, then the spinal nerves, plexuses and, finally, the peripheral nerve trunks.

Peripheral neuron

Peripheral neuron starts from the places where the first one ended: the fibers of the cortic-bulbar tract ended at the nuclei of the cranial nerve, which means they go as part of the cranial nerve, and the corticospinal tract ended in the anterior horns of the spinal cord, which means it goes as part of the anterior roots of the spinal nerves, then peripheral nerves, reaching the synapse.

Central and peripheral paralysis develop with neuron damage of the same name.

8.3. Functional differences of motor neurons

Motor neuron size determines a very important physiological property - the threshold of excitation. The smaller the motor neuron, the easier it is to excite. Or, in other words, in order to excite a small motor neuron, it is necessary to exert less excitatory influence on it than on a large motor neuron. The difference in excitability (thresholds) is due to the fact that the action of excitatory synapses on the small motor neuron is more effective than on the large motor neuron. Small motor neurons are low-threshold motor neurons, and large motor neurons are high-threshold motor neurons.

Pulse frequency motor neurons, like other neurons, is determined by the intensity of excitatory synaptic influences from other neurons. The higher the intensity, the higher the pulse frequency. However, the increase in the frequency of motor neuron impulses is not unlimited. It is limited by a special mechanism found in the spinal cord. From the axon of the motor neuron, even before exiting the spinal cord, a recurrent lateral branch departs, which, branching in the gray matter of the spinal cord, forms synaptic contacts with special neurons - inhibitory cellsRenshaw. Renshaw cell axons terminate at inhibitory synapses on motor neurons. The impulses arising in the motor neurons propagate along the main axon to the muscle, and along the return branch of the axon to the Renshaw cells, exciting them. Excitation of Renshaw cells leads to inhibition of motor neurons. The more often motor neurons begin to send impulses, the stronger the excitation of Renshaw cells and the greater the inhibitory effect of Renshaw cells on motor neurons. As a result of the action of Renshaw cells, the firing frequency of motor neurons decreases.

The inhibitory effect of Renshaw cells on small motor neurons is stronger than on large ones. This explains why small motor neurons fire at a lower rate than large motor neurons. The firing rate of small motor neurons usually does not exceed 20–25 impulses per 1 second, and the firing frequency of large motor neurons can reach 40–50 impulses per 1 second. In this regard, small motor neurons are also called “slow”, and large motor neurons are called “fast”.

8.4. Mechanism of neuromuscular transmission

Impulses propagating along the terminal branches of the axon of a motor neuron reach almost simultaneously all muscle fibers of a given motor unit. The propagation of an impulse along the terminal branch of the axon leads to depolarization of its presynaptic membrane. In this regard, the permeability of the presynaptic membrane changes and the transmitter acetylcholine located in the terminal branch is released into the synaptic cleft. Enzyme contained in the synaptic cleft acetylcholinesterase destroys within a few milliseconds acetylcholine. Therefore, the effect of acetylcholine on the muscle fiber membrane is very short-lived. If a motor neuron sends impulses for a long time and with high frequency, then the reserves of acetylcholine in the terminal branches are depleted and transmission through the neuromuscular junction stops. In addition, when impulses along the axon follow with high frequency, acetylcholinesterase does not have time to destroy acetylcholine released into the synaptic cleft. The concentration of acetylcholine in the synaptic cleft increases, which also leads to the cessation of neuromuscular transmission. Both of these factors can occur during intense and prolonged muscular work and lead to a decrease in muscle performance (fatigue).

The action of acetylcholine causes a change in the ionic permeability of the postsynaptic membrane of the muscle fiber. An ionic current begins to flow through it, which leads to a decrease in the muscle fiber membrane potential. This decrease leads to the development of an action potential that propagates across the muscle fiber membrane. Simultaneously with the propagation of the action potential, a wave of contraction runs along the muscle fiber. Since the impulse from the motor neuron arrives at all terminal branches of the axon almost simultaneously, the contraction of all muscle fibers of one motor unit also occurs simultaneously. All muscle fibers of a motor unit work as a single unit.

8.5. Single cut

In response to an impulse from a motor neuron, all muscle fibers of the motor unit respond single contraction. It consists of two phases - the rise phase voltage(or shortening phases) and phases relaxation(or extension phases). The tension developed by each muscle fiber during a single contraction is a constant value for each muscle fiber. Therefore, the tension developed by a motor unit during a single contraction is also constant and is determined by the number of muscle fibers that make up a given motor unit. The more muscle fibers a motor unit contains, the more tension it develops. Motor units also differ from each other in the duration of a single contraction. The duration of a single contraction of the slowest motor ones can reach 0.2 seconds; the duration of a single contraction of fast motor units is much shorter - up to 0.05 sec. In both types of motor units, the tension-rising phase lasts less than the relaxation phase. Thus, with a total duration of a single contraction of a slow motor unit of 0.1 sec. the tension-rising phase lasts approximately 0.04 seconds, and the relaxation phase lasts about 0.06 seconds. With a single contraction duration of a fast motor unit of 0.05 sec. The duration of the tension rise phase is approximately 0.02 seconds, and the relaxation phase is 0.03 seconds.

The speed of muscle contraction generally depends on the ratio of slow and fast motor units in it. Muscles in which slow motor units predominate are referred to as slow muscles, and muscles in which the majority are fast motor units are referred to as fast muscles.

The ratio of the number of fast and slow motor units in a muscle depends on its function in the body. Thus, the inner head of the gastrocnemius muscle is involved in locomotor movements and jumping and is one of the fast muscles, the soleus muscle plays important role while maintaining a vertical posture in humans and is one of the slow muscles.

8.6. Tetanic contraction

Motor neurons usually send a series of impulses to the muscles rather than a single impulse. The response of muscle fibers to a series of impulses depends on the frequency of impulses of the motor neuron.

Let us consider the features of the response to a series of impulses of muscle fibers of a slow motor unit with a single contraction duration of 0.1 sec. As long as the frequency of impulses of the motor neuron of this motor unit does not exceed 10 impulses per 1 second, that is, the impulses follow each other with an interval of 0.1 seconds. and more, the slow motor unit operates in the mode of single contractions. This means that each new contraction of muscle fibers begins after the end of the relaxation phase in the previous contraction cycle.

If the impulse frequency of a slow motor neuron becomes more than 10 impulses per 1 second, i.e. impulses follow each other with an interval of less than 0.1 second, the motor unit begins to work in the mode tetanic abbreviations. This means that each new contraction of the muscle fibers of the motor unit begins even before the end of the previous contraction. Successive contractions superimpose each other, so that the tension developed by the muscle fibers of a given motor unit increases and becomes greater than with single contractions. Within certain limits, the more often the motor neuron sends impulses, the more tension the motor unit develops, since each subsequent increase in tension begins against the background of increasing tension remaining from the previous contraction.

