Cerebellar mutism (CM) is a group of transient clinical syndromes most often seen in children after posterior cranial fossa tumor surgery, occasionally secondary to cerebellar hemorrhage, inflammatory reactions and trauma, with predominantly language impairment, often combined with oropharyngeal dyskinesia and psychiatric changes. This paper reviews the clinical characteristics, pathogenesis, prognosis and prevention. The overall incidence is about 5%-10%, with about 90% occurring in children. The incidence of CM and secondary dysarthria is as high as 11%-29%. 2. Preferred site: CM mostly occurs after extensive resection of tumors in the posterior cranial fossa, and about 90% of the tumors are located in the near midline of the cerebellum. In early studies, it was thought that the size of tumor was related to the occurrence of CM, but in recent years, it was thought that brainstem compression, involvement of cerebellar peduncle, earthworm and periaqueductal structures were related to the occurrence of CM. 3. Latency and duration: The significant clinical characteristics of CM are latency and self-limiting, the latency period is mostly 1-3d after surgery, and the average duration is 7-8 weeks. In general, those who developed CM immediately after surgery showed slow recovery of neurological function and relatively long duration of mutism, which could be several months; those with long latency period showed relatively fast recovery of neurological function and short duration of mutism, which could be several days. There was no significant difference in the latency period and duration between the child and adult groups. 4, clinical manifestations: (1) mental symptoms and behavioral changes: there may be refusal to eat, agitation, mood changes, flexion in bed, laziness, crying, screaming and other manifestations, and the incidence is high; (2) the patient is conscious during mutism, but lack of behavioral initiative, memory, comprehension and problem processing ability is reduced; (3) oropharyngeal muscle movement can not: mainly manifested by the reduction of transoral feeding, swallowing and masticatory motor incoordination, no initial movement, but basically normal function after the movement starts; (4) symptoms of bulbar palsy: characterized by three main signs of speech difficulty, vocal disturbance, and feeding difficulty, pathological brainstem reflexes, positive cone bundle sign, urinary discontinuity and urinary retention may appear. II. Anatomical basis of the cerebellum related to language The normal speech production process is divided into five basic elements, namely: arousal; emotion and desire; cognition; initiation, planning and coordination; and implementation. Normal speech depends on the integrity of six anatomical structures that together comprise the supplementary motor area, Broca’s area, basal ganglia, thalamus, brainstem, and cerebellum and the coordination of the intermuscular movements involved in speech production. Of these, the cerebellum plays a coordinating and planning role. The middle and lower earthworms, the earthpituitary, the earthcone and the hillside are the representative areas of the head and face, and there are representative areas of the lingual and oropharyngeal muscles in the middle earthworm cortex, which are extensively connected to the nucleus accumbens of the neocerebellum and via this to the motor and sensory cortex of the brain. This loop is as follows: cerebral cortex (including the upper part of prefrontal area 8 and the lower part of Broca’s language areas 44 and 45) – internal capsule – medial and lateral parts of the peduncle – pontine nuclei – middle peduncle – neocerebellar cortex – dentate nucleus – superior peduncle, partly via the red nucleus – red nucleus spinalis bundle to the anterior horn of the spinal cord, and partly via the thalamus to the frontal cortex. From this loop, the neocerebellar cortex integrates the information received and sends nerve impulses to the dentate nucleus, which then influences the cerebral cortex upward and the spinal cord downward. In addition, there is a neural loop in the brainstem: red nucleus – inferior olivary nucleus – neo-dentate nucleus – red nucleus, in which the red nucleus receives fibers from the cortical language area, making this loop involved not only in the cognitive but also in the motor expression of language. In addition, the development of the neo-dentate nucleus coincides with the development of the prefrontal cortex of the brain and is presumably related to the reception of fibers from the neo-dentate nucleus in the prefrontal area of the brain, which is involved in the completion of cognitive and linguistic functions. Therefore, if there is an extensive bilateral cerebellar lesion or a disruption of the bilateral intercerebellar fiber connection that regulates the speech muscle movement through the earthworm, speech dysfunction may occur. The exact site of the lesion and the pathophysiological mechanism of CM remain unknown. Any lesion that may cause disruption of the cerebellar-brain “language pathway” may lead to the development of mutism, and may involve factors such as injury or edema of the cerebellopontine nucleus, brainstem invasion or compression, earthworm incision, nature of the tumor, cerebrospinal meningitis or encephalomyelitis, hydrocephalus, and psychiatric factors. Early on, surgery was considered necessary for the development of CM. In recent years, studies have found that most patients with postoperative mutism in the posterior cranial fossa have varying degrees of preoperative language dysfunction. The literature summarizes 225 cases of CM: 90% occurred after tumor resection, 4 or 4% were secondary to vascular lesions, 2 or 2% were due to trauma, and 3 or 1% were secondary to infectious lesions. It is evident that surgery is not necessary to cause CM. We hypothesize that when slow and progressive lesions do not completely destroy the structures and fiber connections of the cerebellum, only language dysfunction may occur, but not mutism, and that only when the relevant structures are suddenly and completely damaged may mutism appear. 