Observation of neutron spectrum produced by fast deuterons via ultraintense laser plasma interactions.

We report the first precise spectral measurement of fast neutrons produced in a deuterated plastic target irradiated by an ultraintense sub-picosecond laser pulse. The 500-fs, 50-J, 1054-nm laser pulse was focused on the deuterated polystyrene target with an intensity of 2 x 10(19) W/cm(2). The neutron spectra were observed at 55 degrees and 90 degrees to the rear target normal. The neutron emission was 7 x 10(4) per steradian for each detector. The observed neutron spectra prove the acceleration of deuterons and neutron production by d(d,n)3He reactions in the target. The neutron spectra were compared with Monte Carlo simulation results and the deuteron's directional anisotropy and energy spectrum were studied. We conclude that 2% of the laser energy was converted to deuterons, which has an energy range of 30 keV up to 3 MeV.

Herpes simplex virus type 1 reactivation and antiviral therapy in patients with acute peripheral facial palsy.

OBJECTIVE: Recent studies provide compelling data for the hypothesis that herpes simplex virus type I (HSV-1) is implicated in the pathogenesis of idiopathic peripheral facial palsy (Bell's palsy). The present study analyzed the severity of facial palsy in patients with HSV-1 reactivation and sought to determine the efficacy of acyclovir-prednisone therapy for these patients. MATERIALS AND METHODS: In total, 176 patients, clinically diagnosed with Bell's palsy. were divided into three groups by polymerase chain reaction (PCR) and serological tests--31 patients with HSV-1 reactivation, 45 patients with VZV reactivation (zoster sine herpete) and 100 patients without HSV-1 or VZV reactivation (Bell's palsy). RESULTS: The difference in the worst grade of facial palsy between patients with zoster sine herpete and Bell's palsy was significant (P = 0.01 10, Mann-Whitney U-test). In contrast, no difference in the severity of palsy was observed between patients with HSV-1 reactivation and Bell's palsy. Twelve patients received acyclovir-prednisone treatment within 7 days of onset based on positive PCR results and ten of the 12 (83%) recovered completely. In contrast, 14 patients with HSV-1 reactivation received prednisone treatment because their PCR tests were performed at a later date; ten of these 14 (71%) recovered completely. The difference in the cure rate between the two treatment groups was not significant (P > 0.05, Fisher exact test). CONCLUSIONS: The results indicate that the severity of palsy in patients with HSV-1 reactivation is similar to that in patients with Bell's palsy and suggest that early diagnosis of HSV-1 reactivation by PCR and subsequent acyclovir-prednisone therapy do not improve recovery from facial palsy.

Herpes virus reactivation and serum tumor necrosis factor-alpha levels in patients with acute peripheral facial palsy.

Recent studies have shown that tumor necrosis factor-alpha (TNF-alpha) plays an important regulatory role in several inflammatory and infectious diseases. In the present study, we evaluated serum TNF-alpha levels of patients with acute peripheral facial palsy using an ELISA method. We examined sera from each group (n = 25 per group) of patients with herpes simplex virus type 1 reactivation (HSV-1). varicella-zoster virus (VZV) reactivation, and with no HSV or VZV reactivation. We also tested the sera of 25 normal controls. No significant difference was found between the serum TNF-alpha levels in facial palsy and controls. No correlation was found between serum TNF-alpha levels in cases with HSV-1 or VZV reactivation and with no HSV-1 or VZV reactivation. These results indicate that serum TNF-alpha levels are not affected by HSV-1 or VZV reactivation in patients with facial palsy.

Quantitation of varicella-zoster virus DNA in patients with Ramsay Hunt syndrome and zoster sine herpete.

