Features of spasticity after SCI
The prevalence of SCI is increasing every year. Spasticity caused by SCI seriously affect a individual’s mood, sleep, disease prognosis and quality of life. The mechanism of spasticity is unclear; currently, it is thought to be a complete γ-loop stretch reflex caused by abnormal muscle tone due to the cone system, extrapyramidal system, brainstem reticular formation and cerebellar participation. When the cone system or extrapyramidal system is damaged, excessive γ motor neuron activity occurs and can present as cramps. Studies have suggested that spasticity are caused by changes in the network excitability of interneurons after SCI and the adaptive changes of motor neurons below the injury plane, such as the decrease in the levels of inhibitory neurotransmitter γ-aminobutyric acid (GABA)[8], the change in the number of 5-HT receptors[9] and the decrease in the presynaptic inhibitory activity of Class Ia proprioceptive afferent fibre terminals[10] .
Analysis of the factors related to spasticity
Relationship between the disease course and spasticity
This study’s findings suggest that the duration of the SCI is one of the risk factors for spasticity(when the course of disease was 3 to 6 months and 6 months or more, the incidence of spasticity was 2.441 times (95% CI, 0.968 ~ 6.157) and 5.090 times (95% CI, 1.883 ~ 13.76), compared with a disease course of less than 3 months), and as the duration is prolonged, the incidence of spasticity increased. Previous studies have shown that the incidence of spasticity gradually increases with the prolongation of the course of SCI[11, 12]. Those results are consistent with the present study’s findings. Moreover, relevant animal experiments have explored the relationship between spasticity and the course of disease or the formation of chronic spasticity in individuals with SCI. Kapitza et al.[13] reached the same conclusion. They performed complete sacral spinal cord transection in rats at the S2 level of the spinal cord, and the rats gradually showed signs of tail spasm one week after surgery; that study also found that the number of inhibitory GABA neurons was significantly reduced one week after injury. Therefore, one of the possible causes of spasticity after SCI could be the main structural changes in the interneuronal circuit connections in the spinal cord below the transection level. Emre et al. [14] reported that the denervation structure at the spinal cord level restructured and changed the upper and lower conduction fibre bundles, leading to the formation of chronic spasticity in individuals with SCI.
At present, it is unclear which neural pathways or substances play a key role in the formation of chronic spasticity. Therefore, researchers should continue to conduct more studies on the relationship between various substances in the spasticity -related pathways and the disease course after SCI, and conduct early interventions of spasticity in high-risk individuals with SCI to prevent limb spasticity from seriously affecting their daily life.
Relationship between injury segment and spasticity
The protective factor for spasticity increases when the SCI occurs at lower the level of the spinal cord (the incidence of spasticity in thoracic and lumbar spinal cord injuries was 0.363 times (95% CI, 0.154 ~ 0.855) and 0.034 times (95% CI, 0.004 ~ 0.268) higher than that in cervical spinal cord injuries). In the present study, the incidence of spasticity was significantly lower in individuals with a lumbosacral SCI in comparison to individuals with thoracic and cervical SCIs. This conclusion is consistent with the research results of Holtz et al. [5]. At present, there are few reports on the mechanism between spasticity and injured spinal cord segments after SCI. We hypothesised that the possible reason for spasticity was that the upper motor nerve damage weakened the inhibitory effect on the lower motor neurons. The incidence of spasticity was higher in individuals with a cervical SCI segment than those with a thoracolumbral SCI segment. Thus, the inhibitory effect was more obvious in the cervical SCI individuals, resulting in a higher proportion of spasticity. Some individuals with a high SCI (above C4), especially those with complete SCI, may die due to severe respiratory complications in the process of clinical diagnosis and treatment and may fail to be transferred to a rehabilitation department of a hospital; however, that does not affect the final statistical results of our study. It is worth noting that our study also found that individuals with cervical SCI with the same degree of injury had a higher probability of organ and limb dysfunction due to the higher injury segment, so the prognosis and the ability to function in their daily lives were worse for individuals with cervical SCI than those with an SCI in another segment of the spine. Some individuals with cervical SCI have diaphragmatic and upper limb spasticity, which significantly affects their airway clearance, respiratory function. Therefore, we should pay more attention to the spasticity of individuals with cervical SCI and actively address it to prevent more serious complications from affecting the quality of their daily life.
