|Year : 2022 | Volume
| Issue : 4 | Page : 300-304
Modified Technology for a New Generation Stroke Rehabilitation Module by Transcutaneous Vagal Nerve Stimulation Therapy − A Critical Analysis
Leena Chacko1, Janseya Delani2, Rajaram Prabhu2, Uma Maheshwari Raman3, Hanan Fahad Alharbi4, Yoga Rajamani5, Mullaicharam Bhupathyraaj6
1 Bioanalytical Lab, Meso Scale Diagnostics LLC, Rockville, MD, USA
2 Madurai Medical College, Madurai, Tamil Nadu, India
3 ESI Dispensary, Tallakulam, Madurai, Tamil Nadu, India
4 Dept of Maternity and Child Health Nursing, College of Nursing, Princess Nourah Bint Abdulrahman University, Riyadh, Saudi Arabia
5 College of Computer, Mathematics, and Natural Sciences, University of Maryland, College Park, MD, USA
6 College of Pharmacy, National University of Science and Technology, Muscat, Oman
|Date of Submission||18-Aug-2022|
|Date of Decision||27-Sep-2022|
|Date of Acceptance||03-Oct-2022|
|Date of Web Publication||30-Nov-2022|
Bioanalytical Lab, Meso Scale Diagnostics LLC, 1601 Research Blvd, Rockville, MD 20850
College of Pharmacy, National University of Science and Technology, Muscat
Source of Support: None, Conflict of Interest: None
| Abstract|| |
An important goal of stroke rehabilitation is to improve the quality of life, enhancing functional independence, and active participation in daily routine activities. Stroke is a cerebral vascular event with rapidly developing clinical signs of global disturbances with no apparent cause other than a vascular origin. A stroke occurs when the blood vessels in the brain are blocked or burst, which prevents the blood and oxygen from reaching brain tissues. Symptoms of stroke in body parts are controlled by damaged areas of the brain and the main symptoms show involuntary muscle tightening, paralysis, and restricted physical abilities. Other complications depend upon the damage to part of the brain. Enhancing plasticity by triggering neuromodulators with paired motor training provides the basis for transcutaneous vagal nerve stimulation (TVNS) therapy. TVNS to activate the neuromodulatory networks of cortical neurons shall be achieved by the battery-powered device with electrodes and adhesive backing which can be positioned on the skin in specific areas. The device delivers electrical impulses which activate the vagal nerve and enhance the plasticity of cortical neurons. This article emphasizes vagal nerve stimulation paired with rehabilitation therapy, which combines a device that stimulates vagal function which promotes motor function, and rehabilitation training to facilitate a speedy recovery. This technology is precise and consistent in developing pro plasticity neuromodulators and improves the daily performance of the affected individual.
Keywords: Device, neuromodulation, stroke, TVNS therapy
|How to cite this article:|
Chacko L, Delani J, Prabhu R, Maheshwari Raman U, Fahad Alharbi H, Rajamani Y, Bhupathyraaj M. Modified Technology for a New Generation Stroke Rehabilitation Module by Transcutaneous Vagal Nerve Stimulation Therapy − A Critical Analysis. Int J Nutr Pharmacol Neurol Dis 2022;12:300-4
|How to cite this URL:|
Chacko L, Delani J, Prabhu R, Maheshwari Raman U, Fahad Alharbi H, Rajamani Y, Bhupathyraaj M. Modified Technology for a New Generation Stroke Rehabilitation Module by Transcutaneous Vagal Nerve Stimulation Therapy − A Critical Analysis. Int J Nutr Pharmacol Neurol Dis [serial online] 2022 [cited 2023 Jan 29];12:300-4. Available from: https://www.ijnpnd.com/text.asp?2022/12/4/300/362420
| Introduction|| |
A stroke or brain attack occurs when blood on a network of blood vessels in the brain is blocked or bursts. The brain cannot store oxygen so it relies upon vessels to provide it with blood that is rich in oxygen. A stroke results in a lack of blood supply, causing surrounding nerve cells to be cut off from their supply of nutrients and oxygen. When tissue is cut off for more than 3 to 4 minutes, it begins to die., Nerve cells in the brain tissue communicate with other cells to control functions including memory, speech, and movement. When a stroke occurs nerve cells in the brain tissue become injured. As a result of this injury, nerve cells cannot communicate with other cells, and functions are impaired. If a stroke occurs on the right side of the brain, the left side of the body is affected and vice versa. Disability from neurologic conditions like a stroke can greatly increase health care costs. Because there is no permanent cure for neurodegenerative disorders, hence, there is growing interest in establishing therapeutic and dietary strategies to combat oxidative stress-induced damage to the central nervous system. The use of technological advancements to augment health care services provides one such method called transcutaneous vagal nerve stimulation (TVNS).
Lasting effects of stroke
The effects of a stroke depend on the extent and the location of damage in the brain. The disabilities resulting from a stroke are:
- Inability to move part of the body
- weakness in part of the body
- numbness in part of the body
- inability to speak or understand words
- difficulty in communication
- difficulty in swallowing
- vision loss
- memory loss, confusion, or poor judgment
- personality change.
