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Spasticity Treatment Options

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Presentation on theme: "Spasticity Treatment Options"— Presentation transcript:

1 Spasticity Treatment Options
Andrea P. Toomer, M.D. Physical Medicine and Rehabilitation Culicchia Neurological Clinic

2 Objectives Review the prevalence of spasticity
Discuss the functional implications of spasticity Review oral, intramuscular and intrathecal treatments for spasticity Discuss the interdisciplinary approach necessary to improve function in a patient with spasticity

3 Spasticity VELOCITY DEPENDENT INCREASE IN RESISTANCE TO PASSIVE MOVEMENT FOLLOWING DAMAGE TO THE UPPER MOTOR NEURON SYSTEM Spasticity of cerebral origin results from lack of descending inhibitory input from subcortical nuclei in brain Spasticity of spinal origin results from interruption of descending tracts that inhibit or modulate alpha and gamma motor neurons

4 Distribution of Spasticity
Focal Isolated local motor disturbance affecting a single body part Regional Motor disturbance involving a large region of the body Generalized Motor disturbance involving widespread regions of the body

5 Prevalence of Spasticity
Brain injury 20% of brain injury survivors experience severe spasticity Cerebral palsy (CP) 45% of individuals with cerebral palsy have severe spasticity Stroke 58% experience spasticity according to a survey of stroke survivors or primary caregivers of a stroke survivor (N = 504)

6 Prevalence of Spasticity
Multiple sclerosis (MS) 34% of MS patients experience severe spasticity Spinal cord injury (SCI) Between 53% and 78% of SCI patients report spasticity Approximately 41% of these individuals list spasticity as one of the major medical obstacles to community and workplace re-integration

7 Spasticity is under treated
National Stroke Association survey of 504 stroke survivors (or caregivers) Up to 58% of stroke survivors develop spasticity1 Of the 292 patients in the study with spasticity: 51% (149 patients) were receiving treatment 49% (143 patients) were untreated

8 Treatment Goals Prevention of contracture Improved seating position
Improved hygiene Improved mobility Improved ADL function Decrease pain Prevent pressure wounds Improve quality of life

9 Pharmacologic Treatment

10 Baclofen Binds to GABA receptors in the spinal cord, suppressing release of excitatory neurotransmitters Side effects Sedation Weakness GI symptoms Confusion Tremor Insomnia

11 Benzodiazepines Acts on GABA receptors to facilitate post-synaptic GABA effects to inhibit muscle contraction Side effects Sedation Memory impairment Abuse potential

12 Dantrium Acts on muscle tissue to block calcium release from sarcoplasmic reticulum thereby inhibiting muscle contraction Side effects Hepatotoxicity Frequent monitoring of LFTs required Not centrally acting- does not cause sedation

13 Tizanidine Central α-2 agonist
Decreases release of excitatory amino acids, inhibiting spinal neurons Side effects Hypotension Sedation

14 Chemodenervation Localized therapy

15 Chemodenervation Phenol
Causes demyelination of the nerve Immediate onset of relaxation Effects last up to 36 months (average 6 months) Complications Difficulty with administration Dysesthesias If injected intravascular can cause convulsions, CNS depression, cardiovascular collapse

16 Chemodenervation Botulinum Toxin
Acts at the neuromuscular junction Blocks release of acetylcholine from the presynaptic neuron Injected with audio EMG guidance Maximum effect in 7-10 days, lasts 3 months Complications Focal weakness Distal spread of toxin

17 Intrathecal Therapy Global therapy

18 Intrathecal Baclofen Binds to GABA receptors in the spinal cord, suppressing release of excitatory neurotransmitters Implanted pump delivers baclofen to the intrathecal (subarachnoid) space Effective at substantially lower doses than are required orally Significantly less sedation seen as compared to oral dosing

19 Intrathecal Baclofen Screening Test
Trial dose of baclofen is given intrathecally PT/OT exam prior to administration PT/OT exams after administration Quantify effects of ITB If trial is positive patient proceeds to implantation

20 Intrathecal Baclofen Pump Implantation
Implanted by a neurosurgeon Same day surgery Treatment is initiated at the time of implant Patient wears an abdominal binder for about a month to prevent edema at the pump site Begin PT and OT after the post op visit

21 Intrathecal Baclofen Dosing is adjusted slowly Continuous or bolus
dosing options

22 Commitment to ITB therapy
Frequent PT/OT sessions Daily HEP Daily use of static and/or dynamic bracing Frequent doctor visits for dose titration Visits 2-4 times a year for pump refills Pump replacement every 7 years

23 Summary Spasticity occurs as result of damage to the central nervous system Spasticity can be present with TBI, SCI, CVA, MS, CP Spasticity can develop gradually and can change over time Spasticity can limit function, causing difficulty in performing ADLs and mobility skills Medical complications of spasticity include contracture and skin breakdown Treating spasticity as a part of an interdisciplinary rehab program can lead to improved function and improved quality of life

24 Treatment Goals Prevention of contracture Improved seating position
Improved hygiene Improved mobility Improved ADL function Decrease pain Prevent pressure wounds Improve quality of life

25 Interdisciplinary Treatment
Medical treatments will decrease the muscle tone PT/OT is necessary to improve function PT/OT feedback helps us to make determinations in dosing titration

26 Patient Presentations

27 Questions ?

28 Thank You Andrea P. Toomer, M.D. Culicchia Neurological Clinic
(504) (504) fax


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