A.M.'s initial MRIs performed on September 29, 2007, and October 10, 2007, did not reveal any abnormality. Pet. Ex. 4 at 438. The interpreting radiologist noted that these were limited studies due to the presence of braces on her teeth, which frequently cause artifact obscuring the images. Id. Respondent's expert, Dr. Venkatesan, reviewed the films himself and found them adequate to conclude that they did not show inflammation. Tr. at 367. Her third MRI, after the braces were removed, showed increased signal in the temporal lobe with atrophy in the hippocampus. Pet. Ex. 4 at 457; Tr. at 19-20. A PET scan done in November 2007 demonstrated hypometabolism of glucose in the temporal lobe. Pet. Ex. 4 at 461; Tr. at 20-21. While these two results do not verify an instigating cause of the seizures, they do localize the damage caused by the seizures to her temporal lobes, particularly on the left.
With that clinical underpinning, Dr. Blitshteyn opined that A.M.'s clinical symptoms, including severe seizures, status epilepticus, subsequent memory deficits, severe learning disabilities, and behavioral problems, were consistent with ALE. Tr. At 24. She testified the EEG findings were quite consistent with limbic encephalitis and the MRI and PET scans helped to localize the damage to the temporal lobes. Tr. at 21-23, 17-20. She also noted that the operative biopsy after A.M.'s temporal lobe was removed ruled out cortical dysplasia and cancer, and found gliosis consistent with a reaction to seizures. Tr. at 20-23. Further, a flu-like prodromal illness has been reported in case reports on limbic encephalitis. Tr. at 30 (referencing Pet. Ex 25A at 392).22