The diagnosis and treatment of adults with acquired cerebral and/or spinal spasticity are significantly influenced by factors such as time since injury (acute, subacute, or chronic phase), the patient's age, and their current stage of life. Several reasons underline the importance of considering the temporal dimension in the assessment and management of spasticity:

• Phenotypic evolution over time following the onset of spastic paresis, particularly with respect to the manifestation of spasticity and the resulting functional limitations.
• Variations in the incidence and prevalence of spasticity across different stages of life.
• Differences in treatment objectives depending on the phase of life or recovery.

The first part of this module focuses on the temporal development of spasticity-related features in relation to the time elapsed since the neurological insult (Key Question 1). The second part addresses the role of age and life stage in the development, diagnosis, and treatment of spasticity (Key Question 2).

The subquestions were addressed narratively, having used studies known to the working group. For subquestion 2, additional references were identified through an exploratory literature search.

Subquestion 1: Influence of time period after onset of spasticity

Following a stroke, both neural and non-neural (tissue) components undergo changes over time. In addition to the neural component, changes in (non-)contractile tissues also play a role in spasticity. The most significant tissue changes include muscle shortening and connective tissue stiffening, which can result in limited range of motion (ROM) in joints (contractures). Research on the progression of spasticity over time is scarce, but distinguishes three phases: the acute (< 7 days post stroke, early subacute phase (<3 months), late subacute phase (3-6 months) and the chronic phase (>6 months).

(Sub-)acute phase

a. Natural course

Several studies suggest that both neural and non-neural (tissue) stiffness increase within the first six months after a stroke, particularly in patients without neurological recovery in the subacute phase (see Table 1) (De Gooijer, 2018; Andringa, 2020).

Table 1. Study design and findings on changes in neural and non-neural components in the acute phase after stroke

b. Effect of interventions over time: botulinum toxin

Wissel (2023) compared early intervention (mean 2.6 ± 1.8 months); median intervention (mean 17.2 ± 11.1 months); and late intervention (mean 138.6 ± 90.9 months) in 303 participants, and found a reduction in MAS scores in all study groups without significant differences between groups. Picelli (2021) compared early (<3 months) with late (>3 months <12 months) BoNT treatment after stroke onset (n = 83), and found significant lower MAS scores in the early treatment group 12 weeks after intervention (OR 2.87; 95% CI 1.46 to 5.65). Research on interventions in the acute phase (<7 days post stroke) is lacking (Tilborg, 2024).

Chronic phase

a. Natural course

Prospective longitudinal studies on the natural progression of spasticity over the long term are unavailable. However, cross-sectional studies suggest structural muscle changes over time in a subgroup of stroke patients:

• A significantly lower number of sarcomeres and a smaller physiological cross-sectional area in the biceps brachii compared to the contralateral side and age-matched controls (mean age of patients: 59 years [SD 10]; mean age of controls: 62 years [SD 6]), after an average follow-up of 13 ± 10 years post-stroke (Adkins, 2021).
• A shift from slow (MHC type I) to fast muscle fibers (MHC type IIA and IIX) (De Deyne, 2004; Hafer-Macko, 2008).
• Myosteatosis: infiltration of fat tissue into the muscle. This is also seen in physiological aging, but is more pronounced in paretic limbs (Carda, 2013).

In spinal cord injury, atrophy can occur rapidly due to damage to motorneurons of the anterior horn at the level of the lesion. The extent of atrophy depends on the completeness of the injury and occurs earlier than the described muscle fiber shifts.

b. Effect of interventions over time: botulinum toxin

In addition to natural progression, the evolution of spasticity can be inferred from the effectiveness of interventions over time. Several studies have examined this (Table 2). Repeated botulinum toxin treatments appear to result in long-term reductions in spasticity without a decrease in effectiveness (and sometimes even increasing effectiveness) over time.

Table 2. Study design and findings on BoNT-A injections in stroke patients with spasticity

Mohammadi (2010) found in 1227 treatments in 137 patients with spasticity of various etiologies a significant negative correlation between the time from spasticity onset to BoNT-A treatment initiation and the degree of improvement post-treatment, with a stable effect over time (treatment duration averaged 7.5 years, ranging from 2 to 12 years). An earlier start of treatment in the chronic phase of spasticity appears to be associated with better outcomes.

c. Effect of interventions over time: ITB

Small studies (with 14 to 41 patients) indicate stable effectiveness of ITB with long-term use (>10 years) in patients with multiple sclerosis or chronic spasticity due to spinal cord or brain injury (Azouvi, 1996; Mathur, 2014; Rekand, 2011; Plassat, 2004, Draulans, 2013; Stampacchia, 2016). This is further supported by studies in children and young adults with cerebral spasticity (prospective research; Albright, 2003).

However, dosage adjustments over time may be necessary (Coffey, 1993; Maneyapanda, 2017; Kawano, 2018).

Subquestion 2: Influence of age and stage of life

Prevalence of spasticity in the elderly

In the review by Sommerfeld (2012), various prevalence rates of spasticity after stroke are presented, using a definition of a MAS score of 1 or higher. The prevalence of spasticity after stroke is initially higher in younger patients (<65 years), but this difference in prevalence disappears after 18 months (Sommerfeld, 2012). The scoping review by Jensen (2013), which focuses on patients with spinal cord injury, reports a high prevalence of muscle spasms (53–87%) and severe spasms (37%). Spasms were associated with higher age and longer time since spinal cord injury.