The goal of stroke rehabilitation is to regain independence and improve the quality of life. There are many approaches to stroke rehabilitation., This review article emphasizes technology-assisted physical activities for stroke rehabilitation.
| Background|| |
Vagal nerve stimulation paired with rehabilitation is a potential novel treatment for stroke vagal nerve is one of 12 pairs of cranial nerves that originate in the brain and is part of the autonomic nervous system, which controls involuntary body functions.,, The nerve passes through the neck as it travels between the chest and abdomen and the lower part of the brain. It is connected to both motor and sensory functions. Vagal nerve stimulation sends regular mild pulses of electrical energy to the brain via the vagal nerve, through a device that is similar to a pacemaker. There is no physical involvement of the brain in this surgery and the patient cannot feel the pulses.
Effects of vagal nerve stimulation in stroke
- Trigger the release of acetylcholine and norepinephrine.
- Improve synaptic recognition of cortical motor networks controlling the impaired limbs.
- Transmitting and mediating sensory information from all parts of the body to the brain.
- Reduce the extent of a stroke-induced lesion of brain parenchyma.
- Neuroinflammation and neuroplasticity are influenced by vagal nerve.
- Enhancing plasticity by triggering neuromodulators with paired motor training provides the basis for TVNS therapy.
| Materials|| |
- An implantable pulse generator (implantable device) that is implanted under an individual chest wall [Figure 1].
- An implantable lead [Figure 2].
- Wireless transmitter (for communication between device and computer).
- Hand-held magnet [Figure 5].
- Custom programming software.
| Methods|| |
In TVNS therapy the vagal nerve is stimulated by a therapist using a button timed with a task-specific movement. Pressing the button delivers a brief burst (0.5 seconds) of drug goal-directed movement.
Post-stroke recovery is associated with plasticity in motor networks. Transcutaneous vagal nerve stimulation (vagal nerve − 10th cranial nerve) to activate the neuromodulatory networks of cortical neurons shall be achieved by a battery-powered device with electrodes and adhesive backing which can be positioned on the skin in specific areas. Numerous studies have revealed that cortical representation areas are constantly modified by sensory inputs and motor experiences, which play a major role in the subsequent physiological reorganization that occurs in the adjacent intact brain tissue after stroke. The device [Figure 3] delivers electrical impulses, which activate the vagal nerve and enhance the plasticity of cortical neurons. This method emphasizes vagal nerve stimulation with paired rehabilitation therapy, which combines a device that stimulates vagal function which promotes motor function, and rehabilitation training to facilitate recovery. TVNS excites large diameter afferents which include sensory and motor fibers. Because increased sensory input could facilitate cortical synaptic reorganization and motor output.,, This technology was precise and consistent in developing pro plasticity neuromodulators and improves the daily performance of the affected individual as it has practical implications for administration therapy. Given a fixed duration for a session of rehabilitation, a therapist would need to determine whether a patient receives a greater number of stimulation pairings during a more constrained set of rehabilitative exercises.,
| Mechanism|| |
Structural plasticity in descending cortical spinal circuits has been associated with recovery after stroke. TVNS paired with rehabilitative training influenced the reorganization of the corticospinal tract. Vagal nerve stimulation engages a variety of molecular and neuronal mechanisms via the ascending neuromodulatory system that may underlie the observed reorganization of observed networks. After a stroke, treatment with brain-derived neurotrophic factor (BDNF) increases functional recovery, whereas reduction of the BDNF levels prevented the benefits of rehabilitative training. Engagement of neuromodulatory networks that regulate synaptic plasticity also represents a means by which TVNS likely supports recovery. TVNS drives the activation of multiple neuromodulatory networks including the noradrenergic, cholinergic, and serotonergic systems. These neuromodulators in turn act synergistically to alter spike-timing-dependent plasticity properties in active networks. These studies align well with the time scale of the synaptic eligibility trace and provide a means by which TVNS may drive temporally precise neuro modulatory release to reinforce ongoing neural activity related to the paired event.
| Tvns implantation procedure|| |
This procedure performed by a neurosurgeon usually takes about 45 to 90 minutes with the patient most commonly under general anesthesia. This procedure requires two small incisions. The first one is made on the upper left side of the chest where the pulse generator is implanted. A second incision is made horizontally on the left side of the lower neck, along a crease of the skin. This is where the thin, flexible wires that connect the pulse generator to the vagal nerve are inserted. The stimulator is most commonly activated 2 to 4 weeks after implantation, although in some cases may be activated at the time of implantation. The treating neurologist programs the stimulator with a small hand-held computer, and programming software. The strength and duration of electrical impulses are programmed. The amount of stimulation varies by case but is usually initiated at a low level and slowly increased to a suitable level for an individual. The device continuously runs and is programmed to turn on and shut off for specific periods − for example, 30 seconds on and 5 minutes off [Figure 4].
|Figure 4 (a) In clinic rehabilitation with TVNS, (b) home-based TVNS therapy.|
Click here to view
Patients are provided with the hand-held magnet [Figure 5] to control the stimulator at home (activated by the physician to magnet mode) when the magnet is swept over the pulse generator site, extra stimulation is delivered regardless of the treatment schedule. Holding the magnet over the pulse generator will turn the stimulation off while the magnet is in position. Removing it will resume the stimulation cycle.
