Course Objectives - Optometric Extension Program · Case report: MBH • A 91 years old recently retired optometrist suffered a massive stroke while attending a birthday party for
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Stroke of Fortune Found in the
V.T. Room
Holly Harlow, COVTT Marilyn Brenne Heinke, OD, FAAO, FCOVD
Vision‘s purpose is to guide actions, growth, understanding and the quality of life. The sensory component of vision is to serve as a feedback mechanism to evaluate the adequacy of our actions. Vision problems should be explained in terms of performance. John Streff, OD, DOS, FCOVD,FAAO
Patients in the slow-to-recover subset of brain injury benefit from longer trials of rehabilitation, with functional recovery continuing to improve months or years after injury.
Neurons increase connections with other neurons through sensory stimulation, learning with complex, interesting experiences that are novel coupled with motivation.
• Eye movements • Double Pursuits and Saccades • Eye throw • Saccade into neglect • Optokinetic stimulation
Eye Movements
Oculomotor visual rehabilitation affects the visual system at early visuo-cortical levels, as well as other pathways which are involved in visual attention.
Optokinetic Stimulation• Kerkhoff, Keller 2006, Restorative Neurology and
Neuroscience • Helps direct attention into neglected space • Increases exploration of left space • Positive influence on spatial perception • Valler 1997: arm posiiton • Strum 2006: reactivates cortical areas
Minimize Screen Time• Inhibits neuronal growth!• Passive vs active stimulus!• Decreases tone!• Increases visual stress!• Sleep like state!• Blue light exposure!• Brain needs to heal!• Apps for visual recognition and reaction time
An Effective NOVTR Program…1. Complies with the VISUAL DEVELOPMENT Process!2. Uses VISUAL MOTOR to guide VISUAL SENSORY!3. Has VISUALLY GUIDED Sensory Integration Activities to
Improve Orientation and Organization of Visual Space!4. Builds VISUAL MEMORY and REACTION TIME to
improve daily living activities !5. Incorporates Good POSTURE and BREATHING into all
activities!6. Works AMBIENT to FOCAL!7. Uses OCCLUSION, LENSES and PRISMS for Enhanced
Visual Experience!8. ASKS doesn’t tell how to create self discovery!9. Is based on patient GOALS, rehabilitation and remediation
• Be sure activity provides feedback!• Keep level of complexity at appropriate level!• Increase demand slowly!• Integrate activities into daily living activities (ADL)!• Give lots of reinforcement of even very small gains
Neurons increase connections with other neurons through sensory stimulation, learning with complex, interesting experiences that are novel coupled with motivation.
Neuroplasticity provides patients with a brain that can adapt not only to changes from damage, but allows adaptation to any and all experiences and changes we may encounter.
NeurogenesisTo change the wiring of one skill, one must engage in an activity that is unfamiliar, novel but related to the skill. Simply repeating the same activity only maintains established connections. Practice helps rewire the brain. John Ratey, MD: Users guide to the brain.
• Reduced ability to attend to meaningful sensory stimuli presented in the affected hemi-field.!
• Geniculo-striate pathway is intact.!• With or without hemianopsia and hemiplegia.!• CVA of middle cerebral artery is most common.!• Competitive process.!• Extinction phenomenon: only happens with
simultaneous perception.!• Can occur with any combination of visual, auditory or
Right Versus LeftRight VFD ! ! ! ! ! ! !• Left insult!• No word recognition!• Poor cognition!• Aware of VFD!• Left egocentric shift!• Base Rt. Yoked prism
Left VFD! ! ! ! ! ! !• Right insult!• Intact word recognition!• Intact cognition!• Unaware of VFD!• Right egocentric shift!• Base Lt. yoked prism
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Visual Neglect• Ignores food on left side of plate!• Shaves right side of face!• Ignores left side of body !• Denies ignoring left space and items in left space!• Rotates head and body away from area of neglect!• Inattentiveness!• Imperception!• Unawareness!• No knowledge the space exists!• Object permanence!• Occurs with or without a VFD
Studies of Treatments for Neglect• Hemispatial Sunglasses!
• Arch Phys Med Rehabil. 1997 Feb;78(2):230-2.Hemispatial sunglasses: effect on unilateral spatial neglect.Arai T1, Ohi H, Sasaki H, Nobuto H, Tanaka K.!
• Prism Adaptation!• JBO 2009, 20:101-105 by Massucci: Prism Adaptation in
USI.!• Mirror Therapy!
