tendon tap
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Author(s):  
Timothy S. Pulverenti ◽  
Gabriel S. Trajano ◽  
Benjamin J. C. Kirk ◽  
Vanesa Bochkezanian ◽  
Anthony J. Blazevich

Author(s):  
Volker Dietz ◽  
Thomas Sinkjaer

The relationship between clinical spasticity and spastic movement disorder in human adults is covered in this chapter. Exaggerated tendon tap reflexes associated with muscle hypertonia are the clinical signs of central nervous system lesions. Therefore, most antispastic treatments are directed at the reduction of reflex activity. However, a discrepancy exists between spasticity as measured in the clinic and movement disorder. Central motor lesions are associated with a loss of supraspinal drive and defective use of afferent input. These changes lead to paresis and maladaptation of the movement pattern. Secondary changes in mechanical muscle fibre and collagen tissue result in spastic muscle tone, which in part compensates for paresis and allows functional movements on a simpler level of organization. In mobile patients, functional training should be applied to improve both function and spasticity. Antispastic drugs can accentuate paresis and should primarily only be applied in non-ambulatory subjects.


2018 ◽  
Vol 9 (2) ◽  
pp. 85-89
Author(s):  
Yaemi Koshino ◽  
Koki Yamaguchi ◽  
Yuki Takahashi ◽  
Yusuke Takahashi ◽  
Jun Watabe

2018 ◽  
Vol 3 ◽  
pp. 1-5 ◽  
Author(s):  
Lale A. Ertuglu ◽  
Ilhan Karacan ◽  
Gizem Yilmaz ◽  
Kemal S. Türker

2016 ◽  
Vol 17 (1) ◽  
Author(s):  
James Maurini ◽  
Paul Ohmsen ◽  
Greg Condon ◽  
Rodney Pope ◽  
Wayne Hing

2016 ◽  
Vol 43 ◽  
pp. 182-186 ◽  
Author(s):  
Robyn L. Mildren ◽  
Martin Zaback ◽  
Allan L. Adkin ◽  
James S. Frank ◽  
Leah R. Bent
Keyword(s):  

Author(s):  
Volker Dietz ◽  
Thomas Sinkjaer

The relationship between clinical spasticity and spastic movement disorder in human adultsis covered in this chapter. Signs of exaggerated tendon tap reflexes with muscle hypertonia are the consequence of central nervous system lesions. Most antispastic treatments are directed at the reduction of reflex activity. In recent years, a discrepancy between spasticity as measured in the clinic and movement disorder was noticed. Central motor lesions are associated with a loss of supraspinal drive and defective use of afferent input. These changes lead to paresis and maladaptation of the movement pattern. Secondary changes in mechanical muscle fibre and collagen tissue result in spastic muscle tone, which in part compensates for paresis and allows functional movements on a simpler level of organization. In mobile patients functional training should be applied to improve both function and spasticity. Antispastic drugs can accentuate paresis and should primarily only be applied in non-ambulatory subjects.


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