Mild Traumatic Brain Injury (mTBI) and concussion syndromes have been a subject of increasing interest in both medicine and the media.
Notably, a report by the World Health Organization, International Collaboration on Mild Traumatic Brain Injury Prognosis 2014, states it is now considered a “prominent public health problem.”
As neuromuscular specialists, chiropractors see a significant percentage of a patient population with a history of traumatic head and neck injuries resulting in mTBI. These practitioners are uniquely positioned to diagnose and treat this health problem. Post-mTBI care, however, is plagued by limited treatment modalities.
An undiagnosed, untreated, and undertreated problem
In cases of mild TBI, the term “mild” refers to the severity of the initial physical trauma and does not indicate the degree of brain trauma or the severity of the consequences of the injury. These consequences frequently manifest as impairment of working memory and information processing speed.
Secondary symptoms include chronic headaches, anxiety, depression, insomnia, social withdrawal, seizures, and other indications of CNS dysfunction. These consequences may lead to long-term impairment in the perform- ance of activities of daily living (ADL) or even employability. An additional concern is neurodegeneration, which has become a serious concern in some subsets of mTBI patients.
The WHO report recommends that DCs only “facilitate a path to good recovery for mTBI patients through early education and positive reassurance as well as by providing treatments aimed at reducing associated spine and headache-related pain.” And it warns against “excessive diagnostic testing or applying diagnostic labels,” and suggests “integrating care with a patient’s primary medical physician is recommended if additional symptom- specific treatments are required (e.g., pain medication or neurocognitive testing).”
There are no effective alternatives in the pharmacological realm. Various anti-inflammatory, anti-depressant, and anti-apoptotic modalities may address symptoms, but there are no specific pharmacological agents to prevent the progression of secondary brain damage that may occur.
Compounding the matter, the AMA Guides to the Evaluation of Permanent Impairment, 6th ed., regarding “symptoms of mild traumatic brain injury,” indicates they “generally resolve in days to weeks, and leave the patient with no impairment.” This diminishes the legal and clinical importance of mTBI, especially in many work-related and motor-vehicle accident cases.
The impact of these factors may lead some clinicians to disregard or ignore the importance of proper diag- nosis, documentation, and treatment in cases of mTBI. This is especially problematic in cases that exhibit continuing post-concussion symptoms (PCS) that go undocumented or under- treated, leading to unrecognized impairment and preventable long-term disability.
During the evaluation of all patients with head or neck trauma, mTBI should be included in the differential diagnosis. It must be stressed that early recognition is key. Often the first clues are the symptoms a friend or a family member reports during the history.
Imaging studies such as MRIs, CTs, and X-rays, while often clinically indicated, are frequently negative. The definitive test is quantitative EEG (qEEG), or “brain mapping,” to evaluate and locate areas of injury to the brain.
Any history of head and neck trauma should include an evaluation for brain injury. Along with a detailed history, medical record review, and examination, a qEEG scan should be considered if mTBI is suspected. Early clues to an mTBI diagnosis can be gained from the history and patient symptoms.
Therefore, patients should be educated in the signs of mTBI and encouraged to report them to the treating physician. These may include:
- Any loss of consciousness up to 30 minutes
- Any loss of memory of events immediately before or after the accident (up to 24 hours)
- Any alteration of mental state at the time of the accident (e.g., dazed, disoriented, or confused)
- A Glasgow Coma Scale score falling below 13 after 30 minutes (review ER records)
- Dizziness or vertigo
- Lack of awareness of surroundings
- Nausea with or without memory dysfunction
- Persistent low-grade headache
- Poor attention and concentration
- Excessive or easy fatigue
- Intolerance of bright light or difficulty focusing
- Intolerance of loud noises
- Ringing in the ears
- Anxiety and depressed mood
- Irritability and low frustration tolerance
DCs have attempted to address mTBI through alternatives to pharmacological agents. Research has shown that a ketogenic diet and supplementary support, such as PQQ, reduced CoQ10, hydroxyl and adenosylcobalamin, NAC, magnesium threonate, curcumin, pregnenolone, DHA, riboflavin, L- carnitine, and resveratrol work well in supporting the brain’s recovery from an injury.
Post-graduate programs and the functional neurology paradigm focus on considerations for metabolic and neurological functioning. They address biochemical variables that are critical for brain recovery and combine with rehabilitation, positive neuroplasticity, and neural reprograming. While these are promising and targeted at the underlying disturbances of brain chemistry and function, this approach can be complex and require expensive training limited to a relatively few chiropractic specialists.
