History

Concussions have existed as an important observation for hundreds of years, with a current PubMed search yielding articles from 1799 [1]. Sports Related Concussions (SRC) separated itself from the general term as a sports specific occurrence of concussion with articles arising by the late 1970's. Within the last 20 years concussions as a mild traumatic brain injury has been strongly correlated to certain neurodegenerative processes. In combat sports (primarily boxing) a phenomenon known as the ‘punch drunk’ phenomenon has been observed  for more than 100 years with a PubMed search today yielding the earliest records of medical 'punch-drunk syndrome' or traumatic encephalopathy accounts in 1934 [2]. It is described as having limited lower limb motor control, often in the right leg that remained, but didn't worsen, once boxing participation ended [2].
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This observation only existed in boxing group at the time, with the science machine ticking away looking for an explanation. By the mid 1950's concussion was identified as a risk factor.  Since then more connections between concussion and traumatic encephalopathy began surfacing, and early understandings of the disease process behind the punch-drunk syndrome emerged. By the early 2000's risk factors including concussions or mild traumatic brain injuries, genetic predispositions and lifestyle choices (i.e., opioid addiction, alcoholism and obesity) were identified as main drivers behind this degenerative progression [3]. Luckily, when excluding genetics the remaining risk factors (excluding the environmental impact of the epigenetic phenomenon) are modifiable, with lifestyle choices and concussion frequency being adjustable drivers behind this degenerative disease development. This blog will discuss the concussion risk factor.

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Mechanism

Initially, the concussion mechanism was thought to be one of coup contra-coup. That is, an impact to the head will cause an injury site at that location (figure 1: 2), with the momentum of this blow shifting the brain to the other end of the skull where it causes a secondary injury (figure 1: 4). This momentum shift results in two locations of injury in the affected individual after a single impact. (see figure 1)

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The observations into the mechanisms of concussion began to improve by the early 21st with modern investigations suggesting a 'shearing' between grey and white nerve cells during this 'coup contra-coup' occurrence as the primary mechanism of concussion [4]. In short, this impact would stretch the sensitive white matta or myelin based nerve cells. This stretch distorts and forces an electrical release by these cells, that triggers the surrounding cells in a domino's like fashion. Eventually this accumulated, fast electrical release sends the body into a shock state where unconsciousness can occur [4]. As the body attempts to return to homeostasis (or normal) the body has to work hard to balance the cells again chemically and metabolically, it is in this period that the body needs to heal unhindered by any further trauma [4].

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The pathology for concussion is explored further in the below text.

1)     Impact is made bending the spinal cord. This results in a vibration and stretch of both grey and white matta.

2)    Due to the different densities between the grey and white matta, two separate vibrations occur causing a shear between the two tissues mainly effecting the white matta. The white matta, the communication nerves in the brain, then release its neurotransmitter material into its surroundings. The neurotransmitter then tells other neural cells to excite and release their chemicals for action potential. This builds until a full neural cascade (a huge dominos collapse) of electrical signals have occurred [3].

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3)     This action potential cascade results in a mass efflux potassium and a mass influx of calcium and sodium. This initial change results in a sensory overload i.e., shaky legs. Additionally, inflammation mediators and fluid accumulate at the locations of over-stretch/damage resulting in an accumulation of excess fluid in the skull increasing skull pressure [4].

4)     CHEMICALLY: Once the Calcium enters the cell it successfully begins competing with magnesium. The calcium does this by attaching itself to the surrounding mitochondria more efficiently than the magnesium. This then reduces the cells capacity for normal ATP (energy) production [4].

5)     METABOLICALLY: The cells of the brain begin undergoing anaerobic respiration. This promotes lactate (as mentioned above) with potential to alter the blood brain barrier permeability (the barrier's filter capacity reduces) resulting in cerebral/brain oedema adding to the inflammatory fluid further increasing pressure in the skull. It is thought the accumulated oedema pressure reduces blood flow to the brain by up to 50%. This places the working mitochondria under further metabolic stress [4].

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6)    Once the cerebral blood flow has returned to normal and calcium levels begin to return to normal, all the magnesium ‘maned’ mitochondria are correctly operating the sodium pump ‘machines’ to remove the last bits of the residual calcium.

