What is the etiology and pathology of cervical spondylosis

  The etiology of cervical spondylosis is very complex, and although different types of cervical spondylosis have their own unique pathogenic factors, they still have their commonality. Cervical spondylosis starts slowly and is predominant in middle-aged and elderly people, especially in long-term accounting, sewing, computer operation, desk-bound workers and drivers. According to some statistics, the incidence of cervical spondylosis in different populations can range from 1.7% to 17.6%, and the incidence increases with age, with 40-60 years old as the high incidence age; the incidence of cervical spondylosis has increased, and there is a trend of youth.
  Etiology]
  The cervical spine is in a very special position, located between the more fixed thoracic vertebrae and the extremely flexible head, and is the concentration of various stresses, so it is easy for trauma, strain and degeneration to occur and lead to the occurrence of cervical spondylosis.
  1, bad habits and posture This is an important factor in the occurrence of cervical spondylosis. The posture of the human body is affected by three main factors: one is genetics, the second is disease, and the third is habit. The first two are obvious, the third factor is more hidden and difficult to intervene, which includes the influence of feelings, habits and training. To a large extent, it can be said that posture is a self-portrayal of emotions by the body. People sit, stand, walk, and lie in a way that consciously or unconsciously describes their demeanor and their response to the environment. It has been said that “posture is the organ of speech”, and this expression is very apt. Posture can show people’s inner emotions outside. For example, people who are depressed or fatigued, sitting and standing will hang their shoulders and bend their backs. When hanging the head is bound to flex the neck, so that the head moved forward, away from the center of gravity. This posture indicates fatigue and can cause fatigue, and ligament strain, increasing the burden on the neck muscle, which causes fatigue. Emotional tension and excessive movement of people, because there is no relaxation and can not lift the muscle tension, muscle is in isometric contraction, the motor function of the neck unit is a “clamp” effect; long and tedious mental activities, long time fixed position of labor, in all parts of the body is most likely to cause tension in the neck nerve – muscle – skeletal system. Such as often continuously engaged in sewing, turning, accounting, computer and playing mahjong people often have neck, back, part of the pain. Tall people try to become shorter on their own for fear of ridicule, adopting a posture of drooping shoulders and flexing the back. Girls with oversized breasts may adopt a posture of drooping shoulders. This posture can last a lifetime. Abnormal postures adopted in childhood, if not corrected consistently, may not be corrected due to structural stereotypes and have a subtle effect on the cervical spine.
  Pillows and sleep have a non-negligible impact on the cervical spine. Do not pay attention to rest and sleep science is an important cause of cervical spondylosis. The pillow is very important to people. People have to have at least 1/3 of their lives with the pillow companion. Under normal conditions, the physiological convexity of the cervical spine is the basic condition for maintaining the dynamic balance within and outside the spinal canal. High pillow, such as pillow in the occipital part of the head and neck forward flexion, can make the cervical spine curvature inversion, easy to cause fatigue of the muscles and ligaments behind the cervical spine, then the posterior wall of the dural sac in the spinal canal is stretched tight, and displaced to the front; in the long run will damage the morphology of the cervical spine and the soft tissue inside and outside the spinal canal. So the saying “no worries about high pillows” is not justified. Free pillow, so that the cervical spine in a suspended state, will also produce the same damage as the high pillow. The pillow is too low, the head and neck in supine position, especially in the lateral position, because it can not maintain the neutral position of the neck and lead to more complex physiological or pathological changes in the neck, resulting in increased neck convexity, not only the muscle in front of the vertebral body and the anterior longitudinal ligament fatigue due to excessive tension, and can cause chronic injury. The ligamentum flavum posterior to the vertebral canal can then protrude forward into the vertebral canal, increasing the pressure on the posterior part of the vertebral canal. As the spinal canal is elongated and the volume becomes smaller, the spinal cord and nerve roots become shorter instead, so that the spinal canal is in a full state. At this point, symptoms are likely to occur due to various complex factors (such as herniated nucleus pulposus or bone spur formation), and in severe cases, the nerve roots or spinal cord may be directly compressed. All poor postures aggravate the hunchback and sagging shoulders, and this posture causes the head to move forward and increases the cervical anterior convexity. The increase in neck curvature puts the cervical spine in a hyperextended position, which is the main cause of neck pain and cervical spondylosis disability.
