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CHAPTER 5

Key Elements that Define Concussion

ONE OF THE best definitions provided for concussion is based on a consensus statement provided at the 4th International Conference on Concussion in Sports held in November 2012 in Zurich. This very progressive definition evolved from the changing evidence that we now have on concussion. The definition is as follows: “Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. Several common features that incorporate clinical, pathologic, and biomechanical injury constructs that may be utilized in defining the nature of a concussive head injury include:

1. Concussion may be caused by a direct blow to the head, face, neck, or elsewhere on the body with an ‘impulsive’ force transmitted to the head.

2. Concussion typically results in the rapid onset of short-lived impairment of neurologic function that resolves spontaneously. However, in some cases, symptoms and signs may evolve over a number of minutes to hours.

3. Concussion may result in neuropathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury, and as such, no abnormality is seen on standard structural neuroimaging studies.

4. Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course. However, it is important to note that in some cases symptoms may be prolonged” (McCrory 2013).

BHET defined: Concussion occurs when mechanical forces affect the brain in such a manner that it disrupts the structural and physiological hierarchical organization and the associated functioning of the brain to the point that the patient experiences signs and symptoms that we now know are characteristic of concussions. In TBI/concussion, signs are what the healthcare providers find and symptoms are what the patients report.

These signs and symptoms include the following:

• Physical or somatic – fatigue, dizziness, spinning sensation, headaches, sleep disturbance, and lack of energy. Headache is the most commonly reported symptom in TBI/concussion, followed by dizziness, vertigo, and fatigue. A hallmark reported somatic symptom suggesting a disruption in the brain cycle is difficulty falling asleep and staying asleep.

• Cognitive – mental fog, memory and attentional impairment, and word-finding and visual perception problems. The hallmark feature of TBI/concussion is the inadequacy in executive functions, manifested by diminished insight, speed of processing, trouble with social graces, and in one’s ability to shift from one set of cognitive tasks to another.

• Neurobehavioral – anxiety, OCD, depression, low self-esteem, disinhibition (loss of filter), fear, short fuse, and personality changes that could include aggression, emotional lability (inappropriate laughter or crying), impulsivity (lack of impulse control), and irritability (Riggio 2009).

• According to Riggo (2009), neuropsychiatric or neurobehavioral symptoms actually are correlated with the severity, type, and duration of the somatic symptoms. This issue of which comes first the chicken or the egg, i.e. the physical somatic symptoms causing the cognitive and behavioral symptoms or vice versa is critical to understand TBI and concussions and how to treat such conditions.

Signs and symptoms in the immediate and chronic phases Immediate:

• Impaired attention – vacant stare, delayed responses, inability to focus

• Slurred or incoherent speech

• Gross incoordination

• Disorientation

• Emotional reactions out of proportion

• Memory deficits

• Any loss of or alteration of consciousness

Within one hour to days:

• Persistent headache

• Dizziness/vertigo

• Poor attention and concentration

• Memory dysfunction

• Nausea or vomiting

• Frequent fatigue

• Irritability

• Intolerance of bright lights

• Intolerance of loud noises

• Anxiety and/or depression

• Sleep disturbances

Concepts on Classification – It is now commonly believed that a proper classification system is necessary for the allocation of resources, treatment, and for determining the severity, prognosis, and outcomes. However, due to our recent understanding from new pathological studies, imaging, and new emerging clinical evaluation and treatment methods, we now can revisit how we define and classify TBI and concussion.

For years, experts in the field of TBI/concussion have applied many classification systems to better define the condition. However, these systems that worked previously may not be as relevant given the new understanding we have of injury and the science of the body. Many of the very strict classification systems used in the past that supported research initiative and clinical evidence required the patient to have suffered LOC and in some cases hospitalization. In fact, many of the older publications on concussion stipulated that one had to have a loss of consciousness as a criterion for establishing a concussion. No wonder many physicians (including neurologists), attorneys, and sports medicine programs still hold on to that belief.

Here is a classification system utilized for concussion, based on the acute severity at the time of the injury, which has been utilized by the VA and Department of Defense.

Table # 2 -- Classification of TBI Severity

Criteria	Mild	Moderate	Severe
Structural imaging	Normal	Normal or abnormal	Normal or abnormal
Loss of consciousness (LOC)	0–30 min	> 30 min and < 24 hrs	> 24 hrs
Alteration in consciousness/mental state (AOC)	a moment up to 24 hrs	> 24 hours; severity based on other criteria
Post-traumatic amnesia (PTA)	0-1 day	> 1 and < 7 days	> 7 days
Glasgow Coma Scale (GCS) (best available score in first 24 hours)	13–15	9–12	< 9

Source: O’Neal 2013

Note that PTA refers to a period of time following an injury when the patient is confused and unable to form new memories.

So, the question is: when does a concussion end or get resolved?

