Herpes simplex virus type 1 (HSV-1) enters sensory neurons and can remain latent there until reactivation. During latency restricted HSV-1 gene expression takes place in the form of latency-associated transcripts (LAT). LAT has been demonstrated to be important not only for latency but also for reactivation, which may cause cranial nerve disorders. Tissue sections of the trigeminal ganglia (TG), geniculate ganglia (GG), and the vestibular ganglia (VG) from seven subjects were examined for the presence of LAT using the in situ hybridization technique. LAT was found on both sides in allTG (100%), on both sides of five subjects (70%) in the GG, and in none of the VG. Using a second more sensitive detection method (RT-PCR), we found LAT in the VG of seven of ten other persons (70%). This is the first study to demonstrate viral latency in the VG, a finding that supports the hypothesis that vestibular neuritis is caused by HSV-1 reactivation. The distribution of LAT in the cranial nerve ganglia indicates that primary infection occurs in the TG and GG and subsequently spreads along the faciovestibular anastomosis to the VG.

Reactivation of herpes simplex virus type 1 (HSV-1) in the vestibular ganglion (VG) is the suspected cause of vestibular neuritis (VN). Recent studies reported the presence of HSV-1 DNA not only in human VGs but also in vestibular nuclei, a finding that indicates the possibility of viral migration to the human vestibular labyrinth. Distribution of HSV-1 DNA was determined in geniculate ganglia, VGs, semicircular canals, and macula organs of 21 randomly obtained human temporal bones by nested PCR. Viral DNA was detected in 48% of the labyrinths, 62% of the VGs, and 57% of the geniculate ganglia. The potential significance of this finding is twofold: (1) Inflammation in VN could also involve the labyrinth and thereby cause acute unilateral vestibular deafferentation. (2) As benign paroxysmal positional vertigo often occurs in patients who have had VN, it could also be a sequel of viral labyrinthitis.

The changes in the cerebellar activation pattern of two successive fMRI scanning runs were determined for visually guided to-and-fro saccades in 12 healthy volunteers familiar with the study paradigm. Group and single subject-analyses revealed a constant activation of the paramedian cerebellar vermis (uvula, tonsils, tuber, folium/declive), which reflects constant ocular motor activity in both runs. A significant decrease in activation of the cerebellar hemispheres found in the second run is best explained by either a decrease in attention or the effects of motor optimization and learning. The significant, systematic changes of the cerebellar activation pattern in two successive runs were not expected, because the ocular motor task was simple, familiar, and highly automated. These findings indicate that similar effects may bias other cerebellar activation studies, in which sensorimotor tasks are repeated in a single session.

Background The aim of this retrospective study was to document the long-term clinical efficacy of a surgical-prosthetic technique (the flat one-bridge technique) involving the immediate restoration of both postextraction and nonpostextraction implants supporting full-arch restorations. Methods Implants were placed by adapting the axis to the available bone. Flat definitive abutments were connected during surgery and never disconnected to compensate for eventual implant disparallelism. Bone grafting was performed when needed. The patients received a screw-retained provisional restoration within 48 h of surgery and a final screw-retained prosthesis within 1 year. Results Sixty-six patients received 494 implants distributed in 75 prostheses. The median follow-up was 86 months (range 82–168 months). Only three implants had failed at the last follow-up. Implant survival was 99.6%. Conclusion The flat one-bridge prosthetic protocol is a viable procedure with excellent long-term outcomes. No difference in clinical success could be observed between postextractive and nonpostextractive implants.

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