Any motor unit develops maximum tetanic tension in cases where its motor neuron sends impulses at a frequency at which each new contraction begins at the phase, or peak, of the increase in tension of the previous contraction. It is easy to calculate: the peak increase in voltage during a single contraction is reached in a slow motor unit after approximately 0.04 sec. after the start of contraction. Therefore, the maximum summation will be reached when the next contraction occurs after 0.04 sec. after the beginning of the previous one, i.e., at intervals between impulses of the “slow” motor neuron of 0.04 seconds, which corresponds to an impulse frequency of 25 impulses per 1 second.

So, if a slow motor unit motor neuron sends impulses at a frequency of less than 10 impulses/sec, then the motor unit operates in a single contraction mode. When the motor neuron impulse frequency exceeds 10 impulses/sec, the motor unit begins to work in the tetanic contraction mode, and within the range of an increase from 10 to 25 impulses/sec, the higher the motor neuron impulse frequency, the greater the voltage the motor unit develops. In this frequency range of motor neuron impulses, the muscle fibers controlled by it operate in the mode dentate tetanus(alternating rise and fall of voltage).

The maximum tetanic tension of the slow motor unit is achieved at a motoneuron firing rate of 25 impulses/sec. At this frequency of motor neuron impulses, the muscle fibers of the motor unit operate in the mode smooth tetanus(there are no sharp fluctuations in muscle fiber tension). An increase in the frequency of motor neuron impulses beyond 25 impulses/sec no longer causes a further increase in the tension of slow muscle fibers. Therefore, for a “slow” motor neuron there is no “sense” to work with a frequency of more than 25 impulses/sec, since a further increase in frequency will still not increase the tension developed by its slow muscle fibers, but will be tiring for the motor neuron itself.

It is easy to calculate that for a fast motor unit with a total duration of a single contraction of muscle fibers of 0.05 sec. the single contraction mode will be maintained until the motor neuron impulse frequency reaches 20 impulses/sec, i.e., at intervals between impulses of more than 0.05 sec. When the motor neuron impulse frequency is more than 20 impulses/sec, the muscle fibers operate in the dentate tetanus mode, and the higher the motor neuron impulse frequency, the greater the tension the muscle fibers of the motor unit develop. The maximum voltage of a fast motor unit occurs when the motor neuron impulse frequency is 50 impulses/sec and higher, since the peak voltage rise in such a motor unit is reached after approximately 0.02 sec. after the start of a single contraction.

8.7. Comparison of single and tetanic contractions

At single contraction in the phase of increasing tension, some energy potential of the muscle is consumed, and in the relaxation phase it is restored. Therefore, if each subsequent contraction of muscle fibers begins after the end of the previous one, then during work in this mode the muscle fibers have time to restore the potential wasted in the contraction phase. In this regard, the mode of single contractions for muscle fibers is practically non-fatiguing. In this mode, motor units can operate for a long time.

At tetanic mode contractions, each subsequent contraction begins before the end of the relaxation phase (or even before the start of the relaxation phase) of the previous contraction. Therefore, work in the tetanic mode is work in “duty” and, therefore, cannot last long. Unlike the single contraction mode, tetanic contraction is tiring for muscle fibers.

The ratio of the maximum tetanic tension that a motor unit develops in the mode of maximum (smooth) tetanus to the tension during its single contraction is called tetanic index. This index shows what increase in the magnitude of tension in the muscle fibers of a motor unit can be obtained by increasing the frequency of motor neuron impulses. The tetanic index for different motor units ranges from 0.5 to 10 or more. This means that by increasing the frequency of motor neuron impulses, the contribution of one motor unit to the total tension of the entire muscle can increase several times.

8.8. Regulation of muscle tension

Movement control is associated with the regulation of muscle tension that carries out movement.

Muscle tension is determined by the following three factors:

1) the number of active motor units;

2) the mode of operation of motor units, which, as is known, depends on the frequency of impulses of motor neurons;

3) connection in time of activity of different motor units.

8.8.1. Number of active motor units

Active motor unit is a unit in which 1) a motor neuron sends impulses to its muscle fibers and 2) the muscle fibers contract in response to these impulses. How larger number active motor units, the greater the muscle tension.

The number of active motor units depends on the intensity of the excitatory influences to which the motor neurons of a given muscle are exposed from neurons of higher motor levels, receptors and neurons of their own spinal level. To develop a small muscle tension, a correspondingly low intensity of exciting influences on its motor neurons is required. Since small motor neurons are relatively low-threshold, their activation requires relatively low level stimulating influences. Therefore, from the totality of motor units that make up a muscle, its weak tensions are provided mainly by the activity of relatively low-threshold, small, motor units. The greater the tension a muscle must develop, the greater the intensity of the exciting influences on its motor neurons. Moreover, in addition to low-threshold, small motor units, increasingly high-threshold (larger in size) motor units become active. As the number of active motor units increases, the tension developed by the muscle increases. Significant muscle tension is provided by the activity of different motor units, ranging from low-threshold (small) to high-threshold (large). Consequently, the smallest motor units are active at any (both small and large) muscle tension, while large motor units are active only at large muscle tension.

8.8.2. Mode of motor unit activity

Within certain limits, the higher the frequency of motor neuron impulses, the greater the tension the motor unit develops and, therefore, the greater its contribution to the total muscle tension. Thus, along with the number of active motor units (motoneurons), an important factor in the regulation of muscle tension is the frequency of motor neuron impulses, which determines the contribution of the active motor unit to the total tension.

The frequency of motor neuron impulses is known to depend on the intensity of the excitatory influences to which the motor neurons are exposed. Therefore, when the intensity of excitatory influences on motor neurons is low, then low-threshold, small motor neurons work and the frequency of their impulses is relatively low. Accordingly, small motor units work in this case in the mode of single contractions. This activity of motor units provides only weak muscle tension, which, however, is sufficient, for example, to maintain an upright body posture. In this regard, it is clear why postural muscle activity can last for many hours in a row without fatigue.

Greater muscle tension occurs due to increased excitatory influences on its motor neurons. This enhancement leads not only to the inclusion of new, higher-threshold motor neurons, but also to an increase in the firing rate of relatively low-threshold motor neurons. At the same time, for the highest-threshold working motor neurons, the intensity of the exciting influences is insufficient to cause their high-frequency discharge. Therefore, from the totality of active motor units, the lower threshold ones work with a relatively high frequency for themselves (in the tetanic contraction mode), and the highest threshold active motor units work in the single contraction mode.

At very high muscle tensions, the vast majority (if not all) of the active motor units operate in the tetanic mode, and therefore large muscle tensions can be maintained for a very short time.

