Spasticity after stroke
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Transcript of Spasticity after stroke
04/09/2023 1
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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