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Hvad er spasticitet?

Hvad er spasticitet?. Jens Bo Nielsen Department of Physical Exercise and Sport Science & Department of Neuroscience and Pharmacology Panum Københavns Universitet E-mail: JBNielsen@sund.ku.dk. Jakob Lorentzen Department of Neurorehabilitation, Hvidovre hospital &

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Hvad er spasticitet?

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  1. Hvad er spasticitet? Jens Bo Nielsen Department of Physical Exercise and Sport Science & Department of Neuroscience and Pharmacology Panum Københavns Universitet E-mail: JBNielsen@sund.ku.dk Jakob Lorentzen Department of Neurorehabilitation, Hvidovre hospital & Department of Neuroscience and Pharmacology Panum E-mail: Jlorentzen@ifi.ku.dk

  2. Hvorfra stammer begrebet? • Lat. Spasticus; at trække mod sig selv.(http://zeus.atilf.fr/tlf.htm) • 1753 Gout, defined to be a spastic and painful affection (http://www.oed.com/) • 1822-7 A spasticity or want of pliancy in the muscular fibres. (http://www.oed.com/)

  3. Spasticitet – tidlig historie • 1841 – Marshall Hall: Decapitated frogs Automatiske bevægelser i ellers paretiske ben – kaldet reflekser (introduceret af Willis). Tonus: Certain degree of firmness. Tonus forårsaget af reflekser • 1863 – Sechenev foreslår release of reflex function fra cerebral inhibition • 1855 Bentley Todd beskriver early and late rigidity • 1880: Brissaud differentierer mellem reflex medieret stivhed og kontrakturer ved hjælp af ischæmi • 1885-1915 Sherrington beskriver forøgede strækreflekser ved decerebreret rigiditet

  4. Spasticitet – senere historie • 1950-1970 Eccles, Lundberg o.a. – introduktion af intracellulær registrering i motorneuroner. Analyse af netværk på dyr. • 1960-1970: Farmakologisk behandling af spasticitet introduceres (benzodiazepiner, baklofen o. a.) • 1970- : Introduktion af elektrofysiologiske metoder til undersøgelse af patofysiologiske grundlag for spasticitet hos mennesker • 1978-: Introduktion af første isokinetiske dynamometre til spasticitetsevaluering • 1990erne: Introduktion af Botox

  5. Definition af spasticitet 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

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

  7. Den kliniske hverdag SPASM: Definition ”disordered sensi-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles” Kilde: Pandyan et al. Spasticity , clinical perceptions and neurological realities and meaningful measurements. Disabil Rehabil 2005;27:2-6. • Forøget muskel tonus • Hyperexcitable strækreflekser • Forøgede flexor reflexer • Spasmer • Babinski • Kontrakturer?

  8. 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 (and without provocation). Lesion of basal ganglia? Inability to ´relax´ • Contractures. Alteration of passive muscle properties • Spastic Gait ??

  9. 5 minutters pause til diskussion • Hvilken definition på spasticitet skal vi bruge?

  10. Back to basics: Hvad bestemmer muskel ´tonus´? • Passive properties (tendon, • connective tissue etc) • 2. Active properties (how many • cross-bridges?)

  11. Muskel tonus ”the sensation of resistance felt as one manipulation of a joint through a range of motion, with the subject attempting to relax” Lance and McLoud 1981

  12. Hvordan trækker musklen sig sammen? Hvordan forlænger musklen sig?

  13. Kontraktur Ref: Singer B et al. Reflex and non-reflex elemanet of hypertonia in triceps surae muscles following acquired brain injury: implications for rehabilitation. Disabil Rehab, 2001; vol.23 no.17, 749-757.

  14. Ændring i antallet af sacromer TA SOL Ref: Shah SB et al. Sacromere number regulation maintained After immobilization in desmin-null mouse skeletal muscle. The Journal of experimental biology 204, 1703-1710 (2001).

  15. Behandling • Evidens for øget ROM • Ingen ændring i spasticitet • Ikke øget funktionsniveau Ref: Mortenson PA, Janice JE. The use of casts in the management of joint mobility And hypertonia following brain injury in Adults: a systematic review. Physical Therapy Vol 83 number 7, July 2003.

  16. Behandling - udspænding Ikke evidens for effekt. • ”Four weeks of daily stretch has little or no effect on wrist contracture after stroke: a randomised controlled trial Ref: Horsley SA et al. Four weeks of dayily stretch has little or no effect on wrist contracture after stroke: a randomised controlled trial. 2007 Australian Journal of physiotherapy 53: 239-245. Anbefaling – langvarigt stræk > 20 min – 12 timer pr dag Ref: Harvey LA, Herbert RD. Muscle stretching for treatment and prevention of contracture in people with spinal cord injury. Spinal Cord. 2002 Jan; 40(1):1-9.

