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Somatosensory Stimulation (RPSS)

What is it?​

Somatosensory Evoked Potentials (SSEP) are a neurophysiological assessment technique invented to measure the speed and quality of electrical information carried from a peripheral nerve to the parietal, or somatosensory cortex, to help a clinician to identify neurological disorders. However, over the decades, researchers realized that these electrical potentials were capable of facilitating neuroplasticity through the manipulation and adaptation of somatosensory maps (1-3) via a non-invasive, electrical, neuromuscular stimulator delivering an asymmetrical biphasic pulse (4,5) over a specific point on the skin. This therapy has been termed Non-Invasive Neuromodulation (NINM), or more specifically, Repetitive Peripheral Somatosensory Stimulation (RPSS). Regardless of what it is called, the stimulation does not cause pain, but instead is reported to feel like a light tapping, tingling, or thumping over the contact point.

Somatosensory-stimulation

Why is it important?

The targeted area of the brain, called the somatosensory system, is comprised of modalities of touch, vibration, temperature, pain and kinesthesia (sense of movement). Because the perception of all external and internal stimuli is integrated in the brain, the evoked potentials generated in the periphery are relayed through pathways involving receptors in the skin, nuclei in the spinal column, brainstem, thalamus, and cerebral cortex (primary somatosensory cortex, primary motor cortex) (5-7). Located in the primary somatosensory cortex (parietal lobe), as well as the primary motor cortex (frontal lobe), is a topographical map, known as the homunculus, reflecting the amount of cortex dedicated to a to a specific body part and its particular function (8,9).

It is important that these body maps be accurate because of the many subsequent areas associated, coordinated and integrated with the sensations mentioned above. These areas include, but are not limited to, the vestibular system (balance/sensing motion), frontal lobe (executive function/motor planning) (1-3,10), posterior parietal cortex (spatial orientation), and cerebellum (motor coordination/error processing) (11). Dysfunction in any of these areas may cause these maps to be altered, skewed, or misrepresented, resulting in symptomology of spatial disorientation, postural abnormalities, dizziness, oculomotor dysfunction, movement disorders, motor planning, etc. (1.3,10,11).

somatosensory-stimulation-rpss

How does it work?

In addition to modulating and correcting somatotopic maps, NINM stimulation has also been researched and proven to have a positive effect on cognitive states (24-26), blood pressure/autonomic function, balance and stability (21,22), and even visual acuity, when applied to specific areas, such as, locations on the face tongue, and wrist. This phenomenon occurs through a series of reflex-arcs that integrate in the brainstem, the primary region for consciousness and autonomic regulation.

somatosensory-stimulation-rpss

In addition to modulating and correcting somatotopic maps, NINM stimulation has also been researched and proven to have a positive effect on cognitive states (24-26), blood pressure/autonomic function, balance and stability (21,22), and even visual acuity, when applied to specific areas, such as, locations on the face tongue, and wrist. This phenomenon occurs through a series of reflex-arcs that integrate in the brainstem, the primary region for consciousness and autonomic regulation.

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The median nerve, located on the palmar, thumb-side of the wrist (12,13), when stimulated, provides a peripheral entryway to the Ascending Reticular Activating System (consciousness center) located in the brainstem (autonomic regulation). It makes sense then, that stimulation to this pathway has been shown to be sufficient to cause clinical improvement in many conditions involving altered states of consciousness, such as, Alzheimer’s Disease and even comatose patients (12-15).

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The Trigeminal Nerve (Cranial Nerve 5), originating in the brainstem, innervates the face through three separate branches. Stimulation of any of these branches (Ophthalmic, Maxillary, Mandibular) stimulates a reflex known as the Trigeminal-Cardial Reflex (TCR). Within seconds after initiation or stimulation, powerful and differentiated activations of sympathetic pathways are engaged, attenuating physiological homeostatic responses, such as baroreceptors and chemoreceptor reflexes for blood pressure regulation (16-20).

