Subscription is FREE for qualified healthcare professionals in the US.
10 Articles in Volume 13, Issue #4
Traumatic Brain Injury
US Service Members With Polytrauma
Cancer Patient: Controlling The Pain
Pharmaceutical Treatment of the Cancer Pain Patient
Drug Interactions in Cancer Patients Requiring Concomitant Chemotherapy and Analgesics
How Do We Get Enough Physicians to Medically Manage The Difficult (High-dose Opioid) Pain Patient?
Ultra-high Dose Opioid Therapy: Uncommon and Declining, But Still Needed
Head Trauma: More Than A Headache
Ask the Expert May 2013
Letters to the Editor May 2013

Traumatic Brain Injury

With millions of traumatic brain injuries occurring in the United States each year, it is becoming more crucial for pain practitioners to understand the biomechanics, pathophysiology, and symptomatology of these conditions.
Page 1 of 5

Traumatic brain injuries (TBIs) are on the rise in the United States, and most TBIs (the mild form of which is also referred to as a concussion) are not treated in hospitals or emergency departments. According to the Centers for Disease Control and Prevention (CDC), approximately 1.4 million TBIs occur in the United States each year.1 For military personnel, TBIs also are an increasingly common injury, with blasts in combat zones being the most frequent causes for military service members.2 Added to this are the rising medical costs of treating TBIs, which the CDC estimates at $12 billion.2 Since more TBI patients are being seen by private practice clinicians, as opposed to hospital emergency departments, this article discusses the importance of clinicians understanding the biomechanics, pathophysiology, and symptomatology of these injuries, especially since highly variable symptom durations are such a common occurrence following TBIs. Part 2 of this article series will discuss treatments for TBI-related headaches. Part 3 discusses the evaluation, treatment and rehabilitation

Concussion Biomechanics

There are a number of variables to consider when a TBI occurs. The two main types of forces are inertial and contact. Inertial acceleration loading occurs without actual head contact.3 Contact loading may result in injuries directly at the site of impact, such as a skull fracture, as well as at distant areas in the brain. Milder TBI rarely results in linear or depressed fractures.

With milder TBI, the inertial forces (acceleration) are responsible for most of the symptoms. Acceleration forces are divided into two types: 1) rotational, and 2) linear.4 After a blow to the head, there is a temporary rise in pressure within the cranium. Neuronal injury somewhat correlates with the height of the peak pressure. Rotational forces produce more serious damage than do acceleration ones. When the head rapidly rotates, shear-induced damage to brain tissue ensues.5 Rotational impacts produce the unconsciousness associated with more severe concussions.

The important question in understanding the biomechanics of concussion is: How does energy from a blow to the head get transferred into the brain? Brain tissue is soft, consisting mostly of water. If a shearing force hits the skull, the brain is easily deformed. Models have been able to predict how much pressure is generated in the brain by various forces.6 Pressure gradients lead to deformation of the cerebrum and brainstem. Rotational accelerations produce much more profound effects than do linear accelerations.

Experiments have proven that coronal (lateral) rotational accelerations produce the most profound effects deep within the brain. These coronal accelerations often produce loss of consciousness.7 Other factors enter into the effects of head trauma, such as the ventricular system, which may dampen the effect of the trauma. Detailed 3-D computerized modeling of different rotational forces will help to predict the extent of neural and vascular deformations from various blows.

Concussion Pathophysiology

A complex series of neurometabolic and neurochemical changes occur immediately following a concussion. Axons are stretched and cell membranes disrupted. This results in ionic flow that is largely unregulated. The result is a release of various neurotransmitters, in particular the excitatory amino acids (EAAs).8 The ATP-dependent pump works overtime to restore sodium (Na+) and potassium (K+) balance, all of which take a tremendous amount of energy. With most concussions, these molecular changes are short lived, but they can be permanent, particularly in the setting of multiple head traumas.

After the concussion, K+ flows out of the neuron, along with EAAs such as glutamate. N-methyl-D-aspartate (NMDA) receptors are activated, and calcium ions rush into the neuron.9 Neurons are suppressed, similar to the situation we encounter with spreading depression. Spreading depression (originally described by Leao) is important in epilepsy and migraine.

The Na+ and K+ pumps kick into high gear, which requires increased glucose metabolism. Oxidative metabolism is compromised, and lactate accumulates. Lactate adds to local acidosis, and contributes to cerebral edema.

Directly following a concussion, hyperglycolysis is observed, followed by a glucose hypometabolism. This glucose hypometabolism may last weeks or months (after a severe TBI). The influx of calcium (Ca++) into mitochondria leads to glucose oxidative dysfunction.10

All of the above problems set the brain up for the deadly or disabling second impact syndrome. The exact reasons why second impact syndrome occurs are not clear. Second impact syndrome involves cerebral edema after a second concussion, and often is catastrophic.11 The first concussion leaves the brain in a vulnerable state, with depleted energy stores, activation of neurotransmitters, and altered ionic balance. Dysfunction in the mitochondria adds to the increased vulnerability. With repeated blows to the head, axonal disruption may be permanent.

After a severe TBI, the effect on cerebral blood flow has been described in 3 phases. Initially there is a cerebral hypoperfusion, followed by hyperemia, and finally a cerebral vasospasm. Edema may occur. The axons are stretched during a blow to the head, resulting in depolarization, mitochondrial dysfunction, calcium influx, and flux of other ions.12

Axonal injury occurs even after a milder TBI. The myelin and cell bodies are relatively untouched after milder injuries. Diffusion tensor imaging (DTI) has been able to detect subtle axonal changes after mild TBI.13> In addition to DTI, functional MRI may become clinically useful in helping to predict recovery time.

With repeated concussions and subconcussive hits, the dreaded progression in chronic traumatic encephalopathy (CTE) may occur. Tau and amyloid deposition occurs.14 CTE has previously been a post-mortem diagnosis, but a PET study in 2012 was able to detect signs of CTE in living individuals.15 To prevent tauopathy and CTE, it is crucial to limit the total hits, concussive and lesser, in the young athletes.

Post-concussion Syndrome

Mild and so-called minor TBIs produce well-documented post-concussion symptoms, including migraines and other headaches. These individual symptoms are quite treatable, and should be documented and worked up objectively using an interdisciplinary approach.16

Post-concussion syndrome is when a set of symptoms occurs following an initial concussion and lasts for extended periods of time. The symptoms can occur for weeks, months, or years; are quite frequent; and are seen in the majority of patients with so-called mild or minor brain trauma. Often, these TBIs are of the whiplash type, without contact of the head against a solid and immovable object. Frequently, no loss of consciousness is reported by the patient, but many will speak about being dazed or “dinged” at the time of the injury. Table 1 outlines the symptoms commonly exhibited following a TBI.

Last updated on: April 15, 2015

Join The Conversation

Register or Log-in to Join the Conversation