What type of sensitivity disorder is characteristic of lesions of the dorsal horns of the spinal cord (1)? Symptom complexes of damage to the cortical-muscular tract at different levels
Spinal cord(medulla spinalis) - part of the central nervous system located in the spinal canal. The spinal cord has the appearance of a white cord, somewhat flattened from front to back in the area of thickenings and almost round in other parts.
In the spinal canal it extends from the level of the lower edge of the foramen magnum to the intervertebral disc between the I and II lumbar vertebrae. At the top, the spinal cord passes into the brain stem, and at the bottom, gradually decreasing in diameter, it ends with the conus medullaris.
In adults, the spinal cord is much shorter than the spinal canal, its length varies from 40 to 45 cm. The cervical thickening of the spinal cord is located at the level of the third cervical and first thoracic vertebra; The lumbosacral thickening is located at the level of the X-XII thoracic vertebra.
The anterior median (15) and posterior median sulcus (3) divide the spinal cord into symmetrical halves. On the surface of the spinal cord, at the exit sites of the ventral (anterior) (13) and dorsal (posterior) (2) roots, two shallower grooves are revealed: anterior lateral and posterior lateral.
A segment of the spinal cord corresponding to two pairs of roots (two anterior and two posterior) is called a segment. The anterior and posterior roots emerging from the segments of the spinal cord unite into 31 pairs of spinal nerves. The anterior root is formed by processes of motor neurons of the nuclei of the anterior horns of the gray matter (12). The anterior roots of the VIII cervical, XII thoracic, and two upper lumbar segments, along with the axons of somatic motor neurons, include neurites of the cells of the sympathetic nuclei of the lateral horns, and the anterior roots of the II-IV sacral segments include the processes of neurons of the parasympathetic nuclei of the lateral intermediate substance of the spinal cord. The dorsal root is represented by the central processes of false unipolar (sensitive) cells located in the spinal ganglion. The central canal passes through the gray matter of the spinal cord along its entire length, which, expanding cranially, passes into the fourth ventricle of the brain, and in the caudal part of the conus medullaris forms the terminal ventricle.
The gray matter of the spinal cord, consisting mainly of nerve cell bodies, is located in the center. In cross sections, it resembles the shape of the letter H or has the appearance of a “butterfly”, the anterior, posterior and lateral sections of which form the horns of gray matter. The anterior horn is somewhat thickened and located ventrally. The dorsal horn is represented by a narrow dorsal part of the gray matter, extending almost to outer surface spinal cord. The lateral intermediate gray matter forms the lateral horn.
Longitudinal collections of gray matter in the spinal cord are called columns. The anterior and posterior columns are present throughout the entire length of the spinal cord. The lateral column is somewhat shorter, it begins at the level of the VIII cervical segment and extends to the I-II lumbar segments. In the columns of gray matter, nerve cells are united into more or less distinct groups-nuclei. Around the central canal there is a central gelatinous substance.
White matter occupies the peripheral parts of the spinal cord and consists of processes of nerve cells. The grooves located on the outer surface of the spinal cord divide white matter on the anterior, posterior and lateral funiculi. Nerve fibers, uniform in origin and function, within the white matter are combined into bundles or tracts that have clear boundaries and occupy a specific position in the cords.
There are three systems of pathways functioning in the spinal cord: associative (short), afferent (sensitive) and efferent (motor). Short association fascicles connect segments of the spinal cord. Sensory (ascending) tracts are directed to the centers of the brain. The descending (motor) tracts provide communication between the brain and the motor centers of the spinal cord.
Along the spinal cord there are arteries supplying it with blood: the unpaired anterior spinal artery and the paired posterior spinal artery, which are formed by large radiculomedullary arteries. The superficial arteries of the spinal cord are interconnected by numerous anastomoses. Deoxygenated blood It flows from the spinal cord through the superficial longitudinal veins and anastomoses between them along the radicular veins into the internal vertebral venous plexus.
The spinal cord is covered with a dense cover of the dura mater, the processes of which, extending from each intervertebral foramen, cover the root and the spinal ganglion.
The space between the dura mater and the vertebrae (epidural space) is filled with venous plexus and fatty tissue. In addition to the dura mater, the spinal cord is also covered by the arachnoid and pia mater.
Between the pia mater and the spinal cord is the subarachnoid space of the spinal cord, filled with cerebrospinal fluid.
There are two main functions of the spinal cord: its own segmental reflex and conductor, which provides communication between the brain, torso, limbs, internal organs, etc. Sensitive signals (centripetal, afferent) are transmitted along the dorsal roots of the spinal cord, and motor signals are transmitted along the anterior roots ( centrifugal, efferent) signals.
The spinal cord's own segmental apparatus consists of neurons for various functional purposes: sensory, motor (alpha, gamma motor neurons), autonomic, interneurons (segmental and intersegmental interneurons). All of them have direct or indirect synaptic connections with the conduction systems of the spinal cord. Neurons of the spinal cord provide muscle stretch reflexes - myotatic reflexes. They are the only spinal cord reflexes in which there is direct (without the participation of interneurons) control of motor neurons using signals transmitted along afferent fibers from muscle spindles.
RESEARCH METHODS
Myotatic reflexes are manifested by shortening of the muscle in response to its stretching when the tendon is struck with a neurological hammer. They differ in locality, and according to their condition, the topic of spinal cord damage is determined.
The study of superficial and deep sensitivity is important. When the segmental apparatus of the spinal cord is damaged, sensitivity in the corresponding dermatomes is impaired (dissociated or total anesthesia, hypoesthesia, paresthesia), and vegetative spinal reflexes change (viscero-motor, vegetative-vascular, urinary, etc.).
According to condition motor function limbs (upper and lower), as well as by muscle tone, the severity of deep reflexes, the presence of pathological hand and foot signs, one can assess the safety of the functions of the efferent conductors of the lateral and anterior cords of the spinal cord. Determining the zone of disturbance of pain, temperature, tactile, joint-muscular and vibration sensitivity allows us to assume the level of damage to the lateral and posterior cords of the spinal cord. This is facilitated by the study of dermographism, sweating, and vegetative-trophic functions.
To clarify the topic of the pathological focus and its relationship with surrounding tissues, as well as to determine the nature of the pathological process (inflammatory, vascular, tumor, etc.), solutions to issues of therapeutic tactics are carried out additional research. During a spinal puncture, the initial cerebrospinal fluid pressure and patency of the subarachnoid space are assessed (liquid dynamic tests); cerebrospinal fluid is subjected to laboratory testing.
Important information about the state of motor and sensory neurons of the spinal cord is obtained through electromyography and electroneuromyography, which make it possible to determine the speed of impulses along sensory and motor nerve fibers and to record evoked potentials of the spinal cord.
Using X-ray examination, damage to the spine and the contents of the spinal canal (the membranes of the spinal cord, blood vessels, etc.) are detected.
In addition to survey spondylography, if necessary, tomography is performed, which makes it possible to detail the structures of the vertebrae, the size of the spinal canal, and detect calcification meninges etc. Highly informative methods of X-ray examination are pneumomyelography, myelography with radiocontrast agents, as well as selective spinal angiography, venospondylography.
The anatomical contours of the spine and structures of the spinal canal of the spinal cord are well visualized using computed tomography, magnetic resonance imaging.
The level of block of the subarachnoid space can be determined using radioisotope (radionuclide) myelography. Thermography is used in the diagnosis of various spinal cord lesions.
Topical diagnostics
Lesions of the spinal cord are manifested by symptoms of irritation or loss of function of motor, sensory and autonomic-trophic neurons. Clinical syndromes depend on the localization of the pathological focus along the diameter and length of the spinal cord; the topical diagnosis is based on a set of symptoms of dysfunction of both the segmental apparatus and the conductors of the spinal cord. When the anterior horn or anterior root of the spinal cord is damaged, flaccid paresis or paralysis of the corresponding myotome develops with atrophy and atony of the innervated muscles, myotatic reflexes fade, fibrillation or “bioelectric silence” is detected on the electromyogram.
With a pathological process in the area of the dorsal horn or dorsal root, sensitivity in the corresponding dermatome is disrupted, deep (myotatic) reflexes, the arc of which passes through the affected root and segment of the spinal cord, decrease or disappear. When the dorsal root is damaged, radicular shooting pains first appear in the area of the corresponding dermatome, then all types of sensitivity are reduced or lost. When the posterior horn is destroyed, as a rule, sensitivity disorders are of a dissociated nature (pain and temperature sensitivity is lost, tactile and articular-muscular sensitivity is preserved).
Bilateral symmetrical dissociated sensitivity disorder develops with damage to the anterior gray commissure of the spinal cord.
When the neurons of the lateral horns are damaged, autonomic-vascular, trophic disorders and disturbances in sweating and pilomotor reactions occur (see Autonomic nervous system).
Damage to the conduction systems leads to more common neurological disorders. For example, when pyramidal conductors in the lateral cord of the spinal cord are destroyed, spastic paralysis (paresis) develops of all muscles innervated by neurons located in the underlying segments. Deep reflexes increase, pathological hand or foot signs appear.
If sensory conductors in the lateral cord are damaged, anesthesia occurs downward from the level of the pathological focus and on the side opposite to the lesion. The law of eccentric arrangement of long conductors (Auerbach - Flatau) allows us to differentiate the development of intramedullary and extramedullary pathological processes in the direction of spread of sensitivity disorders: the ascending type of sensitivity disorders indicates an extramedullary process, the descending type indicates an intramedullary process. The axons of the second sensory neurons (dorsal horn cells) pass into the lateral cord of the opposite side through two overlying segments of the spinal cord, therefore, when identifying the upper limit of conduction anesthesia, it should be assumed that the pathological focus is located two segments of the spinal cord above the upper limit of sensitivity disorders.
When the posterior cord is destroyed, joint-muscular vibration and tactile sensitivity on the side of the lesion is disrupted, and sensitive ataxia appears.
When half the diameter of the spinal cord is affected, central paralysis occurs on the side of the pathological focus, and on the opposite side - conduction pain and temperature anesthesia (Brown-Séquard syndrome).
Symptom complexes of spinal cord lesions at its various levels
There are several main symptom complexes of damage at different levels. Damage to the entire diameter of the spinal cord in top cervical spine (I-IV cervical segments of the spinal cord) is manifested by flaccid paralysis of the neck muscles, paralysis of the diaphragm, spastic tetraplegia, anesthesia from the level of the neck and downwards, dysfunction of the pelvic organs of the central type (urinary and fecal retention); Possible radicular pain in the neck and back of the head.
A lesion at the level of the cervical thickening (segments CV-ThI) leads to flaccid paralysis of the upper extremities with muscle atrophy, disappearance of deep reflexes in the arms, spastic paralysis of the lower extremities, general anesthesia below the level of the lesion, dysfunction of the pelvic organs of the central type.
Destruction of lateral horn cells at the CVIII-ThI level causes Bernard-Horner syndrome.
Damage to the thoracic segments is characterized by lower spastic paraplegia, conduction paraanesthesia, the upper limit of which corresponds to the level of the location of the pathological focus, urinary and fecal retention.
When the upper and middle thoracic segments are affected, breathing becomes difficult due to paralysis of the intercostal muscles; damage to the TX-XII segments is accompanied by paralysis of the abdominal muscles. Atrophy and weakness of the back muscles are detected. Radicular pain is girdling in nature.
Damage to the lumbosacral thickening (segments LI-SII) causes flaccid paralysis and anesthesia of the lower extremities, urinary and fecal retention, impaired sweating and pilomotor reaction of the skin of the lower extremities.
Damage to the segments of the epiconus (Minor's epiconus syndrome) is manifested by flaccid paralysis of the muscles of the LV-SII myotomes with the disappearance of Achilles reflexes (with preservation of the knee reflexes), anesthesia in the area of the same dermatomes, urinary and fecal retention, and impotence.
Damage to the conus segments (segments (SIII - SV)) is characterized by the absence of paralysis, peripheral dysfunction of the pelvic organs with true urinary and fecal incontinence, absence of the urge to urinate and defecate, anesthesia in the anogenital zone (saddle anesthesia), impotence.
