Osteochondrosis

Ultrasound diagnosis of femoral and sciatic neuropathy in neurological practice

Etiology: infection or intoxication, diseases of the pelvic organs, fracture of the spine and pelvic bones.

Clinic: characterized by pain in the buttocks, the back of the thigh, the lateral surface of the leg and back of the foot, pain of the sciatic nerve on palpation (midway between the greater trochanter and sciatic bulge) and tension, Lesag's symptom, decrease or absence of the Achilles reflex, flabbiness of the gluteus and triceps of the lower leg , disorders of sensitivity in the lateral region of the leg and on the back of the foot, lumbar scoliosis, with severe damage to the sciatic nerve - pronounced paresis and paralysis of the muscles of the leg, are affected by either unbig whether the feet and fingers (patients cannot stand on their heels, the foot hangs down - “horse” foot) or flexors of the foot and fingers (bending of the foot and fingers is impossible, standing on the toes - “heel” foot), in some muscles of the lower legs are affected (patients they cannot stand on their toes or on their heels - a “dangling” foot; the muscles of the lower leg and trophic disorders (hypertrichosis, skin atrophy or hyperkeratosis, trophic ulcers on the plantar surface of the first finger and heel) atrophy.

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Peripheral nerve damage and tunneling neuropathy are among the most common types of pathology of the nervous system. The incidence of soft tissue injuries with involvement of peripheral nerves, according to different authors, is 25-65% among all injuries, and the incidence of tunnel neuropathies - 30-40% of all diseases of the peripheral nervous system [1, 2]. The choice of the most rational methods for diagnosing lesions and diseases of the peripheral nerves of the limbs is currently a difficult problem. Existing methods of instrumental diagnostics either do not produce a nerve trunk image (electromyography), or are laborious, requiring complex expensive equipment (magnetic resonance imaging - MPT). According to a number of foreign authors [3, 4], ultrasound scanning can be quite successfully used in the diagnosis of injuries and diseases of the peripheral nerves.

Electrophysiological methods, such as electromyography and neuromyography, are traditionally recognized as the "gold standard" for identifying the pathology of the peripheral nervous system. However, it should be noted that the information obtained in the course of the above examinations does not give an idea of ​​the state of the surrounding tissues, does not indicate the nature and cause of damage to the nerve trunk, and does not always accurately reflect the localization of changes. At the same time, it is this information that helps determine the tactics of conservative or surgical treatment. Ultrasound examination (ultrasound) of the peripheral nervous system was first used to diagnose diseases of the nerve trunks in the late 90s of the last century, and thanks to indisputable advantages compared with other diagnostic methods, has developed rapidly.

However, despite the publications in this country on this issue, it should be recognized that the possibilities of ultrasound diagnostics in the assessment of peripheral nerves in chronic pain in the lower extremities remain poorly understood.

The aim of the work was to assess the possibilities of ultrasound sciatic and femoral nerves in the syndrome of chronic pain in the lower extremities.

Material and methods

The present study is based on the analysis of the ultrasound results of 27 patients (18 women, 9 men) aged 30 to 65 years (mean age 47.2 ± 2.4 years) suffering from chronic lower extremity pain.

All patients underwent a comprehensive clinical and instrumental examination, which included a thorough, scrupulous analysis of complaints and anamnesis of the disease, examination by a neurologist, rheumatologist, urologist and / or gynecologist, ultrasound of the femoral and sciatic nerves.

Patients complained of pain bearing all the features of neuropathic pain, which were often accompanied by the presence of related phenomena, such as paresthesia, dysesthesia, allodynia, hyperpathy, hyperesthesia and hypoesthesia. Patients described pains as burning, shooting, stitching, as "electric shock", burning, chilling, piercing with increasing intensity in the buttock, inguinal and popliteal areas, limiting the amount of movement of the leg. Along with a change in sensitivity, vegetative disturbances in the relevant area were often detected - discoloration of the skin (hyperemia or cyanosis), disturbance of tissue trophism, sweating, and swelling. As a result, patients had disturbed sleep, there were depressive and anxiety disorders. The average duration of pain and movement restrictions ranged from 1 to 3 months.

In terms of diagnostic search to identify possible causes of pain in the pelvic area, 17 patients underwent a radiography of the hip joints (16 (94%) patients showed signs of coxarthrosis), 9 patients had MRI of the lumbosacral spine (7 (78%) patients were degenerative -distrophic processes). Ultrasound of the pelvic organs was performed in 15 cases, with pathology detected in 14, including 3 in uterus myoma, in 4 - signs of external endometriosis, which could be the cause of pain in the buttock and thigh, radiating to the foot, the severity of which depended on phases of the menstrual cycle. 4 men showed signs of chronic prostatitis in combination with benign prostatic hyperplasia of various degrees.

Ultrasound was performed on modern ultrasound devices with linear sensors with a frequency of 5-13 MHz. In the course of the study, the thickness, structure, and echogenicity of the nerve were evaluated. In order to determine the echogenicity of the nerve, it was compared with the healthy contralateral side and with the adjacent muscles.

It is known that the femoral nerve begins with three branches of the II-IV lumbar spinal nerves, which form a single trunk, going down between the large lumbar and iliac muscles, and then along the lateral edge of the first. There are several sites in which the anatomical and topographic features of the femoral nerve predispose to an increased risk of its compression or traumatization - in the iliopsoas muscle, under the inguinal ligament, in the Gunther canal area and at its exit.

Fig. one. Anatomy of the femoral nerve, the zone of innervation and the place of its most frequent damage (http://mfvt.ru/wp-content/uploads/2012/06/19.png).

Depending on the level of the lesion, the clinical manifestations of femoral neuropathy vary considerably.

Ultrasound examination of the femoral nerve was performed with the patient lying on his back. The femoral nerve was visualized in the groin area lateral to the vascular bundle from the level of the inguinal ligament to the upper third of the thigh (Fig. 2, 3). The study was carried out in the transverse and longitudinal scanning planes (Fig. 2, 4).

Fig. 2 In-mode. Examination of the right femoral nerve in the transverse plane of the scan at the level of the inguinal region: BN - femoral nerve, BA - femoral artery.

Fig. 3 DDC mode. Examination of the right femoral nerve in the transverse plane of the scan at the level of the inguinal region: BN - femoral nerve, BA - femoral artery.

Fig. four. In-mode.Examination of the right femoral nerve in the longitudinal plane of the scan at the level of the groin and upper third of the thigh: arrows - femoral nerve.

The sciatic nerve is the largest of the peripheral nerves in the human body, which emerges from the pelvic cavity through the large sciatic opening under the pear-shaped muscle. In the area of ​​the gluteal fold, the sciatic nerve is located close to the broad fascia of the thigh, is displaced laterally and then lies under the long head of the biceps of the thigh, located between it and the large adductor muscle. Depending on the level (height) of the lesion, the following options for neuropathy of the sciatic nerve are possible: very high level, piriformis syndrome (at the level of the subvaroidal opening), at the level of the thigh (above the site of division into the tibial and common peroneal nerves). The topical differential diagnosis of sciatic nerve syndrome often has to be performed with LV-SII discogenic compression radiculopathy.

Ultrasonography of the sciatic nerve was performed with the patient lying on his stomach. The sciatic nerve was visualized distal to the sciatic tuber in the interval under the tendons of the semi-membranous and semitendinosus muscles and the long biceps head from the gluteal region to the site of division into the tibial and common fibular nerves. The study was carried out in the transverse and longitudinal plane of the scan (Fig. 6, 7).

Fig. 6 In-mode. Examination of the left sciatic nerve in the transverse scanning plane in the upper third of the posterior surface of the thigh: CH - the sciatic nerve.

Fig. 7 In-mode. Examination of the left sciatic nerve in the longitudinal plane of the scan in the upper third of the posterior thigh: arrows - the sciatic nerve.

results

According to the ultrasound, signs of neuropathy were detected in 24 (88.9%) patients. The distribution of identified neuropathies by location and sex of patients based on the results of ultrasound is presented in Table 1.

In females, the femoral nerve on the right prevailed (31.2%), and the sciatic nerve on the left (31.2%), in men, the sciatic nerve on the right was more common, which is consistent with literary data.

Normally, the thickness of the femoral nerve at the level of the hip joint in men and women is 0.31 ± 0.08 cm, the thickness of the sciatic nerve in the upper and middle third of the posterior surface of the thigh is 0.4 ± 0.05 cm.

As can be seen from the data in Table 2, with neuropathy, a uniform increase in nerve thickness was observed: femoral - on average up to 0.56 ± 0.09 cm in women and 0.62 ± 0.20 cm in men, sciatic - on average up to 0 , 62 ± 0.06 cm in women and 0.66 ± 0.04 cm in men. Local thickening (suspicious for neuromas, schwannomas) or thinning (suspicious for injury) of the nerve trunks in our study was not identified. In 50% of cases, the echogenicity of the nerve trunks decreased, in 37.5% it was not changed, in 12.5% ​​it was increased. When comparing the thickness of the femoral and sciatic nerves obtained during the examination of healthy men and women, as well as in the study of the right and left lower extremities, the bilateral and sexual differences of parameters were insignificant.

Pathogenetic therapy (muscle relaxants, nonsteroidal anti-inflammatory drugs (NSAIDs), group B vitamins, anticonvulsants, antidepressants, acupuncture reflexology, laser puncture) was carried out to all patients, as a result of which 22 had improved. With the control ultrasound in patients with clinical improvement, nerve thickness was reduced: femoral - on average up to 0.39 ± 0.04 cm in women and 0.40 ± 0.04 cm in men, sciatic - on average up to 0.43 ± 0 , 02 cm in women and 0.45 ± 0.03 cm in men.

Discussion

Femoral and sciatic neuropathies are fairly frequent mononeuropathies of the lower extremities [9-11]. Symptoms of femoral neuropathy and other neuropathies are often mistakenly regarded as manifestations of vertebral pathology.According to some studies, approximately 9% of patients referred to the clinic with a diagnosis of "radiculopathy" caused pain, sensory and motor disorders in the lower extremities, in fact were traumatic and compression-ischemic neuropathies, a significant portion of which (more than 10%) were various options for femoral neuropathy.

Diagnosis of lesions of the femoral nerve is primarily based on a thorough neurological study and analysis of the distribution of sensory and / or motor disorders, revealing their correspondence to the area of ​​innervation of the femoral nerve or its individual branches. At the same time, the topography of the femoral nerve is determined, which, along with anamnestic data, suggests the etiology of the disease. In practice, femoral neuropathy most often has to be differentiated from vertebral radiculopathy L2-L4. Radiography of the joints of the lower extremities is not very important for diagnosing the state of the femoral and sciatic nerves due to the impossibility of their image. MRI makes it possible to clearly assess the condition of the corresponding section of the spine, suspect the presence of neuropathy, but does not give an image of the nerves over.

