Concussion – A Therapeutic Solution

Author: Fred Kahn MD, FRCS (C)

Source: Meditech International Inc.

Currently episodes of concussion, also known as Traumatic Brain Injury (TBI), continues to present a major therapeutic challenge. Characterizing its underlying, somewhat complex pathologies remains a central topic in the never-ending quest to find an effective solution. Brain injuries are more prevalent than is statistically recorded and are not always followed by a visit to the practitioner’s office. When the latter does occur, all too frequently the patient is advised to “take some aspirin for the headaches and not to worry too much about the other symptoms as they will get better over the course of time”. Unfortunately, complete recovery occurs in less than 50% of the cases that demonstrate symptoms and the severity of the incident can often impact the patient’s cognitive abilities and impair their quality of life for indeterminate periods of time.

Immediate and chronic symptoms can include headaches, an inability to focus, short and long term memory loss, visual disturbances, depression and coma1. The Glasgow coma scale classifies concussions based upon the level of consciousness of the patient1,3. Mild concussion typically allows for full neurological recovery; moderate concussion can result in stupor, lethargy and a comatose state and severe concussion patients have experienced a comatose state, heightened risk of hypotension, hypoxaemia and brain edema3. Sometimes symptoms are simply described as “brain fog”. It should be noted that associated pain may often be most pronounced over the cervical spine, accompanied by radiation of pain to the upper extremities. Generally, mild, moderate and severe concussion results in varying degrees of inflammation and consequential pain affecting both physical function and the patient’s intellectual status3. Moreover, it has been determined that MRI, PET and EEG scans may not reveal any obvious abnormalities as macroscopic changes in the brain do not always accompany the symptoms of concussion. Many therapies are available, yet few are effective on a scalable basis; most typically these include analgesics that relieve the pain without addressing the underlying causes of the primary and secondary injuries. Whereas, diagnostic measures have improved in recent years, therapeutic solutions are either non-existent or remain elusive, at best.

In the era of neuroplasticity, retraining of neurological pathways can be achieved over time but this approach can only be applied in a somewhat limited manner.

glasgow_scale Table 1. The Glasgow Coma Scale. This scale is utilized to distinguish the severity of injury such that Mild Injury results in a score of 13-15 Points; Moderate Injury results in a score of 9-12 Points and Severe Injury results in a score of 3-8 Points.

At Meditech, based on our experience and the results achieved in a growing number of cases, we stipulate that Laser Therapy applied in the 660-1000 nm range, encompassing both Red and Near Infrared LEDs incorporated in large surface arrays and laser diodes in proper sequence, enables us to demonstrate a higher than anticipated level of relief in the majority of patients treated. To continue on this path of endeavor, properly engineered Laser Therapy Systems must be utilized. These devices require standardization and light-emitting diodes that can deliver an accurate, reproducible photon stream at each treatment session. Only in this manner can complete resolution of symptoms be realized. Whereas standard treatment protocols have been determined, considerable individualization of application must occur. In addition, the process requires co-operation between the clinician and the patient. The latter in particular must understand that the course and direction of the therapy inevitably leads to improvement if the rules of compliance are followed.

At our clinics we have been able to accommodate a significant number of patients and have increased the scope of our therapeutic initiatives. We fully appreciate the opportunity to develop effective treatment plans supported by a number of neuroscientists, neurologists and clinicians interested in finding better solutions. Much has been accomplished and more remains to be done. Notwithstanding these factors, an effective course of action has been charted and clearly this is a significant first step in the right direction.

The Pathophysiology of Concussion

Primary focal damage to the cranium and/or the cervical spine comprise the initial injury, characterized by contusion, laceration and possibly haemorrhage1,2. Mechanical shaking of the head including acceleration; deceleration and rotational movements can induce a cascade of neurochemical changes within the first 24-48 hours following the incident2. These types of mechanical challenges can occur with or without direct impact3. Neuronal cell membranes are disrupted and these cells experience axonal stretching which contributes to a disruption in ionic homeostasis1–3. There is an indiscriminate release of neurotransmitters and excitatory amino acids which contribute to a disruption in ionic homeostasis and ion flux, including calcium influx and consequent disruption of membrane depolarization and oxidative phosphorylation2,3. The disruption of the electron transport chain is accompanied by a depletion of nicotinic coenzymes and the exhaustion of the Na+/K+ adenosine triphosphate pumps5–7. There is a diminished ATP supply from oxidative phosphorylation, heightened oxygen-independent energy production by glycolysis and a consequent accumulation of lactic acid5. Calcium and sodium ion influxes coupled with malfunctions in the mitochondria contribute to an increased production of lipid peroxidase, proteases, phospholipases and a heightened state of oxidative stress2. The release of caspases can also occur, which collectively contributes to increased potential for damage or death of cells4.

