Patients with epileptic G are frequently comorbid with cognitive dysfunction, especially in children, and the relationship between the two is multifactorial. Previous studies have suggested that the development of cognitive dysfunction is mainly related to epileptic G seizures, site of epileptogenic foci, socio-environmental factors, and antiepileptic G medications; however, recent studies have increasingly found that certain aspects of cognitive deficits are also present in patients without epileptic G seizures and neuroanatomical abnormalities, but with frequent subclinicinal epileptiform discharges (SEDs). The occurrence and development of SED and its relationship with cognitive function are gradually being emphasized by clinicians. Historical review: Epileptiform discharges are occasionally seen in the normal population, partly in combination with psychiatric, behavioral, and cognitive disorders. 1939 Schwab first described the relationship between SED and prolonged response time to stimuli. Subsequent studies have gradually found that different forms of SED can lead to different degrees and contents of cognitive deficits, and the course and prognosis of the disease are also different. Cognitive function assessment of various types of epilepsy G patients has been widely carried out abroad, and there is still a lack of unified understanding and evaluation scale in China, but it has received increasing attention. The relationship between age-related epileptic G-like discharges and cognitive function: Benign childhood epileptic G with central temporal spikes (BECTS), acquired epileptic G aphasia syndrome (LKS), and persistent spikes and slow waves during slow-wave sleep (CSWS) are similar in clinical features, most of them start in childhood, and the clinical manifestations are sparse transient partial seizures, with frequent restricted epileptic episodes in the inter-ictal period of the electroencephalogram (EEG), especially the EEG of the sleep period. Frequent limiting epileptiform discharges, with no obvious abnormalities on neuroimaging, and spontaneous remission before puberty; an excellent model for studying SED and cognitive function. Previous studies have concluded that BECTS does not have neuropsychological deficits, but recent studies have found selective cognitive impairment in some patients; Shafrir has also found that the large number of discharges during the waking interictal period and the frequent spike discharges during the slow-wave sleep period of LKS are associated with fluctuating cognitive dysfunction.Binnie’s study confirms that transient cognitive impairment ( Binnie’s study confirmed a direct link between the development of transitory cognitive impairment (TCI) and frequent SED. At present, the relationship between EEG abnormalities and neuropsychological deficits is not completely clear, one viewpoint believes that the two are two results of the same etiology, and more believe that the two have a causal relationship, which may be related to the long-term, frequent SED caused by brain maturation disorders impairing the establishment and modification of neuronal circuits. Physiological mechanisms of epileptic G-like discharges affecting cognitive function: Age-related epileptic G-like discharges are generally age-dependent, with EEG abnormalities and clinical symptoms resolving spontaneously during puberty. Before puberty, the brain is in a period of high synaptic and axonal pruning, and focal SEDs during the developmental period may cause structural and functional abnormalities in the focal area and its connective tissues. SPECT and PET studies on CSWS have confirmed that some areas of cerebral blood flow hypoperfusion and glucose hypermetabolism are consistent with the sites of spike wave issuance shown on EEG, and that cortical metabolism is higher than subcortical metabolism, which shows the metabolic characteristics of immature brain. The localized hypermetabolism may be a result of the disease itself or may be related to epileptic G-like discharge. 4. Characteristics of cognitive impairment due to epileptic G-like discharges: Frequent epileptic G-like discharges can cause TCI and chronic cognitive impairment. Mild visuospatial and auditory impairment, decreased attention, learning difficulties, and behavioral deficits have been found in many patients with BECTS. This cognitive impairment occurs only for a certain period of time during the course of the disease; it does not occur in conjunction with EEG changes and clinical episodes, and sometimes the symptoms are so mild that they can only be detected by statistical comparisons between the two groups. A routine neuropsychological examination hardly meets the clinical requirements and can be detected only by using a highly selective examination. Such an examination must meet the following conditions: the task process cannot inhibit epileptic G activity; there should be enough examination time, at least more than half an hour; the examination items must be completed consecutively; the degree of difficulty of the examination should be adapted to the patient’s level; the purpose of the examination should be practical; and different examinations should be developed according to different neuropsychological functions and functional brain areas. Commonly used tests abroad include Digits Forward, RAVLT, Story Recall, Spatial Learning test, Verbal Fluency, Tower of London, etc. Each of these tests is designed for a different cognitive task, focusing on verbal structure, reading and reciting fluency, picture naming, visual-spatial short-term memory, visual-motor coordination, cognitive flexibility, attention, etc., with high sensitivity. Due to the differences between domestic and foreign education systems and cultural differences, the domestic neuropsychological scale assessment cannot mechanically transpose foreign data, and a set of cognitive assessment methods adapted to Chinese people, especially children, should be established. 