Spasticity pp 239-250 | Cite as

Pathological Changes in Spastic Muscle Reflexes Evoked by Passive Stretch or Tendon Taps

  • A. F. Thilmann
  • S. J. Fellows
  • H. F. Ross


Spasticity is a motor disorder which occurs after CNS lesions. Although in diagnostic terms clinicians worldwide would largely agree over the term spasticity, no totally satisfying physiological definition has been agreed upon (see Thilmann, this volume). The most widely accepted definition is that of Lance (1980): ‘Spasticity is a motor disorder characterized by the velocity-dependent increase in tonic stretch reflexes (‘muscle tone’) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex as one component of the upper motor neurone syndrome.” This definition contains two assumptions: (a) spasticity is a disorder mainly affecting reflex systems, and (b) it is defined by a passive movement in which increased muscle tone correlates with the velocity of a passive muscle stretch. Implicitly it is often assumed that the disability of the patient is correlated to the degree of disturbance in reflexes and to muscle tone (for literature see Feldman et al. 1980). During voluntary activation of muscles, however, the disability may differ greatly from that seen during passive disturbance. This issue is discussed further in the chapters by Fellows et al. and Dewald and Rymer in this volume.


Reflex Response Displacement Velocity Biceps Brachii Muscle Spastic Muscle Increase Muscle Tone 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. Ashby P, Burke D (1971) Stretch reflexes in upper limb of spastic man. J Neurol Neurosurg Psychiatry 34:765–771PubMedCrossRefGoogle Scholar
  2. Ashworth B (1964) Preliminary trial of Carisoprodol in multiple sclerosis. Practitioner 192: 540–542PubMedGoogle Scholar
  3. Bathien N, Rondot P (1985) Assessment of motor functions in extrapyramidal disorders. In: Eccles J, Dimitrijevic MR (eds) Upper motor neuron functions and dysfunctions. Karger, Basel (Recent achievements in restorative neurology, vol 1), pp 211–221Google Scholar
  4. Burke D, Gandevia SC, McKeon B (1984) Monosynaptic and oligosynaptic contributions to human ankle jerk and H-reflex. J Neurophysiol 52:435–448PubMedGoogle Scholar
  5. Dietz V, Quintern J, Berger W (1981) Electrophysiological studies of gait in spasticity and rigidity: evidence that altered mechanical properties of muscle contribute to hypertonia. Brain 104:431–449PubMedCrossRefGoogle Scholar
  6. Feldmann RG, Young RR, Koella KP (1980) Spasticity: disordered motor control. Year Book Medical Publishers, ChicagoGoogle Scholar
  7. Fellows SJ, Thilmann AF (1989) The role of joint biomechanics in determining stretch reflex latency at the normal human ankle. Exp Brain Res 77:135–139PubMedCrossRefGoogle Scholar
  8. Fellows SJ, Ross HF, Thilmann AF (1993) The limitations of the tendon jerk as a marker of pathological stretch reflex activity in human spasticity. J Neurol Neurosurg Psychiatry 56:531–537PubMedCrossRefGoogle Scholar
  9. Katz RT, Rymer WZ (1989) Spastic hypertonia: mechanisms and measurement. Arch Phys Rehabil 70:144–155Google Scholar
  10. Lance JW (1980) Pathophysiology of spasticity and clinical experience with baclofen. In: Feldmann RG, Young RR, Koella KP (eds) Spasticity: disordered motor control. Year Book Medical Publishers, Chicago, pp 185–203Google Scholar
  11. Müller H, Zierski J, Dralle D, Hoffmann O, Michaelis G (1988) Intrathecal baclofen in spasticity. In: Müller H, Zierski J, Penn RD (eds) Local-spinal therapy of spasticity. Springer, Berlin Heidelberg New YorkGoogle Scholar
  12. Powers RK, Marder-Meyer J, Rymer WZ (1988) Quantitative relations between hypertonia and stretch reflex threshold in spastic hemiparesis. Ann Neurol 23:115–124PubMedCrossRefGoogle Scholar
  13. Rondot P, Dalloz JC, Tardieu G (1958) Mesure de la force des réactions musculaires à L’étriment passiv au cours des radieurs pathologiques par lésion cérébrales. Rev Fr Etud Clin Biol 3:585–592PubMedGoogle Scholar
  14. Thilmann AF, Fellows SJ (1991) The time-course of bilateral changes in the reflex excitability of relaxed triceps surae muscle in human hemiparetic spasticity. J Neurol 238:293–298PubMedGoogle Scholar
  15. Thilmann AF, Fellows SJ, Garms E (1990) Pathological stretch reflexes on the “good” side of 250 hemiparetic human subjects. J Neurol Neurosurg Psychiatry 53:208–214PubMedCrossRefGoogle Scholar
  16. Thilmann AF, Fellows SJ, Garms E (1991) The mechanism of spastic muscle hypertonia: variation in reflex gain over the time course of spasticity. Brain 114:233–244PubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1993

Authors and Affiliations

  • A. F. Thilmann
    • 1
  • S. J. Fellows
    • 1
  • H. F. Ross
    • 2
  1. 1.Alfried Krupp von Bohlen und Halbach KrankenhausNeurologische Klinik mit Klinischer NeurophysiologicEssenDeutschland
  2. 2.Dept. of Physiology, The Medical SchoolUniversity of BirminghamBirminghamEngland

Personalised recommendations