Hypertonia
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Hypertonia is a term sometimes used synonymously with spasticity and rigidity in the literature surrounding damage to the central nervous system, namely upper motor neuron lesions.[1] Impaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles, and decreased synaptic inhibition.[2] These consequences result in abnormally increased muscle tone of symptomatic muscles.[3] Some authors suggest that the current definition for spasticity, the velocity-dependent over-activity of the stretch reflex, is not sufficient as it fails to take into account patients exhibiting increased muscle tone in the absence of stretch reflex over-activity. They instead suggest that "reversible hypertonia" is more appropriate and represents a treatable condition that is responsive to various therapy modalities like drug or physical therapy.[4]

Presentation

Symptoms associated with central nervous systems disorders are classified into positive and negative categories. Positive symptoms include those that increase muscle activity through hyper-excitability of the stretch reflex (i.e., rigidity and spasticity) where negative symptoms include those of insufficient muscle activity (i.e. weakness) and reduced motor function.[5] Often the two classifications are thought to be separate entities of a disorder; however, some authors propose that they may be closely related.[6]

Pathophysiology

Characteristic features, analogy, and pathophysiology of common types of hypertonia. GTO – Golgi Tendon Organ

Hypertonia is caused by upper motor neuron lesions which may result from injury, disease, or conditions that involve damage to the central nervous system. The lack of or decrease in upper motor neuron function leads to loss of inhibition with resultant hyperactivity of lower motor neurons. Different patterns of muscle weakness or hyperactivity can occur based on the location of the lesion, causing a multitude of neurological symptoms, including spasticity, rigidity, or dystonia.[3]

Spastic hypertonia involves uncontrollable muscle spasms, stiffening or straightening out of muscles, shock-like contractions of all or part of a group of muscles, and abnormal muscle tone. It is seen in disorders such as cerebral palsy, stroke, and spinal cord injury. Rigidity is a severe state of hypertonia where muscle resistance occurs throughout the entire range of motion of the affected joint independent of velocity. It is frequently associated with lesions of the basal ganglia. Individuals with rigidity present with stiffness, decreased range of motion and loss of motor control. Rigidity is a nonselective increase in the tone of agonist and antagonist without velocity dependence, and the increased tone remains uniform throughout the range of movement. On the contrary, spasticity is a velocity-dependent increase in tone resulting from the hyper excitability of stretch reflexes.[7] It primarily involves the antigravity muscles – flexors of the upper limb and extensors of the lower limb. During the passive stretch, a brief “free interval” is appreciated in spasticity but not in rigidity because the resting muscle is electromyographically silent in spasticity. In contrast, in rigidity, the resting muscle shows firing.[8] Dystonic hypertonia refers to muscle resistance to passive stretching (in which a therapist gently stretches the inactive contracted muscle to a comfortable length at very low speeds of movement) and a tendency of a limb to return to a fixed involuntary (and sometimes abnormal) posture following movement.

Management

Therapeutic interventions are best individualized to particular patients. Basic principles of treatment for hypertonia are to avoid noxious stimuli and provide frequent range of motion exercise.

Physical interventions

Physiotherapy has been shown to be effective in controlling hypertonia through the use of stretching aimed to reduce motor neuron excitability.[9] The aim of a physical therapy session could be to inhibit excessive tone as far as possible, give the patient a sensation of normal position and movement, and to facilitate normal movement patterns. While static stretch has been the classical means to increase range of motion, PNF stretching has been used in many clinical settings to effectively reduce muscle spasticity.[10]