8.8.3. Relationship in timing of activity of different motor units

In addition to the two factors already discussed, muscle tension to a certain extent depends on how the impulses sent by different motor neurons of the muscle are related in time. To make this clear, consider a simplified example of the activity of three motor units of one muscle operating in single contraction mode. In one case, all three motor units contract simultaneously, since the motor neurons of these three motor units send impulses simultaneously (synchronously). In another case, the motor units do not work simultaneously (asynchronously), so that the phases of contraction of their muscle fibers do not coincide in time.

It is absolutely clear that in the first case the total muscle tension is greater than in the second, but the fluctuations in tension are very large - from maximum to minimum. In the second case, the total muscle tension is less than in the first, but the voltage fluctuations are much smaller. From this example it is clear that if the motor units work in the mode of single contractions, but asynchronously, then the overall tension of the entire muscle fluctuates slightly. The more asynchronously working motor units, the less fluctuation in muscle tension, the more smoothly the movement occurs or the less fluctuation in posture (the less amplitude of physiological tremor). Under normal conditions, most of the motor units of one muscle work asynchronously, independently of each other, which ensures smooth contraction. With fatigue associated with large and prolonged muscular work, the normal activity of motor units is disrupted and they begin to work simultaneously. As a result, movements lose smoothness, their accuracy is disrupted, and tremor of fatigue.

If motor units operate in the mode of smooth tetanus or close to it serrated tetanus, then the interconnectedness of the activity of motor units over time is no longer of serious importance, since the voltage level of each of the motor units is maintained almost constant. Consequently, the moments of the beginning of each subsequent contraction of the motor unit are also unimportant, since their coincidences or mismatches have almost no effect on the overall tension and fluctuations in muscle tension.

8.9. Energy of muscle contraction

Muscle work is the result of the conversion of the chemical energy of energy substances contained in the muscle into mechanical energy. The main energy substance in this case is adenosine triphosphoric acid(otherwise adenosine triphosphate), which is usually denoted by three letters - ATP. It is capable of easily splitting off one molecule of phosphoric acid, turning into adenosine diphosphoric acid (ADP); this releases a lot of energy (about 8 kcal). The breakdown of ATP occurs under the influence of an enzyme, the role of which, when the muscle is excited, is performed by the muscle protein itself - myosin. Thanks to the breakdown of ATP, the released chemical energy is converted into mechanical energy, manifested in the mutual movement of actin and myosin filaments. It is characteristic that chemical energy is transformed in the muscle directly into mechanical energy without an intermediate stage - conversion into thermal energy. This makes muscle as an engine different from other known engines created by man. Chemical energy is used very fully, with negligible losses.

The amount of ATP in muscle is limited - 0.75% of muscle weight. At the same time, even with continuous work, ATP reserves are not depleted, because it is continuously re-formed in muscle tissue. The source of its formation is its own decay product, i.e. ADP. For the reverse conversion of ADP to ATP, phosphoric acid must be added to ADP again. This is what actually happens. However, if the breakdown of ATP is accompanied by the release of energy, then its synthesis requires the absorption of energy. This energy can come from three sources.

1 – breakdown of creatine phosphoric acid, or, otherwise, creantine phosphate (CrP). It is a combination of a nitrogen-containing substance - creatine with phosphoric acid. When CrP decomposes, phosphoric acid is released, which, when combined with ADP, forms ATP:

2 – anaerobic breakdown of glycogen(glycogenolysis) or glucose (glycolysis) to lactic acid. It is not the carbohydrate itself that undergoes decomposition, but its compound with phosphoric acid – glucose phosphate. This compound sequentially breaks down into a series of intermediate substances, with phosphoric acid cleaved off and added to ADP to synthesize ATP. The end product of carbohydrate breakdown is lactic acid. Some of the resulting lactic acid can be further subjected to aerobic oxidation to carbon dioxide and water. The energy generated in this case is used for the reverse synthesis (resynthesis) of carbohydrate from other parts of lactic acid. Typically, due to the energy of aerobic oxidation of one lactic acid molecule, 4–6 other lactic acid molecules are resynthesized into carbohydrate. This indicates the great efficiency of using carbohydrate energy. It is believed that the resynthesis of carbohydrates to glycogen due to the energy of aerobic oxidation of lactic acid occurs mainly in the liver, where lactic acid is delivered by blood from working muscles.

3 – aerobic oxidation of carbohydrates and fats. The process of anaerobic breakdown of carbohydrates may not be completed to lactic acid, but at one of the intermediate stages oxygen is added. The energy generated in this case is used to add phosphoric acid, released during the breakdown of carbohydrates, to ADP. The energy from aerobic fat oxidation is also used for ATP resynthesis. Fat is broken down into glycerol and fatty acids, and the latter, through appropriate transformations with the addition of phosphoric acid, become capable of aerobic oxidation, in which phosphoric acid is added to ADP and ATP is resynthesized.

During single short-term muscle tension (jumping, throwing, lifting a barbell, boxing punch, rapid wrestling techniques, etc.), ATP resynthesis occurs due to the energy of KrF. During longer work, requiring 10–20 seconds. (running 100–200 m), ATP resynthesis occurs with the participation of anaerobic breakdown of carbohydrates, i.e., glycolysis processes. With even longer work, ATP resynthesis can be determined by aerobic oxidation of carbohydrates.

If respiration is excluded or insufficient, i.e. if work is performed only or predominantly due to anaerobic processes, then an accumulation of anaerobic decomposition products occurs. These are mainly ADP, creatine and lactic acid. The elimination of these substances after work is carried out with the participation of oxygen. The increased amount of oxygen absorbed after work is called oxygen debt. That part of the oxygen debt that goes to the oxidation of lactic acid is called lactate oxygen debt. The other part of the oxygen debt is spent on reactions necessary for the restoration of CrP and ATP. It is called alactic oxygen debt. Thus, oxygen consumed after work promotes the resynthesis of the main energy substances: ATP, CrP and glycogen.

Training and metodology complex

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Educational and methodological complex for the discipline (222)

Training and metodology complex

... Educational-methodicalcomplexBydisciplinePhysiology plants (name) Specialty: 020201.65 “Biology” (code By OKSO) Agreed: Recommended by the department: Educational-methodical ...

Educational and methodological complex for the discipline of general professional training “Theory and Methods of Teaching Biology”, specialty “050102 65 – Biology”

Training and metodology complex

Educational-methodicalcomplexBydiscipline general professional training “... 1978. Brunovt E.P. etc. Lessons By anatomy, physiology and human hygiene. – M.: Education..., 1970. 6. Experimental methodology Byphysiology plants, manual for teachers; ...

Neurology and neurosurgery Evgeniy Ivanovich Gusev

3.1. Pyramid system

3.1. Pyramid system

There are two main types of movements: involuntary And arbitrary.

