In 1975, PedersoYl and Afzelius respectively observed that some male infertility patients had viable but non-motile sperm, and found that sperm motility was due to structural abnormalities of the axoneme in the sperm flagellum. Later, it was also noted that sperm axoneme abnormalities were combined with ciliary motility disorders in the respiratory tract and other parts of the body, i.e., inability to swing in a directional manner, loss of transport, and signs of obstructive respiratory disease and infection. Since axoneme is the core structure of both sperm flagellum and cilia, Eliasson called the series of symptoms caused by abnormal sperm flagellum and cilia axoneme as cilia immobility syndrome. A, the occurrence and pathology of cilia immobility syndrome human body has cilia epithelial parts of the nasal cavity, pay sinus, trachea, bronchus, middle ear, ventricular canal, inner surface of the cornea, in the male reproductive tract is limited to the testicular output duct. Each cell has one cilium, and the cilia in each region have a directional oscillation so that the contents of the duct can be transported. Although sperm flagella and cilia differ in length and movement, the core structure is the axoneme, so axoneme abnormalities can lead to sperm flagellar oscillation and ciliary dyskinesia. According to statistics, cilia immobility syndrome accounts for 1.14% of male infertility. The axoneme is composed of 9+2 structural units, with nine microtubule pairs in the shape of a garden barrel surrounding two separate central microtubules, the latter two partially surrounded by a central sheath (see Chapter 6 for details). The microtubule units are linked by three structures: (1) the nexi-n link is an elastic bridge that connects adjacent microtubules and serves to stabilize the axoneme so that it remains as a single unit. (2) The dynein arm allows the relative sliding of nine microtubule pairs and transforms the sliding restricted by the nexi-n link into the oscillation of cilia or flagella. (3) Radial spokes can change the distance between the peripheral microtubule pairs and the central sheath, thus preventing excessive bending of the axoneme and converting the sliding of microtubules into bending of cilia in concert with the linker protein chains. Because of the complexity of the axoneme structure, abnormalities in any one of them can cause dysfunction. (1) Ciliary protein arm abnormalities: This is the most common pathological change in ciliary immobility syndrome, which can be the absence of inner or outer arms, or both. (2) Abnormal radiating spokes: absence of radiating spokes with two central microtubules off-center; or absence of the head of the radiating spokes (thickened part of the center of the radiating spokes) and the central sheath. (3) Central microtubule abnormality: the central microtubule disappears or there is a short central microtubule at the base of the axoneme, which disappears at the middle and distal end of the axoneme, when the peripheral microtubules move in, forming a regular symmetrical 8+l composite structure, similar to the connection structure of the radial spokes to connect the moved in central microtubules with the peripheral microtubules. (4) Other: cilia or flagella without central microtubules and axonemes. Another pathological feature of the cilia in patients with this syndrome is the disorganized pointing without uniform orientation, which can be observed by cross-sectioning the axoneme, where the central microtubule is the most readily observable pointing marker. In addition, there are also pathological changes that can be seen in this syndrome, such as compound cilia and flaccid ci lia, but this may be a non-specific manifestation of the syndrome, as these changes can also be seen in some airway inflammatory conditions. It is now generally accepted that cilia immobility syndrome is an autosomal recessive disorder based on the following; (1) Patients with the syndrome are commonly found in siblings, and there can be affected or non-affected individuals in the same family, but no intermediate ones. (2) The incidence is higher in areas where consanguineous marriages take place. (3) The cilia of patients resemble those of rats and lower animal biogenetic mutants. (4) Respiratory disorders occur as early as young age, and about 50% of patients have visceral translocation. Second, the diagnosis of cilia immobility syndrome 1, clinical features in the distribution of cilia can occur in the parts of the performance of certain corresponding disorders, the most prominent of which is the respiratory tract disorders. Initially, it was thought that the respiratory cilia in patients with this syndrome were completely immobile, but later studies found that the cilia were not completely immobile, only that the movement was abnormal and ineffective, i.e., they could not send the mucus out of the respiratory tract, thus losing the ability to resist the invasion of foreign harmful factors. Therefore, the patient is prone to infection. Patients often begin to show signs of respiratory infections at an early age, with chronic cough, sputum, pneumonia and pulmonary atelectasis being very common, and developing into childhood with bronchiectasis, etc., with severe impairment of lung function, increased coughing, recurrent fever and hemoptysis. Loss of clearance of airway mucus clearance tests is a characteristic feature of the syndrome. Patients often have chronic rhinitis and nasal polyps with markedly diminished sense of taste. Chronic or recurrent upper collar sinusitis and septal sinusitis are seen in any patient, and examination may reveal nonexistent or undeveloped anterior nasal sinuses and poor ventilation within the mastoid process. In addition, patients may have otitis media and neurological symptoms such as headache. Respiratory tract disorders are most severe in childhood and adolescence and tend to decrease in adulthood, and many are in good health and have a normal work life. About 50% of patients have visceral transposition, which is thought to be due to ciliary defects. If the cilia fail to act, the rotation of the embryo to the right or to the left (visceral transposition) depends on chance, which explains why about 50% of patients with this syndrome have visceral transposition. Patients have normal development of secondary sexual characteristics and sexual organs, semen volume and sperm count are in the normal range, but semen staining shows that sperm are viable but not motile or rarely motile, and the aforementioned pathological changes can be found under ultrastructure. 2, diagnostic points in the male infertility clinic for live but immobile sperm in the semen and the patient has a history of chronic bronchitis or sinusitis that occurred in early life, the diagnosis can be made basically, if combined with any one or more of the following manifestations, the diagnosis is clearer: (1) the patient or siblings or close relatives who have visceral transposition. (2) Absence or basic absence of bronchial mucus clearance. (3) The nasal or bronchial cilia or sperm flagellum ultrastructure has the aforementioned pathological features. Kartagener’s syndrome is also known as Kartagener’s syndrome when the above diagnosis is met and there is visceral translocation. Kartagener’s syndrome is included in the ciliary immobility syndrome but is different from it. Sturgess et al. found that cilia and spermatozoa with abnormal axoneme central microtubules still had some motility, with lO% of them moving normally, which he attributed to the symmetrical 8+1 composite structure that converts the sliding of the double microtubules into axoneme motion. Sturgess referred to these two conditions as multiple forms of ciliary dyskinesia, which he considered inappropriate to be expressed by the term ciliary dyskinesia, and suggested that all dyskinesias caused by congenital abnormalities of the cilia (or sperm flagellum) be collectively referred to as ciliary dyskinesia, which includes ciliary dyskinesia, Kartagener’s syndrome, Kartagener’s syndrome, and Kartagener’s syndrome. It includes ciliary dyskinesia, Kartagener’s syndrome, and multiple forms of ciliary dyskinesia. The name classification is complicated by the fact that some patients have cilia defects but have unaffected sperm and are fertile. Therefore, it may be better to use the term ciliary dyskinesia, which is widely accepted, to express these conditions. Because the syndrome is likely to be congenital, there is a lack of specific and effective treatment for immobile sperm. Some studies have shown that sperm from patients with this syndrome have a range of functions for fertilization such as capacitation, acrosome reaction, fusion with the egg membrane and nuclear depolymerization, but whether they can be used for in vitro insemination to produce IVF and thus solve fertility problems is a topic that remains to be studied. The current treatment of ciliary dyskinesia is mainly non-specific and directed at respiratory infections to prevent its further development.