## 1 Introduction  
Stroke is the second leading cause of death, the third cause of disability worldwide and the leading cause of disability in the elderly. The consequences of a stroke depend on the location and size of the lesion. These may involve functional and self-care abilities, speech, vision, spatial perception and several cognitive abilities [1]. Approximately 15 million people worldwide are affected by a stroke yearly, either ischemic or haemorrhagic. Among them, 5 million people remain permanently disabled, and approximately 35% of post-stroke patients develop a severe disability, resulting in a loss of motor functions and/or the impairment of activities in daily living (ADL) [2]. One of the most frequent functional problems that arise over time after a stroke and hinder motor recovery is the onset of muscle overactivity. The prevalence of localised limb spasticity is between 25% and 45% in the first year after a stroke [3; 4; 5; 6], depending on the stroke aetiology, and is higher in patients needing to be admitted in acute neurorehabilitation wards [7]. Among the negative consequences of muscle overactivity the development of muscular-tendinous deformities [8; 9] is decisive in developing a negative impact on the patient's quality of life [10; 11]. In particular, the equinovarus foot deviation (EVFD), the most frequent lower limb deviation in stroke survivors [12], can hinder walking ability and, consequently, autonomy. EVFD can cause inadequate foot clearance during the swing phase of gait, thus increasing the risk of falling [10; 11]. During the stance phase, EVFD can limit or prevent both the weight-bearing and the progression ability, reducing stability and propulsion [13]. This typically results in the need for assistance and/or the use of orthoses and/or assistive devices [14]. The lack of ankle dorsiflexion and the excessive foot supination that characterises EVFD can result from several levels of weakness, imbalance, overactivity and the contracture of muscles whose tendons surround the ankle joint. The main causes reported in the literature are the overactivity of muscles, weakness of the tibialis anterior (TA) and strength deficits of the peroneus longus (PL) and peroneus brevis (PB) [15; 16]. These can sometimes be associated with the contractures and/or spasticity of the triceps surae (TS) and other plantar flexors, including the tibialis posterior (TP), the flexor hallucis longus (FHL) and the flexor digitorum longus (FDL) [10; 11; 17; 18; 19; 20; 21; 22]. Already in the nineteenth century, [PERSON] conducted experiments on selective muscle electrostimulation. He clearly described that the action of the extensor digitorum longus (EDL) balanced the TA varus component and favoured neutral dorsiflexion [23]. In the current literature, there is a lack of studies addressing the contribution of EDL weakness in the genesis of EVFD. Only three papers mention the necessity of EDL activity to generate sufficient ankle dorsiflexion during the swing phase. [PERSON] and colleagues [24] assessed the balance between the TA and EDL in stroke patients during gait. Conversely to the TA, both the duration and EMG amplitude of EDL activity were reduced when compared to a control group and determined the varus deformity during swing. In their study for the assessment of the equinovarus foot, [PERSON] and colleagues [25] stated that the imbalance between the TA and anterior lateral muscles, including the EDL, is responsible for the varus deformity and leads to ankle sprains and falls in stroke patients. [PERSON] and colleagues [26] reported that an absent or weak EDL activity combined with a normal TA activation during the loading response, pre-swing and swing phases results in EVFD in patients with shortened or inextensible calf muscles. It is noteworthy that studies dealing with the evaluation and treatment of EVFD do not suggest assessing the EDL during walking [16; 27]. Skipping this step could negatively influence the choice of EVFD treatment.