Clinically, patients with the classic presentation of ALE usually manifest with "rapidly progressive short-term memory deficits, psychiatric symptoms, and seizures." Resp. Ex. J at 1. However, the literature acknowledges that traditional hallmarks of ALE—the short-term memory deficits and behavioral changes—can be overshadowed by other dominant symptoms, such as refractory seizures.17 In fact, the literature suggests that the first signs to be recognized in childhood cases of ALE are often non-psychiatric symptoms, such as seizures and status epilepticus. "[I]n children, the first symptom to be recognized is often non-psychiatric — e.g. seizures, status epilepticus, dystonia, verbal reduction or mutism." Pet. Ex. 25N at 64.18 As there has never been a suggestion that A.M. suffered from any type of cancer, the focus of this analysis is on those studies that have examined more recently recognized patterns of limbic encephalitis where the agent appears to be antibodies to neuronal cell surface antigens. See Resp. Ex J at 1. The Tuzin and Dalmau article states "[s]tudies have now shown that many of [ALE patients] do in fact have antibodies to neuronal cell surface antigens. These antigens may be ubiquitously expressed in the nervous system but usually are distinctively enriched in the hippocampus and sometimes the cerebellum. They include voltage-gated potassium channels, N-methyl-D-aspartate receptors and others that remain uncharacterized." Id.