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In recent years, the development of primate models of Parkinson’s disease has made it possible to clarify some of the pathophysiological mechanisms underlying parkinsonian symptoms (akinesia, rigidity, tremor and dopa-induced dyskinesia=DID)(Crossman, 1987). A sophisticated functional architecture of basal ganglia circuits has been proposed(Alexander and Crutcher, 11990), and parkinsonian symptoms can be accounted for by postulating specific disturbances within the basal ganglia-thalamocortical motor circuit(DeLong,1990). Lesion experiments in monkeys have revealed that parkinsonian-like tremor was the result of damage to the nigrostriatal dopaminergic pathways in combination with damage to the rubro-olivo-cere-bello-rubral and cerebello-thalamic pathways(Larochelle et al., 1970). Based on experimental studies in monkeys and depth microelectrode studies in the human thalamus, a closed tremor-mediating neuronal circuit has been proposed(Ohye, 1988a; Ohye et al., 1993). However, the data in living humans remain inconsistent. We have recorded spontaneous neuronal activity in the thalamus or pallidum with the aid of microelectrodes during the course of stereotactic thalamotomy or pallidotomy, clarifying several characteristic features in Parkinson’s disease(Ohye et al., 1979, 1989). On the other hand, positron emission tomography(PET) allows measurements of regional cerebral glucose metabolism(rCMRGlu)(Sokoloff et al., 1977; Phelps et al., 1979) and cerebral blood flow(rCBF) (Frackowiak et al., 1980), which is related to the local functional activity of the central nervous system(Sokoloff, 1981). Combining both independent techniques, we have studied the neural mechanisms or on-going changes underlying movement disorders of Parkinson’s disease(Ohye et al., 1991; Hirato et al., 1991, 1993). The present study was conducted to elucidate the possible neural pathway mediating parkinsonian symptoms in human beings.

A simple and rapid ultraviolet spectrophotometric method is proposed for the determination of trace amounts of tungsten(VI) with ammonium 1-pyrrolidinecarbodithioate (APDC). The method is based on measurement of the absorbance of the tungsten APDC complex in fairly concentrated hydrochloric acid medium; no extraction is required. The complex is formed at an initial acidity of 6 M hydrochloric acid and has an absorption maximum at 250 nm. The high absorption of the reagent blank at 250 nm disappears on decomposition of excess of reagent by heating. Beer's law is obeyed over the range 0.43–3.2 ppm of tungsten(VI). The molar absorptivity of the complex is 4.5 × 10 4 l.mole −1 .cm −1 at 250 nm. Tenfold amounts of aluminium, magnesium, calcium, cobalt, iron(II), lead, silver, sodium and titanium do not interfere in the determination of 50 μg of tungsten (VI).