A multimodal investigation in eye movements

While functional magnetic resonance imaging (fMRI) has identified which regions of interest (ROIs) are functionally active during a vergence movement (inward or outward eye rotation), task-modulated coactivation between ROIs is less understood. This study tests the following hypotheses: (1) significant task-modulated coactivation would be observed between the frontal eye fields (FEFs), the posterior parietal cortex (PPC), and the cerebellar vermis (CV); (2) significantly more functional activity and task-modulated coactivation would be observed in binocularly normal controls (BNCs) compared with convergence insufficiency (CI) subjects; and (3) after vergence training, the functional activity and task-modulated coactivation would increase in CIs compared with their baseline measurements. A block design of sustained fixation versus vergence eye movements stimulates activity in the FEFs, PPC, and CV. fMRI data from four CI subjects before and after vergence training are compared with seven BNCs. Functional activity is assessed using the blood oxygenation level dependent (BOLD) percent signal change. Task-modulated coactivation is assessed using an ROI-based task modulated coactivation analysis that reveals significant correlation between ROIs

Visual problems associated with traumatic brain injury:Vision with traumatic brain injury

Traumatic brain injury (TBI) and its associated concussion are major causes of disability and death. All ages can be affected but children, young adults and the elderly are particularly susceptible. A decline in mortality has resulted in many more individuals living with a disability caused by TBI including those affecting vision. This review describes: (1) the major clinical and pathological features of TBI; (2) the visual signs and symptoms associated with the disorder; and (3) discusses the assessment of quality of life and visual rehabilitation of the patient. Defects in primary vision such as visual acuity and visual fields, eye movement including vergence, saccadic and smooth pursuit movements, and in more complex aspects of vision involving visual perception, motion vision (‘akinopsia’), and visuo-spatial function have all been reported in TBI. Eye movement dysfunction may be an early sign of TBI. Hence, TBI can result in a variety of visual problems, many patients exhibiting multiple visual defects in combination with a decline in overall health. Patients with chronic dysfunction following TBI may require occupational, vestibular, cognitive and other forms of physical therapy. Such patients may also benefit from visual rehabilitation, including reading-related oculomotor training and the prescribing of spectacles with a variety of tints and prism combinations

Eye movements in mild traumatic brain injury: Ocular biomarkers

Mild traumatic brain injury (mTBI, or concussion), results from direct and indirect trauma to the head (i.e. a closed injury of transmitted forces), with or without loss of consciousness. The current method of diagnosis is largely based on symptom assessment and clinical history. There is an urgent need to identify an objective biomarker which can not only detect injury, but inform prognosis and recovery. Ocular motor impairment is argued to be ubiquitous across mTBI subtypes and may serve as a valuable clinical biomarker with the recent advent of more affordable and portable eye tracking technology. Many groups have positively correlated the degree of ocular motor impairment to symptom severity with a minority attempting to validate these findings with diffusion tract imaging and functional MRI. However, numerous methodological issues limit the interpretation of results, preventing any singular ocular biomarker from prevailing. This review will comprehensively describe the anatomical susceptibility, clinical measurement, and current eye tracking literature surrounding saccades, smooth pursuit, vestibulo-ocular reflex, vergence, pupillary light reflex, and accommodation in mTBI

Diplopia and eye movement disorders.

Published versio

Role of Primary Care Optometrists in the Assessment and Management of Patients with Traumatic Brain Injuries in Canada

Traumatic brain injury (TBI) results from a strong blow or jolt to the head that disrupts the normal function of the brain.1 The severity of a TBI can range from mild to severe, depending on the patient’s mental status, con-sciousness level and amnesia following the injury. The annual incidence of TBI in North America and Europe is conservatively estimated to be ap-proximately 600/100,000.2,3 This translates to at least 200,000 TBI cases in Canada every year. According to the Centers for Disease Control and Prevention, and the Canadian Institute for Health Information, the leading cause of TBIs that result in hospital admission is falls (35%-45%), followed by motor vehicle accidents (17%-36%), collision-related events (struck by or against) (10-17%) and assaults (9-10%).4,5 Head injuries are more common in the 0- to 19-year age group, followed by those who are aged 60+. Males are more highly represented in every age group than females. However, it should be noted that the demographics of patients who present in an op-tometrist’s office may differ from those based on hospital admissions [...

