## 4 Discussion  
To date, we have not found a publication that addresses all three measures (Lovett Scale, Ashworth Scale, and sEMG) in patients with incomplete spinal cord injury and presents correlations proving the relationship between the various parameters. These relationships, while seeming obvious in clinical work and based on intuition, have so far not had their scientific proof in numbers and data presented based on cases of patients after incomplete spinal cord injuries. This study supports the notion that a negative relationship exists between increased muscle tension and decreased muscle strength in patients following iSCI with injuries at varying levels, as indicated by standard clinical scale assessments and validated by non-invasive electromyographic testing. If a negative correlation exists between spasticity levels and muscle strength, this might suggest that interventions aimed at reducing spasticity (e.g., pharmacological treatments or stretch therapies) could be beneficial for improving muscle strength. However, it is important to note that correlations do not necessarily indicate causation and that other factors may be influencing the relationship between variables. Therefore, clinical decisions should be based on a comprehensive evaluation of all relevant factors and individual patient characteristics. The results might strongly depend on two additional pathological factors in addition to the spinal injury itself, namely pain reported by the patients limiting the ability of maximal muscle contraction and changes in transmission of neural impulses within the motor fibres of upper and lower extremity nerves, influencing the number of recruited muscle motor units. The patients in our study reported similar low pain scores on the VAS, with an average of 1.78 \(\pm\) 1.0; the axonal changes in motor fibres were confirmed as moderate in ENG studies (see Table 2). Therefore, both pain and abnormal neural transmission have a very similar impact on muscle tension and contractile muscle properties in all patients analysed in this study. However, it should be remembered that the iSCI patients in our study were just after the injury incidence. The consequences of the spasticity and the pathological, secondary changes in the motor nerve fibres usually occur after three months from the spinal trauma [6; 15; 36]. Previous studies utilising sEMG and clinical scales for evaluation of the iSCI patients' motor functional status did not provide similar correlations to the ones presented in this study [37; 38]. Increased muscle tension is mostly related to the consequences of lower motoneuron dysfunction, which is caused by disturbances in the neural transmission of impulses coming from the supraspinal centres. Therefore, similar observations on the relationship between increased spasticity and decreased muscle strength have been found in patients after ischemic stroke [22]. The lack of the spinal motor centres' control from the excitatory and inhibitory influences of cortico-spinal centres leads to the spontaneous generation of neuronal impulses from the lower motoneuron to the effectors at the rate of 5 Hz [39]. This creates an increase in the amplitude parameter in rsEMG recordings of  
Figure 3: Graphical presentation of relationships presented in Table 5; spasticity scores (MAS) vs. resting sEMG amplitude recordings (**A**), muscle strength scores (Lovett) vs. maximal contraction sEMG amplitude recordings (**B**), rsEMG amplitude recordings vs. maximal contraction sEMG amplitude recordings (**C**). Most points on charts are overlapped multiple times with their Y–X locations. more than 25 \(\upmu\)V (see Table 3), which neurophysiologically defines the increased muscle tension [40]. Our current study on iSCI patients seems to confirm the above hypothesis.