The clinic of cervical osteochondrosis is largely due to the anatomophysiological features of the cervical spine. Degenerative changes in the disk are more common in the most mobile lower cervical spine (C5, C6, C7). There are some features in the mechanism of compression of nerve and vascular formations in cervical osteochondrosis. Due to the high density of the central section of the posterior longitudinal ligament, posterior hernias in the cervical region are extremely rare. The slip of the disk is characteristic in the lateral and posterior-lateral directions. The growth of osteophytes in the region of the hook-shaped processes of the cervical vertebrae is directed towards the channel a. vertebralis and often causes its irritation or squeezing. The latter position is confirmed by vertebral angiography. In this regard, cerebrovascular insufficiency is often triggered by turning the head and neck extension.
An important factor causing root compression is flattening of the disc, leading to a decrease in the vertical and horizontal diameters of the intervertebral foramen. At the same time, flattening of lordosis, its straightening, and even local kyphosis appear reflexively. Normally, when the neck is bent and extended, the rear edges of the bodies form a regular arc. In osteochondrosis, accompanied by a decrease in the height of the disk, such movements lead to subluxation (subluxation) in the intervertebral joints – the front corner of the upper articular process moves forward, which creates additional conditions for deformation a. vertebralis. That is why at the cervical level the clinic of osteochondrosis more often depends not on hernial protrusions, but on changes in bone structures – mainly in the form of uncovertral arthrosis.
Cervical vertebral pathology almost always makes its debut with pain or discomfort in the neck. The pain is more often paroxysmal in type of cervical backache. Lumbago is an acute pain.
Sub-arising pains are longer in time and are called cervicalgia. The active duration of the cervical muscles during periods of exacerbation of osteochondrosis enhances pain. The severity of pain in vertebral syndrome is of 3 degrees: the first degree – pain occurs only with the maximum volume and strength of movements in the spine, the second degree – the pain calms down only in a certain position of the spine, the third degree – the pain is constant.
In the clinic of cervical extravertebral pathology, so-called reflex syndromes are often found. In the origin of these syndromes, the main role is given to irritation of nerve endings in the discs. It is believed that trauma or dystrophy of the intervertebral disc does not always lead to direct compression of the roots. And in the absence of radicular symptoms, pain is possible due to sharp irritation of the ends of the synuvertebral nerve, embedded in the outer fibers of the fibrous ring and in the posterior longitudinal ligament. The result is a clear reflex muscle contracture, and pain often has the character of sympathalgia. The appearance of muscular reflex compression syndromes is also possible due to irritation of the spinal roots or paravertebral sympathetic ganglia. The most common reflex-muscular compression syndrome is Nuffziger syndrome. Among the causes of Nuffziger syndrome are osteochondrosis of the spine in the first place, the presence of an additional cervical rib in the second, and occupational overstrain of the scalene muscles in third.
Compression radicular cervical vertebrogenic syndromes
Compression of the root or radicular artery is performed by various structures. The anterior intervertebral foramen narrows due to disc herniation or osteo-cartilaginous growths with uncovertral arthrosis. The posterior part of the opening narrows with spondylarthrosis and cervicospondyloperiarthrosis. With osteochondrosis, the vertical size of the intervertebral foramen decreases. The root can also suffer with sclerosis of the vertebral artery, aseptic inflammation in the area of spider muffs, dural sacs and cuffs with an excess of the root.
Certain motor, sensory and reflex disturbances are associated with the compression of each root. Spine C1 (cranio-vertebral vertebral-motor segment) lies in the groove of the vertebral artery. It is very rarely injured with calcification of the latter, with subluxation of the atlant or Kimmerle anomaly. It manifests itself in the clinic with pain and a violation of sensitivity in the parietal region.
Spine C2 (diskless vertebral-motor segment C1-2). It is rarely involved. With damage, pain appears in the parieto-occipital region. Hypotrophy of the hyoid muscles is possible. It is accompanied by a violation of sensitivity in the parietal-occipital region.
Spine C3 (disc, joints and intervertebral foramen CII-III). It rarely affects. In the clinical picture, there is pain in the corresponding half of the neck and a feeling of swelling of the tongue on this side, language proficiency is difficult (speech and movement of food in the mouth worsen). Paresis and hypotrophy of the hyoid muscles. These disorders are caused by anastomoses of the root with the hyoid nerve. Violation of the sensitivity of the skin in the neck.
