Dizziness, commonly known as lightheadedness, is a common medical condition. Vertigo differs from dizziness in that dizziness is a feeling of dizziness, while vertigo is a sensation of constant rotation of the body and surrounding matters on top of dizziness. The essence of vertigo is the subjective sensation of disruption of the central nervous system’s judgment of the body’s own spatial position or change in motion. The signals that provide changes in the body’s own spatial position or movement come mainly from three different sources of the sensory system, namely, visual signals, vestibular nerve signals, and cervical proprioceptive signals. Therefore, any cause that affects one, two or three of these sensory systems can cause vertigo. In clinical practice, we find that vertigo is related to cervical spondylosis in many patients, and there is a trend of younger and younger patients. Some of these patients have symptoms and signs of cervical spondylosis and corresponding X-ray manifestations, but there are also many patients with dizziness that do not conform to the manifestations of conventional cervical spondylosis, and the X-ray often only shows loss of curvature, but the dizziness symptoms are obviously relieved after treatment according to cervical spondylosis treatment methods, which suggests that there may be cervical spondylosis related, but whether to classify these patients as cervicogenic cervical spondylosis may need further study. The pathogenesis of cervical vertigo is relatively complicated, and generally speaking, there are the following: 1. Cervical spine osteophytes Osteophytes and soft tissue hypertrophy gradually appear in the late stages of cervical spine degeneration, which affect the vertebral artery from two aspects: 1) Osteophytes around the transverse foramen cause narrowing of the transverse foramen. Under normal circumstances, the transverse foramen of the cervical spine is larger than the outer diameter of the vertebral artery. When the surrounding osteophytes compress the transverse foramen surface below the transverse foramen and directly compress the vertebral artery, vertigo mostly occurs, and when the osteophytes occupy 1/3 of the transverse foramen, obvious clinical symptoms appear; ② the osteophytes of the anterior-internal hook vertebral joint and the posterior small joint of the vertebral artery can compress the vertebral artery or hit the vertebral artery with the proliferated part when moving. When the contralateral vertebral artery is insufficiently compensated, it leads to insufficient blood supply to the vertebrobasilar artery. 2, sympathetic nerve theory In 1926, Barre first reported that stimulation of the sympathetic plexus of the vertebral artery by the cervical joints could induce symptoms such as vertigo, headache and neck pain, and named it Barre-Lieou syndrome. Currently, there are two theories for the mechanism of vertigo caused by stimulation of the cervical sympathetic plexus: the vertigo is caused by insufficient blood supply to the vertebrobasilar artery due to hyper tension in the sympathetic nervous system caused by cervical instability and spinal stenosis, in which the sympathetic nerve acts on the blood vessels mainly through the chemical transmitters released from the postganglionic fibers of the sympathetic nerve that bind to the receptors in the vessel wall to produce a constricting effect. Some scholars believe that abnormal mechanical and inflammatory stimuli affect the cervical sympathetic nerve endings, resulting in sympathetic nerve dysfunction causing intracranial vasoconstriction and transient cerebral ischemia. 3.The theory of cervical medullary injury (1) cervical trauma. In clinical work, it can be seen that cases with severe vertigo undergo vertebral arteriogram and there is no sign of compression. The vertigo was also not abnormal in the vertebral artery when the film was taken immediately after making the rotation of the head to induce vertigo, but the vertigo disappeared immediately after performing anterior decompression intervertebral implant or posterior open-door decompression. Therefore, vertigo in such patients is not caused by compression of the vertebral artery. After the degeneration or herniation of the intervertebral disc causes narrowing of the intervertebral space and loosening of the posterior longitudinal ligament and the ligamentum flavum, resulting in instability of the intervertebral joints of the cervical spine, the cervical medulla is constantly bumped or compressed during frequent neck activities, damaging the vestibular spinal cord bundle and the medial longitudinal bundle in the cervical medulla and causing vertigo inversely. (2) Cervical spinal stenosis. In cases with heavy degeneration of the cervical spine, there are not only disc