How NeuroFlex®

works

NeuroFlex® uses Virtual Reality (VR) technology to provide scientifically validated and precise measurements of Brain Health.

Why use NeuroFlex®

The technology consists of a laptop, VR goggles and the NeuroFlex® Software. It is light, portable and easy to use.

The NeuroFlex® Test is under 8 minutes of eye-tracking and head movement in VR focused on a set of scientifically validated ocular motor functions. Within seconds, the NeuroFlex® Software analyses the test data with its proprietary algorithms and deidentified data bank to generate an accurate, quantitative and metrics-based report.

The NeuroFlex Report establishes the individuals longitudinal record of their brain health and provides objective data that measures an individual’s oculomotor response to visual stimuli, supporting the identification of visual tracking deficiencies for the healthcare professional when they are determining a diagnosis.

NeuroFlex® Software digitally records eye reflexes of stationary, moving and disappearing targets, eye and head position data and uploads this data to a secure site in the cloud for analysis.

NeuroFlex® Training incorporates over 20 NeuroFlex® VR training exercises for rehabilitation and performance that are derived from the NeuroFlex® Test for personalised programs.

Our Test protocols

In just a few minutes, get objective and accurate indexes of brain health in a report. Each of our test protocols targets specific functions to produce metric based results. Read below about our nine test protocols.

Smooth Pursuit

Head-Fixed & Head-Free

Smooth pursuit eye movements serve an important role in vision by maintaining fixation on a selected moving target as it moves randomly across their visual field. For example, following a ball with your eyes and catching it requires a stable vision as well as good speed perception.

Smooth pursuit is commonly studied with a fixed head position and a given pattern; however, people use both head and eyes in coordination to track objects that move randomly across their visual field. The head free test offers a randomized target path and is a better functional representation of real life movement. The head fixed test isolates the oculomotor functions to a greater degree and may be a better choice for patient with cervical issues.

A high number of corrective saccades during smooth pursuit reflects poor speed perception meaning a catch-up saccade will make the object appear to move faster, while a backward saccade will make it appear slower. There are two possible reasons for generating saccades during pursuit: compensating for the offset between gaze and target position or failing to inhibit saccades when there was no need to initiate them. The former is present in patients with concussion. The latter is present in Parkinson patients.

The smooth pursuit neural pathway uses large areas of the brain to map the target movement as well as to process vision namely, the middle temporal area, the vestibular nuclei, the dorsolateral pontine nuclei, the frontal eye field, and the visual cortex. Lesions to these areas can affect smooth pursuit.

References:
1. Han BI, Song HS, Kim JS.   Vestibular Rehabilitation Therapy: Review of Indications, Mechanisms, and Key Exercises. J Clin Neurol. 2011 Dec;7(4):184-196.
https://doi.org/10.3988/jcn.2011.7.4.184 
2. Ranjbaran M. & H.L. Galiana, Hybrid model of the context dependent vestibulo-ocular reflex: Implications for vergence-version interactions, Frontiers in Computational Neuroscience 9:6: 1-14 (invited Paper for Special Research Topic: Neural and Computational Modeling of Movement Control.
http://dx.doi.org/10.3389/fncom.2015.00006 
3. Eye movements and speed perception, Alexander Goettker, Doris I. Braun, Alexander C. Schütz, Karl R. Gegenfurtner, Proceedings of the National Academy of Sciences Feb 2018, 115 (9) 2240-2.245; 
https://doi.org/10.1073/pnas.1704799115
  
4. Thier, Peter and Uwe J. Ilg. “The neural basis of smooth pursuit eye movements.” Current Opinion in Neurobiology 15 (2005): 645-652.
https://doi.org/10.1016/j.conb.2005.10.013
  
5. Wu C, Cao B, Dali V, Gagliardi C, Barthelemy OJ, Salazar RD, Pomplun M, Cronin-Golomb A, Yazdanbakhsh A. 2018. Eye movement control during visual pursuit in Parkinson’s disease. PeerJ 6:e5442
https://doi.org/10.7717/peerj.5442  
6. Nicholas G. Murray, Brian Szekely, Arthur Islas, Barry Munkasy, Russell Gore, Marian Berryhill, and Rebecca J. Reed Jones. 2019. Smooth Pursuit and Saccades after Sport-Related Concussion. Journal of Neurotrauma 36:1-7.
http://doi.org/10.1089/neu.2019.6595   

Saccades

2D

A saccade refers to a “fast conjugate eye movement that shifts the eyes from one target to another, bringing an object of interest into focus on the fovea where visual acuity is highest.”⁴

During the saccade task, the subject is instructed to move his eyes rapidly to randomly appearing targets. Slow saccade latency or reaction time or other saccade dysfunctions may indicate diseases involving higher brain functions such as Parkinson, Attention Deficit Disorders, Schizophrenia, dementia, or concussion.