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The degree of injury is linked to the specifics of the initial traumatic blow (punch or other). The location of the strike and the force behind it i.e., rotational (a hook punch landing on the chin) or peak force (a straight right landing on the nose) offer different injury mechanisms and potentially types of concussions [5-7]. The hook punch to the chin may deliver a more rotational force that stresses the spinal cord in a whiplash fashion as compared to the straight right that may predominately influence the white matta in the brain. The difference in punch location may explain why not all concussions are the same, and the similarity between long lasting post-concussion syndrome and whiplash disorders [5].

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Management

Irrespective of injury mechanism, once a concussion has occurred the body attempts to return itself to homeostasis. If any further trauma were to be placed on the system whilst the body is non-homeostatic (i.e., from another concussion between steps 1 and 6) the calcium influx will be much greater than the initial concussion. This is academically considered a 'second impact scenario' where the recovery period is extended for months and can often prove to be fatal. It is believed the reduced cerebral blood flow lingers for longer, lactic acid continues to build ultimately prolonging the entire healing process [4]. Multiple concussions in a short window requires extended healing times in order to return the athlete back to normal. Identifying a concussion early not only encourages a better healing environment, but it allows athletes to return to competition sooner with much less complication.

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The return to sport after concussion and head trauma management is complex as these injuries involve the most complex organ of the body. The brain holds influence over general nerve function, mood, perception, balance, social inclination, pain, sleep and others [8-11]. Any suffers of concussion, especially symptoms associated with post-condition syndrome, should consult experts for management and treatment of these lingering conditions. The best settings includes a variety of treatment approaches involving a variety of healthcare professionals including Chiropractors, Dieticians, Physiotherapists, Optometrists, and Medical Doctors. Often these symptoms are very manageable, including symptoms that have been lingering for years.

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For individuals looking to minimise symptoms or reduce the risk of severe concussive episodes there is emerging data for certain dietary compounds including vitamin E, vitamin D, Omega 3, specific Magnesium supplements, isometric neck exercises and low intensity aerobic based exercise [12-16]. Neck strength has been demonstrated to reduce concussion risk, low intensity exercise promotes cerebral blood flow and the dietary compounds paired with exercise enact an anti-inflammatory effect that reduces the damage of neuro-inflammation. Other less tested treatments are showing promise but require more research to identify dosage, contraindications, and possible side effects in each group of people [17]. Current best practice guidelines suggest that exercise within certain heart rate thresholds have been excellent in the concussion recovery process. Whilst under supervision from a professional, it should be noted that once a concussion has occurred in most cases 2 - 4 days of active recovery i.e., walks etc should be encouraged before delving into light aerobic exercising [18].

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Future

The future of the management of concussions and traumatic brain injury is looking promising. As research continues into this space, we are identifying strategies to minimise its burden in contact and combat sports. As of the 24th of October (Australia time) the US National Institute of Health (NIH) has formally acknowledged a causal link between repeated blows to the head and Chronic Traumatic Encephalopathy (CTE). It is stated that symptoms of cognitive deterioration can occur years after impact exposure, so it is imperative in this time healthy lifestyle habits are maintained. Scientifically, we are able to identify risk factors, discuss mechanisms and are progressing to an efficienct way to diagnose CTE during life (as all cases have been confirmed on death). Because of CTE's connections between sub-concussive impacts it will be soon obligatory for contact and combat sporting governing bodies to minimise the rates of unnecessary head impact. Notwithstanding this preventive thinking, it is my opinion that the MANAGEMENT of CTE and probable CTE (and most brain health practices) will involve a similar trajectory to the osteoarthritis management.

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Formally, the presentation of degeneration in knees/hips etc use to warrant treatment and instil patient panic where, perhaps ignorant but manipulative clinicians would exploit for treatment. The current best practice guidelines now avoid or delay early invasive treatments and encourage the priority of healthy lifestyle living. Current best practice protocols like the GLA:D protocol offers an exercise, lifestyle based program with excellent non-surgical, non-panic based results. Further emerging research on the nature of inflammation suggests diet, habits and lifestyle greatly influence the residual inflammation (inclusive of neurodegenerative neuroinflammation) in a persons body. Further, it is known that exercise can reduce inflammation in the body and improve coordination, with a current popular form of management for parkinsonian patients includes a boxing exercise therapy that aims to rebuild this coordination [19].
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Recently I published an article titled ‘Epidemiology of injuries in amateur boxing: a systematic review and meta-analysis’ detailing the injury burden in amateur boxing [20]. In the article one of the main points raised was the very high likelihood that concussion injuries are being under-reported. By now I hope the importance of early intervention as the best form of intervention for currently affected persons is clear.

