Management of Spasticity

Transcription

1 Management of Spasticity Stephen P. Moran, M.D. Department of Physical Medicine and Rehabilitation Ochsner Medical Center Outline Review pathophysiology of spasticity Discuss epidemiology of spasticity Discuss functional limitations associated with spasticity Describe the appropriate management of spasticity Non-pharmacological Pharmacological Oral Chemodenervation Intrathecal 1

2 What is spasticity? Most commonly cited definition a motor disorder characterized by VELOCITY dependentincrease in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motorneuron syndrome What is spasticity? Decq recently has suggested the use of modified definition. Spasticity is defined as symptom of upper motor neuron syndrome characterized by an exaggeration of stretch reflex secondary to hyper excitability of spinal reflexes Separates spasticity into various components intrinsic tonic spasticity intrinsic phasic spasticity 2

3 Positive Signs Spasticity Rigidity Hyperreflexia Primitive reflexes Clonus Negative Signs Lack of strength Lack of Motor Control Lack of Coordination UMN Syndrome stretch reflex a monosynaptic reflex pathway that originates in the muscle spindles embedded parallel to the muscle fibers and travel via a Ia afferent to the spinal cord synapses either first with an interneuron or directly with alpha motor neuron innervating the muscle from which the stimulus originated. 3

4 stretch reflex The Ia afferent fibers also transmit signals via interneurons (Renshaw cells) which inhibit alpha motor neuron of antagonist muscles causing them to relax. This is mediated by GABAergic mechanism Inhibitory interneurons are also mediated by descending supraspinal pathways 4

5 intrinsic tonic spasticity exaggeration of the tonic component of the stretch reflex manifests as increased tone velocity dependent with faster stretching velocities being associated with greater amounts of reflex activity 5

6 intrinsic tonic spasticity development of tonic stretch reflex hyper excitability could be due to a lower threshold, increased gain of stretch reflex, or combination of the two 1. Denervation leading to hyperexcitability of alpha motor neuron 2. Collateral sprouting results in loss of inhibitory input 3. Increased Gamma fiber activity increase sensitivity of muscle spindle 4. Decreased spinal inhibitory mechanism from brain centers intrinsic tonic spasticity Bottom line: Imbalance of excitatory & inhibitory mechanisms leading to disinhibition of alpha motor neuron at the agonist and antagonist muscles 6

7 intrinsic phasic spasticity encapsulates symptoms such as tendon hyperreflexia and clonus tendon hyperreflexia is identified as exaggerated muscle response to an externally applied tap of deep tendons reduced presynaptic Ia inhibition is thought to play an important role in this hyperreflexia intrinsic phasic spasticity Clonus involuntary rhythmic muscle contraction that can result in distal oscillation theory is that activation of the stretch reflex of the calf muscle results in plantar flexion of the ankle. the disinhibition of stretch reflex due to interruption of the descending influences with SCI that is thought to cause exaggeration of reflex, thus causing clonus 7

8 Positive Effects of Spasticity Spasticty may: Be used to help with transfers, standing, walking, and ADLs Help prevent muscle atrophy Negative Effects of Spasticity Decrease ROM Restrict ADLs inhibit effect walking and self care cause pain and fatigue sleep disturbance compromise safety 8

9 Negative Effects of Spasticity Can contribute to the development of contractures pressure ulcers infections negative self image complications for role of caretaker impeding rehabilitation efforts Management of Spasticity Decisions must be based on the goal of achieving balance between the useful and detrimental effects of spasticity on an individual s quality of life passive problems preventing contracture reduce pain facilitate splint wearing easing positioning and hygeine functional problems ability to perform useful work (ie ambulation, transfers) 9

10 Management of Spasticity Progression of management Physical Rehab Modalities > Pharmacologic Interventions > Injection Techniques > Intrathecal Baclofen > Surgical Procedure Physical Techniques Positioning In bed and during sitting Important for maintenance of muscle length Passive Range of Motion Prevents contractures May cause plastic changes within the central nervous system Weight bearing Using tilt table or standing frame Suggest mechanism is modulating influence from cutaneous and joint receptor input in the spinal motor neurons, results in decreased excitability 10

