Defining and Measuring Spasticity
Transcription
Defining and Measuring Spasticity
Defining and Measuring Spasticity Anand D Pandyan (behalf of a much bigger team) Professor of Rehabilitation Technology School of Health and Rehabilitation Keele University, UK Motor control / capacity … Lost/disordered control after an UMN lesion… UMN lesion Independence threshold 0 Life span (years) Twilight zone The paradoxical symptoms Increased activity Reduced activity •Increased reflexes •Weakness •Spasticity •Fatigueability •Altered tone •Loss of fine •Spasm & Clonus motor control •Abnormal movement patterns & co-contraction A brief history 1. 1st occurrence - Spastic Paralysis (this is a term I have seen in the literature since 1890’s) 2. Spasticity then used in the context of the positive symptoms (Sherrington & Hughlings Jackson) 3. First form of a clinical definition produced by Denny-Brown 1960’s 4. The Lance definition of the 1980’s The Lance definition…. A motor disorder characterised by a velocity dependent increase in the tonic stretch reflex (muscle tone) with exaggerated tendon reflexes, resulting from the hyper-excitability of the stretch reflex, as one component of the upper motor neurone syndrome. Lance (1980): 51-55, 185 – 204, 485-494. Malhotra et al 2009 Clin Rehbail Lance 31% Muscle Tone 35% None 31% Other 3% clinician Nurse Therapist Carer Patient Researcher Spasticity There was an attempt at splitting • Spastic hypertonia: Velocity dependent increase in hypertonia with a catch when a threshold is exceeded. (no abnormal resting position) Dystonic hypertonia: After testing the limb will return to fixed resting posture that can vary with state of mind or attempted movement. (stiffness is independent of direction) • Rigid hypertonia: Resistance to passive movement is not velocity dependent and no consistent abnormal posture is observed. (stiffness is independent of direction) • Sanger et al 2003 Paediatrics – North American Task Force Updating the definition (SPASM - consortium) Disordered sensori-motor control, resulting from an upper motor neurone lesion, presenting as intermittent or sustained involuntary activation of muscles Pandyan et al 2005 Disabili & Rehab – SPASM consortium The obvious first step Spasticity Increased activity •Increased reflexes •Increased reflexes •Altered tone •Spasticity •Spasm & Clonus •Altered tone •Abnormal •Spasm & Clonus movement •Abnormal movement patterns patterns & cocontraction & co-contraction The splitting Spasticity •Increased reflexes •Altered tone/Stretch induced muscle activity •Spasm •Clonus •Abnormal movement patterns & cocontraction The splitting Spasticity •Increased reflexes (Not necessarily abnormal but modulation may be altered) •Altered tone/Stretch induced muscle activity •Spasm •Clonus •Abnormal movement patterns & cocontraction The splitting Spasticity •Increased reflexes •Altered tone/Stretch induced muscle activity •Spasm •Clonus •Abnormal movement patterns & cocontraction Altered tone 1. Resistance one feels when stretching the joint This is a confounded measure so cannot contribute to a definition 2. Readiness of the muscle to act This is reduced and is no different to the definition of paralysis or weakness – so there is a problem Stretch induced muscle activity Increase in the gain and/or reduction in threshold velocity dependent responses to a stretch Velocity response is nonstationary and its influence on stiffness is variable The start of the splitting Spasticity •Increased reflexes •Altered tone/Stretch induced muscle activity •Spasm •Clonus •Abnormal movement patterns & cocontraction The start of the splitting Spasticity •Stretch induced muscle activity •Spasm •A transient but continuous muscular contraction (cutaneous/visceral triggers) •Clonus •Abnormal movement patterns & cocontraction The start of the splitting Spasticity •Stretch induced muscle activity •Spasm •Clonus •A transient but intermittent / rhythmic / cyclical muscle contraction (proprioceptive and/or cutaneous) •Abnormal movement patterns & cocontraction The start of the splitting Spasticity •Increased reflexes •Altered tone/Stretch induced muscle activity •Spasm •Clonus •Abnormal movement patterns & cocontraction There is a need to resolve the pathology and physiology conundrum SWING PHASES Unimpaired walking Gastroc-soleus muscles Anterior tibial ? Spastic response Newcastle 2004 - SPASM EMG Walk 3 - Right 12 Walk 1 - Left R Rectus 2.0 L Rectus F V V -2.0 -12 12 R Vastus 2.0 L Vastus L V V -2.0 -12 12 2.0 L Vastus M R Hamstrings V V -2.0 2.0 -12 12 R Peroneus L V -2.0 V 2.0 -12 10 L Hams L R Tib Ant L Hams M V -2.0 4.0 V L Tib Ant V -10 12 R Gastroc -4.0 4.0 L EDL V V -12 12 R Soleus -4.0 4.0 V L EHL V -4.0 -12 Child with CP Normal Attempt 1 50 10 0.1 5 0 0 0 0 2.742 5.484 8.226 10.968 0 - 0.1 13.71 Time (s) Grip (Kg) Extensor EMG (mV) Flexor EMG (mV) Stroke patient – ipsilateral Non-impaired adult is similar 0.2 40 30 0.1 EMG activity 0.2 Grip Strength Grip (Kg) 15 -5 Muscle activity in the contralateral arm 0.3 maxrc1a EMG activity (mV) 20 20 10 0 0 - 10 - 0.1 15 20 25 Time (s) Grip Strength (Kg) Arm Flexor EMG Arm Extensor EMG Elbow Flexor EMG Elbow Extensor EMG Non-impaired adult contralateral Current “state of the art” Spasticity •Spasm •Clonus •Stretch induced muscle activity •Abnormal movement patterns & cocontraction still remain unresolved A brief introduction to measurement & classification Stiffness not spasticity! Neural Spasticity Voluntary In-voluntary* (SPASTICITY) Non-neural Contracture Current “state of the art” Spasticity •Spasm •Clonus •Stretch induced muscle activity •Abnormal movement patterns & cocontraction still remain unresolved Score Penn spasm frequency scale Spasm frequency score 0 No spasms No spasms 1 Mild spasms at stimulation One or fewer spasms per day 2 Irregular strong spasms less than one time/hour Between one and five spasms per day 3 Spasms more often than one time/hour Five to less than 10 spasms per day 4 Spasms more than 10 times/hour Ten or more spasms per day, or continuous contraction Source of information: Penn RD et al 1989 Intrathecal baclofen for severe spinal spasticity. N Engl J Med, 320: 1517 – 1521. Snow BJ et al 1990 Treatment of spasticity with botulinum toxin: a double blind study. Ann Neurol, 28: 512 – 515. Biering-Sørensen et al 2005 Spasticity-assessment: a review. Spinal Cord, 44: 708 – 722. Current “state of the art” Spasticity •Spasm •Clonus •Stretch induced muscle activity •Abnormal movement patterns & cocontraction still remain unresolved Measuring Clonus – the original Tardieu classification method Held & Pierrot-Deseilligny (1969) No resistance throughout the course of the passive movement Slight resistance throughout the course of the passive movement, with no clear catch at precise angle Clear catch at precise angle, interrupting the passive movement, followed by release Fatigable clonus (< 10 seconds when maintaining pressure) occurring at precise angle Infatigable clonus (> 10 seconds when maintaining pressure) occurring at precise angle Current “state of the art” Spasticity •Spasm •Clonus •Stretch induced muscle activity •Abnormal movement patterns & cocontraction still remain unresolved Biomechanical & Neurophysiological Force to move limb Measuring stretch induced muscle activity EMG EMG Joint Angle Displacement Muscle activity extensors Muscle activity flexors Force/Moment Outcome Threshold angle Wartenberg Spasticity may be a potential epiphenomenon Evidence for an epiphenomenon NF Muscle activity at a slow F stretch NF Muscle activity at a fast F stretch W0 W6 W12 W24 W32 1.1 0.97 0.73 0.74 0.7 (0.2) (0.3) (0.2) (0.2) (0.1) 1.1 (0.4) 1.2 (0.3) 1.0 (0.4) 1.1 (0.5) 1.1 (0.3) 1.3 (0.6) 1.4 (0.6) 0.9 (0.2) 1.3 (0.7) 0.82 (0.2) 0.7 (0.1) 1.1 (0.3) 1.7 (0.6) 0.8 (0.1) 1.9 (0.7) Are you as confused as I? My funders Action Medical Research, N.Staffs Medical Institute, EU, DoH (NIHR), Biometrics Ltd, Allergan. My many colleagues Garth, Chris, Hermie, Caroline, Sybil, Sandra, Rasheed, Venu My many students Jose, Liz, Shweta, Leanne, Cameron