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​Stimulation to the tongue has been shown to provide stimulation to an area of the brainstem specifically within the region of the pons (33). This region is important because of the nuclei that originate here, including vestibular, trigeminal, and solitary nuclei. The trigeminal nuclei receive somatosensory information from the tongue while the solitary nuclei receive information about taste, but because of such complex and coordinated interactions between these structures, including but not limited to, co-modulation of visual, vestibular (balance/stability), visceral sensory (sensations from organs) and pain signals, SSEP to the tongue could be involved in the resolution of various symptoms such as hypersensitivity to visual stimuli in balance, anxiety disorders, balance dysfunction in migraine disorders, and interoception (physiological sense of well-being) (21,22, 27-32).

How does it help?

Likewise, the presence of any of the aforementioned symptomatology could be a subclinical que or biomarker indicating the need for somatosensory evoked potential over a specific area of the body.

References

  1. Haavik-Taylor H, Murphy B. Cervical spine manipulation alters sensorimotor integration: a somatosensory evoked potential study. Clin Neurophysiol. 2007;118:391–402. [PubMed]

  2. Haavik-Taylor H, Murphy B. Altered sensorimotor integration with cervical spine manipulation. JMPT. 2008;31:115–126. [PubMed]

  3. Haavik H, Murphy B. The role of spinal manipulation in addressing disordered sensorimotor integration and altered motor control. J Electromyogr Kinesiol. 2012;22:768–776. [PubMed]

  4. Hayashi, N. (1997). Prevention of vegetation after severe head trauma and stroke by combination therapy of cerebral hypothermia and activation of immune-dopaminergic nervous system. Society for Treatment of Coma, 6, 133–147.

  5. Leeman SA. SSEPs: from limb to cortex. Am J Electroneurodiagnostic Technol. 2007;47:165–177. [PubMed]

  6. Leeman SA. SSEPs: from limb to cortex. Am J Electroneurodiagnostic Technol. 2007;47:165–177. [PubMed]

  7. Leyton ASF, Sherrington CS. Observations on the excitable cortex of the chimpanzee, orang-utan, and gorilla. Exp Physiol 1917; 11: 135–222.

  8. Leyton ASF, Sherrington CS. Observations on the excitable cortex of the chimpanzee, orang-utan, and gorilla. Exp Physiol 1917; 11: 135–222.

  9. Foerster O. The motor cortex in man in the light of Hughlings Jackson's doctrines. Brain 1936; 59: 135–59.

  10. Dringenberg, H. C., & Olmstead, M. C. (2003). Integrated contributions of basal forebrain andthalamus to neocortical activation elicited by pedunculopontine tegmental stimulation in urethane-anesthetized rats. Neuroscience, 119, 839–853.

  11. Restuccia D, Valeriani M, Barba C, Le Pera D, Capecci M, Filippini V, et al. Functional changes of the primary somatosensory cortex in patients with unilateral cerebellar lesions. Brain 2001;124:757–68

  12. Cooper, J., Jane, J., Alves, W., & Cooper, E. (1999). Right median nerve electrical stimulation to hasten awakening from coma. Brain Injury, 13, 261–267.

  13. Cooper, E., & Cooper, J. (2003). Electrical treatment of coma via the median nerve. ActaNeurochirurgica Supplement, 87, 7–10.

  14. Moriya, T., Hayashi, N., Utagawa, A. et al. (1999). Median nerve stimulation method for severe brain damage, with its clinical improvement. Society for Treatment of Coma, 8, 111–114.

  15. Doraiswamy, M. (2003). Alzheimer’s disease and the glutamate NMDA receptor. Psycho-pharmacology Bulletin, 37, 41–49.

  16. Cha ST, Eby JB, Katzen JT, et al. (2002) Trigeminocardiac reflex: a unique case of recurrent asystole during bilateral trigeminal sensory root rhizotomy. J Cran Maxillofac Surg 30:108-111. (50, 51, 56)

  17. Schaller B, Baumann A (2003) Headache after removal of vestibular schwannoma via the retrosigmoid approach: A long-term follow-up-study. Otolaryngol Head Neck Surg 128: 387-395.

