Playing football in high school was an amazing time for me; being part of a team, developing strong self-esteem and getting bigger and stronger. These are all terrific things for a young man to experience, but all of this positivity sometimes comes at a price. I clearly remember many times during 'hitting drills' where there would be a clash of helmets and someone would be left dazed and confused. We called it "getting your bell rung." What was worse was that you never wanted anyone to know that it happened for fear of being taken out of a game, or your teammates thinking that you weren't tough enough to play. Unfortunately this is still a very common occurrence. The difference is that now we have evidence clearly showing just how devastating multiple head traumas can be over time.
'Getting your bell rung' is actually a description of a mild Traumatic Brain Injury (mTBI) or Concussion. A concussion results from a significant 'jarring' of the brain in any direction and temporarily interferes with the way the brain works. Mild concussions can cause immediate confusion, drowsiness, feelings spaciness or not being able to think straight and headache. More prolonged symptoms can be persistent headaches, memory problems, altered judgment, reflex and speech changes, balance and coordination problems and sleep disturbances.
In more severe cases, an injured person could experience a loss of consciousness, memory loss (amnesia) of events before the injury or immediately after, nausea and vomiting, visual disturbances like seeing flashing lights, feeling like they have "lost time", changes in alertness and consciousness, persistent confusion, seizures and even death.
Head injuries do not have to result in a loss of consciousness to be serious. In fact, most people who have a concussion never black out. Recent studies find that repeated minor concussions can be more dangerous than a single, serious head injury and that these seemingly minor head injuries can cause lifelong neurological problems.
The American Academy of Neurology straightforwardly defines concussion as a "trauma- induced alteration in mental status that may or may not involve a loss of consciousness. Studies show there are more than 300,000 sports related concussions per year.
The initial injury begins a result of a traumatic distortion of the brain. But, in mild cases, this trauma actually causes a limited amount of mechanical brain injury at the time of impact. Research studies have found shown that most of the damage from brain concussion is delayed and occurs after the head is injured.
According to a 2005 study by the Center for the Study of Retired Athletes, former NFL players who suffered three or more concussions are five times more likely to have mild cognitive impairment and three times more likely to have significant memory problems than players who do not have a history of concussions. In addition, there appears to be a link between multiple concussions and the early onset of Alzheimer's. The study's disturbing conclusion: "Our findings suggest that the onset of dementia-related syndromes may be initiated by repetitive cerebral concussions in professional football players." Dr. Julian Bailes, the CSRA's medical director goes on to state that a player who suffers three or more concussions is three times more likely to suffer from depression than a player without a history of concussions.
There is an unfortunate pattern developing among former athletes of contact sports; an Alzheimer's-like neurodegenerative disease called Chronic Traumatic Encephalopathy (CTE). According to researchers, CTE has a clear environmental cause - repeated brain trauma. Originally termed "dementia pugilistica" otherwise known as "punch drunk", this disorder was first described in 1928 in boxers because boxers suffered from slowed movement, confusion, speech problems, and tremors (Sports Legacy Institute, 2010).
The disease is characterized by a number of neurological and physiological changes in the brain including the buildup of an abnormal protein called tau. This protein builds up in places in the brain where it is not supposed to be and congregates in clumps in and around the brain disrupting its function.
A person with CTE may progress through three stages of the disease beginning in the first stage with emotional regulation disturbances and psychotic symptoms. As the disease progresses to stage two, the individual may suffer from social instability, erratic behavior, memory loss, and the initial symptoms of Parkinson's disease (McKee, A.C., et.al., 2009) . The final stage consists of a progressive deterioration to dementia and may have other symptoms including the signs associated with Parkinson's disease, speech difficulties, gait abnormalities, dysarthria (speech disorder characterized by neuromuscular weakness or lack of control of facial muscles), dysphagia (difficulty swallowing), and ptosis (drooping eyelid) (McKee, A.C., et.al., 2009).