In the longitudinal study by Haisma (2007), the course of spasticity is described during the first year after admission to a rehabilitation center due to spinal cord injury (patients <65 years). At all measurement points, most patients showed signs of spasticity during physical examination (67% after one year). Higher age was associated with a lower prevalence of spasticity (OR 0.97; 95% CI 0.96–0.99 per year of age increase). In a large cross-sectional study by Hitzig (2008), which used questionnaires from 781 participants following a specialized program for adults with spinal cord injury, a spasticity prevalence of 71% was observed. Again, higher age was associated with a lower prevalence of spasticity (OR 0.98; 95% CI 0.97–0.99 per year of age increase). This study had no age restrictions for inclusion (median age 51.3 years, range 18–92 years). The studies do not speculate further on the causes of a lower prevalence of spasticity with increasing age. However, the Sommerfeld (2012) study suggests that lower reflex activity with aging, including reduced pathological reflexes, may be a contributing factor.

Prevalence of contractures in nursing home residents

Lam (2022) investigated the prevalence and incidence of joint contractures, defined as a functional limitation in range of motion (ROM), in 1915 residents of nine long-term care facilities (674 men [35%], mean age 83.4 years). During the first five years after admission, the prevalence of upper limb contractures increased from 29.8% to 36.5%, and lower limb contractures from 41.5% to 57.4%. Reduced mobility, presence of neurological diseases, and higher age were the main risk factors for the development of new joint contractures.

Spasticity in relation to physiological aging

The reason for the higher prevalence of spasticity in patients <65 years is not well understood. This may partly be explained by the reduction of tendon reflexes with increasing age as part of normal physiological aging (Chung, 2005). Additionally, muscle quality changes with aging, which may alter the interaction between neural and non-neural tissue components, leading to changes in the presentation of spasticity. Fast-twitch muscle fibers (type II) decline in both size and number with physiological aging. The narrative review by Carda (2013) describes further physiological changes related to age in neurological diseases. Sarcopenia—the decline in muscle mass and quality with aging (Dhillon, 2017)—can influence the manifestation of spasticity. Initially, there is a loss of muscle mass, followed by a decline in muscle quality due to increased fibrosis and myosteatosis, changes in muscle metabolism, and degeneration of the neuromuscular junction.

When combined with the previously described changes in muscle architecture following central neurological injury (subquestion 1), which also occur with physiological aging, diagnosing and treating spasticity at older age becomes more complex and may necessitate alternative therapeutic strategies. Increased age and immobilization may shift the phenotype from spasticity-dominant to contracture-dominant presentation.

Diagnosis and underrecognition

The literature suggests a striking underrecognition and undertreatment of spasticity in nursing home settings. This particularly affects the older population with severe neurological disorders, but younger individuals with such neurological conditions may also reside in nursing homes. The Dutch study by Meijer (2017) focused on the added value of rehabilitation physicians assessing and co-managing nursing home residents with pyramidal tract damage. The 77 included participants underwent physical examination by a rehabilitation physician, and 56 (73%) were found to have spasticity. Most participants were examined for spasticity for the first time, had no documentation of spasticity symptoms in their records, and would not have been identified without the involvement of the rehabilitation physician. This study showed a high prevalence of spasticity, a high burden of disease (increased dependency in ADL, increased burden of care, sleeping problems and many complaints) and thereby a need for extra treatment (mainly targeting the reduction of painful spasms and improvement of care needs). The study by Gill (2020), conducted in a 240-bed nursing home, showed a prevalence of 22% spasticity among all residents, but only 11% of those with spasticity had a documented diagnosis and treatment plan.

The MAS remains the most widely used tool in research and clinical practice, but its interpretation is influenced by muscle and connective tissue changes related to aging. Assessment of spasticity in older subjects should also include measurements of passive range of motion of relevant joints. Additionally, age (a possible declining prevalence) and setting (higher prevalence due to patient selection) impact the observed prevalence (a priori likelihood of spasticity).

Treatment

The study by Shah (2006) describes principles of stroke rehabilitation, specifically in geriatric patients. The author highlights the need for caution with oral medications due to their mild effect on spasticity and significant adverse effects on cognitive function. Even dantrolene, which is believed to act primarily peripherally, causes sedation and muscle weakness. In general, older patients are at increased risk of side effects.

Age-specific challenges arise due to patient selection in nursing homes, where individuals tend to have more severe diseases, greater immobility, more comorbidities, and (as a consequence) increased frailty. Severe movement restrictions (ROM) should be taken into account when considering treatment, which occur primarily due to tissue shortening and stiffening. For this population, there is insufficient data on the long-term effects of early spasticity interventions.

This module focuses on describing differences in the diagnosis and treatment of spasticity between various durations since onset and life stages. A systematic literature search was not considered to add significant value, and the subquestions were addressed narratively. Studies known to the working group were used to elaborate on the acute, subacute and chronic phases of cerebral or spinal spasticity.

Only to further support the elaboration of subquestion 2, an exploratory literature search was conducted. The PICO  below was used. The search targeted systematic and narrative reviews, as well as longitudinal studies, published after the year 2000.