Because it has been confirmed that the vanadyl(IV) ion and its complexes act as insulin mimetics, a new organic vanadyl complex, (N-pyridylmethylaspartate)oxovanadium (VOPASP) with VO(N2O2) coordination mode, was prepared. Development of a simple and rapid in-vitro assay is needed for recognition of potent insulin-mimetic complexes. Treatment of Ehrlich ascites tumour cells with 2-deoxyglucose in the presence of vanadyl sulphate, or other vanadyl complexes with the same coordination mode (VOPASP, bis(picolinate)oxovanadium (VOPA) and bis(6-methyl picolinate)oxovanadium (VOMPA)), in the presence of 2-deoxy-D-[1-3H]glucose ([3H]deoxyglucose), resulted in concentration-dependent uptake of 2-deoxyglucose by the cells. The responses of the cells to the vanadyl complexes were reflected, in part, by results obtained from the free fatty acid-releasing assay using rat adipocytes. These results show that the in-vitro assay with Ehrlich ascites tumour cells provides an accurate and rapid assessment of glucose uptake by the cells. The assay is proposed as a means of predicting the insulin-mimetic activity of the vanadyl complexes and for studying the mechanism of action of the complexes.

A 52‐year‐old schizophrenic patient acutely showed blepharospasm and oromandibular dystonia following neuroleptic‐induced akathisia. She had suffered from schizophrenia and been treated with neuroleptics for 15 years and had manifested tardive dyskinesia 5 years ago. Following a change in her neuroleptic medication, severe akathisia developed. Two days after the appearance of akathisia, blepharospasm and oromandibular dystonia appeared. After the disappearance of akathisia, the disorder continued. The frequency of blepharospasm ranged from 30 to 40 (times/min). The oral administration of trihexyphenidyl (6 mg/day), perphenazine (12 mg/day), and fluphenazine (12 mg/day) significantly decreased the frequency of blepharospasm, whereas carbamazepine (600 mg/day) and sulpiride (1200 mg/day) did not. These results suggest that overactivity of both cholinergic and dopaminergic functions in the striatum may be involved in this patient. Our patient, who showed acute onset of Meige's syndrome following neuroleptic‐induced akathisia, is of interest to those studying the pathogenesis of Meige's syndrome.

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