References:
1. Han BI, Song HS, Kim JS.  Vestibular Rehabilitation Therapy: Review of Indications, Mechanisms, and Key Exercises. J Clin Neurol. 2011 Dec;7(4):184-196.
https://doi.org/10.3988/jcn.2011.7.4.184
2. Termsarasab, P., Thammongkolchai, T., Rucker, J.C. et al. The diagnostic value of saccades in movement disorder patients: a practical guide and review. J Clin Mov Disord 2, 14 (2015).
https://doi.org/10.1186/s40734-015-0025-4
3. Stefano Ramat, R. John Leigh, David S. Zee, Lance M. Optican, What clinical disorders tell us about the neural control of saccadic eye movements, Brain, Volume 130, Issue 1, January 2007, Pages 10–35,
https://doi.org/10.1093/brain/awl309
4. McDowell, Jennifer E et al. “Neurophysiology and neuroanatomy of reflexive and volitional saccades: evidence from studies of humans.” Brain and cognition vol. 68,3 (2008): 255-70.
https://doi.org/10.1016/j.bandc.2008.08.016

Optokinetic Nystagmus

Horizontal & Vertical

The Optokinetic Reflex (OKR) is a reflex that detects relative motion of the scenery on the retina. Helmholtz first observed the OKN by looking at the eyes of passengers on a moving train. Optokinetic nystagmus (OKN) response to a repetitive stimulus combines two types of eye movements: a slow pursuit stabilizing the image on the retina followed by rapid saccadic refixations.

The OKN is tested by fixating a target while a visual field of dots (a star-field) provides a visual slip in horizontal or vertical directions at variable velocities. The result is a nystagmus in the direction of the induced visual slip (field velocity). Thus, the patient makes pursuits in the direction of the target movement, and corrective saccades back to center.

Large parts of the brain are active during OKN stimulus: the occipitotemporal cortex, posterior parietal cortex, precentral, and posterior median frontal gyrus, the anterior and the posterior insula, the prefrontal cortex, and the medial part of the superior frontal gyrus. OKN dysfunctions are present in Multiple Sclerosis patients. It is also a symptom provocateur in concussion and vestibular patients.

References:
1. Ranjbaran M. & H.L. Galiana, Hybrid model of the context dependent vestibulo-ocular reflex: Implications for vergence-version interactions, Frontiers in Computational Neuroscience 9:6: 1-14 (invited Paper for Special Research Topic: Neural and Computational Modeling of Movement Control)
http://dx.doi.org/10.3389/fncom.2015.00006 
2. Han BI, Song HS, Kim JS. Vestibular rehabilitation therapy: review of indications, mechanisms, and key exercises. J Clin Neurol. 2011;7(4):184–196. doi:10.3988/jcn.2011.7.4.184
3. Marousa Pavlou, The Use of Optokinetic Stimulation in Vestibular Rehabilitation, Journal of Neurologic Physical Therapy. 34(2):105-110, JUN 2010, DOI: 10.1097/NPT.0b013e3181dde6bf
4. Improvements in Gait Speed and Weight Shift of Persons With Traumatic Brain Injury and Vestibular Dysfunction Using a Virtual Reality Computer-Assisted Rehabilitation Environment
5. Pinata H &al., Improvements in Gait Speed and Weight Shift of Persons With Traumatic Brain Injury and Vestibular Dysfunction Using a Virtual Reality Computer-Assisted Rehabilitation Environment, Military Medicine, Volume 180, Issue suppl_3, March 2015, Pages 143- 149,
https://doi.org/10.7205/MILMED-D-14-00385
6. Penelope S. Suter, Lisa H. Harvey. Vision Rehabilitation: Multidisciplinary Care of the Patient Following Brain Injury. Routledge – Feb 2 2011 (p.433-4)
7. London, Richard. (1982). Optokinetic nystagmus: a review of pathways, techniques and selected diagnostic applications. Journal of the American Optometric Association. 53. 791-8. PMID: 7142632
8. Gottlob, I. “Ups and downs of optokinetic nystagmus.” The British journal of ophthalmology vol. 84,5 (2000): 445-6. 
https://doi.org/10.1136/bjo.84.5.445

Vestibulo-Ocular Reflex

Horizontal & Vertical

Coordination of the eyes with head movement is a function of the Vestibular Ocular Reflex (VOR). During brief, rapid head motion, the semicircular canals of the inner ear will elicit compensatory eye movements to maintain the image on the fovea. In order to test the active visual VOR, the patient will fixate a target during active head turns. This functional test includes sensory signals from both the neck and the visual system.

