Disorders of craniofacial muscles (CFM) frequently arise from various conditions and injuries affecting the central and peripheral nervous systems, as well as from neurosurgical, reconstructive, and cosmetic interventions. The principal clinical manifestations include facial asymmetry, lagophthalmos, paralytic strabismus, synkinesis, contractures, trismus, bruxism, temporomandibular joint dysfunction, chronic facial pain, and sialorrhea. Such disorders not only restrict daily functioning but also lead to significant psychosocial maladjustment, a decline in quality of life, and increased disability among affected individuals. Despite the high prevalence of CFM dysfunction, contemporary methods for the medical rehabilitation of patients remain inconsistent, with poor regulation governing continuity among the various stages of care. This paper posits the establishment of «facial rehabilitation» as a distinct interdisciplinary approach within medical rehabilitation, integrated into the established three-stage medical rehabilitation framework in the Russian Federation. A thorough review of current literature and pertinent Russian regulatory documents has been conducted. The objectives of facial rehabilitation across the first, second, and third stages are analyzed, along with the role of botulinum therapy in comprehensive rehabilitation programs aimed at restoring impaired functions. The potential of this method for a wide range of functional, structural, and autonomic disorders of the face is considered, given the multifaceted mechanisms of action of botulinum toxin type A (BTA), including muscle-relaxant, antinociceptive, neuromodulatory, and anti-inflammatory effects. The authors present their own clinical experience demonstrating the effective use of botulinum therapy to treat trismus, paralytic strabismus, lagophthalmos, and pronounced facial asymmetry in patients with complications from neurological conditions and injuries. The findings underscore the efficacy of integrating botulinum therapy into three-stage medical rehabilitation programs, highlighting its role in preventing complications and enhancing rehabilitation potential and quality of life for patients.

Although laser-assisted drug delivery (LADD) technology is well established, its clinical application has now expanded to include a broader range of energy-based devices (EBDs). This review aims to evaluate the use of energy-based device-assisted drug delivery (EADD) in the treatment of hypertrophic scars (HTS) and keloids. Following a comprehensive search of English and Chinese databases, 30 relevant studies were included. These studies evaluated the combined application of various EBDs-including ablative and non-ablative fractional lasers, micro-plasma radiofrequency (MPR), ultrasound, and thermomechanical fractional injury-with pharmacological agents such as corticosteroids, 5-fluorouracil (5-FU), verapamil, botulinum toxin type A (BTXA), and photosensitizers (5-aminolevulinic acid). The results indicate that for corticosteroids, EADD achieves efficacy comparable to that of intralesional injection while significantly reducing pain and lowering the risk of skin atrophy and telangiectasia, offering particular benefits for pediatric patients. The combination of EADD with 5-FU effectively improves scar thickness, whereas CO2 AFL-assisted photosensitizers delivery shows an exceptionally low recurrence rate in the treatment of acne-induced HTS. In contrast, for keloids, intralesional BTXA injections remain superior to CO2 AFL-assisted BTXA delivery. Furthermore, emerging strategies such as the triple-modality "light-light-sound" therapy, which combines intense pulsed light, CO2 ablative fractional laser, and ultrasound, provide promising prospects for recalcitrant cases. In summary, EBDs enhance drug delivery through micropore formation or acoustic effects, establishing it as a key therapeutic strategy that balances efficacy with improved safety and patient compliance compared to monotherapy. However, standardized treatment protocols still require further validation through future research.

Ketamine is a potent anaesthetic drug that has been used for decades. Ketamine abuse is an increasingly common problem, particularly among young people. Over one quarter of ketamine users will have at least one bothersome urological symptom, with heavier and longer use leading to potentially irreversible damage to the lower and upper urinary tract. Hence, this study carried out a narrative review focusing on ketamine-induced uropathy pathophysiology, clinical presentation, and treatment options. It was found that ketamine uropathy is an inflammatory condition affecting predominantly the bladder but also the upper urinary tracts. A hypersensitivity reaction to the drug has been proposed as the potential pathophysiological mechanism that causes inflammatory reaction, muscle hypertrophy, and non-reversible fibrosis in the advanced stages of the disease. Abstinence from ketamine use is the cornerstone of treatment at any stage of the disease, with effective pain management and psychological support being critical to reduce ketamine seeking behaviours. For mildly symptomatic patients, minimally invasive options such as bladder instillations and intravesical Botox injections can provide symptomatic relief. For more severe cases with refractory symptoms and upper urinary tract involvement, reconstructive urological operations might be necessary, including augmentation cystoplasty, cystectomy, or ureteric reconstruction. Ongoing surveillance of the upper tracts is recommended for both groups of patients. Ketamine induced uropathy is an increasingly prevalent condition, and ketamine abuse should always be inquired about in people with unexplained lower urinary tract symptoms. Adequate information of the public regarding ketamine abuse and early consultation with a urologist might prevent irreversible damage.