Varicella-zoster virus (VZV) reactivation causes facial nerve palsy in Ramsay Hunt syndrome (RHS) and zoster sine herpete (ZSH) with and without zoster rash, respectively. In the present study, we analyzed the VZV DNA copy number in saliva samples from 25 patients with RHS and 31 patients with ZSH using a TaqMan PCR assay to determine differences in the viral load between the two diseases. VZV copy number in saliva peaked near the day of the appearance of zoster in patients with RHS. Consequently, VZV DNA was less frequently detected in patients with RHS who exhibited facial palsy several days after the appearance of zoster. These findings suggest that the VZV load in saliva samples reflects the kinetics of viral reactivation in patients with RHS. In addition, VZV DNA was equally detected in saliva from patients with RHS and ZSH, and there was no significant difference in the highest viral copy number between patients with RHS and those with ZSH. The VZV load does not appear to reflect a major difference between RHS and ZSH.

Herpes virus reactivation and gadolinium-enhanced magnetic resonance imaging in patients with facial palsy.

OBJECTIVE: This study investigated whether magnetic resonance imaging (MRI) patterns were different between patients with Bell's palsy and those with herpetic facial palsy in whom varicella-zoster virus (VZV) or herpes simplex virus type 1 (HSV-1) reactivation had been confirmed by polymerase chain reaction (PCR) or serologic assay. STUDY DESIGN: A retrospective study of 15 patients with acute peripheral facial palsy was performed to compare virologic tests and gadolinium (Gd)-enhanced MRI findings. RESULTS: Ramsay Hunt syndrome was diagnosed in one patient. By use of virologic tests, zoster sine herpete (VZV reactivation without zoster) was diagnosed in four patients and HSV-1 reactivation in three. Bell's palsy was diagnosed in the remaining seven patients. No significant difference in the frequency of Gd-enhanced MRI was observed between herpetic facial palsy and Bell's palsy. However, in those patients who underwent MRI on the day viral reactivation was confirmed by PCR, Gd enhancement of the meatal fundus was observed infrequently. In addition, when MRI was performed within 10 days of the onset of palsy, Gd enhancement was not detected at the geniculate ganglion in any patients with herpetic facial palsy. By contrast, both the meatal fundus and the geniculate ganglion were enhanced in all patients with Bell's palsy, regardless of when MRI was performed with respect to the onset of palsy. CONCLUSION: This study shows a difference in the pattern of Gd enhancement at the meatal fundus and the geniculate ganglion between patients with Bell's palsy and those with herpetic facial palsy. The results suggest that the meatal fundus or the geniculate ganglion may be affected first by virus reactivation in patients with herpetic facial palsy.

Western blot analysis for diagnosis of Lyme disease in acute facial palsy.

BACKGROUND: Lyme borreliosis has been implicated in the pathogenesis of acute peripheral facial palsy (APFP). Few studies, however, have used Western blot analyses to confirm the serological diagnosis. PURPOSE: To analyze the prevalence of anti-Borrelia antibodies in patients with APFP compared with healthy control subjects living in Hokkaido Island, Japan. PATIENTS AND METHODS: In total, 113 patients with APFP were analyzed. They included 32 patients with varicella zoster virus (VZV) reactivation (Ramsay Hunt syndrome and zoster sine herpete) and 81 patients with Bell's palsy. Fifty-eight healthy control subjects were also included. IgM and IgG antibodies to Borrelia garinii and afzelii were tested by Western blot, and diagnoses were made according to the Centers for Disease Control and Prevention criteria. RESULTS: Five of 81 (6.2%) patients with Bell's palsy, 1 of 32 (3.1%) patients with VZV reactivation, and 1 of 58 control subjects (1.7%) were judged to have both IgM and IgG antibodies to Borrelia. This difference was not significant (P >.05, chi2 test). Patients with Bell's palsy who had herpes simplex virus type 1 (HSV-1) reactivation at the onset of palsy had a higher IgM-immunoreactivity to Borrelia afzelii. CONCLUSIONS: Although it is one of the endemic areas of Lyme disease in Japan, the prevalence of APFP caused by Lyme borreliosis is low in Hokkaido Island. In addition, cross-reactivity to B. afzelii in IgM blots is often observed in patients with HSV-1 reactivation, suggesting that careful interpretation of Borrelia IgM immunoblot data are needed for accurate serological diagnosis.