Relationship between pressure ulcers and spasticity
Pressure ulcers are one of the common complications in individuals with SCI, especially in individuals with high SCI who are in bed for a prolonged period. In this study, pressure ulcers were an important risk factor for spasticity in individuals with SCIs (the incidence of spasticity in patients with pressure ulcers was 2.481 times (95% CI, 0.961 ~ 6.406) higher than that without pressure ulcers. Previous studies have also shown that the presence of spasticity in the chronic stage of SCI is associated with an increased prevalence of pressure ulcers[15]. In individuals with SCI, pressure ulcers and spasticity also affect each other. Jaul et al.[16] found that the damage to skin and muscle soft tissues caused by pressure ulcers results in a series of changes in the neurons innervated by pressure ulcers and promote the occurrence of spasticity. After spasticity occurs, the muscle tension increases in the limbs and the soft tissue of the spasm muscle group and skin cells are damaged, which can promote the reoccurrence of pressure ulcers. Both are common and serious complications after SCI; this not only significantly interferes with the rehabilitation process of individuals with SCI, but also increases the economic burden of the individuals’ families. Therefore, in the early stage of SCI, it is important to pay attention to pressure ulcers that may develop in individuals, increase the nursing care for of individuals with pressure ulcers and, as much as possible, reduce the risk of spasticity caused by those sores in the later stage of SCI.
Relationship between age of onset and spasticity
Previous studies have shown that in the analysis of related factors of spasticity in individuals with SCI, there is a significant correlation between the age of onset and spasticity; the incidence of spasticity is relatively low in elderly individuals. In the study by Mills et al.[17], For every 10 years increase in onset age, the probability of spasticity limiting function at community follow-up decreased by 4%; Field-Fote[18] and DiPiro[12] also reached the same conclusion. In their study on post-stroke muscle spasm, Béseler et al. [19] found that the incidence of spasticity was lower in elderly individuals than younger individuals; the possible reason for this was that the muscle stretch reflex and tension related to spasticity in the elderly were weak, so the incidence of spasticity was lower. It is worth noting that, in the univariate analysis of SCI individuals with spasticity in this study, although there was no statistical difference between the age factor and the occurrence of spasticity(p = 0.762), the probability of spasticity is higher in young individuals with SCI than in elderly individuals. The reason may be that the sample size is too small, which leads to the bias of statistical results. However, the relevance and specific mechanism of this are still unclear. Therefore, this provides a new direction for future research on the factors related to spasticity in SCI individuals. It also suggests that clinicians should pay more attention to the prevention and management of spasticity in young individuals with SCI during diagnosis and treatment.
Other factors related to spasticity after SCI
Neuropathic pain
Neuropathic pain and spasticity may occur together. In this study, the incidence of spasticity was higher in individuals with neuropathic pain (31.17%) than that in individuals without neuropathic pain (21.70%), but the difference was not statistically significant(p = 0.148). A large cross-sectional study conducted by Müller et al.[20] showed that the probability of chronic pain problems in individuals with spasticity increased by 2.38 times. Heijmans[21] found that the 5-HT system plays an important role in chronic neuropathic pain, indicating that 5-HT may simultaneously contribute to the occurrence of spasticity and neuropathic pain. However, we also paid attention to the cases in which neuropathic pain was significantly reduced after some individuals were treated with anti-spasticity medications; this indicates that there may be a relationship between them.
Lower extremity deep venous thrombosis
The results of this study showed that the proportion of individuals without lower limb deep vein thrombosis combined with spasticity was (29.06%), which was relatively higher than that of those with thrombosis (18.33%)(p = 0.217). This conclusion is consistent with the findings of Do et al.[22]. Gaber[23] reported that the spasticity of calf muscles can improve the efficiency of calf intramuscular pump and promote the emptying of lower limb venous blood; thus, the probability of individuals with spasticity suffering from deep venous thrombosis of the lower extremities is relatively low. From this point of view, spasticity may be beneficial to individuals. Therefore, in clinical work, the risk of spasticity can also be predicted by colour Doppler ultrasound and coagulation indicators of the deep veins of both lower limbs.
Limitations
In this study, the proportion of individuals with spasticity after SCI is lower than that reported in previous studies. There may be several reasons for this difference. First, most of the individuals included in the present study were in the acute stage and subacute stage of SCI, of which 83.06% had a disease course of less than 6 months, so the incidence rate of spasticity was low. Second, all the individuals with SCI were treated with manipulation and physical factors while being hospitalised in our department. During hospitalisation, the individuals were actively taught some occupational therapy to prevent spasticity and they were assigned homework. Previous studies have clearly shown that rehabilitation treatment can help improve the spasticity symptoms of individuals with SCI, thus delaying or reducing the occurrence of spasticity[24]. Third, we use the modified Ashworth evaluation scale to evaluate the degree of spasticity of the individuals in our study. During hospitalisation, some individuals may have some symptoms of spasticity, but they cannot meet the standard of the modified Ashworth evaluation scale to evaluate the spasticity, so the proportion of individuals with spasticity is low. However, this does not affect the judgment of the incidence and the trend of spasticity. Finally, there is a lack of follow-up in community hospitals or in families for discharged individuals in the later period of SCI, which is not conducive to obtaining more comprehensive and detailed data on spasticity after SCI.