Spine C4 (disc, joints and intervertebral foramen CIII-IV). It is struck infrequently. Pain in the shoulder girdle, collarbone. Weakness, decreased tone and hypotrophy of the belt, trapezius, raising the scapula and the longest muscles of the head and neck. In connection with the presence of fibers of the phrenic nerve root, respiratory function disorders, as well as the presence of pain in the region of the heart and liver, are possible. There may be dysphonia and hiccups. Sensitive disorders in the shoulder girdle.
Spine C5 (disc, joints and intervertebral foramen CIV-V). Amazed quite rarely. Pain radiates from the shoulder to the shoulder girdle and the external surface of the shoulder. Weakness and malnutrition of the deltoid muscle. Violation of sensitivity on the outer surface of the shoulder.
Spine C6 (disc, joints and intervertebral foramen CV-VI). Frequent localization. The pain spreads from the neck to the shoulder blade, shoulder girdle along the outer surface of the shoulder to the radial edge of the forearm and to the thumb, accompanied by paresthesia of the distal area of the dermatome. Weakness and malnutrition of the biceps. Decreased or lack of reflex from the specified muscle. Sensory impairment from the lower third of the forearm along the radial edge, along the front-side surface of the thumb.
Spine C7 (disc, joints and intervertebral foramen CVI-VII). The pain radiates from the neck under the scapula along the outer-posterior surface of the shoulder and the dorsal surface of the forearm to the II and III fingers, parasthesia in the distal part of this zone is possible. Weakness and malnutrition of the triceps muscle, a decrease or disappearance of the reflex from it. Violation of the sensitivity of the skin along the outer surface of the forearm onto the hand to the back surface of the second and third fingers.
Spine C8 (disc, joints and intervertebral foramen CVII-TI). The pain radiates from the neck to the elbow edge of the forearm and to the little finger; parasthesia in the distal parts of this zone. Partial hypotrophy and a decrease in the reflex from the triceps muscle, atrophy of the muscles of the elevation of the little finger are possible. Loss of stylo-radial and instep reflexes. Violation of the sensitivity of the skin from the upper edge of the scapula along the outer surface of the shoulder and forearm to the little finger.
A characteristic feature of radicular pathology is an acute painful debut and intensification of the pain pattern with active neck movements and with the triggering of the phenomenon of the intervertebral foramen (passive tilt of the neck to the sore side).
In the treatment of radicular compression, the main focus is on root decompression and the fight against edema. To do this, it is advisable to use the extension of the cervical spine, as well as dehydrating and diuretics in the initial stages of the disease and its stationary course. Biostimulants and neurotropic drugs are prescribed in the middle of the stationary stage and with regression of the syndrome.
A – cervicalgia – intense piercing, boring or dull pain in the deep parts of the neck. This pain is most pronounced in the morning, after sleep, aggravated by turning the head, coughing, sneezing, laughing;
B – cervicocranialgia – the pain is localized in the neck and occipital region;
B – cervicobrachialgia – pain in the neck is combined with aching pain in the deep parts of the shoulder and forearms (autonomic, sclerotomic pain).
II. Muscle-tonic syndromes. Due to the constant irritation of pain receptors around degenerated intervertebral discs and joints, excitation of the segmental apparatus of the spinal cord occurs, including motor neurons (especially in the gamma-motor neuron system). This is manifested by muscle tension (in certain myotomes). Prolonged tonic muscle tension leads to a deterioration in metabolic processes, hypoxia, swelling and changes in trophic muscle areas. Palpation in such a muscle reveals areas of painful seals, heaviness. These pain points are a source of reflected pain within the segmental vegetative innervation (Zakharyin-Ged zone) and are designated as trigger zones.
Syndrome of the lower oblique muscle of the head. This muscle attaches to the transverse process of the vertebra CI and the spinous CII, providing rotation in the vertebral segment of CI-CII. The clinical picture was described by Y. Yu. Popelyansky In 1961: constant breaking pain in the cervical-occipital region, paresthesia in the back of the head, hyperalgesia in the area of the major occipital nerve invasion, painful palpation of the points of attachment of the lower oblique muscle of the head, increased pain in the cervical-occipital region head rotation in a healthy way.
Shoulder-raising syndrome (scapular-rib syndrome). This muscle is attached to the posterior tubercles of the transverse processes of the four upper cervical vertebrae and to the upper part of the medial edge of the scapula. Clinic: (aching, braining) in the neck and in the region of the upper inner corner of the scapula, in the shoulder girdle, radiating to the shoulder joint, shoulder or along the lateral surface of the chest. The pain intensifies with intense pronation of the hand, wound behind the lower back (E. S. Zaslavsky).