  2, prolonged bumps and whipping-like injury car drivers account for a large proportion of patients with cervical spondylosis and lumbar disc herniation. Such as cab drivers, often in a highly concentrated state, the cervical spine is often in a forced position. The cervical vertebrae are subjected to light and heavy whip-like injuries due to emergency braking, and long-term chronic injuries accumulate various lesions of the cervical vertebrae, which eventually lead to the occurrence of cervical spondylosis. Clinically, we see young drivers of 20 years old suffering from cervical spondylosis, and X-rays show that the intervertebral space has been narrowed and changed.
  3, chronic strain Chronic cumulative injury is the root cause of cervical spondylosis. In daily activities, the cervical spine has to perform two heavy tasks of static and kinetic balance. The so-called static balance refers to maintaining the normal posture of the head and neck, standing, sitting and lying, etc.; the so-called kinetic balance refers to how to balance the pressure, tension, shear force, etc. when the neck is active. Under normal circumstances static upright spine has four physiological curves, anterior cervical convexity, posterior thoracic convexity, anterior lumbar convexity and posterior sacral convexity, in order to maintain the static balance of the spine. The cervical vertebrae 1 to 7 usually form a uniform anterior convex curve; while above C1 they are at an acute angle to keep the head in a horizontal position. Once one part of the spine is altered, the rest of the spine changes with it, thus breaking the normal static balance. When physical work and mental activity for a long time, this conjugation phenomenon will inevitably cause adverse reactions and damage to the muscle-ligament-bone because the muscle is always in a state of isometric contraction. All the bad postures, including the postures of work, life and labor, will increase the dynamic balance disorder of the neck. Especially the change of neck curvature will further cause strain on the neck muscles, tendons, ligaments, bone and joint tissues; directly or indirectly damage the intervertebral discs, ligaments, joint capsule, intervertebral joints and produce changes such as degeneration and contracture. This is the main cause of cervical spondylosis and neck pain, and is also the main factor of disability. Among intellectuals, the proportion of cervical spondylosis is very high. The reason for this is that they are too involved in their work and do not pay attention to the rhythmic way of working; or do not pay attention to the adjustment of work posture, etc., which accumulates over time and unknowingly casts cervical spondylosis. The author has seen 18-year-old students suffering from cervical spondylosis to the extent that they could not insist on attending classes.
  4.Trauma Both minor and major trauma can lead to changes in the neck tissue. In mild cases, the patient has forgotten the details of the trauma, but it has caused pathological changes in the bone and joint of varying severity, which is one of the important reasons for the occurrence of cervical spondylosis. For example, in the case of impact injury, the patient has a rapid forward displacement of the cervical vertebrae under a sudden impact that stops instantly, such as a whip-like injury, and a certain intervertebral displacement change is produced. Another example is cervical contusions caused by first landing on the head etc. during falls or cartwheels, which later produced symptoms of cervical spondylosis and visible clear changes in imaging.
  5, congenital anomalies Deformities of the bony joints, such as fused vertebrae, split vertebrae, spina bifida and other deformities can affect the morphology of the cervical spine, stress and other changes and lead to cervical spondylosis. Such as developmental spinal stenosis, although it can be peaceful for life, once there is interference (such as mild trauma, etc.), it may attack and show serious symptoms.
  There are many other factors that can lead to cervical spondylosis, so a specific analysis should be done on the patient to facilitate treatment and prevention.
