The Role for Chiropractic Evaluation
and Treatment of Concussion Patients

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On November 14, 2015 favored Ultimate Fighting Champion Ronda Rousey was knocked unconscious by her underdog opponent Holly Holm. The internet is littered with video of the knockout. It occurred as a consequence of a single kick by Holm to Rousey. The kick was not delivered to Rousey’s head. It was delivered to her neck.

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The principles of inertia have always been with us, but they were not officially acknowledged through publication until Sir Isaac Newton wrote the book Mathematical Principles of Natural Philosophy in the year 1687.

Inertia is the resistance of a physical object to any change in its state of motion or to its state of rest. As often stated, an object in motion will remain in motion unless an outside force acts upon that object. Likewise, an object at rest will remain at rest unless an outside force acts upon that object.

It is now accepted that Newton’s Laws of Inertia apply to the human body. Different parts of the human body have different inertias between them. Specific to this discussion are the inertial differences between a human’s trunk and head. A classic actual-life example of these inertial concepts is the rear-end motor vehicle collision.

In a rear-end motor vehicle collision, the struck vehicle, its seat, and trunk of the occupant are quickly propelled forward, while the head, having its own inertial mass, will remain at rest. Thus, the head remains still while the body is moved forward, under the head. This gives the appearance that the head is extending upon the trunk, the so-called “hyperextension” phase of a rear-end motor vehicle collision.

Neck Hyperextension As Trunk Is Pushed Under Head

Under these circumstances, the most vulnerable body part to injury is not the trunk nor the head, but rather the part of the body that balances these two larger inertial masses to each other, the neck. Because of the large inertial masses of the trunk and the head, the neck is historically very vulnerable to “inertial injury.” In this context, an “inertial injury” means that there is no direct blow or contact injury to the neck.

The inertial loads to the neck occur in both extension and flexion directions. In a rear-end collision the neck/head complex first extends, followed by a “rebound” flexion (1, 2, 3). Or, in a head-on collision (or the hitting of a stationary object such as a tree or wall), the neck/head complex first goes into flexion (1, 2, 3).

Also specific to this discussion is the fact that in the neck exists the spinal cord and the spinal cord is attached to the brainstem and brain. As the neck experiences inertial loading, so does the spinal cord and tissues the spinal cord are contiguous with. In flexion, whether rebound or initial, there is a significant tractional/tension load to the spinal cord (4).

History

1867 and 1885 and 1928

With the dawn of moving humans around in wheeled vehicles there has been a paralleling increase in the reports of inertial injuries to the neck from accidents involving those vehicles. In 1867, a book detailing these inertial injuries subsequent to train crashes was published (5). In 1885, a surgeon from London, England, published a 397-page book titled (6):

Injuries of the Spine and Spinal Column
Without Apparent Mechanical Lesion, and Nervous Shock
in their Surgical and Medico-Legal Aspects

As there were no automobiles in 1885, this book also highlighted injuries from train accidents. This book includes chapters on “Concussion of the Spinal Cord” and “Concussion of the Spine.”

The first official medical paper pertaining to automobile collision cervical spine inertial injuries was published in 1928 (7).

1940 and 1941

Derek Denny-Brown (1901-1981) was a New Zealand-born physician and neurologist whose distinguished career took him to Oxford, Yale, and Harvard. In 1940, Dr. Denny-Brown and colleague published a study in the Journal of Physiology titled (8):

Experimental Cerebral Concussion

In this study, the authors note that the signs and symptoms of a brain concussion could be established in animals subjected to acceleration/deceleration loads and in animals (monkeys) in which their brain had been surgically removed (the decerebrate animal). The authors reported that the injury had to be to the spinal cord and/or the brain stem. They stated:

“Acceleration in movement resulting from the blow is the essential factor in the stimulus, for if the head is prevented from moving when struck the phenomenon fails to occur.”

“The nervous effect of a blow is thus considered to be due to the physical acceleration directly transmitted to each and every centre.”

The authors further stated that the following structures played no part in the post concussive syndrome:

• Deformity of the skull
• Labyrinthine stimulation
• Rise of intracranial pressure

The following year, 1941, Dr. Denny-Brown and colleague update these concepts the Proceedings of the Royal Society of Medicine (9). In this study they coin “acceleration concussion” which “occurs in all brain-stem mechanisms examined and is brought about at and beyond a threshold value of change in velocity [acceleration]”.

1957

Kirk V. Cammack, MD, from the Hurley Hospital, Flint, Michigan evaluated 50 consecutive whiplash cases. He published the results in the American Journal of Surgery in an article titled (10):

Whiplash Injuries to the Neck

Dr. Cammack notes:

Cerebral concussion primarily occurs during the deceleration (flexion) phase to the occipital areas of the brain, “accompanied by the torsion of the brain stem.”