There are two main things that happen to the brain with concussion. First, there is the actual mechanical trauma where the brain bangs around inside the skull. Believe it or not, the body has a built in shock absorbing system of soft tissues and fluid that protects the brain from most bumps and bruises. In the case of a mild TBI or concussion, the forces exceed the body's ability to absorb the blow and injury occurs to the brain tissue from the impact. A common pathological feature of TBI includes distributed injuries to the subcortical white matter, or diffuse axonal injury (DAI). mTBI may involve DAI as well. In blunt closed head injury, these diffuse axonal damages have been attributed to shear strain and tissue deformation caused by the rotational accelerations of the brain as an external force is applied to the head.
Second, there is a biochemical reaction that involves inflammation and swelling. Scientific studies have shown that there is a slow buildup in the injured brain of free radicals, prostaglandins, lipid peroxidation products, inflammatory cytokines and excitotoxins that damage the connections between brain cells, the synapses, axons and dendrites.
In the body, this inflammatory reaction is part of the healing process which is activated by our white blood cells. In the brain, the process is mediated by cells called microglia. The main difference is that once the microglial cells are activated, they tend to persist in this state and can actually create even greater neuroinflammation over time.
Chronic neuroinflammation causes most if not all of the long term effects of concussion. If symptoms do not resolve after 10 days of rest, postconcussive syndrome (PCS) may be diagnosed. PCS is a constellation of symptoms that can be categorized as cognitive, affective, or somatic and may lead to chronic disability. Post-concussion syndrome (PCS) can affect up to 20% - 30% of patients with concussions, comprising incomplete recovery and debilitating persistence of post-concussion symptoms. It has been shown that eye movements relate closely to the functional integrity of the injured brain and eye movement function is impaired post-acutely in mTBI. The greater the defect in various eye movement analysis testing, the greater degree of functional brain impairment and potential for long term disability.
Since this a traumatic event, the initial assessment is usually performed by emergency medical specialists or athletic trainers on sports fields. With awareness of concussion and its long term ramifications at an all-time high, most first responders err on the side of caution. Athletes should be immediately removed from the field of play.
Currently, the method of mTBI diagnosis is highly dependent upon information obtained through patients' subjective self-report about the acute characteristics of their injury or from the description of an observer. Unlike moderate or severe Traumatic Brain Injuries, which are more easily diagnosed acutely by loss of or alteration in consciousness or abnormality in CT images, mTBI is much more ambiguous during the acute phases and may not be diagnosed until the affected individual complains of postconcussive symptoms or experiences difficulties in their social interactions or in job or school performance. Difficulties exist in truly judging the full extent of the concussion for many reasons. Oftentimes lesser blows cause more symptoms where more aggressive blows cause lesser symptoms. Adding to the complexity, as a consequence of cognitive impairments that result from their injury, mTBI patients may have a reduced awareness of their deficits. Every concussion is different in its mechanism of injury and is also influenced by the status of the nervous system prior to the injury.
Currently neuropsychological testing is considered to be one of the most important assessment tools during both the acute and chronic phases of Post Concussive Syndrome, although it may not be sensitive enough to evaluate mTBI early on. Typical neuropsychological batteries assess attention, working memory, and executive functions.Another valuable assessment for patients with mTBI is the evaluation of eye movements like visual tracking, saccades and smooth pursuits. Predictive visual tracking shows promise as an attention metric to assess severity of mTBI. Deficits seen during predictive visual tracking correlate with observed damage to neural pathways known to carry out cognitive and affective functions that are vulnerable to mTBI. These assessments can be done using advanced diagnostic technology called Video Nystagmography.
Remember, the head is connected to the neck Head injuries that result in concussion often are associated with injury to the neck and spine. The body reacts to a blow to the head by creating spasm throughout the intrinsic and extrinsic cervical spine muscles. This is an innate attempt to reduce motion in the region which might increase the damage. After a period of time, the large outer muscles will loosen up, but the deep intrinsic muscle spasm commonly persists and can lead to mechanical neck pain and headaches.
