Traumatic Brain Injury (TBI) can occur with either direct or indirect contact to the head. For example, a whiplash when rear-ended is an indirect injury to the brain and can result in a concussion or mild TBI. Key contributors to concussions are the starting, stopping, and rotational forces on the brain from the acceleration and deceleration of the head and neck. Since brain tissue is soft, it is particularly vulnerable to these shearing forces. If the forces are strong and widespread throughout the brain, loss of consciousness can occur. TBIs can be categorized as mild (also termed concussion), moderate, or severe. The brain needs to repair itself but it has run out of resources, leading to an energy deficit. Following a TBI, there is a neurometabolic cascade:1) ionic changes to K+, Ca2+, Na-K-ATPase channels 2) Excitatory channels are activated 2) reduced cerebral blood flow (40% less blood flow to area of injury) 3) less glucose and water impacting cellular energy 4) mitochondrial dysfunction due to lack of glucose, less ATP (energy molecules) 5) prolonged depolarization sending "injury impulses". The brain goes into overdrive for producing energy (in the form of ATP), however there is still lack of ATP production and ability for it reach the neurons due to constricted blood flow. Increase in free radicals and shifts in metabolic capacity results in greater vulnerability to repetitive injury. In addition, structural proteins (cytoskeleton) and neuronal axons are physically compromised. Up-regulation of inflammatory markers occur, leading to greater risk of developing long-term neurological conditions such as Parkinsons or Alzheimers Disease. Cell and neuronal death can occur in chronic cases leading to Chronic Traumatic Encephalopathy.
Concussion/mTBI recovery is variable and will depend on the severity of injury and type of symptoms. However, there are general concussion/MTBI recovery timelines:
85-90% of the time, all symptoms are gone within 7-10 days. It’s no surprise that this 7-10 day timeline parallels the 7-10 days that it takes for the brain to get out of its energy crisis.
It is not uncommon for healing to take 2-4 weeks for symptoms to resolve.
If recovery takes over 4+ weeks, this is termed “post concussion syndrome” (PCS). PCS means that it will take longer and more therapeutic intervention is frequently needed.
Seek medical care to rule out an injury that could be more severe than a concussion; concussions should be diagnosed, not assumed.
Rest for 48 hours. This includes no screen-time, reading, exercise, and definitely no activities that increase your risk for a subsequent concussion. Avoid bright lights, loud noises, and manage stress.
Sleep well and eat for better brain recovery. Avoid sugars, alcohol, and drugs. Consume healthy fats high in omega-3s: walnuts, wild salmon, flaxseed, pasture-raised eggs. Consider adding a fish oil supplement (2000-4000mg daily).
Other promising supplements to consider based on your doctor's treatment plan: curcumin, vitamin D, progesterone, n-acetylcysteine (NAC) and n-acetylecysteine amide (NACA), alpha-lipoic acid (ALA), branched-chain amino acids, glutathione, vitamin Bs, zinc, magnesium, selenium, and phytochemicals (sulforaphane, flavenoids, resveratrol, polyphenols, gingko biloba)
If symptoms persist after 4 weeks, seek medical care for further evaluation including Neuro-optometrist, Functional Neurologist, and other concussion/TBI specialists.
There is no one-size-fits all treatment approach. The treatment must be tailored to the individual based on diagnoses and test results.
Evidence for Vision Rehabilitation
The Vision Conditions and Symptoms due to TBI can be treated and resolved with a successful program of vision rehabilitation. A multitude of research has proven the effects of concussion on vision and the success of vision rehabilitation including:
Master CL, Scheiman M, Gallaway M, et al. Vision Diagnoses Are Common After Concussion in Adolescents. Clinical Pediatrics 2015;1-8.
Ciuffreda KJ, Kapoor N, Rutner D. Occurrence of oculomotor dysfunctions in acquired brain injury: A retrospective analysis. Optometry 2007;78:155-61.
Groce A, Bansal S. Optometric Management of Sports-related Post-concussion Visual Symptoms in Teenagers with Vision Therapy: A Case Series. Vision Development & Rehabilitation 2016;2(1):34-53.
Ciuffreda KJ, Kapoor N. Vision Disturbances Following Traumatic Brain Injury. Current Treatment Options in Neurology 2002;4:271-80.
Weiss LM. Visual-Vestibular Interaction in the Acquired Brain Injured Patient. J Optom Vis Devel 2002;33:33-41.
Suter p, Harvey l. (eds). Vision Rehabilitation: Multidisciplinary Care of the Patient Following Brain Injury. CRC Press:2011
Suchoff I, Han E, Craig S, Rutner,D, Kapoor N, Ciuffreda K. The Frequency of Occurrence, types and Characteristics of Visual Field Defects in Brain Injury: A Retrospective Analysis. J Am Optom Assoc 5/2008;79: 259-256.
Proctor A. Traumatic brain injury and binasal occlusion. OptVis Dev 2009;40(1):45-50.
Maino D. Neuroplasticity: Teaching an old brain new tricks. Rev Optom, 2009; 46(1):62-64,66-70.
Lachapelle, J., Bolduc-Teasdale, J., Ptito, A., McKerral, M., Deficits in complex visual information processing after mild TBI: electrophysiological markers and vocational outcome prognosis, Brain Inj, 2008;22, 265.
Ciuffreda KJ, Ludlam, Kapoor N. Clinical oculomotor training in traumatic brain injury. Optom Vis Dev 2009;40(1):16-23.
Craig S, Kapoor N, et al. Profile of Selected Aspects of Visually Symptomatic Individuals With Acquired Brain Injury: A Retrospective Study. J Behav Optom 2008;19:1-10.
Ciuffreda KJ, Kapoor N, Han Y. Reading-related ocular motor deficits in traumatic brain injury. Brain Inj/Professional 2005;2:16-20.