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Spasticity After StrokeAdeagbo, Caleb A

B.Physiotherapy (Lagos)Department of Physiotherapy,

National Hospital, Abuja

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Outline IntroductionDefinitionsTypes of

spasticityPathophysiologyOther Types of

HypertonicityAdvantages of

Spasticity

Measurement Tools

Treatment ConclusionReferences

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Introduction

Stroke is the leading cause of morbidity and mortality (Lundstrom et al, 2008; Urban et al, 2012).

Spasticity is a common complication of stroke that lead to impaired gait characteristics in the upper and lower extremities (Karadag-Saygi et al, 2010).

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Introduction contOptimum management of spasticity

is dependent on an understanding of its underlying physiology, an awareness of its natural history, an appreciation of the impact on the patient and a comprehensive approach to minimizing that impact which is both multidisciplinary and consistent over time (Thompson et al, 2012).

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Definitions

Stroke is an acute/sudden focal/global disturbance of the cerebral function with symptoms lasting for more than 24hours or sometimes leading to death with no other cause than vascular origin.

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Definitions contSpasticity (meaning to draw or tug)Spasticity is abnormal muscle tone

recognized clinically as resistance to passive muscle stretch which increases with velocity of stretch. It is defined as 'a motor disorder characterized by velocity dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex

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Types of spasticityLEAD PIPE: presents as a uniform

resistance to movement throughout the range of movement.

COGWHEEL: presents as an intermittent on/off resistance throughout the range of movement, making the movements jerky.

CLASP KNIFE: presents as increase in extensors of a joint when its passively flexed given way suddenly on exertion of further pressure.

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Pathophysiology

The pathophysiologic basis of spasticity is incompletely understood.

Spasticity is loss of inhibitory control over the gamma motor neuron

This inhibitory influence is in turn controlled by descending and peripheral inputs.

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Pathophysiology contdLack of descending control over spinal

cord interneuronal circuits results in a decrease in the effectiveness of spinal inhibitory circuits such as those mediating reciprocal, presynaptic, and recurrent inhibition.

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Pathophysiology contd

The changes in muscle tone probably result from

alterations in the balance of inputs from reticulospinal and other descending pathways to the motor and interneuronal circuits of the spinal cord

the absence of an intact corticospinal system.

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Pathophysiology contd

Loss of descending tonic or phasic excitatory and inhibitory inputs to the spinal motor apparatus,

alterations in the segmental balance of excitatory and inhibitory control

denervation supersensitivity neuronal sprouting

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Other Types of Hypertonicity

RIGIDITY - Involuntary, bidirectional, non–velocity-dependent resistance to movement

CLONUS - Self-sustaining, oscillating movements secondary to hypertonicity

DYSTONIA - Involuntary, sustained contractions resulting in twisting, abnormal postures

ATHETOID - Involuntary, irregular, confluent writhing movements

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Other Types of Hypertonicity contd

CHOREA - Involuntary, abrupt, rapid, irregular, and unsustained movements

BALLISMS - Involuntary flinging movements of the limbs or body

TREMOR - Involuntary, rhythmic, repetitive oscillations that are not self-sustaining

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Advantages of Spasticity

Maintenance of Muscle tone or Muscle Bulk

Tone Effect on MobilityTone effect on ADL's Improved CirculationPrevention of DVTMay assist with postural control

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Measurement Tools

Ashworth scaleModified Ashworth scale: Spasm frequencyReflex scalePain scale

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Ashworth scale

0 – no increase in tone1 – slight increase in tone given a

catch 2 – more marked increase in tone 3 – considerable increase in tone PM

difficult4 – limb rigid in flexion and extension

(Ashworth scale, 1964)

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Modified Ashworth Scale 0 = no increase in muscle tone1 = slight increase in muscle tone (catch

or min resistance at end range)1 + = slight increase in muscle resistance

throughout the range.2 = moderate increase in muscle tone

throughout ROM, PROM is easy3 = marked increase in muscle tone

throughout ROM, PROM is difficult4 = marked increase in muscle tone,

affected part is rigid (Bohannon & Smith 1987)

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Spasm Frequency

Spasm Frequency Scale: How many spasms in the last 24 hours in the affected extremity?

0 = no spasms1 = 1 / day2 = 1-5/ day3 = 5-9 / day4 = >10/day (Penn et al, 1989)

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Pain scale

Numerical rating pain intensity scale: a verbal analogue scale. Scale 0 – 10 (Kremer et al, 1981).

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Treatment Goals Improve functional ability, Quality

of Life and MobilityDecrease pain associated with

spasticity Prevent or decrease incidence of

contractures Ease of care are possibleDecrease Cost of CareFacilitate hygieneEase rehabilitation procedures

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Remove noxious stimuli

Identify the “triggering” stimulusEliminate the factors that increase

sensory input to the central nervous system

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Rehabilitation therapy

Positioning Joint mobilization Stretching Strengthening

Exercises Modalities:

Cryotherapy, Hydrotherapy, Thermotherapy

Soft tissue manipulation

EMG biofeedback Electrical

stimulation Orthotics Splinting-

static/dynamic Casting: including

serial casting

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Oral medications

Lioresal: BaclofenBenzodiazepams: Diazepam (Valium)Dantrolene SodiumTizanidineGabapentin (Neurontin)

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Neurolysis

Botulinum toxin Injections Phenol Injections

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Orthopedic approach

TenotomyTendon lengtheningMyotomyTendon transfers

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Neurosurgical approach

NeurectomyMyelotomy/Cordectomy/ Chordotomy RhizotomySelective Dorsal Rhizotomy Implantable dural electric stimulator Intrathecal Baclofen Pump

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Conclusions

While spasticity management can be difficult, it may also improve patient’s quality of life

Spasticity is not necessarily the enemy, but is part of a pattern of abnormal motor control

The choice of treatment depends on pattern of involvement

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References

Akosile CO, Fabunmi AA (2011). Pathophysiology, Functional Implications and Management of Spasticity in Stroke – A Review. AJPARS 3(1):6-12

Ashworth B (1964). Preliminary trial of crisoprodol in multiple sclerosis. The practitioners 192:540-2

Bohannon RW, Smith MB (1987). Interrater reliability of a modified Ashworth scale of muscle spasticity. PhysTher 67: 206-7.

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References cont

Karadag-Saygi E, Cubukcu-Aydoseli K, Kablan N, Ofluoglu D (2010). The role of Kinesiotaping combined with Botulinum Toxin to reduce plantar flexors spasticity after stroke. Top Stroke Rehabil; 17(4):318–322

Lundstromac E, Terentb A, Borgc J (2008). Prevalence of disabling spasticity 1 year after first-ever stroke. European Journal of Neurology 15: 533–539

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References contUrban PP, Wolf T, Uebele M, Marx JJ, Vogt

T, Stoeter P, Bauermann T, Weibrich C, Vucurevic GD, Schneider A, Wissel J (2010). Occurence and Clinical Predictors of Spasticity after Ischemic Stroke. Stroke 41:2016-2020

Thompson AJ, Jarrett L, Lockley L, Marsden J, Stevenson VL (2012). Clinical management of spasticity. Available @ www.jnnp.bmj.com Retrieved on August 06 2012, Published by group.bmj.com

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Thank youQuestions

&contributions