Local muscle cramps in cervical osteochondrosis occur in other muscles of the neck and shoulder girdle, in particular, in the trapezius, supraclavicular, sternocleidomastoid, deltoid, etc. In the study of such patients, deep palpation of all the muscles of this region is necessary.
Neurodystrophic syndromes develop with prolonged irritation of the vegetative-trophic structures of the segmental and suprasegmental apparatus.
In addition to neuromyodystrophic lesions of the muscles of the neck and shoulder girdle mentioned above, shoulder-scapular periarthrosis is quite common. In this case, the clinical picture consists of symptoms of osteochondrosis itself or deforming spondylarthrosis (straightening of the cervical lordosis, limitation of the mobility of the cervical spine, radiological data) and impaired function of the shoulder joint due to pain and contracture. Pain in the joint area intensifies at night and during movements (abduction of the arm and laying it behind the back), radiating to the neck. Palpation of the external surface of the shoulder in the area of its tubercles, coracoid process, upper edge of the trapezius muscle is painful.
With the prolonged existence of pain and limited mobility in the shoulder joint, atrophy of the deltoid, supraspinatus, and infraspinatus, subscapularis muscles develops. Hypalgesia on the outer surface of the shoulder.
Brachial epicondylosis – neurodystrophic changes in the area of the epicondyle of the shoulder, where many muscles are attached (long and short radial extensor of the hand, brachioradialis muscle, etc.). Clinic of external brachial epicondylosis: pain with contraction of the attached muscles and soreness with local palpation. The pains are intense, crippling, aggravated by jerking in the elbow or hand, especially when resisting the passive bending of an unfolded hand or supination from the position of extreme pronation. Muscle weakness in epicondylosis is determined by Thomsen’s symptoms (when trying to hold a hand clenched in a fist in the back flexion position, it quickly drops, moving to the position of palmar flexion) and Belsh (the patient simultaneously extends and supines both forearms, initially at the level of the chin in the flexion position and pronation; while on the sore side, extension and supination noticeably lags compared with the healthy side).
Vertebral artery syndrome
One of the most important structural features of the cervical spine is the presence of holes in the transverse processes of the VI-II cervical vertebrae. These holes form a channel through which the main branch of the subclavian artery passes – the vertebral artery with the sympathetic nerve of the same name (Frank’s nerve).
When the vertebral artery exits the canal, it goes to the large occipital foramen, making bends. Then, at the lower edge of the Varolian bridge, both vertebral arteries are connected, forming the main artery. The vertebral-basilar basin is connected with the carotid through the Willis circle. The vertebral artery vascularizes a vast territory: segments of the spinal cord from CI to DIII inclusive (upper medullary vascular pool), inner ear, stem structures of the brain with its reticular formation and vital centers, occipital lobes, mediobasal temporal lobes, cerebellum, posterior hypothalamic region .
The vertebral nerve (posterior cervical sympathicus or Frank’s nerve) departs from the stellate ganglion formed by the sympathetic centers of the CIII – DI segments of the spinal cord. The latter enters the canal of the transverse processes, densely braiding with its branches the vertebral artery. In addition, branches participating in the formation of Lyushka’s synuvertebral nerve depart from the vertebral nerve. The latter innervates the capsule-ligamentous apparatus of the cervical vertebral-motor segments, periosteum of the vertebrae and intervertebral discs.
Irritation of the efferent sympathetic plexus fibers causes spasm of the vessel – a compression-irritative version of the syndrome is formed. If spasm occurs in response to irritation of the receptors in the area of affected PDS, i.e., in a reflexive manner, it indicates a reflex angiospastic cerebral syndrome.
In the compression-irritative variant, the narrowing of the vessel is possible not only due to its spasm, but also as a result of mechanical action on its wall – compression of the artery. With the appearance of organic disorders from the side of brain function, they speak of the organic stage of the syndrome, and in their absence, the functional stage.
The functional stage of the vertebral artery syndrome is characterized by three groups of symptoms: headache (and concomitant autonomic disorders), cochleovestibular disorders, and visual disorders. Headache, throbbing or cerebral, aching, burning, constant and intensifying paroxysmally, especially with movements of the head, with its prolonged forced position, spreads from the back of the head to the forehead.
The patient, showing this zone on himself, makes a movement with his palm, as if removing a gas mask – a symptom of removing the helmet. The pain is reproduced or aggravated by pressure, and especially when thrashing along the vertebral artery. Other vascular points, the external carotid artery, especially the temporal branch, the orbital branch along the inner-upper corner of the orbit, are also painful on the sick side. The scalp is often painful even with a light touch, combing the hair.
