Relation between abnormal synergy and gait in patients after stroke

Yes, yes, we know synergy exists after stroke and is a problem. What do you suggest we do about this f*cking problem? Solutions anyone?
http://www.jneuroengrehab.com/content/11/1/141

Kaoru Sakuma^12*, Koji Ohata¹, Keisuke Izumi³, Yu Shiotsuka⁴, Tadashi Yasui⁵, Satoko Ibuki¹ and Noriaki Ichihashi¹

• * Corresponding author: Kaoru Sakuma sakuma.kaoru.27u@st.kyoto-u.ac.jp

Author Affiliations

¹ Department of Physical Therapy, Human Health Sciences, Graduate School of Medicine, Kyoto University, 53, Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan
² Japan Society for the Promotion of Science, 5-3-1 Kojimachi, Chiyoda-ku, Tokyo 102-0083, Japan
³ Department of Rehabilitation, Biwako Gakuen Medical and Welfare Center, Kusatsu, 8-3-113 Kasayama, Kusatsu-shi, Shiga 525-0072, Japan
⁴ Department of Rehabilitation, Hakuhoukai Tagawashinsei Hospital, 3638 Ooazanatsuyoshi, Tagawa-shi, Fukuoka 825-0004, Japan
⁵ Manufacturing Technology Section, Kawamura Gishi Co., Ltd, 1-12-1 Goryo, Daito-shi, Osaka 574-0064, Japan

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Journal of NeuroEngineering and Rehabilitation 2014, 11:141  doi:10.1186/1743-0003-11-141
The electronic version of this article is the complete one and can be found online at: http://www.jneuroengrehab.com/content/11/1/141

Received:	11 June 2014
Accepted:	18 September 2014
Published:	25 September 2014

© 2014 Sakuma et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Abstract

Background

The abnormal synergy seen in patients after stroke is considered to limit the ability of these patients. However, in the lower extremity, antigravity torque generation rather than precise movement is needed for functions such as sit-to-stand movement and gait. Therefore, the ability to generate torque may be important either as a primary movement or as an abnormal synergy. We attempted to quantify the torque generation in the lower limb, selectively and as an abnormal synergy, and its relation with gait.

Methods

Selectively generated plantar flexion torque in the ankle and plantar flexion torque secondarily generated accompanying maximal hip extension (i.e., torque generated with abnormal synergy) were measured in subjects after stroke and control subjects. In subjects after stroke, secondary torque generation while controlling hip extension torque as 25%, 50%, and 75% of the maximal hip extension was also measured. The relation of torque generation with the gait speed and timed-up-and go test (TUG) was also analyzed.

Results

In subjects after stroke, there was no difference between the amount of plantar flexion torque generated secondarily and the selectively generated torque, whereas the selective torque was significantly greater in control subjects. Pearson product–moment correlation coefficient analysis revealed that TUG speed is related to secondarily generated torque accompanying maximal hip extension but not with selectively generated torque.

Conclusion

Secondarily generated torque was found to be a factor that affects TUG speed, and the ability to generate torque even through abnormal synergy may help for gait ability in subjects after stroke. 

Discussion

The results of this study revealed that in subjects after stroke, the increase in the percentage of maximum hip extension torque generated by the subjects increased the%STo. The subjects after stroke exhibited lower torque than the control group in the PTo but not in the STo. The PTo was significantly higher than the STo in the control group but not in the subjects after stroke. Our hypothesis was supported by the observation that there is a correlation between TUG and the STo in the subjects after stroke, and the principal finding of this study is that the STo was the determinant of TUG, as revealed by stepwise analysis. This is the first study that quantitatively demonstrated the inability to selectively generate voluntary torque in the lower limb, and showed that STo affects TUG in patients after stroke.

Relation between secondary torque generation and percent hip extension torque in the subjects after stroke

Controlling agonist activity is a fundamental function required in activities of daily living. Therefore, in this study, we chose a task that requires generating a certain percentage of maximum voluntary torque. The subjects after stroke showed explicit increase in the %STo as the percentage of required hip extension increased, which is consistent with the characteristics of abnormal synergy described in previous studies [8,9]. Therefore, the STo measured in this study is considered to reflect the feature of abnormal synergy.