Utilizing the VA/DOD criteria, it was found that approximately 12–23% of service members returning from Iraq and Afghanistan suffered a TBI while deployed with most of the injuries being mild to moderate. Overall, only 10–20% of the individuals following a TBI experienced symptoms beyond 30 days. However, returning military has a larger percentage of individuals that remain symptomatic beyond 30 days. Moreover, one must consider the limited reporting of those conditions at the time (O’Neal 2013).

Consensus statements from the 4th International Conference on Concussion and the National Athletic Trainers Association estimated that most athletes recover within 7–10 days of a concussion (McCrory 2013, Broglio 2014).

Signs and symptoms have been viewed as the major evidence of when a concussion or TBI occurs and when it is resolved. But is it ever completely resolved?

The new markers of injury and the tools that are emerging may provide better answers to those questions. We now understand that the brain changes every day and every moment that we exist. I don’t know if there is a saying out there for this one, but I will go ahead and say, “We never have the same brain as yesterday.” These changes are accelerated by age and injury and result in the reorganization of the brain and its capacity to continue to reorganize. Current findings have suggested that these issues are more complex than we first realized. On the micro level, just thinking of the impact of injury in the disorganization of the brain is a challenge. The disruption of over a hundred million neurons with over a thousand trillion connections presents a problem of exponential magnitude. It is also highly challenging to look at the recovery process and the subsequent reorganization of the relationships between the many trillions of nerve terminal connections that exist together with all of the neurotransmitter (neurochemicals) substances that are responsible for creating and maintaining the complex messaging system that makes us human. We are far from understanding how much reorganization the brain experiences before a patient cease to experience the signs and symptoms. This certainly begs the question of when and how clinicians know from the signs and symptoms that the concussion or TBI is cured or treated, even if the symptoms have dissipated and the patient reports not experiencing the effects of TBI/concussion. This phenomenon of injury and the miracle of recovery will remain a mystery for a long time. However, we continue to make major strides in our understanding of these mysteries of the human brain.

Pathophysiology of a concussion

At its core, a concussion is highly related to an imbalance between energy utilization and availability throughout the brain or in certain parts of the brain. These delicate structures in the brain that are responsible for producing energy to ensure the appropriate functioning of the nerve cells working in a complex array become impaired. After an injury, the brain remains impaired until there is a recovery of the hierarchical organization of the array of neurons on a physiological and anatomic basis to manage energy efficiently to facilitate appropriate human functioning.

Energy-mismatched neuro-metabolic changes in concussion, as described by Hovda, represent a mismatch period where the demand for fuel (glucose) is high, while the blood flow to bring the glucose to the cell and the oxygen required to cause combustion is low. This results in a mismatch where sufficient energy is not created to keep the cells going. In other words, there is a gap in supply and demand, where demand is much higher than the supply (Giza 2001).

Utilizing physiological studies following severe brain injury in humans called Positron Emission Tomography (PET), Bergsneider and Hovda showed rapid uptake and utilization of glucose up to 8 days following TBI. (Bergsneider 1997). Kawamata was able to use a certain technique known as microdialysis and attenuate the increased glucose utilization seen after concussive brain injury (Kawamata 1992).

In animal studies, a rapid increase in glucose uptake has been evidenced after TBI. A second injury before the recovery of the first causes worse physiological changes in brain functioning and prolonged symptoms. After the second injury, this condition is a result of the greater mismatch in energy supply and demand than that from the first injury. The presence of signs and symptoms of concussion generally means that the energy mismatch is ongoing, and a second injury should be avoided at all cost.

The study reported by Prins in 2013 in the Journal of Neuro-trauma, evaluating vulnerability in the brain based on the timing of injury, showed that a second concussion during the period of metabolic impairment (glucose utilization) results in worse metabolic (brain physiological functioning) disruption and cognition impairment in the memory areas of the brain. This is the main reason the return-to-play policy is so critical (Prins 2013).

Second Impact Syndrome (SIS) is a result when another concussion occurs while a person is still symptomatic and in the process of healing from a previous injury that occurred days or weeks or months earlier. The condition occurs during a period of vulnerability before the symptoms from a prior injury are resolved.

SIS can result in the following:

• Massive swelling of the brain shortly after impact, known as diffuse cerebral edema, can cause the brain to be pushed through very narrow structures, a condition called brain herniation. Shifting of the brain and herniation cause increased pressure in the brain, and this can result in a collapse of the blood vessels that supply blood, nutrients, and oxygen to the brain. Any limitation in blood supply to the brain can result in further damage to brain cells, causing cell dropout or the death of nerve cells and their supporting cells. Due to the fact that the brains of younger individuals are without atrophy (with less space) when compared to older individuals, the “full” younger brain is more vulnerable to this condition. SIS generally occurs in young athletes under the age of 20 (Cantu 1998, Field 2003, Scramstad 2017).

• During the vulnerable period, there is an abject failure of the brain’s ability to regulate blood flow (also known as failure of autoregulation), and thus, wide fluxes in blood pressures can be seen.

• This condition can be fatal or result in death in 50% of cases, and severe disability in 100% of cases, as we saw in the instance of Mario (Case #1) (Stovitz 2017).

• There is also a higher risk of long-term cognitive dysfunction.