Involuntary movements include simple automatic movements carried out by the segmental apparatus of the spinal cord and brain stem as a simple reflex act. Voluntary purposeful movements are acts of human motor behavior. Special voluntary movements (behavioral, labor, etc.) are carried out with the leading participation of the cerebral cortex, as well as the extrapyramidal system and the segmental apparatus of the spinal cord. In humans and higher animals, the implementation of voluntary movements is associated with the pyramidal system. In this case, the impulse from the cerebral cortex to the muscle occurs through a chain consisting of two neurons: central and peripheral.

Central motor neuron. Voluntary muscle movements occur due to impulses traveling along long nerve fibers from the cerebral cortex to the cells of the anterior horns of the spinal cord. These fibers form the motor ( corticospinal), or pyramidal, path. They are the axons of neurons located in the precentral gyrus, in cytoarchitectonic area 4. This zone is a narrow field that stretches along the central fissure from the lateral (or Sylvian) fissure to the anterior part of the paracentral lobule on the medial surface of the hemisphere, parallel to the sensitive area of ​​​​the postcentral gyrus cortex .

Neurons innervating the pharynx and larynx are located in the lower part of the precentral gyrus. Next, in ascending order, come the neurons innervating the face, arm, torso, and leg. Thus, all parts of the human body are projected in the precentral gyrus, as if upside down. Motor neurons are located not only in area 4, they are also found in neighboring cortical fields. At the same time, the vast majority of them are occupied by the 5th cortical layer of the 4th field. They are “responsible” for precise, targeted single movements. These neurons also include Betz giant pyramidal cells, which have axons with thick myelin sheaths. These fast-conducting fibers make up only 3.4-4% of all fibers of the pyramidal tract. Most of the fibers of the pyramidal tract come from small pyramidal, or fusiform (fusiform), cells in motor fields 4 and 6. Cells of field 4 provide about 40% of the fibers of the pyramidal tract, the rest come from cells of other fields of the sensorimotor zone.

Area 4 motor neurons control fine voluntary movements skeletal muscles the opposite half of the body, since most of the pyramidal fibers pass to the opposite side in the lower part of the medulla oblongata.

The impulses of the pyramidal cells of the motor cortex follow two paths. One, the corticonuclear pathway, ends in the nuclei of the cranial nerves, the second, more powerful, corticospinal tract, switches in the anterior horn of the spinal cord on interneurons, which in turn end on large motor neurons of the anterior horns. These cells transmit impulses through the ventral roots and peripheral nerves to the motor end plates of skeletal muscles.

When the pyramidal tract fibers leave the motor cortex, they pass through the corona radiata of the white matter of the brain and converge towards the posterior limb of the internal capsule. In somatotopic order, they pass through the internal capsule (its knee and the anterior two-thirds of the posterior thigh) and go in the middle part of the cerebral peduncles, descending through each half of the base of the pons, being surrounded by numerous nerve cells bridge nuclei and fibers of various systems. At the level of the pontomedullary junction, the pyramidal tract becomes visible from the outside, its fibers forming elongated pyramids on either side of the midline of the medulla oblongata (hence its name). In the lower part of the medulla oblongata, 80-85% of the fibers of each pyramidal tract pass to the opposite side at the decussation of the pyramids and form lateral pyramidal tract. The remaining fibers continue to descend uncrossed in the anterior funiculi as anterior pyramidal tract. These fibers cross at the segmental level through the anterior commissure of the spinal cord. In the cervical and thoracic parts of the spinal cord, some fibers connect with the cells of the anterior horn of their side, so that the muscles of the neck and trunk receive cortical innervation on both sides.

The crossed fibers descend as part of the lateral pyramidal tract in the lateral funiculi. About 90% of the fibers form synapses with interneurons, which in turn connect with large alpha and gamma neurons of the anterior horn of the spinal cord.

Fibers forming corticonuclear pathway, are directed to the motor nuclei (V, VII, IX, X, XI, XII) of the cranial nerves and provide voluntary innervation of the facial and oral muscles.

Another bundle of fibers, starting in the “eye” area 8, and not in the precentral gyrus, also deserves attention. Impulses traveling along this beam provide friendly movements eyeballs in the opposite direction. The fibers of this bundle at the level of the corona radiata join the pyramidal tract. Then they pass more ventrally in the posterior leg of the internal capsule, turn caudally and go to the nuclei of the III, IV, VI cranial nerves.

Peripheral motor neuron. Fibers of the pyramidal tract and various extrapyramidal tracts (reticular-, tegmental-, vestibular, red-nuclear-spinal, etc.) and afferent fibers entering the spinal cord through the dorsal roots end on the bodies or dendrites of large and small alpha and gamma cells (directly or through intercalary, associative or commissural neurons of the internal neuronal apparatus of the spinal cord) In contrast to the pseudounipolar neurons of the spinal ganglia, the neurons of the anterior horns are multipolar. Their dendrites have multiple synaptic connections with various afferent and efferent systems. Some of them are facilitative, others are inhibitory in their action. In the anterior horns, motoneurons form groups organized into columns and not divided segmentally. These columns have a certain somatotopic order. In the cervical region, the lateral motor neurons of the anterior horn innervate the hand and arm, and the motor neurons of the medial columns innervate the muscles of the neck and chest. In the lumbar region, neurons innervating the foot and leg are also located laterally in the anterior horn, and those innervating the trunk are located medially. The axons of the anterior horn cells exit the spinal cord ventrally as radicular fibers, which gather in segments to form the anterior roots. Each anterior root connects to a posterior one distal to the spinal ganglia and together they form the spinal nerve. Thus, each segment of the spinal cord has its own pair of spinal nerves.

The nerves also include efferent and afferent fibers emanating from the lateral horns of the spinal gray matter.

Well-myelinated, fast-conducting axons of large alpha cells extend directly to the striated muscle.

In addition to alpha motor neurons major and minor, the anterior horn contains numerous gamma motor neurons. Among the interneurons of the anterior horns, Renshaw cells, which inhibit the action of large motor neurons, should be noted. Large alpha cells with thick, fast-conducting axons produce rapid muscle contractions. Small alpha cells with thinner axons perform a tonic function. Gamma cells with thin and slow-conducting axons innervate muscle spindle proprioceptors. Large alpha cells are associated with giant cells of the cerebral cortex. Small alpha cells have connections with the extrapyramidal system. The state of muscle proprioceptors is regulated through gamma cells. Among the various muscle receptors, the most important are the neuromuscular spindles.

Afferent fibers called ring-spiral, or primary endings, have a rather thick myelin coating and belong to fast-conducting fibers.

