This literature marketed report as received from a other health professional refers to a 22 year old male patient. Further examination of his childhood medical records disclosed that his older sister had varicella when the patient was 6 months old. The patient did not have an obvious varicella exanthema at that time. However, at 27 months of age, the patient developed a left-sided T6/T7 dermatomal rash. He was seen by his pediatrician and a dermatologist at a clinic, both of whom documented in his medical record a clinical diagnosis of herpes zoster. The patient was not given any varicella vaccinations during his childhood. The patient was healthy with a normal body mass index when he completed his college education in June 2012. Because of a requirement for new employment in a hospital, he was serotested and found to have a negative varicella zoster virus (VZV) antibody titer on 20-SEP-2012. As per regulation, he received his first varicella vaccination (manufacturer unknown) on 11-DEC-2012 and his second vaccination on 24-JAN-2013. He did not recall any side effects of the 2 varicella immunizations. Between 11-FEB-2013 and 15-FEB-2013, he developed intermittent headaches, mainly in the left temporal area, and took ibuprofen to reduce pain. On 16-FEB-2013, he had a headache earlier in the day and, later, a seizure that was witnessed by another person in the same room. He was taken to a local emergency department, where an initial assessment was negative. On 19-FEB-2013, he was seen in follow-up by the neurology service; they found no remarkable findings but did order magnetic resonance imaging (MRI) and electroencephalography (EEG). The MRI demonstrated a small T2/FLAIR hyperintense and T1 mildly hypointense lesion (14 x 15 x 9 mm) involving the cortex and adjacent subcortical white matter centered at the left inferior temporal sulcus. There was no associated restricted diffusion, hemorrhage, calcification, or contrast enhancement. A routine EEG recorded 2 subclinical left temporal lobe seizures; levetiracetam (500 mg twice daily) was prescribed to prevent further seizure activity. Differential considerations favored a neoplasm, such as a low-grade astrocytoma or oligodendroglioma. On 12 March 2013, neurosurgeons performed an MRI guided left temporal craniotomy and resected the lesion. He recovered quickly and was walking within 3 days of surgery; he had no further seizures. On 18-MAR-2013, the initial pathology report indicated an absence of tumor in the resected tissue. However, perivascular inflammation was present, involving many small leptomeningeal vessels. This finding suggested that a viral etiology could have caused the gliosis. On 21-MAR-2013, the patient developed recurrent headache that continued for another week. Because of the recent history of 2 varicella vaccinations, VZV immunostaining was performed on the brain tissue and was interpreted as positive on 22-MAR-2013. On 23-MAR-2013, the patient initiated valacyclovir treatment 1000 mg 3 times daily, even though he was greatly improved symptomatically and had already returned to work. Subsequent hematologic screening studies on 25-MAR-2013 for a variety of autoimmune/rheumatology disorders were negative, but VZV serology was now positive. Serum immunoglobulin levels as well as absolute numbers of CD3+, CD4+, CDS+, CD19+, and CD16+CD56+ lymphocytes were within normal ranges. At a follow-up examination 1 year after the seizure episode, the patient was completely free of any central nervous system symptoms. Neuropathology Studies: After neurosurgical excision, the cortex showed severe gliosis and diffuse microglial activation without microglial nodule formation. A chronic lymphocytic inflammatory infiltrate was present with a predominant perivascular distribution, involving cortex and small leptomeningeal vessels. The infiltrate was composed predominantly of CD3+ cells and only a few CD20+ cells. The findings were consistent with an inflammatory reactive process and raised the possibility of viral etiology, but no viral inclusions were observed. The edges of the excised brain tissue were free of inflammation. The final intriguing aspect of this unusual case was the proximity of the VZV reactivation in the temporal lobe with 2 varicella vaccinations during the preceding months. Since our virology sequencing data indicated that the VZV infection in the brain was caused by wild-type VZV, the most likely explanation was a coincidental association. On an unknown date, the patient recovered from herpes zoster meningoencephalitis and herpes zoster. In March 2013 the patient recovered from craniotomy. The reporter considered herpes zoster meningoencephalitis, herpes zoster and craniotomy to be related to VARIVAX (Merck). Upon internal review, Herpes zoster meningoencephalitis and Craniotomy were considered other important medical events. Additional information has been requested.