  [Pathology
  1. Disorders of force balance Abnormally high stress in certain muscles, tendons, ligaments, joint capsules and other soft tissues is the most important etiology of cervical spondylosis. The neck is characterized by a weighty head on it. The neck must be supported by strong ligaments and muscle tissues in order to support the weight of the head, ensure the movement of the head and neck, and maintain the balance of the center of gravity. The function of the neck muscles can be divided into two groups, namely the head-acting muscles (extension and flexion of the head) and the neck-acting muscles (extension and flexion of the neck). The head flexors, mainly the short straight head muscles and the long head muscles. Head extension muscles, including the vertebral occipital muscles and walking longer head pinch muscles, cervical pinch muscles, and head semispinal muscles. They are rotators when contracted unilaterally and extensors when contracted bilaterally at the same time. Other muscles associated with the head and neck are extensions of the entire erector spinae muscle, acting on the cervical spine. The cervical extensors are characterized by the fact that the main muscle coverage is in the atlantoaxial region, indicating that this is the site of greater extensor stress. In contrast, the largest volume of flexor muscles is concentrated at the level of the 4th cervical vertebra, suggesting that this is the site of greatest flexion stress.
  The cervical ligaments are characterized by toughness to maintain a strong connection of the head and neck; they also have good elasticity to control the movement of the neck, and the elasticity of the ligaments has a protective effect, which protects the spinal cord and nerves from pressure and elasticity damage during movement. The head above the slender cervical spine not only has a certain weight, but also is in an eccentric position. In order to maintain the balance of the center of gravity of the head, the cervical spine, as a support, must often move to change the posture; such as balance disorders, it is easy to cause different degrees of acute and chronic injury. Among them, the muscles and ligaments bear the brunt of the impact of various stresses at all times. When the muscle fatigue and can not adapt to its load, only the ligament burden its supporting role. As a result, ligaments under abnormally high stress conditions will degenerate.
  Studies have proven that soft tissues under the continuous action of abnormally high stress, the blood vessels inside the soft tissues are squeezed and become ischemic, leading to partial tearing and bleeding of the muscle fibers and finally mechanization, forming adhesions, scarring, contractures, and even bone growth. In clinical practice, nodular and striated changes are felt in the muscle belly, and there is obvious pressure pain due to muscle injury; while tendon injury is manifested by partial rupture of degenerated tendon fibers and formation of scar; at the same time of tendon injury, the tendon peripheral structure is the first to be damaged, producing edema, congestion, inflammatory cell infiltration and other sterile inflammation. The joint capsule may thicken, and the anterior longitudinal ligament, posterior longitudinal ligament, and ligamentum flavum may also undergo hypertrophy, adhesions, contractures, and other changes. Due to the abnormally high stress pulling and squeezing of soft tissues, protective and reactive osteophytes are produced in bone tissues; ligaments and joint capsules produce pathological changes such as hypertrophy and calcification: calcification and ossification of posterior longitudinal ligaments; hyperplasia of synovial joints, vertebral labrum and posterior osteophytes. At the same time, such stress changes and spasm and contracture of soft tissues inevitably cause changes in bone structure: changes in curvature, anterior-posterior, left-right, rotational and other misalignments in mild cases; in severe cases, obvious slippage of the vertebral body is visible, resulting in changes in the morphology and position of the spinal canal, intervertebral canal, adjacent transverse foramen, hook vertebral joint and articular eminence joint, which directly affect the morphology and size of the spinal canal, intervertebral canal and transverse foramen, and thus produce effects on the They directly affect the morphology and size of the spinal canal, intervertebral canal and transverse foramen, thus producing a series of pathological changes on the spinal cord, nerve roots, vertebral artery, sympathetic nerve and the accompanying vascular traction and extrusion. The consequence of soft tissue adhesions and scar contractures is a contractural displacement of the cervical spine. Currently, the term “instability” is commonly used to express this, but what is the cause of “instability”? Is it relaxation instability, or is it spasticity or contracture instability?
  Some people divide the “instability” of the cervical and lumbar spine into three stages.
  The first stage is the dysfunctional stage, that is, the early stage of the lesion. The affected lumbar planes do not function normally, and pathological anatomy reveals slight laxity of the small joint capsule ligaments, mild fibrosis of the small joint surfaces, and mild changes in the intervertebral discs. Biomechanical testing reveals a decrease in lumbar spine stiffness and a large displacement can occur under external forces. The clinical manifestations of this stage are the least typical, and x-ray examination may reveal narrowing of the intervertebral space and manifestations of osteoarthritis in the small joints.