Incorrect diagnosis leads to partially or completely inadequate therapy, which, naturally, adversely affects the course of the disease and contributes to its chronicity. Meanwhile, the overwhelming majority of cases of femoral neuropathy, subject to the timely commencement and adequacy of therapeutic measures, are potentially curable. Elimination of the cause of the lesion of the femoral nerve and early pathogenetic therapy make it possible to avoid disabling outcomes, including intractable complex pain syndromes of the pelvic girdle and paresis of the anterior group of the thigh muscle with persistent impairment of the walking function.

Pathological tension of the pear-shaped muscle during compression of the root of L1 or S1, as well as due to injury, unsuccessful injection, prolonged lying on the back and side (during prolonged operations), syndrome of the posterior thigh muscular bed may be a manifestation of the sciatic nerve neuropathy. The sciatic nerve may be subjected to compression by a tumor or hematoma in the pelvic region, aneurysm of the iliac artery.

Therefore, cooperation between neurologists, urologists, gynecologists, rheumatologists, and ultrasound diagnostics doctors is more important for a more accurate and detailed differential diagnosis of neuropathies of the femoral and sciatic nerves.

The use of methods for radiological diagnosis of the peripheral nerves of the lower limb is limited by the technical capabilities of the equipment and the anatomical features of the location of the nerves [6, 12, 13].

The decisive advantage of ultrasound of the peripheral nerves is non-invasiveness, the absence of radiation load on the patient, the conduct of research in real time, as well as minimal economic costs for the study. Ultrasound allows not only to visualize the sciatic and femoral nerve throughout, but also to assess its location, thickness and structure, in turn, helps the neurologist to choose and promptly start an adequate treatment.

Conclusion

Thus, the use of an ultrasound nerve research method in neurologist's practice allows optimizing the differential diagnostic diagnosis of the causes of pain in the lower extremities, as well as minimizing the number of studies performed on a patient with neurological symptoms of peripheral genesis, avoiding unnecessary manipulations and studies, reducing radiation load indicators on a patient, reduce the cost of its examination and thereby increase the diagnostic effectiveness of the research.

Literature

  1. Popelyansky I.Yu. Orthopedic neurology (vertebral neurology). M .: MEDpress-inform, 2003.
  2. Popelyansky I.Yu. Diseases of the peripheral nervous system. M .: MEDpress-inform, 2005.
  3. Bianchi S., Martinoli C.Ultrasound of the Musculoskeletal System. Springer-Verlag Berlin Heidelberg New York 2007.
  4. Peer S., Bodner G. High-resolution ultrasound of the peripheral nervous system. Springer-Verlag Berlin Heidelberg 2008.
  5. Eskin N.A. Ultrasound diagnosis in traumatology and orthopedics / / Ed. Mironova S.P. M .: Publishing house "Socio-political thought", 2009.
  6. Saltykova V.G. Ultrasound technique and normal echographic picture of the sciatic nerve // ​​Ultrasound and Functional Diagnostics. 2009. N 6. S. 75-81.
  7. Shtulman D.R., Levin OS Neurology: Reference practitioner. 5th ed., Ext. and pererabat. M .: MEDpressinform, 2007. p. 91-95.
  8. Samoilov V.I. Syndromological diagnosis of diseases of the nervous system. Volume 1, 2nd ed. St. Petersburg, "SpecLit", 2001.
  9. Khabirov F.A. Guide to clinical neurology of the spine. Kazan: Medicine, 2006.
  10. Elman L., McCluskey L. Occupational and Sport Related Traumatic Neuropathy // The Neurologist. 2004. V. 10. P. 82-96.
  11. Durrant D.H., True J.M., Blum J.W. Myelopathy radiculopathy, and peripheral entrapment syndromes. CRC Press, 2002.
  12. Jacobson J.A. Fundamentals of musculoskeletal ultrasound, second edition 2013, 2007 by Saunders, an imprint of Elsevier Inc.
  13. McNally Eugene. Ultrasound studies of the musculoskeletal system: A Practical Guide // Per. from English Khitrova A.N. / Ed. Nazarenko G.I., Heroev I.B. M .: Vidar M Publishing House, 2007.

Types of reflexes

Countless reflexes are divided into groups according to a particular attribute.

According to their biological significance, there are food reflexes, defensive, sexual, orienting, motor and posotonic reflexes (supporting postures of the body). The location of the receptors (causing a certain reflex) is exteroceptive (receptors on the outer surface of the body), interoceptive (receptors in the internal organs) and proprioceptive (receptors in the muscles, tendons, joints).

By the nature of the response - motor (muscle contraction), secretory (secretion by the glands) and vasomotor (dilation and vasoconstriction). According to the duration of the flow - physical and tonic (fast and slow).

Conventionally, there are several options for neurological disorders:

Symptoms of loss, which are a consequence of organic lesions of the nervous system, are characterized, as a rule, by the constancy of the function disorder, which is confirmed by the data of an objective study, these symptoms occur when one or another nerve center or pathways that connect this center to the periphery are destroyed (video 1).

With the defeat of the efferent centers and systems, the symptoms of loss are often combined with the so-called plus-symptoms or symptoms of release. The more complex the level of organization of the nerve center, the more regulatory mechanisms it unites, and when it is damaged, the variety of plus-symptoms increases significantly. The emergence of symptoms of release is associated with the disintegration of the regulatory activity of the nervous system, when low-order automatisms come into play, in parallel, compensatory reactions are formed, which can also be attributed to the symptoms of release (video 2).

Symptoms of irritation occur when excitation of the nerve centers, irritation of the pathways by various pathological processes (brain tumors, encephalitis, meningitis, general infections, intoxication, etc.), and they are intermittent, such as scratching the neck in dogs with syringomyelia. In the development of these symptoms an important role belongs to disorders of hemo - and liquorodynamics, metabolic disorders in the brain tissue.

Symptoms of prolapse and irritation are often observed simultaneously, therefore, to establish their true nature and determine the value for topical diagnosis, detailed knowledge of the anatomy and structural and functional relationships in the nervous system is necessary.

Diaschis (Greek diaschizō split, divide, synonymous diaskhiz) - the state of inactivity of the nerve centers, developing as a result of a sudden cessation of stimulatory impulses to them, is expressed in the first days after acute extensive intracerebral hemorrhage, spinal cord injury leading to the defeat of the pyramidal system on various levels.The lack of excitatory impulses after damage to the conductors translates the structurally preserved nerve cells to a different level of reactivity, which is clinically manifested by various functional disorders.

The term “diashiz” was proposed in 1914 by Monakov (S. Monakow), who singled out associative, commissural and cerebrospinal diaschises. Disorder of functions in intact structures, but connected to the pathological focus in the same hemisphere of the large brain, he called associative, and with the pathological focus in the other hemisphere, the commissural diasis. In cerebrospinal diasis, patients with hemiplegia resulting from hemorrhage develop dysfunction of the cells of the ventral horns of the spinal cord. Clinically, it is manifested by the absence of tendon reflexes and a decrease in muscle tone instead of tendon hyperreflexia and spastic muscle hypertension characteristic of hemiplegia.

When diasis is eliminated and the excitability of motoneurons is restored, an increase in muscle tone and tendon reflexes is observed in the paralyzed muscles. The duration of diasis depends on the size, nature, localization of the lesion and the compensatory capabilities of the central nervous system. Of great importance is the patient's age and the state of his cardiovascular system. Under adverse conditions, diaschis can be long lasting, while the so-called permanent sluggish hemiplegia is maintained. (Sorokhtin G.N. 1968). It is precisely because of this phenomenon that the assessment of neurological status after injury does not fully correspond to the real picture of damage.

With the slow development of the pathological process (for example, with the growth of glioma of the brain) focal symptoms may not be detected for a long time due to compensatory brain mechanisms. A tumor may occupy a significant part of the brain, and at the same time the dog may look completely normal or have minimal neurological disorders (video 3, 4).


It is worth noting that in this patient the tumor in the brain remains, but the use of anti-edema therapy completely eliminated the symptoms of brain damage.

The development of focal symptoms is associated not only with direct damage to one or another area of ​​the brain, but also with the displacement of brain structures, with liquorodynamic disorders. Diffuse damage to the nervous system, as a rule, is characterized by symptoms caused by the damage not only to one or several specific areas of the brain, but to a widespread damage to the nervous system.

Along with organic symptoms in diseases of the nervous system, so-called functional disorders are also observed. At the same time, it is not possible to detect objective signs of focal brain damage, but the regulation of the functions determined by it is disturbed. This kind of dysregulatory manifestations often occur after severe somatic diseases, mental shocks, and traumatic brain injuries, as well as due to physiological changes in the body. Sometimes functional disorders may be early manifestations of organic lesions of the nervous system.

The formulation of a topical diagnosis requires knowledge of the main symptom complexes and their variants arising from the defeat of certain parts of the nervous system. It is important to determine the degree of neurological disorders immediately, as the choice of further actions will depend on this: the method of treatment and diagnosis.

I degree - pain.

Grade II - pain, impaired limb setting, (impaired proprioception) paresis. Saved ability to walk.

Grade III - pain, impaired limb setting, (impaired proprioception) paresis. There is no ability to walk.

IV degree - lack of sensory and motor functions (paralysis). Saved perception of deep pain.

V degree - lack of sensory and motor functions (paralysis).There is no perception of deep pain (spinal cord rupture syndrome).

And also to determine the type of paralysis, after a neurological examination.

There are only two types of paralysis. Having identified on the basis of 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, determine its nature: is it due to a lesion of central or peripheral motor neurons.

The defeat of the central motoneurons at any level of the cortical-spinal tract causes the emergence of central or spastic paralysis.

Central motoneuron. The defeat of the motor area of ​​the cerebral cortex or pyramidal path leads to the cessation of the transmission of all impulses to perform voluntary movements from this part of the cortex to the ventral horns of the spinal cord. The result is paralysis of the corresponding muscles. If the break in the pyramidal path occurs suddenly, the stretch reflex is suppressed. This means that paralysis is initially flaccid. Days and weeks may pass before this reflex is restored.

Peripheral motoneuron. Damage can capture ventral horns, ventral roots, peripheral nerves. In the affected muscles, neither voluntary nor reflex activity is detected. Muscles are not only paralyzed, but also hypotonic, areflexia is observed due to interruption of the monosynaptic reflex arc of stretching. After a few weeks, atrophy occurs, as well as the reaction of rebirth of paralyzed muscles. This suggests that the cells of the ventral horns have a trophic effect on muscle fibers, which is the basis for normal muscle function..

The main symptoms of central paralysis (spastic paralysis always indicates damage to the central nervous system - the brain or spinal cord):

  • Reduced strength combined with the loss of subtle movements.
  • Spastic increase in tone (hypertonia).
  • Enhancement of proprioceptive reflexes with or without clonus.
  • The appearance of pathological reflexes (tibia, on the greater spit, etc.).
  • Pathological friendly movements.

The main symptoms of peripheral paralysis (flaccid paralysis). It occurs when peripheral motoneurons are damaged at any site (ventral horn, root, plexus and peripheral nerve):

  • Lowering the tone of the innervated muscles (there is neither arbitrary nor reflex activity).
  • Muscle atrophy (for two three weeks).
  • Weakening of reflexes (up to complete absence).

A topical diagnosis of spinal cord injury includes an assessment of segmental movement disorders, sensitivity and vegetative functions, as well as conduction disorders of movement and sensitivity below the level of the lesion.