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The future of concussion and traumatic brain management sits in good hands with the continuation of good research and research transparency. If you have any questions or queries on concussions for yourself or a friend family member don't hesitate to reach out.

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Regards,

Alex
Combatsportschiro

The Combat Sports Chiropractor

References;

1)     Brown C. A Case of Concussion of the Brain, Which Terminated Fatally. Journal of Medical Physics. 1799;2(10):407-408.

2)     Parker HL. Traumatic Encephalopathy (`Punch Drunk') of Professional Pugilists. Journal of Neurological Psychopatholgy.1934;15(57):20-8.

3)     Phelps A, Mez J, Stern RA, Alosco ML. Risk factors for chronic traumatic encephalopathy: a proposed framework. In Seminars in Neurology. 2020;40(04):439-449.

4)     Giza CC & Hovda DA. The neurometabolic cascade of concussion. Journal of Athletic Training. 2001;36(3):228.

5)     Leslie O & Craton N. Concussion: purely a brain injury? Clinical Journal of Sport Medicine. 2013;23(5):331-2.

6)     Elkin BS, Elliott JM & Siegmund GP. Whiplash injury or concussion? A possible biomechanical explanation for concussion symptoms in some individuals following a rear-end collision. Journal of Orthopaedic& Sports Physical Therapy. 2016;46(10):874-85.

7)     Rebbeck T, Evans K, Elliott JM. Concussion in combination with whiplash-associated disorder may be missed in primary care: key recommendations for assessment and management. Journal of Orthopaedic & Sports Physical Therapy. 2019;49(11):819-28.

8)   Wetjen NM, Pichelmann MA & Atkinson JL. Second impact syndrome: concussion and second injury brain complications. Journal of the American College of Surgeons. 2010;211(4):553-7.

9)     Jaffee MS,Winter WC, Jones CC, et al. Sleep disturbances in athletic concussion. Brain Injury. 2015;29(2):221-7.

10)     Sandel N,Reynolds E, Cohen PE, et al. Anxiety and mood clinical profile following sport-related concussion: From risk factors to treatment. Sport, Exercise, and Performance Psychology. 2017;6(3):304.

11)     Valovich McLeodTC & Hale TD. Vestibular and balance issues following sport-related concussion. Brain Injury. 2015;29(2):175-84.

12)   Lewis MD. Concussions, traumatic brain injury, and the innovative use of omega-3s. Journal of the American College of Nutrition.20163;35(5):469-75.

13)   Lawrence DW, Sharma B. A review of the neuroprotective role of vitamin D in traumatic brain injury with implications for supplementation post-concussion. Brain Injury. 2016;30(8):960-8.

14)   Trojian TH, Wang DH & Leddy JJ. Nutritional supplements for the treatment and prevention of sports-related concussion—evidence still lacking. Current Sports Medicine Reports. 20171;16(4):247-55.

15)   Standiford L, O'Daniel M, Hysell M, et al. A randomized cohort study of the efficacy of PO magnesium in the treatment of acute concussions in adolescents. The American Journal of Emergency Medicine.2021;44(1):419-22.

16)   Leddy JJ, Haider MN, Ellis M et al. Exercise is medicine for concussion. Current Sports Medicine Reports. 2018;17(8):262.

17)   Khan SM, Carter GT, Aggarwal SK, et al. Psychedelics for brain injury: A mini-review. Frontiers in Neurology. 2021:1260.

18)  Ventresca M. The curious case of CTE: Mediating materialities of traumatic brain injury. Communication & Sport. 2019 Apr;7(2):135-56.

19)   Dawson RA, Sayadi J, Kapust L, et al.  Boxing exercises as therapy for Parkinson disease. Topics in Geriatric Rehabilitation. 2020;36(3):160-5.

20)   Alevras AJ, Fuller JT, Mitchell R, et al. Epidemiology of injuries in amateur boxing: a systematic review and meta-analysis. Journal of Science and Medicine in Sport. [pre-release].

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