A bio-inspired neuromuscular model to simulate the neuro-sensorimotor basis for postural-reflex-response in humans

Author(s):  
Fady Alnajjar ◽  
Tytus Wojtara ◽  
Shingo Shimoda ◽  
Hidenori Kimura
1992 ◽  
Vol 12 (4) ◽  
pp. 229-241
Author(s):  
Richard P. DiFabio ◽  
Mary Beth Badke ◽  
Ann Breunig

Gaps in the recruitment of postural muscles to correct body sway may be a limiting factor in the rehabilitation of patients with stroke. The purpose of this study was to determine how the onset of a postural reflex compares to the conscious identification of body sway in patients with hemiplegia and in a comparison group of able-bodied subjects. All subjects stood on a movable force platform that was unexpectedly displaced backwards inducing a forward body sway. The excursion and velocity of the platform displacements were varied systematically and the frequency of activation of postural muscles was recorded. A hand held response key was used to measure the time required to react to the postural disturbance (RT). In addition, the onset time of a long-loop “stretch” reflex was measured in the gastrocnemius muscles bilaterally. Subjects with hemiplegia failed to recruit a reflex response in 53% of the trials, whereas able-bodied subjects had an absent response in only 3% of the trials. The upper extremity RT for subjects with hemiplegia was not significantly delayed compared to able-bodied subjects, and the onset of a stretch reflex response in the gastrocnemius muscles was not different between groups. In addition, there was no correlation between reflex onset and conscious reaction time for control or disabled groups. These results have implications for the practice of occupational therapy because lower extremity recruitment deficits may persist and require treatment even though the recognition of body sway and the onset of reflex muscle discharge (when recruited) was similar to that of able-bodied subjects.


2006 ◽  
Vol 2006.2 (0) ◽  
pp. 337-338
Author(s):  
Tatsuya OKUNAKA ◽  
Shinichiro YAMAMOTO ◽  
Yukio KAWAKAMI

Author(s):  
Kazumasa HIROSAWA ◽  
Shinichiro YAMAMOTO ◽  
Hiroyuki KOYAMA ◽  
Takashi KOMEDA ◽  
Yukio KAWAKAMI

Author(s):  
Kouhei MISHIMA ◽  
Shin-ichiro YAMAMOTO ◽  
Hiroyuki KOYAMA ◽  
Takashi KOMEDA ◽  
Yukio KAWAKAMI

2005 ◽  
Vol 2004.17 (0) ◽  
pp. 103-104
Author(s):  
Kazumasa HIROSAWA ◽  
Shin-ichiro YAMAMOTO ◽  
Hiroyuki KOYAMA ◽  
Takashi KOMEDA ◽  
Yukio KAWAKAMI

Author(s):  
Takeshi OBARA ◽  
Shin-Ichiro YAMAMOTO ◽  
Tasuku MIYOSHI ◽  
Yukio KAWAKAMI ◽  
Tatsuya OKUNAKA

Author(s):  
L. Vacca-Galloway ◽  
Y.Q. Zhang ◽  
P. Bose ◽  
S.H. Zhang

The Wobbler mouse (wr) has been studied as a model for inherited human motoneuron diseases (MNDs). Using behavioral tests for forelimb power, walking, climbing, and the “clasp-like reflex” response, the progress of the MND can be categorized into early (Stage 1, age 21 days) and late (Stage 4, age 3 months) stages. Age-and sex-matched normal phenotype littermates (NFR/wr) were used as controls (Stage 0), as well as mice from two related wild-type mouse strains: NFR/N and a C57BI/6N. Using behavioral tests, we also detected pre-symptomatic Wobblers at postnatal ages 7 and 14 days. The mice were anesthetized and perfusion-fixed for immunocytochemical (ICC) of CGRP and ChAT in the spinal cord (C3 to C5).Using computerized morphomety (Vidas, Zeiss), the numbers of IR-CGRP labelled motoneurons were significantly lower in 14 day old Wobbler specimens compared with the controls (Fig. 1). The same trend was observed at 21 days (Stage 1) and 3 months (Stage 4). The IR-CGRP-containing motoneurons in the Wobbler specimens declined progressively with age.


2001 ◽  
Vol 120 (5) ◽  
pp. A718-A718
Author(s):  
C DIENEFELD ◽  
L WANG ◽  
K NEUFELD ◽  
Y MAO ◽  
S HOLLERBACH ◽  
...  

1999 ◽  
Vol 86 (1) ◽  
pp. 294-297 ◽  
Author(s):  
Elizabeth M. Wagner ◽  
David B. Jacoby

To determine whether methacholine causes vagally mediated reflex constriction of airway smooth muscle, we administered methacholine to sheep either via the bronchial artery or as an aerosol via tracheostomy into the lower airways. We then measured the contraction of an isolated, in situ segment of trachealis smooth muscle and determined the effect of vagotomy on the trachealis response. Administering methacholine to the subcarinal airways via the bronchial artery (0.5–10.0 μg/ml) caused dose-dependent bronchoconstriction and contraction of the tracheal segment. At the highest methacholine concentration delivered, trachealis smooth muscle tension increased an average of 186% over baseline. Aerosolized methacholine (5–7 breaths of 100 mg/ml) increased trachealis tension by 58% and airways resistance by 183%. As the bronchial circulation in the sheep does not supply the trachea, we postulated that the trachealis contraction was caused by a reflex response to methacholine in the lower airways. Bilateral vagotomy essentially eliminated the trachealis response and the airways resistance change after lower airways challenge (either via the bronchial artery or via aerosol) with methacholine. We conclude that 1) methacholine causes a substantial reflex contraction of airway smooth muscle and 2) the assumption may not be valid that a response to methacholine in humans or experimental animals represents solely the direct effect on smooth muscle.


1957 ◽  
Vol 40 (3) ◽  
pp. 435-450 ◽  
Author(s):  
David P. C. Lloyd

An assemblage of individual motoneurons constituting a synthetic motoneuron pool has been studied from the standpoint of relating monosynaptic reflex responses to frequency of afferent stimulation. Intensity of low frequency depression is not a simple function of transmitter potentiality. As frequency of stimulation increases from 3 per minute to 10 per second, low frequency depression increases in magnitude. Between 10 and approximately 60 per second low frequency depression apparently diminishes and subnormality becomes a factor in causing depression. At frequencies above 60 per second temporal summation occurs, but subnormality limits the degree of response attainable by summation. At low stimulation frequencies rhythm is determined by stimulation frequency. Interruptions of rhythmic firing depend solely upon temporal fluctuation of excitability. At high frequency of stimulation rhythm is determined by subnormality rather than inherent rhythmicity, and excitability fluctuation leads to instability of response rhythm. In short, whatever the stimulation frequency, random excitability fluctuation is the factor disrupting rhythmic response. Monosynaptic reflex response latency is stable during high frequency stimulation as it is in low frequency stimulation provided a significant extrinsic source of random bombardment is not present. In the presence of powerful random bombardment discharge may become random with respect to monosynaptic afferent excitation provided the latter is feeble. When this occurs it does so equally at low frequency and high frequency. Thus temporal summation is not a necessary factor. There is, then, no remaining evidence to suggest that the agency for temporal summation in the monosynaptic system becomes a transmitting agency in its own right.


Sign in / Sign up

Export Citation Format

Share Document