Clinical trial NCT06898242: Early Myofascial Manual Treatment in Subjects With Spasticity Following Acquired Brain Injury
Official title: Early Myofascial Manual Treatment in Subjects With Spasticity Following Acquired Brain Injury
Study type: INTERVENTIONAL
Overall status: ACTIVE_NOT_RECRUITING
Phase: NA
Conditions: Brain Injury
Brain Injury, Vascular
Brain Injuries, Traumatic
Keywords: acquired brain injury
traumatic
spasticity
myofascial manual treatment
Lead sponsor: Fondazione Policlinico Universitario Agostino Gemelli IRCCS
Sponsor class: OTHER
First posted: 2025-03-27
Enrollment: 24
Sex: ALL
Minimum age (years): 18
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: no
Allocation: RANDOMIZED
Intervention model: CROSSOVER
Primary purpose: TREATMENT

Brief summary: Spasticity is characterized by an increase in muscle tone that is velocity-dependent and caused by the exaggeration of the stretch reflex. Clinically, it is found in 70-85% of patients with spinal cord injury at one year, 40-45% in patients with stroke at 12 months, and 25% in patients with traumatic brain injury at one year.

The term 'Severe Acquired Brain Injury' refers to a condition characterized by brain damage that causes a coma with an acute phase score of 8 on the Glasgow Coma Scale (GCS), lasting more than 24 hours. It may be caused by vascular, traumatic, anoxic, infectious, toxic-metabolic, or neoplastic damage, which can cause multiple and complex sensory, cognitive, and behavioral impairments that lead to significant disability. Spasticity occurs frequently in patients with GCA, often at an early stage, with serious repercussions on the rehabilitation process and outcome.

Numerous studies indicate that spasticity due to neurological damage is supported, in addition to hyperexcitable stretch reflexes, by changes in the connective tissues of the peripheral limbs that increase muscle resistance to passive movement. After neurological damage, and starting 1 week after immobilization, alterations in the muscles and connective tissue can be observed: changes in the muscle fibers, changes in the collagen tissue, and changes in the properties of the tendons. It is believed that the quantitative and qualitative changes in the intramuscular connective tissue contribute to the deterioration of the properties and functions of the immobilized muscle, which contributes to the establishment and progression of spasticity.

In patients with spastic paresis, therapeutic interventions are intended to prevent prolonged shortening of the muscles and mobilize the affected areas. According to recent research, the connective tissue is particularly sensitive to mechanical stress, particularly deep manual manipulation and vibration. Several studies have suggested that myofascial release therapy can be a complementary treatment in patients with neurological disorders to reduce muscle spasticity and increase joint mobility.

Myofascial release techniques can be hypothesized to be a valid integrated treatment for spasticity in patients with sequelae from GCA, but their use in this area has been little studied and no studies have been conducted in the post-acute period of intensive hospitalization.

The purpose of the present study is to determine whether manual myofascial release techniques, applied to the upper and lower limbs, are safe, tolerable, and effective in modifying the degree of spasticity and improving functional activity in patients with GCA. Additionally, changes in muscle structure will be evaluated by ultrasound: cross-sectional area, anteroposterior diameter, and pennation angle.

Finally, we will measure the effects of manual myofascial treatment stimulation by measuring electrodermal activity (EDA), which is a non-invasive method in which an electrode bracelet is applied to the patient's right wrist to measure the electrical conductance of the skin, which is a function of the autonomic nervous system, which is controlled by the sweat glands. Various sensory stimulations, including visual, auditory, olfactory, tactile, vestibular, and proprioceptive stimulations, can produce a physical sensation that can influence the patient's sensorimotor output, resulting in physiological changes in the activity of the ANS as a consequence of the processing of sensory afferents. A response to an appropriate sensory stimulus can be regarded as a manifestation of a change in consciousness.


Eligibility criteria: Inclusion Criteria:

* Aquired brain injuries from 40 days to 6 months after the event
* Spasticity at upper orvlower limbs quantified at MAS scale \>= than 1
* Age \>= 18 years
* Patient/Caregiver ability to understand and sign the informed consent

Exclusion Criteria:

* Spasticity at MAS scale \> 2
* Non consolidatetd fracture and/or muscle injuries to the limbs
* Deep vein thrombosis
* Neoplasms
* Hemodynamic instability
* Local infections to the limbs
* Recent treatment with botulinum toxin (within 40 days)

Primary outcomes:
measure: Modification of spasticity through Modified Ashworth Scale
timeFrame: Changes from baseline (T0), 4 weeks of treatment (T1), 4 weeks of follow up (T2)
Secondary outcomes:
measure: Tolerance and safety of treatment
timeFrame: Changes from baseline (T0), 4 weeks of treatment (T1), 4 weeks of follow up (T2)
measure: Evaluation of changes in the degree of functional use of the upper and lower limbs through Motricity Index Scale
timeFrame: Changes from baseline (T0), 4 weeks of treatment (T1), 4 weeks of follow up (T2)
Other outcomes:
measure: Changes in muscle echostructure
timeFrame: Changes from baseline (T0), 4 weeks of treatment (T1), 4 weeks of follow up (T2)
measure: Changes in muscle echostructure
timeFrame: Changes from baseline (T0), 4 weeks of treatment (T1), 4 weeks of follow up (T2)
measure: Changes in muscle echostructure
timeFrame: Changes from baseline (T0), 4 weeks of treatment (T1), 4 weeks of follow up (T2)
measure: Changes in muscle echostructure
timeFrame: Changes from baseline (T0), 4 weeks of treatment (T1), 4 weeks of follow up (T2)
measure: Evaluation of electrodermal activity
timeFrame: Changes from baseline (T0), 4 weeks of treatment (T1), 4 weeks of follow-up (T2)
Locations:
city: Roma
country: Italy
facility: UOC Neuroriabilitazione ad Alta Intensità COD. 75 Policlinico Gemelli
state: RM
Study officials:
affiliation: Fondazione Policlinico Universitario A. Gemelli, IRCCS
name: Luca Padua, MD, phD
role: PRINCIPAL_INVESTIGATOR
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