Effects of posterior parietal lesions on visually guided movements in monkeys

Abstract

Four monkeys were trained to position, with either hand, a vertical rod in front of one of 5 target lights spaced 20 degrees apart on a semicircular screen. After the monkeys had reached the preoperative criterion (80% trials correct per session) they received a 1- or 2-stage bilateral lesion of posterior parietal cortex restricted to area 7. The lesion produced in all the monkeys considerable but temporary changes in movement latency, accuracy, velocity and duration. Latency increase appeared to be independent of changes in the other parameters. After the first lesion, movement latency increased for the contralateral arm in both left and right working spaces, from 100 ms up to 400 ms depending on the animal. A second lesion symmetrical to the first one increased movement latency of the arm contralateral or ipsilateral to the last lesion, depending on the time interval between the two lesions. In addition, unilateral lesions of area 7 induced a gross inaccuracy in movements of the arm contralateral to the lesion, more marked in the contralateral working space. These lesions also increased movement peak velocity and simultaneously decreased movement duration for the arm contralateral to the lesion. The increase in velocity appeared to be related to the decrease in duration. A second lesion of area 7 in the opposite hemisphere similarly affected accuracy, velocity and duration but for the arm contralateral to the second lesion.

Volumetric effects of motor cortex injury on recovery of dexterous movements

“…Interrupting corticocortical projection fibers disconnects cortical areas that normally coordinate sensorimotor activities during control of hand/digit function and may create greater lasting impairments of function than lesions limited primarily to gray matter (Haaxma and Kuypers, 1975). Indeed, monkeys with surgically induced lesions of posterior parietal cortex that were limited primarily to gray matter have reported recovery of visually guided hand function occurring 2–3 weeks after injury (Battaglini, et al, 2002; Faughier-Grimaud, et al, 1985; Faughier-Grimaud, et al, 1978). Moreover, some studies of surgical lesions to motor areas of the frontal lobe in humans for treatment of cancer, epilepsy and arteriovenous malformations have found relatively minor lasting motor function deficits in most cases (Chamoun, et al, 2007; Da Pian, et al, 1980; Laplane, et al, 1977; Mikuni, et al, 2005; Rostomily, et al, 1991).…”

Response Properties of Motor Equivalence Neurons of the Primate Premotor Cortex

“…This was indeed the case, the difference being nearly 50 ms ( t = 2.5, p < 0.05), even though in both cases the eyes were moving in the same direction (Fisk and Goodale, 1985). The notion that movements of the eyes and hand are coupled (at least temporally) is supported by one of the symptoms of the parietal syndrome, directional hypokinesia, which leads to an increase of the reaction time of both hand movements (Faugier-Grimaud et al, 1985; Mattingley et al, 1994) and saccades (Girotti et al, 1983) to contralateral targets. The same is true of the monkey where LIP lesions delay the onset of both the saccadic and the reaching components of coordinated eye-hand movements (Yttri et al, 2013).…”

Optic ataxia as a model to investigate the role of the posterior parietal cortex in visually guided action: evidence from studies of patient M.H.

“…In other words the normal pre-calibration of grip size in advance of contact with an object is typically lost in patients with optic ataxia: they open their hands widely and indiscriminately, without regard for the size of the target object. As mentioned in the Introduction, grasping impairments have been associated with optic ataxia since the earliest reports of misreaching following parietal damage, in both monkeys and humans (La Motte and Acuna, 1978; Damasio and Benton, 1979; Faugier-Grimaud et al, 1985; Ferrier, 1886, 1890; Jeannerod, 1986b; Perenin and Vighetto, 1988). …”