On the basis of the existing symptoms, the level of the pathological focus and its distribution in the transverse and longitudinal directions are determined. Data acquisition is based on knowledge of the location of the spinal cord segments relative to the spine and the passage of the spinal cord pathways.

The layout of the lower motor centers in dogs.

Distribution of pathways and gray matter nuclei in the area of ​​the second cervical segment in dogs.

1 central canal - central channel

2 ventral median fissure

3 dorsal median septum - dorsal median septum

4 dorsolateral sulkus - lateral dorsal trough

Gray matter

5 dorsal horn - dorsal horn

6 substantia gelatinosa - gelatinous substance

7 nucleus proprius - dorsal nucleus

8 lateral cervical nucleus - lateral cervical nucleus

9 intermediate region - intermediate region

10 accessory n. spinal nucleus

11 central gray substance - central gray substance

12 ventral horn - ventral horn

White matter

13 dorsal funiculus - dorsal cord

14 fasciculus gracilis - a bundle of Goll

15 lateral funiculus - lateral funicular

16 ventral funiculus - ventral cord

17 fasciculus cuneatus - wedge-shaped bundle (Burdakh bundle)

18 lateral corticospinal tract (crossed pyramidal, rubrospinal)

19 wentral white commissure - white bundle

The posterior cord, funiculus dorsalis (posterior) (13) at the level of the cervical and upper thoracic segments of the spinal cord of the posterior intermediate sulcus is divided into two beams:

the medial bundle, or thin bundle (Gaulle bundle), fasciculus graciiis (14), is directly adjacent to the posterior longitudinal groove. (F. Goll, Friedrich Goll, 1829-1903, Swiss anatomist),

a wedge-shaped bundle (Burdakh bundle), fasciculus cuneatus (17), is adjacent on the medial side to the posterior horn lateral to the medial bundle. (KF Burdach, Karl Friedrich Burdach, 1776-1847, German anatomist and physiologist).

The thin bundle consists of longer conductors running from the lower parts of the body and lower limbs of the corresponding side to the medulla oblongata. It includes the fibers that make up the dorsal roots of the 19 dorsal segments of the spinal cord and occupy the more medial part of the posterior cord.
By entering into the 12 cranial segments of the spinal cord fibers belonging to neurons innervating the forelimbs and the anterior part of the body, a wedge-shaped bundle is formed, which occupies a lateral position in the dorsal cord of the spinal cord.
Thin and wedge-shaped bundles are the conductors of information due to proprioceptive sensitivity (joint and muscular feeling). These beams carry information about the position of the body and its parts in space into the cerebral cortex. Dorsal cord fibers are conductors of skin and mechanical sensitivity.

The lateral motor system of the spinal cord is a system of descending pathways of the spinal cord, which includes phylogenetically younger motor paths (crossed pyramidal, rubrospinal (18). Well developed in primates. They are located mainly in the lateral columns of the spinal cord and are responsible for providing thin differentiated movements distal muscles of the limbs, as well as the extensors of the body. The lateral spinal-thalamic pathway (tr. spinothalamicus lateralis) is located in the lateral cord (15), formed Assumption in the posterior horns of the second neuron pain and temperature, as well as part of tactile sensitivity.

The ventral spinotalamic path passes into the ventral component of the STP; it is also called the ventral STP. The cell bodies of the neurons of this pathway are located in the plates I, IV-VII. The path rises in the ventral bundle of the spinal cord (16 ventral funiculus) and ends in various nuclei of the trunk and thalamus.

The spinal-reticular-talamic pathway, the spinal-reticular pathway, the spinal-mesencephalic pathway and the medial bundle of the forebrain are sometimes combined into a functionally single entity called the spinal-reticular-thalamic pathway. It forms pathways with many synaptic connections between the spinal cord, the reticular formation of the spinal cord, the thalamus and the hypothalamus. Since these pathways end in the paraventricular nuclei of the hypothalamus, continuing into the medial bundle of the forebrain, the dorsal-reticular-thalamic pathway is undoubtedly involved in the neuroendocrine responses to pain.

Scheme: a cross section of the spinal cord, in which all the basic structures are combined, which are normally at different levels.

(s - innervation of the same side of the body, o - innervation of the opposite side of the body).

Descending (motor) ways:
1 - anterior corticospinal tract (o)
2 - medial longitudinal bundle (s)
3 - vestibulospinal tract (s)
4 - medullary (ventrolateral) reticulospinal tract (s)
5 - Rubrospinal tract (s)
6 - lateral corticospinal (pyramidal) tract (s)

Bidirectional paths:
7 - dorsolateral bundle
8 - fasciculus propriu (s)

Ascending (sensitive) ways:
9 - fasciculus gracilis (s)
10 - fasciculus cuneatus (s)
11 - posterior spinocerebellar tract (s)
12 - lateral spinothalamic tract (o)
13 - anterior spinocerebellar tract (o)
14 - spinotectal tract (o)
15 - front spinothalamic tract (o)

Neurological examination

Inspect, palpate and measure muscle volume. Atrophy or hypertrophy is determined. Measuring in centimeter the volume of the muscles of a limb, it is possible to identify the severity of trophic disorders, fibrillary and fascicular twitches, the configuration of the muscles, their tension.Determine the amount of active and passive movements, muscle strength, muscle tone, the rhythm of active movements and reflexes. Spinal (segmental) reflex apparatus, afferent innervation, reticular formation, as well as cervical tonic, including vestibular centers, cerebellum, system of the red nucleus, basal nuclei, affect the muscle tone.

Hypotension and atony of muscles occur in peripheral paralysis or paresis (violation of the efferent reflex arc with nerve, root, spinal cord horn cells), damage to the cerebellum, brain stem, striatum, and posterior spinal cord.

Muscle hypertension is the tension felt by the patient during passive movements.
Contracture is a persistent tonic tension of the muscles causing a restriction of movement in the joint.

The complete absence of active movements is called paralysis, the restriction of movements or the weakening of their strength is called paresis. Paralysis or paresis of one limb is called monoplegia or monoparesis (video 5). Paralysis or paresis of two limbs of the same name are called hemiplegia or hemiparesis (video 6).

Paralysis of the three limbs - triplegia, four limbs - quadriplegia or tetraplegia (video 7)

Reflex is a reaction in response to receptor irritation in the reflexogenic zone: muscle tendons, skin of a specific area, mucous membrane, pupil. As reflexes are judged on the state of various parts of the nervous system. In the study of reflexes determine their level, uniformity, asymmetry.

Pathological reflexes appear when the pyramidal pathway is affected, when spinal automatisms are disturbed. Pathological reflexes, depending on the reflex response is divided into extensor and flexor. Pathological protective (or spinal automatism) reflexes on the thoracic and pelvic limbs - involuntary shortening or lengthening of the paralyzed limb at a prick, pinching. Protective reflexes often have a flexing nature (involuntary flexion of the limb in the knee and hip joints). The extensor protective reflex is characterized by involuntary extension of the limb in the hip, knee joints and flexion of the tarsus. Cross defense reflexes — flexion of the irritated limb and extension of the other, are usually noted in the combined lesion of the pyramidal and extrapyramidal tracts, mainly at the level of the spinal cord (video 8).

An extreme manifestation of increased tendon reflexes are the so-called clonuses. Clonuses are the rhythmic contractions of a muscle resulting from the stretching of its tendon. In essence, clonus is a chain of successive tendon reflexes caused by uninterrupted tendon stretching. The most frequent are clonus of the knee-cup reflex (video 8).

Patellar reflex A blow is struck on the knee-cup tendon (video 9). Manifests itself normally in all animals, there is an extension of the knee joint, quadriceps, femoral nerve, localization of the reflex arc L3-L6 segment of the spinal cord. Which corresponds to half of the third and fully fourth lumbar vertebrae in dogs. And the third-seventh lumbar vertebrae in cats. Very reliable reflex. Strengthening, weakening or pseudo-reinforcement of the knee jerk is possible. Pseudo-enhancement is observed when the sciatic nerve is broken.

Reflex on the sciatic nerve A hammer is struck between the greater trochanter of the femur and the ischial tubercle (video 10). Reliable reflex. The reflex on the sciatic nerve manifests itself in all animals. Strengthening, weakening or absence of a reflex is possible. When testing this reflex, contraction of the opposite limb indicates a syndrome of transverse lesion of the spinal cord.

Achilles tendon reflex Affects L5-L7, S1 spinal cord segments located in the fourth and fifth lumbar vertebrae in dogs. And in the area of ​​the fifth-seventh in cats. Involved sciatic nerve and gastrocnemius muscle. The reflex is not very pronounced in healthy dogs.

When describing reflexes, the following gradations are used:

  • live reflexes (normal)
  • hyporeflexia
  • hyperreflexia (with extended reflexogenic zone)
  • areflexia (lack of reflexes).

Reflexes can be:

  • deep (proprioceptive - tendinous, periosteal, articular)
  • superficial (skin, mucous membranes).

Reflex on the shin A hammer is struck on the inner surface of the shin (video 11). Involved periosteum receptors shin. Reflex is expressed in pathology. Reflex on the big spit (Trohanter major). Reflex enlargement of the reflex zone on the sciatic nerve. Called only in pathology. Indicates hyperreflexia. Causes contraction and straightening of the thigh muscles.

Reflex with Panniculus - a panicular reflex (video 12). The subcutaneous muscle of the torso participates, segments C7-Th1 are involved. It is expressed in twitching of the skin in the area of ​​irritation.

Pull-up reflex - affected L6-S1 spinal cord segments located in the fifth lumbar vertebra in dogs (video 13). And the sixth and seventh lumbar vertebrae in cats. Reliable reflex. Often this reflex is confused with conscious pain sensitivity (the dog tries to bite or free itself. Video 14). All muscle flexors are involved. In the case of testing this reflex, straightening the opposite limb indicates the syndrome of transverse lesion of the spinal cord. We must remember that deep pain sensitivity and reflex are not the same thing. On the front paw, sensitivity depends on the radial nerve, and C6 - Th1 segments are involved. On the hind paw, the sensitivity of the (second) finger is provided by the branch of the femoral nerve, and the rest of the fingers by the branch of the sciatic nerve.

On the pectoral limb - a reflex with the triceps muscle of the shoulder. Expressed in muscle contraction. The radial nerve (N. radialis) and the triceps muscle of the shoulder are affected. Affected C7- Th1 spinal cord segments. Reliable reflex.
Reflex with biceps muscle of the shoulder. The biceps muscle of the shoulder C6-C8 segments of the spinal cord are affected. Called with difficulty, is estimated with hyperreflexia. Pull-up reflex is also evaluated.
The reflex on the muscles of the abdominal wall - estimated the reduction of the muscles of the abdominal wall.
The reflex from the anal area - the anal contraction is estimated (video 15). Affected S1-S2 segments of the spinal cord, located in the region of the fifth - sixth lumbar vertebrae in dogs and in the region of the seventh lumbar and first sacral - in cats.