figure2 Figure 2. The Mechanics of Concussion. A normal healthy brain exists cushioned by cerebrospinal fluid within the skull. While cerebrospinal fluid facilitates some lubrication and support to mitigate the impact of normal movements it is less effective at preventing the consequences of a more significant impact (b). Furthermore, secondary impacts can result following a concussion event, exacerbating the preliminary effects (c). These acceleration; deceleration and rotational movements can induce a cascade of neurochemical changes and an increased potential for neuronal cell loss (d).

Low Intensity Laser Therapy

Over the past seven years there has been a growing interest in the efficacy of Low Intensity Laser Therapy (LILT) in the treatment of concussion. LILT utilizes light energy to produce biological effects in tissues. LILT has been recognized for its high safety profile and has been used therapeutically in humans for more than 4 decades without the report of any adverse side effects8–10. While the therapeutic potential has not yet been fully established for pathologies of the brain, there have been a growing number of promising studies to date providing insight into the long-range therapeutic potential of Laser Therapy for TBIs.

A case study published in 2012 by Stephan et al., presented the efficacy of administering five treatments at a wavelength of 905nm and an average power of 50mW over a two week period to address the migraines that developed in a 25 year old male as a consequence of a TBI that had occurred two years prior12. Naeser et al (2011), also present two case studies describing the effective utility of concurrent administration of 870nm and 633nm light to the midline sagittal area of the head to address sustained attention deficits and deficits in executive function11. These secondary injuries from concussions were treated with laser therapy 7 years and 3 years post trauma respectively11. These preliminary investigations support the utilization of LILT in the treatment of the secondary injuries commonly associated with concussion and therein its capacity to assist with rehabilitation leading to normal lifestyles. Herein, we discuss two clinical cases of individuals who had suffered the long term disabling consequences of concussion and clearly demonstrate the efficacy of LILT to alleviate their symptoms.

figure3 Figure 2. Axonal Shearing. The brains rotational movement in concussion can result in damage to both axons and their myelin coverings.


June 9, 2014:

The Patient, a 17-year-old student, who complained of concussion-type symptoms since September 2013. At that time, she headed a soccer ball, which resulted in the diagnosis of concussion. In March 2014 while skiing downhill, she collided with another individual. The contact was head-on. She did not recall whether there was a specific loss of consciousness after the second event, however symptoms became acute shortly after this episode and had persisted. They consisted of daily headaches, memory loss, irritability, inability to concentrate, vertigo, fatigue, irregular sleeping patterns and blurry vision. Following the second concussion, this patient was unable to continue to attend school and missed a total of 16 weeks of attendance.

She consulted several specialists including a neurosurgeon who provided some vitamins and trained her in meditation. This was helpful in relieving symptoms to some degree and occasionally arresting the headaches. The latter were primarily located in the fronto-temporal area and were predominant on the right side. She generally goes to bed around 11 pm but is unable to sleep until 3 am and then sleeps until 10 am, with periodic interruptions. The patient had also undergone a course of acupuncture over a 5 week period, osteopathic manipulation, massage and chiropractic therapy, none of which provided any benefit.

Physical Examination:

The patient was right-handed. The right grip was 70 lbs and the left, 50 lbs. There was a normal range of motion of both shoulders. Flexion, extension, lateral rotation and lateral flexion of the cervical spine was only 60% of normal. A moderate degree of paracervical muscle spasm was noted to be present. There was no evidence of motor impairment or sensory deficit. Reflexes were within normal limits.


  • Cerebral Concussion.
  • Myofascitis – Cervical Spine.