Cochleovestibular disorders are also in the form of paroxysmal non-systemic dizziness (instability, swaying) or systemic dizziness. They can be combined with paracusias (noise in the ear), a slight decrease in hearing and give rise to confusion with Meniere’s disease.
Visual disturbances are limited to disorders: darkening in the eyes, sensation of sand, sparks and other photopsies, slight changes in the tone of the vessels of the fundus.
In conditions of prolonged and intense vascular spasms, it is possible to develop foci of persistent ischemia – the organic stage of the vertebral artery syndrome.
The organic stage of the vertebral artery is manifested by transient and persistent circulatory disorders in the brain and spinal cord. Transient circulatory disorders in the vertebrobasillar system are possible, as is the case with such non-vertebral disorders: short atactic disorders, nausea, impaired articulation and other loss of function from the IX-X or other cranial nerves. However, there are forms of transient cerebral ischemia, most often observed with vertebral lesions of the vertebral arteries. They often occur at the time of turning or tilting the head. This is, firstly, bouts of a sudden fall while maintaining consciousness and fainting (syncope). The first lasts for one to two minutes, the second – longer. The return of consciousness comes faster in a horizontal position. After the attack, in addition to general weakness, headaches are observed; tinnitus, photopsies, pronounced vegetative lability. Attacks are caused by paroxysmal ischemia of the brain stem, its reticular formation (with syncopal attacks) and in the area of the intersection of the pyramids (with attacks of falling).
With persistent circulatory disorders in the vertebrobasillar system, the symptoms of stem and cerebellar pathology remain persistent for at least longer than a day.
Although the clinical manifestations of both forms of vertebral artery syndrome are similar, nevertheless, reflex angiospastic syndrome has its own distinctive features. It is characterized by:
Bilateral and diffuse cerebral vegetative-vascular disorders;
The predominance of vegetative manifestations over focal;
Relatively less connection of attacks with a turn of the head;
Compression-irritation syndrome is more common in pathologies of the lower cervical spine and is combined with brachial pectoral syndromes, reflex syndrome in lesions of the upper and middle cervical levels.
Radiological data are essential. The presence of compressing factors (deformed hook-shaped processes, subluxations, etc.) indicate a possible compression of the vertebral artery.
Cervical compression myelopathy
The cervical segments of the spinal cord “bulging” or the fallen part of the disk, by the proliferation (“osteophytes”) of the vertebral body or the posterior longitudinal ligament are compressed. In most patients, the disease proceeds for a long time (for years), the symptoms increase over months and even years. In typical cases with ventral compression, the first complaints are pain, a feeling of cold or numbness, weakness in the arms and legs. The weakness of the muscles of the hands gradually increases, hypotension, atrophy and fascular twitching appear, that is, signs of damage to peripheral motor neurons for the upper extremities are detected. At the same time, pyramidal disorders are detected. Different degrees of severity of sensitivity disorder (temperature, pain) are determined by the conductor and segmental type. Vibrational sensitivity often suffers, disorders of the pelvic organs are intermittent and insignificant.
There may be mild cerebellar symptoms due to a violation of the spinocerebellar pathways. When squeezing segments C 1-2 due to damage to the trigeminal nucleus at this level, sensory impairment on the face in the caudal zones of Zelder and loss of corneal reflexes often occur. A number of authors consider Lermitt’s phenomenon of cordonal pain (the phenomenon of “electric current”) pathognomic for this suffering. When moving the head, there are unpleasant sensations of the passage of electric current from the neck in both hands, along the spine, in both legs. These painful paresthesias are regarded as symptoms of involvement of the posterior cords. With paramedian localization of compression, when the precipitated hernia is small in size and compresses the front surface of the spinal cord, the front horn, spinothalamic and pyramidal tracts are involved, on the same side. Peripheral paresis in the arm, fascicular jerking of the arm muscles on the side of the outbreak, spastic paresis of the leg are detected. Decrease in surface types of sensitivity on the side opposite to the focus. Muscular-articular feeling, as a rule, is not upset, that is, there is no complete Brown-Sekarovsky syndrome.
Cranio-vertebral anomalies (KA) are fraught with the development of various neurological complications. Intravital diagnostics of spacecraft became possible after the introduction of x-ray research methods.