  The second stage is the instability stage. The affected small joint capsule is obviously relaxed, the articular cartilage is severely damaged, the disc nucleus pulposus is dehydrated, and the fibrous ring expands in all directions. At this stage, the patient may have clear clinical symptoms such as low back pain and some nerve root irritation, and increased motion of the affected segment is found on radiographic power radiographs. Biomechanical studies show that this stage is prone to disc herniation.
  The third stage is the restabilization stage. Pathological examination shows further degeneration of the small joint cartilage and discs, significant osteophytes around the small joints and discs, fixation of the deformity, and regained stability of the motion segment. Kinetic radiographs show a reduction in the range of motion of the affected segment and a re-increase in lumbar stiffness as measured by in vitro mechanics. The problem at this stage is that the various pathological changes caused by the deformed lesions and osteophytes, etc. produce irritation and compression of the various blood vessels and nerves of the spine (including the spinal cord), which can produce a series of complex clinical manifestations, commonly including spinal stenosis.
  In short, the end result remains osteophytes and soft tissue scar contractures. From the clinical point of view, trauma of different severity and strain can cause muscle spasm and stiffness of soft tissues in the neck; spasm of muscles, tendons, ligaments, and joint capsule occurs when the innervated nerves are stimulated, which in turn creates abnormally high stress in soft tissues, causing bleeding and mechanization, which can also develop into bone spurs and form osteophytes; leading to herniated discs compressing the spinal cord and nerve roots, causing nerve irritation of the anterior or posterior branch of the spinal nerve, which also The spastic response of the corresponding part of the soft tissue is also caused. The result is scar contracture of soft tissues, thickening, calcification and ossification of ligaments and joint capsule, and abnormal proliferation of bone tissue. How can the resulting displacement of the bones and joints be the result of joint laxity?! Patients often have symptoms such as stiffness, sore plate, inflexibility of movement and spasmodic pain in the neck; various shifts of the cervical spine of varying degrees can be detected, commonly rotational shifts, but also anterior-posterior, left-right and lateral rotational shifts, etc.; changes such as narrowing of the intervertebral space, narrowing of the hook vertebral joint, calcification and ossification of the ligaments can also be detected. Combining these lesions together, it is not difficult to conclude that the appearance of these pathological changes is not the result of soft tissue laxity! Quite the contrary, the information on these symptoms, signs and imaging examinations indicate that they are due to spasm or contracture of the tissues.
  It is also important to point out that the so-called re-stabilized area is no longer the original normal state, but has, as it were, a state after the joint has been fixed (fused). This inevitably produces another change in biomechanics, namely the problem of stress concentration in the joint. The stress concentration in the joint increases the tendency for separation and new instability in the area. The more segments that are fused and fixed, the amount of deformation that should have occurred in the intervertebral joints of the fixed segment has to be transferred to multiple joints above and below the fixed segment, resulting in increased deformation of these segments, especially for segments close to the region of tonicity. This inevitably leads to the development of more segmental lesions. It has been found that damage to the spine in Luque devices always occurs in the spine at the ends of the devices. It can also cause a medically induced “flat back” and the patient will almost always suffer from back pain. This is a serious consequence of stress concentration.
  Fixation and fusion of the joint can produce further damage to the small joints. Due to the long-term fixation of the small joints, the articular cartilage is not stimulated by normal physiological stresses, resulting in cartilage nutritional disorders and bone thinning, joint capsule contracture, joint stiffness, ankylosis, and eventually arthritic lesions of the small joints. This may be one of the reasons for pain after extensive spinal fixation.