Many muscle spindles have not only primary but also secondary endings. These endings also respond to stretch stimuli. Their action potential spreads in the central direction along thin fibers communicating with interneurons responsible for the reciprocal actions of the corresponding antagonist muscles. Only a small number of proprioceptive impulses reach the cerebral cortex; most are transmitted through feedback rings and do not reach the cortical level. These are elements of reflexes that serve as the basis for voluntary and other movements, as well as static reflexes that resist gravity.

Extrafusal fibers in a relaxed state have a constant length. When a muscle is stretched, the spindle is stretched. The ring-spiral endings respond to stretching by generating an action potential, which is transmitted to the large motor neuron via fast-conducting afferent fibers, and then again via fast-conducting thick efferent fibers - the extrafusal muscles. The muscle contracts and its original length is restored. Any stretch of the muscle activates this mechanism. Percussion on the muscle tendon causes stretching of this muscle. The spindles react immediately. When the impulse reaches the motor neurons in the anterior horn of the spinal cord, they respond by causing short cut. This monosynaptic transmission is basic for all proprioceptive reflexes. The reflex arc covers no more than 1-2 segments of the spinal cord, which is of great importance in determining the location of the lesion.

Gamma neurons are influenced by fibers descending from the motor neurons of the central nervous system as part of tracts such as pyramidal, reticular-spinal, and vestibular-spinal. The efferent influences of gamma fibers make it possible to finely regulate voluntary movements and provide the ability to regulate the strength of the receptor response to stretching. This is called the gamma neuron-spindle system.

Research methodology. Inspection, palpation and measurement of muscle volume are carried out, the volume of active and passive movements, muscle strength, muscle tone, rhythm of active movements and reflexes are determined. To identify the nature and localization motor disorders, as well as when clinically insignificant severe symptoms Electrophysiological methods are used.

The study of motor function begins with an examination of the muscles. Attention is drawn to the presence of atrophy or hypertrophy. By measuring the volume of the limb muscles with a centimeter, the degree of severity of trophic disorders can be determined. When examining some patients, fibrillary and fascicular twitching is noted. By palpation, you can determine the configuration of the muscles and their tension.

Active movements are checked consistently in all joints and performed by the subject. They may be absent or limited in volume and weakened in strength. Complete absence active movements are called paralysis, limitation of movements or weakening of their strength is called paresis. Paralysis or paresis of one limb is called monoplegia or monoparesis. Paralysis or paresis of both arms is called upper paraplegia or paraparesis, paralysis or paraparesis of the legs is called lower paraplegia or paraparesis. Paralysis or paresis of two limbs of the same name is called hemiplegia or hemiparesis, paralysis of three limbs - triplegia, paralysis of four limbs - quadriplegia or tetraplegia.

Passive movements are determined when the subject’s muscles are completely relaxed, which makes it possible to exclude a local process (for example, changes in the joints) that limits active movements. Along with this, determining passive movements is the main method for studying muscle tone.

The volume of passive movements in the joints of the upper limb is examined: shoulder, elbow, wrist (flexion and extension, pronation and supination), finger movements (flexion, extension, abduction, adduction, opposition of the first finger to the little finger), passive movements in the joints of the lower extremities: hip, knee, ankle (flexion and extension, rotation outward and inward), flexion and extension of fingers.

Muscle strength determined consistently in all groups with active resistance of the patient. For example, when studying muscle strength shoulder girdle the patient is asked to raise his hand to a horizontal level, resisting the examiner’s attempt to lower his hand; then they suggest raising both hands above the horizontal line and holding them, offering resistance. To determine the strength of the shoulder muscles, the patient is asked to bend his arm in elbow joint, and the examiner tries to straighten it; The strength of the shoulder abductors and adductors is also examined. To study the strength of the forearm muscles, the patient is instructed to perform pronation, and then supination, flexion and extension of the hand with resistance while performing the movement. To determine the strength of the finger muscles, the patient is asked to make a “ring” from the first finger and each of the others, and the examiner tries to break it. Strength is checked by moving the fifth finger away from the fourth finger and bringing the other fingers together, while clenching the hands into a fist. The strength of the pelvic girdle and hip muscles is examined by performing the task of raising, lowering, adducting, and abducting the hip while exerting resistance. The strength of the thigh muscles is examined by asking the patient to bend and straighten the leg at the knee joint. The strength of the lower leg muscles is checked as follows: the patient is asked to bend the foot, and the examiner holds it straight; then the task is given to straighten the foot bent at the ankle joint, overcoming the resistance of the examiner. The strength of the muscles of the toes is also examined when the examiner tries to bend and straighten the toes and separately bend and straighten the first toe.

To identify paresis of the limbs, a Barre test is performed: the paretic arm, extended forward or raised upward, gradually lowers, the leg raised above the bed also gradually lowers, while the healthy one is held in its given position. With mild paresis, you have to resort to a test for the rhythm of active movements; pronate and supinate your arms, clench your hands into fists and unclench them, move your legs like on a bicycle; insufficient strength of the limb is manifested in the fact that it gets tired more quickly, movements are performed less quickly and less dexterously than with a healthy limb. Hand strength is measured with a dynamometer.

Muscle tone– reflex muscle tension, which provides preparation for movement, maintaining balance and posture, and the ability of the muscle to resist stretching. There are two components of muscle tone: the muscle’s own tone, which depends on the characteristics of the metabolic processes occurring in it, and neuromuscular tone (reflex), reflex tone is often caused by muscle stretching, i.e. irritation of proprioceptors, determined by the nature of the nerve impulses that reach this muscle. It is this tone that underlies various tonic reactions, including anti-gravity ones, carried out under conditions of maintaining the connection between the muscles and the central nervous system.

Tonic reactions are based on a stretch reflex, the closure of which occurs in the spinal cord.

Muscle tone is influenced by the spinal (segmental) reflex apparatus, afferent innervation, reticular formation, as well as cervical tonic centers, including vestibular centers, the cerebellum, the red nucleus system, basal ganglia, etc.

The state of muscle tone is assessed by examining and palpating the muscles: with a decrease in muscle tone, the muscle is flabby, soft, doughy. at increased tone it has a denser consistency. However, the determining factor is the study of muscle tone through passive movements (flexors and extensors, adductors and abductors, pronators and supinators). Hypotonia is a decrease in muscle tone, atony is its absence. A decrease in muscle tone can be detected by examining Orshansky's symptom: when lifting up (in a patient lying on his back) the leg straightened at the knee joint, hyperextension in this joint is detected. Hypotonia and muscle atony occur with peripheral paralysis or paresis (disturbance of the efferent part of the reflex arc with damage to the nerve, root, cells of the anterior horn of the spinal cord), damage to the cerebellum, brain stem, striatum and posterior cords of the spinal cord. Muscle hypertension is the tension felt by the examiner during passive movements. There are spastic and plastic hypertension. Spastic hypertension - increased tone of the flexors and pronators of the arm and extensors and adductors of the leg (if the pyramidal tract is affected). In case of spastic hypertension, the “penknife” symptom is observed (obstruction of passive movement in the initial phase of the study), in case of plastic hypertension, the “penknife” symptom is observed. gear wheel"(feeling of tremors during examination of muscle tone in the limbs). Plastic hypertension is a uniform increase in the tone of muscles, flexors, extensors, pronators and supinators, which occurs when the pallidonigral system is damaged.