Early diagnosis of zoster sine herpete and antiviral therapy for the treatment of facial palsy.

The effect of antiviral agents on recovery from facial palsy in patients with zoster sine herpete (ZSH; varicella zoster virus reactivation without zoster) has not been evaluated because ZSH is difficult to diagnose early after onset. In this study, all 13 patients who received acyclovir-prednisone treatment within 7 days of onset, as confirmed by a positive PCR result, showed complete recovery. PCR-based early diagnosis of ZSH and antiviral therapy elicited an excellent outcome for recovery from facial palsy due to ZSH.

Rapid strip assay for detection of anti-herpes simplex virus antibodies: application to prediction of varicella-zoster virus reactivation in patients with acute peripheral facial palsy.

Varicella-zoster virus (VZV) reactivation causes acute peripheral facial palsy in the majority (88%) of patients who lack anti-herpes simplex virus (HSV) antibodies, suggesting that an absence of anti-HSV antibodies is a reliable serological marker for the diagnosis of VZV reactivation in patients who are diagnosed initially as idiopathic peripheral facial palsy (Bell's palsy) [Furuta et al., 2000] Clinical Infectious Diseases]. A simple and rapid immunoassay for detection of anti-HSV antibodies based on HSV type 1 glycoprotein D was developed by modifying the conventional Western blot technique. The assay was evaluated by comparing the results with those of conventional Western blot. In total, 100 sera obtained from patients with acute peripheral facial palsy were tested and judged blindly by two investigators. Twenty-four of 26 HSV-seronegative sera were obtained from patients with VZV reactivation (Ramsay Hunt syndrome or zoster sine herpete). The sensitivity of the assay was over 95% and the specificity was 100%. The two investigators agreed on the diagnosis in 99 of the 100 sera. These results indicate that the rapid strip assay is applicable to prediction of VZV reactivation in patients diagnosed clinically with Bell's palsy before zoster lesions appear or PCR using saliva samples indicates VZV reactivation.

Reactivation of varicella-zoster virus in delayed facial palsy after dental treatment and oro-facial surgery.

In rare cases, acute peripheral facial palsy occurs several days after dental treatment and oro-facial surgery. Surgical procedures have been known to trigger reactivation of varicella-zoster virus (VZV) and herpes simplex virus type 1 (HSV-1). The present study examined eight patients who exhibited delayed facial palsy after dental treatment or oro-facial surgery. Ramsay Hunt syndrome was diagnosed in three patients and varicella-zoster virus (VZV) reactivation without zoster lesions (zoster sine herpete) was diagnosed in three patients either by PCR or serological assay. Therefore, VZV reactivation was detected in 75% (6 of 8) of patients who exhibited delayed facial palsy after dental or oro-facial treatment. The results suggest that VZV reactivation is a major cause of delayed facial palsy after dental treatment or oro-facial surgery.

High prevalence of varicella-zoster virus reactivation in herpes simplex virus-seronegative patients with acute peripheral facial palsy.

Varicella-zoster virus (VZV) and herpes simplex virus (HSV) are considered to be the major causes of acute peripheral facial palsy (APFP). One hundred and forty-two patients with APFP were analyzed by serological assays and polymerase chain reaction analysis. Ramsay Hunt syndrome was diagnosed in 21 patients. Of the remaining 121 patients clinically diagnosed with Bell's palsy, VZV reactivation without zoster (zoster sine herpete) was detected in 35 patients (29%). The prevalence of antibodies to HSV among patients with Bell's palsy was significantly higher than the prevalence among those with VZV reactivation (Ramsay Hunt syndrome or zoster sine herpete). In contrast, a high incidence (88%) of VZV reactivation among HSV-seronegative patients with APFP was observed. Our data indicate that VZV is one of the major etiologic agents of clinically diagnosed Bell's palsy and that VZV reactivation causes APFP in most patients who lack antibodies to HSV.