  More important is the clinical practice. Among the cervical spine patients treated with acupuncture, there are quite a number of people with small joint stenosis, calcification, ossification, and total closure of the joint space. Do not do not know, with acupuncture practice doctors will certainly understand what is “contracture”, what is calcification, can also understand the cervical spine misalignment and other pathological changes in the cause. Of course, there are pathological changes in the body where a joint can relax; what is meant here is that the cause of pathological displacement in cervical spondylosis is not due to soft tissue relaxation, but rather that the real cause of such pathological displacement is due to spasm and contracture of the soft tissues of the cervical spine. The establishment of this view is important, and it is the theoretical basis for the treatment of the disease by closed-loop decompression with acupuncture. And this viewpoint is not imagined out of thin air, it is based on the significant efficacy achieved in the treatment of cervical spondylosis by needle knife closed type surgery (i.e. release decompression), and the medical practice of needle knife closed type surgery proves the correctness of this viewpoint.
  2. Alteration of the intervertebral disc Among the soft tissues of the cervical spine, the intervertebral disc is an important component. The neck is the most flexible part of the whole body, plus the cervical vertebral body is small, and the intervertebral disc is smaller than the vertebral body, so the unit force area of the cervical intervertebral disc is larger than the force of the thoracic and lumbar vertebrae. By measurement, the bearing pressure of L5-S1 is 9.5kg/cm2, while C5-7 is 11.5kg/cm2, so it can be seen that the cervical spine bears a huge pressure on the head; especially the C4-7 segment, which is the most active part of the body, the stress is naturally very high; because the disc itself has no direct blood supply and innervation, the cervical disc is more vulnerable to damage. When the disc is degenerated and damaged, the function of the nucleus pulposus decreases and the role of the disc in absorbing shocks decreases; at this time, the disc will expand in all directions under the action of minor external forces, resulting in narrowing of the intervertebral space and various mild displacements of the vertebral body. The ligaments around the disc (including the Sharpey fibers of the disc) are in spasm for a long time, so the abnormally high stresses produce the corresponding osteophytes. C4-6 is the apex of the cervical curvature, the site of the greatest stress, and the best site for cervical labyrinthine hyperplasia. According to statistics, on the lateral X-ray of the cervical spine, the cases of labral proliferation at the anterior edge of the vertebral body are: C5 64.9%, C6 62.9%, C4 33.3%, C7 18.3%, C3 11.1%; while the bony proliferation at the posterior edge of the vertebral body is most frequent in C6, respectively: C6 35.3%, C5 24.5%, C4 18.8%. The proliferation and development of these labrums at the anterior edge of the vertebral body and the posterior edge of the vertebral body are a defensive mechanism under high stress, a repair process to the injury. However, this repair is not only of physiological significance, but may become pathological, as it will have a great impact on the size of the spinal canal and intervertebral canal, on the spinal cord, nerve roots and adjacent tissues and organs. Studies have concluded that all herniated discs are caused by trauma, only the size of the trauma varies. On top of the degeneration and herniation of the disc, a mixed herniation consisting of bone rash at the posterior edge of the vertebral body, degenerative hypertrophy, edematous posterior longitudinal ligament, and locally proliferated capillary network squeezes the nerve roots, irritates the vertebral artery and sympathetic plexus in the posterior lateral aspect, thus producing a series of complex cervical spondylosis symptoms. From the pathological changes of the resected cervical discs, it was found that the early lesions were swelling of the intervertebral disc fibrous rings, cell enlargement, some nucleus-free or nuclear necrosis, decreased cell count, and transverse or longitudinal fissures and cavities in the fibrous rings. In the later stage, increased chondrocytes and calcification at the vertebral body margin were seen; the cartilage plate was fissured and some nuclei disappeared, but no granulation tissue was seen to grow into the disc; no giant cell reaction was seen in the anterior longitudinal ligament. From the above pathological changes, it can be understood that disc degeneration and rupture in cervical spondylosis are due to local strain caused by frequent cervical extension and flexion activities, and the damaged disc has a series of histological and biochemical changes and is a multi-segmental lesion. These changes can be confirmed on the x-ray of hyperextension and hyperflexion, and the most obvious place of displacement is also the most important lesioned segment.