The associated resultant joint dysfunction may further impair brain function, due to the alteration in the mechanical axis of rotation and reduced afferent input from the cervical joint and muscle spindle receptors in the neck.
Understanding the complexity of post-injury pathophysiology is critical for optimal management of Post concussive patients. Initial concussions aren't usually serious. It's the second ones that do real damage, especially if they occur before the brain has recovered. If an injured brain has a repeat injury too soon, permanent brain damage — and even death — can result. After an injury, the brain needs time to heal. Until it does, it is prone to more serious injury the second time called a "second-impact syndrome."
First, there is a biomechanical 'injury' to the brain as a result of the initial trauma, followed by a series of biochemical events that can create the Post-Concussive Syndrome.
The biomechanics of a concussion or mTBI involve both linear and rotational forces. Linear forces result from straight ahead acceleration-deceleration and can be associated with cerebral cortex injury at the site of contact (coup), as well as injury to the opposite side of the contact to the head (contra-coup).
While most high-speed head injuries involve some linear component, rotational forces will almost always also play a role. It is these rotational forces that lead to twisting and shearing injuries in the brain tissue, particularly in the white matter fiber tracts resulting in diffuse axonal injury. Rotational forces of lower magnitude are also present in milder forms of TBI such as sports-related concussion.
From a metabolic perspective, there are several things that happen following a concussion.
- Increased glutamate levels
- Altered glucose utilization
- Mitochondrial dysfunction
- Reduced available Magnesium
Acute injury to the brain causes a rapid release of glutamate, the predominant excitatory neurotransmitter in the central nervous system. This indiscriminate release occurs as a result of extensive triggering of action potentials, synaptic neurotransmitter release, and membrane disruption. This massive release of glutamate is a major source of potassium efflux into the extracellular space. The rise in the extracellular concentration of potassium also results from nonspecific breakdown of the plasma membrane, especially in areas of the brain damaged by localized contusion. This increase in extracellular potassium, in turn, may lead to increased energy demand, causing greater rates of glycolysis with a parallel rise and accumulation of lactate.
There is also a significant increase of glucose utilization within the first 30 minutes following a head injury, after which glucose uptake diminishes and then remains low for about 5-10 days. In fact, globally decreased glucose metabolism has been demonstrated persisting chronically for weeks to months post-injury in human patients. The initial hyperglycolysis described above results from disruption of ionic gradients across the neuronal cell membrane, activating energy-dependent ionic pumps. In experimental animal models the increase in glucose utilization is almost instantaneous following injury and lasts up to 30 minutes in the ipsilateral cortex and hippocampus. As cerebral oxidative metabolism at baseline is already near or at maximum levels, this increased energy demand may be dealt with by augmenting glycolysis, which in turn increases lactate production.
There is also increasing evidence for impairment of oxidative metabolism following brain trauma. This may lead to depletion of high-energy phosphates (adenosine triphosphate, ATP), with a subsequent rise in anaerobic metabolism, and yet further accumulation of lactate. Increased lactate may generate neuronal dysfunction as a result of acidosis, membrane damage, disruption of the blood brain barrier and cerebral edema. There is also some evidence suggesting lactate accumulation post-injury may render the neurons more susceptible to secondary ischemic insults.
Glutamate also induces opening of calcium channels. A significant calcium accumulation for up to four days following injury in the ipsilateral cortex, hippocampus, striatum, and thalamus of experimental animals has been shown. We know that an accumulation of calcium inside neurons has been an indicator mitochondrial dysfunction and for impending cell death.
A marked decrease in brain magnesium concentration lasting up to 4 days post injury has also been shown. Magnesium is one of the electrolytes that play a significant role in maintaining ionic balance within the injured cell and plays a pivotal role in maintaining the integrity of the mitochondrial inner membrane. Additionally, magnesium has a significant role in influencing the degree of excitotoxic damage as a result of TBI, as intra- and extracellular magnesium concentration affects the opening and closing of sodium and calcium ion channels.