Horse's tail (cauda equina) - damage to it gives a symptom complex very similar to damage to the lumbar enlargement and conus medullaris. Peripheral paralysis of the lower extremities occurs with urinary disorders such as retention or true incontinence. Anesthesia on the lower extremities and perineum. Severe radicular pain in the legs is characteristic and for initial and incomplete lesions - asymmetry of symptoms.
When a pathological process destroys not all, but only part of the diameter of the spinal cord, the clinical picture consists of various combinations of disturbances in movement, coordination, superficial and deep sensitivity, disorders of the function of the pelvic organs and trophism (bedsores, etc.) in the denervated area.
The most common types of incomplete damage to the diameter of the spinal cord are:
1) damage to the anterior (ventral) half of the diameter of the spinal cord, characterized by peripheral paralysis of the corresponding myotomes, central paralysis and conduction pain and temperature anesthesia below the level of the pathological focus, dysfunction of the pelvic organs (Preobrazhensky syndrome);
2) damage to one half of the diameter of the spinal cord (right or left), clinically manifested by Brown-Séquard syndrome;
3) damage to the posterior third of the diameter of the spinal cord, characterized by impaired deep, tactile and vibration sensitivity, sensory ataxia, conduction parasthesias (Williamson syndrome);
4) damage to the anterior horns of the spinal cord, causing peripheral paralysis of the corresponding myotomes (poliomyelitis syndrome);
5) damage to the centromedullary zone or posterior horn of the spinal cord, manifested by dissociated segmental anesthesia in the corresponding dermatomes (syringomyelic syndrome).
In the topical diagnosis of spinal cord lesions, it is important to remember the discrepancy between the level of location of the spinal cord segments and the vertebral bodies. It should be taken into account that in case of acute damage to the cervical or thoracic segments (trauma, hematomyelia, myeloischemia, etc.), developing paralysis of the lower extremities is accompanied by muscle atony, absence of knee and Achilles reflexes (Bastian's law). The slow development of the process of such localization (for example, with a tumor) is characterized by symptoms of spinal automatism with protective reflexes.
With some lesions of the posterior cords at the level of the cervical segments of the spinal cord (tumor, plaque multiple sclerosis, spondylogenic myelischemia, arachnoiditis) at the moment of tilting the head forward, a sudden pain piercing the whole body occurs, similar to an electric shock (Lhermitte’s symptom). For topical diagnosis, the sequence of symptoms of dysfunction of the spinal cord structures is important.
Determining the level of spinal cord damage
To determine the level of damage to the spinal cord, in particular its upper border, radicular pain, if any, is of great importance. When analyzing sensory disorders, it should be taken into account that each dermatome, as noted above, is innervated by at least 3 segments of the spinal cord (in addition to its own, another upper and one lower neighboring segments). Therefore, when determining the upper limit of anesthesia, it is necessary to consider the affected level of the spinal cord, located 1 - 2 segments higher.
Changes in reflexes, distribution of segmental movement disorders and the upper limit of the conductors. Sometimes it can also be useful to study sympathetic reflexes. For example, in areas of the skin corresponding to the affected segments, there may be an absence of reflex dermographism, piloarrector reflex, etc.
The so-called “mustard plaster” test can also be useful here: narrow strips of dry mustard plaster paper are cut, moistened and applied to the skin (you can fix them with transversely glued strips of adhesive plaster), one below the other, along the length, in a continuous strip. Differences in vascular reactions above the level of the lesion, at the level of segmental disorders and below them, in the territory of conduction disorders, can help clarify the topic of spinal cord damage.
For spinal cord tumors, the following techniques can be used to determine their level of location:
Herniation symptom. During a lumbar puncture, if there is a blockage of the subarachnoid space, as the cerebrospinal fluid flows out, a difference in pressure is created and it decreases in the lower part of the subarachnoid space, below the block. As a result, a “movement” downwards, “wedging” of the tumor is possible, which determines increased radicular pain, worsening conduction disorders, etc. These phenomena can be short-term, but sometimes they are persistent, determining deterioration in the course of the disease. The symptom is more typical for subdural extramedullary tumors, for example, for neuromas, which often arise from the dorsal roots and are usually somewhat mobile (Elsberg, I.Ya. Razdolsky).
Close to described cerebrospinal fluid rush symptom(I.Ya. Razdolsky). Again, in the presence of a block, and more often also with subdural extramedullary tumors, increased radicular pain and worsening of conduction disorders occur when the head is tilted to the chest or when the jugular veins are pressed with hands on both sides of the neck (as with the Queckenstedt maneuver). The mechanism of occurrence of the symptom is almost the same; only here it is not the decrease in fluid pressure in the subarachnoid space below the block that affects, but its increase above it due to venous stagnation inside the skull.
Spinous process symptom(I.Ya. Razdolsky). Pain when tapping the spinous process of the vertebra, at the level of which the tumor is located. The symptom is more typical for extramedullary and extradural tumors. It is best caused by shaking not with a hammer, but with the hand of the examiner (“the flesh of the fist”). Sometimes, not only do radicular pains appear (exacerbate), but also peculiar paresthesias occur: “a feeling of electric discharge” (Cassirer, Lhermitte) - a feeling of electric current (or “goosebumps”) passing down the spine, sometimes into the lower extremities.
May also have a known significance radicular positional pain(Dandy - Razdolsky). In a certain position, which causes, for example, tension in the posterior root from which the neuroma arises, radicular pain of the corresponding level arises or intensifies.
Finally worthy of attention Elsberg-Dyck sign(x-ray) - abnormal increase in the distance between the roots of the arches from 2 to 4 mm at the level of tumor localization (usually extradural).
When projecting the affected segments of the spinal cord onto the vertebrae, it is necessary to take into account the discrepancy in the length of the spinal cord and spine and carry out the calculation according to the instructions given above. For orientation in the spinous processes of the vertebrae, the following data can be used:
- the highest vertebra visible under the skin is the VII cervical, i.e. the lowest cervical vertebra;
- the line connecting the lower corners of the shoulder blades passes above the VII thoracic vertebra;
- the line connecting the tops of the iliac crests (cristae lliacae) runs in the space between the III and IV lumbar vertebrae.
In processes leading to filling of the cavity of the intravertebral canal (for example, with tumors) or causing adhesions in the subarachnoid space (with arachnoiditis), valuable data for localizing the process can sometimes be obtained by myelography, i.e., radiography when contrast solutions are introduced into the subarachnoid space. It is preferable to administer “heavy” or descending solutions (oil) by suboccipital puncture; contrast agent, descending down in the cerebrospinal fluid, in case of obstruction in the subarachnoid space, it stops or is temporarily delayed at the level of the block and is detected on radiography in the form of a shadow (“stop” contrast).
Less contrast images are obtained with pneumomyelography, i.e., when air is injected through a lumbar puncture in a sitting patient; the air, rising upward through the subarachnoid space, stops under the “block” and determines the lower border of the existing obstruction.
To determine the level of the “block” (for tumors, arachnoiditis, etc.), a “staircase” lumbar puncture is sometimes used, usually only in the spaces between the LIV - LIII - LII vertebrae (puncture of higher sections can be dangerous due to possible injury from the needle to the spinal brain). Below the blockade of the subarachnoid space, protein-cell dissociation is observed, above - the normal composition of the cerebrospinal fluid; Below the blockade there are symptoms of Queckenstedt and Stuckey, above - their absence (the norm).
Lesson 1
Topic: Clinical anatomy of the spinal cord. Spinal reflex ring. Reflexes and methods for their study. Voluntary movements, types of paralysis, movement disorder syndromes. Symptoms of damage to the cortico-muscular pathway at different levels.
Practical skills.
Spinal cord
Spinal cord ( medulla spinalis) is located in the spinal canal. At the level of the I cervical vertebra and occipital bone, the spinal cord passes into the medulla oblongata, and extends downwards to levels I-II lumbar vertebra, where it thins out and turns into a thin final thread. The length of the spinal cord is 40-45 cm, thickness 1 cm. The spinal cord has cervical and lumbosacral thickenings, where nerve cells providing innervation to the upper and lower extremities are localized.
The spinal cord consists of 31-32 segments. A segment is a section of the spinal cord that contains one pair of spinal roots (anterior and posterior).
The anterior root of the spinal cord contains motor fibers, the posterior root contains sensory fibers. Connecting in the area of the intervertebral node, they form a mixed spinal nerve.
The spinal cord is divided into five parts: 1) cervical (8 segments); 2) thoracic (12 segments); 3) lumbar (5 segments); 4) sacral (5 segments); 5) coccygeal (1-2 rudimentary segments).
The spinal cord is slightly shorter than the spinal canal. In this regard, in the upper parts of the spinal cord, its roots run horizontally. Then, starting from the thoracic region, they descend somewhat downwards before emerging from the corresponding intervertebral foramina. In the lower sections, the roots go straight down, forming the so-called ponytail.
On the surface of the spinal cord, the anterior median fissure, posterior median sulcus, and symmetrically located anterior and posterior lateral sulci are visible. Between the anterior median fissure and the anterior lateral groove is the anterior cord (funiculus anterior), between the anterior and posterior lateral grooves - the lateral cord (funiculus lateralis), between the posterior lateral groove and the posterior median groove - the posterior cord (funiculus posterior), which is in the cervical part The spinal cord is divided by a shallow intermediate groove into a thin fasciculus (fasciculus gracilis), adjacent to the posterior median sulcus, and a wedge-shaped fascicle (fasciculus cuneatus) located lateral to it. The funiculi contain pathways.
The anterior roots emerge from the anterior lateral sulcus, and the dorsal roots enter the spinal cord in the region of the posterior lateral sulcus.
Rice. Cross section of the spinal cord (diagram).
1 - anterior median fissure; 2 - posterior horn: a - top; b - head; c - neck; 3 - gelatinous substance; 4 - posterior cord; 5 - posterior median groove; 6 - thin beam; 7 - wedge-shaped bundle; 8 - posterior median septum; 9 - lateral cord; 10 - central channel; 11 - front horn; 12 - anterior cord.
Rice. Transverse section of the spinal cord at the level of the upper thoracic region (conducting tracts).
1 - posterior median septum; 2 - thin beam; 3 - wedge-shaped bundle; 4 - posterior horn; 5 - posterior spinocerebellar tract; 6 - central channel; 7 - side horn; 8 - lateral spinothalamic tract; 9 - anterior spinocerebellar tract; 10 - anterior spinothalamic tract; 11 - front horn; 12 - anterior median fissure; 13 - olivospinal tract; 14 - anterior corticospinal (pyramidal) tract; 15 - anterior reticular-spinal tract; 16 - vestibulospinal tract; 17 - bulboreticular-spinal tract; 18 - anterior white commissure; 19 - gray commissure; 20 - red nucleus-spinal tract; 21 - lateral corticospinal (pyramidal) tract; 22 - posterior white commissure; 23 - chest column (Clark's column).
In a cross-section of the spinal cord, the gray matter located in the central parts of the spinal cord and the white matter lying on its periphery are clearly distinguished. Gray matter in a cross section resembles the shape of a butterfly with open wings or the letter “H”. In the gray matter of the spinal cord, more massive, wide and short anterior horns and thinner, elongated posterior horns are distinguished. In the thoracic regions, the lateral horn is especially clearly visible, which is also less pronounced in the lumbar and cervical regions of the spinal cord. Right and left half spinal cord are symmetrical and connected by commissures of both gray and white matter. Anterior to the central canal is the anterior gray commissure (comissura grisea anterior), followed by the anterior white commissure (comissura alba anterior); posterior to the central canal, the posterior gray commissure and the posterior white commissure are located successively.
Large polygonal motor nerve cells are localized in the anterior horns of the spinal cord, the axons of which go to the anterior roots and innervate the striated muscles of the neck, trunk and limbs. The motor cells of the anterior horns are the final authority in the implementation of any motor act, and also have trophic effects on the striated muscles.