30% of the subjects had signs of cerebral concussion.

Initial concussion symptoms range from mental confusion or headache to loss of consciousness.

20% of the subjects had persistent symptoms (lasting more than a month) consisting of headache, vertigo and inability to concentrate.

Concussion symptoms may still be present after two years.

1960

An article was published in the Journal of Neuropathology and Experimental Neurology titled (11):

Specific Cord Damage at the Atlas Level as a
Pathogenic Mechanism in Cerebral Concussion

Thirty-two cats were purposefully head injured with the following findings/conclusions:

“Considerable damage was found in the thick fibers at the ventral surface of the upper segments of the cervical spinal cord.”

“These changes decreased considerably towards the medulla oblongata and showed maximal damage caudally from the first spinal segment. This typical distribution implies a confined damage at the level of the atlas.”

“X-ray investigations revealed flexion or strain of the cervical cord around the odontoid process. This flexion acts in forced changes of position of the head and may operate as a damaging mechanism. It is suggested that a subluxation of the odontoid process might enhance this mechanism.”

These findings “agree with the findings of Denny-Brown and Russel (9) who obtained concussion even in the decerebrate animal. The term ‘brain’ concussion would definitely be wrong if the above assumptions are correct.”

“Significant fiber damage was found in serial studies of the cervical spinal cord,” and “the damage was maximal at the atlas level but sparse above this level.”

“It seems more than reasonable to assume a specific cord injury at the atlas level is behind at least many instances of so called ‘brain’ concussion.”

“A specific mechanism of cord injury at the atlas level seems responsible for many instances of so called ‘brain’ concussion.”

1998

Researchers from the Department of Bioengineering, University of Pennsylvania, published a study in the journal Spine titled (12):

In Vivo Human Cervical Spinal Cord
Deformation and Displacement in Flexion

The human cervical spinal cord was measured in five volunteers during flexion of the neck using a magnetic resonance imaging technique. Animal studies demonstrate that at full flexion that the entire cervical cord elongates approximately 10% of its length from a neutral position. This is the first such study measuring spinal cord tension performed on living human subjects. The authors concluded:

“The cervical cord elongates and displaces significantly during head flexion in human volunteers, offering valuable information regarding the normal milieu of the cord.”

2018

Researchers from Wayne State University, Detroit, Michigan, published a study in the journal BMJ Open Sport & Exercise Medicine titled (13):

Concussion with Primary Impact to the
Chest and the Potential Role of Neck Tension

These authors note that most biomechanical research on brain injury focuses on direct blows to the head. Yet, they propose that a blow to the chest could cause an inertial flexion of the head/neck complex resulting in concussion-type injury. They also note that there are few studies on concussion with primary impact to the chest resulting in neck injury. They state:

“Studies that indicate craniocervical stretch could be a factor in concussion by causing strain in the upper spinal cord and brainstem.” 

The objective of this study was to assess the biomechanical responses to strain in the upper cervical spine and brainstem from impact to the chest in American football. The study involved four phases:

• Chest impact testing on a helmeted stationary anthropomorphic test device (ATD).
• Chest impact testing on an un-helmeted stationary anthropomorphic test device (ATD).
• A study of two NFL game collisions resulting in concussion to estimate the biomechanical forces in real-life collisions.

In these cases, the primary impact was to the chest, and the player experienced a concussion with a delayed return to play.

• A finite element study was also conducted to estimate the elongation of the cervical spine under tensile and flexion loading conditions.

Studies show that during maximum cervical spine flexion there is a caudal (downward) displacement of the spinal cord relative to the spinal column, “indicating that stretch of the spinal cord (above C5) and brainstem occurs.”

Animal studies have shown signs of neuropathology in the upper spinal cord and brainstem in response to a distraction load in a non-impact condition. These studies “concluded that craniocervical distraction (tension) and flexion are the most important factors in concussion.”

“Studies have produced signs of cerebral concussion, hemorrhages on and contusions over the surface of the brain and upper cervical cord by rotational flexion displacement of the head on the neck, without direct head impact.” These studies concluded that rotational flexion-extension acceleration of the head, flexion-extension-tension of the neck and subsequent intracranial pressure gradients development are causative factors in concussion.

Human studies have also shown concussion with loss of consciousness without impact to the head. These injuries often showed primary shoulder-to-chest contact. The proposed mechanism is angular accelerations (flexion/extension) to the head-neck complex, such as would be experienced in a whiplash inertial injury.