Amplification of RNA from archival human temporal bone sections.

BACKGROUND: The amplification of DNA from celloidin-embedded human temporal bone sections by polymerase chain reaction (PCR) has been applied to some auditory diseases, such as herpes zoster oticus and hearing loss caused by the mutations of mitochondrial DNA. However, few studies have reported detection of RNA from temporal bone sections. OBJECTIVES: Because RNA analysis from temporal bone sections may elucidate the development of the diseases in the auditory, vestibular, and facial nerves, the authors investigated whether RNA in these sections can be amplified by reverse transcription (RT)-PCR. METHODS: Sections that were formalin-fixed, decalcified, and embedded between 1972 and 1986 were used. Nucleic acid was extracted from the celloidin-embedded temporal bone sections and subjected to RT-PCR. Human alpha-tubulin RNA was reverse transcribed to cDNA and amplified by nested PCR using two sets of primers that were designed to distinguish cDNA from genomic DNA based on the presence of an intron between the primers. RESULTS: Human alpha-tubulin RNA was detected in 11 of 14 temporal bone sections (79%) by RT-PCR. RNA was detected in even the oldest sections, which were processed in 1972. CONCLUSIONS: These results indicate that RNA can be analyzed from archival celloidin-embedded human temporal bone sections.

Reactivation of herpes simplex virus type 1 in patients with Bell's palsy.

Reactivation of herpes simplex virus type 1 (HSV-1) has been implicated in the pathogenesis of idiopathic peripheral facial palsy (Bell's palsy). The present study used the polymerase chain reaction (PCR) to analyze the saliva of patients with Bell's palsy for the presence of shed HSV-1. The study involved 47 patients with Bell's palsy, 24 patients with Ramsay Hunt syndrome, and 16 healthy HSV-seropositive volunteers. HSV-1 DNA was not detected in the saliva samples from HSV-seronegative patients. The prevalence of shed HSV-1 in patients with Bell's palsy (50%) was significantly higher than that in healthy volunteers (19%, p<0.05). When saliva samples were tested within 7 days after the onset of palsy, the prevalence of shed HSV-1 in patients with Bell's palsy (40%) was significantly higher than that in patients with Ramsay Hunt syndrome (7%, p<0.05). Furthermore, HSV-1 usually became undetectable by the second week after the onset of Bell's palsy when HSV-1 was detected during the acute phase of the disease. These findings strongly suggest that reactivation of HSV-1 is involved in the pathogenesis Bell's palsy, and indicate that PCR is a useful tool for early diagnosis of HSV-1 reactivation in patients with Bell's palsy.

Acetazolamide challenge for three-dimensional time-of-flight MR angiography of the brain.

PURPOSE: We compared three-dimensional time-of-flight MR angiograms obtained before and after acetazolamide administration to evaluate whether use of this drug could improve visualization of small peripheral intracranial arteries and atherosclerotic stenosis. METHODS: For evaluation of small peripheral arteries, 10 patients with clinical diagnosis of ischemic cerebrovascular disease and 10 healthy volunteers were investigated, and for evaluation of stenosis, another 6 patients were investigated. Vascular images were obtained by three-dimensional time-of-flight MR angiography. After a baseline scan, 17 mg/kg acetazolamide was injected intravenously and the second scan was performed 20 minutes later. RESULTS: Several small peripheral arteries that had not been seen on the baseline images were visible on the acetazolamide images without any augmentation of the background signals. Stenotic lesions in the main trunks of the major cerebral arteries were detected more clearly on acetazolamide images. CONCLUSIONS: Acetazolamide improves visualization of small peripheral intracranial arteries and sensitivity in detecting atherosclerotic stenosis in the main trunk of major cerebral artery by three-dimensional time-of-flight MR angiography without changing MR apparatus and software.