Reflexes. A reflex is a reaction that occurs in response to irritation of receptors in the reflexogenic zone: muscle tendons, skin of a certain area of ​​the body, mucous membrane, pupil. The nature of the reflexes is used to judge the state of various parts of the nervous system. When studying reflexes, their level, uniformity, asymmetry are determined: when elevated level mark the reflexogenic zone. When describing reflexes, the following gradations are used: 1) living reflexes; 2) hyporeflexia; 3) hyperreflexia (with an expanded reflexogenic zone); 4) areflexia (lack of reflexes). Reflexes can be deep, or proprioceptive (tendon, periosteal, articular), and superficial (skin, mucous membranes).

Tendon and periosteal reflexes are caused by percussion with a hammer on the tendon or periosteum: the response is manifested by the motor reaction of the corresponding muscles. To obtain tendon and periosteal reflexes in the upper and lower extremities, it is necessary to evoke them in an appropriate position favorable for the reflex reaction (lack of muscle tension, average physiological position).

Upper limbs. Biceps tendon reflex caused by a hammer blow to the tendon of this muscle (the patient’s arm should be bent at the elbow joint at an angle of about 120°, without tension). In response, the forearm flexes. Reflex arc: sensory and motor fibers of the musculocutaneous nerve, CV-CVI. Triceps brachii tendon reflex is caused by a hammer blow on the tendon of this muscle above the olecranon (the patient’s arm should be bent at the elbow joint at almost an angle of 90°). In response, the forearm extends. Reflex arc: radial nerve, СVI-СVII. Radiation reflex caused by percussion of the styloid process radius(the patient’s arm should be bent at the elbow joint at an angle of 90° and be in a position midway between pronation and supination). In response, flexion and pronation of the forearm and flexion of the fingers occur. Reflex arc: fibers of the median, radial and musculocutaneous nerves, CV-CVIII.

Lower limbs. Knee reflex caused by a hammer hitting the quadriceps tendon. In response, the lower leg is extended. Reflex arc: femoral nerve, LII-LIV. When examining the reflex in a horizontal position, the patient’s legs should be bent at the knee joints at an obtuse angle (about 120°) and rest freely on the examiner’s left forearm; when examining the reflex in a sitting position, the patient's legs should be at an angle of 120° to the hips or, if the patient does not rest his feet on the floor, hang freely over the edge of the seat at an angle of 90° to the hips, or one of the patient's legs is thrown over the other. If the reflex cannot be evoked, then the Jendraszik method is used: the reflex is evoked when the patient pulls towards the hand with the fingers tightly clasped. Heel (Achilles) reflex caused by percussion of the calcaneal tendon. In response, plantar flexion of the foot occurs as a result of contraction of the calf muscles. Reflex arc: tibial nerve, SI-SII. For a lying patient, the leg should be bent at the hip and knee joints, the foot should be bent at the ankle joint at an angle of 90°. The examiner holds the foot with his left hand, and with his right hand percusses the heel tendon. With the patient lying on his stomach, both legs are bent at the knee and ankle joints at an angle of 90°. The examiner holds the foot or sole with one hand and strikes with the hammer with the other. The reflex is caused by a short blow to the heel tendon or to the sole. The heel reflex can be examined by placing the patient on his knees on the couch so that the feet are bent at an angle of 90°. In a patient sitting on a chair, you can bend your leg at the knee and ankle joints and evoke a reflex by percussing the heel tendon.

Joint reflexes are caused by irritation of receptors in the joints and ligaments of the hands. 1. Mayer - opposition and flexion in the metacarpophalangeal and extension in the interphalangeal joint of the first finger with forced flexion in the main phalanx of the third and fourth fingers. Reflex arc: ulnar and median nerves, СVII-ThI. 2. Leri – flexion of the forearm with forced flexion of the fingers and hand in a supinated position, reflex arc: ulnar and median nerves, CVI-ThI.

Skin reflexes are caused by line irritation with the handle of a neurological hammer in the corresponding skin area in the patient's position on the back with slightly bent legs. Abdominal reflexes: upper (epigastric) are caused by irritation of the skin of the abdomen along the lower edge of the costal arch. Reflex arc: intercostal nerves, ThVII-ThVIII; medium (mesogastric) – with irritation of the skin of the abdomen at the level of the navel. Reflex arc: intercostal nerves, ThIX-ThX; lower (hypogastric) – with skin irritation parallel to the inguinal fold. Reflex arc: iliohypogastric and ilioinguinal nerves, ThXI-ThXII; the abdominal muscles contract at the appropriate level and the navel deviates towards the irritation. The cremasteric reflex is caused by irritation of the inner thigh. In response, the testicle is pulled upward due to contraction of the levator testis muscle, reflex arc: genital femoral nerve, LI-LII. Plantar reflex - plantar flexion of the foot and toes when the outer edge of the sole is stimulated by strokes. Reflex arc: tibial nerve, LV-SII. Anal reflex - contraction of the external sphincter anus with tingling or streak irritation of the skin around it. It is called in the position of the subject on his side with his legs brought to the stomach. Reflex arc: pudendal nerve, SIII-SV.

Pathological reflexes . Pathological reflexes appear when the pyramidal tract is damaged, when spinal automatisms are disrupted. Pathological reflexes, depending on the reflex response, are divided into extension and flexion.

Extensor pathological reflexes in the lower extremities. Highest value has a Babinsky reflex - extension of the first toe when the skin of the outer edge of the sole is irritated by strokes; in children under 2-2.5 years old - a physiological reflex. Oppenheim reflex - extension of the first toe in response to running the fingers along the ridge tibia down to the ankle joint. Gordon's reflex - slow extension of the first toe and fan-shaped divergence of the other toes when the calf muscles are compressed. Schaefer reflex - extension of the first toe when the heel tendon is compressed.

Flexion pathological reflexes in the lower extremities. The most important reflex is the Rossolimo reflex - flexion of the toes during a quick tangential blow to the pads of the toes. Bekhterev-Mendel reflex - flexion of the toes when struck with a hammer on its dorsal surface. The Zhukovsky reflex is the flexion of the toes when a hammer hits the plantar surface directly under the toes. Ankylosing spondylitis reflex - flexion of the toes when hitting the plantar surface of the heel with a hammer. It should be borne in mind that the Babinski reflex appears with acute damage to the pyramidal system, for example with hemiplegia in the case of cerebral stroke, and the Rossolimo reflex is a later manifestation of spastic paralysis or paresis.