Most clinical neuropsychologists are taught a cortico-centric model of cognition. From this viewpoint, the neocortex is considered to play the most important role in generating human thinking and behavior.
However, we now understand that subcortical structures that have traditionally been considered only as co-processors of movement, Basal Ganglia & Cerebellum, also contribute to cognition and emotion.
There are two vertically organized re-entrant brain systems that interface the cortex and the descending systems; the cortico-basal ganglia system and the cerebro-cerebellar system. They are termed reentrant systems because their circuitries form a ''loop''—the circuit re-enters a region near its point of origin. The circuits originate in the cerebral cortex, sends information through the various subcortical structures within each respective system, and signals are sent back to the cortex terminating very near the same region in which the circuit originated.
Within the nervous system, loops of interaction of this type are considered to have a modulatory function. In these two systems, the cortical inputs are always excitatory. Outputs from these subcortical regions are largely inhibitory. This means that these subcortical circuits are regulating or modulating — and thus changing — the nature of input received from various cortical domains.
So much of the brain's activity occurs with the cortex itself, one region communicating with another. Once the cortex is released from thalamic inhibition, it has two major final output pathways; a lesser one it to the corticospinal system to control voluntary motion, and the majority is to the corticobulbar system (brainstem). Altered cortical function due to mTBI can change the integration to both internal and output systems.
Once the mechanical and metabolic insult takes place following an injury, there are many ways that neurological cells and systems are linked and can be affected by mTBI.
- Altered corticobulbar output
- Altered rhythmic firing of neural networks
- Neurotransmitter alterations
Altered corticobulbar output
The Pontomedullary System in the brainstem receives massive input from the ipsilateral cerebral cortex and it is responsible for many of the body's internal functions. Cranial nerves 5-10 are in this region, so alteration in functions involving motion to the face, balance and coordination, swallowing and digestive functions may all be impacted by mTBI.
Altered rhythmic firing of neural networks
Changes in intrinsic, voltage-gated ionic conductance at the level of thalamic relay cells are thought to create thalamocortical dysrhythmia. In recent years it has become evident that rhythmic neuronal firing and neuronal oscillation are deeply related to the emergence of brain functions. Prominent in these studies was the linking of high-frequency oscillations (25 - 50 Hz) with sensorimotor and cognitive functions. Currently, there is little doubt that slow oscillatory activity, as observed in phase four of the sleep cycle, cannot presently be correlated with normal levels of cognition. In fact, neurological and psychiatric conditions have been correlated with the presence of slow thalamocortical oscillation (4 - 8 Hz) in awake patients (2). Suprachiasmatic Nuclues (SCN) The SCN, located in the hypothalamus, is the central circadian clock in humans and other mammals and controls not only the timing of the sleep-wake cycle but also many other rhythmic and non-rhythmic processes in the body. Patients with TBI show significantly lower levels of evening melatonin production which may indicate disruption to circadian regulation of melatonin synthesis. It is now felt that elevated depression in mTBI patients is associated with reduced sleep quality, and increased slow wave sleep is attributed to the effects of mechanical brain damage (3).
Long-term deficits in memory and cognition in a setting of minimal anatomic change are often seen after concussion. These may result from dysfunctional excitatory neurotransmission. Postconcussive alterations have been reported in glutamatergic (NMDA), adrenergic, and cholinergic systems. Long-term potentiation, an NMDA-dependent measure of plasticity, may be persistently impaired in the hippocampus after concussive brain injury. Concussive brain injury also leads to early changes in choline acetyltransferase activity and later loss of forebrain cholinergic neurons. Impaired cholinergic neurotransmission leads to learning and spatial memory deficits in animals. Inhibitory neurotransmission is also altered after TBI. A loss of g-aminobutyric acid-producing (GABAergic) hilar neurons can compromise normal inhibition of hippocampal dentate granule cells. This loss of inhibitory neurons may predispose the traumatized brain to subsequent development of seizures (4).
