Lakhasly

Stroke events in EU countries are estimated to increase by 30% by 2025. The most common deficit is contralateral upper limb hemiparesis, affecting over 80% acutely and 40% chronically. This causes motor impairments like weakness, contracture, and impaired control, leading to disabilities in daily activities such as reaching and gripping. Associated neurological issues include somatic sensory deficits (11–85% prevalence), which impede sensory detection, disturb motor tasks, and diminish rehabilitation outcomes, impacting safety. Up to 50% of patients experience upper extremity pain in the first year, particularly shoulder pain or CRPS-type I, hindering early rehabilitation; joint subluxation and contractures also cause pain. Neglect syndrome and spasticity further affect functional outcomes. Neurological recovery follows a nonlinear, logarithmic pattern, with most occurring within the first three months, but continuing for many years. Recovery combines spontaneous and learning-dependent processes like restitution, substitution, and compensation. Spontaneous recovery in the initial three months can confound rehabilitation. While some once believed recovery was intrinsic, improvements after three months primarily depend on learning adaptation strategies. Evidence shows neurological repair via brain reorganization, supporting true recovery or compensation, continues into subacute and chronic phases, with initial contralesional activation shifts.

INTRODUCTION The World Health Organization (WHO) estimates that stroke events in EU countries are likely to increase by 30% between 2000 and 2025 (Truelsen et al., 2006). The most common deficit after stroke is hemiparesis of the contralateral upper limb, with more than 80% of stroke patients experiencing this condition acutely and more than 40% chronically (Cramer et al., 1997). Commonmanifestations of upper extremity motor impairment include muscle weakness or contracture, changes in muscle tone, joint laxity, and impaired motor control. These impairments induce disabilities in common activities such as reaching, picking up objects, and holding onto objects (for a review on precision grip deficits, see Bleyenheuft and Gordon, 2014). Motor paresis of the upper extremity may be associated with other neurological manifestations that affect the recovery of motor function and thus require focused therapeutic intervention. Deficits in somatic sensations (body senses such as touch, temperature, pain, and proprioception) after stroke are common with prevalence rates variously reported to be 11–85% (Carey et al., 1993; Yekutiel, 2000; Hunter, 2002). Functionally, the motor problems resulting from sensory deficits after stroke can be summarized as (1) impaired detection of sensory information, (2) disturbed motor tasks performance requiring somatosensory information, and (3) diminished upper extremity rehabilitation outcomes (Hunter, 2002). Sensation is essential for safety even if there is adequate motor recovery (Yekutiel, 2000). Also, up to 50% of patients experience pain of the upper extremity during the first year after stroke, especially shoulder pain and complex regional pain syndrome-type I (CRPS-type I), which may impede adequate early rehabilitation (Jönsson et al., 2006; Kocabas et al., 2007; Sackley et al., 2008; Lundström et al., 2009). Furthermore, joint subluxation and muscle contractures can lead to nociceptive musculoskeletal pain (de Oliveira et al., 2012). Among other complications of stroke the neglect syndrome (Ringman et al., 2004) and spasticity (Sommerfeld et al., 2004; Welmer et al., 2010) affect motor and functional outcomes. The neurological recovery after stroke displays a nonlinear, logarithmic pattern (Figure 1; Kwakkel et al., 2006; Langhorne et al., 2011). The greater part of recovery is reported to take place in the first 3 months following stroke (Wade et al., 1983). However, there is evidence that recovery is not limited to this time period; hand and upper extremity recovery has been reported many years after stroke (Carey et al., 1993; Yekutiel and Guttman, 1993). Improvement probably occurs through a complex combination of spontaneous and learning-dependent processes including: restitution, substitution, and compensation (Kwakkel et al., 2004; Langhorne et al., 2011). Until the third month after stroke onset, a variable spontaneous neurological recovery can be considered a confounder of rehabilitation intervention (Kwakkel et al., 2006). In the past, the observation of spontaneous recovery after stroke has misled some authors to believe that recovery of upper extremity function is intrinsic and that little can be done by therapists to influence it (Wade et al., 1983; Heller et al., 1987). Progresses in functional outcome appearing after 3 months seem largely dependent on learning adaptation strategies (Kwakkel et al., 2004). Evidence suggests that neurological repair through brain reorganization supporting true recovery or, alternatively through compensation, may also take place in the subacute and chronic phase after stroke (Krakauer, 2006). Functional imaging of stroke recovery corroborates this temporal pattern of activation shifts. Shortly after stroke, an initial contralesional shift of activation toward the “unaffected"