Cranial nerve reflexes

Corneal reflex. Involved eye branch of the left trigeminal nerve (fifth pair, afferent part of the reflex). The orbital branch of the trigeminal nerve is a sensitive reflex arc. The motor way is the facial nerve (the seventh pair. The efferent part of the reflex), providing a blink, and the abducent nerve (the sixth pair), retracting the eyeball. The center of the reflex is located in the brain stem (corneal reflex, absent nystagmus). (Video 16)

Pupillary reflex to light. Afferent part of the second pair (optic nerve). Efferent part of the third pair (oculomotor nerve) cranial nerves. It is expressed in the constriction of the pupil on the effect of light, the degree of constriction and the friendly reaction in the opposite eye are evaluated. With the defeat of the parasympathetic additional nuclei of the oculomotor nerve, mydriasis develops - reducing the reaction of the pupil to light. Irritation of the parasympathetic fibers causes constriction of the pupil.
Facial sensitivity (video 17) depends on the fifth (trigeminal nerve) and the seventh pair (facial nerve) cranial nerves. The response to skin irritation of the muzzle, twitching of the skin and blinking of the eyes is evaluated (video 18).


Video 18 Violation of the facial sensitivity of a cat.

Video 19 Damage to the facial nerve in a dog.

Reflex threat (video 20). Afferent part of the second pair (optic nerve).The efferent part of the seventh pair (facial nerve) of the cranial nerves, motor nucleus in the middle and rhombic brain, and motor cells in the ventral horns of the cervical segments. Conscious proprioception (video 21). Affected receptors of the joints, muscles, pathways of the spinal cord. Thin and wedge-shaped bundles and centers of the brain. Normally, the animal must straighten the limb immediately after it has been placed on the outer surface.

Tonic or postural reflexes (reflexes of the situation. Video 22) are manifestations of a special complex innervation system that automatically regulates muscle tone to maintain body position. There are mechanisms that reflexively regulate the balance, both at rest and in motion. The redistribution of muscle tone largely depends on changes in the position in the head space (labyrinth and cervical tonic reflexes). As shown by an animal experiment, vestibular and red nuclei in the brainstem are of major importance in the regulation of muscle tone during standing and movement. Normally, tonic reflexes are significantly inhibited by the higher parts of the brain and are detected with particular intensity when they are turned off.
The inclination of the head depends on the eighth pair (the precursor is the cochlear) and can develop with a unilateral lesion of the stem or nuclei of the eleventh pair of cranial nerves (additional motor nerve only). With the defeat of the eleventh pair (video 23), signs of peripheral paralysis develop muscle atrophy innervated by the nerve (trapezoidal, clavicular-mastoid clavicle-cervical muscle). In case of unilateral lesion of the accessory nerve, the head is deflected to the affected side. Turning the head to a healthy side is limited.

Syndrome of lesion of half the diameter of the spinal cord (Brown-Sekar syndrome)

On the side of the lesion, central paralysis develops; the deep pain sensitivity shuts down, all types of segmental sensitivity are disturbed, peripheral paresis of the muscles of the corresponding myotoma, dissociated anesthesia on the opposite side (associated with impaired blood circulation in the spinopalamic tract). Occurs in ischemic spinal strokes, impaired blood circulation in the sulco-commissural artery, as a result of embolism, trauma, etc. This artery supplies with blood almost the entire lateral half of the spinal cord diameter, with the exception of the posterior cords, so in this case the Broun-Sekar syndrome will be incomplete during ischemia, since there will be no conduction disorders of epicritical sensitivity on the affected side.

The leading clinical signs of Brown-Sekara syndrome (video 24) are:

  • Spastic (central) paralysis (paresis) on the ipsilateral side (lesion side) below the level of damage as a result of interruption of the descending corticospinal tract, which has already made the transition to the opposite side at the level of the medulla oblongata to the spinal cord.
  • Flaccid (peripheral) paralysis or paresis in the myotome on the ipsilateral side due to the destruction of peripheral motoneurons that innervate it.
  • Loss of deep sensitivity (touch, touch, pressure, vibration, body weight, position and movement) on the affected side. Symptomatology arises ipsilaterally, since the beams of Gaulle and Burdah at the level of the spinal cord carry out afferent impulses of their own side, and the transition of their fibers to the opposite side occurs only after they leave the brain stem nuclei in the inter-brewing layer.
  • Loss of pain and temperature sensitivity of the conductor type on the contralateral side due to the lesion of the neo-spin-thalamic tract, and more important is the defeat of the lateral spinal-thalamic tract.The contralateral localization of the process is connected with the fact that the axons of the second neurons of the lateral spinal-talamic path pass to the opposite side of the spinal cord through the anterior gray commissure and enter the lateral columns of the spinal cord of the opposite side. It should be noted that the fibers are not strictly horizontally, but obliquely and upwards. Thus, the transition is carried out 1–2 segments higher, which leads to the “overlapping” of the segments. This must be considered when determining the level of damage to the spinal cord. So, when determining the horizontal level of sensitivity damage in the area of ​​a certain dermatome, it is necessary to compare it with a segment of the spinal cord and “rise” by 1–2 segments, and at the level of the pectoral ones - 3 segments higher. With the extramedullary nature of the process, it is necessary to take into account the law of the "eccentric arrangement of conductors": newly entering conductors push back the outwardly entering ones. Thus, the conductors from the hind limbs are located laterally, and from the front - medially. Therefore, with the extramedullary character of the process, taking into account the somatotopic representation during the fibers of the spinal-talamic tract, an “ascending” type of sensitivity disturbance takes place (from distal limbs and higher with the presence of a horizontal lesion level).
  • Disorder of all types of segmental sensitivity on the affected side, if two or more segments are damaged.
  • Vegetative (vascular-trophic) disorders are detected on the affected side and in the zone of the corresponding segments.
  • The absence of disorders of urination and bowel movements, as arbitrary sphincters of the bladder have bilateral cortical innervation.

Wobbler syndrome. Cervical Spondylopathy or Dog Syndrome Wobblers

Dog dogs have a true wobbler usually noticed between the ages of 3-12 months. The leading symptoms of the disease are the slow development of progressive impairments of coordination and paralysis of the hind limbs. This paresis and / or impaired coordination is caused by compression of the spinal cord in the cervical part of the medullary canal in the region of the 3 lower cervical vertebrae, which normally are the most prominent areas. In this disease, the animal may seem clumsy, "loose", which is difficult to maintain balance with its hind legs. Such animals hardly move on a smooth floor or cannot walk on it at all. The dog may fall when trying to turn its head, and the toes of the hind legs may “shuffle” on the floor while walking. Proprioception is violated. Paresis or paralysis is diagnosed with symptoms of lesions of the upper motor neuron for the fore and hind limbs. Dogs usually spread their legs as much as possible in order to balance themselves better. Initially, forelimb involvement is minimal or not at all. As the disease progresses further, a characteristic shortening of the step appears with a characteristic jerky step at the expense of the forelimbs. As spinal cord compression becomes more severe, the front legs may have the same symptoms as the hind legs. The pain in the neck is usually minimal or absent, but the dog prefers to keep the neck bent (ie, down). This position of the neck reduces the compression of the spinal cord and facilitates the well-being of the animal. Many dogs resist any manipulation of the neck and can even fall from committing violent acts that change the position of the neck. Sometimes, there may be an acute onset of symptoms. Such an onset of the disease has more severe clinical manifestations and consequences than the gradually progressive course of the disease. Involvement of the front limbs is usually always present at this beginning. With an acute onset, neck pain is more common.This type of wobbler syndrome is most common in five to seven year old Doberman Pinchers and rarely in young dogs. If the acute onset of cervical neurological symptoms still happens in mastiff, then the cause of the acute onset of the disease is most often a fracture of the cervical spine or displacement of the intervertebral disc into the lumen of the spinal canal. The compression of the spinal cord is due to the asynchronous formation of the anatomical parts surrounding the spinal cord during its growth.

Compression can occur due to a single cause or a combination of them:

  • Weak ligaments, which normally should hold the vertebrae in place, allow the vertebrae to perform excessive movements with displacement relative to each other when the position of the neck changes, which leads to compression of the spinal cord.
  • Hyperplasia (excessive growth) of the yellow ligaments, normally represented by thin free elastic plates that attach between the arches of adjacent vertebrae. Under them (ligaments) is a narrow slit of the epidural space, behind which is located the spinal cord itself with its shells. The excess tissue of these ligaments can squeeze the spinal cord.
  • Malformation of the vertebrae themselves. This can happen in various ways:
    · A. the bone spinal canal is too small for the spinal cord,
    · B. asymmetric intervertebral cartilage defects causing subluxation (displacement) of the vertebrae,
    · C. changes in the articular surfaces of cartilage, which also lead to subluxation,
    · D. stenosis of the cranial vertebral foramen, causing compression of the spinal cord (Bruce R. Wittels, D.V.M.).

The clinical symptoms of cervical disc herniation are associated with the dynamic force of compression and mechanical displacement of the spinal cord and cervical nerve roots displaced disc material. (Olsson SE 1951). Symptoms may include neck hyperesthesia, painful spasms of the neck muscles, paresis, ataxia, or tetraplegia. Despite the great compression, only constant or intermittent pain can be present. (Bailey CS, Holliday TS 1975, Hoerlein BF 1978, Shores A 1982) The pain may be caused by compression of the roots, sheaths of the brain, or it may be discogenic. (Prata RG, Stroll SG1973). Similar symptoms can occur with myelitis and meningitis, as well as tumors of the spinal cord and vertebral bodies. For differential diagnostics spend myelography. Myelography is also useful in determining the location of a lesion (Bartels JE, Hoerlein BF, Boring JG: 1978 Morgan JP 1972)

Horner syndrome. (Ocular sympathetic paralytic)

It is manifested by narrowing of the palpebral fissure of the eyelids, miosis of the pupil, enophthalmia (failure of the eye into orbit). Causes of Horner's syndrome - sympathetic nerve damage from the manifestation of the syndrome:

  • First order - damage to the cervical and cranial parts of the spinal cord.
  • The second order is damage to the roots of the brachial plexus nerves and the soft tissues of the neck.
  • The third order is damage to the middle ear.

Syndromes of lesion of different segments of the spinal cord of a dog (spinal cord segments and vertebrae do not match)

Upper cervical region (C1-C5)

Paralysis of the diaphragm
Spastic tetraplegia
Loss of all types of sensitivity
Central bladder dysfunction (delay with periodic incontinence and imperative urges (urgent))
Pain in the neck and neck

Cervical thickening (C5-Th1-3) (Video 25, 26)
Peripheral paralysis of the forelimbs
Central hind limb paralysis
Bernard-Horner syndrome
Pain in the area of ​​damage
Loss of all types of sensitivity
Central dysfunction of the bladder (delay with periodic incontinence and imperative urges (urgent)).

Fig. 1 Damage to the neck and the onset of flaccid paralysis in the cat's chest.

Thoracolumbar (Th1-3 - L 2)

Rear spastic paraplegia (Central hind limb paralysis)
Disturbance of superficial and deep sensitivity below the level of damage. Lack of a panicular reflex below the level of damage.
Central bladder dysfunction (delay with periodic incontinence and imperative urges (urgent))
Pain in the area of ​​damage hyperesthesia.