Course Of Therapy:

Laser Therapy was applied to the cervical spine, including the brainstem and cerebellum. Treatment was administered from June 13, 2014 until July 5, 2014.

Outcome Of Treatment:

After the initial 3 treatment sessions, the patient indicated that she had not experienced any headaches in the past 2 days. She also was able to sleep for 6 hours without interruption. After 5 treatments, the headaches had disappeared completely and the range of motion of the cervical spine had improved to 80% of normal.

The final evaluation was performed on July 5, 2014. After 10 Laser Therapy treatments all symptoms relating to the episodes of brain trauma had disappeared completely, with the exception of a mild degree of persisting long-term memory loss. Overall, the loss of memory had been reduced by 80% and improvement was continuing. The range of motion of the cervical spine had returned to normal and no tenderness or muscle spasm was evident. The patient was obtaining 8 hours of deep sleep each night without interruption and returned to the gym 4 days ago resuming her exercise programme. She planned to return to school in September and was not utilizing any medication at that time.


July 9, 2014

The patient, a 53-year-old bank executive specializing in marketing strategies at a major bank. Her history revealed that while at work she forcefully extended the cranium and the cervical spine when she laughed explosively and in moving these structures backwards rapidly, the occiput collided forcibly with the unyielding sharp edge of a corner in the wall. This event occurred four years ago. The noise generated by the contact could be heard two offices away. She has not been able to work subsequently.

After this event she was momentarily dazed, however the majority of her symptoms began gradually over the next 48 hours and additional symptoms continued to develop over the course of the first year. These included disruptive sleep patterns, progressive fatigue, memory loss both short and long-term, difficulty finding appropriate words, an inability to focus or concentrate and fuzzy vision, sometimes so severe that it felt as if she were going blind. Her thought processes were often confused and she began to experience “silent headaches” that presented on most days and would last for many hours, sometimes extending to the following day. The patient described these episodes as an “aura-type” syndrome where she would see small coloured lines that expanded from a central small area to a large C as time progressed. This process had a debilitating effect, however the problem was partially controlled with a variety of medications including Nortriptyline, Gabapentin, etc. These events, which occurred at least 5 times each week, were quite disturbing and caused severe depression. The headaches, although relatively acute early on, were largely disregarded. Moreover, the patient complained of fatigue most of the time.

Physical Examination:

The patient was right handed. The right grip was 32 lbs and the left 5 lbs. Range of motion of the cervical spine with regard to flexion, extension, lateral rotation and lateral flexion was less than 20% of normal. Significant paracervical muscle spasm was noted to be present extending over both the cervical and thoracic spine. The degree of tenderness over the occiput and cervical spine was relatively severe and extended to the T6 level. Lateral abduction of both shoulders was to 50° only. There was significant tenderness over both shoulder joints. No overt neurological abnormalities were identified.


  • Cerebral Concussion.
  • Myofascitis/Degenerative Osteoarthritis – Cervical, Thoracic and Lumbar Spine.
  • Diabetes Mellitus (the patient had diabetes which was under control utilizing Metformin).
  • Multiple Soft Tissue Injuries.

This case is somewhat unusual as none of the physicians who initially attended the patient entertained the diagnosis of concussion, despite the fact that the latter was the most significant component of her injury. Not until she consulted a specialist almost a year post-trauma was this diagnosis seriously considered. Initially the primary injury had been described as a severe sprain of the soft tissues of the neck. Analgesics and anti-inflammatory medications, along with a prolonged course of injections to the cervical spine region at frequent intervals were utilized to treat her problems and no particular attention was given to the brain injury.

The patient herself, although she agreed with the diagnosis of the neck problem, thought that the primary damage had occurred in what she believed to be the “pain centre” of her brain and this was partially confirmed by the symptoms of acute pain in the neck with subsequent extension to the thoracic and lumbar spine and radiation to all the extremities.

Course Of Therapy:

Initially Laser Therapy was applied to the cervical spine, including the brain stem and cerebellum and gradually extended to the thoracic spine and eventually the lumbar spine. Therapy was instituted on May 14, 2014, on the date of presentation and is still continuing at time of writing, July 19, 2014, on a bi-weekly basis.

