The mechanism of complement fixation on cell surfaces by whole antiserums, and by 19S and 7S fractions has been studied with a new comple-ment-fixation test. This test is based on the fixation and transfer of the activated first component of complement (C1a). We have concluded that a single molecule of 19S antibody in combination with antigen at the cell surface is sufficient to bind one molecule of C1a. For 7S antibodies at least two molecules in close proximity at the cell surface are required to fix one molecule of C1a.

Patients suffering from Parkinson's disease (PD) are more dependent on visual feedback during movement than are normals. Studying two-dimensional pointing movements, we recently found that PD patients undershoot targets when vision of their own moving hand is occluded but not when complete vision is provided or when the target is extinguished immediately before movement onset. In the absence of vision, information about position of the moving hand may originate from peripheral kinesthetic feedback and from corollary discharges derived from the efferent motor signal. To find out which of both mechanisms--kinesthetic feedback or corollary discharge--is defective in PD, we compared active movements with imposed movements in which the hand is passively moved by the experimenter, whereas vision of the hand was occluded under either condition. In agreement with our earlier findings, slow, active pointing movements of PD patients were hypometric. In addition, PD patients terminated passively imposed movements of comparable speed earlier than did normals, with the consequence that imposed movements were equally hypometric. Our results make it unlikely that disturbed corollary discharge is responsible for hypometria under nonvisual conditions. Instead, the data suggest that PD patients have a defect of kinesthesia in slowly executed movements.

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