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A 63-year-old Japanese female in an immunocompetent state developed right Ramsay Hunt syndrome and left shoulder pain, and left upper limb motor paresis with herpes zoster (HZ) duplex in the right auricle and left shoulder regions. With her Ramsay Hunt syndrome, neural deafness, tinnitus and vestibular symptoms were observed, and she lacked facial nerve palsy. Cerebrospinal fluid (CSF) findings revealed an increase in lymphocytes (21 cells/μl) and protein content (29 mg/dl), and polymerase chain reaction for varicella-zoster virus DNA in CSF was negative. Cervical root MRI using 3D Nerve VIEW (Philips) imaging showed high-intensity lesions on the C5-C8 spinal roots with contrast enhancements. No abnormalities were observed in the median or ulnar motor sensory nerve conduction velocity conduction studies including the F wave. PubMed search revealed no report of a patient with this profile, and to the best of our knowledge HZ duplex with concomitant neurological impairments has not been reported. We compare our present case with several similar cases from the literature.

A 34-year-old man developed right-dominant lower limb paraplegia, and then upper limb paresis with radicular pain following disseminated herpes zoster (HZ) in his right forehead, back of the trunk, and lumbar and right lower limb regions. Cerebrospinal fluid (CSF) findings revealed an increase in lymphocytes (32 cells/μl) and protein content (50 mg/dl), and polymerase chain reaction (PCR) for varicella-zoster virus (VZV) DNA was negative in CSF, but VZV antigen was positive in the patient's vesicle smear. Lumbar root MRI using 3D Nerve VIEW (Philips) imaging showed high-intensity lesions on the L2-L5 spinal roots with contrast enhancements, and cervical MRI showed similar findings on both sides at the C4-Th1. Peripheral nerve conduction study revealed prolonged distal latency to 4.9 ms, decreased MCV to 38 m/s, and complete loss of F-wave was seen in the right peroneal nerve study. Minimal F-wave latency was prolonged in the right tibial nerve. Thus, the patient was diagnosed with VZV polyradiculoneuritis caused by disseminated HZ. Regarding the possible pathogenesis of polyradiculoneuritis in this patient with disseminated HZ, we speculate that VZV reached by retrograde transmission from the involved peripheral nerves to the spinal ganglia, which, then, produced polyradiculoneuritis.

A 76-year-old Japanese female who was treated with long-term use of prednisolone at 10 mg/day for interstitial pneumonia developed acute right-dominant lower limb paralysis and then upper limb paralysis with herpes zoster eruptions on the right C7-Th1 dermatomes. On admission, right predominant quadriplegia was observed with sensory symptoms; Hughes functional grade was level 4; the hand grip power was right, 0, and left, 7 kg, the deep tendon reflexes were abolished throughout without pathologic reflexes. Twenty days after the onset of the symptoms, the cerebrospinal fluid (CSF) revealed mild increases of lymphocytes (13 cells/μl) and protein content (73 mg/dl). Varicella-zoster virus (VZV) PCR was negative in the CSF, but an enzyme immunoassay for VZV was positive in her serum and CSF, and the high titers were prolonged. Peripheral nerve conduction and F wave studies suggested right-dominant demyelinating polyradiculoneuropathy. A T 1 -weighted MR contrast image exhibited right-dominant high-intensity lesions on the C7-Th1 spinal roots and similar lesions on the L4-5 spinal roots. We compared with several similar cases from the literature and proposed that VZV itself involves the pathogenesis of the polyradiculoneuritis in immunocompromised hosts.

Carbon ion radiotherapy (CIRT) is a promising modality because of its excellent dose localization and high biological effect on the tumor. Our clinical trials led us to conclude that irradiation with heavy particle beams, notably carbon ion beams, offers a significant potential for improving tumor control without increasing toxicity risks. In lung cancer treatment, between 1994 and 1999, a phase I/II study of the treatment for stage I non-small cell lung cancer by CIRT was first conducted using a dose escalation method to determine the optimal dose. Furthermore, definite tumor control was also confirmed by the autopsies of CIRT-treated patients and in cases treated by surgery. In the present study, a phase II clinical trial and a phase I/II dose escalation clinical trial are reported.

A 60-year-old man with surgically treated nocardia pyothorax was referred to our hospital since he became drowsy. Brain MRI revealed multiple brain abscesses. His cerebrospinal fluid (CSF) showed increase in polymorphonuclear cells and decrease in glucose. Since he was allergic to sulfamethoxazole * trimethoprim, ceftriaxone and then minocycline were given. Minocycline resulted in dramatic improvement of neurological symtoms, MRI findings and CSF cell count. PCR analysis of 16S ribosomal DNA using his resected thoracic wall revealed that nocardia from his tissue was strain IFM0860. Strain IFM0860 nocardia was found to be sensitive to minocycline but not to sulfamethoxazole * trimethoprim and ceftriaxone. Intravenous administration of minocycline was followed by three-year per os administration of minocycline during which he had no recurrence of brain abscess. Thus, brain nocardiosis could be successfully treated with appropriate antibiotics. The lesson from the present case is that identification of the type of nocardia by PCR analysis of 16S ribosomal DNA could help accomplish tailor-made antibiotic therapy.

A rapid and excessive increase in extracellular dopamine(DA) after L-DOPA administration is considered one of the major causes for L-DOPA-induced peak-dose dyskinesia. Therefore, inhibition of excessive rise in L-DOPA-derived DA is likely to be an ideal treatment for L-DOPA-induced dyskinesia. Based on our previous experimental studies that 8-OH-DPAT, a potent 5-HT1A agonist, attenuates an increase in L-DOPA-induced extracellular DA in the striatum of the rat model of Parkinson's disease, we hypothesized that L-DOPA-induced dyskinesia in patients with Parkinson's disease is alleviated by a 5-HT1A agonist. In the present study, we administered tandospirone citrate, a selective 5-HT1A agonist, to patients with Parkinson's disease suffering from L-DOPA-induced dyskinesia. Tandospirone(15-60 mg/day) was administered to 10 patients with L-DOPA-induced peak-dose dyskinesia. Twelve weeks after tandospirone treatment, duration of dyskinesia, subjective and objective severity of dyskinesia, and parkinsonian features were evaluated. Severity of dyskinesia was decreased in 5 patients; among these, 3 patients experienced slight worsening of parkinsonian features. Four patients showed no change in dyskinesia; among these, 2 patients showed worsening of parkinsonian features. One patient had slight worsening of dyskinesia without any change in parkinsonian features. The present study demonstrated that tandospirone is effective in alleviating L-DOPA-induced dyskinesia in 50% of the patients. However, at the same time 50% patients showed slight worsening of parkinsonian features. Both the anti-dyskinetic effect and the worsening of parkinsonian features are thought to be induced by tandospirone's potent 5-HT1A agonistic activity. Diverse effect of tandospirone may be caused by its partial agonist activity on 5-HT1A receptors, or may indicate that other causes for the expression of dyskinesia exist apart from excessive rise in brain DA levels. Administration of a 5-HT1A agonist is a choice for patients with dyskinesia if the care is taken so as not to induce worsening of parkinsonian features. Further studies such as double-blind trials are needed to confirm the usefulness of a 5-HT1A agonist for L-DOPA-induced dyskinesia.