Outcome Of Treatment:

At the time of this patient’s most recent evaluation on July 19, the majority of her symptoms had either disappeared or have been substantially reduced. Her chronic fatigue, which was at times almost paralyzing, is gone and has been replaced by new found energy expressed by resuming driving, trips to the gym and travel to more distant points. Sleep patterns have normalized as anxiety and depression have been completely relieved. Her memory loss and ability to concentrate continue to improve and recovery is in excess of 75% of normal capacity. The headaches had diminished in intensity since her 10th treatment session out of a total of 20 treatments to date. The periods of complete relief between headache incidence has increased to several days.

At the time of her initial presentation, the patient was ingesting a total of 9 medications daily in various dosages. Currently, she is only utilizing 4 of these pharmaceuticals and another 2 should be eliminated over the next month. There have been no withdrawal symptoms.

Her recovery process at this time is 85% complete from a global perspective and is continuing to improve with ongoing treatment. The prognosis, both short and long term, is positive and should result in a normal state of health based on the encouraging progress to date.

It is anticipated that the patient should be able to return to work, if she so desires, in a year at most. The most salient feature of this case is the frequent failure to diagnose concussion at the time of injury and institute effective therapeutic solutions at an early stage.

Review Of Research Articles:

The parameters that were selected for use in these cases are founded on our clinical experience. However, there are a number of pre-clinical investigations that have been performed that strongly support our choice of protocols and the regimen of therapy applied. While continuous and pulsed light have both demonstrated efficacy in a mouse model of TBI, 10Hz pulsing has been shown to be particularly advantageous relative to 100Hz or continuous wave producing reduced neurological severity scores22. It has been determined that a one time LILT administration at 810nm and 660nm are the most effective wavelengths to elicit a therapeutic response13–15. 730nm and 980nm were less effective14,15. In two subsequent studies, it was determined that one time laser treatment or three treatments (over three days) provided accelerated healing in mice who had experienced a controlled cortical focal impact16,17. However, when the treatment is continued for 14 days this therapeutic effect is lost16. These studies emphasize the need for monitoring the patient response to therapy and not prolonging treatment beyond the necessary period required to produce an optimal clinical response. In clinical practice, we often experience significant variations in the patient population treated.


Light energy at 660nm and 830nm have been shown to be absorbed by cytochrome c of the electron transport chain, wherein it facilitates ATP production providing the necessary energy for the healing and repair of tissues18. There is a large foundation of evidence that has demonstrated that LILT can alleviate inflammation and offer an analgesic effect19,20. In addition, it has also been shown to promote neuron regeneration21. Collectively, these features of LILT suggest that its therapeutic effect is well aligned to resolve the signs and symptoms resulting from primary injuries to the brain. This paper should serve to stimulate wider utilization of Laser Therapy in the treatment of TBIs and associated injuries.


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  2. Werner, C. & Engelhard, K. Pathophysiology of traumatic brain injury. British Journal of Anaesthesia 99, 4–9 (2007).
  3. Greve, M. W. & Zink, B. J. Pathophysiology of traumatic brain injury. (2009). doi:10.1002/msj.20104
  4. Ghajar, J. Traumatic brain injury. (2000). at
  5. Barkhoudarian, G., Hovda, D. & Giza, C. The molecular pathophysiology of concussive brain injury. Clinics in sports medicine 30, 33–48, vii–iii (2011).
  6. Mustafa, A. G. & Alshboul, O. A. Pathophysiology of traumatic brain injury. (2013). at
    Signoretti, S., Lazzarino, G., Tavazzi, B. & Vagnozzi, R. The pathophysiology of concussion. (2011). doi:10.1016/j.pmrj.2011.07.018
  7. Mester, E, Spiry, T, Szende, B & Tota, J. G. Effect of laser rays on wound healing. The American Journal of Surgery 122, 532–535 (1971).
  8. Avci, P. et al. Low-level laser (light) therapy (LLLT) in skin: stimulating, healing, restoring. Seminars in cutaneous medicine and surgery 32, 41–52 (2013).
  9. Tuby, H., Hertzberg, E. & Maltz…, L. Long-term safety of low-level laser therapy at different power densities and single or multiple applications to the bone marrow in mice. (2013). doi:10.1089/pho.2012.3395
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