The condition is mediated by autoantibodies that target<unk><unk> s in the brain. These can be produced by cross reactivity with<unk><unk> s in teratomas, which contain many cell types, including brain cells, and thus present a window in which a breakdown in immunological tolerance can occur. Other autoimmune mechanisms are suspected for patients who do not have tumors. Whilst the exact pathophysiology of the disease is still debated, empirical evaluation of the origin of<unk> -NMDA<unk> <unk> bodies in serum and cerebrospinal fluid leads to the consideration of two possible mechanisms. These mechanisms may be informed by some simple observations. Serum<unk><unk> <unk> bodies are consistently found at higher concentrations than cerebrospinal fluid<unk> bodies, on average ten times higher. This strongly suggests the<unk> body production is systemic rather than in the brain or cerebrospinal fluid. When concentrations are normalized for total IgG, intrathecal synthesis is detected. This implies that there are more<unk><unk> <unk> bodies in the cerebrospinal fluid than would be predicted given the expected quantities of total IgG. # Passive access involves the diffusion of<unk> bodies from the blood across a pathologically disrupted blood-brain barrier (BBB). This cellular filter, separating the central nervous system from the circulatory system, normally prevents larger molecules from entering the brain. A variety of reasons for such a collapse in integrity have been suggested, with the most likely answer being the effects of acute inflammation of the nervous system. Likewise, the involvement of corticotropin releasing hormone on mast cells in acute stress has been shown to facilitate BBB penetration. However, it is also possible that the autonomic dysfunction manifested in many patients during the later phases of the condition aids<unk> body entry. For example, an increase in blood pressure would force larger proteins, such as<unk> bodies, to extravasate into the cerebrospinal fluid. # Intrathecal production (production of<unk> bodies in the intrathecal space) is also a possible mechanism. Dalmau et al. demonstrated that 53 out of 58 patients with the condition had at least partially preserved BBBs, whilst having a high concentration of<unk> bodies in the cerebrospinal fluid. Furthermore, cyclophosphamide and rituximab, drugs used to eliminate dysfunctional immune cells, have been shown to be successful second-line treatments in patients where first-line immunotherapy has failed. These destroy excess<unk> body-producing cells in the thecal sac, thus alleviating the symptoms. A more sophisticated analysis of the processes involved in<unk> body presence in the cerebrospinal fluid hints at a combination of these two mechanisms in tandem.<unk> bodies Once the<unk> bodies have entered the CSF, they bind to the NR1 subunit of the<unk><unk> . There are three possible methods in which neuronal damage occurs. # A reduction in the density of<unk><unk> s on the post synaptic knob, due to<unk>  internalization once the<unk> body has bound. This is dependent on<unk> bodies cross linking. # The direct antagonism of the<unk><unk>  by the<unk> body, similar to the action of the classic dissociative anesthetics phencyclidine and ketamine. # The recruitment of the complement cascade via the classical pathway <unk> body-antigen interaction). Membrane attack complex (MAC) is one of the end products of this cascade and can insert into neurons as a molecular barrel, allowing water to enter. The cell subsequently lyses. Notably, this mechanism is unlikely as it causes the cell to die, which is inconsistent with current evidence.
Anti-NMDA receptor encephalitis
Neuroleptic malignant syndrome
Anti-Hu associated encephalitis
Psychosis
Anti-VGKC-complex encephalitis
Viral encephalitis
Powassan encephalitis
Autoimmune encephalitis