| Abstract: | Healthy sleep is implicated in cognitive functioning, especially sleep-dependent memory consolidation (SDC). Insomnia, a common sleep disorder mainly characterized by sleep disturbances, has become a prominent problem in modern society. Its impact on SDC has also attracted increased attention. Therefore, this paper aimed to review previous studies on the effects of primary insomnia (PI) on SDC of different types of memory, and to elucidate the neural mechanism of SDC changes in PI, so as to provide theoretical support for improving the SDC of PI patients.According to previous studies, the influence of PI on SDC mainly focused on declarative memory (semantic memory) and non-declarative memory (procedural memory), and the conclusions seem to be inconsistent. Generally speaking, SDC of procedural memory was found to be more susceptible to PI, while the influence of PI on SDC of declarative memory was relatively mild. Most existing studies found that PI patients had greater impairment in procedural memory consolidation than healthy sleepers. However, only one study showed that SDC of declarative memory in patients with PI was defective. Moreover, SDC of declarative memory in patients with PI was more vulnerable to interference learning than that of procedural memory. The differences in experimental design, SDC paradigm type, first-night effect, sample characteristics, and sleep structure may be the reasons for this inconsistency.To date, the mechanisms of the effects of PI on the SDC of declarative and procedural memories are still unclear. Some polysomnographic studies have demonstrated that the influence of PI on SDC is linked to certain macrostructures and microstructures of sleep. Specifically, a previous study showed that the amount of slow wave sleep (SWS) decreased significantly in PI patients, and the compensatory increase in rapid eye movement sleep (REM) had a positive correlation with SDC of declarative memory in patients. In another study, PI patients had a diminished amount of REM, but there was no correlation between SDC impairments of procedural memory and REM in the PI group. Furthermore, no SWS compensation was observed in patients, indicating that REM may play an irreplaceable role in SDC of procedural memory. In addition, the damage of different functional brain regions in insomnia patients may hinder SDC of declarative or procedural memory, which is mainly due to the relationships between SDC of different memory types and different brain structures. However, there is no direct evidence to support this hypothesis. Overall, based on the disruption of sleep structure and abnormal brain structures in insomnia patients and the relationships between these changes and SDC in PI, it can be speculated that the effect of PI on SDC of declarative and procedural memories could be consistent with the system consolidation hypothesis and synaptic homeostasis hypothesis. In essence, the potential brain mechanisms of PI on SDC are dependent on system consolidation and synaptic consolidation.Future studies could be conducted on the synchronous acquisition of behavioral, electroencephalographic, and brain imaging data to explore the neural pathways of SDC associated with insomnia, and on the prevention and treatment of SDC impairment in patients with PI through transcranial current stimulation, transcranial magnetic stimulation, or targeted memory reactivation. |
