Managing Spasticity with a Focus on Rehabilitation

Konstantina Petropoulou, MD, PhD
Member, International Neuromodulation Society
Head of 2nd PRM Department
National Rehabilitation Center
Athens, Greece

Note: A thorough 2017 version of the document appears at Spasticity Management with a Focus on Rehabilitation

Introduction

Spasticity as a motor disorder is a result of injury to the brain and/or the spinal cord. Its gradual development is caused by a group of neurophysiologic mechanisms emerging after central nervous system (CNS) injury.

Loss of descending inhibitory (reticulospinal) influences leads to exaggerated excitability of dynamic gamma neurons and alpha motor neurons. Other spinal tracts such as the vestibulospinal and rubrospinal tracts become more active. Essentially, spasticity can result from injury to the cortex, basal ganglia, thalamus, brainstem, cerebellum, central white matter, or spinal cord.

It affects patients with cerebrovascular episodes, traumatic brain injury, spinal cord injury, multiple sclerosis (MS), and others. (1)

In order to study “spasticity” and provide the right treatment at the right time, we must first analyze all aspects of the phenomenon, such as:

a) The nature of spasticity, b) its differentiation from other clinical syndromes of muscle tone disorders, c) its different development according to the site and degree of the injury, d) the modification it shows in time, e) its changes throughout the day and during sleep, f) its coexistence with other symptoms such as pain, and g) its changes in intensity due to external and internal sensory stimuli.

Definition and clinical particularities of spasticity

In the traditional sense of the term, James Lance, MD, described spasticity in 1980 as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexitability of the stretch reflex as one component of the upper motor neurone syndrome.” (2)

Nine years later, Robert R. Young, MD introduced the clinical entity ‘‘spastic paresis,’’ which included extensor plantar responses, a velocity-dependent increase in tonic stretch reflexes, exaggerated phasic stretch reflexes, increased autonomic reflexes, and abnormal postures. (3)

Spasticity is only one of several components of the upper motor neurone (UMN) syndrome, known collectively as “positive” signs and characterized by muscle overactivity. Other components include tendon hyper-reflexia, clonus, the clasp-knife phenomenon, flexor and extensor spasms, a Babinski sign, and spastic dystonia. (4)

Even though the positive signs of the upper motor neurone syndrome, such as clonus, should not be confused with spasticity, their production during an attempt to voluntarily move affects the motor pattern and contributes to its abnormal expression. During a voluntary movement, spontaneous movements often emerge, including flexor or extensor spasms, co-contraction, synergies, synkinesis and/or associated reactions. These movements are stereotypical, massive and irregular with no functional importance.

The development and degree of spasticity, especially during the execution of a movement, activate these “immature” motor patterns, negatively affecting the normal movement, posture, and balance of the torso.

In CNS lesion, there is a combination of involuntary muscle overactivity, i.e. “spasticity,” with the emergence of immature movements leading to the so-called “pathological motor syndrome.”

“Pure spasticity” could be defined as the early involuntary muscular overactivity, taking place during the fast passive movement manifested as a “catch”, while the elasticity of soft tissues is preserved and the passive movement is fully completed.

This type of spasticity is clinically observed in the acute phase of CNS lesion, where during the recovery process there is a transition from the flaccid to the “spastic” phase. During this phase the degree of spasticity is low, grade 1 or 1+ in the mod. Ashworth scale, while the joint range of motion remains intact. (5)

On the other hand, when there is spontaneous muscle overactivity at rest without a primary triggering factor, parts of the body assume abnormal positions, which are a major cause of disfigurement and social handicap in these patients. (6) Denny-Brown has defined this condition as “spastic dystonia.” (7)

In time, there are rheological changes in muscle composition, so the muscle becomes shortened and the range of joint motion limited, possibly reaching permanent fixation (contracture) or even ankylosis.

The shortening of soft tissues initiates chain reactions such as the activation of clonus in walking, causing massive bending or extensional muscle spasm of the lower limbs and abnormal gait. That is called “secondary spasticity,” or hypertonia. This condition includes a neural component secondary to spasticity and a biomechanical component secondary to the soft tissue changes.

At the same time, the constant contraction of “spastic” muscles renders the antagonists inactive, resulting in the latter developing muscular atrophy due to disuse.

So, a vicious circle is created; in a typical example, the permanent contraction of the biceps brachialis and the inability to extend the elbow renders the triceps brachialis inactive due to disuse.

The state of hypertonia in a muscle or group of muscles is the commonest condition we encounter in patients with subacute spasticity.

Depending on which of the two components (spasticity or tendon shortening) is prevalent and to what degree, treatment can be either conservative, e.g. local injection of botulinum toxin, or operative, to lengthen or even transfer tendons. The coexistence of spasticity, either local or generalized, must be taken into account in the operative decision, and usually the spasticity must first be managed with either local or generalized intervention in order for the operative results to be satisfactory.