Lumbar Thickening (L2-3-S3) (Video 28)

Sluggish lower paraplegia
Anesthesia of the hind limbs and tail
Dysfunction of the bladder (possibly flaccid paralysis of the wall and spastic sphincter)
Pain in the area of ​​damage hyperesthesia.

Horsetail (cauda equin) (Video 29)

Pain in the area of ​​damage
Peripheral paralysis of the hind limbs
Disorders of all kinds of sensitivity in the hind limbs and perineum
Peripheral bladder dysfunction
Reduction of the anal reflex until the anal opening, incontinence of feces
Trophic disorders in the sacrum and hind limbs.

Structural abnormalities localized in the medulla oblongata, the bridge and the legs of the brain involve the nucleus of the cranial nerves in the pathological process. Symptoms of damage to certain nuclei indicate the level of localization of the focus. The lesion of the motor core or the fibers emanating from it is usually combined with the lesion of closely located motor or sensory pathways. Peripheral paresis of the muscles innervated by the cranial nerves on the side of the lesion and conduction disorders of movement and sensitivity on the opposite side are characteristic of half lesions of the brain stem and are called alternating syndromes.

Damage to the medulla oblongata is accompanied by, among other symptoms, bulbar paralysis. Bilateral supranuclear pathological processes cause pseudobulbar palsy. Bulbar palsy is a peripheral palsy that develops when the ninth, tenth, and twelfth pairs of cranial nerves are affected and manifested by dysarthria, dysphonia, and dysphagia.

On examination, atrophies of the tongue, muscles of the larynx and soft palate, fibrillary twitches (especially in the muscles of the tongue), reduction of pharyngeal reflexes and identification of the reaction of rebirth in the muscles of the tongue are detected.

Pseudobulbar palsy is a central paralysis that develops with lesions of the corticonuclear pathways of the ninth, tenth and twelfth pairs of cranial nerves and is manifested by dysarthria, dysphonia, and dysphagia.

When viewed, unlike bulbar paralysis, with pseudobulbar palsy, there are no atrophies and fibrillations, there is no reaction of rebirth during ENMG. The pharyngeal reflex is preserved or enhanced. Acutely developed bulbar paralysis can result in death as a result of respiratory disorders and cardiac abnormalities, since bulbar syndrome develops when the medulla oblongata is affected, where along with the centers responsible for swallowing and vocalization, there are vital centers regulating the act of breathing and cardiac activity thirty).

Video 30 Paralysis of the tongue

Fig. 2 neoplasm of cerebellum with symptoms of lesion of medulla oblongata in labrador

A topical diagnosis of cerebellar lesions is made in coordination disorder in the form of static and locomotor ataxia, observed on the side of the lesion, as well as nystagmus and cerebellar dysarthria (video 31).

Lesions of the thalamus. Characteristic disorders of sensitivity, especially expressed in the distal extremities, are characterized by the so-called talamic pains and hyperpathy on the opposite side of the hearth. Musculo-articular disorders are manifested by sensitive ataxia.

Syndromes of lesion of the basal nuclei of the brain consist of complex changes in muscle tone and motor activity.

Topical diagnosis of lesions of various parts of the hypothalamus is based on the analysis of disorders of water-salt, fat, protein and carbohydrate metabolism, sleep functions, thermoregulation, endocrine and internal organs, disorders of emotional reactions.

The lesion of the inner capsule is manifested by hemiplegia, hemianesthesia and hemianopia on the side opposite to the lesion focus.

Topical diagnosis of lesions of the cerebral cortex in the presence of symptoms of irritation, a combination of signs of violation of the cortical parts of the analyzers with a disorder of higher cortical functions. Due to the fact that the higher cortical functions reflect the complex integrative activity of the brain as a whole, determining the location of the pathological focus in the cerebral cortex presents great difficulties, which can sometimes be overcome only through comprehensive studies.

Topical diagnosis of peripheral nervous system lesions is made on the basis of motor, sensory and autonomic disorders, corresponding to the anatomical distribution of the innervation zones of the peripheral nerves, plexuses, spinal nerve roots.

Modern topical diagnostics has, in addition to the neurological examination, such research methods as computed tomography of the spinal cord and brain, nuclear magnetic resonance imaging, angiography, echoencephalography, electroencephalography, radionuclide scanning, electromyography, neuro-ophthalmologic methods of investigation, with the help of which data can be obtained , clarifying the localization of the pathological focus and the nature of neurological symptoms.

The study of pupillary reactions in the differential diagnosis of damage to the optic nerve.

Possible combined damage to the optic and oculomotor nerves, both homolateral and contralateral with respect to each other, while there are various options for violations of pupillary reactions to light.

With combined homolateral damage to the optic and oculomotor nerves, anisocoria will be observed, on the side of injury, mydriasis with no direct and friendly reaction (due to a violation of the afferent and efferent parts of the pupillary reflex), the direct side will be caused and no friendly reaction will occur. With a combined contralateral damage to the oculomotor and optic nerves, another picture is noted: anisocoria, on the side of the damage to the oculomotor nerve - mydriasis with no direct and friendly reaction (violation of the efferent link), on the side of the damage of the optic nerve - changing pupil sizes depending on the light of the opposite retina, no direct reaction with the safety of the friendly (violation of the afferent link).

In all these cases, the key to diagnosing damage to the optic nerve will be the state of a friendly reaction to light on its or opposite side.

Undoubtedly, clinical detection of optic nerve damage is possible at a stage when there are only unilateral pupillary disorders.

Fig. 3 Pupillary reactions in normal and damage to the optic and oculomotor nerves (Yeolchiyan SA, 1996)

Sensitivity - the body's ability to perceive irritation emanating from the environment or from its own tissues and organs. Teaching I.P. Pavlov on analyzers laid the foundation for a natural science understanding of the nature and mechanisms of sensitivity. Each analyzer consists of a peripheral (receptor) department, a conductor part and a cortical department.

Receptors are special sensitive formations that can sense any changes inside or outside the body and transform them into nerve impulses.

Thanks to the specialization of receptors, the first stage of the analysis of external stimuli is carried out - decomposition of the whole into parts, differentiation of the nature and quality of signals. In this case, all types of external energy, transforming into nerve impulses, enter the brain in the form of signals.Depending on the functional characteristics, receptors are divided into exteroreceptors (located in the skin and informed about what is happening in the environment), telereceptors (contained in the ears and eyes), proprioceptors (provide information about muscle and tendon tension, movements and body position) and interoceptors (“ reporting "condition inside the body). There are also osmo-, chemo-, baroreceptors, etc.

Skin receptors are divided into mechanoreceptors (touch, pressure), thermoreceptors (cold, heat) and nociceptive receptors (pain). These receptors are many in the skin, especially between the epidermis and connective tissue, so the skin can be considered as a sensitive organ covering the entire surface of the body. It contains free nerve endings and encapsulated terminal formations. Free nerve endings are located between the epidermal cells and perceive pain irritations. Lamellar calves Vater-Pacini, located in the deep layers of the skin, perceive pressure. Krause flasks are considered cold receptors, and Ruffini bodies are thermal.

Receptors are also found in deeper tissues: muscles, tendons, fascia, joints. Muscle receptors include several types, the most important of which are neuromuscular spindles. They respond to stretching the muscles and are responsible for the implementation of the stretching reflex.

Golgi-Mazzon bodies are thick myelin fibers, “wound” around groups of collagen tendon fibers, surrounded by a connective tissue capsule. They are located between the tendon and the muscle. Like muscle spindles, they respond to tension, but the threshold of their sensitivity is higher.

The encapsulated, more differentiated bodies, obviously, provide epicritical sensitivity, a sense of light touch, vibration, pressure. Free nerve endings provide protopathic sensitivity, such as differences in pain or temperature.

Receptors are peripheral endings of afferent nerve fibers, which are peripheral processes of pseudounipolar neurons of the spinal ganglia. In this case, the fibers emanating from the neuromuscular spindles and having a thick myelin sheath, occupy the most medial part of the dorsal root. The middle part of the spine is occupied by fibers emanating from encapsulated receptors. The most lateral fibers are almost not myelinated and carry out pain and temperature impulses. Only some of the impulses coming from the muscles, joints, fascia and other tissues reach the level of the cerebral cortex and are realized, most of the impulses are needed to automatically control the motor activity necessary for standing or walking.

Passing into the spinal cord through the dorsal roots, the individual fibers are divided into numerous collaterals, which provide synaptic connections with other spinal cord neurons. All afferent fibers passing through the entrance area of ​​the dorsal roots lose the myelin coating and go in different paths depending on their sensitive modality.

The conductor part of the analyzer is represented by spinal nodes, nuclei of the spinal cord, brain stem, various thalamic nuclei, as well as such formations as the reticular formation, structures of the limbic system, and the cerebellum. The afferent impulses received by the central nervous system propagate, primarily, along specific projection paths of a given sensory modality and are switched in the corresponding nuclei of the diencephalon. The axons of the neurons of these nuclei reach the sensory zones of the cortex, where the highest analysis of afferent information occurs within the limits of this analyzer. In the cortical parts of the analyzer, there are neurons that react only to one sensory stimulation. These are specific projection neurons.Next to them are non-specific nerve cells that respond to various sensory stimuli. At the level of the midbrain, collaterals depart from the fibers of specific sensory pathways, along which excitation radiates to the reticular formation and non-specific nuclei of the thalamus and hypothalamus. It has been established that the reticular formation, as well as other subcortical structures, has an ascending activating generalized effect on the cerebral hemisphere. After processing at the level of the cortical end of the analyzer, the impulses can radiate both horizontally via the intercortical and intracortical pathways, and vertically along the corticofugal paths to the nonspecific structures of the trunk. The activity of the analyzer includes the reverse effect of higher departments on the receptor and conductor parts of the analyzer. The sensitivity of the receptors (the sensing part), as well as the functional state of the transfer relays (the conductor part) are determined by the downward effects of the cerebral hemispheres cortex, which allows the body to actively select the most adequate sensory information at a given moment.

The most common during the neurological examination is the following classification of sensitivity:

  • surface (exteroceptive) - pain, temperature and tactile sensitivity,
  • deep (proprioceptive) - musculo-articular, vibration sensitivity, feeling of pressure, body weight, determining the direction of movement of the skin fold (kinesthesia),
  • complex forms of sensitivity: a sense of localization of the injection, touch,
  • sensation due to stimulation of receptors of internal organs (interoceptive sensitivity).

Exteroceptive sensations are those that form in sensitive formations of the skin or mucous membranes in response to external influences or environmental changes. Otherwise they are called superficial (or skin) and emanating from the mucous membranes, types of sensitivity. There are three leading varieties: pain, temperature (cold and heat) and tactile (with a light touch).

Proprioceptive sensitivity comes from the deep tissues of the body: muscles, ligaments, tendons, joints and bones.