The risk of TVNS includes injury to the vagal nerve or nearby blood vessels, including the carotid artery and jugular vein. In addition, there are risks associated with any surgical procedure, such as bleeding and an allergic reaction to anesthesia.
| Conclusion|| |
This technology is precise and consistent in developing pro plasticity neuromodulators and improves the daily performance of the affected individual.
This review article emphasizes vagal nerve stimulation for stroke therapy, which combines a device that stimulates vagal function which promotes motor function, and rehabilitation training to facilitate recovery.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Vermeer SE, Longstreth WT,Jr., Koudstaal PJ. Silent brain infarcts: a systematic review. Lancet Neurol 2007;6:611-19.
Adams HPJr., Bendixen BH, Kappelle LJ et al.
Classification of subtype of acute ischemic stroke. Definitions for use in multicenter clinical trials. Toast. Trial of org 1017 2 in acute stroke treatment. Stroke 1993;24:35-41.
Simons LA, Mc Callum J, Friedlander Y, Simons J. Risk factors for ischemic stroke. Stoke 1998;29:1341-46.
Feigin VL, Lawes CM, Bennett DA, Barker-Collo SL, Parag V. Worldwide stroke incidence and early case fatality reported in 56 population-based studies: a systematic review. Lancet Neurol 2009;8:355-69.
Ara G, Afzal M, Jyoti S, Siddique YH. Effect of myricetin on the oxidative stress markers in the brain of transgenic flies expressing human alpha-synuclein. Int J Nutr Pharmacol Neurol Dis 2017;7:101-6. [Full text]
O’Donnellnel MJ, Xavier D, Liu L et al.
Risk factors for ischemic and intracerebral hemorrhagic stroke in 22 countries (the Inter stroke study): a case-control study. Lancet 2010;376:112-23.
Baggs S, Pombo AP, Hopman W. Effect of age on functional outcomes after stroke rehabilitation. Stroke 2002;33:179-85.
Kwakkel G, Kollen B, Twisk J. Impact of time on improvement of outcome after stroke. Stroke 2006;37:2348-53
Baumann M, Le Bihan E, Chau K, Chau N. Associations between quality of life and socioeconomic factors, functional impairments, and dissatisfaction with the received information and home-care services among survivors living at home two years after stroke on set. BMC Neurol 2014;14:92.
Rangel ES, Belasco AG, Dicinni S. Quality of life in patients with stroke rehabilitation. Acta Paul Enferm 2013;26:205-12.
Civelek GM, Atalay A, Turhan N. Medical complications experienced by first-time ischemic stroke patients during inpatient, tertiary level stroke rehabilitation. J Phys Ther Sci 2016;28:382-91.
Sveen U, Bautz-Holter E, Sodring KM, Wyller TB, Laake K. Association between impairments, self-care ability and social activities 1 year after stroke. Disabil Rehabil 1999;21:372-7.
Engineer ND, Kimberley TJ, Prudente CN, Dawson J, Tarver WB, Hays SA. Targeted vagus nerve stimulation for rehabilitation after stroke. Front Neurosci 2019;13:280.
Ng SSM, Hui-Chan CWY. Transcutaneous electrical nerve stimulation combined with task-related training improves lower limb functions in subjects with chronic stroke. Stoke 2007;38:2953-9.
Rana M, Upadhyay J, Rana A, Durgapal S, Jantwal A. A systematic review on etiology, epidemiology, and treatment of cerebral palsy. Int J Nutr Pharmacol Neurol Dis 2017;7:76-83. [Full text]
Borland MS, Vrana WA, Moreno NA et al.
Cortical map plasticity as a function of vagus nerve stimulation intensity. Brain Stimul 2016;9:117-23.
Wolf T, Koster J. Perceived recovery as a predictor of physical activity participation after a mild stroke. Disabil Rehabil 2013;35:1143-8.
Boon P, Moors I, De Herdt V, Vonck K. Vagus nerve stimulation and cognition. Seizure 2006;15:259-63.
Franck JA, Smeets RJEM, Seelen HAM. Changes in arm-hand function and arm-hand skill performance in patients after stroke during and after rehabilitation. Plus One 2017;12:1.
Ay I, Sorensen AG, Ay H. Vagus nerve stimulation reduces infarct size in rat focal cerebral ischemia. Neurosci Lett 2009;459:147-51.
Bauer S, Baier H, Baugartner C et al.
Trans cutaneous Vagus Nerve stimulation (tvns) for treatment of drug-resistant epilepsy: a randomized, double-blind clinical trial (cMPsE02). Brain Stimul 2016;9:356-63.
Langhorne P, Coupar F, Pollock A. Motor recovery after stroke: a systematic review. Lancet Neurol 2009;8:741-54.
Bailey RR, Klaesner JW, Lang CE. Quantifying real-world upper limb activity in non-disabled adults and adults with chronic stroke. Neurorehabil Neural 2015;29:969-78.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]