Characteristics of primary torque and secondary torque in the subjects after stroke and the control group

In a previous study that measured the secondary torque in the ankle joint during maximum voluntary hip extension in both controls and subjects after stroke, the secondary torque was seen in both groups and no differences were found in the rate of the secondary torque to maximum voluntary ankle plantar flexion torque between the groups [13]. Similarly in this study, there were concurrent ankle plantar flexion torques measured as the STo during the generation of the maximum voluntary hip extension torque in both the controls and the subjects after stroke, and there were no differences between the controls and subjects after stroke in the STo torque normalized to body weight. In the current study, the control group could generate considerably higher PTo than STo, whereas the subjects after stroke could only generate PTo torque equivalent to their STo torque. Moreover, the gastrocnemius and the soleus, which are the agonist muscles in ankle plantar flexion, were more activated during STo than during PTo in the subjects after stroke; the opposite was observed in the controls. This is probably due to the disorganization of motor unit recruitment, rate modulation patterns [31,32], antagonist muscle weakness [33], and the abnormal corticospinal responses [34-36] that might affect the contribution of agonist activity to the voluntary torque seen in the subjects after stroke. It should also be noted that the tibialis anterior muscle activity during STo was higher than that during PTo in the subjects after stroke. The co-activation of the antagonist muscle, i.e., the tibialis anterior muscle might have inhibited the generation of plantar flexion torque as STo. However, the gastrocnemius and soleus activities during STo were not higher than those during PTo. Therefore, we conclude that the tibialis anterior muscle activity did not affect the results of this study. In the subjects after stroke, because of the inability to selectively activate the agonist muscle, the STo becomes relatively higher than the PTo.

Correlation with gait ability

The stepwise analysis revealed that the STo, and not the PTo, was the determinant of TUG. Although there was no significant relation between the STo and gait speed, the correlation coefficient was high. Therefore, we consider that there might be a relation between the STo and gait ability. In previous studies, the relation between the Brunnstrom recovery stage [19] or the Fugl-Meyer assessment [23] and gait speed was reported. However, because these clinical assessments evaluated both recovery from abnormal synergy and improvement of voluntary movement, it was unclear whether abnormal synergy or voluntary movement was related to gait speed. In this study, by quantifying the abnormal synergy measuring the joint torque, the relation between abnormal synergy and gait was revealed for the first time, showing that STo was the determinant of TUG. On the other hand, a previous study showed that the paretic ankle plantar flexion torque was correlated with gait speed in the patients after stroke [27]. We consider that because TUG consists not only of gait but also of sit-to-stand movement, which requires a large torque [37,38], abnormal synergy might be a related factor. Our results suggest that in subjects after stroke, STo might be adopted to compensate for the inability to generate the voluntary torque during gait.

Limitation

Three limitations of this study need to be mentioned. First, the PTo and STo measured in this study might be affected by other factors such as co-activation and spasticity. Nevertheless, we could at least assess one aspect of abnormal synergy quantitatively as the joint torque generated concurrently with the intended voluntary torque.

Second, the subjects after stroke recruited in our study were community-dwelling, able to walk. Therefore, our results may not be applicable to patients in a more severe condition after stroke who are unable to live in the community or have greater disability in gait.

Finally, this study did not evaluate abnormal synergy during gait, or the relation of abnormal synergy with each element in gait. Therefore, the influence of abnormal synergy on each factor in gait remains unknown.

Conclusion

We found that the amount of secondarily generated plantar flexion torque (STo) was as large as the selectively generated plantar flexion torque (PTo), and that the STo was negatively correlated to TUG speed. This suggests that torque generation as abnormal synergy may help for patients after stroke who cannot sufficiently generate selective torque.

 

More details at link since you will need to figure out how to solve this yourself.