Primary sensory cells are located in the spinal (intervertebral) nodes. Such a nerve cell has one process, which, moving away from it, is divided into two branches. One of them goes to the periphery, where it receives irritation from the skin, muscles, tendons or internal organs, and through the other branch these impulses are transmitted to the spinal cord. Depending on the type of irritation and, therefore, the pathway along which it is transmitted, the fibers entering the spinal cord through the dorsal root may end on the cells of the dorsal or lateral horns or directly pass into the white matter of the spinal cord. Thus, the cells of the anterior horns carry out motor functions, the cells of the posterior horns carry out the sensitivity function, and the spinal vegetative centers are localized in the lateral horns.
The white matter of the spinal cord consists of fibers of the pathways that interconnect both the different levels of the spinal cord with each other, and all overlying parts of the central nervous system with the spinal cord.
In the anterior cords of the spinal cord there are mainly pathways involved in the implementation of motor functions: 1) the anterior corticospinal (pyramidal) tract (uncrossed), coming mainly from the motor area of the cerebral cortex and ending on the cells of the anterior horns; 2) vestibulospinal tract, coming from the lateral vestibular nucleus of the same side and ending on the cells of the anterior horns; 3) tegnospinal tract, starting in the upper colliculi of the quadrigeminal tract of the opposite side and ending on the cells of the anterior horns; 4) the anterior reticular-spinal tract, coming from the cells of the reticular formation of the brain stem of the same side and ending on the cells of the anterior horn.
In addition, near the gray matter there are fibers that connect different segments of the spinal cord with each other.
The lateral cords of the spinal cord contain both motor and sensory pathways. The motor tracts include: 1) the lateral corticospinal (pyramidal) tract (crossed), coming mainly from the motor area of the cerebral cortex and ending on the cells of the anterior horns of the opposite side; 2) the red nucleus-spinal tract, coming from the red nucleus and ending on the cells of the anterior horns of the opposite side; 3) reticular-spinal cord tracts, coming mainly from the giant cell nucleus of the reticular formation of the opposite side and ending on the cells of the anterior horns; 4) the olivospinal tract, connecting the inferior olives with the motor neuron of the anterior horn.
The afferent, ascending conductors include the following paths of the lateral cord: 1) posterior (dorsal uncrossed) spinocerebellar path, coming from the cells of the dorsal horn and ending in the cortex of the superior cerebellar vermis; 2) anterior (crossed) spinocerebellar tract, coming from the cells of the dorsal horns and ending in the cerebellar vermis; 3) the lateral spinothalamic tract, coming from the cells of the dorsal horns and ending in the thalamus.
In addition, the spinopectoral tract, spinoreticular tract, spinoolivary tract and some other conduction systems pass through the lateral funiculus.
The afferent thin and cuneate fasciculi are located in the posterior cords of the spinal cord. The fibers included in them begin in the intervertebral nodes and end, respectively, in the nuclei of the thin and wedge-shaped fasciculi, located in the lower part of the medulla oblongata.
Thus, part of the reflex arcs is closed in the spinal cord and the excitation coming through the fibers of the dorsal roots is subjected to a certain analysis and then transmitted to the cells of the anterior horn; the spinal cord transmits impulses to all overlying parts of the central nervous system up to the cerebral cortex.
The reflex can be carried out in the presence of three successive links: 1) the afferent part, which includes receptors and pathways that transmit excitation to the nerve centers; 2) the central part of the reflex arc, where the analysis and synthesis of incoming stimuli occurs and a response to them is developed; 3) the effector part of the reflex arc, where the response is carried out through skeletal muscles, smooth muscles and glands. The spinal cord is thus one of the first stages at which the analysis and synthesis of stimuli both from internal organs and from receptors of the skin and muscles are carried out.
Rice. Spinal nerve.
I - posterior horn; 2 - posterior cord; 3 - posterior median groove; 4 - posterior root; 5 - spinal node; 6 - trunk of the spinal nerve; 7 - internal branch of the posterior branch; 8 - external branch of the posterior branch; 9 - posterior branch; 10 - anterior branch;
II - white connecting branches; 12 - shell branch; 13 - gray connecting branches; 14 - node of the sympathetic trunk; 15 - anterior median fissure; 16 - front horn; 17 - anterior cord; 18 - anterior root; 19 - anterior gray commissure; 20 - central channel; 21 - lateral cord; 22 - postganglionic fibers. Sensory fibers are indicated in blue, motor fibers in red, white connecting branches in green, and gray connecting branches in purple.
The spinal cord exerts trophic influences, i.e. damage to the nerve cells of the anterior horns leads to disruption of not only movements, but also the trophism of the corresponding muscles, which leads to their degeneration.
One of important functions The spinal cord regulates the activity of the pelvic organs. Damage to the spinal centers of these organs or the corresponding roots and nerves leads to persistent disturbances in urination and defecation.
PYRAMID SYSTEM
Movement is one of the main manifestations of life. There are two main types of movements: involuntary and voluntary. 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 (praxia). Special voluntary movements - behavioral, labor, etc. - are carried out with the leading participation of the cerebral cortex, as well as extra pyramid system and segmental apparatus of the spinal cord. In humans and higher animals, the implementation of voluntary movements is associated with a special department nervous system- pyramid system.
Central motor neuron. Voluntary muscle use involves long nerve fibers that originate from cortical neurons and travel down to the anterior horn cells of the spinal cord. These fibers form the corticospinal, or pyramidal, tract. They are axons of neurons located in the medullary zone, the precentral gyrus, in the 4th cytoarchitectonic field. 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, opposite the sensory cortex of the postcentral gyrus.
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. This somatotopic projection corresponds to a person standing on his head. The distribution of motor neurons is not limited to fields; they are also found in neighboring cortical fields. At the same time, their vast majority occupies the 5th cortical layer of area 4. They are “responsible” for precise, targeted single movements. These neurons also include Betz giant pyramidal cells, which give off axons with a thick myelin coating. These fast-conducting fibers make up only 3.4-4% of all pyramidal tract fibers. Most pyramidal fibers arise from small pyramidal, or fusiform (spindle-shaped) cells in motor fields 4 and 6. Cells in field 4 provide about 40% of the fibers of the pyramidal tract, the rest come from other fields of the sensorimotor zone.
Area 4 mononeurons control fine voluntary movements of the skeletal muscles of the opposite half of the body, since most pyramidal fibers pass to the opposite side in the lower part of the medulla oblongata.
Rice. Pyramid system.
A - pyramidal tract: 1 - cerebral cortex; 2 - internal capsule; 3 - cerebral peduncle; 4 - bridge; 5 - intersection of pyramids; 6 - lateral corticospinal (pyramidal) tract; 7 - spinal cord; 8 - anterior corticospinal tract; 9 - peripheral nerve; III, VI, VII, IX, X, XI, XII - cranial nerves. B - convexital surface of the cerebral cortex (fields 4 and 6). Topographic projection of motor functions: 1 - leg; 2 - torso; 3 - hand; 4 - brush; 5 - face. B - horizontal section through the internal capsule. Location of the main pathways: 1 - visual and auditory radiation; 2 - temporopontine fibers and parieto-occipital-pontine fascicle; 3 - thalamic fibers; 4 - corticospinal fibers to the lower limb; 5 - corticospinal fibers to the muscles of the trunk; 6 - corticospinal fibers to the upper limb; 7 - cortical-nuclear pathway; 8 - frontal-pontine tract; 9 - corticothalamic tract; 10 - anterior leg of the internal capsule; II - knee of the internal capsule; 12 - hind leg internal capsule. G - anterior surface of the brain stem: 1 - decussation of the pyramids.
The impulses of the pyramidal cells of the motor cortex follow two paths. One - the corticonuclear tract - ends on the nuclei of the cranial nerves of the trunk, the second, thicker, 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 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 of the pons nuclei and fibers of various systems. At the level of the pontomedullary junction, the pyramidal tract becomes externally visible and forms 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 the lateral pyramidal tract. The remaining fibers continue to descend uncrossed in the anterior funiculi as the 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 probably 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. The lateral pyramidal tract becomes thinner and thinner as the fibers extend. About 90% of the fibers form synapses with interneurons, which in turn connect with large alpha and gamma motor neurons of the anterior horn.
The fibers forming the corticonuclear tract leave the rostral part of the pyramidal fasciculus at the level of the midbrain. On the way to the nuclei of the cranial motor nerves, some of them intersect. Those nerves that provide voluntary innervation of the facial and oral muscles are supplied: V, VII, IX, X, XI, XII.
Another bundle of fibers, starting in the “eye” area 8, and not in the precentral gyrus, also deserves attention. Impulses traveling along this bundle provide conjugal eye movements. When the fibers of this bundle leave field 8, they join the pyramidal path in the corona radiata. Then they pass more ventrally in the posterior leg of the internal capsule, turn caudally and go to the nuclei of the motor nerves of the eye: III, IV, VI. Field 8 impulses act synergistically, causing friendly movements eyeballs in the opposite direction.
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 cells and gamma cells. 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 part, the lateral motor neurons of the anterior horn innervate the hand and arm, and 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 more 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 the posterior root immediately 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 consist not only of afferent sensory (somatic) and efferent motor (somatic), but also efferent autonomic fibers emanating from the lateral horns of the spinal gray matter, and afferent autonomic fibers.
The well-myelinated, rapidly conducting axons of the large alpha cells go directly to the striated muscle and give off more and more branches as they spread distally.
In addition to alpha motor neurons major and minor, the anterior horn contains numerous gamma motor neurons. Among other interneurons of the anterior horns, Renshaw cells should be noted, which in turn reconnect with the cells of the anterior horn, inhibiting their action. This is an example of spinal negative feedback that inhibits the action of large motor neurons. Large alpha cells with thick and rapidly conducting axons, performing a phasic function, carry out rapid muscle contractions. Small alpha cells with thinner axons perform a tonic function. Gamma cells with a thin and slowly conducting axon innervate muscle fibers located inside the muscle spindles - muscle proprioceptors. Large alpha cells are associated with giant cells of the cerebral cortex. Small alpha cells have connections with the extrapyramidal system.
Rice. Transverse sections of the spinal cord.
A - conductive tracts of the spinal cord: 1 - wedge-shaped bundle; 2 - thin beam; 3 - posterior spinocerebellar tract; 4 - anterior spinocerebellar tract; 5 - lateral spinothalamic tract; 6 - back-cover path; 7 - spinoolivary path; 8 - anterior spinothalamic tract; 9-anterior own bundles; 10-anterior corticospinal tract; 11 - tegnospinal tract; 12 - vestibular spinal cord; 13 - olivospinal tract; 14 - red nuclear spinal tract; 15 - lateral corticospinal tract; 16 - rear own bundles. B - topography of the white matter of the spinal cord: 1 - anterior cord. Paths from the cervical, thoracic and lumbar segments are indicated in blue, and from the sacral segments in purple; 2 - lateral cord. Paths from the cervical segments are indicated in blue, from the thoracic segments in blue, and from the lumbar segments in purple; 3 - posterior cord. The paths from the cervical segments are indicated in blue, from the thoracic segments in blue, and from the thoracic segments in dark blue.
lumbar, purple - from the sacral. B - cross section of the spine and spinal cord: 1 - spinous process of the vertebra; 2 - synapse; 3 - skin receptor; 4 - afferent (sensitive) fibers; 5 - muscle; 6 - efferent (motor) fibers; 7 - vertebral body; 8 - node of the sympathetic trunk; 9 - spinal (sensitive) node; 10 - gray matter of the spinal cord; 11 - white matter of the spinal cord. D - topographic distribution of motor nuclei in the anterior horns of the spinal cord at the level of the lower cervical segment. On the left - the general distribution of cells of the anterior horn, on the right - the nuclei: 1 - posteromedial; 2 - anteromedial; 3 - front; 4 - central; 5 - anterolateral; 6 - posterolateral; 7 - posterolateral; I - gamma efferents from small cells of the anterior horns to the neuromuscular spindles; II - somatic efferent fibers, giving collaterals to medially located Renshaw cells; III - gelatinous substance.