Other functional domains like balance and eye movements are also found to be aberrant in these patients leading to feelings of dizziness or unsteadiness. Eye movements relate closely to the functional integrity of the injured brain and eye movement function is impaired post-acutely in mTBI. Changes in the interplay between the three sensory systems that govern balance; the vestibular system, the visual system and the proprioceptive system, can cause this. This can result from initial injury to the vestibular system or as an after effect from metabolic changes in the integration between regions (5).
We are sometimes asked if someone with a mild concussion should receive ongoing evaluation and care. Our immediate reaction is that there is NOTHING mild about a concussion, period. However media, teams, players and even medical staffs continue to use this nomenclature with this injury. It is simply counterproductive to label this injury with a "mild" tag, and hampers the effort of everyone trying to increase awareness. Even what may be considered a 'mild' injury can lead to Post Concussive Syndrome and especially a 'Second Impact Syndrome.' Take it seriously!
If you have had a concussion or have a child who has had one or more, it is very important to work with a professional team of experts. It is imperative to balance the desire to return to the activity where the injury occurred with the knowledge of the long term consequences of repeated injuries. There is a test battery called IMPACT which can be used to determine a 'baseline' for which any traumatic injury can be compared.
At our center in Chester County, we take do not provide acute TBI care. There are many outstanding brain injury sites at major hospitals around the country that do that work better than anyone. We focus on patients who have not responded to treatment, are dealing with post concussive syndrome or have a long term history of head injuries and want to do everything they can to avoid Chronic Traumatic Encephalopathy.
We are functional specialists and we strive to create a dynamic entry point for our patients, defining exactly where potential functional neurological lesions may be. Through a thorough history, structural assessment, neurological examination and Video Nystagmography testing, we can determine the system(s) that may be compromised. Additionally, we can develop a nutritional and supplementation strategy to reduce the long term effects of neuroinflammation.
Once the assessment is complete, we can implement a series of modalities aimed at restoring functional integrity to the system and reduce long term impairment.
No other facility in Pennsylvania provides our unique approach, enabling us to provide the very best assessment possible, exceptional continuity of patient care, and convenience for the patient.
- 1. Indian Journal of Neurotrauma (IJNT) 2006, Vol. 3, No. 1, pp. 9-17
A Clinician's Guide to the Pathophysiology of Traumatic Brain Injury
Andranik Madikians MD, Christopher C Giza MD*
- 2. Thalamocortical dysrhythmia: A neurological and neuropsychiatric syndrome characterized
Rodolfo R. Llina' s*†, Urs Ribary*, Daniel Jeanmonod‡, Eugene Kronberg*, and Partha P. Mitra§ *Department of Physiology and Neuroscience, New York University School of Medicine, 550 First Avenue, New York, NY 10016; ‡Universitätsspital Zurich, Neurochirurgische Klinik, Sternwartstrasse 6, CH-8091 Zurich, Switzerland; and §Bell Laboratories, Lucent Technologies, 600 Mountain Avenue, Murray Hill, NJ 07974
Contributed by Rodolfo R. Llina's, October 21, 1999
- 3. Neurology May 25, 2010 vol. 74 no. 21 1732-1738
Sleep disturbance and melatonin levels following traumatic brain injury
J.A. Shekleton, BBNSc (Hons), D.L. Parcell, DPsych, J.R. Redman, PhD,
4. Journal of Athletic Training 2001;36(3):228 - 235q by the National Athletic Trainers' Association, Inc.
The Neurometabolic Cascade of Concussion
Christopher C. Giza; David A. Hovda
Neurotrauma Laboratory, Division of Neurosurgery, University of California, Los Angeles School of Medicine, Los Angeles, CA
5. Brain 2009: 132; 2850 - 2870
Impaired eye movements in post-concussion syndrome indicate suboptimal brain function beyond the influence of depression, malingering or intellectual ability
Marcus H. Heitger,1,2 Richard D. Jones,1,2,3 A. D. Macleod,4 Deborah L. Snell,4