  Anatomically, the functional unit of the cervical spine consists of five joints: two synovial joints, two hook joints and the intervertebral joints (discs). The synovial joints are in a relatively horizontal position and are arranged in a cephalocaudal direction. The curve in front of the disc allows for lateral bending and flexion of the cervical spine. The lateral aspect is the hook vertebral joint. The crooked vertebral joints and discs are aligned tangentially with the emanating nerve roots and play an important role in the development of clinical symptoms. The hook vertebral joint is also known as the neural arch vertebral joint. On the one hand, it has a protective effect, separating the disc from the intervertebral foramen and preventing the disc from protruding laterally and posteriorly; on the other hand, the lateral surface of the hooked process is slightly inclined inward, and the posterior lateral surface can be straightened or inclined outward in case of injury or hyperplasia, i.e., vertical hyperplasia or transverse hyperplasia, compressing the lateral vertebral artery and stimulating the sympathetic plexus or the posterior external nerve roots. The foramen is closer, especially the lateral growths, and the nerve roots and vertebral arteries are most vulnerable to stimulation and compression. The small joints (synovial joints) of the cervical spine are rounded and smoothly arranged, and there is no step phenomenon. When hyperflexion or posterior extension occurs, the intervertebral foramen is reduced to a certain extent due to the forward or backward movement of the upper and lower vertebral bodies by 1~2mm, and the nerve roots are easily compressed. The joint capsule of the small joints is thickened, fibrotic and calcified by repeated pulling and squeezing, which can also lead to the proliferation of synovial bones. Both of them not only cause stenosis of the intervertebral canal, but also narrow the lateral saphenous fossa and the spinal canal. Stenosis of the lateral saphenous fossa is an important factor in nerve root compression.
  In his study of neck and shoulder back pain, Kellett noted that because “the nerve root is firmly fixed in the intervertebral foramen, it does not slide in or out of the foramen or within the foramen during neck flexion and extension, but only when the foramen is narrowed and the nerve root or the foramen itself becomes inflamed or fibrotic, does the nerve root become impaired. When the neck is extended, the intervertebral foramen is narrowed and the nerve root becomes relaxed; when the neck is flexed, the nerve root becomes tense and moves to the upper part of the intervertebral foramen; this has a protective effect on the nerve root. Thus, the pathology of nerve root damage must include narrowing of the intervertebral foramen lumen, whether due to degenerative disc degeneration, anterior invasion due to bone spurs or disc herniation, posterior invasion due to inflammation of the synovial joint, or compression of the nerve by inflammation or fibrosis within the nerve root sheath.” This study specifies that in cervical spondylosis, pathological changes in the intervertebral canal of the cervical spine play a pivotal role in the development of cervical spondylosis.
  4. Changes in the spinal canal, intervertebral canal and its filling The narrowing of the cervical intervertebral canal is closely related to the degeneration of the intervertebral disc. The presence of the leptomeningeal joint makes it impossible for the disc to protrude into the lateral intervertebral canal, but the thinning of the disc causes stress changes in the intervertebral and leptomeningeal joints leading to osteophytes and direct compression of the nerve roots and vertebral arteries by the articular and leptomeningeal osteophytes. Another consequence of disc degeneration is that the superior vertebra slides backward, causing deformation and narrowing of the intervertebral canal, compressing the nerve roots and vertebral arteries. The thickening of the intervertebral joint capsule and the hooked vertebral capsule also exacerbates the narrowing of the intervertebral joint. In summary, compression factors in the intervertebral canal region will lead to the development of nerve root type, vertebral artery type and even sympathetic cervical spondylosis.
  The main contents of the spinal canal are the spinal cord, nerve roots and their perineurium, which occupy only a portion of the spinal canal space (the maximum diameter of the cervical spinal cord is 10 mm, and the anterior and posterior diameters of the spinal canal are 14 to 17 mm). In the cervical region, the ratio of the spinal canal area to the dural sac is about 1:0.7; and the volume of the nerve roots in the intervertebral canal occupies only 1/2 to 1/5 to 1/8. The rest of the space is filled by the intravertebral venous plexus and adipose tissue. The pathological changes in these tissues cannot be ignored and will have a significant impact on the spinal cord and nerve roots. The internal and external stresses, especially the aseptic inflammatory response, will produce a series of changes in the blood circulation: the
  Vertebral vein → congestion → stasis → venous pressure ↑ → arterial blood supply ↓ → arterial ischemia
  This is a vicious circle.
