Clinical assessment and management of spasticity: a review


  • Conflicts of interest : none.

T. Rekand, Department of Neurology, Haukeland University Hospital, Bergen, Norway
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Rekand T. Clinical assessment and management of spasticity: a review. Acta Neurol Scand: 2010: 122 (Suppl. 190): 62–66. © 2010 John Wiley & Sons A/S.

Spasticity is a sign of upper motor neurone lesion, which can be located in the cerebrum or the spinal cord, and be caused by stroke, multiple sclerosis, spinal cord injury, brain injury, cerebral paresis, or other neurological conditions. Management is dependent on clinical assessment. Positive and negative effects of spasticity should be considered. Ashworth score and the modified Ashworth score are the most used scales for assessment of spasticity. These and other spasticity scales are based on assessment of resistance during passive movement. The main goal of management is functional improvement. A novel 100-point score to assess disability, function related to spasticity (Rekand disability and spasticity score) is proposed.

Management of spasticity should be multimodal and should always include physiotherapy or exercise. Oral medications such as baclofen and tizanidine have limited efficacy and considerable side effects, but are easiest to use. Botulinum toxin combined with physiotherapy and/or orthopaedic surgery is effective treatment of localized spasticity. Treatment with intrathecal baclofen via programmable implanted pump is effective in generalized spasticity, particularly in the lower extremities. Neurosurgical and orthopaedic procedures may be considered in intractable cases.


Spasticity is one of the signs indicating damage of upper motor neurone system on spinal or cerebral level. It may cause disability in numerous neurological conditions such as cerebral paresis, multiple sclerosis, brain injury and spinal cord injury.

Lance defined spasticity in 1980 (1). Later, Young developed further the definition as ‘a velocity dependent increase of muscle tone with exaggerated tendon jerks resulting in hyper-excitability of the stretch reflex in association with other features of upper motor neuron syndrome’ (2). Young also divided the signs indicative of upper motor neurone damage to the positive and negative ones. The positive ones include increase of muscle tone and tendon jerks, clonus, extensor stretch reflexes and released flexor reflexes such as Babinski reflex. The negative ones are paresis, loss of fine motor control and loss of dexterity, increased fatigability of muscles and hypotonia in early phase of upper motor neurone damage.

Pathophysiologically, spasticity is not a stable condition. The neural insult itself causes paresis, and the consequent immobilization of the paretic body part may cause adaptive shortening of the muscles and joint contractures (3). These changes lead to the chronic disuse of the paretic body part, which will induce plastic rearrangements in the nervous system. To optimize motor recovery, it is necessary to disrupt the vicious circle of paresis, disuse and more paresis (3, 4). Therefore, management of disabling spasticity is necessary to prevent further deterioration of function.

Assessment of spasticity

Management of spasticity is based upon clinical evaluation of the patient.

Spasticity may not exclusively have negative consequences for the patient. In a paretic limb, spasticity may yield better function, enabling walking, standing, transfer, which may also protect against deep venous thrombosis. However, pronounced spasticity may be a hindrance to functions and cause problems in activities in daily living. In these cases, management options should be considered (5).

Clinical assessment of spasticity should include quantification through a validated scoring system. The most used score is the Ashworth scale or the modified Ashworth scale (6, 7). These scales measure passive resistance in the joint, as the examiner perceives it. The resistance is scored from 0 to 4 (Ashworth scale) and from 0 to 5 (modified Ashworth scale) (4, 5). The modified Ashworth scale has proved to be useful for assessing spasticity in clinical settings (7, 8). Other scales are the Tardieu scale and the modified Tardieu scale (9–11). These consider passive range of motion, quality of muscle reaction to passive stretch at the fastest stretching velocity and angle of muscle reaction at the point of resistance to the fastest stretching velocity when the overactive stretch reflex produces a first catch (11). Priebe and Penn have developed a scale based on counting of spasm frequency (12, 13). In the pendulum test defined by Wartenberg knee spasticity is assessed by extending the patient’s leg, hanging over the end of couch, to the horizontal position and then measuring the swing of the leg may be evaluated using goniometers (14, 15). The shortcomings of all these scales are that they are dependent on the examiner’s impression of spasticity on passive movement. Previous studies have shown that spasticity scales provide insufficient information about muscles involved in spastic movement, and the reliability and validity of the scales has been questioned in clinical practice (16, 17). The self-report of scales of perceived spasticity (visual analogue scale or numeric rating scale may provide additional information, bur are not sufficient alone for clinical assessment (18, 19).

In the decision about treating spasticity or not, one should take into consideration how much the spasticity interferes with the functioning and influences disability (5). Therefore, the scales described above have limited value in the clinical decision-making process. A good spasticity assessment scale should primarily take into consideration disability caused by the spasticity itself, but also the pain and dystonia related to spasticity.

The scale considering the important aspects of treatment indication should consider the disability related to daily activities, pain, dystonia and the presence of spasticity. As there are no such scores available, the following disability and spasticity score (Rekand disability and spasticity score) is proposed:

1. Independence of all daily activities

0 – completes independence in all daily activities

5 – needs more time or help in some daily activities. Patient is independent with regard to at least one daily activity.