• Neurology. 2014 Sep 9; 83(11): 1012–1017.Mirror Therapy in Unilateral Neglect After Stroke (MUST trial) A randomized controlled trial J.D. Pandian, et al
References for Fatigue, Brain Injury and Blue Light!
•Assessment and treatment of mental fatigue after a traumatic brain injury. Birgitta Johansson & Lars Rönnbäck. Published online: 01 Mar 2017: Pages 1047-1055 , http://dx.doi.org/10.1080/09602011.2017.1292921 !!
•Description of a multifaceted intervention program for fatigue after acquired brain injury: a pilot study J. Stubberud, Espen Edvardsen, Anne-Kristine Schanke, Anners Lerdal, Anita Kjeverud, Andreas Schillinger. Pages 1-23 Published online: 05 Jul 2017. http://dx.doi.org/10.1080/09602011.2017.1344132
Randomized controlled trial of light therapy for fatigue following traumatic brain injury.
The current study aimed to investigate the efficacy of 4 weeks of light therapy for fatigue in patients with TBI.!
METHODS: We undertook a randomized, placebo-controlled study of 4-week, 45 min/morning, home-based treatment with short wavelength (blue) light therapy (λmax = 465 nm, 84.8 µW/cm(2), 39.5 lux, 1.74 × 10(14) photons/cm(2)/s) compared with yellow light therapy (λmax = 574 nm, 18.5 µW/cm(2), 68 lux, 1.21 × 10(12) photons/cm(2)/s) containing less photons in the short wavelength range and a no treatment control group (n = 10 per group) in patients with TBI who self-reported fatigue and/or sleep disturbance. Assessments of fatigue and secondary outcomes (self-reported daytime sleepiness, depression, sleep quality, and sustained attention) were conducted over 10 weeks at baseline (week -2), midway through and at the end of light therapy (weeks 2 and 4), and 4 weeks following cessation of light therapy (week 8).!
RESULTS:After controlling age, gender, and baseline depression, treatment with high-intensity blue light therapy resulted in reduced fatigue and daytime sleepiness during the treatment phase, with evidence of a trend toward baseline levels 4 weeks after treatment cessation. These changes were not observed with lower-intensity yellow light therapy or no treatment control conditions. There was also no significant treatment effect observed for self-reported depression or psychomotor vigilance performance.!
CONCLUSIONS: Blue light therapy appears to be effective in alleviating fatigue and daytime sleepiness following TBI and may offer a noninvasive, safe, and nonpharmacological alternative to current treatments.
Naveen K. Yadav, Preethi Thiagarajan & Kenneth J. Ciuffreda. Pages 922-929 Published online: 24 Feb 2014, http://dx.doi.org/10.3109/02699052.2014.887227 !Abstract: Primary objective: The purpose of the experiment was to investigate the effect of oculomotor vision rehabilitation (OVR) on the visual-evoked potential (VEP) and visual attention in the mTBI population.!Research design and methods: Subjects (n = 7) were adults with a history of mild traumatic brain injury (mTBI). Each received 9 hours of OVR over a 6-week period. The effects of OVR on VEP amplitude and latency, the attention-related alpha band (8–13 Hz) power (µV2) and the clinical Visual Search and Attention Test (VSAT) were assessed before and after the OVR.
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Effect of oculomotor vision rehabilitation on the visual-evoked potential and visual attention in mild traumatic brain injury !
Results: After the OVR, the VEP amplitude increased and its variability decreased. There was no change in VEP latency, which was normal. Alpha band power increased, as did the VSAT score, following the OVR.!Conclusions: The significant changes in most test parameters suggest that OVR affects the visual system at early visuo-cortical levels, as well as other pathways which are involved in visual attention.
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Effect of oculomotor vision rehabilitation on the visual-evoked potential and visual attention in mild traumatic brain injury !
Dusting• Dust safe areas • Hand/eye coordination • Judgments beyond reach • Fixation and eye movements • Sitting or Standing • Fixate objects working around • Place important object on side
• Safe areas • Hand/eye coordination • Judgments beyond reach • Fixation and eye movements • Sitting or Standing • Fixate objects working around • Place important object on side of VFD
• Calorie-protein deficits are found 6 months post acute stroke
• Reduced plasma levels of tyrosine occurs this is the amino acid precursor of brain adrenergic neurotransmitters (epinephrine, norepinephrine, dopamine).
