Motor and nonmotor behavioral deficits in monkeys made hemiparkinsonian by intracarotid MPTP infusion

• Published in: Neurology Vol. 42; no. 8; p. 1565
• Main Authors: Schneider, J S, McLaughlin, W W, Roeltgen, D P
• Format: Journal Article
• Language: English
• Published: United States 01.08.1992
• Subjects: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Animals; Attention; Behavior, Animal - physiology; Carotid Arteries; Functional Laterality; Injections, Intra-Arterial; Macaca mulatta; Male; Motor Activity - physiology; Parkinson Disease, Secondary - chemically induced; Parkinson Disease, Secondary - psychology; Photic Stimulation; Reward; Visual Fields
• ISSN: 0028-3878
• DOI: 10.1212/wnl.42.8.1565

We tested five monkeys (three Macaca mulatta, two Macaca nemistrina) made hemiparkinsonian by internal carotid artery infusion of 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) for lateralized motor function using a bar press task and a reaction time/movement time task and for hemispatial neglect or hemi-inattention using a double simultaneous stimulation (DSS) task, a lateralized reward retrieval task, and a task that assessed response to lateralized moving stimuli. All monkeys had impaired bar press performance and prolonged reaction and movement times with the limb contralateral to the lesion. However, using the limb ipsilateral to the lesion, all animals showed extinction to DSS, that is, they responded to single stimuli presented on the impaired side (contralateral to the MPTP lesion) more often than to stimuli presented on the impaired side that were presented simultaneously with stimuli on the unimpaired side (ipsilateral to the lesion). There was a response bias toward the side ipsilateral to the lesion in the lateralized retrieval task and a deficit in the ability to direct attention toward the side contralateral to the lesion when moving stimuli were employed. These latter results could not be explained by primary motor or sensory impairments. We conclude that unilateral MPTP-induced dopamine depletion in monkeys causes a complex syndrome characterized by overt motor disturbances contralateral to the side of lesion and less overtly apparent sensorimotor integration deficits.