I promised to post on spasticity in MS a while back. Hope you find this post useful…

Firstly, here is the wikepedia version [click].

And now mine – as clinicians when we say there’s spasticity in an arm/leg we mean that there’s increased resistance to movement of the arm/leg at the level of it’s joint. For example, this is the knee joint for the lower leg, or the hip for the upper leg.

This happens due to increased muscle tone (termed a high tone/hypertonus) and varies with the speed of movement at the joint. This is opposed to rigidity which is present throughout the range of movement, and is seen in conditions such as Parkinson’s disease.

Spasticity can be mild with simply a catch on bending and extending the leg at the knee joint or severe where the leg may remain in a flexed posture even at rest and lead to contractures (permanent shortening of the muscle) and painful spasms. Spinal cord lesions as opposed to brain lesions tend to have more spasticity than brain lesions.

Spasticity often does not occur in isolation and is commonly seen together with:

  • Abnormal reflex transmission with increased gain on reflexes
  • Clonus (muscle spasm with repeated, rhythmic contractions – on flexing a muscle or simply on movement) 
  • Painful muscle spasms (which are sudden involuntary [i.e. happen without any planned intention] movements involving multiple muscles in response to movement or touch)
  • Dystonia (tonic muscle overactivity without triggers due to an inability of the nerve innervating the muscle to stop firing after voluntary movement or reflex activity)
  • Co-contraction (inappropriate activation of the opposing muscles during voluntary movement leading to loss of dexterity and slowed movements)

Cross-section through the spinal cord (ascending and descending tracts to and from the brain).

In the spinal cord for sometime the wildly held belief was that spasiticity was caused by damage to the corticospinal tract (all of these pathways except the medial reticulospinal tract and vestibulospinal tract are held under INHIBITORY control by the brain), but it is now understood that other motor tracts may also play a role:
  • The lateral reticulospinal tract which is adjacent to the corticospinal tract (see diagram above) may be involved in MS where lesions have a predilection for the lateral surface of spinal cord. This pathway has an inhibitory effect on stretch reflexes. 
  • The medial reticulospinal tract and vestibulospinal tract (see diagram above) which have excitatory effects on extensor muscle tone.

The over activity of the spinal neurones leads to involuntary activation of muscles.

Whereas lesions affecting the brain leads to increased excitation of the spinal pathways and a lowering of the threshold (i.e. easily triggered) to respond to stimuli such as stretch.

There are certain things which worsen spasticity:

  • skin ulcers, ingrown toenails, skin infections
  • constipation, UTIs, kidney stones, and pain 
  • improper seating, ill fitting orthotics
  • rapid withdrawal of anti-spasticity medication
  • other- deep vein thrombosis/DVT, injuries, stress

Pharmacological medications commonly used include Baclofen (GABAergic drug which relieves spasms) often in combination with Tizandine (centrally acting alpha2-noradrengic drug) as their mechanism of action is complimetary. Gabapentin is also a useful anti-spasmodic but limited by its sedative side effects, the latter also occurs with Baclofen. Botox is useful when individual muscles are involved. When oral anti-spasticity medications are of limited use, intrathecal Baclofen which delivers Baclofen into the spinal space may be used. Rarely, drastic measures are taken for painful immobile spastic legs with reflex spasms using intrathecal phenol or alcohol which causes irreversible nerve damage. Other measures include relief of pain and discomfort, improvement in posture, stretch exercises, facilitation of sitting, standing and walking, and prevention of complications such as contractures and pressure sores. Contractures which are not severe can be corrected using sequential casting (see below).

Stretch exercises (left) and manual sequential casts (right)

About the author

Neuro Doc Gnanapavan


  • Other things that I have experienced worsening spasticity are hunger and a full blatter. Which makes you hobble to the bathroom and walk back out of it. Very bad for my credibility. People think your faking it.

  • Seeing a physiatrist helped me immensely. She altered the way I was taking baclofen, tizanidine and lyrica in combination and has made things much smoother.

    The list of other things that worsen spasticity were labelled 'noxious stimuli' by my physiatrist. I like the term 'noxious' to describe anything to do with MS!

  • @ Johanna, Good points, also I have noticed outdoor air temperature extremes have worsened spasticity. By the way are there any new anti-spastic drugs in the pipeline? MD mentioned that Bart's was investigating a new drug.

    • COI yes we are and have the drug ready for the first MSer sometime very soon, we aim to be finished around May 2016

    • I experience spasms in extreme temperatures. Haven't has spasms for many months then last night my night storage heater in my bedroom got very warm, also too many bedcovers I was very hot.
      My feet and legs were moving a lot when I was trying to sleep. Need to keep my bedroom cooler.

  • Very enlightening your text Neuro Doc Gnanapavan. I recover after the outbreak and the transition of Interferon Beta 1a for Glatiramer come to feel a sense of heaviness in the legs uncomfortable. Every time I went to the gym weight training to piorova feeling, but I decided to "risk" and insist on physical activity. I searched the medical literature and found about the possible causes of this feeling could be a form of spasticity, muscle weakness and a result of fatigue. I came to report to my neurologist in more than one routine visit, she assessed me but did not quite give me an answer as to what caused this feeling. Then I started me to consult with a nutritionist in order to let her pass me an anti inflammatory diet (an attempt to holistic therapy for MS). I reported that I was practicing bodybuilding, so she gave me to take isolated from milk protein (either beef, soy, or egg white too) to take immediately after physical activity. You know, I do not know if it was "placebo effect", or instead be suffering from dystonia (which was what I personally think it was the cause of feeling) I was suffering from muscle weakness … Anyway I feel very relieved and I just come back to feel her menstrual period or when I'm very tired …

  • Thankyou for that. In 2008 I was diagnosed with a CIS – one lesion on the spinal cord. I recovered but a year later started to notice heaviness in leg after a long walk and foot drop. The spasticity has gradually got worse. I have had no further attacks or lesions on spine and/or brain. I have had an attack which has started the onset of spasticity in the one leg. My question why does it take years to manefest itself after one attack.

    • This is tricky but our imaging sensitivity is not as good in the spinal cord as for the brain – so easy to miss new lesions or sub clinical MS activity. In the meantime in the background spasticity can increase. The lesion itself also maybe very large and longitudinally extensive and can affect a larger surface area of pathways, i.e. the very large transverse myelitis which have a greater likelihood of spasticity. Age can affect plasticity/recovery capacity – so as you age this also creeps up. And sometimes simply not treating it makes it gradually worse.

    • Hi doctor Neuro Doc Gnanapavan
      i hope you can help me
      i was diagnostic with an uveitis a year ago , and everything was normal in tests except two things, i had CMV and MS when i made MRI . the ophtamologist told me that its because of MS not cmv but the neurologist said i dont have MS because my lesions arent so bad like his other patients
      so is it possible to have lesions in brain without having ms ? and is it cmv that caused me the uveitis or MS ?
      then i had to take corticosteroids for 3 days in hospital by (serum) and then 60 mg everyday "pills" for almost 5 months.
      but after one week of getting out of hospital i had another problem , it was trendelenburg gait , my left hip starts to shrinks which make my left leg bends towards the right leg which causes a strange way of walking with every step, its not because of pain but it just happens ,and i have it now since a year ago .
      the neurologist who said i dont have MS said also i was pretending and acting
      im afraid i have a sarcoma or something , or is it because of MS ?
      i also doubt of AVN cause i have scoliosis since i was four & bad circulation too " im only 20 "
      my x ray showed nothing
      i do have pain in my hip and it burns specially at night and i feel knives hurt my leg sometimes
      what can i do ? please help



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