Diagnosis and intervention with LLLT
When patients report these symptoms, additional evaluation should include a detailed neurological examination and qEEG. This will bring out clinical evidence of brain injury. A neuropsychological assessment is typically used to assess the functional impact of a mild brain injury. A cognitive evaluation by a skilled clinician with formal neuropsychological training can be helpful.
Diagnostic studies such as brain imaging with CAT scan, MRI, and single-photon emission computed tomography (SPECT) often add little diagnostic information and are generally not recommended without other concerns (e.g., hemorrhage or hemorrhagic stroke). History, examination, and symptoms may correlate with and help identify areas of brain injury and confirm with qEEG brain mapping.
With the areas of injury suspected or identified, begin early and aggressive intervention to limit damage and reduce the long-term effects of brain trauma. Research has demonstrated low level laser therapy (LLLT) delivered transcranially to be both safe and effective in the treatment of mTBI and other conditions of the central nervous system.
Moreover, suspected areas of injury can be safely addressed with LLLT before they are confirmed by qEEG. The effects of near-infrared light are only manifested in injured or hypoxic neurons; they do not adversely affect healthy tissue.
Many chiropractors recognize the effectiveness of LLLT in treating neuromusculoskeletal conditions but have not realized its transcranial potential. Current research is a wake-up call for doctors of chiropractic to consider transcranial LLLT in mTBI cases.
Daniel J. Bourassa, DC graduated summa cum laude from Life College in 1989 and is currently in the medical studies program at USAT. He is a past expert medical advisor for the Florida Division of Worker Compensation. He was a member of the editorial review board of the Journal of Sports, Chiropractic and Rehabilitation and has authored several articles on nutrition, rehabilitation, and low level laser therapy. He can be contacted at email@example.com.
1 Donovan J, Cancelliere C, Cassidy JD. Summary of the findings of the International Collaboration on Mild Traumatic Brain Injury Prognosis. Chiropractic and Manual Therapies. 2014;22:38.
2 Crownfield P. Understanding the Injured Brain—J. David Cassidy, DC, PhD, DrMedSc, talks mild traumatic brain injury and the latest findings. Dynamic Chiropractic. 2014;32(13).
3 Dean P, et al. Long-term effects of mild traumatic brain injury on cognitive performance. Front Hum Neurosci. 2013;7:30.
4 Gavett B, et al. Mild traumatic brain injury: a risk factor for neurodegeneration. Alzheimers Res Ther. 2010;2(3):18.
5 Roozenbeek B, et al. Changing patterns in the epidemiology of traumatic brain injury., Nature Reviews Neurology. April 2013;9:231-236.
6 Karu TI. (2003). “Low-power laser therapy.” In: Vo-Dinh T, editor. Biomedical Photonics Handbook. Vol. 48. (pp. 7-20). London: CRC Press.
7 Karu T. Molecular Mechanism of the Therapuetic Effect of Low-Intensity Laser Radiation. Lasers in Life Sciences. 1988;2(1):53-74.
8 Xuan W, et al. Low-level laser therapy for traumatic brain injury in mice increases brain derived neurotrophic factor (BDNF) and synaptogenesis. J. Biophoton., 2015;8(6):502-11.
9 Carroll L, et.al. Systematic Review of the Prognosis after Mild Traumatic Brain Injury in Adults: Cognitive, Psychiatric, and Mortality Outcomes: Results of the International Collaboration on Mild Traumatic Brain Injury Prognosis. Archives of Physical Medicine and Rehabilitation. 2014;95(3 Suppl 2):S152-73.
10 Bikson M, et al. Safety of Transcranial Direct Current Stimulation: Evidence Based Update 2016. Brain Stimulation. 2016;9:641–661.
11 Huang Y, et al. Low-level laser therapy (810 nm) protects primary cortical neurons against excitotoxicity in vitro. J. Biophoton. 2014;7(8):656-64. doi:10.1002/jbio.201300125.
12 Gonzalez-Lima F, et al. Protection against neurodegeneration with low- dose methylene blue and near-infrared light. Front Cell Neurosci. 2015;9:179.
13 Hernandez-Ontiveros DG, et al. Microglia activation as a biomarker for traumatic brain injury. Front. Neurol., 2013;26(4):30.doi: 10.3389/fneur.2013.00030.
14 Khuman J, et al. Low-Level Laser Light Therapy Improves Cognitive Deficits and Inhibits Microglial Activation after Controlled Cortical Impact in Mice. J Neurotrauma. 2012;29(2):408-17.doi: 10.1089/neu.2010.1745.