  17. Elektromekanisk kobling

  18. Cross-bridge formation

  19. Hvis der ikke findes aktivitet i nerverne (ingen AP) er der heller ikke ret meget Ca i muskelcellerne og derfor ingen dannelse af krydsbroer – dødsstivhed bidrager med andre ord ikke til musklernes stivhed (tonus) i hvile – dvs udelukkende bindevæv o.a. bestemmer stivheden i hvile

  20. NB: Motorneuronerne er pr definition langt fra deres fyringstærskel i hvilesituationen – og sender således ingen aktionspotentialer til musklerne. Men er vi i den kliniske situation altid sikre på at patienten er i hvile? Findes der forskellige grader af hvile? • Hvad har betydning for det?

  21. Hvad bestemmer aktiviteten i motorneuroner? Den forenklede model. Descenderende supraspinalt input Mn egenskaber Mn er ikke aktive spontant! (men: kramper + spasmer?) Sensorisk input

  22. Hvad bestemmer aktiviteten i motorneuroner?

  23. Budskabet er at der ikke er øget tonus i musklerne medmindre der er forandringer i musklernes bindebæv olign (kontrakturer og forstadier) eller aktivitet i motorneuronerne. Aktiviteten i motorneuronerne kan være ´spontan´ - slapper patienten af? – er der tale om dystoni? – eller provokeret af voluntær aktivitet eller sensorisk input (spasticitet) Klassifikation: Passiv Aktiv Reflex medieret Supraspinalt medieret Slapper patient af? Patologisk årsag – fx affektion af basal kerner

  24. Behandling afhænger af symptom • Spasticitet: Behandling nødvendig/hensigtsmæssig.? Fysioterapi, træning, antispastisk medicinering (ikke botox!) • Dystoni: Muligvis Botox, men langsigtet virkning ikke klart dokumenteret • Kontrakturer: Udstrækning , gipsning, men dokumentation for langsigtet effekt mangler • Spasmer: Behandling nødvendig/Hensigtsmæssig? Antispastisk medicinering

  25. Hvad er årsagen til spastictet?

  26. Dystoni Parese Ataxi Spasticitet

  27. Årsager til spasticitet i DK • Apopleksi (12.000 pr år – stigende – 50 % varigt mén) – heraf ca. 30-50 % spasticitet • Hjernetraumer (100-200 pr år) – heraf 30-60 % spasticitet • MS (150-200 pr år) – heraf 75-95 % spasticitet • Rygmarvslæsion (100-150 pr år) – heraf 60-80 % spasticitet • Cerebral parese o.lign. (125 pr år) - ?

  28. Spasticitet skyldes ikke læsion af pyramidebanen • 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. 1968 Mar;91(1):1-14. • Evidence from human • NO: Sherman et al. J Neurol Sci. 2000 Apr 15;175(2):145-55. • NO: Nathan PW Effects on movement of surgical incisions into the human spinal cord. Brain. 1994 Apr;117 ( Pt 2):337-46. • Yes: Paulson et al. Arch Neurol. 1986 Jan;43(1):93-5.

  29. Hjernelæsion involverer almindeligvis mange strukturer

  30. Pathophysiological mechanisms in spasticity Gr. II pathways Postactivation depression

  31. Control of reciprocal inhibition in healthy human subjects

  32. Reciprocal inhibition in patients with spasticity Crone C, Nielsen J, Petersen N, Ballegaard M & Hultborn H. (1994). Brain 117, 1161-1168. Crone C, Johnsen LL & Nielsen J (2000). Clinical neurophysiology suppl 53, 160-178 Morita H, Crone C, Christenhuis D, Petersen NT & Nielsen JB. (2001). Brain. 124(Pt 4), 826-37 Crone C, Johnsen LL, Biering-Sørensen F & Nielsen JB (2003). Appearance of reciprocal facilitation in patients with spasticity. Brain, 126(Pt 2):495-507.

  33. Reciprocal inhibition in stroke patient Before stroke After stroke

  34. Reciprocal inhibition is impaired in the legs but not the arms in ADPSP subjects

  35. In spastic patients reciprocal inhibition cannot be appropriately modulated during extension-flexion movements Patients Healthy subjects Healthy subjects without reciprocal inhibition Morita H, Crone C, Christenhuis D, Petersen NT, Nielsen JB Modulation of presynaptic inhibition and disynaptic reciprocal Ia inhibition during voluntary movement in spasticity. Brain 2001;124:826-37

  36. Turning off plateau potentials by reciprocal inhibition. Towards a functional understanding of spasticity? Hounsgaard J, Hultborn H,Jespersen B, Kiehn O. J. Physiol. 1988; 405:345-367

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