Swallowing is a process of fine muscular activity that requires multiple sets of muscles to be activated in different sequences and with precise timing and force, such as opening the mouth on demand, pushing the tongue backward to deliver food, contracting of the cricopharyngeal muscle groups, airway closure, and opening of the esophageal sphincter. Errors in any of these stages can result in the patient developing dysphagia. This includes the control of swallowing movements by the brainstem swallowing center, the cerebral cortex, subcortical fibers, and the extrapyramidal system. The brainstem swallowing centers include not only the coordinated motor abilities and sensory inputs from multiple pairs of cerebral nerves to the swallowing muscles [6] , but also the medullary swallowing centers that integrate and process the information from cerebral nerves and supramedullary inputs to elicit a swallowing response [7] ; therefore, lesions of the brainstem are critical to the control of swallowing. The cortical swallowing centers of the brain play a key role in the initiation of swallowing [8] , and a large number of studies now suggest that cortical swallowing centers are present in the frontal lobe, parietal lobe, temporal lobe, and anterior cingulate gyrus [9] . Dysfunction of many subcortical regions can also lead to dysphagia, such as the thalamus, the internal capsule, the insula, and the amygdala, which can also participate in the process of swallowing movements through the extrapyramidal system [10] [11] . Cerebellar and extrapyramidal damage may also cause swallowing dysfunction, which may be caused by dystonia in the muscles corresponding to swallowing movements [12] .

A complete sensory input-output link is essential during swallowing, and sensory decline in the oral cavity and pharynx may have difficulty in inducing the production of the swallowing reflex [13] , and the input of sensory stimuli also causes an increase in the excitability of the corresponding areas of the cerebral cortex, which demonstrates the inextricable link between movement and sensation, and that sensory deficits have a significant impact on swallowing movements [14] .

The interhemispheric inhibition (IHI) model refers to the fact that the two cerebral hemispheres are connected via the corpus callosum [17] which not only transmits information directly to each other between the two hemispheres, but also dynamically regulates their reciprocal inhibitory or excitatory effects to a dynamic equilibrium, and after a stroke, this inhibitory equilibrium is broken, which will cause the healthy hemisphere’s inhibition of the affected hemisphere to be enhanced while the affected hemisphere’s inhibition of the healthy hemisphere to be weakened, leading to dysphagia [18] . Based on this theory, a large number of studies have demonstrated that the balance can be maintained by inhibiting the excitability of the healthy hemisphere or increasing the excitability of the affected hemisphere, thus improving the symptoms of post-stroke dysphagia.

After stroke, the brain will organize the nerves around the damaged area to re-establish new circuits, which is mainly manifested in the re-awakening of the nerves in the uninjured area, connection, and the occurrence of new dendrites and spines [19] . When the swallowing center on the affected side is destroyed, the remodeling ability of the remaining neurons cannot meet the functional recovery needs, the healthy side of the swallowing center will compensate for the increase in the neural pathways of the region, in order to improve the recovery of swallowing function. When the affected side is the healthy side of the swallowing center, the healthy side will increase the neural pathways of the region, so as to improve the symptoms of dysphagia and function recovery, and when the affected side is the dominant hemisphere of the swallowing center, it will also promote the transfer of the dominant hemisphere to the healthy side [20] .

Di Pino G [18] argued that the interhemispheric connection as inhibition or compensation after stroke is related to the neural pathways that survived the stroke and the reserve of neural remodeling in the region, and that the healthy-side compensatory model may be more helpful for functional recovery if the surviving tissues and reserve of the lesion area are low, and the interhemispheric inhibitory model may be more helpful for functional recovery if the lesion area is sufficiently well endowed with the neural pathways and reserves, which has implications for this will help us to develop individualized plans for rTMS, but this model needs more imaging and neurological examinations to monitor and judge before treatment, so as to develop individual treatment plans, and there are fewer studies in this direction now.

After stroke, neuroplasticity is the basis for the recovery of brain function, and brain plasticity will follow a fixed time line and also increase in a limited period of time [21] , and rTMS is one of the factors that regulate the enhancement process, and high-frequency repetitive transcranial magnetic stimulation (HF-rTMS) will elevate the excitability of the cerebral cortex, and when the cerebral cortex excitability is elevated, it will be more favorable for this process to take place [22] , therefore, in the recovery period of stroke, rTMS can be used to enhance neuroplasticity, promote the compensation of the cerebral cortex, improve central nerve conduction, and help the recovery of swallowing function [23] .

After stroke, the release of neurotransmitters will be affected [24] , which will cause a series of clinical symptoms, including cognition, memory, motor, swallowing dysfunction, etc. Therefore, regulating the release of neurotransmitters and the expression of the corresponding genes can improve the swallowing dysfunction after stroke, and the study of Ikeda T [25] showed that rTMS can regulate the mRNA expression level of some neurotransmitter genes in the mouse brain, thereby regulating the neurotransmitter expression level, thereby regulating neurotransmitter secretion levels and affecting neuronal activity. At the same time, studies have shown that rTMS can also affect the release level of cholinergic neurons [26] , which has a more obvious effect on improving the excitability of neurons. In addition, rTMS also has a more significant effect on some other neurotransmitters, such as brain neurotrophic factor [27] , which can improve post-stroke dysfunction.

Astrocytes are the most abundant glial cells in the body, and they are activated in two different phenotypes after stroke, type A1 and type A2. Type A1 astrocytes secrete inflammatory cytokines and neurotoxic mediators, which trigger neuroinflammation and further aggravate craniocerebral injuries after stroke, while type A2 astrocytes secrete anti-inflammatory cytokines and nerve growth factors to promote nerve regeneration, in order to protect neurological function. Studies have shown that rTMS inhibits the production of type A1 astrocytes [28] , promotes the transformation of type A1 astrocytes to type A2 and increases the secretion of trophic factors by type A2 astrocytes [29] . Therefore, rTMS can alleviate the neuroinflammatory response, minimize the exacerbation of brain injury, and promote the regeneration of the nerves to assist in post-stroke rehabilitation.

The secretion of inflammatory cytokines will be rapidly activated after stroke, which includes two types: pro-inflammatory cytokines such as IL-1, IL-6, IL-11, IL-17, IL-23 and interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), etc., and anti-inflammatory cytokines, including IL-4, IL-6, IL-10 and TGF-β, etc. [30] . Among them, IL-6 has both anti-inflammatory and pro-inflammatory properties [31] . rTMS can simultaneously inhibit the secretion of pro-inflammatory cytokines and promote the production of anti-inflammatory cytokines after stroke [32] - [35] , thus reducing the damage of inflammation and promoting tissue repair after stroke. At the same time, pro-inflammatory cytokines can also affect synaptic plasticity, thereby influencing neurological recovery after stroke [36] .