Different types of sensitivity correspond to different paths. In the spinal nodes located cells of peripheral neurons of all types of sensitivity. The first neuron conducting impulses of pain and temperature sensitivity are pseudo-unipolar neurons of the spinal nodes, the peripheral branches of which (dendrites) are thin myelin and non-myelin fibers directed to the corresponding skin (dermatome). The central branches of these cells (axons) enter the spinal cord through the lateral part of the dorsal roots. In the spinal cord, they are divided into short ascending and descending collaterals, which after 1-2 segments form a synaptic contract with the nerve cells of the gelatinous substance. This is the second neuron that forms the lateral spin-talamic pathway.

The fibers of this path pass through the anterior commissure into the opposite half of the spinal cord and continue in the outer part of the lateral cord, and then up to the thalamus. The fibers of both spinal-thalamic pathways have somatotopic distribution: those that come from the pelvic limbs are located laterally, and those that come from the more cranial parts, the medial-eccentric arrangement of long conductors. The lateral spinal-thalamic path ends in the ventrolateral nucleus of the thalamus. From the cells of this nucleus originate the fibers of the third neuron, which are directed through the posterior third of the back leg of the inner capsule and the radiant crown to the cortex.In the postcentral gyrus there is a somatotopic distribution, similar to the somatotopic projection of certain parts of the body in the precentral gyrus.

The course of the fibers conducting pain sensitivity from internal organs is the same as that of somatic pain sensitivity fibers.

Conducting tactile sensitivity provides spinal thalamic tract. The first neuron is also the cells of the spinal node. Their moderately thick myelinated peripheral fibers terminate in certain dermatomes, and the central branches pass through the posterior root to the posterior cord of the spinal cord. Here they can climb 2-15 segments and form synapses with neurons of the posterior horn on several levels. These nerve cells make up the second neuron, which forms the spinal-talamic tract. This tract intersects the white commissure ventrally from the central canal, goes to the opposite side, continues in the ventral cord of the spinal cord, rises through the brainstem and ends at the ventrolateral thalamus nucleus. The thalamic nerve cells are the third neuron that conducts impulses to the postcentral gyrus through the thalamocortum.

The animal is aware of the position of the limbs, movement in the joints, feels the pressure of the body on the limbs. Proprioceptive impulses emanate from the receptors of muscles, tendons, fascias, joint capsules, deep connective tissue and skin. They go to the spinal cord first along the dendrites, and then along the axons of the pseudo-unipolar neurons of the spinal nodes. After giving collaterals to the neurons of the dorsal and ventral horns of the gray matter, the main part of the central branches of the first neuron enters the dorsal cord. Some of them go down, others go upward in the medial thin bundle (Gaulle) and lateral wedge-shaped bundle (Burdaha) and terminate in their own nuclei: thin and wedge-shaped, located on the dorsal side of the tire of the lower part of the medulla. The fibers rising in the composition of the dorsal cords are arranged in somatotopic order. Those of them that conduct impulses from the rear half of the body, go in a thin beam, adjacent to the rear median sulcus. Others conducting impulses from the chest, forelimbs and neck, are held in the composition of the wedge-shaped bundle, and the fibers from the neck are located most laterally. Nerve cells in the thin and wedge-shaped nuclei represent the second neuron conducting impulses of proprioceptive sensitivity. Their axons form the bulbotalamic path. It first goes anteriorly over the cross of the descending pyramidal paths, then crosses the midline as a medial loop and rises backwards from the pyramids and medially from the lower olives through the tire of the medulla oblongata, the bridge and the midbrain to the ventrolateral thalamus nucleus. The nerve cells of this nucleus are the third neuron. Their axons form the thalamocortical path that passes through the posterior third of the posterior pedicle of the inner capsule and the radiant crown of the white matter of the brain and ends in the postcentral gyrus (fields 1, 2, 3) and the upper parietal lobe (fields 5 and 7). Somatotopic organization persists throughout the course of the fibers to the thalamus and cortex.

Not all afferent impulses are transmitted by the thalamus to the sensitive area of ​​the cortex. Some of them end in the motor area of ​​the cortex. To a certain extent, motor and sensory cortical fields overlap, so we can speak of the central gyrus as a sensorimotor area. Sensitive signals here can be immediately converted into motor reactions. This is due to the existence of sensorimotor feedback loops. The pyramidal fibers of these short circles usually terminate directly on the cells of the ventral horns of the spinal cord without intercalary neurons.

Impulses emanating from the muscle spindles and tendon receptors are transmitted by more rapidly conducting myelinated fibers. Other proprioceptive impulses emanating from the receptors in fascia, joints and deep layers of connective tissue are carried along less myelinated fibers. Only a small portion of proprioceptive impulses reach the cortex of the cerebral hemispheres and can be analyzed. Most pulses propagate through feedback loops and do not reach this level. These are elements of reflexes that serve as the basis for voluntary and involuntary movements, as well as static reflexes opposing gravity.

Part of the impulses from the muscles, tendons, joints and deep tissues goes to the cerebellum along the spinal cerebellum. In addition, cells are located in the dorsal horn of the spinal cord, the axons of which occupy the lateral cord, along which they ascend to the neurons of the brain stem. These pathways — the dorsal-buccal, dorsal-reticular, dorsal-olivic, and dorsal-predoor — are connected to the feedback rings of the extrapyramidal system.

The reticular formation plays the role in conducting sensitive impulses. In its entirety, spinal-reticular axons and collaterals of the spinal-thalamic pathways approach the reticular formation. Spinal-reticular pathways, conducting impulses of pain and temperature sensitivity and certain types of touch, discharging into the reticular formation, enter the thalamus and then into the cerebral cortex. The difference between proto-and epicritic sensitivity may be partly due to the quantitative difference and distribution of fibers of the reticular formation between sensory pathways.

In the thalamus pain, temperature and other types of sensitivity are perceived as vague, indefinite sensations. When they reach the cortex of the big hemispheres, they are differentiated by consciousness into different species. Complex types of sensitivity (discrimination - distinguishing between two points, precise determination of the location of a separate irritation, etc.) are the product of cortical activity. The main role in the conduct of these modalities of sensitivity belongs to the dorsal cords of the spinal cord.

Research methodology

The study of surface sensitivity. To check pain sensitivity, pinching the skin and phalanges of the fingers. They use a conventional needle or hemostatic clamp, which is much more effective. Pay attention to the behavior of the animal - its desire to bite the verifier.

The study of deep sensitivity. Musculo-articular feeling is checked as follows: it is necessary to put the animal on the limb, the checked limb is placed not on the fingertips, but on the back side. Normally, the dog resists trying to put the limb wrong.

Disorders of sensitivity. Pain sensation is the most frequent symptom of the disease and the reason for seeking medical attention. Pain in diseases of the internal organs occurs due to impaired blood flow, spasm of smooth muscles, stretching the walls of hollow organs, inflammatory changes in organs and tissues. The defeat of the brain substance is not accompanied by pain, it occurs when the irritation of the membranes, intracranial vessels. Pain sensitivity is practically not represented at the cortical level (irritation of the cortex does not cause pain), therefore, they believe that the thalamus is the highest center of pain sensitivity, where 60% of neurons in the respective nuclei clearly respond to pain stimulation. Thus, the spinotalamic system plays an important role in organizing generalized responses to the action of pain, temperature and tactile stimuli.

Pains occur in various pathological processes in organs and tissues due to the stimulation of sensitive fibers (somatic and vegetative) of the nerve trunks and roots, have a projective nature, i.e.they are felt not only in the place of irritation, but also distally, in the region innervated by these nerves and roots. Phantom pains in the missing limb segments after amputation and central pains, especially agonizing with the defeat of the thalamus, are also projective. Pain can be radiating, i.e. extending from one of the branches of the nerve to the other, not directly affected. The pain can manifest itself in the zone of segmental innervation or in a remote area, in the zone directly connected with the pathological focus, as reflected. Painful repercussion is carried out with the participation of cells of the spinal nodes, gray matter of the spinal cord and brain stem, the autonomic nervous system and receptors in the area of ​​irritation. Repercussion is manifested in the reflection zone by various phenomena: vegetative, sensitive, motor, trophic, etc. Reflected painful zones Zakharyin - Geda occur during irradiation of irritation to the corresponding zone on the skin for diseases of internal organs

It is important to study the muscles and nerve trunks by their palpation and stretching. When neuralgia and neuritis can be detected their pain. Palpation is produced in those places where the nerves are located close to the bones or to the surface (pain points).

Sensory impairment can be described as hypoesthesia - decrease in sensitivity, anesthesia - lack of sensitivity, dysesthesia - distortion of perception of irritation (tactile or thermal irritation is felt as pain, etc.), analgesia - loss of pain sensitivity, topanesthesia - lack of localization, thermoesthesia - lack of temperature sensitivity, hyperesthesia or hyperalgesia - increased sensitivity, hyperpathy - increased excitability threshold (mild irritation not perceived at higher - there is an excessive intensity and persistence of sensations), paresthesia - incorrect recognition irritation, phantom pain - a feeling of missing part of the limb.

Topical diagnosis of sensitivity disorders. Syndromes of sensitivity disorders vary depending on the localization of the pathological process. The defeat of the peripheral nerves causes the neural type of sensitivity disorder: pain, hypoesthesia or anesthesia, the presence of pain points in the innervation zone. All kinds of sensitivity are violated. The zone of hypoesthesia that is detected in case of damage to this nerve is usually smaller than the zone of its anatomical innervation, due to overlap by the adjacent nerves. Neuralgia is noted - pain in the area of ​​the affected nerve, sometimes hyperpathy, hyperalgesia or causalgia. The pain intensifies with pressure on the nerve, agitation (trigeminal neuralgia). Pleksalgichesky type (with defeat plexus) - pain, symptoms of nerve tension coming from the plexus, sensitivity disorders in the area of ​​innervation. Usually, there are also movement disorders. Radicular type (with damage to the dorsal roots) - paresthesia, pain, impairment of all types of sensitivity in the corresponding dermatomes, symptoms of root tension, pain in the paravertebral points and in the area of ​​the spinous processes. If damaged roots innervate the limb, hypotension, areflexia and ataxia will also be noted. For the loss of sensitivity on the radicular type requires the defeat of several adjacent roots.

With damage to the central nervous system (spinal cord, brainstem, thalamus, cortex of the postcentral gyrus and parietal lobe), the following sensitivity disorders are observed:

  • Segmental sensitivity disorders, a dissociated type of sensitivity disorder - a violation of pain and temperature sensitivity in the corresponding dermatomes with the preservation of deep and tactile sensitivity. Usually observed with syringomyelia.
  • Dermatomes correspond to certain segments of the spinal cord, which is of great diagnostic value in determining the level of its lesion.
  • The tabular type of sensitivity disorder (with the defeat of the dorsal cords) is a violation of deep sensitivity with the preservation of surface sensitivity, sensitive ataxia.
  • Sensory disorders in Brown-Sekar syndrome (in the case of a lesion in half of the spinal cord) are a violation of deep sensitivity and movement disorders on the affected side, and surface sensitivity on the opposite side.