Studies on the head and neck of pilots who ditch in the ocean showed that the “added weight of a helmet” resulted in spinal “cord concussion due in part to upper cervical cord stretch during the combined vertical acceleration and forward deceleration of the aircraft.” This would be a spinal cord tension and flexion mechanism. Studies show that the “mass of the helmet aggravates the potential for injury by adding bending, axial and shear loads at the craniocervical junction. There is a 40% increase in upper neck tensile forces in the helmeted compared with un-helmeted impacts of equal severity. This suggests that wearing a helmet increases the loading on the brainstem and cervical spinal cord.

Neck tension increases with flexion of the head relative to the torso. The helmeted anthropomorphic test device had a 40% increase in neck tensile force and an 8% increase in neck flexion angle when compared with an un-helmeted anthropomorphic test device. This case study indicated that the neck tension in the injured players exceeded tolerable levels from volunteer studies. The helmet mass increased the effective mass of the head by 47% compared with the un-helmeted head. “This resulted in significantly greater neck forces and movements when compared with the un-helmeted impacts.” “The mass of the helmet added to the head can increase the strain at the craniocervical junction.”

The finite element analysis estimated that the strain along the axis of the upper cervical spinal cord and brainstem was 10%–20% for the combined flexion and tension loading in the two cases presented, indicating that the “strain in the upper spinal cord and brainstem from neck tension is a factor in concussion.” The maximum strain in the vertebral column occurred in the upper cervical spine (C1–C2).

These authors note:

“The axonal strain in the spinal cord and brainstem exceeds the levels that have been documented to cause changes in functional and structural response in spinal nerve roots when stretched in tension at varying strain rates.”

“The strains are similar to those documented in in vivo tests with primates which resulted in functional changes in the spinal cord as well as changes in heart rate and respiration.”

“Craniocervical stretch resulting from tension and flexion in the upper cervical spine has been reported to be an important factor in concussion.”

“Neck tension and head flexion have each been shown to result in strain of the upper cervical spinal cord and the brainstem.”

“Tension generated in the spinal cord can be transmitted from the spinal cord to the brainstem.” “The largest elongation occurred in the medulla.”

The loss of consciousness in football players is consistent with these injuries to the brainstem.

The neck tensions documented in this study “apparently resulted in injury to the upper cervical spinal cord and medulla.”

Other studies “have indicated that strains in the upper spinal cord and brainstem are important factors in concussion.”

“Neck tension or strain along the axis of the upper cervical spinal cord and brainstem is a possible mechanism of brain injury.”

This study is quite important for chiropractors as it suggests that tackle impacts can cause head-neck flexion-tractional inertial injuries to the brainstem and upper cervical spinal cord, resulting in the concussion syndrome. In such cases, management of the cervical spine may greatly improve clinical outcomes. This appreciation and approach was published in a study in 2015 in the journal The Physician and Sports Medicine titled (14):

The Role of the Cervical Spine
in Post-concussion Syndrome

This paper reviews the existing literature surrounding the numerous proposed theories of post-concussive syndrome and introduces another potential, and very treatable, cause of this chronic condition; cervical spine dysfunction due to concomitant whiplash-type injury.

The authors discuss the cases of 5 patients with diagnosed post-concussive syndrome, who experienced very favorable outcomes following various treatment and rehabilitative techniques aimed at restoring cervical spine function. The treatment included chiropractic spinal manipulation.

These authors propose that a cervical injury, suffered concurrently at the time of the concussion, acts as a “major symptomatic culprit in many post-concussive syndrome patients.”

Concussion injuries, or mild traumatic brain injury, have an estimated prevalence of 3.8 million per year in the United States. Concussions are one of the least understood injuries facing sports medicine and neuroscience today.

The post-concussion syndrome is the chronic phase of concussion. The patient is considered to be chronic when symptoms persist longer than 4-12 weeks. This occurs in about 10–15% of concussed patients. These patients may develop persistent symptomatology lasting weeks, months or even years after injury.

Significant concepts in this study include:

“Any significant blunt impact and/or acceleration/deceleration of the head will also result in some degree of inertial loading of the neck potentially resulting in strain injuries to the soft tissues and joints of the cervical spine.”

“Acceleration/deceleration of the head–neck complex of sufficient magnitude to cause mild traumatic brain injury is also likely to cause concurrent injury to the joints and soft tissues of the cervical spine.”

It is “well established that injury and/or dysfunction of the cervical spine can result in numerous signs and symptoms synonymous with concussion, including headaches, dizziness, as well as cognitive and visual dysfunction; making diagnosis difficult.”

It has been known since 2006 that brain-injured athletes concurrently injure their cervical spines. Injury or dysfunction of the cervical spine has been shown to cause headaches, dizziness and loss of balance, nausea, visual and auditory disturbances, reduced cognitive function, and many other signs and symptoms considered synonymous with concussion.