Icing and other topical anesthetics may decrease the reflexive activity for short period of time in order to facilitate motor function. Inhibitory pressure (applying firm pressure over muscle tendon) and promoting body heat retention and rhythmic rotation (slow repeated rotation of affected body part to stimulate relaxation)[11] have also been proposed as potential methods to decrease hypertonia. Aside from static stretch casting, splinting techniques are extremely valuable to extend joint range of motion lost to hypertonicity.[12] A more unconventional method for limiting tone is to deploy quick repeated passive movements to an involved joint in cyclical fashion; this has also been demonstrated to show results on persons without physical disabilities.[9] For a more permanent state of improvement, exercise and patient education is imperative.[11] Isokinetic,[13][14][15][16] aerobic,[17][18][19] and strength training[20][21][22][23] exercises should be performed as prescribed by a physiotherapist, and stressful situations that may cause increased tone should be minimized or avoided.[11]

Pharmaceutical interventions

Baclofen, diazepam and dantrolene remain the three most commonly used pharmacologic agents in the treatment of spastic hypertonia. Baclofen is generally the drug of choice for spinal cord types of spasticity, while sodium dantrolene is the only agent which acts directly on muscle tissue. Tizanidine is also available. Phenytoin with chlorpromazine may be potentially useful if sedation does not limit their use. Ketazolam, not yet available in the United States, may be a significant addition to the pharmacologic set of options. Intrathecal administration of antispastic medications allows for high concentrations of drug near the site of action, which limits side effects.[12]

