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Muscle stiffness and spasm

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Muscle stiffness and spasm in MS Miranda Olding RGN MSCN November 2012
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Page 1: Muscle stiffness and spasm

Muscle stiffness and spasm in MS

Miranda Olding RGN MSCNNovember 2012

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Neurones

http://www.bbc.co.uk/schools/gcsebitesize/science/aqa/nervesandhormones/thenervoussystemrev2.shtml

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http://www.childrenshospital.org/research/_neuron/index.html

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Anatomy of a cell

• neurone

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Action Potential at work

• link

http://www.apstherapy.co.nz/wpimages/wpfe373a51.gif

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•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.

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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.

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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.

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and new theories often emerge ...

• Is multiple sclerosis a mitochondrial disease?Peizhong Maoa and P. Hemachandra Reddya,b

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PatientIntrathecalBaclofen

(ITB™)Therapy

OralMedications

Non Pharmacological

OrthopedicSurgery

Neurosurgery

InjectionTherapy

Clinical practice interventionscourtesy of the UKMSSNNA

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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

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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.

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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

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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

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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.

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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.com/medical-use-of-cannabis-video/marijuana-tincture

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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

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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

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Intrathecal Baclofen (ITB™)

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Injectable therapies

• Anaesthetic / Diagnostic Nerve Blocks– Procaine– Lignocaine

• Neurolytic Nerve Blocks– Ethanol– Phenol

• Botulinum Toxin• Intrathecal Baclofen• Intrathecal Phenol

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InjectionsAdvantages• 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

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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

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Botulinum toxinSide 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

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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

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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

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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

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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.

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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)

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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

syndromeBaker, Pryce, Givanni & Thompson Neurology 2003

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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

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Exciting possibilities

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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

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Stay in touch!

• www.mirandasmsblog.wordpress.com• Visit my blog to find out how we do!


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