protrusion, osteophytes and bone redundancy, but also thickening of the posterior longitudinal ligament or ligamentum flavum, resulting in narrowing of the cervical spinal canal, so that the ventral and dorsal parts of the cervical medulla are compressed, especially when the ventral part of the spinal cord is compressed, the medial longitudinal bundle and the vestibular spinal cord bundle in the anterior cord are easily compressed directly and vertigo symptoms appear. It is reported that the narrower the cervical spinal canal is, the more obvious the compression of cervical medulla, cervical nerve root or vertebral artery is. Therefore, some scholars believe that most of the vertigo symptoms are not caused by a single vertebral artery compression, but by various factors such as cervical medullary compression, ligamentous laxity and intervertebral joint instability. 4.The theory of proprioception The human body mainly depends on the balance triad consisting of vestibular system, vision and proprioception to maintain balance, and any damage to one of the three localized senses and abnormal impulses can cause vertigo. Among the proprioceptors, especially the afferent impulses from the neck are most closely related to balance. The cervical proprioceptive information comes from the skeletal muscles (muscle shuttle), tendons (Golgi tendon apparatus) and joints (small joint receptors) in the neck. The cervical collar muscles are rich in high-density muscle shuttle, which is more densely distributed than other skeletal muscles, and the mechanoreceptors of small joints in the cervical spine are also the most abundant in the spine. Injuries to the cervical muscles and small joints disrupt the afferent cervical proprioceptive information from the cervical muscles, tendons and small joints, and incorrect cervical proprioceptive afferent information causes errors in the central nervous system’s analysis of vestibular and visual signals, making it difficult to make an accurate assessment of one’s head position and producing a subjective feeling of vertigo. 5. Vascular lesion and abnormal hemodynamic theory The occurrence of cervical vertigo is not only related to the above-mentioned factors, but also related to the lesion of vertebral artery itself and hemodynamic factors. The main cause is atherosclerosis, which causes narrowing of the lumen of the vertebral artery and reduces the elasticity of the closed lumen of the vertebral artery, and if there are other factors related to the development of vertigo, the lack of blood supply to the vertebral artery is aggravated. This can lead to the development of vertigo. (1) Under normal conditions, changes in the radius of blood vessels have a great influence on blood flow, but when the vertebral artery is squeezed by bone or atherosclerosis and distortion, the compensatory expansion of the vertebral artery is limited, so it is unlikely that the blood flow in the vertebral artery can be improved by adjusting the internal diameter of the vessel. A slight increase in blood viscosity can significantly reduce the blood flow in the vertebral artery, thus aggravating the ischemia of the vertebrobasilar system. (2) The increase in blood viscosity directly affects the microcirculatory perfusion of brain tissue. The increase of blood viscosity and the increase of capillary radius further aggravate the ischemia and cause vertigo attacks. In conclusion, we can see that cervical vertigo is not only related to cervical osteophytes (hyperplasia of the hook vertebral joint, supra-articular eminence, transverse foramen, etc.), disc degeneration leading to narrowing of the intervertebral space, displacement, fracture or slippage of the vertebral body, transverse synovial lesions (fracture or displacement under external force), soft tissue lesions of the neck, but also related to sympathetic nerve dysfunction and cervical proprioceptive disorders. Other factors such as tumor, subclavian steal syndrome and suprathoracic syndrome can cause cervical vertigo. Although the research on cervical vertigo has been intensifying, the clinical efficacy is not satisfactory, and as the disease is getting younger and younger, the clinicians have higher requirements. That is why good prevention is the most effective way. The best way to prevent cervicogenic vertigo is to slow down the process of degenerative changes in the cervical spine. All people with high incidence of cervical spondylosis, such as accountants, teachers, text workers and computer operators, should start to avoid prolonged low head work from young age, advocate cervical spine exercises or cervical spine resistance exercise between jobs, and advocate scientific use of pillows. Those who suffer from cervical vertigo and are in remission should get enough sleep and avoid overexertion.