The state of muscle proprioceptors is regulated through gamma cells. Muscle receptors include several types, the most important of which are the neuromuscular spindles. They respond to passive stretching of the muscle and are responsible for the stretch reflex, or myotatic reflex. These thin, spindle-shaped structures are covered by a sheath of connective tissue and are located between the striated fibers of skeletal muscle. They contain 3-10 very thin striated fibers called intrafusal muscle fibers, as opposed to the other extrafusal fibers.
Afferent fibers, called anulospiral or primary endings, coil around the middle of the muscle spindle. These fibers have a fairly thick myelin coating and are classified as fast-conducting fibers. The nuclei of some intrafusal fibers of the spindle are grouped in the equatorial part, forming a nuclear bag, while the nuclei of others are located in a chain along the entire spindle.
Many muscle spindles, especially nuclear chain fibers, have not only primary but also secondary endings. These endings also respond to stretch stimuli, and their action potential propagates centrally along thin fibers communicating with interneurons responsible for reciprocal actions. Through these neurons, flexors or extensors can be activated, inhibiting the corresponding antagonist muscles.
Only a small number of proprioceptive impulses reach the cortex and, accordingly, the level of consciousness, while the majority are transmitted through feedback rings and do not reach this level. These are elements of reflexes that serve as the basis for voluntary and other movements, as well as static reflexes that resist gravity.
Thus, the spindle is considered to be a stretch receptor responsible for maintaining constant muscle length. Extrafusal fibers in a relaxed state have a constant length. When a muscle is stretched, the spindle is stretched. The anulospiral endings respond to stretch 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 triggers this mechanism. Light percussion on the muscle tendon instantly stretches the muscle. The spindles react immediately. When the impulse reaches the anterior horn motor neurons, they respond by causing a short contraction. This monosynaptic transmission is basic for all proprioceptive reflexes. 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 motor neurons are influenced by fibers descending from motor neurons localized in the rostral part of the central nervous system as part of tracts such as the pyramidal, reticular-spinal, and vestibular-spinal tracts. Thus, the muscle is under the direct influence of the brain, which is important for performing any voluntary movement. The efferent actions of gamma fibers make it possible to finely regulate voluntary movements and provide the ability to regulate the strength of the “response” of the receptors to stretch. This is called the gamma neuron-spindle system. Contraction of intrafusal muscle fibers causes a decrease in the threshold for the action of stretch receptors. In other words, a small stretch of the muscle itself causes the activation of stretch receptors. Under normal circumstances, muscle length is automatically adjusted through this reflex arc.
Research methodology. Inspect, palpate and measure muscles, determine the volume of active and passive movements, muscle strength, muscle tone, rhythm of active movements and reflexes. To identify the nature and localization motor disorders, as well as for clinically mild symptoms, electrophysiological methods are important.
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 can be detected. By palpation, you can determine the configuration of the muscles and their tension.
Active movementsare checked consistently in all joints and performed by the subject. They may be absent or limited in volume and weakened in strength. The complete absence of active movements is 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 both legs is called lower paraplegia or paraparesis. Paralysis or paresis of two limbs of the same name is called hemiplegia or hemi-paresis, paralysis of three limbs - triplegia, paralysis of four limbs - quadriplegia or tetraplegia.
Passive movementsare determined at complete relaxation muscles to the subject, which makes it possible to exclude a local process (changes in joints, other reasons causing limb immobility) that limits active movements. Along with this, passive movements are the main method of studying muscle tone.
The volume of passive movements of the upper limb is examined: in the shoulder, elbow, wrist joints (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 are studied: hip, knee, ankle (flexion and extension, outward and inward rotation), flexion and extension of fingers.
Muscle strength is determined consistently in all their groups with active resistance of the patient. For example, when studying the strength of the muscles of the shoulder girdle, the patient is asked to raise his arm to a horizontal level, resisting the examiner’s attempt to lower his arm; then it is proposed to raise both hands above the horizontal line and hold them, offering resistance. Shoulder muscle strength: the patient is asked to bend his arm at the elbow joint, and the examiner tries to straighten it; the strength of the abductors and adductors of the shoulder is also examined. Forearm muscle strength: the task is given to perform pronation, and then supination, flexion and extension of the hand with resistance in the movement performed. Strength of the muscles of the fingers: the patient is asked to make a ring from the first finger with each of the others, and the examiner tries to straighten it. Strength is checked when the fifth finger is moved away from the fourth finger and when the other fingers are brought together, when the hands are clenched into a fist. The strength of the pelvic girdle and hip muscles is tested by lifting, 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 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, the Barre test is examined - the paretic arm, extended forward or raised upward, is gradually lowered, the leg raised above the bed is gradually lowered, while the healthy one is held in its given position. In mild cases of paresis, you have to resort to testing 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 a limb will result in the limb becoming more likely to get tired; movements are not performed as quickly and less dexterously than with a healthy limb. Hand strength is measured with a dynamometer.
Muscle tone - involuntary, constantly changing in intensity muscle tension, not accompanied by a motor effect. Muscle tone creates preparation for movement, ensures muscle resistance and elasticity, and maintains balance and posture. The term “muscle tone” refers to the ability of a muscle to resist stretching or maintain tension for a long time.
Buddha test (paretic hand falls faster)
Muscle tone is a postural reflex and is maintained by asynchronous activity of motor units. There are two components of muscle tone: plastic and reflex. Plastic tone is muscle tension, its turgor, which persists under conditions of denervation. This term defines the tone of individual muscle cells, depending on the characteristics of their structure, metabolism, blood and lymph circulation, the content of connective tissue, etc. Reflex tone is understood as reflex muscle tension, most often caused by its stretching, i.e. irritation of proprioceptors. 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. The implementation of these reactions is possible only in the presence of appropriate impulses to the muscle from the motor cells of the anterior horns of the spinal cord. Tonic reactions are based on a stretch reflex, or myotatic reflex, the closure of which occurs in the spinal cord. The peripheral system for regulating muscle tone is the gamma system.
Muscle tone is influenced by the spinal (segmental) reflex apparatus, afferent innervation, reticular formation and a whole complex of tonic formations (cervical tonic, including vestibular, centers, cerebellum, red nucleus system, basal ganglia, etc.).
To judge the state of muscle tone, the muscles of segmental areas of the body are directly felt. With hypotension, the muscle is flabby, soft, and doughy; with hypertension, it has a denser consistency. However, the determining factor is the study of muscle tone through passive movements in the 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 studying Orshansky's symptom: when lifting up (in a lying patient) a leg straightened at the knee joint, it is overextended in this joint and the heel lags behind the bed. Hypotonia and muscle atony occur with peripheral paralysis or paresis (disruption 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 muscle tone in the flexors and pronators of the arm and in the extensors and adductors of the leg (if the pyramidal tract is affected). With spastic hypertension, during repeated movements of the limb, muscle tone does not change, and sometimes decreases; with plastic hypertension, muscle tone increases. With spastic hypertension, a “penknife” symptom is observed (an obstacle to passive movement in the initial phase of the study), with plastic hypertension, a “gear wheel symptom” (a sensation of jolts during the study of muscle tone in the limbs). Plastic hypertension is an increase in muscle tone, uniform in both flexors and extensors, pronators and supinators (with damage to the pallidonigral system).
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. Reflexes allow us to judge the state of various parts of the nervous system. When studying reflexes, their character, uniformity, and asymmetry are determined; when they increase, a reflexogenic zone is noted. 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 reflexesarise when 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).
Rice. Tendon reflex (diagram).
1- gamma central pathway; 2- alpha central pathway; 3- spinal (sensitive) node; 4 - Renshaw cell; 5 - spinal cord; 6 - alpha motor neuron of the spinal cord; 7 - gamma motor neuron of the spinal cord; 8- alpha efferent nerve; 9- gamma efferent nerve; 10 - primary afferent nerve of the muscle spindle; 11 - afferent nerve of the tendon; 12 - muscle; 13- muscle spindle; 14-nuclear bag; 15 - pole of the spindle. The plus sign denotes the process of excitation, and the minus sign denotes inhibition.
On the upper limbs. The reflex from the tendon of the biceps brachii muscle is caused by hitting the tendon of this muscle with a hammer (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, Cy - Cyj segments. The reflex from the tendon of the triceps brachii muscle (Fig. 8) is caused by hitting the tendon of this muscle above the olecranon with a hammer (the patient’s arm should be bent at the elbow joint at an angle of almost 90°). In response, the forearm extends. Reflex arc: radial nerve, CVi - Suts. The carporadial or metacarpal radial reflex (Fig. 9) is 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, Su - Noun.
Rice. Inducing the flexion-elbow reflex.
Rice. 8. Inducing the ulnar extension reflex.
On the lower extremities. The knee, or patellar, reflex is caused by hitting the quadriceps tendon with a hammer. In response, the lower leg is extended. Reflex arc: femoral nerve, bc - Ljy. 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.
The heel (Achilles) reflex is caused by percussion on the Achilles tendon. In response, plantar flexion of the foot occurs as a result of contraction of the calf muscles. Reflex arc: tibial nerve, Si-Sn- In a lying patient, the leg should be bent at the hip and knee joints, the foot 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 Achilles 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 percussion on the Achilles tendon or on 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 Achilles tendon.
Rice. Inducing the metacarpal radial reflex.
Rice. Inducing a knee reflex (a, b).
Rice. Inducing the heel reflex (a, b).
Joint reflexes (caused by irritation of the receptors of the joints and ligaments on 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, Sup - Thj; 2) Leri - flexion of the forearm with forced flexion of the fingers and hand in a supinated position. Reflex arc: ulnar and median nerves, Cyi - Th[.
Skin reflexes (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 - upper (epigastric) is caused by irritation of the abdominal skin along the lower edge of the costal arch (intercostal nerves, Tup - Tush), middle (mesogastric) - by irritation of the abdominal skin at the level of the navel (intercostal nerves, Tjx-Tx) and lower (hypogastric) - with irritation of the skin parallel to the inguinal fold (iliohypogastric and ilioinguinal nerves, Txi - Txp); 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 cremasteric muscle. Reflex arc: genital femoral nerve, Lj - bc. Plantar reflex: plantar flexion of the foot and toes upon stroke stimulation of the outer edge of the sole. Reflex arc: tibial nerve, Ly - S\\. 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, Sni - Sy.
Pathological reflexes. Pathological reflexes appear when the pyramidal tract is damaged, when spinal automatisms are disinhibited. Pathological reflexes Depending on the reflex response, they are divided into extension and flexion.
Rice. Inducing abdominal reflexes.
Rice. Inducing the Babinski reflex (a) and its diagram (b).
Rice. Inducing the Oppenheim reflex.
Rice. Inducing the Gordon reflex.
Rice. Inducing the Schaefer reflex.
Extensor pathological reflexes in the lower extremities. The most important is the Babinski reflex - extension of the first toe during line irritation of the skin of the outer edge of the sole, in children under 2-2"/2 years - a physiological reflex. Oppenheim reflex - extension of the first toe in response to running the fingers down along the crest of the tibia To 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 Achilles tendon is compressed.
Rice. Inducing the Rossolimo reflex.
Rice. Inducing the Bekhterev-Mendelian reflex.
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-Mendelian 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 - late manifestation spastic paralysis or paresis.
Flexion pathological reflexes in the 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 (II-IV fingers of the patient). Jacobson's reflex - Weasel - 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.
Rice. Inducing the Zhukovsky reflex.
Rice. Inducing the heel reflex of Bekhterev
Pathological protective, or spinal automatism, reflexes on 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-Foix method (the researcher performs
sharp active flexion of the toes). Protective reflexes are often of a flexion nature - involuntary bending 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. When inducing protective reflexes, the form of the reflex response, the reflexogenic zone, is noted, i.e., the boundary of inducing the reflex and the effectiveness of the stimulus.
Rice. Study of the postural reflex (shin phenomenon).
Rice. Clonus.
a - patella; b - feet.
Cervical tonic reflexes occur in response to stimulation associated with changes in the position of the head in relation to the body. Magnus-Klein reflex - when turning the head, the extensor tone in the muscles of the arm and leg, towards which the head is turned with the chin, increases, the flexor tone in the muscles of the limbs, to which the back of the head is turned; flexion of the head causes an increase in flexor tone, and extension of the head - extensor tone in the muscles of the limbs.