Flexion pathological reflexes on upper limbs . Tremner reflex - flexion of the fingers in response to rapid tangential stimulation with the fingers of the examiner examining the palmar surface of the terminal phalanges of the patient's II-IV fingers. The Jacobson-Weasel reflex is a combined flexion of the forearm and fingers in response to a blow with a hammer on the styloid process of the radius. The Zhukovsky reflex is the flexion of the fingers of the hand when hitting the palmar surface with a hammer. Carpal-digital ankylosing spondylitis reflex - flexion of the fingers during percussion of the back of the hand with a hammer.

Pathological protective, or spinal automatism, reflexes in the upper and lower extremities– involuntary shortening or lengthening of a paralyzed limb during injection, pinching, cooling with ether or proprioceptive stimulation according to the Bekhterev-Marie-Foy method, when the examiner performs a sharp active flexion of the toes. Protective reflexes are often of a flexion nature (involuntary flexion of the leg at the ankle, knee and hip joints). The extensor protective reflex is characterized by involuntary extension of the leg at the hip and knee joints and plantar flexion of the foot. Cross protective reflexes - flexion of the irritated leg and extension of the other - are usually observed with combined damage to the pyramidal and extrapyramidal tracts, mainly at the level of the spinal cord. When describing protective reflexes, the form of the reflex response, the reflexogenic zone, is noted. area of ​​evocation of the reflex and intensity of the stimulus.

Cervical tonic reflexes arise in response to irritations associated with changes in the position of the head in relation to the body. Magnus-Klein reflex - when the head is turned, the extensor tone in the muscles of the arm and leg, towards which the head is turned with the chin, increases, and the flexor tone in the muscles of the opposite limbs; flexion of the head causes an increase in flexor tone, and extension of the head - extensor tone in the muscles of the limbs.

Gordon reflex– delay of the lower leg in the extension position when inducing knee reflex. Foot phenomenon (Westphalian)– “freezing” of the foot during passive dorsiflexion. Foix-Thevenard tibia phenomenon– incomplete extension of the lower leg in the knee joint in a patient lying on his stomach, after the lower leg was held in extreme flexion for some time; manifestation of extrapyramidal rigidity.

Janiszewski's grasp reflex on the upper limbs - involuntary grasping of objects in contact with the palm; on the lower extremities - increased flexion of the fingers and toes when moving or other irritation of the sole. The distant grasping reflex is an attempt to grasp an object shown at a distance. It is observed with damage to the frontal lobe.

Expression sharp increase tendon reflexes serve clonus, manifested by a series of rapid rhythmic contractions of a muscle or group of muscles in response to their stretching. Foot clonus is caused by the patient lying on his back. The examiner bends the patient's leg at the hip and knee joints, holds it with one hand, and with the other grabs the foot and, after maximum plantar flexion, jerks the foot into dorsiflexion. In response, rhythmic clonic movements of the foot occur while the heel tendon is stretched. Clonus of the patella is caused by a patient lying on his back with straightened legs: fingers I and II grasp the apex of the patella, pull it up, then sharply shift it in the distal direction and hold it in this position; in response, there is a series of rhythmic contractions and relaxations of the quadriceps femoris muscle and twitching of the patella.

Synkinesis– a reflex friendly movement of a limb or other part of the body, accompanying the voluntary movement of another limb (part of the body). Pathological synkinesis is divided into global, imitation and coordinator.

Global, or spastic, is called pathological synkinesis in the form of increased flexion contracture in a paralyzed arm and extension contracture in a paralyzed leg when trying to move paralyzed limbs or during active movements with healthy limbs, tension in the muscles of the trunk and neck, when coughing or sneezing. Imitative synkinesis is the involuntary repetition by paralyzed limbs of voluntary movements of healthy limbs on the other side of the body. Coordinator synkinesis manifests itself in the form of additional movements performed by paretic limbs in the process of a complex purposeful motor act.

Contractures. Persistent tonic muscle tension, causing limited movement in the joint, is called contracture. They are distinguished by shape as flexion, extension, pronator; by localization - contractures of the hand, foot; monoparaplegic, tri- and quadriplegic; according to the method of manifestation - persistent and unstable in the form of tonic spasms; according to the period of occurrence after the development of the pathological process - early and late; in connection with pain – protective-reflex, antalgic; depending on the damage to various parts of the nervous system - pyramidal (hemiplegic), extrapyramidal, spinal (paraplegic), meningeal, with damage to peripheral nerves, such as the facial nerve. Early contracture – hormetonia. It is characterized by periodic tonic spasms in all extremities, the appearance of pronounced protective reflexes, and dependence on intero- and exteroceptive stimuli. Late hemiplegic contracture (Wernicke-Mann position) – adduction of the shoulder to the body, flexion of the forearm, flexion and pronation of the hand, extension of the hip, lower leg and plantar flexion of the foot; when walking, the leg describes a semicircle.

Semiotics of movement disorders. Having identified, based on a study of the volume of active movements and their strength, the presence of paralysis or paresis caused by a disease of the nervous system, its nature is determined: whether it occurs due to damage to central or peripheral motor neurons. Damage to central motor neurons at any level of the corticospinal tract causes the occurrence of central, or spastic, paralysis. When peripheral motor neurons are damaged at any site (anterior horn, root, plexus and peripheral nerve), peripheral, or sluggish, paralysis.

Central motor neuron : damage to the motor area of ​​the cerebral cortex or pyramidal tract leads to the cessation of the transmission of all impulses for voluntary movements from this part of the cortex to the anterior horns of the spinal cord. The result is paralysis of the corresponding muscles. If the pyramidal tract is interrupted suddenly, the muscle stretch reflex is suppressed. This means that the paralysis is initially flaccid. It may take days or weeks for this reflex to return.

When this happens, the muscle spindles will become more sensitive to stretching than before. This is especially evident in the arm flexors and leg extensors. Stretch receptor hypersensitivity is caused by damage to the extrapyramidal tracts, which terminate in the anterior horn cells and activate gamma motor neurons that innervate intrafusal muscle fibers. As a result of this phenomenon, the impulse through the feedback rings that regulate muscle length changes so that the arm flexors and leg extensors are fixed in the shortest possible state (minimum length position). The patient loses the ability to voluntarily inhibit overactive muscles.

Spastic paralysis always indicates damage to the central nervous system, i.e. brain or spinal cord. The result of damage to the pyramidal tract is the loss of the most subtle voluntary movements, which is best seen in the hands, fingers, and face.