5. The relationship between epileptic G-like discharge sites and cognitive dysfunction: The brain is an extremely complex and precise organization, and different functional representative areas have corresponding specific functions. neuropsychological deficits of BECTS are often consistent with the focal functions of abnormal EEG. The left hemisphere is the linguistically dominant area in the vast majority of people, and its abnormal discharges mostly cause impairments in language cognition, while right hemisphere discharges cause deficits in visuospatial cognition; the earliest spiking foci of the LKS are located in the vicinity of the cortex of the lateral fissure, and so it manifests itself as a distinct aphasia. Poor attention and impulsivity suggest that the abnormalities are far from the rolandic/central temporal area, and that a balance between frontal and hemispheric function contributes to attention, which is an anatomical area that should mature in childhood and before puberty. 6. Relationship between type of epileptic G-like discharges and cognitive dysfunction: Focal spikes can cause difficulty with reaction time and short-term visual memory tasks in patients with BECTS, suggesting that the discharges only cause focal specific TCIs and that the result is equivalent to the damage caused by the surgical foci rather than a generalized decline in cognitive function. Massa et al. concluded that the combined presence of three or more of the EEG abnormalities of bilateral asynchronous spike-slow wave syndrome, periodic focal slow waves, long-range bursts of spike-slow wave rhythms, and global symmetrical 3-4 Hz spike-slow wave discharges, and their persistence for more than 6 months, are risk factors for the development of neuropsychological deficits in BECTS, and Aarts et al. demonstrated that paroxysmal bursts of slow waves caused a lower rate of TCIs compared to spikes. Bilateral independent spike-wave foci are closely related to the development of cognitive deficits. The relationship between the frequency, morphology and duration of epileptic G-like discharges and cognitive function has been neglected in previous studies: Staden found that a spike wave index (SWI) (the number of spikes per minute) of >10 was associated with verbal dysfunction and may be the only relevant risk factor. Some studies have found that the duration of epileptic status epilepticus during sleep (ESES) is related to intellectual disability, and the higher the SWI and the longer the duration (more than 2 years), the more severe the degree of intellectual disability. The relationship between them is not yet well understood, and further research is needed. The effect of epileptic G-like discharges on sleep: As the brain synchronization mechanism plays a dominant role in the NREM period, the epileptic G activity is easily generalized and the epileptic G-like discharges are more obvious in this period, whereas the brain desynchronization mechanism plays a dominant role in the REM period and the awakening period, so that it produces an inhibitory effect on the epileptic G activity. In patients with epileptic G, changes in the sleep-wake cycle are common to varying degrees, with frequent transitions between sleep phases and an increase in the number of awakenings, which are associated with epileptic G episodes and epileptic G-like discharges affecting the sleep structure. Even in the absence of epileptic G episodes, sleep structure can still be destabilized and sleep disruption can occur, independent of the duration of the disease, its severity, and the application of anti-epileptic G drugs. Some patients with epileptic G experience daytime sleepiness and fatigue as a result, which may also have an impact on cognitive function. 9. Impact of cognitive function on epileptic G-like discharges: Similarly, complex cognitive tasks can affect epileptic G-like discharges. The most obvious example is reflex epilepsy G. The frequency and total duration of epileptic G-like discharges increase when reading and calculating compared to rest. The frequency of discharges is higher in the right hemisphere than in the left hemisphere during reading, whereas the difference between the two hemispheres during computation is not significant. The possible mechanism is that reading is a left hemisphere function and computation is a bi-hemispheric function, and cognitive tasks associated with epileptic G foci inhibit epileptic G-like discharges in this region but have a facilitating effect on discharges in the contralateral hemisphere. 10.Treatment: If frequent SED has caused significant cognitive impairment, then anti-epileptic G medication should be given. The purpose of treating SED is not simply to inhibit epileptic G-like discharges, but ultimately to reduce the degree of cognitive impairment and improve the prognosis. Carbamazepine, valproic acid and benzodiazepines are generally used clinically. Most studies have concluded that anti-epileptic G drugs themselves have adverse effects of varying degrees of cognitive impairment, such as phenobarbital, phenytoin sodium, clonidine, etc., mainly affecting attention, alertness, and psychomotor speed; however, some studies have concluded that carbamazepine has no impairment of psychomotor function and memory in patients at normal doses, or only minor effects of no clinical significance. In general, some of the newer anti-epileptic G drugs have less effect on cognitive function. Therefore, the pros and cons should be weighed when choosing the timing of treatment, in order to avoid the aggravation of cognitive impairment by antiepileptic G drugs on the one hand, and to be wary of the cognitive impact of social prejudice and family attitudes of concern on the patient on the other hand.