Gordon's reflex - holding the lower leg in the extension position while inducing the knee reflex. Foot phenomenon (Westphalian) - “freezing” of the foot during passive dorsiflexion. The Foix-Thevenard shin phenomenon is incomplete extension of the shin at the knee joint in a patient lying on his stomach after the shin has been held in extreme flexion for some time; manifestation of extrapyramidal rigidity.
Janiszewski's grasping reflex - in the upper extremities, 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. Distant grasping reflex - an attempt to grab an object shown at a distance. It is observed with damage to the frontal lobe.
An expression of a sharp increase in tendon reflexes is clonus, which manifests itself as 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, she makes rhythmic clonic movements for as long as the Achilles tendon continues to stretch. 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 is 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 synkinesia in the form of increased flexion contracture in the paralyzed arm and extension contracture in the 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.
Rice. Wernicke-Mann pose
Imitative synkinesis is the involuntary repetition by paralyzed limbs of voluntary movements of healthy limbs on the other side of the body. Coordinative synkinesis manifests itself in the form of paralyzed limbs performing movements in the process of a complex purposeful motor act that they cannot produce in isolation.
Contractures. Persistent tonic muscle tension, causing limited mobility - tightening of limbs or individual muscle groups. They are distinguished: by shape - 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 (hormetonia); 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 of all extremities, increased 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 the central or peripheral motor neurons. Damage to central motor neurons at any level of the corticospinal tract causes central, or spastic, paralysis. When peripheral motor neurons are damaged at any site (anterior horn, root, plexus and peripheral nerve), peripheral or flaccid paralysis occurs.
Central motor neuron: Damage to the motor cortex or pyramidal tract stops transmission of all voluntary movement stimuli from the motor cortex to the anterior horn of the spinal cord. The result is paralysis of the muscles supplied by these cells. 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 position (minimum length position). The patient loses the ability to voluntarily inhibit overactive muscles.
Inhibitory and activating fibers should be differentiated. It is assumed that inhibitory fibers are closely intertwined with pyramidal fibers. This is the reason that they are also always damaged when the pyramidal tract is affected. Activating fibers are involved to a lesser extent and may still influence muscle spindles. The consequence of this is spasticity and hyperreflexia, accompanied by clonus.
Spastic paralysis always indicates damage to the central nervous system, i.e., the 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.
Symptomatology varies 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 one 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 radiate) lesion: contralateral hemiparesis with a predominance in the arm or leg, depending on which part of the precentral gyrus the lesion is located 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, contralateral damage to the facial and hypoglossal nerves is observed. 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 hours or days as the extrapyramidal fibers are also affected.
Brain stem (brain peduncle, cerebral pons, medulla oblongata): involvement of the cranial nerve on the side of the lesion in the pathological process and hemiplegia on the opposite side - alternating hemiplegia. Cerebral peduncle: the result of a lesion in this area is contralateral spastic hemiplegia, 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. On the other hand, ipsilateral involvement of the abducens or trigeminal nerve is possible. 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 the medulla oblongata and remain intact. When the intersection of the pyramids is damaged, a rare syndrome develops - cruciate, or alternating, hemiplegia (right arm and left leg and vice versa).
To recognize focal brain lesions in patients in a comatose state, 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.
Rice. Rotation of the foot with hemiplegia.
If the pyramidal tract is damaged below the chiasm, hemiplegia occurs with involvement of the ipsilateral limbs. Bilateral damage to the brain or upper cervical segments of the spinal cord causes tetraplegia. Unilateral damage to the upper cervical segments of the spinal cord (involvement of the lateral pyramidal tract) causes spastic hemiplegia on that side, since the pyramidal tract is already crossed. The paralysis is spastic, since the extrapyramidal fibers mixed with the pyramidal fibers are also damaged. 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 may involve the anterior horns, several anterior roots, and peripheral nerves. Neither voluntary nor involuntary, or 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 of the paralyzed muscles occurs. It can be so severe that after months and years only connective tissue remains. This indicates that the cells of the anterior horns have a trophic effect on muscle fibers, which is the basis of normal muscle function.
The following symptoms are characteristic of peripheral paralysis: 1) hypotension or muscle atony; 2) hypo-or areflexia; 3) hypo- or muscle atrophy; 4) neurogenic muscular degeneration with degeneration reaction. These features are characteristic of peripheral paralysis, regardless of the level of damage to the peripheral neuron. However, 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 there are fast contractions individual muscle fibers and their bundles - fibrillar and fascicular twitching, resulting from 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 rare, since the anterior horn cells supplying the various muscles are grouped in 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 muscular atrophy, syringomyelia, hematomyelia, myelitis, and disorders of the blood supply to the spinal cord. Lesions of the anterior roots give almost the same picture as lesions of the anterior horns, because the distribution 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 painful processes in the membranes or vertebrae, which simultaneously involve the posterior roots, movement disorders are 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 mixed peripheral nerve 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 attributed to mechanical causes (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 damaged, bringing its ends together with a suture can lead to complete regeneration.
Damage to many peripheral nerves results in widespread sensory, motor and autonomic disorders, most often bilateral, mainly in the distal segments of the limbs. Patients complain of paresthesia and pain. Sensitive disturbances of the “socks” or “gloves” type, flaccid muscle paralysis with atrophy, and trophic disturbances on the skin are detected. Polyneuritis or polyneuropathy are noted, arising due to many reasons: intoxication (lead, arsenic, etc.), nutritional deficiencies - as a result of alcohol intake, cachexia, cancer of internal organs, etc., infectious (diphtheria, typhus, etc.), metabolic (diabetes mellitus, porphyria, pellagra, uremia, etc.). Sometimes the cause cannot be determined, and this state is regarded as idiopathic polyneuropathy.
SCHEME FOR DIAGNOSTIC SEARCH FOR MOTOR DISORDERS
I STAGE. Target. Determine the presence or absence of movement disorders.
To do this you should
1. Use the information provided in the patient’s complaints; the main criteria necessary to identify the issue of interest to us are limitations in active movements and weakness in the limbs.
2. Examine the strength and volume of active movements in the patient.
3. Formulate a conclusion about the presence or absence of paresis or paralysis.
II STAGE. Target. Identify the nature of paralysis.
For this it follows.
1. Examine the patient and analyze the examination data based on the criteria below.
|
/criteria/ |
Flaccid paralysis /criteria/ |
|
Muscular hypertension |
Atony |
|
Hyperreflexia |
Atrophy |
|
Pathological reflexes |
Areflexia |
2. Formulate a conclusion about the presence of flaccid or spastic paralysis.
III STAGE Purpose. Identify the level of damage to the motor pathway.
To do this, you should: use the results of an objective examination and use the following criteria:
|
Damage level |
Criteria |
|
Peripheral nerve. Complaints of muscle weakness in the area of nerve innervation, muscle loss in this area. |
Flaccid paralysis in the zone of innervation of the peripheral nerve. |
|
Anterior horns of the spinal cord at the cervical level. Complaints of weakness in the arms, weight loss. |
Flaccid paralysis of the arms, there may be fascicular twitching in the muscles. |
|
Anterior horns at the level of the lumbar enlargement. Complaints of weakness in the legs, weight loss. |
Flaccid paralysis of the legs, there may be fascicular twitching in the muscles. |
The most common mistake at this stage is incorrect differential diagnosis between damage to the anterior horns of the spinal cord and the peripheral nerve. Mistakes can be avoided by taking into account that if the peripheral nerve is damaged, there will be pain and sensory disturbances. Electromyography and nerve conduction velocity testing can provide significant assistance in diagnosis. Electromyography reveals lesions of the anterior horns, and a “picket fence” rhythm is detected. A decrease in nerve conduction velocity is found with peripheral nerve damage.
|
Level of the thoracic segments of the spinal cord. Complaints of weakness in the legs. |
Spastic paralysis of the leg on the affected side. Abdominal reflexes are absent on the side of the lesion, below the level of its location. |
|
Level of cervical thickening. Complaints of weakness in the arm and leg, weight loss in the arm. |
Flaccid paralysis of the arm and spastic paralysis of the leg on the affected side, abdominal reflexes are absent. |
|
Level of the upper cervical segments. |
Spastic paralysis of the arm and leg on the affected side, abdominal reflexes are absent. |
|
Level of the internal capsule. Complaints of weakness in the arm and leg. |
Spastic paralysis of the arm and leg on the side opposite to the lesion. Smoothness of the nasolabial fold, deviation of the tongue towards paralysis. |
|
Level of the anterior central gyrus. Complaints of weakness in the arm and leg. |
Spastic paralysis of leg or arm, motor jackson in leg or arm. |
2. Formulate a conclusion about the level of damage to the motor pathway.
At this stage, it is difficult to differentiate between lesions of the motor pathway at the level of the internal capsule and at the upper cervical level. Mistakes can be avoided if we take into account that when the lesion is not at the level of the internal capsule, damage to the cranial nerves joins the clinic of spastic paralysis of the arm and leg.
IV STAGE Purpose. Carry out differential diagnosis using an algorithm for the differential diagnosis of movement disorders and compare the results obtained with the conclusions II - III stages.
Formulate a final topical diagnosis with justification using the formula of the diagnosis protocol, which reflects the nature of paralysis /spastic, flaccid/, the level of damage to the motor pathway /peripheral nerve, anterior horns of the spinal cord at what level, internal capsule, anterior central gyrus/.
SIGNS OF INJURY IN DIFFERENT PARTS OF THE MAIN MOTOR PATH
Damage to various parts of the main motor pathway, consisting of central and peripheral neurons and providing the possibility of voluntary movements, has its own characteristics, the identification of which helps to clarify the topic of the pathological focus.
Damage to the motor cortex of the cerebral hemisphere. The motor zone of the cortex occupies the precentral (anterior central) gyrus, mainly fields 4 and 6, according to Brodmann, its continuation on the medial surface of the hemisphere - the paracentral lobe, as well as adjacent territories of the frontal lobe - the so-called precentral region (field 8) and a section of the parietal lobe (fields 5 and 7), as well as fields 23c and 24c of the cingulate cortex. In view of large sizes area of the motor cortex, its total destruction is rare. Usually it is partially damaged, which leads to the development of movement disorders in that part of the opposite half of the body that is projected onto the affected area of the cortex. Therefore, with the cortical localization of the pathological focus, the development of movement disorders in a limited part of the opposite half of the body is characteristic: they usually manifest themselves in the form of monoparesis or monoplegia. Since the opposite half of the body is projected upside down onto the motor cortex, dysfunction of, for example, the upper parts of the right precentral gyrus leads to movement disorders in the left leg, and damage to the lower parts of the left motor cortex leads to central paresis of the muscles of the right half of the face and language. If the pathological focus is located at the level of the central convolutions in the interhemispheric fissure, for example, a tumor growing from the large falx process (falx meningioma), the paracentral lobules of both hemispheres adjacent to the falx process may be affected, which leads to the development of central inferior paraparesis, usually in combination with violation of control over pelvic functions.
In cases of irritation of the motor zone of the cerebral cortex in the muscles of the corresponding part of the opposite half of the body m Convulsive paroxysms may occur, which is characteristic of focal epilepsy of the Jacksonian type. These convulsions are usually not accompanied by a disorder of consciousness, but they can spread to adjacent parts of the body, sometimes turning into a secondary generalized convulsive seizure, which, starting as a focal seizure, transforms into a grand mal seizure with a disturbance of consciousness. If the zone of the posterior central gyrus adjacent to the affected area of the anterior central gyrus is also involved in the pathological process, in part of the opposite half of the body - the muscles of which are in a state of paresis or paralysis, attacks of paresthesia are possible - sensitive Jacksonian seizures, often hypoesthesia, and to a greater extent proprioceptive sensitivity and complex types of sensitivity are impaired. With Jacksonian epilepsy, during a seizure, a combination of local convulsions and paresthesia in a certain part of the body on the side opposite the pathological focus is possible.
