Transcript 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: [email protected]
Jakob Lorentzen
Department of Neurorehabilitation, Hvidovre
hospital
&
Department of Neuroscience and Pharmacology
Panum
E-mail: [email protected]
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/)
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
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
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
But in the clinic ”spasticity” is used more broadly:
Increased muscle tone
Hyperexcitable tendon jerks
(stretch reflexes)
Spasms
Spastic gait
Babinski
Increased flexor reflexes
and contractures
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Multiple sclerosis
Stroke
Spinal cord injury
Amyotrophic lateral sclerosis
Traumatic brain injury
Cerebral palsy
Tumors
Hereditary spastic paraparesis
(Neurolatyrism)
(hyperekplexia (startle disease)?)
Den kliniske hverdag
SPASM: Definition
• Forøget muskel tonus
• Hyperexcitable
strækreflekser
• Forøgede flexor reflexer
• Spasmer
• Babinski
• Kontrakturer?
• ”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.
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 ??
Factors causing hypertonicity
Active stiffness
Passive stiffness
(Contracture)
Afferent (disinhibited spinal reflexes)
Efferent (tonic
supraspinal drive)
Proprioceptive
reflexes
Spasticity (tonic)
Cutaneous and
nociceptive reflexes
Flexor withdrawal
reflexes
(Spastic) dystonia
Tendon
hyperreflexia and
Clonus (phasic)
Clasp knife
syndrome
Flexor spasms
Clasp knife (with
tonic stretch reflex)
Extensor reflexes
Extensor spasms
Arthrogenetic
changes
Intra-articular
adhesion formation
Associated reactions Adaptive shortening
?synkinesia
of periarticular
connective tissue
Cocontraction
Reduced lubrication
between collagen
fibres
Increased immature
collagen
Myogenetic
changes
Loss of sacromers in
series
Increased intra
muscular collagen
Disuse atrophy
Muscle fibre
transformation ST to
FT
Degenerative
changes in muscletendinous junction
Increased actinemyosin cross-bridge
linkage
5 minutters pause til diskussion
• Hvilken definition på spasticitet skal vi bruge?
Back to basics: Hvad bestemmer muskel ´tonus´?
1. Passive properties (tendon,
connective tissue etc)
2. Active properties (how many
cross-bridges?)
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
Hvordan trækker musklen sig sammen?
Hvordan forlænger musklen sig?
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.
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).
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.
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
on wrist contracture after stroke: a randomised controlled trial.
Australian Journal of physiotherapy 53: 239-245.
effect
2007
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.
Elektromekanisk kobling
Cross-bridge formation
• 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
• 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?
Hvad bestemmer aktiviteten i motorneuroner? Den
forenklede model.
Descenderende
supraspinalt input
Sensorisk input
Mn egenskaber
Mn er ikke aktive spontant!
(men: kramper + spasmer?)
Hvad bestemmer aktiviteten i motorneuroner?
10.000 synapses
Rubrospinal
Corticospinal
Vestibulospinal/tectospinal/
reticulospinal
Ib afferent
Mn
Ia afferent
Gr. II afferent
Renshaw inhibition
Ib inhibition
Reciprocal inhibition
Muscle
• 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
Reflex medieret
Aktiv
Supraspinalt
medieret
Slapper patient af?
Patologisk årsag – fx affektion af basal kerner
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
Hvad er årsagen til spastictet?
F
Feedback from
Skin
Reflex gating
Muscles
Joints
Phase-dependent gain
E
Dystoni
Parese
Ataxi
Spasticitet
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) - ?
Spasticitet skyldes ikke læsion af pyramidebanen
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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.
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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.
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Hjernelæsion involverer almindeligvis mange strukturer
Pathophysiological mechanisms in spasticity
Gr. II pathways
Postactivation depression
Control of reciprocal inhibition in healthy human
subjects
Reciprocal inhibition in patients with spasticity
Healthy subjects (n=25)
Hemiplegic patients (n=11)
Paraplegic patients (n=11)
MS patients (n=30)
Size of conditioned reflex
(% of control reflex)
130
120
110
100
90
80
70
0
2
4
6
8
10
12
Conditioning-test interval (ms)
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.
Reciprocal inhibition in stroke patient
Size of condiitoned reflex (% of control reflex)
A
Before stroke
120
110
100
90
80
70
0
2
Size of condiitoned reflex (% of control reflex)
B
After stroke
4
6
8
10
12
10
12
Conditioning-test interval (ms)
140
130
120
110
100
90
80
70
0
2
4
6
8
Conditioning-test interval (ms)
Reciprocal inhibition is impaired in the legs but not
the arms in ADPSP subjects
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
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