See also

References

  1. ↑ "Archived copy". Archived from the original on 2013-06-18. Retrieved 2012-12-17.{{cite web}}: CS1 maint: archived copy as title (link)
  2. ↑ O'Sullivan, Susan (2007). Physical Rehabilitation. Philadelphia, Pennsylvania: F.A Davis Company. p. 234. ISBN 9780803612471.
  3. 1 2 Sheean, Geoffrey; McGuire, John R. (2009). "Spastic Hypertonia and Movement Disorders: Pathophysiology, Clinical Presentation, and Quantification". PM&R. 1 (9): 827–33. doi:10.1016/j.pmrj.2009.08.002. PMID 19769916. S2CID 30715890.
  4. ↑ Bakheit, A.M.; Fheodoroff, K.; Molteni, F. (2011). "Spasticity or Reversible Muscle Hypertonia?". Journal of Rehabilitation Medicine. 43 (6): 556–7. doi:10.2340/16501977-0817. PMID 21491075.
  5. ↑ Sanger, T. D.; Chen, D.; Delgado, M. R.; Gaebler-Spira, D.; Hallett, M.; Mink, J. W. (2006). "Definition and Classification of Negative Motor Signs in Childhood". Pediatrics. 118 (5): 2159–67. doi:10.1542/peds.2005-3016. PMID 17079590. S2CID 1974796.
  6. ↑ Damiano, Diane L; Dodd, Karen (2002). "Should we be testing and training muscle strength in cerebral palsy?". Developmental Medicine & Child Neurology. 44 (1): 68–72. doi:10.1111/j.1469-8749.2002.tb00262.x. PMID 11811654.
  7. ↑ Rushton, David N. (2008-04-24), "Intrathecal baclofen for the control of spinal and supraspinal spasticity", Upper Motor Neurone Syndrome and Spasticity, Cambridge University Press, pp. 181–192, doi:10.1017/cbo9780511544866.011, ISBN 9780521689786, retrieved 2023-07-31
  8. ↑ Ramanathan, Venkateswaran; Baskar, Dipti; Pari, Hariswar (2022). "'Seatbelt Effect' of spasticity: Contrasting velocity dependence from the clasp knife phenomenon". Annals of Indian Academy of Neurology. 25 (3): 517–519. doi:10.4103/aian.aian_817_21. ISSN 0972-2327. PMC 9350785. PMID 35936584.
  9. 1 2 Chang, Ya-Ju; Fang, Chia-Ying; Hsu, Miao-Ju; Lien, Hen-Yu; Wong, Mei-Kwan (2007). "Decrease of hypertonia after continuous passive motion treatment in individuals with spinal cord injury". Clinical Rehabilitation. 21 (8): 712–8. doi:10.1177/0269215507079137. PMID 17846071. S2CID 12538385.
  10. ↑ Sharman, Melanie J; Cresswell, Andrew G; Riek, Stephan (2006). "Proprioceptive Neuromuscular Facilitation Stretching". Sports Medicine. 36 (11): 929–39. doi:10.2165/00007256-200636110-00002. PMID 17052131. S2CID 3123371.
  11. 1 2 3 O'Sullivan, Susan (2007). Physical Rehabilitation. Philadelphia, PA: F.A Davis Company. p. 497. ISBN 9780803612471.
  12. 1 2 Katz, Richard T. (1988). "Management of spasticity". American Journal of Physical Medicine & Rehabilitation. 67 (3): 108–16. doi:10.1097/00002060-198806000-00004. PMID 3288246. S2CID 45292155.
  13. ↑ Giuliani, Carol A. (1997). "The Relationship of Spasticity to Movement and Considerations for Therapeutic Interventions". Neurology Report. 21 (3): 78–84. doi:10.1097/01253086-199721030-00009.
  14. ↑ Light, K E; Giuliani, C A (1992). "Effect of Isokinetic Exercise Effort on the Arm Coordination of Spastic Hemiparetic Subjects". Neurology Report. 16 (4): 19. doi:10.1097/01253086-199216040-00016.
  15. ↑ Giuliani, C A; Light, K E; Rose, D K. (1993). "The Effect of an Isokinetic Exercise Program on Gait Patterns in Patients with Hemiparesis". Neurology Report. 17 (4): 23–4. doi:10.1097/01253086-199317040-00029.
  16. ↑ Brown, D. A.; Kautz, S. A. (1998). "Increased Workload Enhances Force Output During Pedaling Exercise in Persons With Poststroke Hemiplegia". Stroke. 29 (3): 598–606. CiteSeerX 10.1.1.568.9281. doi:10.1161/01.STR.29.3.598. PMID 9506599.
  17. ↑ Hunter, Marque; Tomberlin, JoAnn; Kirkikis, Carol; Kuna, Samuel T (1990). "Progressive exercise testing in closed head-injured subjects: comparison of exercise apparatus in assessment of a physical conditioning program". Physical Therapy. 70 (6): 363–71. doi:10.1093/ptj/70.6.363. PMID 2345780.
  18. ↑ Jankowski, LW; Sullivan, SJ (1990). "Aerobic and neuromuscular training: effect on the capacity, efficiency, and fatigability of patients with traumatic brain injuries". Archives of Physical Medicine and Rehabilitation. 71 (7): 500–4. PMID 2350220.
  19. ↑ Potempa, K.; Lopez, M.; Braun, L. T.; Szidon, J. P.; Fogg, L.; Tincknell, T. (1995). "Physiological Outcomes of Aerobic Exercise Training in Hemiparetic Stroke Patients". Stroke. 26 (1): 101–5. doi:10.1161/01.STR.26.1.101. PMID 7839377.
  20. ↑ Damiano, Diane L.; Abel, Mark F. (1998). "Functional outcomes of strength training in spastic cerebral palsy". Archives of Physical Medicine and Rehabilitation. 79 (2): 119–25. doi:10.1016/S0003-9993(98)90287-8. PMID 9473991.
  21. ↑ Damiano, Diane L.; Vaughan, Christopher L.; Abel, Mark E. (1995). "Muscle response to heavy resistance exercise in children with spastic cerebral palsy". Developmental Medicine and Child Neurology. 37 (8): 731–9. doi:10.1111/j.1469-8749.1995.tb15019.x. PMID 7672470. S2CID 33519087.
  22. ↑ Miller, G T; Light, K E; Kellog, R. (1996). "Comparison of Isometric-Force Control Measures in Spastic Muscle of Poststroke Individuals Before and After Graded Resistive Exercise". Neurology Report. 20 (2): 92–3. doi:10.1097/01253086-199620020-00041.
  23. ↑ Hall, C; Light, K (1990). "Heavy restrictive exercise effect on reciprocal movement coordination of closed-head injured subjects with spasticity". Neurology Report. 14: 19.
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