11 Physical Techniques Cold Application May reduce the reflex excitability for short time (< 1 hr) May cause slowing of nerve conduction May cause decrease in sensitivity of cutaneous receptors Heat Application Subsequent passive stretch is facilitated Facilitation of uptake of release transmitter Return of calcium to the sarcoplasmic reticulum Splinting/Orthoses Continuous application of muscle stretch joint can be maintained in a position that does not elicit a spasm Three functional categories Systemic pharmacological management GABAergic -act at the interneuron that use the neurotransmitter gama-aminobutyric acid (GABA) in the CNS Baclofen and Diazepam alpha-2-adrenergic agonists - act at alpha-2 receptors in CNS Tizanidine and Clonidine peripheral acting - act at neuromuscular junction Dantrolene 11

12 GABAerigic Medications Baclofen (FDA approved) GABA B agonist Side effects: sedation, lowered seizure threshold, toxicity with renal clearance deficiencies Withdrawal: fevers, hallucinations, worsening spasticity, seizures, death 12

13 Baclofen Dosing Initial: 5 mg 3 times daily Increase by 5 mg per dose every 3 days until optimal response is reached Usual dosage range: 40 to 80 mg daily Do not exceed 80 mg daily (20 mg 4 times daily) GABA agonist at GABAb receptors Provides inhibitory effects in the monosynaptic reflex pathway Activates presynaptic GABAb receptors that suppresses release of excitatory neurotransmitters Also activates postsynaptic GABAb receptors which makes it difficult to depolarize the post-synaptic cell, thus dampening effects of excitatory neurotransmitters Baclofen 13

14 GABAergic Medications Benzodiazepines: Diazepam (FDA approved) Facilitates GABA A activity Same side effect profile and withdrawal profile as baclofen GABAergic medications should be avoided in patients with brain injury (stroke, TBI) because of excessive sedation and hinderance of neurological recovery Dosing: 2mg BID starting dose, rapid titration to max dose 60mg/day. Most effective treatment of hyperactive reflexes and painful spasms (in SCI vs stroke or MS) Clonazepam causes less sedation than diazepam and lower risk of dependence. Typically used for night time spasms. alpha-2-adrenergic Clonidine Provides inhibition of sensory afferents reported useful in treatment of supraspinal (brainstem) spasticity activates inhibitory neurons which results DECREASED sympathetic outflow Side effects -hypotension/syncope, nausea, sedation, ankle edema Dosage: Transdermal Patch (more common) -start 0.1mg patch q weekly. Titrate up to 0.3mg. Change patch every 7 days Oral: start 0.05mg BID, increase up to 0.4mg/day 14

15 alpha-2-adrenergic agonist Tizanidine acting primarily to decrease polysynaptic reflex activity overall effect is to reduce facilitation of spinal motor neurons Side effects: sedation/drowsiness, liver damage, bradycardia, dizziness LFT monitoring suggested Dosing: start at 2-4mg/day, usually at bedtime can increase dose and frequency up to max of 36mg/day 15

16 Peripheral Acting Dantrolene acts at the level of muscle itself blocks release of Ca++ from the sarcoplasmic reticulum reduces extrafusal muscle fiber contraction strength and muscle spindle activity fast twitch motor untis are more sensitive than slow twitch motor units Side effects: weakness (affects all muscles), liver toxicity, drowsiness Dosage: start 25mg BID. Can titrate up to total of 400mg/d 16

17 Other PO meds Cyproheptadine a histamine and serotonin antagonist proposed to reduce spasticity via inhibition of motor neurons by neutralizing the spinal and supraspinal seratoninergic excitatory associated with improved walking pattern of SCI patients Dronabinol relaxing effect on muscles some theories believe could potentially inhibit the polysynaptic reflexes Injection Techniques Chemodenervation Treats by simulating a lower motor neuron lesion Preferred treatment of focal spasticity and when agonist muscles have a functional strength once freed from antagonist spasticity Benefit is minimization of systemic side effects 17

18 Injection Techniques Phenol Ethanol Botulinum Toxin Chemoneurolysis Induce demyelination and axonal destruction via protein denaturation and axonal necrosis Phenol: 2-7% concentration. Ethanol: % concentration. Maximum 20-30mL per treatment. Used to disrupt nerves within a trunk or at the motor point where it attaches to the muscle Frequently use nerve stimulation for nerve blocks and EMG for motor point blocks. Can also use ultrasound guidance. 18

