Bibliography: 1. Lance JW. The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurology 1980; 30: 1303 2. Pandyan A, Gregoric M, Barnes M, et al. Spasticity: clinical perceptions, neurological realities and meaningful measurement. Disabil Rehabil 2005; 27:2-6 3. Voerman G, Greporic M, Hermens H. Neurophysiological methods for the assessment of spasticity: the Hoffman reflex, the tendon reflex, and the stretch reflex. Disabil rehabil 2005; 27: 33-68 .4. Ada L, Vattanasilp W, o´Dwyer NJ, Crosbie J. Does spasticity contribute to walking dysfunction after stroke? J Neurol Neurosur Psychiatry 1998; 64: 628-35. 5. DietzV, Sinkjaer T. Spastic movement disorder: impaired reflex function and altered muscle mechanics. Lancet Neurol 2007; 6: 725-33. 6. Malhotra S, Cousins E, Ward A, et al. Na investigation into the agreemente between clinical, biomechanical and neurophysiological measures of spasticity. Clin Rehabil 2008; 22: 1105-15 7. Voerman GEBurridge JH, Hitchcock RA, Hermens HJ. Clinometric properties of a clinical spasticity measurement tool. Disabil Rehabil 2007; 29: 1870-80 8. Pandyan AD, Van Wijck FMJ, Stark S, Vuadens P, Johnson GR, Barnes MP. The construct validity of a spasticity measurement device for clinical practice: an alternative to Ashworth scales. Disabil Rehabil 2006; 28: 579-85 9. Chen JJJ, Wu YN, Huang SC, Lee HM, Wang LY. The use of a portable muscle tone measurement device to measure the effects of botulinum toxine type A on elbow flexor spasticity. Arch Phys Med Rehabil 2005; 86: 1655-60 10. Turk R, Notley SV, Pickering RM, Simpson DM, Wright PA, Burridge JH. Reliability and sensitivity of a wrist rig to measure motor control and spasticity in poststroke hemiplegia. Neurorehabil Neural Repair 2008; 22: 684-96

Materials e methods: A web-based search to identify relevant studies and reviews about spasticity assessment by instruments that combine multidimensional signals (electrophysiological and biomechanical) during manually controlled or motor-driven passive muscle stretches. Six studies were selected (only post stroke patients) (table).The non-invasive devices used consisted on:1.Biomechanical devices (records of angular position/range of movement, velocity, forces used for stretching-resistance):

Dynamometer- hand-held (“user-friendly”) or motor- driven (less common) Force transdutors (single or multiple-axes) or differential pressure sensors: force recomputed to torques based on measures or estimations of moments arms Potentiometers or electrogoniometers (sometimes using inertial sensors containing an accelerometer and gyroscope or a velocity sensors): angular position, ROM,

velocity2. Surface EMG: Records of agonist and antagonist (additionally): muscle activity: 1. slope/angle and angular velocity onset 2. average root mean square sEMG signal- area under the the angle muscle activity (RMS-EMG). Stretches at 2,3 or 4 velocites ( 2º a 720º/seg). Low velocity velocity below the stretch reflex threshold (SRT) (non-neural elastoviscous muscle properties). High-velocity activation of muscle additionally influenced any increase in torque – identification of SRTs (reduced in UMN syndrome). The decreased SRTs may be related to: spasticity severity, type of motor deficit, risk of developing contractures. Identification of patterns of muscle activation “velocity-dependent”- afferents Ia- and “position-dependent”- afferents II (curve torque-velocity and curve torque-angle slope of the curve torque-angle is better used as a measure of non-neural related stiffness better differentiation of neural and non-neural related stiffness. Clinical assessment of spasticity: Modified Ashworth scale (MAS) and Modified Tardieu scale (MTS).

Results/Discussion: Parameters based on RMS-EMG (full ROM or as a function of velocity) fulfil aspects of validity to be used as a quantifiable measure of spasticity (however in some studies the electrophysiological response was occassionally found to be variable and unstable, which may also be a true phenomenon of spasticity which is on its own worthy of further investigation). Few torque-related parameters possess convincing validity to be used as clinical measures of spasticity (slope of torque-velocity curve better used to measure spasticity, and slope of torque-angle curve better used to measure non-neural related stiffness). The articles reviewed reported poor correlations between the electrophysiological findings and the scores of the MAS and MTS (lack of any sign of hyperactive H-reflexes) , confirming the inadequacy of clinical tests (+++ mid-range severities) The current papers covered reports on the measurement of passive-state spasticity only. The exact pathophysiology of spasticity during active motion remains debatable, and consequently, the literature related to its impact on function is divided (4,5). With advances in musculoskeletal modelling (improved accuracy, synchronization and portability of equipment- wireless inertial measurements units combined with EMG sensor technology), kinematic data can be used to calculate muscle lengths and lengthening velocities, essential for spasticity interpretation (6).