Macular pigment optical density is related to cognitive function in older people. Rohini Vishwanathan, Alessandro Iannaccone, Tammy M. Scott, Stephen B. Kritchevsky, Barbara J. Jennings, Giovannella Carboni, Gina Forma, Suzanne Satterfield, Tamara Harris, Karen C. Johnson. Age and Ageing, Volume 43, Issue 2, 1 March 2014, Pages 271–275
Mol Med Rep. 2017 Oct;16(4):4235-4240. 2017 Jul 20.!Lutein protects against severe traumatic brain injury through anti‑inflammation and antioxidative effects via ICAM‑1/Nrf‑2. Tan D1, Yu X1, Chen M1, Chen J1, Xu J1.
Relationship of Lutein and Zeaxanthin Levels to Neurocognitive Functioning: An fMRI Study of Older Adults. J or Internatl. Neuropsychological Soc., 2016; 1 Cutter A. Lindbergh, CM Mewborn et al. !
•Lutein and other carotenoids are fat-soluble, so to optimize absorption, be sure to add a little bit of healthy fat to your meal. !
•Research shows that adding a couple of eggs, which contain both lutein and healthy fats, to your salad can increase the carotenoid absorption from the whole meal as much as nine-fold.
Traumatic brain injury causes a long-lasting calcium (Ca2+)-plateau of elevated intracellular Ca levels and altered Ca2+ homeostatic mechanisms in hippocampal neurons surviving brain injury!
David A. Sun,1 Laxmikant S. Deshpande,2 Sompong Sombati,2 Anya Baranova,3,5 Margaret S. Wilson,6 Robert J. Hamm,5 and Robert J. DeLorenzo2,3,4!
Fatty AcidNeuroprotectin D1 (NPD1): A DHA-Derived Mediator that Protects Brain and Retina Against Cell Injury-Induced Oxidative Stress Nicolas G. Bazan, LSU Neuroscience Center and Department of Opthamology, Louisiana State University Health Sciences Center School of Medicine in New Orleans. First published: April 2005!
•The biosynthesis of oxygenated arachidonic acid messengers triggered by cerebral ischemia-reperfusion is preceded by an early and rapid phospholipase A2 !
•Activation reflected in free arachidonic and docosahexaenoic acid (DHA) accumulation. These fatty acids are released from membrane phospholipids. !
•Both fatty acids are derived from dietary essential fatty acids; however, only DHA, the omega-3 polyunsaturated fatty acyl chain, is concentrated in phospholipids of various cells of brain and retina. !
•Synaptic membranes and photoreceptors share the highest content of DHA of all cell membranes. DHA is involved in memory formation, excitable membrane function, photoreceptor cell biogenesis and function, and neuronal signaling, and has been implicated in neuroprotection.
Neuroprotectin D1 (NPD1): A DHA-Derived Mediator that Protects Brain and Retina Against Cell Injury-Induced Oxidative Stress Nicolas G. Bazan, LSU Neuroscience Center and Department of Opthamology, Louisiana State University Health Sciences Center School of Medicine in New Orleans. First published: April 2005!!•Omega 3 fatty acid is required for retinal pigment epithelium cell (RPE) functional integrity. !
•In oxidative stress-challenged human RPE cells and rat brain undergoing ischemia-reperfusion, 10,17S-docosatriene (neuroprotectin D1, NPD1) synthesis evolves. !
•In addition, calcium ionophore A23187, IL-1β, or the supply of DHA enhances NPD1 synthesis. !
•Moreover, NPD1 bioactivity demonstrates that DHA is not only a target of lipid peroxidation, but rather is the precursor to a neuroprotective signaling response to ischemia-reperfusion.!
•This opens avenues of therapeutic exploration in stroke, neurotrauma, spinal cord injury, and neurodegenerative diseases, such as Alzheimer disease, aiming to up-regulate this novel cell-survival signaling.
Neuroprotectin D1 (NPD1): A DHA-Derived Mediator that Protects Brain and Retina Against Cell Injury-Induced Oxidative Stress Nicolas G. Bazan, LSU Neuroscience Center and Department of Opthamology, Louisiana State University Health Sciences Center School of Medicine in New Orleans. First published: April 2005
Chocolate•Several recent studies suggest that some types of cocoa contain substances that could enhance blood flow in the brain and improve brain function. !