The facial feedback hypothesis suggests that facial muscle activity contributes to emotion perception, but the developmental origins of this mechanism remain underspecified. This theoretical paper argues that caregiver mirroring - specifically caregivers' contingent imitation of infant facial expressions - plays a critical role in establishing the facial feedback mechanism. Drawing on previous empirical findings, we propose that repeated episodes of being mirrored provide infants with reliable sensorimotor contingencies linking facial action, proprioceptive feedback, and emotional states. We further consider situations that impede caregiver mirroring - such as infant dummy (pacifier) use and caregiver botulinum toxin (Botox) treatment - as naturalistic perturbations of these contingencies. This paper highlights how caregiver facial mirroring may scaffold infants' developing emotion processing, offering a socially embedded perspective on the early development of embodied emotional understanding.

Post-stroke spasticity may interfere with function and rehabilitation and contribute to pain, contracture, care burden, and disability. Botulinum toxin type A is an established focal treatment for post-stroke spasticity, but it is often introduced in the chronic phase, when persistent involuntary muscle overactivity may coexist with secondary musculoskeletal complications. This opinion paper critically examines whether early treatment with botulinum toxin should be considered a myth or an emerging clinical reality. Current evidence from meta-analyses, randomized trials, observational cohorts, and pooled analyses was reviewed with particular attention to treatment timing, treatment triggers, functional outcomes, and prevention of secondary complications. The literature supports the clinical usefulness of earlier treatment in appropriately selected patients, particularly for reducing focal involuntary muscle overactivity and resistance to passive movement, delaying symptomatic progression, slowing contracture development, and reducing pain-related complications. However, a consistent additional effect on active motor recovery has not been demonstrated, and evidence for participation and long-term functional independence remains less definitive. Moreover, "early" is heterogeneously defined across studies, ranging from the first weeks to the first year after stroke. We therefore propose moving from a rigid time-based concept of "early" treatment toward timely, target- and goal-guided intervention, integrating botulinum toxin with rehabilitation when a clinically relevant and modifiable focal neural treatment target emerges. To operationalize this concept, we propose a pragmatic set of clinical variables including the neural treatment target, its clinical impact and trajectory, passive musculoskeletal status, pain and care burden, motor recovery context, rehabilitation goals, and patient priorities.

Post-stroke spasticity involves both neural and non-neural mechanisms, including structural alterations of muscles and surrounding fascia. Although botulinum toxin type A (BoNT-A) is widely used to treat focal spasticity, its effects on fascial tissue remain unclear. This retrospective observational study investigated longitudinal changes in fascial thickness after BoNT-A injection using ultrasonography. Thirty-seven patients with post-stroke spasticity were included. Fascial thickness was measured at baseline, 3 weeks, and 3 months after treatment in the injected muscle regions. Clinical outcomes were assessed using the Modified Ashworth Scale (MAS), Fugl-Meyer Assessment (FMA), and Brunnstrom stages. Repeated-measures analysis demonstrated significant reductions in fascial thickness across all evaluated regions. Pairwise comparisons showed significant decreases from baseline to week 3 and month 3, whereas continued reductions between week 3 and month 3 were observed only in the flexor digitorum superficialis fascia, the flexor digitorum superficialis-flexor digitorum profundus interfascial layer, and the deep brachialis fascia. MAS scores and upper extremity Fugl-Meyer scores improved significantly, whereas Brunnstrom stages remained unchanged. These findings suggest that the therapeutic effects of BoNT-A may extend beyond neural inhibition to include fascial remodeling. Ultrasonographic assessment of fascial thickness may represent a potential imaging biomarker for monitoring structural treatment responses in post-stroke spasticity.