Available in Brazil
Traumatic brain injury (TBI) is a leading cause of death and disability globally,
significantly affecting the quality of life for patients and caregivers.
In the United States, traumatic brain injury is the leading cause of death for people
aged 1 to 45 and a major risk factor for morbidity and mortality in politrauma cases.
Although epidemiological data in Brazil are limited, studies indicate that TBI is a
significant public health issue, primarily impacting the country's young and economically
active population.
Automobile accidents and falls are primary causes of traumatic brain injury, with
incidence rates highest among young adults (20 to 29 years) and individuals over 80 years
old.
TBI is a highly heterogeneous condition, with multiple classification systems that
emphasize distinct aspects such as the underlying mechanism of injury, clinical severity,
radiological characteristics, and pathophysiological processes. These classifications
play an important role in standardizing data collection, identifying prognostic factors,
and informing the selection of appropriate therapeutic approaches tailored to individual
cases.
From a pathophysiological perspective, traumatic brain injury (TBI) causes damage through
primary lesions-direct energy transfer to the brain at trauma-and secondary effects,
which involve cellular and molecular changes occurring for hours to weeks post-injury.
Diffuse axonal injury (DAI) is a type of lesion in TBI that leads to significant brain
dysfunction and affects roughly 40% of patients, making it a leading cause of
neurological problems in survivors.
Clinically, it is defined as a coma lasting more than 6 hours after TBI, excluding cases
caused by ischemic brain injury or intracranial masses.
Detecting this condition during routine exams in TBI patients can be challenging, as
DAI-related abnormalities are often missed by standard CT or MRI scans and may require
advanced imaging techniques to identify structural changes in the central nervous system.
From a neurological perspective, TBI can result in a wide range of cognitive, behavioral,
and sensory-motor changes that may affect the patient's quality of life. Cognition
encompasses the processes involved in acquiring knowledge and includes factors such as
thought, language, memory, reasoning, and task execution, which are considered important
for intellectual development.
Although TBI is strongly linked to cognitive dysfunction, effective treatment remains
difficult. While cognitive rehabilitation therapies have shown benefits in some studies,
results are inconsistent.
Drug therapies for post-TBI cognitive disorders have proven ineffective. The limited
effectiveness of conventional cognitive rehabilitation in DAI patients has led to the
exploration of new therapies. Neuromodulation techniques, both invasive and noninvasive,
offer promising options by targeting specific brain regions to alter activity and support
recovery.
Radio-electric asymmetric conveyer (REAC) technology is a noninvasive technique that was
first described by Rinaldi and Fontani. REAC neurobiological modulation with specific
protocols such as neuro-postural-optimization (NPO) and
neuro-psycho-physical-optimization - brain wave optimization-G (NPPO-BWO-G) is a safe,
established technique with proven therapeutic benefits for various neurological and
psychiatric disorders.
Given the significant brain damage and multiple disabling neurological sequelae, in
severe TBI patients, combined with the limited efficacy of conventional pharmacological
and cognitive rehabilitation interventions, REAC may be a promising therapeutic approach
for affected patients. We will conduct a randomized clinical trial to assess REAC's
effects in patients with DAI.
GOALS Primary Endpoint
• To evaluate the qEEG changes in patients with subacute/chronic DAI, following REAC
neuromodulation.
Secondary Endpoint
- To evaluate the qEEG changes in adults free of neurological conditions, following
REAC neuromodulation.
- To evaluate cognitive and humor changes in adults free of neurological conditions,
following REAC neuromodulation.
1Research sites
60Patients around the world