Muscle stiffness and spasm
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Spasticity or muscle stiffness and spasm in MS. Cause, treatment and management of this common symptom of MS and other neurological disorders.
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Muscle stiffness and spasm
- 1. Muscle stiffness and spasm in MS Miranda Olding RGN MSCN November 2012
- 4. Anatomy of a cell • neurone
- 5. Action Potential at work • link http://www.apstherapy.co.nz/wpimages/wpfe373a51.gif
- 6. •The Biology of muscle stiffness & spasm • The nerve pathway connecting the brain and spinal cord is made of upper motor neurones. • The pathway between the spinal cord and muscles is made of lower motor neurones. • In MS, spasticity is thought to be due to nerve conduction being affected by lesions located in the brain or spinal cord. • This means that the upper motor neurones struggle to regulate messages to the lower motor neurones. • The lower motor neurones can then become overactive and hypersensitive, causing stiffness or spasms in the muscles.
- 7. Biology of muscle spasm & stiffness • Spasticity occurs as a result of an imbalance between the excitatory and inhibitory signals from the brain and/or spinal cord. • Excitatory signals send messages to other neurons, firing them into action, whereas inhibitory signals stop neurons firing and suppress a response • The primary theory is that there is an interruption of the inhibitory signals along the spinal cord and in the brain which results in an increased excitation and therefore an imbalance.
- 8. However – Much about MS remains unknown… • Will the real multiple sclerosis please stand up? • Peter K. Stys, Gerald W. Zamponi, Jan van Minnen & Jeroen J. G. Geurts • Abstract • Multiple sclerosis (MS) is considered to be an autoimmune, inflammatory disease of the CNS. In most patients, the disease follows a relapsing–remitting course and is characterized by dynamic inflammatory demyelinating lesions in the CNS. Although on the surface MS may appear consistent with a primary autoimmune disease, questions have been raised as to whether inflammation and/or autoimmunity are really at the root of the disease, and it has been proposed that MS might in fact be a degenerative disorder. We argue that MS may be an 'immunological convolution' between an underlying primary degenerative disorder and the host's aberrant immune response. To better understand this disease, we might need to consider non-inflammatory primary progressive MS as the 'real' MS, with inflammatory forms reflecting secondary, albeit very important, reactions.
- 9. and new theories often emerge ... • Is multiple sclerosis a mitochondrial disease? Peizhong Maoa and P. Hemachandra Reddya,b
- 10. Patient Intrathecal Baclofen (ITB™) Therapy Oral Medications Non Pharmacological Orthopedic Surgery Neurosurgery Injection Therapy Clinical practice interventionscourtesy of the UKMSSNNA
- 11. Trigger or aggravating factors: • Sensory stimuli – chafing clothes, splints, straps, ingrown toenails, sore skin, constipation • Infection – can be silent UTI • Patterns of movement • Posture and position • Stress or emotional issues
- 12. My clinic sheet part 1! •http://www.mssociety.org.uk/ms- resources/muscle-spasms-and-stiffness-ms- essentials-19 •Check you don’t have a urine infection – get your urine dipsticked, and get treatment if leucocytes/nitrites present •Check you don’t have any infection, sore skin, ingrown toenails, clothing/splint/shoes that are chafing, or constipation – treat immediately if so, as all these things can trigger muscle spasm.
- 13. My clinic sheet, part 2! • See the Physiotherapist, and Do as much movement exercise as you can, every day, as this has been shown to be the best way to address stiffness physically • Think about how you are sitting and moving • You might need to use pillows in the bed to help get your legs comfortable in a slightly bent position for sleeping
- 14. Part 3…medication • If you need to start or increase muscle relaxant medication, get a tablet cutter, and increase in half tablets, every 3 days, until you find the right dose, a to a max of 90mg a day, in 3 split doses. Ask your GP to adjust your prescription accordingly, and check that you’re not having undue side-effects. • If baclofen causes undue drowsiness, tizanidine could be tried; you’d need a blood test before & for the 1st 3 months to check your liver can process it. • See your MS nurse again if this doesn’t work – there are other options
- 15. part 4 – natural alternatives • Many people ask me about drug-free alternatives. The ones most commonly recommended are calcium 1000mg with magnesium 500mg a day, and GABA as a supplement. ( Baclofen, Gabapentin and Pregabalin all function on altering the levels of GABA in the brain) • Other supplements/natural remedies sometimes recommended are B vitamins, MSM, and the herbal remedies Skullcap and Valerian. • It’s important that you take responsibility for any supplement or herbal medecine that you take, and check that the product and dose is sfe for you to take with any existing conditions or medications.
