Bolaños-Jiménez R, Arizmendi-Vargas J, Calderón-Álvarez TJL, Carrillo-Ruiz JD, Rivera-Silva G, Jiménez-Ponce F

Language: Spanish
References: 45
Page: 141-148
PDF size: 242.46 Kb.

ABSTRACT

Objective: Spasticity is one of the signs described since centuries ago. Nevertheless, this definition per se would be difficult to understand, inclusive for the neurologist, neurosurgeon and therapist. This review pretends to analyze the meaning and clarify the vision of what does it stand for in clinical practice, to differentiate between one patient with spasticity from one that does not. Development: Spasticity is a secondary disease to an insult of the central nervous system. It is defined as an augmentation of muscular stretch reflex that depends of the muscular movement for its manifestation. Pathogenic mechanisms involved in this disorder include an increased neuronal excitation and a decreased neuronal inhibition, that bring as consequence, hyperreflexia and/or hypertonic muscular reflex. Conclusions: Spasticity is the result of the effect of different events occurring in the central nervous system, including trauma, demyelinizant diseases, tumors, etc. Main damage is caused to the pyramidal tract, but is not clear the role of others anatomical pathways, causing hypertonic and hyperreflectic signs as consequence, being these not evident in other nosological entities.

REFERENCES

1. Kim JS, Pope A. Somatotopically located motor fibers in corona radiata: Evidence from subcortical small infarcts. Neurology 2005; 64: 1438-40.

2. Marx JJ, Iannetti GD, Thoemke F, et al. Somatotopic organization of the corticospinal tract in the human brainstem: A MRI-based mapping analysis. Ann Neurol 2005; 57: 824-31.

3. Davidoff RA. The pyramidal tract. Neurology 1990; 40: 332-9.

4. Cuadrado-Pérez ML, Arias-Navalón JA, Palomar MA, Linares R. La vía piramidal: nuevas trayectorias. Rev Neurol 2001; 32: 1151-8.

5. Stecina K, Jankowska E. Uncrossed actions of feline corticospinal tract neurones on hindlimb motoneurones evoked via ipsilaterally descending pathways. J Physiol 2007; 580(1): 119-32.

6. Lacroix S, Havton LA, McKay H, Yang H, Brant A, Roberts J, Tuszynski MH. Bilateral corticospinal projections arise from each motor cortex in the macaque monkey: a quantitative study. J Comp Neurol 2004, 473: 147-61.

7. Stone TW. Cortical Pyramidal Tract Interneurones and their Sensitivity to L-Glutamic Acid. J Physiol 1973; 233: 211-5.

8. Jackson A, Baker SN, Fetz EE, Tests for presynaptic modulation of corticospinal terminals from peripheral afferents and pyramidal tract in the macaque. J Physiol 2006; 573(1): 107-20.

9. Lance JW. What is Spasticity? The Lancet 1980; 335: 606.

10. Meythaler JM. Concept of spastic hypertonia. Phys Med Rehabil Clin N Am 2001; 12: 725-32.

11. Hornby TG, Kahn JH, Wu M, Schmit BD. Temporal facilitation of spastic stretch reflexes following human spinal cord injury. J Physiol 2006; 571(3): 593-604.

12. John R, Sudhof TC. Synaptic vesicles and exocytosis. Annu Rev Neurosci 1994; 17: 219-46.

13. Lance JW. The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurology 1980; 30: 1303-13.

14. Mathews PBC. Evolving views on the internal operation and functional role of the muscle spindle. J Physiol 1981; 320: 1-30.

15. Nielsen JB, Petersen NT, Crone C, Sinkjaer T. Stretch reflex regulation in healthy subjects and patients with spasticity. Neuromodulation 2005; 8: 49-57.

16. Morita H, Shindo M, Momoi H, Yanagawa S, Ikeda S, Yanagisawa N. Lack of modulation of Ib inhibition during antagonist contraction in spasticity. Neurology 2006, 67: 52-6.

17. Katz RT, Rymer WZ. Spastic hypertonia: mechanisms and measurements. Arch Phys Med Rehabil 1989, 70: 144-55.

18. Burke D. Spasticity as an adaptation to pyramidal tract injury. Adv Neurol 1988, 47: 401-22.

19. Gordon LM, Keller JL, Stashinko EE, Hoon AH, Bastian AJ. Can Spasticity and Dystonia Be Independently Measured in Cerebral Palsy? Pediatr Neurol 2006, 35: 375-81.