  Another important tissue is the filler, the adipose tissue, and in aseptic inflammation, changes such as exudation and congestion, edema and swelling of adipocytes are already indisputable. At the same time, the spinal cord, nerve roots, etc., which are under the compression of these fillers, themselves also produce circulatory disturbances, congestion, edema, and other changes. As a result, the pressure in the spinal canal will rise, further compressing the spinal cord and nerve roots, while compressing and stimulating the sympathetic plexus, causing vascular spasm and worse blood flow, resulting in functional stenosis of the spinal canal; and in congenital, developmental spinal stenosis, the spinal cord and the small spinal canal are normally at peace with each other, but with slight trauma, especially cervical hyperextension, hyperflexion plus rotation, some will immediately develop tetraplegia, and herein lies the reason . Thus, many scholars have cautioned, “It must be remembered that many people with significant bone and joint changes never show symptoms; there are also many people with spinal cord symptoms who have little to no radiological findings.” This is often a problem that people tend to overlook.
  5, changes in the vertebral artery The caliber of the vertebral artery is <5mm, and the thickness of the vertebral artery varies on both sides, with the left being thick and the right being thin. The vertebral artery is an important collateral circulation for blood supply in the brain. It supplies 1/6 of the cardiac output (2% of body weight) to the brain, accounting for 11% of the total cerebral blood volume, with 45cm³ of blood entering the brain every minute. In addition to the factors of the atherosclerotic vessels themselves, there are still many factors affecting the intracranial blood supply, which are briefly described below.
  1, the important reason affecting the intracranial blood supply is the extracranial mechanical factors, namely the caliber and curvature of the vertebral artery. Such as vertebral artery start variation, neck deformity, hook vertebral joint bone redundancy, cervical muscle spasm, fascia contracture compression or abnormal bending, angulation, etc.; normal head rotation to one side, the ipsilateral vertebral artery blood flow is reduced, compensated by the opposite side. When the anatomical position of the cervical spine is changed or there is osteophyte, especially because the transverse foramen of C5 is closer to the vertebral body, the stress, torsional force and shear force generated are the greatest, and the vertebral artery is more likely to be directly compressed or stimulated when displacement occurs between the vertebral bodies, and vasospasm occurs, resulting in reduced blood flow to the vertebrobasilar artery. When the blood flow in the visual projection center of the cerebral cortex is lower than the normal metabolic needs of the brain tissue in the visual area, it can cause central visual impairment; if it affects the ischemia of the vagus artery, when the blood flow to the inner ear is impaired, tinnitus and hearing loss can easily occur.
  2. Another important factor is that some sympathetic postganglionic fibers enter the skull along with the vertebral artery and internal carotid artery (the vertebral artery is surrounded by abundant sympathetic nerves). The vertebral artery mainly supplies blood to the occipital lobe (visual cortex), cerebellum, and brainstem; the internal carotid artery innervates the brain and eye vessels and smooth muscle of the eyelids. When the postganglionic fibers of sympathetic nerves are provoked, it can cause vasospasm of vertebral artery or internal carotid artery, or when the vertebrobasilar artery is undersupplied with blood, it can cause lesions of Ⅸ~ Ⅻ cranial nerve, vertebral cross of medulla oblongata and cervical medulla.