- 16. Sativex and cannabis • The cannabinoid medecine Sativex has been licensed and seems to help about 30% of people with MS spasms. As it is so expensive, many PCTs will not fund it. • Some people with MS find using cannabis helps with their spasms, although it is an illegal drug in the UK. This is a link about making cannabis tincture to use as a spray like Sativex. • http://patients4medicalmarijuana.wordpress.co m/medical-use-of-cannabis-video/marijuana- tincture
- 17. Physiotherapy • Self management technique training • Specific techniques; – inhibitory mobilisation techniques – normal patterns of movement – Active and passive movements – Positioning / posture (sitting, lying, standing) – Splinting – Proprioceptive neurological facilitation techniques (PNF) – Bobath technique-uses intensive handling to inhibit abnormal tone and movement patterns
- 19. Self-management techniques • Home exercises/ stretches • Exercise classes • Appropriate strengthening • Regular review • Strengthening exercises for muscle weakness • Improves conditioning, endurance and fitness • Use of: – Free weights – Machines – Theraband – Swiss balls – Aquacise classes
- 25. Injectable therapies • Anaesthetic / Diagnostic Nerve Blocks – Procaine – Lignocaine • Neurolytic Nerve Blocks – Ethanol – Phenol • Botulinum Toxin • Intrathecal Baclofen • Intrathecal Phenol
- 26. Injections Advantages • Not permanent • Evidence to support efficacy in reducing spasticity and improving function • Effects are localized - not systemic Disadvantages • Not permanent - may need to repeat injections • Ethanol and Phenol: require greater skill to inject, increased risk of paresthesias, dysesthesias • Botulinum toxin: more expensive than other injections, may develop antibodies • Only of use in single muscle spasticity • Not appropriate if contracture already present
- 27. Botulinum toxin therapy • Naturally occurring substance produced by bacterium clostridium botulinum • Powerful neurotoxin (type A) • Blocks release of acetylcholine at neuromuscular junction • Results in muscle weakness - effect in 4-7 days - peak 4-6 weeks - lasts 3-4 months
- 28. Botulinum toxin Side effects • Excessive localised muscle weakness • Flu like symptoms • Fatigue without objective weakness • Dry mouth Follow up • Must be multi disciplinary • Education • Physiotherapy e.g stretching regime • Splinting / casting • Review goals 4-6 weeks post injection • Medical review 3-4 months
- 29. Intrathecal Baclofen • ITB™ /“Lioresal Intrathecal” administered by programmable infusion system • Surgically implanted pump delivers tiny doses of baclofen via intrathecal catheter • Effect 5x greater in legs than in arms • Average dose 300-800 mcgs per day compared to 30-120 mgs oral baclofen
- 30. Why Intrathecal vs Oral? • Intrathecal – Lower doses than those required with oral administration – Potentially fewer systemic side effects • Oral – Low blood/brain barrier penetration, with high systemic absorption and low CNS absorption – Lack of preferential spinal cord distribution – Adverse effects, such as drowsiness, for some patients
- 31. Where I stole these slides from: • A presentation put together by staff from: • The National Hospital for Neurology and Neuro-surgery (otherwise known as Queen’s Square) • Laura Flisher ,Physiotherapist • Dr. Rachel Farrell Consultant Neurologist NHNN
- 32. Cannabis • Comes in different forms and can be smoked with tobacco or baked in food/drunk in tea • Hash is made from plant resin and comes in lumps • Grass is dried leaves of plant and is usually more expensive than hash.
- 33. Cannabis • In a 2009 systematic review of RCT trials on people with MS taking cannabis extracts (THC & CBD) found that 5 out of 6 reported: • a decrease in spasticity & improved mobility • All reported side effects, related to dosage. • Generally the treatment was well-tolerated. • Study on whether cannabis protects against progression found it did not. (Cupid)
- 34. Known effects of Cannabis • Psychoactive, mildly euphoric ‘high’ • Slight changes in psychomotor and cognitive function • Appetite stimulation • Increase in heart rate and decrease in blood pressure • Dry mouth and dizziness • May induce feelings of panic, anxiety and paranoia • Frequent, heavy users may develop an amotivational syndrome Baker, Pryce, Givanni & Thompson Neurology 2003
- 35. Remember… • Do you use the benefits of spasticity for your mobility? • Some other benefits are: maintenance of muscle tone, prevention of DVT and circulation • Maintenance of muscle bulk
- 37. APS therapy • Based on the function of the cell • Electrically simulates Action Potential • Dr. in Hull recently having very positive afffects with people with MS with pain, muscle spasm and fatigue • Clinical research project about to start in Hull • MS Therapy Centre in Bedford investing in machines to pilot therapy clinically
- 39. Stay in touch! • www.mirandasmsblog.wordpress.com • Visit my blog to find out how we do!
