title: Deficits of anticipatory grip force control after damage to peripheral and central sensorimotor systems.
abstract: Healthy subjects adjust their grip force economically to the weight of a hand-held object. In addition, inertial loads, which arise from arm movements with the grasped object, are anticipated by parallel grip force modulations. Internal forward models have been proposed to predict the consequences of voluntary movements. Anesthesia of the fingers impairs grip force economy but the feedforward character of the grip force/load coupling is preserved. To further analyze the role of sensory input for internal forward models and to characterize the consequences of central nervous system damage for anticipatory grip force control, we measured grip force behavior in neurological patients. We tested a group of stroke patients with varying degrees of impaired fine motor control and sensory loss, a single patient with complete and permanent differentation from all tactile and proprioceptive input, and a group of patients with amyotrophic lateral sclerosis (ALS) that exclusively impairs the motor system without affecting sensory modalities. Increased grip forces were a common finding in all patients. Sensory deficits were a strong but not the only predictor of impaired grip force economy. The feedforward mode of grip force control was typically preserved in the stroke patients despite their central sensory deficits, but was severely disturbed in the patient with peripheral sensory deafferentation and in a minority of stroke patients. Moderate deficits of feedforward control were also obvious in ALS patients. Thus, the function of the internal forward model and the precision of grip force production may depend on a complex anatomical and functional network of sensory and motor structures and their interaction in time and space.
authors.affiliation: Neuropsychology Research Group (EKN), Department of Neuropsychology, Germany. joachim.hermsdoerfer@extern.lrz-muenchen.de
authors.forename: Joachim
authors.initials: J
authors.lastname: Hermsdörfer
authors.forename: Elke
authors.initials: E
authors.lastname: Hagl
authors.forename: Dennis A
authors.initials: DA
authors.lastname: Nowak
mesh_terms: D000344:Afferent Pathways / Q000503:physiopathology; D000368:Aged; D004292:Dominance, Cerebral / Q000502:physiology; D005260:Female; D018737:Hand Strength / Q000502:physiology*; D006801:Humans; D020244:Infarction, Middle Cerebral Artery / Q000503:physiopathology*; D007537:Isometric Contraction / Q000502:physiology*; D007699:Kinesthesis / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009044:Motor Cortex / Q000503:physiopathology*; D016472:Motor Neuron Disease / Q000503:physiopathology*; D009046:Motor Neurons / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation; D017933:Peripheral Nervous System / Q000502:physiology*; D011434:Proprioception / Q000502:physiology; D011597:Psychomotor Performance / Q000502:physiology; D011984:Sensory Receptor Cells / Q000503:physiopathology; D012815:Signal Processing, Computer-Assisted; D013003:Somatosensory Cortex / Q000503:physiopathology*; D014110:Touch / Q000502:physiology; D014892:Weight Perception / Q000502:physiology*; D016474:Weight-Bearing / Q000502:physiology*