1. Damage and edema of the dentate nucleus: one of the more recognized mechanisms is the involvement of the dentate nucleus of the cerebellum, leading to the blockage of the dentate nucleus and its associated neural pathways as the pathological-anatomical basis for the occurrence of CM. Mutism immediately after surgery may be caused by direct injury to the dentate nucleus, while mutism a few days later may be caused by postoperative spasm of the arteries supplying the cerebellar hemispheres, causing local ischemia and edema in the dentate nucleus region. Ozimek et al. emphasized that the occurrence of CM is caused by bilateral, rather than unilateral, dentate nucleus injury or edema. 2, brainstem invasion or compression: brainstem injury has also attracted widespread attention in recent years. A large number of studies have confirmed that brainstem invasion or compression is associated with the occurrence of CM, and it is believed that brainstem injury is also an independent risk factor affecting CM. McMillan et al. believe that tumor involvement of the brainstem or cerebellar peduncle is associated with CM, and the possible mechanisms are: (1) intraoperative manipulation and traction causing edema of the brainstem and cerebellar peduncle; (2) preoperative tumor compression caused compression and bending of the conduction bundles in the white matter of the brainstem. Decompression of the white matter of the brainstem after tumor resection and postoperative formation of the tumor cavity may lead to further bending of the conduction bundles, thus causing damage to the axons of the white matter conduction bundles and leading to the occurrence of postoperative CM. The possible mechanism is that the damage to the middle earthworm cortex blocks the afferent and efferent motor-sensory information, resulting in the inability to activate the immobilized oropharyngeal application procedure, which makes the patient show inability to perform speech and swallowing actions, and manifests as oropharyngeal disuse. Dailey et al. emphasized the importance of the relationship between the extent of inferior earthworm dissection for tumors in the posterior cranial fossa and the development of mutism. However, opponents argue that earthworm incision has nothing to do with CM, because CM usually has a 1-3d incubation period, which does not correspond to the time point of earthworm incision, and CM may not appear after surgery even if the earthworm is fully incised. 4. Nature of tumor: The chance of CM after surgery is 2-3 times higher in medulloblastoma than in astrocytoma and ventricular meningioma, and the incidence of CM after surgery is 25% in children with medulloblastoma. If the tumor involves the brainstem, the incidence of postoperative CM is as high as 44%. 5. hydrocephalus and cerebrospinal meningitis: Parrish et al. suggested that encephalomyelitis can lead to CM, but the mechanism is unclear. abekura suggested that the enlargement of the third ventricle and aqueduct in acute hydrocephalus damages the cerebellar-thalamic fibers and reticular superior agonist fibers in the superior midbrain, leading to muteness. In contrast, in the 46 cases of mutism counted by Ersahin et al, only 9 cases had postoperative hydrocephalus and 8 cases had meningitis, while the remaining 29 cases had neither hydrocephalus nor meningitis. Therefore, the above two views need to be further confirmed. 6. Others: It is speculated that the occurrence of CM is related to the postoperative cellular architecture of the cerebellum, cerebellar peduncle and brainstem, axonal damage, and inter-synaptic neurotransmitter changes, and this is used to explain the latency period and self-limiting nature of CM. The silence is not related to the cerebellum itself, but is a psychological response to surgical stress in children, called “verbal dissociation”. The syndrome is more common in children because the initiation and programming of speech established by the learning function of the cerebellum in children is not yet mature and consolidated, and because the neuromyelin development in children is incomplete, making children more susceptible to neurological connections that do not lead to silence. The recovery process starts with gradual improvement of psychiatric symptoms and cerebellar hemispheric dyskinesia, disappearance of urinary retention, followed by increased feeding, recovery of oropharyngeal muscle function, and finally recovery of language function, but after the disappearance of mutism, children are mostly left with varying degrees of dysarthria.Robertson et al. In a prospective study, Robertson et al. graded 98 patients with CM and followed them for a long period of time and found that 92% of those who had severe mutism had ataxia, 66% had language impairment, and 59% had cognitive dysfunction, while the three indicators in the moderate mutism group were 78%, 25%, and 17%, respectively, with statistically significant differences. V. Prevention In view of the possible etiology and mechanism of CM, the author believes that prevention can be achieved from the following points: minimize collateral damage during surgery, reduce the output current of bipolar electrocoagulation when separating the tumor to reduce the damage of heat transfer; be familiar with the anatomical level of the surgical site, separate along the tumor perimeter, and try not to block the blood vessels of the cerebellar hemispheres; operate gently and use automatic retractors to reduce strain injuries; achieve tight dural sutures in all of them In order to avoid cerebrospinal fluid leakage and infection, apply anti-cerebral vasospastic drugs such as nimodipine to prevent vasospasm; moderate dehydration to avoid possible vascular microcirculation disorders caused by insufficient or excessive dehydration; in case of CM, head CT, MRI or SPECT should be performed in a timely manner to understand whether there is postoperative hemorrhage, edema and hydrocephalus, and do corresponding treatment in a timely manner; cooperate with neurotrophic treatment. neurotrophic treatment.