If the VOR is deficient, the eyes do not cancel head movements efficiently and this may result in a loss of gaze stabilization, blurry vision, unsteadiness, dizziness or nausea. To illustrate this, if a runner turns their head as they run, the visual field will appear unsteady or bouncing, and may cause the runner to lose balance.

Traumatic brain injury (TBI) patients (30-60%) will complain of dizziness at their initial visit. Dizziness is a factor for an increase risk of developing persistent concussion symptoms. Vestibular loss appears to impact cognitive functions such as attention, executive function, memory and visuospatial ability (tracking, spatial mental representation). For example, astronauts have reported suffering from “Space stupids” during microgravity adaptation. An association exists between vestibular dysfunction and cognitive impairment such as Alzheimer and dementia. To note: cervicogenic pain with associated dizziness must be differentiated from vestibular deficits.

References:
1. Han BI, Song HS, Kim JS.  Vestibular Rehabilitation Therapy: Review of Indications, Mechanisms, and Key Exercises. J Clin Neurol. 2011 Dec;7(4):184-196.
https://doi.org/10.3988/jcn.2011.7.4.184
2. Ranjbaran M. & H.L. Galiana, Hybrid model of the context dependent vestibulo-ocular reflex: Implications for vergence-version interactions, Frontiers in Computational Neuroscience 9:6: 1-14 (invited Paper for Special Research Topic: Neural and Computational Modeling of Movement Control.
http://dx.doi.org/10.3389/fncom.2015.00006 
3. Wallace B, Lifshitz J.,Traumatic brain injury and vestibulo-ocular function: current challenges and future prospects. Eye Brain. 2016 Sep 6;8:153-164.
https://doi.org/10.2147/EB.S82670
4. Penelope S. Suter, Lisa H. Harvey. Vision Rehabilitation: Multidisciplinary Care of the Patient Following Brain Injury. Routledge – Feb 2 2011 (p.433-4)
5. Skóra, W., Stańczyk, R., Pajor, A., and Jozefowicz-korczyńska, M. (2018). Vestibular system dysfunction in patients after mild traumatic brain injury. Annals of Agricultural and Environmental Medicine, 25(4), pp.665-668.
https://doi.org/10.26444/aaem/81138
6. Bigelow RT, Agrawal Y. Vestibular involvement in cognition: Visuospatial ability, attention, executive function, and memory. J Vestib Res. 2015;25(2):73-89.
https://doi.org/10.3233/VES-150544
7. Harun, Aisha et al. “Vestibular Impairment in Dementia.” Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology vol. 37,8 (2016): 1137-42.
https://doi.org/10.1097/MAO.0000000000001157
8. Diane M. Wrisley, Patrick J. Sparto, Susan L. Whitney, and Joseph M. Furman. Cervicogenic Dizziness: A Review of Diagnosis and Treatment. Journal of Orthopadic & Sports Physical Therapy 2000 30:12, 755-766.
https://doi.org/10.2519/jospt.2000.30.12.755

Antisaccades

Anti-saccade testing evaluates inhibition or the capacity to not react reflexively to a stimulus, as well as the capacity to map peripheral vision.

The subject is first provided with a distracting target and is instructed to look in the opposite direction. For example, if the distracting target is 3 cm to the right, the subject should look 3 cm to the left. This test adds a cognitive stage and visual map orientation before executing the saccade. An error is counted if the saccade is performed in the direction of the target instead of the opposite direction.

The anti-saccade task is used to evaluate the function of the visual cortex. Poor anti-saccades results are found in patients with Schizophrenia, frontal or basal ganglia dysfunction, dorsolateral mesial frontal lobes lesions, dorsolateral prefrontal cortex lesions, Huntington’s disease, progressive supranuclear palsy, Parkinson’s disease, and concussion, to name a few.