Damage to the additional motor area in the superior parietal lobule (areas 5 and 7, according to Brodmann) can cause so-called parietal paresis in a limited area of the opposite half of the body, which is usually not accompanied by a significant increase in muscle tone.
Defeat of the radiant crown. The corona radiata is the subcortical white matter of the brain, consisting of axons of nerve cells carrying impulses in the afferent and efferent directions. When the pathological focus is localized in the corona radiata on the opposite side, central hemiparesis usually occurs, sometimes in combination with hemihypesthesia. Functional disorders in various areas the opposite half of the body are expressed to varying degrees, which depends on which part of the corona radiata is involved in the pathological process.
Damage to the internal capsule. In the internal capsule, the nerve fibers are located compactly, so there is a small pathological focus in the area of the knee and two anterior thirds front thigh internal capsule can cause the development of central hemiplegia or central hemiparesis on the opposite side. With a more extensive pathological process extending to the entire posterior thigh of the internal capsule, hemiplegia or hemiparesis can be combined with hemianesthesia and hemianopsia occurring on the same side (loss of homonymous halves of the visual fields), i.e. The so-called syndrome of three “hemi” develops. Acutely occurring damage to the internal capsule often develops with hemorrhagic stroke, manifested by a medial intracerebral hematoma.
With central hemiparesis on the arm, the muscles that abduct the shoulder, extensors and supinators of the forearm, extensors of the hand and fingers are usually more affected, and on the leg - the hip flexors, extensors of the foot and fingers, which leads to the development of a peculiar posture in patients during the recovery phase, known as the Wernicke-Mann position (Fig. 4.16). Due to the fact that the tone of the flexor muscles predominates in the arm, and the extensor muscles in the leg, the arm in a state of paresis is brought to the body and bent at the elbow joint, its hand is pronated, and the paretic leg is straightened and seems slightly longer than the healthy leg . The gait of patients with central hemiparesis turns out to be peculiar. When walking, the straightened paretic leg of the patient moves in an arc, the arm on the side of the hemiparesis remains bent and pressed to the body. In such cases, they sometimes say that the patient “asks with his hand and mows with his foot.”
Brain stem damage. With unilateral damage to various parts of the brain stem (midbrain, pons, medulla oblongata), alternating (cross) syndromes are characterized, in which signs of damage to individual cranial nerves appear on the side of the pathological focus, and on the opposite side - hemiparesis or hemiplegia of the central type , sometimes - hemihypesthesia. The variant of the alternating syndrome in such cases is determined by the level and extent of damage to the trunk. With bilateral damage to the brainstem, the functions of the cranial nerves can be impaired on both sides, and pseudobulbar or bulbar syndromes, tetraparesis, and conduction-type sensitivity disorders are characteristic.
Transverse lesion of half of the spinal cord - Brown-Sequart syndrome. When half the diameter of the spinal cord is affected, the lateral pyramidal tract is involved in the pathological process below the level of its decussation. In this regard, central paresis or paralysis, occurring below the level of the spinal cord lesion, develops on the side of the pathological focus. Movement disorders in this case are usually combined with sensory disturbances of the conduction type. In such cases, proprioceptive sensitivity is impaired on the side of the pathological process, and superficial sensitivity (pain and temperature) is impaired on the opposite side.
Complete transverse lesion of the spinal cord in the upper cervical region (C1-C4). With bilateral damage to the spinal cord in the upper cervical region, central tetraplegia occurs, while combined damage on both sides of the crossed and uncrossed pyramidal tracts leads to the fact that the muscles of the trunk, including the respiratory muscles, also suffer. In addition, in such cases, below the level of the pathological focus, disturbances of all types of conduction-type sensitivity, as well as pelvic and trophic disorders, usually occur.
Damage to the cervical enlargement of the spinal cord (C5-Th2). Damage to the cervical enlargement of the spinal cord also leads to the development of tetraplegia in combination with disturbances of all types of conduction-type sensitivity below the level of the pathological focus with pelvic and trophic disorders. However, due to damage to the cervical thickening of the spinal cord, paralysis or paresis of the arms develops according to the peripheral type, while paralysis of the trunk and legs develops according to the central type.
Damage to the thoracic spinal cord (Th3-Th12). The consequence of a transverse lesion of the thoracic spinal cord is spastic lower paraplegia in combination with the loss of all types of sensitivity below the level of localization of the pathological focus, impaired pelvic functions and a disorder of tissue trophism.
Lesion of the lumbar enlargement of the spinal cord (L2-S2). When the lumbar enlargement of the spinal cord is damaged, lower paraplegia develops peripheral type in combination with impaired sensitivity and trophism of tissues in the legs and anogenital area, as well as pelvic disorders, usually in the form of urinary and fecal incontinence.
Selective damage to the cells of the anterior horns of the spinal cord and the motor nuclei of the cranial nerves. Due to selective damage to the bodies of peripheral motor neurons, peripheral paralysis of the mouse occurs, the innervation of which they provide, while irritation of individual still preserved peripheral motor neurons can cause spontaneous contraction of muscle fibers or their bundles (fibrillar or fascicular twitching).
Selective damage to peripheral motor neurons is characteristic of epidemic childhood polio and amyotrophic lateral sclerosis, as well as spinal amyotrophies.
Damage to the anterior roots of the spinal cord. When the anterior roots of the spinal cord are affected, peripheral paralysis of the muscles that are part of the myotomes of the same name as the affected roots is characteristic.
Damage to the spinal nerves. The consequence of damage to the spinal nerves is peripheral motor disorders in the muscles innervated by the axons of the motor neurons that make up these nerves, as well as sensitivity disorders (pain, hypalgesia, anesthesia) in the dermatomes of the same name. There are also possible vegetative, in particular trophic, disorders,
Nerve plexus lesions. Damage to the nerve plexus causes the development of motor disorders (paralysis or paresis) of a peripheral type, usually in combination with disturbances of sensitivity and trophism in the area of innervation of peripheral nerves originating from the affected plexus, or part thereof.
Peripheral nerve damage. When a peripheral nerve is damaged, peripheral paralysis or paresis of the muscles innervated by it occurs, usually in combination with a disorder of all types of sensitivity and trophic disorders in the area of innervation of the affected nerve
Symptoms of spinal cord damage at different levels
Cervical region. Damage to the upper cervical spinal cord is life-threatening: with tetraplegia, breathing stops completely, and with paralysis of the diaphragm (innervated by the phrenic nerve, segments C3-C5), breathing can only be carried out by the intercostal and auxiliary respiratory muscles. Widespread damage at the border of the medulla oblongata and spinal cord is usually incompatible with life due to the destruction of the cardiovascular center and respiratory center. Partial damage to this area, usually due to trauma, may be accompanied by interruption of the decussating corticospinal tracts, causing paresis of the legs (the corticospinal tracts innervating the arms decussate above). Compression of the brain at the foramen magnum can cause the paresis to gradually spread from the ipsilateral arm to the ipsilateral leg, then the contralateral leg, and finally the contralateral arm. Sometimes there is pain in the suboccipital region, radiating to the neck and shoulder girdle. Damage to the C4-C5 segments is accompanied by tetraplegia without respiratory impairment. If the C5-C6 segments are damaged, the strength of the muscles of the shoulder girdle remains relatively intact, the biceps reflex and the radial reflex disappear. When the C7 segment is damaged, the strength of the biceps brachii muscle does not decrease, weakness of the extensors of the fingers and wrist develops, and the triceps reflex disappears. Destruction of the C8 segment is accompanied by weakness of the finger and wrist flexors, as well as the disappearance of the metacarpal-carpal reflex. In general, the level of cervical spine involvement is easier to determine based on motor rather than sensory impairment. If the cervical spine is damaged, Horner's syndrome (miosis, ptosis and facial anhidrosis) on the ipsilateral side is possible.
It is useful to know that at the level of the nipples there is a Th4 dermatome, and at the level of the navel - Th10. Damage to the thoracic spine is accompanied by weakness in the legs, dysfunction of the pelvic organs and impaired sexual function. The muscles of the abdominal wall are innervated by the lower thoracic segments. The strength of these muscles is assessed by their participation in breathing, coughing, or by asking the patient to sit from a lying position with his hands behind his head. Damage to the Th9-Th100 segments leads to paresis of the muscles of the lower abdominal wall. Due to the fact that the muscles of the upper abdominal wall in this case remain intact, when the abdominal press is tense, the navel moves upward (Beevor's symptom). The lower abdominal reflex disappears. With a unilateral lesion, tension in the abdominal wall muscles is accompanied by a displacement of the navel to the healthy side; Abdominal reflexes disappear on the affected side. Damage to the thoracic segments is also characterized by pain in the middle of the back.
Lumbar region. The size of the lumbar and sacral segments gradually decreases in the caudal direction, so it is more difficult to determine the exact location of the lesion in these sections than in the cervical or thoracic. Damage at the level of segments L2-L4 is accompanied by paresis of the muscles that adduct and flex the hip, and paresis of the muscles that extend the leg at the knee joint. The knee reflex disappears. Damage to the L5-S1 segments leads to paresis of the foot, as well as paresis of the muscles that flex the leg at the knee joint and paresis of the muscles that extend the hip. The Achilles reflex (S1) disappears. Among the superficial reflexes that help to establish the localization of damage to the lumbar spinal cord, the cremasteric reflex is distinguished. It closes at the level of segments L1-L2.
Sacral region and conus medullaris. The conus medullaris is the terminal section of the spinal cord. It consists of the lower sacral and a single coccygeal segment. There are no disorders of movements and reflexes in the legs with isolated damage to the conus medullaris. Damage to the conus medullaris is manifested by saddle anesthesia (S3-S5), severe dysfunction of the pelvic organs (urinary retention or incontinence, decreased tone of the external anal sphincter) and impaired sexual function. The bulbocavernous reflex (S2-S4) and the anal reflex (S4-S5) disappear. Damage to the conus medullaris must be distinguished from damage to the cauda equina, a bundle of spinal roots starting from the lower segments of the spinal cord and heading to the intervertebral foramina. Cauda equina lesions are characterized by severe pain in the lower back or in the area of innervation of the roots, asymmetric paresis of the legs or sensory disturbances in the legs, disappearance of tendon reflexes in the legs and minimal dysfunction of the pelvic organs. Space-occupying lesions in the lower part of the spinal canal can destroy both the cauda equina and the conus medullaris, causing mixed disorders.
Alternating syndromes
Alternating syndromes (cross syndromes) - dysfunction of the cranial nerves on the side of the lesion in combination with central paralysis of the limbs or sensory conduction disorder on the opposite side of the body. Alternating syndromes occur when the brain is damaged (with vascular pathology, tumors, inflammatory processes).
Depending on the location of the lesion, the following types of alternating syndromes are possible. Paralysis of the oculomotor nerve on the side of the lesion and hemiplegia on the opposite side with damage to the cerebral peduncle (Weber syndrome). Paralysis of the oculomotor nerve on the affected side, hyperkinesis and cerebellar symptoms on the opposite side when the base of the cerebral peduncle is affected (Claude's syndrome). Paralysis of the oculomotor nerve on the side of the lesion, intention tremor and choreoathetoid movements in the limbs of the opposite side with damage to the medial dorsal part of the midbrain.
Peripheral paralysis of the facial nerve on the side of the lesion and spastic hemiplegia or hemiparesis on the opposite side (Millar-Gubler syndrome) or peripheral paralysis of the facial and abducens nerves on the side of the lesion and hemiplegia on the opposite side (Fauville syndrome); both syndromes - with damage to the pons (varoliev). Damage to the glossopharyngeal and vagus nerves, causing paralysis of the soft palate, vocal cords, swallowing disorder, etc. on the affected side and hemiplegia on the opposite side with damage to the lateral medulla oblongata (Avellis syndrome). Peripheral paralysis of the hypoglossal nerve on the side of the lesion and hemiplegia on the opposite side with damage to the medulla oblongata (Jackson syndrome). Blindness on the affected side and hemiplegia on the opposite side due to blockage of the internal carotid artery by an embolus or thrombus (optic-hemiplegic syndrome); absence of pulse in the radial and brachial arteries on the left and hemiplegia or hemianesthesia on the right with damage to the aortic arch (aortic-subclavian-carotid Bogolepov syndrome).