There is considerable overlap of the signs and symptoms of mild traumatic brain injury and of whiplash injury:

The symptoms of headache and dizziness, so prevalent in concussion-type injuries, may actually be the result of cervicogenic mechanisms due to a concomitant whiplash injury suffered at the same time. Numerous brain stem structures receive mono-synaptic inputs from the C2 dorsal root ganglion afferents, including:

• Lateral cervical nucleus
• Central cervical nucleus
• Caudal projections to C5 level
• Cuneate nucleus, lateral cuneate nucleus
• Nucleus tractus solitarius
• Intercalatus nucleus
• Nucleus X of the vestibular system
• Trigemino-cervical nucleus (for headache nociception)

Prior studies have concluded that injuries of the cervical spine are responsible for post-concussion syndrome, and have shown excellent clinical outcomes as a consequence of treatment to the cervical spine. These authors present five case studies of patients diagnosed with post-concussive syndrome who were treated successfully in a chiropractic clinic. Their improvement was rapid and documented using standard measurement outcomes. The improved clinical outcome results were long-lasting.

Treatment included:

• Active Release Therapy
• Localized vibration therapy over the affected muscles
• Spinal manipulative therapy of the restricted joints
• Low-velocity mobilizations (on 1 patient)

The authors concluded:

“Management of persistent post concussive symptoms through ongoing brain rest is outdated and demonstrates limited evidence of effectiveness in these patients.”

Instead, there is evidence that “skilled, manual therapy-related assessment and rehabilitation of cervical spine dysfunction should be considered for chronic symptoms following concussion injuries.”

This study is timely, especially considering the evidence that the cervical spine is involved in concussion has been in the literature for about 150 years. This study highlights the lack of understanding by athletes, the public, and healthcare providers that it is essentially impossible to sustain a traumatic brain injury without also injuring the soft tissues of the cervical spine. It is anatomically/biologically probable that these cervical spine injuries cause many, if not most, of the symptoms of the post-concussion syndrome.

It is also gratifying to see a published study showing that traditional chiropractic management of post-concussive syndrome patients resulted in rapid and sustained improvement in post-concussive signs and symptoms, allowing the athlete to return to full completion.

It is recommended that all patients suffering from the post-concussive syndrome should be referred to a chiropractor for cervical spine evaluation and treatment.

REFERENCES:

1. Jackson R, The Cervical Syndrome, Thomas, 1978.
2. Foreman S, Croft A’ Whiplash Injuries: The Cervical Acceleration / Deceleration Syndrome; Williams & Wilkins; 1988.
3. Cailliet R; Whiplash Associated Diseases; American Medical Association; 2006.
4. White AA, Panjabi MM; Clinical Biomechanics of the Spine; Second Edition; Lippincott; 1990.
5. Erichsen JE; On Railway and Other Injuries of the Nervous System; Philadelphia, PA; Henry C. Lea; 1867.
6. Page HW; Injuries of the Spine and Spinal Column Without Apparent Mechanical Lesion, and Nervous Shock in their Surgical and Medico-Legal Aspects; Second Edition; London; J. A. Churchill; 1885.
7. Todman D; Whiplash Injuries: A Historical Review; The Internet Journal of Neurology; Vol. 8 No 2; 2006.
8. Denny-Brown D, Russell WR; Experimental Cerebral Concussion; Journal of Physiology; Vol. 99; p. 153.
9. Denny-Brown D, Russell WR; Experimental Concussion; Proceedings of the Royal Society of Medicine; September 1941; Vol. 34; No. 11; pp 691-691.
10. Cammack KV; Whiplash Injuries to the Neck; American Journal of Surgery; April 1957; Vol. 93; pp. 663-666.
11. Friede RL; Specific cord damage at the atlas level as a pathogenic mechanism in cerebral concussion; Journal of Neuropathology and Experimental Neurology; April 1960; Vol. 19; pp. 266-279.
12. Yuan Q, Dougherty L, Margulies SS; In vivo human cervical spinal cord deformation and displacement in flexion; Spine; August 1, 1998; Vol. 23; No. 15; pp. 1677-1683.
13. Jadischke R, Viano DC, McCarthy J, King AI: Concussion with Primary Impact to the Chest and the Potential Role of Neck Tension; BMJ Open Sport & Exercise Medicine; October 16, 2018; Vol.4; No. 1; pp. e000362.
14. Marshall CM, Vernon H, Leddy JJ, Baldwin BA; The Role of the Cervical Spine in Post-concussion Syndrome; July 2015; Vol. 43; No. 3; pp. 274-284.