Previous research has shown that low-frequency repetitive transcranial magnetic stimulation over the primary motor area and supplementary motor area can reduce L-dopa-induced dyskinesias in Parkinson's disease; however, it involved only patients with peak-dose or diphasic dyskinesia. We report a case of a patient with severely painful off-period dystonia in the unilateral lower limb who underwent 0.9-Hz subthreshold repetitive transcranial magnetic stimulation over contralateral primary motor area and supplementary motor area. Repetitive transcranial magnetic stimulation over the primary motor area significantly reduced the painful dystonia and walking disturbances but repetitive transcranial magnetic stimulation over the supplementary motor area did not. The cortical silent period also prolonged after repetitive transcranial magnetic stimulation over the primary motor area. At 5 mos of approximately once a week repetitive transcranial magnetic stimulation over the primary motor area, the Unified Parkinson's Disease Rating Scale motor score also improved. This report shows that repetitive transcranial magnetic stimulation over the inhibitory primary motor area can be useful for rehabilitating patients with Parkinson's disease with off-period dystonia and suggests that this treatment should be further verified in such patients.

Measuring PMP parameters with a second lumbrical-interosseous study may be useful for diagnosing CTS.

We present a case of primary orthostatic tremor (OT) responsive to dopaminergic medication. The patient was a 62-year-old woman, who had leg tremor on standing for 2 years. No parkinsonian or other neurological signs were observed. Surface electromyography of the quadriceps muscles showed regular 5-6 Hz muscle discharges. [ 123 I]-FP-CIT DAT-SPECT imaging revealed decreased specific binding ratio values in the striatum compared with age-matched controls. Her leg tremor almost completely disappeared following administration of levodopa 200 mg and pramipexole 0.75 mg. Since her OT with low-frequency discharge was responsive to dopaminergic medication, we speculate that it may be a premotor sign of Parkinson's disease.

We report a 34-year-old female PARK2 patient presenting with dopa-responsive dystonia (DRD). She noticed difficulty in raising her foot while walking at the age of 24. Her lower limb symptoms were identified as dystonia later, and she was started on Menesit, which resulted in improvement of her symptoms. She was diagnosed as DRD and has been on continuous treatment since then. The specific binding ratio (SBR) of ¹²³I FP-CIT SPECT was significantly lower than those of controls of the same age, but ¹²³I-meta-iodobenzylguanidine myocardial scintigraphy showed a normal heart to mediastinum ratio. The Montreal Cognitive Assessment, Japanese version, was normal for her age. DRD is an inherited dystonia that typically begins during childhood and may be caused by mutations of the GCH1 (GTP cyclohydrolase), SPR (sepiapterin reductase), or TH (tyrosine hydroxylase) genes. Our patient was diagnosed as PARK2, known as autosomal-recessive juvenile Parkinson’s disease, based on genetic analysis. Although there was no family history of the disease, the decrease in SBR of ¹²³I FP-CIT SPECT enabled us to diagnose PARK2 and to differentiate this from DRD due to other genetic disorders.

We report herein a rare case of middle lobe syndrome, occurring in two sisters. Since selective aspirations of sputum under bronchoscopic guidance proved ineffective, a middle lobectomy was performed in both cases. Histological findings of the resected specimens showed overgrowth of the bronchial glands, lymphocytic infiltration around the alveoli and glandular metaplasia of the alveoli in both cases. Based on the allergic diathesis, we suggest that in these 2 sisters, middle lobe syndrome was caused by chronic inflammation.