Effect of Initial Lean on Scaling of Postural Feedback Responses

2005 ◽  
Vol 277-279 ◽  
pp. 142-147
Author(s):  
Suk Yung Park ◽  
Fay B. Horak ◽  
Arthur D. Kuo

We examined how the central nervous system adjusts postural responses to an increased postural challenge due to an initial lean. Postural feedback responses scale to accommodate biomechanical constraints, such as an allowable ankle joint torque. Initial forward leaning, which is observed among the elderly who are inactive or afraid of falling, brings subjects near to the limit of stability and makes the biomechanical constraints more difficult to obey. We hypothesized that the central nervous system is aware of body dynamics and restrains postural responses when subjects initially lean forward. To test this hypothesis, fast backwards perturbations of various magnitudes were applied to 12 healthy young subjects (3 male, 9 female) aged 20 to 32 years. The subjects were instructed to stand quietly on a hydraulic servo-controlled force platform with their arms crossed over their chests, then to recover from a perturbation by returning to their upright position, without stepping or lifting their heels off the ground, if possible. Initially, the subjects were either standing upright or leaning forward. The force platform was movable in the translational direction and programmed to move backward with various ramp displacements ranging from 1.2 to 15 cm, all with the duration of 275 msec. For each trial, the kinematics and ground reaction force data were recorded, then used to compute the net joint torques, employing a least squares inverse dynamics method. Optimization methods were used to identify a set of equivalent feedback control gains for each trial so that the biomechanical model incorporating this feedback control would reproduce the empirical response. The results showed that the kinematics, joint torque, and feedback gains gradually scaled as a function of the perturbation magnitude before they reached the biomechanical constraint, and the scaling became more severe with an initial forward lean. For example, the model suggested that the magnitude of the ankle joint angle feedback to ankle torque was smaller in the leaning trials than in the initially upright trials, as if the subjects experienced a larger postural perturbation in the leaning trials. These results imply that the central nervous system restrained the postural responses to accommodate the additional biomechanical constraint imposed by the forward posture, thereby suggesting that the central nervous system is aware of body dynamics and biomechanical constraints. The scaling of the postural feedback gains with the perturbation magnitude and initial lean indicates that the postural control can be interpreted as a feedback scheme with scalable gains.

2009 ◽  
Vol 102 (5) ◽  
pp. 2910-2920 ◽  
Author(s):  
Seyoung Kim ◽  
Fay B. Horak ◽  
Patricia Carlson-Kuhta ◽  
Sukyung Park

Many differences in postural responses have been associated with age and Parkinson's disease (PD), but until now there has been no quantitative model to explain these differences. We developed a feedback control model of body dynamics that could reproduce the postural responses of young subjects, elderly subjects, and subjects with PD, and we investigated whether the postural impairments of subjects with PD can be described as an abnormal scaling of postural feedback gain. Feedback gains quantify how the nervous system generates compensatory joint torques based on kinematic responses. Seven subjects in each group experienced forward postural perturbations to seven different backward support surface translations ranging from 3- to 15-cm amplitudes and with a constant duration of 275 ms. Ground reaction forces and joint kinematics were measured to obtain joint torques from inverse dynamics. A full-state feedback controller with a two-segment body dynamic model was used to simulate joint kinematics and kinetics in response to perturbations. Results showed that all three subject groups gradually scaled postural feedback gains as a function of perturbation amplitudes, and the scaling started even before the maximum allowable ankle torque was reached. This result implies that the nervous system takes body dynamics into account and adjusts postural feedback gains to accommodate biomechanical constraints. PD subjects showed significantly smaller than normal ankle feedback gain with low scaling and larger hip feedback gain, which led to an early violation of the flat-foot constraint and unusually small (bradykinetic) postural responses. Our postural feedback control model quantitatively described the postural abnormality of the patients with PD as abnormal feedback gains and reduced ability to modify postural feedback gain with changes in postural challenge.


Author(s):  
Gladys Harrison

With the advent of the space age and the need to determine the requirements for a space cabin atmosphere, oxygen effects came into increased importance, even though these effects have been the subject of continuous research for many years. In fact, Priestly initiated oxygen research when in 1775 he published his results of isolating oxygen and described the effects of breathing it on himself and two mice, the only creatures to have had the “privilege” of breathing this “pure air”.Early studies had demonstrated the central nervous system effects at pressures above one atmosphere. Light microscopy revealed extensive damage to the lungs at one atmosphere. These changes which included perivascular and peribronchial edema, focal hemorrhage, rupture of the alveolar septa, and widespread edema, resulted in death of the animal in less than one week. The severity of the symptoms differed between species and was age dependent, with young animals being more resistant.


Author(s):  
John L.Beggs ◽  
John D. Waggener ◽  
Wanda Miller ◽  
Jane Watkins

Studies using mesenteric and ear chamber preparations have shown that interendothelial junctions provide the route for neutrophil emigration during inflammation. The term emigration refers to the passage of white blood cells across the endothelium from the vascular lumen. Although the precise pathway of transendo- thelial emigration in the central nervous system (CNS) has not been resolved, the presence of different physiological and morphological (tight junctions) properties of CNS endothelium may dictate alternate emigration pathways.To study neutrophil emigration in the CNS, we induced meningitis in guinea pigs by intracisternal injection of E. coli bacteria.In this model, leptomeningeal inflammation is well developed by 3 hr. After 3 1/2 hr, animals were sacrificed by arterial perfusion with 3% phosphate buffered glutaraldehyde. Tissues from brain and spinal cord were post-fixed in 1% osmium tetroxide, dehydrated in alcohols and propylene oxide, and embedded in Epon. Thin serial sections were cut with diamond knives and examined in a Philips 300 electron microscope.


Author(s):  
Ezzatollah Keyhani

Acetylcholinesterase (EC 3.1.1.7) (ACHE) has been localized at cholinergic junctions both in the central nervous system and at the periphery and it functions in neurotransmission. ACHE was also found in other tissues without involvement in neurotransmission, but exhibiting the common property of transporting water and ions. This communication describes intracellular ACHE in mammalian bone marrow and its secretion into the extracellular medium.


Author(s):  
S.S. Spicer ◽  
B.A. Schulte

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.


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