•Flavanoids have the ability to keep the brain healthy and prevent cognitive decline and dementia. !
•After consumption of the cocoa based liquid, it was noted that there was increased blood flow to the gray matter for two to three hours.
Evidence for ChocolateHow Dark Chocolate May Guard Against Brain Injury From Stroke!May 5, 2010 - Researchers at Johns Hopkins discovered that a compound in dark chocolate may protect the brain after a stroke by increasing cellular signals already known to shield nerve cells from damage.!Ninety minutes after feeding mice a single modest dose of epicatechin, a compound found naturally in dark chocolate, the scientists induced an ischemic stroke by essentially cutting off blood supply to the animals’ brains. They found that the animals that had preventively ingested the epicatechin suffered significantly less brain damage than the ones that had not been given the compound.
Evidence for Chocolate•Sylvain Doré, Ph.D., associate professor of anesthesiology and critical care
medicine and pharmacology and molecular sciences at the Johns Hopkins University School of Medicine, says his study suggests that epicatechin stimulates two previously well-established pathways known to shield nerve cells in the brain from damage. When the stroke hits, the brain is ready to protect itself because these pathways — Nrf2 and heme oxygenase 1 — are activated. !
•In mice that selectively lacked activity in those pathways, the study found, epicatechin had no significant protective effect and their brain cells died after a stroke.!
•Eventually, Doré says, he hopes his research into these pathways could lead to insights into limiting acute stroke damage and possibly protecting against chronic neurological degenerative conditions, such as Alzheimer’s disease and other age-related cognitive disorders.
Evidence for Chocolate•The epicatechin is needed to jump-start the protective pathway that is already
present within the cells. “Even a small amount may be sufficient,” Doré says.!•Not all dark chocolates are created equally, he cautions. Some have more
bioactive epicatechin than others.!•“The epicatechin found in dark chocolate is extremely sensitive to changes in
heat and light” he says. “In the process of making chocolate, you have to make sure you don’t destroy it. Only few chocolates have the active ingredient. The fact that it says ‘dark chocolate’ is not sufficient.”!
•The new study was supported by grants from the National Institutes of Health and the American Heart and Stroke Association.!
•Other Johns Hopkins researchers on the study include Zahoor A. Shah, Ph.D.; Rung-chi Li, Ph.D.; Abdullah S. Ahmad, Ph.D.; Thomas W. Kensler, Ph.D.; and Shyam Biswal, Ph.D.
•The effect of blue light on post-stroke fatigue!•Debilitating fatigue is a problem that is experienced by more than 50% of stroke survivors. !
•A small study in traumatic brain injury showed that patients randomied to a 4-week, 45-minutes per day schedule of blue light therapy had lower fatigue than patients exposed to either longer wavelength (yellow) light or no light.!!
Sinclair, K. L., J. L. Ponsford, et al. (2014). "Randomized Controlled Trial of Light Therapy for Fatigue Following Traumatic Brain Injury." Neurorehabilitation and Neural Repair 28(4): 303-313.
The effect of blue light on post-stroke fatigue!!This project investigated whether exposure to blue light can reduce fatigue in community-dwelling stroke survivors. Participants randomized to the intervention received daily blue light exposure over 4 weeks, while controls will receive daily yellow light exposure.!!Sinclair, K. L., J. L. Ponsford, et al. (2014). "Randomized Controlled Trial of Light Therapy for Fatigue Following Traumatic Brain Injury." Neurorehabilitation and Neural Repair 28(4): 303-313.
Canadian researchers found that stroke patients who exercised were able to improve problems with their memory, thinking, language and judgment by close to 50% in just six months
Exercise•It has been found that treadmill activity, forced limb movement, and other physical activities help promote brain plasticity. !
•A pattern of exercise before an injury promotes a defense against cell death. !
•It is thought that in the chronic stages after brain injury, an exercise program might reactivate mechanism of healing and thus it is recommended to keep victims as physically active as possible. !
•In a related study, recreational therapy was found to improve rehabilitation.
Canadian researchers found that stroke patients who exercised were able to improve problems with their memory, thinking, language and judgment by close to 50 percent in just six months
•Careful with HERBAL REMEDIES!•The use of herbal supplements is common in the U.S. However, following a brain injury, remedies such as St. Johns Wort and Ginko Biloba, SHOULD BE AVOIDED. !
•Studies show that they may induce mania in TBI patients. Spinella M., 2002