Editor's Notes
- To understand muscle stiffness and spasm we need to understand a bit about nerve cells
- And we’ll come back to that later when I talk about things in the pipeline
- Today, several treatment options are available to manage spasticity and more than one option can be used. A complementary approach to the treatment of spasticity may include physical, pharmacological, and surgical interventions. For example, physical therapy and orthopedic treatments may be used in combination with ITB Therapy. An individualized treatment plan is required to manage each patient’s needs. Treatment options may be different for children and adults. Efficacy in children has not been established with most oral medications. Selective dorsal rhizotomy is used almost exclusively in patients with cerebral palsy.
- So lets go into each of these approaches in a little more detail…
- I will now go on to discuss what I consider the different aspect of therapy management of spasticity. I am sure this is not an exhaustive list and as discussed previously the therapist should treat or manage whatever spasticity presentation they are faced with by whatever means they find appropriate. Self management of spasticity This is the concept of patients moving away from theidea of ‘physiotherapy must be done to me by a therapist’, especially in the Community or non-acute settings where patients often expect to have access to on-going hands-on therapy. The physiotherapist has a significant role as an educator to the patient about how their body moves, how spasticity effects them in their daily routine, what can affect their spasticity and how they can monitor this. Even newly diagnosed patients or those with very minimal spasticity will benefit from advice and a specific home programme of activities. This may facilitate better movement patterns and make future management easier – as it is said ‘old habits die hard’ and in the case of spasticity, abnormal movement patterns become established and more difficult to alter. It is therefore important to see these patients early in diagnosis or presentation with spasticity symptoms and educate them. A carefully devised home programme of stretching exercises can maintain muscle length and effectively manage early signs of spasticity. More active and strengthening exercises may also be added if spasticity is at an appropriate management level and selective underlying components of movement can be accessed. The effectiveness of teaching such a programme may need to be checked and the programme may require review if there are any changes in the patient’s condition.
- Stolen from
- The SynchroMed® EL Infusion System allows for accurate and continuous administration of baclofen injection to provide optimal relief from severe spasticity. The SynchroMed EL pump can be noninvasively programmed to deliver a range of infusion rates as well as a number of dosing patterns. This allows the physician to tailor the drug dosage to the individual needs and lifestyle of the patient, especially for those patients who rely on some spasticity or hypertonicity for function. The pump and catheter are surgically placed in the patient’s body during the implant phase of ITB Therapy. The pump is placed under the skin, usually on the patient’s lower abdomen. To surgically place the catheter, a needle is first inserted into the intrathecal space below the spinal cord, usually at L2-L3. The catheter is then advanced to about T10-T11. The catheter is then connected to the programmable pump.
- Injections can be an effective treatment for focal spasticity. Injection therapies are often used in combination with other interventions, such as orthoses, serial casting, stretching, strengthening, and rehabilitation to improve motor control. Anesthetic/Diagnostic Nerve Blocks Useful in identifying presence and extent of contracture May help predict effect of subsequent neurolytic procedure Neurolytic Blocks Injected into motor points of involved muscle Decrease spasticity by damaging nerve, blocking efferent (and sometimes afferent) muscle stimulation Agents used in neurolytic blocks include phenol (3-7%) and ethanol Botulinum Toxin Most commonly administered injection for spasticity
- Advantages The injections are not permanent. Effects of ethanol and phenol may last up to a year, or longer. The effects of botulinum toxin typically last 3-6 months. There is randomized, placebo-controlled evidence to support the efficacy of injections for reducing spasticity and improving function. Disadvantages Since the effects are temporary, the injections may need to be repeated. Injections may be painful, and some physicians do the injections under sedation or light anesthesia. Ethanol and Phenol: These injections require the physician to have greater technical skill because the agents must come in direct contact with the motor points. The alcohol agents also have a risk of paresthesias and dysesthesias. Botulinum toxin: is more expensive than other agents. Botulinum toxin diffuses through small areas of the muscle, thus the exact injection site does not seem to be as critical to successful outcomes. A small percentage of patients may also develop antibodies to the toxin.
- Effective doses of intrathecal baclofen are a small fraction of the effective oral dose. Since the drug is delivered to the CSF, systemic side effects are often decreased because a minimal amount of drug enters the vascular system. Orally-administered baclofen circulates throughout the entire vascular system and only a small portion reaches the target site in the spinal cord. Oral baclofen often isn’t effective in treating severe spasticity because effective doses may produce unacceptable side effects: lethargy, drowsiness, hypotonia.