19 Chemoneurolysis Side effects Dysesthesia pain in distribution of sensory component of mixed nerve muscle pain muscle weakness (may be permanent) DVT (related to decreased motor activity which leads to venous stasis) Systemic reaction if Phenol injected intravascularly convulsions, CNS depression, cardiovascular collapse Toxin Injections Most potent neurotoxin known to humans Product of of anaerobic bacteria clostridium botulinum Initially developed for clinical use in 1980 for eyelid muscle spasms and crossed eyes Formally treated spasticity in

20 Toxin Injections 7 immunologically distinct toxins identified (A to G) Types A and B used for treatment Onabotulinumtoxin A (Botox) Abobotulinumtoxin A (Dysport) Incobotulinumtoxin A (Xeomin) Rimabotulinumtoxin B (Myobloc) Toxin Injections manifest their effects at the neuromuscular junction where they inhibit the release of acetylcholine from presynaptic motor axons Botulinum toxin is injected into a muscle at its end plate region and spreads throughout the muscle and fascia approximately 30mm. 20

21 Toxin Injection Because of complex mechanism of action, chemical denervation develops slowly over course of 24 to 72hrs, peaking at 2 to 6 weeks. (Rule of 3) Collateral sprouting and slow re-innervation of chemical denervated nerve terminals allows for gradual reversal of the clinical response 21

22 Toxin Injections Botulinum toxin has been touted the pharmacological treatment of first choice for focal spasticity because of the evidence for its effectiveness in reducing pain and tone, and improving range of motion, function, brace tolerance, and walking ability. Although not as commonly used in individuals with generalized spasticity (such as in SCI), improvements in pain, nursing care, hygiene, comfort, and functional activities can be induced Intrathecal Baclofen FDA Indications: Spasticity of cerebral or spinal in origin A treatment option for the management of severe spasticity for patients who have had ineffective results or intolerable side effects from oral baclofen at effective doses Contraindications: Pump can not be implanted 2.5 cm or less from the from surface of skin Hypersensitivity to baclofen Spinal anomalies Infection Body habitus not sufficient to accept pump bulk and weight *Safety profile has not been established for children under 4 22

23 Intrathecal Baclofen Allows for direct delivery of Baclofen into the CSF in the intrathecal space Makes it possible to achieve high concentration of Baclofen in spinal cord while reducing unwanted CNS effects associated with high oral doses of Baclofen The ratio of Baclofen concentration at level of spinal cord for IT administration compared to oral administered baclofen is 100:1 Intrathecal Baclofen Consists of two fully implantable components: Synchromed II pump Intraspinal catheter Can deliver medication at either a constant rate or a variable rate Reaches end of service at 7 years 23

24 Intrathecal Baclofen: Trial Establish baseline assessment prior to bolus injection 1. Administer an initial screening test dose of 50mcg (25mcg for smaller patients) Effect usually begins min after bolus Peak effect approximately 4 hours after bolus dose and may last up to 8 hours Reassess spasticity at 1, 2, and 4 hours post injection 2. If clinical response less than desired, then go to second trial bolus of 75 mcg. Second bolus may be administered no less than 24 hours after initial bolus 3. Can then go to 100mcg bolus trial. If the patient does not respond to 100mcg bolus then patient should not be considered for ITB therapy Intrathecal Baclofen Pre-implant considerations: Reinforce realistic goals & expectations with therapy Assess patient s equipment needs to determine optimal pump implant location, ie wheelchair seatbelts, seating equipment, supports Post-implant considerations: Patient should lie flat for 2-3 days post implant to reduce chance of CSF leaks Any rehabilitation movements that require excessive twisting or stretching should be avoided for six weeks Use of heat around the pump implant site should be avoided 24

25 References Lin et al (2010). Spinal Cord Medicine: Princeples and Practice. Spasticity: Pathophysiology, Assessment, and Management 40( ). Braddom et al (2007). Physical Medicine & Rehabilitation, 3 rd edition. Cuccurullo, SJ et al(2010). Physical Medicine & Rehabilitation Board Review, 2 nd edition. Hsieh, Wolfe, Connolly, Townson, Curt, Blackmer, Sequeira, and Aubut (2007) Spasticity After Spinal Cord Injury: An Evidence-Based Review of Current Interventions. Topics in Spinal Cord Injury Rehabilitation: Summer 2007, Vol. 13, No. 1, pp Google Image Search Thank you! 25