As an example, equinus with the knee in the extended position is corrected when the knee is flexed. This is a clinical sign of gastrocnemius spasticity. It occurs over the Achilles tendon, which shrinks in the course of the development of equinus.

The clinical evaluation of spasticity

The clinical signs of “spasticity” vary according to the injury type (sudden or progressive), site and extent of lesion (brain or spinal cord), and whether it is complete or incomplete.

In localized brain injury, such as in a stroke, or an incomplete spinal cord injury, the degree of increased muscular tone is different for various joints, while non-injured antagonist muscles also play an important role for the position of the joint. In this case, the risk of deformation of the joint is higher.

In contrast, when the brain or spinal cord injury is diffuse or complete, spasticity is much more homogeneous.

Another important factor is injury chronicity, where repeated abnormal movement over time leads to the development of permanent contractions in adjacent normal muscles (dystonia), in an effort to balance the body out in a motion that is safe, fast, and aesthetically acceptable (e.g. ipsilateral quadriceps dystonia in equinus walking).

There are four stages of clinical examination, including static and functional evaluation.

Stage 1: Clinical observation. The image presented by the patient’s body as they enter the examination room and when in a sitting and supine position. Any muscular atrophies and/or muscular spasms are also recorded.

Stage 2: In a supine position the examination includes the range of joint motion with passive slow movement; the spasticity degree; the active movement; and the normal and pathological reflexes. At this stage we use the motor test, the Modified Ashworth Scale, the Adductor tone rating, and the Tardieu Scale.

Stage 3: Examination with the patient in a sitting position. Here the examination is supplemented by an upper limb motor skill test.

Stage 4: Examination of body balance in upright position and walking for a short and longer distance. Fatigue is considered as a major factor of movement disturbance.

Spasticity is not a static phenomenon but changes continuously throughout the day, even during sleep, depending on the coexistence of pain or other irritant factors such as inflammation, urolithiasis, or infection, as well as emotional condition and menstruation in women.

Timing and type of treatment

It is important to address the issue of proper timing for the therapeutic management of spasticity.

Early intervention with oral antispastic medication (baclofen and tizanidine or dantrolene) is the method of choice. (8, 9)

Treatment of the focal or regional spasticity with intramuscular injections of botulinum toxin should be started early in the gold time when spasticity occurs and before soft tissues begin to shrink. (10, 11)

At a later stage, even at the chronic stage when a pathological motor pattern has been established, such as the typical arm posture of the hemiplegic upper limb, we can intervene with intramuscular injections of botulinum toxin in selective “key muscles” so as to modify synergic movements. (12)

The repeated injections of botulinum toxin with an absolute interval of three months or more do not constitute a contraindication, as long as they serve a predetermined goal each time. (13)

The time window (the time elapsed between the injury and the beginning of spasticity treatment) and the time plateau (when the treatment will end) must also be defined.

For generalized spasticity not responding to oral medication, or when the therapeutic dosage of botulinum toxin is not sufficient for multiple muscle group injections without exceeding the safe limit, the intrathecal baclofen (ITB) is selected instead. ITB is a long-term treatment with continuous or flexible intra-spinal administration via an implanted pump that reduces spasticity, especially in spinal injury and multiple sclerosis patients.

Several assessments are usually performed before a definitive pump implantation by simple injection (bolus test) via lumbar puncture or via a temporary access device. Efficacy may be evaluated in the following 3-4 hours. The usually recommended first test dose is 50 µg in adults, with a maximum dose of 150 µg that should be reached after 3 days. 

It has been determined that the pump is to be implanted a year after the injury. However, there are cases when implantation is recommended earlier, when advantages outnumber disadvantages. (14)

For example, for an incomplete spinal cord injury where the emergence of voluntary movement is inhibited by significant spasticity, therefore on one hand the rehabilitation programme is delayed and on the other contractures are developed.

The time of intervention cannot be absolute, as it depends on the patient’s clinical condition and overall therapeutic plan. (15)

The stages of spontaneous neurological “recovery” have been described for both cerebral and spinal cord injuries, including the transition from the flaccid phase to the spastic phase.

Brunnstrom describes seven stages of recovery following stroke-induced hemiplegia. In this model of recovery following cerebral lesion, early spasticity management begins during the second stage, when “Spasticity appears. Basic synergy patterns appear. Minimal voluntary movements may be present.” (16)

In the complete traumatic injury of the spinal cord, the transition from spinal shock to spasticity includes four stages, described by J. F. Ditunno. Spasticity develops during the 4th stage, 1-12 months after the injury, when the early management of spasticity will also begin. (17)

Any delays in treating the “spastic syndrome” creates a pathological motor pattern which constitutes the maladaptation of the brain and spinal cord to the changes resulting from bodily injury, thus increasing rehabilitation time and minimize end results.

