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Spasticity after spinal cord injury Jens Bo Nielsen Department of Physical Exercise and Sport Science & Department of Neuroscience and Pharmacology Panum.

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Presentation on theme: "Spasticity after spinal cord injury Jens Bo Nielsen Department of Physical Exercise and Sport Science & Department of Neuroscience and Pharmacology Panum."— Presentation transcript:

1 Spasticity after spinal cord injury Jens Bo Nielsen Department of Physical Exercise and Sport Science & Department of Neuroscience and Pharmacology Panum Københavns Universitet

2 Center for Research in Spasticity and Neurorehabilitation Hans Hultborn Kurt Jørgensen Jens Bo Nielsen Jørgen E. Nielsen Nicolas Petersen Fin Biering-Sørensen Clarissa Crone Christian Krarup Mads Ravnborg Thomas Sinkjær Jørgen Feldbæk Nielsen Terry Jernigan Søren Anker Pedersen Egill Rostrup Stig Sonne-Holm Jesper Bencke Purpose: Coordination of research activities in danish laboratories devoted to research in Spasticity and Neurorehabilitation By: 1) Facilitate transfer of knowledge from basic neurobiology to clinic 2) Facilitate development of new evaluation and rehabilitation techniques with a neuroscientific basis Rigshospitalet Panum Hvidovre hospital

3 Spasticity – short history 1841 – Marshall Hall: Decapitated frogs. Automatic movements in paretic limbs – called reflexes (introduced by Willis). Tone: Certain degree of firmness. Tone caused by reflexes 1863 – Sechenev: release of reflex function from cerebral inhibition 1880: Brissaud differentiates reflex mediated stiffness and contracture with the use of ischemia (blocks reflex) 1885: Gowers argues that stretch reflex and tone are related 1890: Haidenhain concludes that tone is a reflex which depends on resistance : Sherrington describes reflexes and points out that muscle tone is complex and should be carefully described when mentioned.

4 Definition of spasticity Spasticity is a motor disorder characterized by a 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 neuron syndrome. Lance, Spasticity: Disordered Motor Control 1980

5 But in the clinic spasticity is used more broadly: Increased muscle tone Spastic gait Hyperexcitable tendon jerks (stretch reflexes) Babinski Spasms and contractures Multiple sclerosis Stroke Spinal cord injury Amyotrophic lateral sclerosis Traumatic brain injury Cerebral palsy Tumors Hereditary spastic paraparesis (Neurolatyrism) (hyperekplexia (startle disease)?) Increased flexor reflexes

6 Different pathophysiological mechanisms are involved Velocity dependent resistance to stretch. Increased stretch reflexes Spasms – sustained activity after input. Role of flexor reflexes, role of Mn properties? Spontaneous muscle activity at ´rest´. = increased muscle tone at rest. Lesion of basal ganglia? Contractures. Alteration of passive muscle properties Spastic Gait ?? Lance´s definition

7 Does lesion of the corticospinal tract lead to spasticity? Evidence from monkeys NO: Towers 1940 NO: Lawrence & Kuypers. The functional organization of the motor system in the monkey. I. The effects of bilateral pyramidal lesions. Brain Mar;91(1):1-14. Evidence from human NO: Sherman et al. J Neurol Sci Apr 15;175(2): NO: Nathan PW Effects on movement of surgical incisions into the human spinal cord. Brain Apr;117 ( Pt 2): Yes: Paulson et al. Arch Neurol Jan;43(1):93-5.

8 Spasticity is not seen immediately after lesion but develops over several months From Ashby 1973

9 Pathophysiological mechanisms in spasticity

10 Control of reciprocal inhibition in healthy human subjects

11 Reciprocal inhibition in patients with spasticity Crone C, Nielsen J, Petersen N, Ballegaard M & Hultborn H. (1994). Brain 117, Crone C, Johnsen LL & Nielsen J (2000). Clinical neurophysiology suppl 53, Morita H, Crone C, Christenhuis D, Petersen NT & Nielsen JB. (2001). Brain. 124(Pt 4), Crone C, Johnsen LL, Biering-Sørensen F & Nielsen JB (2003). Appearance of reciprocal facilitation in patients with spasticity. Brain, 126(Pt 2):

12 Stretch reflexes are not increased in the active spastic muscle Therefore caution when using antispastic medication: Dietz & Sinkjær Lancet Neurol Aug;6(8):

13 Decreased contribution from afferent feedback to the soleus muscle during walking in patients with spastic stroke. Mazzaro et al. J Stroke Cerebrovasc Dis Jul-Aug;16(4): SInkjær et al Clin Neurophysiol May;110(5): NB

14 Reduced reflex modulation during bicycling in stroke Schindler et al NB

15 Reciprocal inhibition is increased following explosive strength training. Increased ability of producing force quickly. Geertsen et al.; indsendt til J Appl Physiol

16 How to evaluate spasticity? Ashworth scale has generally been found to be reliable for the upper arm, but NOT for the lower limb (Brashear et al. Arch Phys Med Rehabil Oct;83(10): Blackburn et al. Phys Ther Jan;82(1): Gregson et al. Arch Phys Med Rehabil Sep;80(9): )

17 Biomechanical evaluation of spasticity Jakob Lorentzen Hvidovre hosp.

18 Larger resistance to stretch in spastic muscle Healthy range False negative False positive

19 Evaluation of muscle resistance by handheld dynamometer is well correlated to resistance measures by stationary device R 2 :0,711

20 Reasonable intra- and interrater reliability R 2 :0,405 R 2 :0,462 R 2 :0,059 R 2 :0,241

21 But not significantly larger resistance measured by handheld device in patients with spasticity according to Ashworth scale

22 The End Jens Bo Nielsen Institut for Neurovidenskab og Farmakologi Panum Københavns Universitet

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