  3, in the cervical muscle, ligament, joint capsule (including the synovial joint, hook vertebral joint or intervertebral fibrous ring) rich distribution of nociceptive receptors in the tissue, especially the synovial joint capsule for extrusion, pulling and other stimuli and sterile inflammation is extremely sensitive. When the cervical spine moves, certain external forces stimulate the sinus vertebral nerve, sympathetic nerve, posterior branch of spinal nerve and other factors in the spinal canal and cause changes in the cervical muscles, ligaments and joint capsule spasm. In particular, the synovial joints (with capsular receptors) as well as the peripheral blood vessels produce spastic changes (including degeneration of the nucleus pulposus) and cause myospasm due to edema. The peripheral myospasm in turn causes pain and dyskinesia, further contributing to abnormal motion of the intervertebral joints. Thus, the hooked, hooked and articulated vertebral joints and articulating joints around the vertebral artery and nerve roots can constitute causative factors. It is worth proposing that the articular eminence of the first and C3, due to its special morphology, is called vertebral eminence. This protrusion can cause abnormal motion and flexion changes in the cervical spine when the transverse diameter of the intervertebral joint increases in deformity and when the osteophytes of the hook protrusion increase, and can affect the vertebral artery; secondly, the proliferation of the hook protrusion has different morphology in the vertical and horizontal directions, and the horizontal proliferation (most common in C4-5 and C5-6 segments) is most likely to squeeze the vertebral artery and produce dizziness symptoms.
  4. The influence of the vertebral artery around the vertebral artery foramen on the vertebral artery. The gap between the foramen of the vertebral artery (transverse foramen) and the vertebral body (i.e., the hook protrusion) is 3-6 mm, while the spacing between the small joint and the transverse foramen is 2-3 mm, with a large difference between the two. This difference indicates that the most common cause of extrusion of the vertebral artery should be the superior articular eminence, while the change of the hook vertebral joint is a secondary factor.
  5, there is another etiology that can cause vertigo and other symptoms, namely subclavian artery steal syndrome. If the lumen between the proximal part of the subclavian artery and the beginning of the vertebral artery is partially or completely blocked, there is a reverse pressure gradient between the vertebral-basilar artery, which is enough to make the blood of the vertebral artery flow backward and inject into the distal part of the subclavian artery, causing cerebral and brachial ischemia, and the patient can have symptoms such as vertigo, nausea, partial blindness and numbness of the limbs.
  6, changes in the spinal cord and nerves In cervical spine movement, the spinal cord and nerve roots in the spinal canal do not rise and fall, but the spinal cord is unfolded in forward flexion, and gradually elastic deformation occurs, which can be stretched to the maximum physiological limit; while in supination and extension, the spinal cord and dura form folds, and gradually elastic compression is formed, just like the opening and closing of the accordion bellows. When the spinal column is in motion, the nerve roots are not active in the spinal canal, but become tense or relaxed as the dura is stretched or folded. In the neutral position of the neck, especially in flexion, the nerve roots are stretched within the physiological range and are located in the uppermost part of the intervertebral foramen, in contact with the lowermost part of the pedicle; in the extended position of the neck, when the dura is folded in folds, the nerve roots also become relaxed, more perpendicular to the spinal cord, and descend within the intervertebral foramen and out of contact with the pedicle above. In the physiological state, the nerve roots are firmly anchored in the intervertebral canal (foramen). When the neck is extended and flexed, the nerve roots do not slide inward or outward into the intervertebral canal. The nerve roots become dysfunctional only when there is narrowing of the intervertebral canal, inflammation or fibrosis of the nerve roots or the intervertebral canal itself. Therefore, whether it is anterior damage due to degeneration of the intervertebral disc, disc herniation, or osteophytes, posterior damage due to inflammation of the synovial joint, or nerve root compression due to inflammation or fibrosis within the nerve root sheath, the pathology of nerve root damage must include narrowing of the intervertebral canal lumen. Within the intervertebral canal, the motor and sensory portions of the nerve roots are kept separate, with the motor roots (ventral roots) close to the hooked vertebral joints and the sensory roots (dorsal roots) close to the articular eminence and joint capsule. This is one aspect. On the other hand, the nerve roots occupy only 1/5 of the intervertebral canal and the rest of the space is filled with other tissues (adipose tissue, venous plexus, etc.). All these tissues can undergo inflammatory reactions and swelling, thus confining the nerve root to a hard bony canal. This relationship has important clinical implications.