The ‘20/20/20 Rule’ – When Good Intentions and Axiomatic Habit Displace Best Practices

Optometrists often proffer the ‘20/20/20 Rule’ as advice for clients who experience nearpoint visual strain, or who are subjected to prolonged exposure to nearpoint devices. The ‘rule’ is offered in the patient’s best interests: To help alleviate asthenopia and visual stress from nearpoint strain, and to reduce the risk of onset or the progression of myopia and associated ocular disease. Best intentions aside, there is a paucity of clinical and scientific support for the rule. On the other hand, modern optical tools and methods, and vision rehabilitation practices are known to be helpful in addressing mild to severe binocular vision disorders, to promote comfort, and to slow the progression of myopia. While offering trite advice to address potentially serious concerns might appear to be helpful, its continued use could well be displacing other more appropriate management strategies. This paper addresses some concerns regarding the promulgation of this well-meaning, but misguided, advice

Comitant strabismus etiology: extraocular muscle integrity and central nervous system involvement—a narrative review

Strabismus is not a condition in itself but the consequence of an underlying problem. Eye misalignment can be caused by disease, injury, and/or abnormalities in any of the structures and processes involved in visual perception and oculomotor control, from the extraocular muscles and their innervations to the oculomotor and visual processing areas in the brain. A small percentage of all strabismus cases are the consequence of well-described genetic syndromes, acquired insult, or disease affecting the extraocular muscles (EOMs) or their innervations. We will refer to them as strabismus of peripheral origin since their etiology lies in the peripheral nervous system. However, in most strabismus cases, that is comitant, non-restrictive, non-paralytic strabismus, the EOMs and their innervations function properly. These cases are not related to specific syndromes and their precise causes remain poorly understood. They are generally believed to be caused by deficits in the central neural pathways involved in visual perception and oculomotor control. Therefore, we will refer to them as central strabismus. The goal of this narrative review is to discuss the possible causes behind this particular type of eye misalignment and to raise awareness among eyecare professionals about the important role the central nervous system plays in strabismus etiology, and the subsequent implications regarding its treatment. A non-systematic search was conducted using PubMed, Medline, Cochrane, and Google Scholar databases with the keywords “origins,” “causes,” and “etiology” combined with “strabismus.” A snowball approach was also used to find relevant references. In the following article, we will first describe EOM integrity in central strabismus; next, we will address numerous reasons that support the idea of central nervous system (CNS) involvement in the origin of the deviation, followed by listing several possible central causes of the ocular misalignment. Finally, we will discuss the implications CNS etiology has on strabismus treatment.Open Access funding provided thanks to the CRUE-CSIC agreement with Springer Nature.Peer ReviewedPostprint (published version

Central Crosstalk for Somatic Tinnitus: Abnormal Vergence Eye Movements

Frequent oulomotricity problems with orthoptic testing were reported in patients with tinnitus. This study examines with objective recordings vergence eye movements in patients with somatic tinnitus patients with ability to modify their subjective tinnitus percept by various movements, such as jaw, neck, eye movements or skin pressure.Vergence eye movements were recorded with the Eyelink II video system in 15 (23–63 years) control adults and 19 (36–62 years) subjects with somatic tinnitus.1) Accuracy of divergence but not of convergence was lower in subjects with somatic tinnitus than in control subjects. 2) Vergence duration was longer and peak velocity was lower in subjects with somatic tinnitus than in control subjects. 3) The number of embedded saccades and the amplitude of saccades coinciding with the peak velocity of vergence were higher for tinnitus subjects. Yet, saccades did not increase peak velocity of vergence for tinnitus subjects, but they did so for controls. 4) In contrast, there was no significant difference of vergence latency between these two groups.The results suggest dysfunction of vergence areas involving cortical-brainstem-cerebellar circuits. We hypothesize that central auditory dysfunction related to tinnitus percept could trigger mild cerebellar-brainstem dysfunction or that tinnitus and vergence dysfunction could both be manifestations of mild cortical-brainstem-cerebellar syndrome reflecting abnormal cross-modality interactions between vergence eye movements and auditory signals

Dynamics of the disparity vergence fusion sustain component

The stereotypical vergence response to a step stimulus consists of two dynamic components: a high velocity fusion initiating component followed by a slower component that may mediate sustained fusion.  The initial component has been well-studied and is thought to be controlled by an open-loop mechanism. Less is known about the slow, or fusion sustaining component except that it must be feedback controlled to achieve the positional precision of sustained fusion.  Given the delays in disparity vergence control, a feedback control system is likely to exhibit oscillatory behavior.  Vergence responses to 4 deg step changes in target position were recorded in eight subjects. The slow component of each response was isolated manually using interactive graphics and the frequency spectrum determined.  The frequency spectra of all isolated slow vergence movements showed a large low frequency peak between 1.0 and 2.0 Hz and one or more higher frequency components.  The higher frequency components were found to be harmonics of the low frequency oscillation.  A feedback model of the slow component was developed consisting of a time delay, an integral/derivative controller and an oculomotor plant based on Robinson’s model.  Model simulations showed that a direction dependent asymmetry in the derivative element was primarily responsible for the higher frequency harmonic components. Simulations also showed that the base frequencies are primarily dependent on the time delay in the feedback control system. The fact that oscillatory behavior was found in all subjects provides strong support that the slow, fusion sustaining component is mediated by a feedback system

Enhanced Brain and Concussion Recovery: Round 1: Knock Out Brian Injury – An evolving paradigm in healing

Newer modalities are emerging which will allow us to better identify injury. Additionally, multiple techniques exist to assist with brain retraining. Hyperbaric oxygen therapy is now emerging as the key management tool for brain repair when integrated into a comprehensive concussion recovery program