## 1 Introduction  
Spasticity and muscle weakness are prevalent symptoms of incomplete spinal cord injury (iSCI) and can significantly impact patients' quality of life [1]. Weakness results from partial paralysis which occurs when certain motor pathways are disrupted while others remain intact, such as in iSCI cases. This form of weakness can have a profound impact on patients' daily life [2]. Spasticity, frequently observed as a concurrent condition in iSCI, is defined by increased muscle tension and spasm that vary based on the speed of movement. These manifestations occur due to uncontrolled reflex activity in muscles located below the level of the injury [3]. The perplexity surrounding spasticity and its associated phenomenon in clinical practice calls for a more practical and more objective approach to address this matter [4]. Clinical assessments of spasticity and muscle strength, such as the Modified Ashworth Scale (MAS) and the Lovett Scale (manual muscle testing, Lovett), are often used to monitor iSCI patients' progress and plan rehabilitation algorithms [5]. However, these methods of assessment are subjective, may have limited accuracy, and may not provide a detailed understanding of the underlying neurophysiological changes that occur after spinal trauma [6; 7]. Following spinal cord injury, individuals who are experiencing spasticity and decreased muscle strength require targeted interventions during the rehabilitation period. Treatment approaches typically involve a combination of pharmacological and physiotherapeutic interventions aimed at mitigating the symptoms and improving functional outcomes [8; 9; 10; 11; 12]. Some neuromodulation methods also appear to be effective [13; 14; 15; 16]. Clinical assessment of iSCI is a part of the American Spinal Injury Association-ASIA scale (ASIA) [17]. However, it is important to have alternative tools to assess the health status of these patients more accurately in order to be able to modify applied therapy on an ongoing basis and tailor it to one's individual needs [18]. The clinical outcomes of iSCI depend on the severity and location of the lesion and may include partial or complete loss of sensory and/or motor function below the level of injury. Lower thoracic lesions can cause paraplegia, while lesions at the cervical level are often associated with semi or total quadriplegia [19]. This study has been undertaken to verify the above symptoms and dysfunctions in an early post-traumatic period. It can be supposed that the present general picture of the iSCI consequences may differ if the development of pathologies is evaluated in an early or late period after the injury. Most of the pathological symptoms and the spontaneous functional recovery phenomena develop during the first 3 months and, in most cases, reach a plateau by 9 months after injury; additional recovery may also occur up to 12-18 months post-injury [20]. Long-term neurophysiological outcomes of iSCI may be closely related to the level of the injury, the severity of the primary injury, and the progression of secondary injury, and they have been characterised in our previous studies with the usage of sEMG recordings from upper and lower extremities muscles [14; 15; 16]. The description of functional pathological consequences in muscle motor units in patients with iSCI immediately after spinal cord injury has been rarely described, which is another of the main reasons for undertaking the sEMG recordings in this work. Increased muscle tension at rest is commonly associated with the decreased motor units' muscle contractile properties [5]. The precise aetiology of the aforementioned phenomenon remains unclear, as it has not been fully elucidated in both clinical and neurophysiological investigations. Muscle weakness may be the result of spasticity or the consequence of direct injury of the lower motor neuron in iSCI patients.