Blood–brain barrier pathology is recognised as a central factor in the development of many neurological disorders, but much less is known about the role of the blood–brain barrier in psychiatric disorders. We review post-mortem, serum-biomarker, CSF-biomarker, and neuroimaging studies that have examined blood–brain barrier structure and function in schizophrenia and related psychoses. We consider how blood–brain barrier dysfunction could relate to glutamatergic and inflammatory abnormalities, which are increasingly understood to play a part in the pathogenesis of psychosis. Mechanisms by which the blood–brain barrier and its associated solute transporters moderate CNS availability of antipsychotic drugs are summarised. We conclude that the complex nature of blood–brain barrier dysfunction in psychosis might be relevant to many aspects of disrupted neuronal and synaptic function, increased permeability to inflammatory molecules, disrupted glutamate homoeostasis, impaired action of antipsychotics, and development of antipsychotic resistance. Future research should address the longitudinal course of blood–brain barrier alterations in psychosis, to determine whether blood–brain barrier dysfunction is a cause or consequence of the pathology associated with the disorder.

血脑屏障的病理学被认为是许多神经系统疾病发展的重要因素，但是关于血脑屏障在精神疾病中的作用的了解却很少。我们回顾了验尸，血清生物标志物，CSF生物标志物和神经影像学研究，这些研究检查了精神分裂症和相关精神病的血脑屏障结构和功能。我们考虑血脑屏障功能障碍如何与谷氨酸能和炎性异常有关，而谷氨酸能和炎性异常在精神病的发病机理中被越来越多地理解。总结了血脑屏障及其相关溶质转运蛋白调节中枢神经系统抗精神病药供应的机制。我们得出的结论是，精神病中血脑屏障功能障碍的复杂性质可能与神经元和突触功能破坏，炎症分子通透性增加，谷氨酸同稳态破坏，抗精神病药作用受损以及抗精神病药耐药性发展的许多方面有关。未来的研究应解决精神病中血脑屏障改变的纵向过程，以确定血脑屏障功能障碍是与该疾病相关的病理的原因还是后果。