  18. Schaller B, Heilbronner R, Pfaltz CR, Probst RR, Gratz O (1995) Preoperative and postoperative auditory and facial nerve function in cerebellopontine angle meningiomas. Otolaryngol head neck surg 112:228-234.

  19. Sessle BJ, Greenwood LF (1976) Input to trigeminal brainstem neurons from facial, oral tooth pulp and pharyngolaryngeal tissues: I Responses to innoculous and noxious stimuli. Brain Res 117:211-226.

  20. McCulloch PF, Faber KM, Panneton WM (1999) Electrical stimulation of the anterior ethmoidal nerve produces the driving response. Brain Res 830:24-31.

  21. Danilov Y, Tyler M, Skinner K, Hogle R, Bach-y-Rita P. Efficacy of electrotactile vestibular substitution in patients with peripheral and central vestibular loss. Journal of Vestibular Research. 2007; 17(2):119–130. [PubMed: 18413905]

  22. Danilov, YP.; Tyler, ME.; Skinner, KL.; Bach-y-Rita, P. Efficacy of electrotactile vestibular substitution in patients with bilateral vestibular and central balance loss. Conference Proceedings :...Annual International Conference of the IEEE Engineering in Medicine and Biology Society.IEEE Engineering in Medicine and Biology Society; 2006. p. 6605-6609.

  23. Collignon O, Voss P, Lassonde M, Lepore F. Cross-modal plasticity for the spatial processing of sounds in visually deprived subjects. Experimental Brain Research. 2009; 192(3):343–358.

  24. Pietrini, P.; Ptito, M.; Kupers, R. Blindness and consciousness: New light from the dark. In: Laureys, S.; Tononi, G., editors. The Neurology of Consciousness. 1st. Academic Press; 2009. p. 360-374.

  25. Poirier C, De Volder AG, Scheiber C. What neuroimaging tells us about sensory substitution. Neuroscience and Biobehavioral Reviews. 2007; 31(7):1064–1070. [PubMed: 17688948]

  26. Ptito M, Moesgaard SM, Gjedde A, Kupers R. Cross-modal plasticity revealed by electrotactile stimulation of the tongue in the congenitally blind. Brain. 2005; 128(3):606. [PubMed: 15634727]

  27. Balaban CD, Thayer JF. Neurological bases for balance-anxiety links. Journal of Anxiety Disorders. 2001; 15(1-2):53–79. [PubMed: 11388358]

  28. Buisseret-Delmas C, Compoint C, Delfini C, Buisseret P. Organisation of reciprocal connections between trigeminal and vestibular nuclei in the rat. The Journal of Comparative Neurology. 1999;409(1):153–168. [PubMed: 10363717]

  29. Craig AD. How do you feel? interoception: The sense of the physiological condition of the body. Nature Reviews Neuroscience. 2002; 3(8):655–666

  30. Jacob RG, Redfern MS, Furman JM. Optic flow-induced sway in anxiety disorders associated with space and motion discomfort. Journal of Anxiety Disorders. 1995; 9(5):411–425.

  31. Marano E, Marcelli V, Stasio ED, Bonuso S, Vacca G, Manganelli F, Marciano E, Perretti A. Trigeminal stimulation elicits a peripheral vestibular imbalance in migraine patients. Headache the Journal of Head and Face Pain. 2005; 45(4):325–331.

  32. Satoh Y, Ishizuka KI, Murakami T. Modulation of the masseteric monosynaptic reflex by stimulation of the vestibular nuclear complex in rats. Neuroscience Letters. 2009; 466(1):16–20. [PubMed:19781598]

  33. Wildenberg JC, Tyler ME, Danilov YP, Kaczmarek KA, Meyerand ME. Sustained cortical and subcortical neuromodulation induced by electrical tongue stimulation. Brain Imaging and Behavior. 2010; 4(3-4):199–211. [PubMed: 20614202]

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