Treatment of the underlying disease and symptoms of brain damage: breathing problems, swallowing problems, heart problems. During the recovery period, prozerin, vitamins, exercise therapy, massage and other activating methods are used.
Alternating syndromes (Latin alternare - take turns, alternate) are symptom complexes characterized by dysfunction of the cranial nerves on the side of the lesion and central paralysis or paresis of the limbs or sensory conduction disorders on the opposite side.
Alternating syndromes occur when the brain stem is damaged: the medulla oblongata, pons or cerebral peduncle, as well as when the cerebral hemispheres are damaged as a result of circulatory disorders in the carotid artery system. More precisely, the localization of the process in the trunk is determined by the presence of damage to the cranial nerves: paresis or paralysis occurs on the side of the lesion as a result of damage to the nuclei and roots, i.e., of the peripheral type, and is accompanied by muscle atrophy, a degeneration reaction when studying electrical excitability. Hemiplegia or hemiparesis develops due to damage to the corticospinal (pyramidal) tract adjacent to the affected cranial nerves. Hemianesthesia of the limbs opposite to the lesion is a consequence of damage to sensory conductors running through the middle lemniscus and the spinothalamic tract. Hemiplegia or hemiparesis appears on the side opposite the lesion because the pyramidal tract, as well as sensory conductors, intersect below the lesions in the trunk.
Alternating syndromes are divided according to the localization of the lesion in the brain stem into: a) bulbar (with damage to the medulla oblongata), b) pontine (with damage to the pons), c) peduncular (with damage to the cerebral peduncle), d) extracerebral.
Bulbar alternating syndromes . Jackson syndrome is characterized by peripheral hypoglossal palsy on the affected side and hemiplegia or hemiparesis on the opposite side. Occurs due to thrombosis a. spinalis ant. or its branches. Avellis syndrome is characterized by damage to the IX and X nerves, paralysis of the soft palate and vocal cord on the side of the lesion and hemiplegia on the opposite side. Swallowing disorders (liquid food getting into the nose, choking when eating), dysarthria and dysphonia appear. The syndrome occurs when branches of the artery of the lateral fossa of the medulla oblongata are damaged.
Babinski-Nageotte syndrome consists of cerebellar symptoms in the form of hemiataxia, hemiasynergia, lateropulsion (as a result of damage to the inferior cerebellar peduncle, olivocerebellar fibers), miosis or Horner's syndrome on the side of the lesion and hemiplegia and hemianesthesia on the opposite limbs. The syndrome occurs when the vertebral artery is damaged (artery of the lateral fossa, inferior posterior cerebellar artery).
Schmidt syndrome consists of paralysis of the vocal cords, soft palate, trapezius and thoracocleidomastoid muscles on the affected side (IX, X and XI nerves), as well as hemiparesis of the opposite limbs.
Zakharchenko-Wallenberg syndrome is characterized by paralysis of the soft palate and vocal cord (lesion vagus nerve), anesthesia of the pharynx and larynx, sensitivity disorder on the face (damage to the trigeminal nerve), Horner's syndrome, hemiataxia on the side of the lesion with damage to the cerebellar tract, respiratory disorder (with an extensive lesion in the medulla oblongata) in combination with hemiplegia, analgesia and thermaneesthesia on the opposite side . The syndrome occurs due to thrombosis of the posterior inferior cerebellar artery.
Pontine alternating syndromes . Millar-Gübler syndrome consists of peripheral facial palsy on the affected side and spastic hemiplegia on the opposite side. Foville syndrome is expressed by paralysis of the facial and abducens nerves (in combination with gaze paralysis) on the side of the lesion and hemiplegia, and sometimes hemianesthesia (damage to the middle loop) of the opposite limbs. The syndrome sometimes develops as a result of thrombosis of the main artery. Raymond-Sestan syndrome manifests itself in the form of paralysis of combined movements of the eyeballs on the affected side, ataxia and choreoathetoid movements, hemianesthesia and hemiparesis on the opposite side.
Peduncular alternating syndromes . Weber syndrome is characterized by paralysis of the oculomotor nerve on the side of the lesion and hemiplegia with paresis of the muscles of the face and tongue (lesion of the corticonuclear pathway) on the opposite side. The syndrome develops during processes at the base of the cerebral peduncle. Benedict's syndrome consists of paralysis of the oculomotor nerve on the affected side and choreoathetosis and tremors of the opposite limbs (damage to the red nucleus and dentatorubral tract). The syndrome occurs when the lesion is localized in the medial-dorsal part of the midbrain (the pyramidal tract remains unaffected). Nothnagel syndrome includes a triad of symptoms: cerebellar ataxia, oculomotor nerve palsy, hearing impairment (unilateral or bilateral deafness of central origin). Sometimes hyperkinesis (choreiform or athetoid), paresis or paralysis of the limbs, and central palsy of the VII and XII nerves may be observed. The syndrome is caused by damage to the tegmentum of the midbrain.
Alternating syndromes characteristic of the intrastem process can also occur with compression of the brain stem. Thus, Weber syndrome develops not only due to pathological processes (hemorrhage, intrastem tumor) in the midbrain, but also due to compression of the cerebral peduncle. Compression, dislocation syndrome of compression of the cerebral peduncle, which occurs in the presence of a tumor of the temporal lobe or pituitary region, can manifest itself as damage to the oculomotor nerve (mydriasis, ptosis, strabismus, etc.) on the side of the compression and hemiplegia on the opposite side.
Sometimes alternating syndromes are manifested mainly by cross-sensitivity disorder. Thus, with thrombosis of the inferior posterior cerebellar artery and the artery of the lateral fossa, alternating sensory Raymond syndrome can develop, manifested by facial anesthesia (damage to the descending root of the trigeminal nerve and its nucleus) on the side of the lesion and hemianesthesia on the opposite side (damage to the middle lemniscus and spinothalamic tract). Alternating syndromes can also manifest themselves in the form of cross hemiplegia, which is characterized by paralysis of the arm on one side and the leg on the opposite side. Such alternating syndromes occur with a focus in the area of the intersection of the pyramidal tracts, with thrombosis of the spinobulbar arterioles.
Extracerebral alternating syndromes . Optical-hemiplegic syndrome (alternating hemiplegia in combination with impaired function of the optic nerve) occurs when an embolus or thrombus obstructs the intracranial segment of the internal carotid artery, is it characterized by blindness as a result of obstruction of the ophthalmic artery? arising from the internal carotid artery, and hemiplegia or hemiparesis of the limbs opposite to the lesion due to softening of the medulla in the area of vascularization of the middle cerebral artery. Vertigohemiplegic syndrome with discirculation in the subclavian artery system (N.K. Bogolepov) is characterized by dizziness and noise in the ear as a result of discirculation in the auditory artery on the side of the lesion, and on the opposite side - hemiparesis or hemiplegia due to circulatory disorders in the branches of the carotid artery. Asphygmohemiplegic syndrome (N.K. Bogolepov) occurs reflexively with pathology of the extracerebral part of the carotid artery (brachiocephalic trunk syndrome). At the same time, on the side of occlusion of the brachiocephalic trunk and the subclavian and carotid arteries, there is no pulse in the carotid and radial arteries, reduced arterial pressure and spasm of the facial muscles is observed, and on the opposite side - hemiplegia or hemiparesis.
Studying the symptoms of damage to the cranial nerves in alternating syndromes allows us to determine the localization and border of the lesion, i.e., establish a topical diagnosis. Studying the dynamics of symptoms allows us to determine the nature of the pathological process. Thus, with ischemic softening of the brain stem as a result of thrombosis of the branches of the vertebral arteries, the main or posterior cerebral artery, the alternating syndrome develops gradually, not accompanied by loss of consciousness, and the boundaries of the lesion correspond to the zone of impaired vascularization. Hemiplegia or hemiparesis can be spastic. With hemorrhage into the trunk, the alternating syndrome may be atypical, since the boundaries of the lesion do not correspond to the zone of vascularization and increase due to edema and reactive phenomena in the circumference of the hemorrhage. With acutely occurring lesions in the pons, the alternating syndrome is usually combined with respiratory distress, vomiting, disturbances of the heart and vascular tone, hemiplegia - with muscle hypotension as a result of diaschisis.
Isolation of A. s. helps the clinician in making a differential diagnosis, for which the complex of all symptoms is important. In cases of A. caused by damage to the great vessels, it is indicated surgery(thrombinthymectomy, vascular plastic surgery, etc.).
Thinking as an independent form cognitive activity is formed gradually and is one of the most recent psychological formations.
Experience in researching intellectual impairments from the technical point of view. theory of systemic dynamic localization of HMF showed that neuropsychological symptoms of thinking disorders have the same local significance as symptoms of other disorders cognitive processes. Luria, describing neuropsychological syndromes of damage to different parts of the left hemisphere of the brain (in right-handed people) - temporal, parieto-occipital, premotor and prefrontal - identifies several types of disorders of intellectual processes.
In case of defeat left temporal region against the background of sensory or acoustic-mnestic aphasia, intellectual processes do not remain intact. Despite the violation of the sound image of words, their semantic (meaning) sphere remains relatively intact. Verbal paraphasias in the speech of a patient with sensory aphasia arise according to the laws of categorical thinking. But they grossly violate those semantic operations that require constant indirect participation of speech connections or if you need to retain speech material in memory. Partial compensation of these disorders is possible only by relying on visual visual stimuli.
In case of defeat parieto-occipital regions of the brain : difficulties of spatial analysis and synthesis. There is a loss (or weakening) of the optical-spatial factor (visual signs and their spatial relationships are poorly visible). With the intention to complete the task intact, they can amount to overall plan upcoming activity, but are not able to complete the task itself. Characteristic acalculia, difficulties in understanding certain logical-grammatical constructions reflecting spatial and “quasi-spatial” relations.
Defeat premotor parts of the left. half-me GM: premotor syndrome - difficulties in the temporary organization of all mental processes, including intellectual ones. Not only the disintegration of “kinetic patterns” of movements and difficulties in switching from one motor act to another are observed, but also disturbances in the dynamics of the thought process. The curtailed, automated nature of intellectual operations (“mental actions”) is disrupted. These violations are included in dynamic aphasia syndrome(the slowness of the process of understanding stories, fables, and arithmetic problems appears in patients already when listening to them). Consequence - violation of the dynamics of verbal-logical thinking(stereotypical responses when switching to a new operation).
Defeat frontal prefrontal regions of the brain: The disorders are very diverse: from gross defects to almost asymptomatic cases. This inconsistency is explained by the variety of “frontal” syndromes and the insufficient adequacy of the implementation techniques. Happening collapse of the structure of mental activity. The 1st stage of intellectual activity - the formation of an “indicative basis for action” - is either completely absent from them or sharply reduced when performing both non-verbal and verbal-logical tasks. Difficulties also arise when analyzing a complex literary text that requires active orientation and reflection (texts are misunderstood). Violation of selectivity logical operations with side connections (tasks on classifying objects): the logical principle is replaced by a situational one.