The conductive type of disorder of all types of sensitivity below the level of damage (with full transverse damage of the spinal cord) is para-anesthesia. An alternating type of sensitivity disorder (with damage to the brain stem) - hemianesthesia of superficial sensitivity in the opposite limb focus with a lesion of the spinal-talamic path along the segmental type on the face on the side of the focus with defeat of the trigeminal nerve. Thalamic type of sensitivity disorder (with damage to the thalamus) - hemihypesthesia in the extremities opposite to the center on the background of hyperpathy, prevalence of deep sensitivity disorders, If the sensitive paths in the posterior pedicle of the inner capsule are affected, all kinds of sensitivity on the opposite half of the body (hemihypesthesia or hemianesthesia) are affected.

The syndrome of muscular-articular sensitivity may manifest itself as afferent paresis, i.e. disorders of motor functions, which are caused by a violation of muscle and joint feeling. It is characterized by a disorder of coordination of movements, slowness, awkwardness when performing an arbitrary motor act, hypermetry. Afferent paresis syndrome may be one of the signs of damage to the parietal lobe. Afferent paresis with damage to the dorsal cords of the spinal cord is characterized by spinal ataxia: movements become disproportionate, inaccurate, and when performing a motor act, muscles that have no direct relation to the movement performed are included. The basis of these disorders is a violation of the innervation of agonists, synergists and antagonists.

Mechanism of regulation of movement

When starting treatment of patients with neurological disorders, it is first necessary to establish whether there is a history of changes in posture and gait, as well as to investigate these functions during the examination. Changes in posture and gait can occur as a result of damage to the nervous system at various levels, and often the type of clinical change indicates the localization of the lesion.

Formations of the nervous system, controlling standing and movement. The formations of the central nervous system that control the standing position and the setting of the extremities are the basal nuclei, the “locomotor zone” of the midbrain, the cerebellum and the spinal cord. The cerebral cortex undoubtedly plays an important role, however, in animal experiments with complete removal of the cerebral cortex in the neonatal period with preservation of the basal nuclei, the visual mound and the underlying formations, standing and walking remain possible. Electrical stimulation of the so-called locomotive zone of the midbrain leads to the appearance of movements characteristic of walking, and the speed and manner of movements can vary from slow walking to fast walking or running, respectively, according to changes in the intensity of stimulation. This zone receives projections from the basal nuclei, including the subthalamic and endopeduncular nuclei and the black substance.

Nerve formations that coordinate muscle movements are located in the spinal cord. After an experimental transection of the spinal cord at the level of the middle thoracic segments, the hind limbs, placed on a moving walkway, retain the ability to perform coordinated movement.With an increase in the speed of movement, the paths of movement change and resemble those when running. With a high transection of the spinal cord, both upper and lower limbs can generate consistent alternating movements. Thus, the nervous system of the spinal cord can coordinate the movements of all four limbs. Many movements necessary for movement are controlled by the cerebellum, and its removal leads to marked disorders of standing and movement.

Thus, movement is the result of joint activity of the basal nuclei, the midbrain, the cerebellum and the spinal cord.

Brain stem damage

Corticospinal (cortical-cerebrospinal) anterior (straight) and lateral (crossed) from pyramidal neurons of the pyramidal and extrapyramidal cortex, which provide for the regulation of voluntary movements) and the red-core-spinal, or rubrospinal, path (tractus rubrospinalis) consists of axons of the red core neurons. Immediately after leaving the nucleus, these axons pass to the symmetrical side and are divided into three beams. One goes to the spinal cord, the other goes to the cerebellum, the third goes to the reticular formation of the brain stem.

The neurons that give rise to this path are involved in the management of muscle tone. Rubromocerebral and rubroreticular pathways provide coordination of the activity of pyramidal neurons of the cortex and neurons of the cerebellum involved in the organization of voluntary movements. Sensitive signals from the movements of the joints and the afferent apparatus of the muscles provide important components of movement control. Without relevant sensitive feedback-type information, the gait can vary significantly.

PFK - prefrontal cortex. MK - motor cortex. DMK - additional motor cortex. PMK - premotor cortex. LMZ - mesencephalic locomotor zone. LVE - lateral vestibular nucleus. MYFF - medullary reticular formation. PT - pyramidal tract. PCT - reticulospinal tract. VST - vestibular tract.
I - spinal level of regulation. II - stem-cerebellar level of regulation. III - highest (cortical-subcortical) level of regulation.

Cerebellum. The cerebellum itself does not initiate movements, however, interacting with the motor cortex, basal nuclei and certain stem formations, it participates in the control of the performance of most movements. The cerebellum is needed to maintain proper body position and stability when walking and running, to perform subtle targeted movements, eating, to quickly perform alternating repetitive movements to coordinate follow-up targeted eye movements. The cerebellum controls some movement quality indicators, such as direction, speed, and acceleration. Arbitrary motions may also exist when the cerebellum is disturbed, but they will be awkward and disorganized. Movement disorders caused by impaired activity of the cerebellum are called dyssynergies (as well as asnergy or ataxia).

The cerebellum consists of a centrally located worm and two hemispheres adjacent to the medulla oblongata, the bridge and the midbrain, and connecting to them with the help of three legs on each side. The surface of the cerebellum covers the cerebellar cortex or layer of gray matter surrounding the white matter located inside. Inside the cerebellum there are three pairs of deep nuclei of the cerebellum, the order of their arrangement from the center to the periphery is as follows: the nucleus of the tent, the interstitial (corky and spherical) and the dentate nucleus.

The cerebellum consists of three lobes. Klochko-nodular lobe, phylogenetic is the oldest part of the cerebellum, consists of a paired shred and nodule. It receives projections mainly from the vestibular nuclei. The anterior lobe, also the old part of the cerebellum, consists of a worm and formations located near it in the anteroposterior part of the cerebellum. It receives projections mainly from the spinal cord.The posterior lobe is the largest and phylogenetically youngest part of the cerebellum and is located between the two other lobes. The posterior lobe receives projections from the cerebral hemispheres through the nucleus of the bridge.

The cerebellar cortex consists of three layers: the surface molecular layer, the middle layer of Purkinje cells and the inner granular layer. Afferent fibers reaching the cerebellar cortex send collateral projections into the deep nuclei of the cerebellum and end either in the granular layer as moss-like fibers or on Purkinje dendrites in the form of creeping fibers. Afferent signals to moss fibers come from the spinal cord, the nucleus of the bridge, the vestibular receptors, the nucleus of the trigeminal nerve, the reticular formation and the deep nuclei of the cerebellum. Afferent innervation to creeping fibers comes exclusively from the lower olives. The impulses coming to moss and creeping fibers are exciting for the deep nuclei of the cerebellum and the cerebellar cortex. Purkinje cells provide the only way for all information emanating from the cerebellar cortex, and are exciting for the deep cerebellar and vestibular nuclei.

The cerebellum also receives projections from the bluish location and the nuclei of the brain stem seam. Afferent projections to the cerebellum from a bluish site are noradrenergic, from suture nuclei are serotonergic, and both of them have a inhibitory effect. The putative cerebellar neurotransmitters are some amino acids: glutamic, used by granular cells, aspartic, used by creeping fibers, and gamma-aminobutyric, used by Purkinje, Golgi, and basket cells.

The lower leg of the cerebellum (the cord body) consists mainly of afferent fibers. In the pedicle passes one efferent path, tent-bulbar, containing projections to the vestibular nuclei and the final vestibular circle passing through the cerebellum. Afferent fibers come to the lower leg of the cerebellum from at least six sources: fibers from the vestibular nerve and its nuclei, fibers of the olive cerebellar pathway from the lower olivary nuclei, posterior spinal cord pathway, some of the fibers of the posterior spinal cord pathway, sphenoid-cerebellar bundle from the accessory core of the sphenoid beam in the medulla oblongata, reticulocerebellar fibers. The middle leg of the cerebellum consists almost entirely of crossed afferent fibers extending from the nuclei of the bridge in the gray matter of the base of the bridge (bridge-bridge or transverse fibers of the bridge). Leading projections come from the cerebral cortex to the nucleus of the bridge. The upper leg of the cerebellum consists mainly of efferent projections of the cerebellum. From the toothed and intermediate nuclei, projections are directed toward the red nucleus, the optic tubercle, and the reticular formation. Part of the fibers of the tent-bulbar path is also for some time in the upper leg, before it reaches the lower leg of the cerebellum. The upper leg of the cerebellum contains afferent projections of the anterior spinal cerebellar pathway and projections into the cerebellum from the nucleus of the trigeminal nerve.

With the exception of direct projections of Purkinje cells into the vestibular nuclei, the efferent pathways of the cerebellum begin from the deep nuclei. Fibers extend from the tent core to the vestibular nuclei and nuclei of the reticular formation of the brainstem.

These nuclei are projected into the spinal cord and are related to the management of body position in space and stability. Intermediate nuclei from each side send axons through the upper legs of the cerebellum to the red nucleus of the opposite side. The red nucleus communicates with the spinal cord via the red-spinal cord path. This path crosses the midline and goes down to the spinal cord. The beginning of this pathway in the intermediate nuclei and the end of it in the spinal cord are on one side.The dentate and intermediate nuclei send projections through the upper pedicle of the cerebellum to the contralateral ventrolateral nucleus of the optic tubercle. The ventrolateral nucleus gives projections to the motor zones of the frontal lobe on the same side. The endings of the fibers extending from the optic hillock form in the cerebral cortex connections with cortico-spinal neurons, the efferent fibers of which pass through the pyramidal pathway and pass to the opposite side in the spinal cord. Thus, the beginning of the cerebellar-talamokorkov path in the dentate and intermediate nuclei and its end in the spinal cord are on the same side.

For clinical purposes, the method of describing the cerebellum is adopted, based on the presence of longitudinal sagittal zones. Each half of the cerebellum is divided into three longitudinal stripes located in the direction from the center to the periphery, they include the cerebellar cortex, the adjacent white matter and the deep nuclei of the cerebellum. There is a median zone consisting of a worm area and a tent core, an intermediate zone including formations located around the worm and intermediate nuclei, a lateral zone consisting of the cerebellar hemisphere and a dentate nucleus.

Lesions of the median zone lead to changes in posture and gait, body ataxia and instability during movement, as well as forced turning or drooping of the head. Damage to the lateral zone leads to impaired coordination of movements in the limbs (ataxia), dysarthria, hypotension, nystagmus and kinetic tremor. Damage to the intermediate zone causes symptoms characteristic of damage to both (median and lateral) zones.

Ataxia occurs as a result of dismetry and disproportion of movements.

Dismetry refers to a violation of the direction or position of a limb during active movement, in which the limb descends before reaching the goal (hypometry), or advances beyond the goal (hypermetry). Disproportion of movements means errors in the sequence and speed of individual components of the movement. As a result, there is a loss of speed and dexterity of movements that require the smooth joint activity of various muscles. The movements that were so smooth and precise become uneven and inaccurate. Clinically, ataxia is presented as a violation of the pace and volume of individual movements, and usually occurs when the cerebellum is damaged or when various types of sensitivity are impaired. Ataxy of walking is characterized by uneven pace, duration and sequence of movements with swaying from side to side.