Spasticity treatment and rehabilitation

Neurorehabilitation comprises four main categories of spasticity management targets.

The first category involves nursing care: a) Preventing or treating contractures, b) preventing or treating decubitus, c) proper positioning of the body on the bed/wheelchair, d) easy catheterization of the bladder, e) easy orthotics fitting, f) facilitating caregiver work, g) pain relief, and h) improving sleep.

The second category comprises movement improvement: a) The unmasking of voluntary movements previously covered by significant spasticity in cases of incomplete lesions, b) accelerating the “spontaneous” recovery process, c) modifying the “immature” motor pattern, d) using new recovery techniques to promote guided neuroplasticity, e.g. robotic rehabilitation, and e) a new functional pattern in moving and walking.

The third category includes daily life activities: transfers, getting around, putting on clothes, personal hygiene, driving, etc.

The fourth category is about quality of life: a) Independent living, and b) social and professional reintegration. (18)

The goals set by the rehabilitation team in cooperation with patients and their families, should guide the therapeutic intervention for reducing spasticity and are a reliable index for a successful outcome. (19)

References

1. K. B. Petropoulou, I. G. Panourias, C.-A. Rapidi, and D. E. Sakas. The phenomenon of spasticity: a pathophysiological and clinical introduction to neuromodulation therapies. Acta Neurochir Suppl (2007) 97(1): 137–144

2. Lance JW. The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurology 1980;30: 1303–1313.

3. Young RR (1989) Treatment of spastic paresis (editorial). N Engl J Med 320: 1553–1555

4. Ivanhoe CB, Reistetter TA. Spasticity: the misunderstood part of the upper motor neuron syndrome. Am J Phys Med Rehabil (2004) 83 Suppl: S3–S9

5. Gracies JM.  Pathophysiology of spastic paresis. II: Emergence of muscle overactivity. Muscle Nerve 2005;31: 552–571.

6. Alain P. Yelnik, MD, Olivier Simon, MD, PhD, Bernard Parratte, MD, PhD and Jean Michel Gracies, MD, PhD. How to clinically assess and treat muscle overactivity in spastic paresis. J Rehabil Med 2010; 42: 801–807

7. Denny-Brown D. The cerebral control of movement. Liverpool: University Press; 1966, p. 124–143

8. Zafonte R, Lombard L, Elovic E (2004) Antispasticity medications: uses and limitations of enteral therapy. Am J Phys Med Rehabil 83:S50–S58

9. Gracies JM, Nance P, Elovic E, McGuire J, Simpson DM (1997) Traditional pharmacological treatments for spacticity part I: local treatments. Muscle Nerve Suppl 6: S1–S92

10. Hesse S, Mach H, Fröhlich S, Behrend S, Werner C, Melzer I. An early botulinum toxin A treatment in subacute stroke patients may prevent a disabling finger flexor stiffness six months later: a randomized controlled trial. Clin Rehabil. 2012 Mar;26(3):237-45

11. Jörg Wissel, MD1, Anthony B. Ward, BSc,et al. European consensus table on the use of botulinum toxin type a in adult spasticity. J Rehabil Med 2009; 41: 13–25

12. Petropoulou K, Rapidi A-C, Noussias V, Berbatiotou L (2001) Study of the effectiveness of botulinum toxin type A in hemiplegic arm spasticity. Neurorehab Neural Repair 15: 323 (abstract)

13. Elie P. Elovic, MD, Allison Brashear, MD, Darryl Kaelin, MD, Jingyu Liu, PhD, Scott R. Millis, PhD, Richard Barron, MS, Catherine Turkel, PharmD, MBA. Repeated Treatments With Botulinum Toxin Type A Produce Sustained Decreases in the Limitations Associated With Focal Upper-Limb Poststroke Spasticity for Caregivers and Patients. Arch Phys Med Rehabil Vol 89, May 2008

14. Francisco GE, Hu MM, Boake C, Ivanhoe CB. Efficacy of early use of intrathecal baclofen therapy for treating spastic hypertonia due to acquired brain injury. Brain Inj. 2005 May;19(5):359-64.

15. Francisco GE, Saulino MF, Yablon SA, Turner M. Intrathecal baclofen therapy: an update. PM R. 2009 Sep;1(9):852-8

16. Brunnstrom S (1966) Motor testing procedures in hemiplegia: based on sequential recovery stages. Phys Ther 46: 357–375

17. JF Ditunno, JW Little, A Tessler and AS Burns. Spinal shock revisited: a four-phase model. Spinal Cord (2004) 42, 383 – 395

18. K.Petropoulou.«Validation study of subjective spasticity questionnaire.» Annals of Physical and Rehabilitation Medicine, Vol:54 , suppl.1, october 2011 p.e137