The main symptoms of central paralysis are: 1) decreased strength combined with loss of fine movements; 2) spastic increase in tone (hypertonicity); 3) increased proprioceptive reflexes with or without clonus; 4) reduction or loss of exteroceptive reflexes (abdominal, cremasteric, plantar); 5) the appearance of pathological reflexes (Babinsky, Rossolimo, etc.); 6) protective reflexes; 7) pathological friendly movements; 8) absence of degeneration reaction.

Symptoms vary depending on the location of the lesion in the central motor neuron. Damage to the precentral gyrus is characterized by two symptoms: focal epileptic seizures (Jacksonian epilepsy) in the form of clonic seizures and central paresis(or paralysis) of the limb on the opposite side. Paresis of the leg indicates damage to the upper third of the gyrus, the arm to its middle third, half of the face and tongue to its lower third. It is diagnostically important to determine where clonic seizures begin. Often, convulsions, starting in one limb, then move to other parts of the same half of the body. This transition occurs in the order in which the centers are located in the precentral gyrus. Subcortical (corona radiata) lesion, contralateral hemiparesis in the arm or leg, depending on which part of the precentral gyrus the lesion is closer to: if it is in the lower half, then the arm will suffer more, and in the upper half, the leg. Damage to the internal capsule: contralateral hemiplegia. Due to the involvement of corticonuclear fibers, there is a disruption of innervation in the area of ​​the contralateral facial and hypoglossal nerves. Most cranial motor nuclei receive pyramidal innervation on both sides, either completely or partially. Rapid damage to the pyramidal tract causes contralateral paralysis, initially flaccid, as the lesion has a shock-like effect on peripheral neurons. It becomes spastic after a few hours or days.

Damage to the brain stem (cerebral peduncle, pons, medulla oblongata) is accompanied by damage to the cranial nerves on the side of the lesion and hemiplegia on the opposite side. Cerebral peduncle: Lesions in this area result in contralateral spastic hemiplegia or hemiparesis, which can be combined with ipsilateral (on the side of the lesion) lesion of the oculomotor nerve (Weber syndrome). Pontine cerebri: If this area is affected, contralateral and possibly bilateral hemiplegia develops. Often not all pyramidal fibers are affected.

Since the fibers descending to the nuclei of the VII and XII nerves are located more dorsally, these nerves may be spared. Possible ipsilateral involvement of the abducens or trigeminal nerve. Damage to the pyramids of the medulla oblongata: contralateral hemiparesis. Hemiplegia does not develop, since only the pyramidal fibers are damaged. The extrapyramidal tracts are located dorsally in medulla oblongata and remain safe. When the pyramidal decussation is damaged, it develops rare syndrome Cruciant (or alternating) hemiplegia (right arm and left leg and vice versa).

To recognize focal brain lesions in patients in comatose, the symptom of an outwardly rotated foot is important. On the side opposite to the lesion, the foot is turned outward, as a result of which it rests not on the heel, but on the outer surface. To determine this symptom, you can use the technique of maximum outward rotation of the feet - Bogolepov's symptom. On the healthy side, the foot immediately returns to its original position, while the foot on the hemiparesis side remains turned outward.

If the pyramidal tract is damaged below the chiasm in the region of the brain stem or upper cervical segments of the spinal cord, hemiplegia occurs with involvement of the ipsilateral limbs or, in the case of bilateral damage, tetraplegia. Lesions of the thoracic spinal cord (involvement of the lateral pyramidal tract) cause spastic ipsilateral monoplegia of the leg; bilateral damage leads to lower spastic paraplegia.

Peripheral motor neuron : damage can involve the anterior horns, anterior roots, peripheral nerves. Neither voluntary nor reflex activity is detected in the affected muscles. The muscles are not only paralyzed, but also hypotonic; areflexia is observed due to interruption of the monosynaptic arc of the stretch reflex. After a few weeks, atrophy occurs, as well as a reaction of degeneration of paralyzed muscles. This indicates that the cells of the anterior horns have a trophic effect on muscle fibers, which is the basis for normal function muscles.

It is important to determine exactly where the pathological process is localized - in the anterior horns, roots, plexuses or peripheral nerves. When the anterior horn is damaged, the muscles innervated from this segment suffer. Often, in atrophying muscles, rapid contractions of individual muscle fibers and their bundles are observed - fibrillar and fascicular twitching, which are a consequence of irritation by the pathological process of neurons that have not yet died. Since muscle innervation is polysegmental, complete paralysis requires damage to several adjacent segments. Involvement of all muscles of the limb is rarely observed, since the cells of the anterior horn supplying various muscles, are grouped into columns located at some distance from each other. The anterior horns can be involved in the pathological process in acute poliomyelitis, amyotrophic lateral sclerosis, progressive spinal muscle atrophy, syringomyelia, hematomyelia, myelitis, disorders of the blood supply to the spinal cord. When the anterior roots are affected, almost the same picture is observed as when the anterior horns are affected, because the occurrence of paralysis here is also segmental. Radicular paralysis develops only when several adjacent roots are affected.

Each motor root at the same time has its own “indicator” muscle, which makes it possible to diagnose its lesion by fasciculations in this muscle on the electromyogram, especially if the cervical or lumbar region is involved in the process. Since damage to the anterior roots is often caused by pathological processes in the membranes or vertebrae, simultaneously involving the dorsal roots, then movement disorders often combined with sensory disturbances and pain. Damage to the nerve plexus is characterized by peripheral paralysis of one limb in combination with pain and anesthesia, as well as autonomic disorders in this limb, since the trunks of the plexus contain motor, sensory and autonomic nerve fibers. Partial lesions of the plexuses are often observed. When the mixed peripheral nerve is damaged, peripheral paralysis of the muscles innervated by this nerve occurs, combined with sensory disturbances caused by interruption of afferent fibers. Damage to a single nerve can usually be explained mechanical reasons(chronic compression, trauma). Depending on whether the nerve is completely sensory, motor or mixed, disturbances occur, respectively, sensory, motor or autonomic. A damaged axon does not regenerate in the central nervous system, but can regenerate in peripheral nerves, which is ensured by the preservation of the nerve sheath, which can guide the growing axon. Even if the nerve is completely severed, bringing its ends together with a suture can lead to complete regeneration. Damage to many peripheral nerves leads to widespread sensory, motor and autonomic disorders, most often bilateral, mainly in the distal segments of the limbs. Patients complain of paresthesia and pain. Sensory disturbances of the “socks” or “gloves” type are detected, flaccid paralysis muscles with atrophy, trophic skin lesions. Polyneuritis or polyneuropathy are noted, arising due to many reasons: intoxication (lead, arsenic, etc.), nutritional deficiency (alcoholism, cachexia, cancer of internal organs, etc.), infectious (diphtheria, typhoid, etc.), metabolic ( diabetes mellitus, porphyria, pellagra, uremia, etc.). Sometimes the cause cannot be determined and this state is regarded as idiopathic polyneuropathy.

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