Physiological reactions that are important for standing and movement

The position is held by means of numerous mechanisms that react to changes in postural reflexes: local static reactions of individual limbs, segmental static reactions ensuring consistency of movements, general static reactions that occur when the head moves in space. Local static reactions include muscle stretching reactions and positive position holding reactions. The simplest stretch reflex muscle can be represented as muscle tension (deep tendon reflex), a short-term muscle contraction caused by the sharp tension of the muscle tendon. Keeping the muscle in a state of stretching leads to a long-term contraction of this muscle, due to the stretch reflex. The positive reaction of holding the position in animals is due to the contact of the skin of the fingertips, as well as the tension of the intercostal muscles, leading to the emergence of proprioceptive stimulation. As a result of this irritation, an extension push in the limb occurs.

The segmental static reactions include a cross extensor reflex and consistency of limb movements.With a cross extensor reflex, excessive irritation of the limb leads to its flexion and simultaneous extension of the opposite limb. With more intense stimulation, the cross-extensor reflex, triggered by the affected hind limb, can cause flexion of the opposite forelimb and extension of the homolateral forelimb. Thus, the entire torso moves diagonally due to the extension of the contralateral hind limb and the homolateral forelimb, removing the irritated limb from the source of irritation. This diagonal nature of coordinated movements provides a change in body position in various situations.

General static reflex reactions are divided into two types. In the first case, the tonic cervical and labyrinth reflexes jointly regulate the position of the body during various head movements relative to the body, in the second, the reflex reflex occurs during labyrinth, cervical and visual stimuli and helps the animal to restore its vertical position after a fall.

Among other types of general static reactions are reflexes of position and jumping, as well as regulation of body position during movement of the limbs. Damage to the cerebellum and its connections lead to considerable difficulties in standing the animal and moving without assistance. Difficulties are compounded when trying to follow a narrow line. A dog or a cat usually stand with its legs wide apart (especially its hind legs); standing by itself can cause staggering, large-scale movements of the body forward and backward or fall. Some patients can not get food because they do not fall into the bowl muzzle. Instability persists with open and closed eyes. With unilateral cerebellar lesions, the dog falls toward the lesion.

When a lesion is limited to the median formations of the cerebellum (worm), such as cerebellar degeneration, postural changes and gait can occur without other cerebellar disorders, such as ataxia or nystagmus. In contrast, with the lesion of the cerebellar hemispheres, unilateral or bilateral, gait disturbances often occur in combination with ataxia and nystagmus. With the defeat of one hemisphere of the cerebellum gait changes are often accompanied by a violation of postures and movements on the side of the lesion. On the side of the lesion, a decrease in the resistance of the limb in response to passive movements (hypotension) is revealed.

Sensitive ataxia. A characteristic change in gait develops with loss of sensation in the limbs, resulting from damage to the peripheral nerves, dorsal roots, dorsal columns of the spinal cord, or medial loop. The greatest difficulties arise in the loss of the feeling of passive movements in the joints, a certain contribution is also made by the interruption of afferent signals from the receptors of the muscle spindles, vibration and skin receptors. Animals with sensitive ataxia do not feel the position of the extremities, therefore they have difficulties both when standing and moving, they usually stand with widely spaced limbs, depending on the degree of damage, can maintain balance, they stagger and often fall. Dogs and cats with sensitive ataxia spread their paws wide when moving, raise them higher than necessary, and sway back and forth swiftly. The steps are different in length. The defeat of peripheral motoneurons or nerves leads to the appearance of weakness in the distal extremities. With peripheral motoneuron lesions, weakness in the limbs develops in combination with fasciculations and muscle atrophy.

Reflect the results of a neurological examination can be in a similar form of neurological examination.

Neurological Examination Sheet

Owner ___________________________ Species animal _______________________

Nickname ____________ age _______________ Paul ________________________

Patellar reflex LION Nor. Amp, donkey, ots, pseudo-amplification. ETC. Nor Usil, donkey, ots, pseudo-amplification.

Reflex on the sciatic nerve LION Nor. Force, donkey, OTC. Norm ETC. Nor Usil, donkey, ots ,.

Reflex on the big spit LEV Pris, cont. ETC. Pris, Ots.

Reflex with Achilles tendon LEO Usil, donkey, ots, Nor. ETC. Amp, ass, ots ,. Nor

Shin reflex. A LION. Present, absent. ETC. Present, absent

Pull-up reflex

Pelvic limb right Normal Strengthened, weakened, absent,

Thoracic limb right Normal Strengthened, weakened, absent,

Pull-up reflex

pelvic left Normal Strengthened, weak, absent,

chest Normal Strengthened, weak, absent,

Reflex with the triceps muscle of the shoulder. Leo Nor Usil, donkey, ots, PR. Nor Force, ass, ots,

Reflex with the biceps muscle of the shoulder LION Strengthened, donkey, ots, PR. Force, ass, ots,

Reflex with Panniculus (pannicular reflex). A LION ___________________. ETC. __________________

Reflex with the muscles of the abdominal wall LION Nor Usil, donkey, ots, PR. Nor Force, ass, ots,

Reflex from the anal area. Normal Strengthened, weakened, absent,

Corneal reflex. LEO, Nor donkey, Ots, PR. Nor, donkey, ots,

Pupillary reflex to light LION, Nor donkey, Ots, PR. Nor ass, ots,

friendly reaction of pupils to light Normal. Weakened. Missing

Facial sensitivity. Leo Nor Usil, donkey, ots, PR. Nor Force, ass, ots,

Reflex threat Normal, Sluggish. Missing.

Fundus vessels _______________________ Nystagmus __________________________

Conscious proprioception LION pelvic Nor, donkey, ots, PR.tazovaya. Nor, donkey, ots,

Conscious proprioception LION thoracic Nor, donkey, ots, PR. pectoral. Nor, donkey, ots

Reaction to the appeal ____________________________________________________________

Pain sensitivity of the tibial nerve (sciatic branch). (Plantar surface of the foot). LION, donkey, ots, Nor. PR., Donkey, ots, Nor

(peroneal nerve) (cranial surface of the foot). LION, donkey, ots, Nor. PR., Donkey, ots ,. Nor

The subcutaneous nerve is a branch of the femoral nerve (the second finger of the hind paw)). LION, donkey, ots, Nor. PR., Donkey, ots ,. Nor

Radial nerve (thoracic limb.) LEO, Nor. Osl, Ots, Pr.Nor, Ass, Ots,

The state of the muscles of the limbs ___________________________________________________________

Degree of neurological disorders

  • I degree - pain
  • Grade II - pain, impaired limb setting, (impaired proprioception) paresis. Retained the ability to move.
  • Grade III - pain, impaired limb setting, (impaired proprioception) paresis. No ability to move.
  • IV degree - lack of sensory and motor functions (paralysis). Saved perception of deep pain.
  • V degree - lack of sensory and motor functions (paralysis). There is no perception of deep pain (spinal cord rupture syndrome).

How to determine sciatica and what can cause it?

The following signs are characteristic of affection of the sciatic nerve:

  • pain that occurs in the lower body,
  • numbness of the limbs
  • goose bumps, burning, stinging.

An important symptom of sciatica is also paroxysmal nature of pain, when their intensity periodically changes from unbearable to weaker, sometimes up to complete disappearance for a while. A special place in the semiotics of the sciatic nerve lesion is its primary one-sidedness.

Bilateral inflammation of the nerve is quite rare, but such a course of sciatica makes a person's life in continuous torture, when the slightest movement causes a sharp unbearable pain.

Signs of sciatica may differ depending on which root has undergone pathological changes. This nerve is one of the main and most branched nerve trunks of the human body.

The nature of the pain depends on this: sharp or pulling, burning or aching, so-called “shooting-outs”.

A lesion can be caused by many reasons or even a complex of reasons:

  • various vertebral pathologies,
  • abscesses or tumors,
  • viral or toxic damage,
  • hypothermia
  • overvoltage
  • injuries.

Inflammation can also occur after an intramuscular injection into the buttock, made with a violation of the rules (when the needle touches the nerve ending or when a cold solution is injected into the muscle, etc.).

Diagnostic approaches

The symptomatology of ishiastic inflammation is rather blurred, and only a hardware diagnosis can provide an accurate clinical picture. In addition, symptomatic treatment never leads to the elimination of the cause of the disease, but only facilitates its course, especially for anesthesia.

Therefore, at the first symptoms, it is necessary to consult a doctor, who after a thorough examination, which may include fluoroscopy, and even computed or magnetic resonance imaging, will prescribe the appropriate treatment.

In order to correctly determine the etiology of the disease, differential diagnosis is necessary: ​​only after a precise determination of the cause of the pathology can treatment be given, aimed at eliminating the factors of the disease, and not its manifestations.

It is strictly not recommended to engage in self-treatment of sciatica. As already mentioned, pain along the nerve trunk can be caused by a wide variety of reasons, and self-medication can only lubricate the characteristic symptoms, which will later become an aggravating factor in the diagnosis by a specialist and make it difficult to correct treatment.

Also, delayed access to a doctor is fraught with complications, which sometimes have to be eliminated by surgical intervention - this, in particular, concerns intervertebral hernias and tumors.

And running sciatica can lead to partial paralysis of the lower limbs or disability due to the flow of vertebral pathologies into the chronic stage.

How is sciatica treated

A timely visit to the doctor helps to start conservative treatment in time, without resorting to extreme measures. With the defeat of the sciatic nerve the best result can be given only by complex therapy. Prescribed a course of drug treatment, which includes:

  • nonsteroidal anti-inflammatory drugs, mandatory painkillers (up to the injection blockade of the sciatic nerve with analgesics),
  • drugs that enhance microcirculation at the site of injury,
  • muscle relaxants.

In addition, antidepressants and anticonvulsants may be prescribed. If it is found out that sciatica has an infectious etiology, the necessary antiviral or antibacterial drugs are used.

When prescribing medical treatment of sciatica, it is necessary to take into account all side effects, as well as individual intolerance to certain drugs.

Special attention should be paid to anti-inflammatory nonsteroids: these drugs are known for their aggressive effects on the gastrointestinal tract.

In some cases, hormonal drugs are prescribed, but this is done with great care and in case of emergency. It is not recommended to use for the treatment of vitamins of group B in high dosage.

The treatment complex, in addition to medicines, also includes physiotherapeutic procedures, in particular, electrophoresis and UHF. Good effect gives acupuncture, various types of massage. Medical exercises are necessarily assigned, the main task of which is to restore normal blood circulation and muscle tone.

Yoga can also be part of a complex of medical measures in case of a sciatic nerve lesion, but beginners need to do it only under the supervision of a specialist. Necessarily important regular physical therapy exercises.

A selection of my useful materials on the health of the spine and joints, which I recommend you to look at:

Also look at a lot of useful additional materials in my communities and accounts on social networks:

Denial of responsibility

The information in the articles is intended solely for general information and should not be used for self-diagnosis of health problems or for medical purposes. This article is not a substitute for medical advice from a doctor (neurologist, therapist). Please consult your doctor first to know exactly the cause of your health problem.

Watch the video: Sciatic Nerve Pain : How to Test the Sciatic Nerve (January 2020).

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