10 – needs help for all daily activities

2. Personal hygiene and natural functions/catheterization

0 – without any problems

5 – needs help or more time to perform activities. Patient is independent with regard to at least one activity

10 – patient is dependent on help for performing personal hygiene and catheterization

3. Walking

0 – without any problems

5 – needs more time or aids for walking

10 – walking is impossible

4. Moving from chair to chair or from bed to chair

0 – completely independent

5 – needs for help or more time or for moving. Needs aids except lift, no need for extra personnel for moving

10 – completely dependent on personnel or need for lift for moving

5. Getting dressed

0 – without any practical problems

5 – needs aid or more time for getting dressed. Patient manages at least one dressing item without help from other person

10 – patient is not able to dress by him/herself, and must be dressed by another person

6. Aids

0 – no needs for aids

5 – uses aids, but not wheelchair

10 – use of aids, including wheelchair

7. Pain

Patient indicating pain level on a numeric scale ranging from 0 (no pain) to 10 (worst possible pain)

8. Dystonia

0 – no dystonia in addition to spasticity

5 – moderate dystonia in addition to spasticity

10 – pronounced dystonia in addition to spasticity

9. Spasticity

Measured by modified Ashworth score in the two bodily areas with the most pronounced spasticity (maximal score 10).

10. Perceived spasticity

Patients score of perceived spasticity between 0 (no spasticity) and 10 (worst possible spasticity)

The RDSS score is calculated as the sum of the 10 subscores, hence having a maximum 100 points. Its main purpose is to allow an assessment of the main clinical aspects before the management.

The RDSS score has been tested in 78 patients with spasticity. These patients attended for treatment with Botulinum toxin or intrathecal Baclofen to the Spasticity Management Clinic at the Haukeland University Hospital. The mean score for these patients was 51.8 (range 19–90). There is reason to consider treatment if the measured and perceived spasticity subscoresis more than 5 points together. Treatment with intrathecal Baclofen and/or Botulinum toxin injections are indicated if total score is more than 15 according to our tests.

Management of spasticity

Physiotherapy should always be included in the management of spasticity. The aim of physiotherapy is to reduce abnormal sensory inputs and decrease α-motor neurone activity (20).

In the case of disabling spasticity, oral medication is the first choice because of easy administration route. Oral Baclofen is widely used. It may also modulate pain due to its binding to GABA receptors. Not all patients with spasticity benefit from this treatment (21), and oral baclofen may cause considerable side effects such as sedation, respiration problems and muscular weakness in higher doses. Often, the effect on spasticity is insufficient (5). Tizanidine, a centrally acting α-2 adrenergic agonist, is another option for oral treatment. Effect on spasticity has been demonstrated on stroke patients (22), but its use is limited by side effects such as dry mouth, sedation, prolonged QT interval and hallucinations at higher dosages (23–25). Few studies compare effects of oral Baclofen with oral Tizanidine. One study suggested that treatment with a combination of oral Tizanidine and Botulinum toxin is more effective than oral Baclofen combined with Botulinum toxin in patients with cerebral palsy and spastic foot deformity (26). Tizanidine has been shown to be more effective than oral Baclofen on spasticity related to cerebrovascular lesions (27). Other oral medications that may be considered are Dantrolene, Diazepam and Gabapentin (23, 25). A study on hemiplegic patients with spasticity showed better effect and fewer side effects of Tizanidine than Diazepam (28). A meta-analysis concluded that efficacy of oral antispastic drugs is small and evaluation of the effect on patients’ quality of life is lacking from the studies (25). The incidence of adverse drug effects (drowsiness, sedation and muscle weakness) was high.

Patients with localized or multifocal spasticity injections have benefit of Botulinum toxins (5, 29, 30). Botulinum toxins cause reversible block of neuromuscular transmission by inhibiting acetylcholine release. Injections should be targeted to spastic muscles responsible to functional loss using EMG guidance (30). The clinical effect appears 4–7 days after injection, reaches a maximum after about 2 months thereafter the effect tapers off. Effect on spasticity caused by cerebral paresis or stroke is well-documented (29, 31, 32), but treatment is also helpful for spasticity related to multiple sclerosis, injury of the spinal cord and the brain tumours (33–35), cerebral anoxia and degenerative diseases (36). The best outcome will be achieved by combining botulinum toxin injections and physiotherapy (5, 33–36). It is recommended that the treatment should be of limited duration, but the drug seems to be effective and safe also with long time treatment (5, 37, 38). Formation of antibodies against botulinum toxins has been demonstrated in 12% of patients in a group of 42 patients treated more than 2 years (39). However, two of five patients with anti-botulinum toxin antibodies remained clinically responsive to the botulinum toxin therapy. The risk for antibody formation depends on the dose and frequency of treatment (40). Treatment outcome should be carefully evaluated. Improvement of quality of life has been demonstrated in an observational study (41). Botulinum toxin therapy must be restricted to localized spasticity.

Oral Baclofen penetrates poorly blood–brain barrier, and generalized spasticity may be managed more effectively via intrathecal administration (5), that is, directly into CSF via programmable pump, giving higher concentrations in relevant tissues and better therapeutic outcome with less side effects. The dose needed for such treatment is considerably lower than with oral administration (42). The treatment may be effective in spasticity both of cerebral and spinal origin (12, 43), and it is most effective in the lower extremities. Long-term effect on spasticity and dose needed for treatment is stable without development of tolerance (44, 45). Technical complications such as catheter disconnection, migration, kink, obstruction, leakage or fibrosis have been reported to occur frequently (46).

Neurosurgery such as rhizotomy and orthopaedic surgery (tendon lengthening and soft tissue releases) may be the options if other treatments do not give expected results (5). Orthopaedic procedures may be combined with Botulinum toxin therapy for better control of spasticity and improvement of function (47).

In conclusion, spasticity should be clinically assessed, including disability related to spasticity. As spasticity is a chronic that may vary considerably over time, the effect of management should be continuously evaluated. Botulinum toxin and intrathecal Baclofen have well-documented effect on pronounced spasticity.