Aim: Databases search of studies that assess spasticty by simultaneously collecting: cinical assessment measures scales of muscle tone, biomechanical methods of assessment the resistance encountered during passive stretching and neurophysiological methods measures of patterns of abnormal involuntary muscle activity during passive stretching; as well as assessment of reliability and accuracy of clinal scales to quantify pathological muscle activation and stiffness associated.

Measures od spasticity assessment: a literature review

Maria João Leite. Physical and Rehabilitation Medicine Service, Centro Hospitalar do Porto - Hospital Santo António, Portugal

Conclusion: The clinical presentations of spasticity are variable and sometimes inconsistent with the existing definitions. There is evidence that the abnormal muscle activity (not necessarily a proportional change in muscle tone), the primary pathophysiological presentation of spasticity, was observed in a significant proportion of patients with UMN syndrome. In light of inaccuracies and poor interrater reliability of the ordinal clinical scales to isolate spasticity, and their oversimplification of the phenomenon, integration of quantified, instrumented methods (biomechanical and neurophysiological) can provide a more accurate and valid evaluation, differentiating between neural and non-neural causes of increased torque, with great advances in terms of treatment planning and outcome evaluation.

Introduction: Lance was the 1st to define spasticity as “a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting in hyper-excitability” (1). Neverthless, there are other reflex mechanisms (eg. cutaneous, nociceptive- reactive resistance) that can also contribute to increase muscle activaction and are difficult to distinguish from the proprioceptive reflex mechanisms. It´s also too required to distinguish the resistance due to passive stiffness (changes in viscoelastic properties (weakness)) from pathological muscle activation. Thus, it appears that “observed” spasticity encompasses multiple phenomena and is not a single pathophysiological entity. The SPASM consortium (established to develop standardized measures of spasticity) introduced a broader definition: “a disordered sensorimotor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles” (2). The majoraty of clinical scales oversimplify the phenomenon, assessing the level of resistance felt by the examiner during a passive muscle stretch.. Many studies have shown poor correlation between clinical scales (MAS; MTS) and objective indicators of pathologically increased muscle activity during passive stretch (eg: hyperactive H-reflexes) (3).

Author n Agonists Antagonists Instruments Stretch velocities

Comparator tests

Torque SurfaceEMG

Voerman (7)

12 Wrist flexors Wrist extensors Hand-held dynamometer, potentiometer, sEMG, electronicmetronomer

30,60,90 cycles/min (180,360,540º/s)

MAS Slope of torque-angle curve over full ROM

Alt average RMS-EMG over full ROM (≠ velocities)

Pandyan (8)

14 Biceps brachii Triceps brachii Force transducer, electrogoniometer, sEMG

Slow, Fast (median ≠ 34º/seg)

MAS Slope of force-angle curve over full ROM ≠ velocities

Alt average RMS-EMG over full ROM (≠ velocities)

Malhotra (6)

100 Long wrist flexors

Long wrist extensors

Force transducer, electrogoniometer, sEMG

Slow, Fast (median ≠ 87º/seg)

MAS Slope of force-angle curve ROM, ≠ velocities and resistance encountered

Alt average RMS-EMG over full ROM and ≠ veloc (patterns of muscle activity)

Chen (9) 10 Biceps brachii Triceps brachii Differential pressure sensor, angular velocity sensor, sEMG

120,180,360,540º/s MAS Velocity-dependent viscous component of torque

Angle at sEMG onset : ≠ velocities

Turk (10)

12 Flexor carpi ulnaris and radialis

Extensor carpi radialis longu

Force sensor, potentiometer, sEMG

Slow: 14.4 or 28,8º/s Fast: 540 º/s

MAS Force/torque angle index (0º-30º wrist extension)

Stretch index:average RMS-EMG minus resting EMG

Ada (4) 14 Medial gastrocnemius

ᴓ Potentiometer, sEMG 180,360,540,720 º/s ᴓ Changes in torque over 20 º interval

Gain in RMS-EMG over ROM