20. Katz R, Rymer WZ. Spastic hypertonia: mechanisms and management. Arch Phys Med Rehabil 1989; 70: 144-55.

21. Sheean G. The pathophysiology of spasticity. Eur J Neurol 2002; 9(Suppl. 1): 3-9.

22. Ben Smaïl D, Kiefer C, Bussel B. Évaluation clinique de la spasticité. Neurochirurgie 2003, 49(2-3): 190-8.

23. Filipetti P, Decq P, Fontaine D, Feve A, Pirotte A, Barbedette B, Nadeau G. La spasticité des membres inférieurs chez l´adulte. Évaluation clinique et blocs moteurs. Neurochirugie 1998, 44(3): 167-74.

24. Priebe MM, Sherwood AM, Thornby JL, Kharas NF, Markowsi J. Clinical assessment of spasticity in spinal cord injury: a multidimensional problem. Arch Phys Med Rehabil 1996; 77: 713-16.

25. Brown P. Pathophysiology of spasticity. J Neurol Neurosurg Psychiatry 1994, 57: 773-7.

26. Dietz V, Sinkjaer T. Spastic movement disorder: impaired reflex function and altered muscle mechanics. Lancet Neurol 2007, 6: 725-33.

27. Katz R, Rymer WZ. Spastic hypertonia: mechanisms and management. Arch Phys Med Rehabil 1989; 70: 144-55.

28. Iles JF, Roberts RC. Presynaptic inhibition of monosynaptic references in the lower limbs of subjects with upper motoneuron disease. J Neurol Neurosurg Psychiatr 1986; 49: 937-44.

29. Lieber RL, Runesson E, Einarsson F, Fridén J. Inferior mechanical properties of spastic muscle bundles due to hypertrophic but compromised extracellular matrix material. Muscle Nerve 2003; 28: 464-71.

30. Lieber RL, Steinman S, Barash IA, Chambers H. Structural and functional changes in spastic skeletal muscle. Muscle Nerve 2004; 29: 615-27.

31. Graham BA, Brichta AM, Schofield PR, Callister RJ. Altered potassium channel function in the superficial dorsal horn of the spastic mouse. J Physiol 2007; 584(1): 121-36.

32. Biscoe TJ, Duchen MR. Synaptic physiology of spinal motoneurones of normal and spastic mice: an in vitro study. J Physiol 1986; 379: 275-92.

33. Kingsmore SF, Giros B, Suh D, Bieniarz M, Caron MG, Seldin MF. Glycine receptor â-subunit gene mutation in spastic mouse associated with LINE-1 element insertion. Nat Genet 1994; 7: 136-41.

34. White WF, Heller AH. Glycine receptor alteration in the mutant mouse spastic. Nature 1982; 298: 655-7.

35. Graham BA, Schofield PR, Sah P, Callister RJ. Altered inhibitory synaptic transmission in superficial dorsal horn neurones in spastic and oscillator mice. J Physiol 2003; 551: 905-16.

36. Li Y, Bennett DJ. Persistent sodium and calcium currents cause plateau potentials in motoneurons of chronic spinal rats. J Neurophysiol 2003; 90: 857-69.

37. Decq P. Physiophatologie de la Spasticité. Neurochirurgie 2003, 49 (2- 3): 163-84.

38. Tardieu G. Physiopathologie des spasticités. J Belge Méd Phys 1980, 3: 93-9.

39. Sherwood AM, Graves DE, Priebe MM. Altered motor control and spasticity after spinal cord injury: subjective and objective assessment. J Rehabil Res Dev 2000, 37(1): 41-52.

40. Dietz V, Quintern J, Berger W. Electrophysiological studies of gait in spasticity and rigidity. Evidence that an altered mechanical properties of muscles contribute to hypertonia. Brain 1981, 104: 431-49.

41. Sköld C, Harms-Ringdahl K, Hultling C, Levi R, Seiger A. Simultaneous Ashworth measurements and electromyographic recordings in tetraplegic patients. Arch Phys Med Rehabil 1998, 79: 959-65.

42. Haas BH, Crow JL. Towards a clinical measurement of spasticity? Physiotherapy 1995, 81: 474-9.

43. Ghotbi N, Ansari NN, Naghdi S, Hasson S, Jamshidpour B, Amiri S. Inter-rater reliability of the Modified Ashworth Scale in assessing lower limb muscle spasticity. Brain Inj 2009; 23(10): 815-19.

44. Haugh AB, Pandyan AD, Johnson GR. A systematic review of the Tardieu Scale for the measurement of spasticity. Disabil Rehabil 2006; 28(15): 899-907.

45. Hobart JC, Cano SJ, Zajicek JP, Thompson AJ. Rating scales as outcome measures for clinical trials in neurology: problems, solutions, and recommendations. Lancet Neurol 2007, 6: 1094-105.