Damage to various parts of the main motor pathway, consisting of central and peripheral neurons and providing the possibility of voluntary movements, has its own characteristics, the identification of which helps to clarify the topic of the pathological focus. . Damage to the motor cortex of the cerebral hemisphere. The motor zone of the cortex occupies the precentral (anterior central) gyrus, mainly fields 4 and 6, according to Brodmann, its continuation on the medial surface of the hemisphere - the paracentral lobe, as well as the adjacent territories of the frontal lobe - the so-called precentral region (field 8) and a section of the parietal lobe (fields 5 and 7), as well as fields 23c and 24c of the cingulate cortex. Due to the large area of the motor cortex, its total destruction is rare. Usually it is partially damaged, which leads to the development of motor disorders in that part of the opposite half of the body that is projected onto the affected area of the cortex. Therefore, with the cortical localization of the pathological focus, the development of movement disorders in a limited part of the opposite half of the body is typical: they usually manifest themselves in the form of monoparesis or monoplegia. Since the opposite half of the body is projected upside down onto the motor cortex, dysfunction of, for example, the upper parts of the right precentral gyrus leads to movement disorders in the left leg, and damage to the lower parts of the left motor cortex leads to central paresis of the muscles of the right half of the face and language. If the pathological focus is located at the level of the central gyri in the interhemispheric fissure, for example, a tumor growing from the large falx process (falx meningioma), the paracentral lobes of both hemispheres adjacent to the falx process may be affected, which leads to the development of central inferior paraparesis, usually in combination with impaired control of pelvic functions. In cases of irritation of the motor zone of the cerebral hemisphere cortex, convulsive paroxysms may occur in the muscles of the corresponding part of the opposite half of the body, which is characteristic of focal epilepsy of the Jacksonian type. These convulsions are usually not accompanied by a disorder of consciousness, but they can spread to adjacent parts of the body, sometimes turning into a secondary generalized convulsive seizure, which, starting as a focal seizure, transforms into a grand mal seizure with a disturbance of consciousness. If the zone of the posterior central gyrus adjacent to the affected area of the anterior central gyrus is also involved in the pathological process, in part of the opposite half of the body - the muscles of which are in a state of paresis or paralysis, attacks of paresthesia are possible - sensitive Jacksonian seizures, often - hypoesthesia, with this disrupts proprioceptive sensitivity and complex types of sensitivity to a greater extent. With Jacksonian epilepsy, during a seizure, a combination of local convulsions and paresthesia in a certain part of the body on the side opposite to the pathological focus is possible. Damage to the additional motor area in the superior parietal lobule (areas 5 and 7, according to Brodmann) can cause the so-called parietal paresis in a limited area of the opposite half of the body, which is usually not accompanied by a significant increase in muscle tone. . Defeat of the radiant crown. The corona radiata is the subcortical white matter of the brain, consisting of axons of nerve cells carrying impulses in the afferent and efferent directions. When the pathological focus is localized in the corona radiata on the opposite side, central hemiparesis usually occurs, sometimes in combination with hemihypesthesia. Functional dysfunctions in different parts of the opposite half of the body are expressed to varying degrees, which depends on which part of the corona radiata is involved in the pathological process. . Damage to the internal capsule. In the internal capsule, nerve fibers are located compactly, so a small pathological focus in the area of the knee and two anterior thirds of the anterior thigh of the internal capsule can cause the development of central hemiplegia or central hemiparesis on the opposite side. With a more extensive pathological process extending to the entire posterior thigh of the internal capsule, hemiplegia or hemiparesis can be combined with hemianesthesia and hemianopsia occurring on the same side (loss of homonymous halves of the visual fields), i.e. The so-called syndrome of three “hemi” develops. Acutely occurring damage to the internal capsule often develops with hemorrhagic stroke, manifested by a medial intracerebral hematoma. With central hemiparesis on the arm, the muscles that abduct the shoulder, extensors and supinators of the forearm, extensors of the hand and fingers are usually more affected, and on the leg - the hip flexors, extensors of the foot and fingers, which leads to the development in patients during the recovery phase of a peculiar pose known as the Wernicke-Mann position (Fig. 4.16). Due to the fact that the tone of the flexor muscles predominates in the arm, and the extensor muscles in the leg, the arm in a state of paresis is brought to the body and bent at the elbow joint, its hand is pronated, and the paretic leg is straightened and seems slightly longer healthy leg. The gait of patients with central hemiparesis turns out to be peculiar. When walking, the straightened paretic leg of the patient moves in an arc, the arm on the side of the hemiparesis remains bent and pressed to the body. In such cases, they sometimes say that the patient “asks with his hand and mows with his foot.” . Brain stem damage. With unilateral damage to various parts of the brain stem (midbrain, pons, medulla oblongata), the development of alternating (crossed) syndromes is characteristic, in which signs of damage to individual cranial nerves appear on the side of the pathological focus, and hemiparesis or hemiparesis occurs on the opposite side. miplegia of the central type, sometimes hemihypesthesia. The variant of the alternating syndrome in such cases is determined by the level and prevalence of damage to the trunk. With bilateral damage to the brainstem, the functions of the cranial nerves can be impaired on both sides, and pseudobulbar or bulbar syndromes, tetraparesis, and conduction-type sensitivity disorders are characteristic. . Transverse lesion of half of the spinal cord - Brown-Secard syndrome. When half the diameter of the spinal cord is affected, the lateral pyramidal tract is involved in the pathological process below the level of its decussation. In this regard, central paresis or paralysis, occurring below the level of spinal cord damage, develops on the side of the pathological focus. In this case, movement disorders are usually combined with sensory disturbances of the conduction type. In such cases, proprioceptive sensitivity is impaired on the side of the pathological process, and superficial sensitivity (pain and temperature) is impaired on the opposite side. . Complete transverse lesion of the spinal cord in the upper cervical region (C1-C4). With bilateral damage to the spinal cord in the upper cervical region, central tetraplegia occurs, while combined damage on both sides of the crossed and uncrossed pyramidal tracts leads to the fact that the muscles of the trunk, including the respiratory muscles, also suffer. In addition, in such cases, below the level of the pathological focus, disturbances of all types of sensitivity of the conduction type, as well as pelvic and trophic disorders, usually occur. . Damage to the cervical enlargement of the spinal cord (C5—Th2). Damage to the cervical enlargement of the spinal cord also leads to the development of tetraplegia in combination with disturbances of all types of conduction-type sensitivity below the level of the pathological focus with pelvic and trophic disorders. However, due to damage to the cervical enlargement of the spinal cord, paralysis or paresis of the arms develops according to the peripheral type, while paralysis of the trunk and legs develops according to the central type. . Damage to the thoracic spinal cord (Th3—Th12). The consequence of a transverse lesion of the thoracic spinal cord is spastic lower paraplegia in combination with the loss of all types of sensitivity below the level of localization of the pathological focus, impaired pelvic functions and a disorder of tissue trophism. . Damage to the lumbar enlargement of the spinal cord (L2-S2). When the lumbar enlargement of the spinal cord is affected, lower paraplegia of the peripheral type develops in combination with impaired sensitivity and trophism of tissues in the legs and in the anogenital zone, as well as pelvic disorders, usually in the form of urinary and fecal incontinence. 106. PART I. Propaedeutics of diseases of the nervous system. Selective damage to the cells of the anterior horns of the spinal cord and motor nuclei of the cranial nerves. Due to selective damage to the bodies of peripheral motor neurons, peripheral paralysis of the mouse occurs, the innervation of which they provide, while irritation of individual still preserved peripheral motor neurons can cause spontaneous contraction of muscle fibers or their bundles (fibrillar or fascicular twitching). Selective damage to peripheral motor neurons is characteristic of epidemic childhood polio and amyotrophic lateral sclerosis, as well as spinal amyotrophies. . Damage to the anterior roots of the spinal cord. When the anterior roots of the spinal cord are affected, peripheral paralysis of the muscles that are part of the myotomes of the same name as the affected roots is characteristic. . Damage to the spinal nerves. The consequence of damage to the spinal nerves is motor disorders of the peripheral type in the muscles innervated by the axons of the motor neurons that are part of these nerves, as well as sensitivity disorders (pain, hypalgesia, anesthesia) in the dermatomes of the same name. Vegetative, in particular trophic, disorders are also possible there. Nerve plexus lesions. Damage to the nerve plexus causes the development of motor disorders (paralysis or paresis) of a peripheral type, usually in combination with disturbances of sensitivity and trophism in the innervation zone of peripheral nerves originating from the affected plexus, or part thereof. . Peripheral nerve damage. When a peripheral nerve is damaged, peripheral paralysis or paresis of the muscles innervated by it occurs, usually in combination with a disorder of all types of sensitivity and trophic disorders in the area of innervation of the affected nerve (see. chapter 8).
The spinal cord is an integral part of the central nervous system. It is located in the spinal canal formed by the foramina of the vertebrae. It starts from the foramen magnum at the level of the articulation of the first cervical vertebra with the occipital bone. It ends at the border of the first and second lumbar vertebrae. There are two thickenings: cervical, responsible for controlling the upper limbs, lumbosacral, controlling the lower limbs.
There are 8 cervical or cervical, 12 thoracic or thoracic, 5 lumbar or lumbar, 5 sacral or sacral, 1–3 coccygeal segments. The spinal cord itself contains white matter (the pathways for impulses) and gray matter (the neurons themselves). The gray matter contains several groups of neurons, called horns because of their external similarity, responsible for certain functions: the anterior horns contain motor neurons that control muscle movements, the posterior ones are responsible for all types of sensitivity coming from the body and the lateral ones (only in thoracic region), giving commands to all internal organs.
Depending on the type of spinal cord lesion and the affected area, the signs of the disease may differ and have an extremely different clinical picture. It is customary to distinguish symptoms depending on the level of brain damage, its localization and the structures (white and gray matter) that it damaged. Moreover, if the damage does not cross the entire diameter, then sensitivity will disappear on the opposite side, and motor function on the affected side.
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By damaged groups of neurons
Damage to the motor neurons of the anterior horns leads to loss of motor function in the muscle groups controlled by these segments. Disturbances in the area of the posterior groups of neurons cause loss of sensitivity in the areas of the skin corresponding to these segments. Damage to the lateral horns causes dysfunction gastrointestinal tract, internal organs.
If the pathological process has affected the white matter, then the paths through which impulses pass between the higher and lower structures of the central nervous system are interrupted. Following this, a stable disturbance of the innervation of the underlying parts of the human body develops.
Symptoms of spinal cord damage at different levels
Contrary to popular belief, spinal cord injury is not always fatal. Fatalities occur only in the case of a complete or half rupture of the diameter in the first five cervical segments– this is due to the location of the respiratory and cardiovascular centers in them. All complete ruptures are characterized by a total loss of sensitivity and motor activity below the site of injury. Injuries to the coccygeal and last sacral segments will cause loss of control over the pelvic organs: involuntary urination, defecation.
Injuries
Trauma accounts for about 80–90% of all spinal cord diseases. They arise in living conditions, sports, in case of an accident, at work. As a result of exposure to a traumatic factor, compression, displacement or various fractures vertebrae When lifting excessive weights, it is possible to form a herniated disc - protrusion of cartilage into the spinal canal with subsequent compression of both the structures of the central nervous system and the nerve roots.
Depending on the severity of the injury, damage to the spinal column is formed to varying degrees. With minor traumatic impacts, a concussion of the nervous tissue is observed, which leads to motor and sensory disorders and resolves within 2–4 weeks. More serious injuries cause complete or partial rupture of the diameter of the spinal cord with the corresponding symptom complex.
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Displacement of the vertebrae is characterized by the development of a long-term, weakly progressive disorder of all types of sensitivity and movement. Symptoms may worsen with certain body positions or with prolonged sedentary work.
Hernias and infections
Often, the resulting hernia compresses the dorsal roots of the spinal nerves, which leads to severe girdling pain without impairing movement. The pain intensifies when bending over, lifting heavy objects, or resting on an uncomfortable surface. With the development of inflammation of the membranes of the SM, symptoms spread to several, sometimes all, segments are observed. The clinical picture may be similar to radiculitis, but the symptoms extend over more than 2-3 segments. There is an increase in body temperature to 39–40 degrees, often accompanied by manifestations of cerebral meningitis, and the patient may experience delirium and loss of consciousness.
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The viral disease poliomyelitis exclusively affects the anterior horns containing motor neurons - this leads to the inability to control skeletal muscles. And although after 4–6 months some restoration of innervation is possible due to preserved neurons, patients lose the ability to full movements for the rest of their lives.
Spinal strokes
A fairly rare disease associated with circulatory disorders. Each segment has its own artery. When it is blocked, the neurons of the corresponding area die. The clinical picture of spinal strokes may be similar to a rupture of half the diameter of the spinal cord, but they are not preceded by trauma. The development of pathology in most cases occurs in older people with atherosclerotic lesion vessels, hypertension, a history of heart attacks and strokes is possible.
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