In the LenGIDUV clinic over the past 15 years, V. S. Lobzin et al. 1988 studied 62 patients with various types of CA at the age of 20-50 years. Men prevailed. 55 patients were referred to the clinic with the diagnoses of multiple sclerosis, local radiculitis, cerebral arachnoiditis, brain tumor, amyotrophic lateral sclerosis, syringomyelia, and others.
The first signs of the disease appear at the age of 5-48 years,
often at 30-40 years. Patients complain of unsystematic dizziness, pain in the cervical-occipital region associated with head movement, weakness in the limbs, and wiggle and wiggle when walking.
The first assumptions about CA in most patients arose due to the presence of signs such as a short neck with a low border of hair growth in the back, rotational head installation, cervical hyperlordosis, facial asymmetry, spinal kyphoscoliosis, foot deformation, cervical ribs, etc.
All identified neurological symptoms can be grouped into a shooting range group depending on the level of damage: craniocerebral, craniocerebrospinal and spinal. At the first two levels of damage, cerebral symptoms were leading: pyramidal insufficiency, vestibulo-cerebellar symptoms, signs of increased intracranial pressure, autonomic endocrine disorders, impaired cranial nerve function, sensitivity, and a change in psyche. In second place are cerebellar disorders with a predominance of symptoms of damage to the worm and floculonodular complex. Headaches are paroxysmal with predominant localization in the parietal-occipital region and are accompanied by nausea, vomiting, and intensify with a change in head position.
With echoencephalography in some patients, there is an expansion of the third ventricle to 7 mm. The radiological signs of hydrocephalus found in 28 patients included characteristic changes in the Turkish saddle, thinning of the cranial vault, and expansion of the channels of the diploic veins. Symptom Babchina observed in 20 patients. Stagnant changes in the optic nerve disc are rare.
One of the leading symptoms is the vestibular, which is characterized by short-term non-systemic dizziness and ataxia, usually caused by head movement. This syndrome is most often of vascular origin, which is confirmed by characteristic changes in hemodynamics in the vertebro-basilar basin during rheoencephalographic examination.
Of the cranial nerves, the caudal group of nerves most often suffers, less often the optic, oculomotor and auditory nerves.
With CA, vegetative-vascular paroxysms of a more often vaginal character, a violation of carbohydrate and fat metabolism, and growth retardation are also determined. A change in the psychoemotional sphere is often expressed in asthenization, often in the patient’s depression.
Sensitivity disorders are determined by the conductor type and more often they occur with a craniocerebrospinal level of damage.
In the polymorphic structure of the clinic of the lesion of the craniocerebral and craniocerebrospinal levels, pyramidal cerebellar, pyramidal cerebellar hydrocephalic, pyramidal cerebellar-vestibular syndromes come to the fore.
The x-ray picture shows that the spacecraft are mostly combined in nature. Often revealed basilar impression of varying severity. The border lines of MacGregor ranged from 10 to 40 mm. Sometimes basilar impression is combined with complete or partial assimilation of the atlas, sometimes with platybasia, less often with convexobasia or tooth bone.
It has been established that with any type of spacecraft there is Atlas hypoplasia, which is often combined with non-closure of the posterior arch.
Cerebral disturbances in CA were caused by chronic compression of the caudal part of the brain stem due to a decrease in the size of the posterior cranial fossa due to basilar impression with a high position of the dentoid process.
Basilar impression with platibasia or convexobasia contribute to a change in the topography of the brain stem and cranial nerves, the occurrence of their traction and compression at the level of the ramp and large occipital foramen.
Partial or complete assimilation of the atlas contributes to the narrowing and deformation of the large occipital foramen and then to the compression of the medulla oblongata or upper cervical segments of the spinal cord.
In a quarter of the patients examined in the clinic, CA was combined with an Arnold-Chiari anomaly detected by pneumomyelography. An indirect sign of the Arnold-Chiari anomaly was the expansion of the spinal canal at the level of the cervical vertebrae, sometimes with an arcuate indentation along the posterior surface of the axial vertebral body and the thinning of its arc.
These changes were revealed on tomograms in the sagittal plane.
With compensatory hypermobility, a subluxation in the atlanto-axillary joint was determined, which led to a narrowing of the anteroposterior size of the spinal canal.
Consequently, neurological syndromes in CA were determined by its type. X-ray examination of the skull and cervical spine is important. Sometimes it is necessary to carry out targeted images (in the lateral projection and in the rear – through the open mouth) or tomography with functional tests (flexion and extension of the head).
Early clinical and radiological diagnosis prevents severe neurological complications and the unreasonableness of the appointment of certain physical treatment factors such as manual therapy.