References:
1. Lévy-Bencheton D, Pélisson D, Prost M, et al. The Effects of Short-Lasting Anti-Saccade Training in Homonymous Hemianopia with and without Saccadic Adaptation. Front Behav Neurosci. 2016;9:332. Published 2016 Jan 5.
https://doi.org/10.3389/fnbeh.2015.00332
2. Munoz DP, Everling S. Look away: the anti-saccade task and the voluntary control of eye movement. Nat Rev Neurosci 5: 218-228, · April 2004.
https://doi.org/10.1038/nrn1345
3. Guitton, D.; Buchtel, H. A.; Douglas, R. M. (1985). “Frontal lobe lesions in man cause difficulties in suppressing reflexive glances and in generating goal-directed saccades.” Experimental Brain Research 58(3): 455-472.
http://dx.doi.org/10.1007/BF0023586
4. Ting, Windsor Kwan-Chun et al. “Antisaccadic Eye Movements Are Correlated with Corpus Callosum White Matter Mean Diffusivity, Stroop Performance, and Symptom Burden in Mild Traumatic Brain Injury and Concussion.” Frontiers in neurology 6 (2015): 271.
https://doi.org/10.3389/fneur.2015.00271

Spontaneous & Gaze-Evoked Nystagmus

Spontaneous nystagmus in the dark is the involuntary movement of the eyes without any visual, vestibular, or cognitive stimuli and is an indicator of imbalance in the gaze orientation system. During fixation, the eyes continuously produce miniature movements: ocular tremor, nystagmus, and microsaccades.

Ocular tremors are low amplitudes high frequency (40-100Hz) eye position changes over time. Ocular drift refers to lower frequency (less than 40 Hz) meandering movements producing much larger shifts in eye position and eye speeds up to about 18 deg/sec. Microsaccades, sometimes referred as ‘fixational saccades” are smaller saccades in the order of 1 deg.

“Eye position during fixation is actively controlled and depends on bilateral activity in the superior colliculi and medio posterior cerebellum” (Krauzlis &al. 2017). There are many causes to nystagmus. A few of the following cases outline some of the possibilities. Peripheral vestibular imbalance accompanied by vertigo will have a horizontal nystagmus that suppresses with fixation.

Congenital nystagmus usually remains horizontal in all gaze angles. Latent nystagmus, associated with either childhood strabismus or an absent stereopsis, changes direction when the eyes are alternatively covered. Acquired pendular nystagmus occurs most commonly in association with disorders of central myelin, especially multiple sclerosis and after brain stem stroke. The most common form of nystagmus encountered in clinical practice occurs when the eyes are moved into eccentric gaze, especially in lateral and up gaze, and is a sign of cerebellar and brainstem disorders as well as a number of intoxications.

References:
1. Serra A, Leigh RJDiagnostic value of nystagmus: spontaneous and induced ocular oscillationsJournal of Neurology, Neurosurgery & Psychiatry 2002;73:615-618.
https://jnnp.bmj.com/content/73/6/615
2. Ko, Hee-Kyoung et al. “Eye movements between saccades: Measuring ocular drift and tremor.” Vision research vol. 122(2016): 93-104.
https://dx.doi.org/10.1016%2Fj.visres.2016.03.006
3. Krauzlis Richard J., Goffart Laurent and Hafed Ziad M. Neuronal control of fixation and fixational eye movements, Philos Trans R Soc Lond B Biol Sci. 2017 Apr 19; 372(1718): 20160205.
http://doi.org/10.1098/rstb.2016.0205

About our Training

NeuroFlex® Training provides over 20 interactive exercises that are personalised to the individual’s NeuroFlex® Test results.

The personalised brain training exercises are done in VR that can result in, performance enhancement to improve ocular motor reflexes, and in rehabilitation to assist recovery and graduated return school, work and play.

NeuroFlex® Training is currently being further developed to be accessed by multiple VR headset suppliers accessed via app stores.

Want to see it in action?

Click below to set up a personal demo with one of our specialists. They’ll show you the tests, rehab exercises, real results, and how NeuroFlex® integrates into clinics, sports teams, hospitals, and more across Canada and Australia.

Coming soon – myNeuroFlex®

While NeuroFlex® is perfect for clinics and organizations, we want to provide advanced care to patients every step of the way. To better assist you with tracking and understanding your progress, we’re building myNeuroFlex, an app for iOS and Android that can be accessed from anywhere.

Results from testing on NeuroFlex® can be viewed on your smartphone, along with helpful information about brain health. Take your brain health into your own hands!