There exist two modes of injury in TBI. The first of these is the initial mechanical insult as described in the prior post and depicted in Figure 1 of that post. The second mode of injury, potentially the more severe, is the biochemical insult that follows subsequent to the mechanical insult and commences within a period of between 1 and 4 hours. This biochemical insult is triggered by the initial injury.

“The Central nervous system (CNS) is one of the complex systems in the body which consists of brain and spinal cord. Any disease or traumatic assault may lead to the degeneration of CNS including loss of homeostasis [1]. CNS injuries constitute a major cause of morbidity and mortality include the life threatening injuries such as traumatic brain injury (TBI) and spinal cord injury (SCI) [2–4]. TBI and SCI are caused by both primary and secondary injuries influencing the cascades of cellular and molecular events which will cause further damage in the system and loss of body functions. The consequences of the secondary injury include mitochondrial dysfunction, neurotransmitter accumulation, blood-brain barrier (BBB) and blood spinal cord barrier disruption, apoptosis, excitotoxic damage, initiation of inflammatory, and immune processes which is followed by initial primary mechanical trauma [5, 6]. Secondary injury involves the production of highly reactive species, reactive oxygen species (ROS), reactive nitrogen species (RNS), or free radicals which will cause damage to protein structure, DNA, and cell membrane and leads to oxidative stress which plays a major role in the pathophysiology of CNS injury. The progression of the damage starts from the primary impact on brain or spinal cord and will continue for hours, days, and weeks after the initial mechanical insult which will result in tissue damage.”  SOURCE

 

It is noted that this biochemical attack “will continue for hours, days, and weeks after the initial mechanical insult.” Any mechanism which serves to diminish, or mitigate, the effects of the mechanical insult will therefore have profound benefit on the injury victim.

The following material is derived from a paper published in Surgical Neurology International [Surg Neurol Int 18-Jun-2014;5:97 DOI: 10.4103/2152-7806.134731] on June 18th, 2014. Titled “Diminished brain resilience syndrome: A modern day neurological pathology of increased susceptibility to mild brain trauma, concussion, and downstream neurodegeneration”   the paper proposes the pineal gland to play a critical role in mitigating the effects of mechanical trauma through the utilization of UV light to produce “sulphate upon catalysis by sunlight:”

 

“Here, we introduce a novel concept that that the pineal gland, a tiny gland in the center of the brain, appears central to the pathology associated with PCS (Post Concussion Syndrome) and related conditions, most critically with impact trauma. Specifically, deficiencies in heparin sulfate (HS) dramatically impair the buffering ability of the brain against impact injury due to the insufficiently gelled water in the cerebrospinal fluid (CSF). We argue that the pineal gland responds to light stimuli by producing sulfate, and that the sulfate, conjugated to melatonin, is distributed throughout the brain via the CSF. Sulfate plays a critical role in buffering the brain against physical impact, and in degrading and recycling damaged proteins and mitochondria. The pineal gland is outside the blood-brain barrier (BBB), and it is profusely supplied with blood, second only to the kidney. This makes it vulnerable to environmental toxicants. Thus, impaired sulfate supply, due to impaired function of the pineal gland, might explain the increased sensitivity to concussion and inability to recover from concussion observed in modern times.” SOURCE

 

UV Deficiency and Role in Etiology of PCS

Morley and Seneff propose a dietary deficiency in sulphate supply to explain the severity of brain trauma. The present paper alters this emphasis and instead proposes that a deficiency in UV light exposure may impair the ability of the pineal gland to produce the required sulphate, and that it is this UV deficiency which serves to explain the increased severity of brain trauma expressed as PCS.

 

“Exposure to sunlight induces 3-O sulfation of HS in the pineal gland, catalyzed by HS 3-O-sulfotransferase.[94] This unique daytime activity of the pineal gland, which has access to ultraviolet (UV) rays from the sun via the optic chiasma, and which possesses both eNOS and nNOS, offers significant validation for the hypothesis, proposed in Seneff et al.,[181] that eNOS produces sulfate upon catalysis by sunlight. Thus, it can be argued that the pineal gland utilizes eNOS and nNOS to restore supplies of HS by day, which are then broken down during the dark cycle so that melatonin can be conjugated with sulfate and distributed throughout the brain via diffusion in the cerebrovascular fluid of the ventricles. Calcification of the pineal gland, which likely impairs eNOs’ ability to synthesize sulfate, is associated with AD.” SOURCE

Kitchen Sink Analogy

The initial paper first describing Diffuse Axonal Injury (DAI) offered an analogy based on the violent manipulation of a bowl of porridge. It is intended to continue this tradition of kitchen sink analogy with the following set of examples.

An analogy to the buffering described in the prior paragraphs may be found if an egg is immersed in a saucepan full of ordinary tap water. When the saucepan is tilted, or rotated, the egg will move within the water and make contact with the sides of the pan. If the applied force is sufficiently violent, it is possible to fracture the eggshell.

If the saucepan is filled with thick pudding, and a fresh egg placed in the pan, and the identical force applied, it will be evident the increased viscosity of the gelled water inhibits egg movement and greatly reduces the likelihood of its fracture against the side of the pan.

While the author is frequently of the opinion that his inter-cranial spaces are filled with thick pudding, it is clear from material science that while viscosity is critical, the fluid damping of mechanical force does not necessarily require a great degree of material depth in order to produce significant effect. Thin films may demonstrate physical properties out of proportion to their dimensions. A thin film may be equal, or superior to, a much thicker layer of the identical material.

An excellent example is found in the accident description contained in this prior post. The subject’s vehicle was positioned on a black ice roadway. The tires were heated as a result of the friction generated in the course of a 100 foot ABS controlled skid. The heated tires would have melted the top surface of the black ice, creating a water film which served to lubricate the ice and greatly reduce its co-efficient of static friction. This water film may have been no more than a few molecules thick. Despite the fact of a thin, barely perceptible film, it had the power to create a surface with a friction co-efficient representing the lowest friction co-efficient of any known material including materials such as Teflon which have been engineered precisely to maximize their low friction properties.

Thixotropy

Certain gels, or fluids, demonstrate a time dependent viscosity. As the fluid undergoes shear stress its viscosity will be lowered and it will commence to flow more easily. In the case of brain injury, such thixotropy would increase the degree of neurological insult due to trauma. Using the prior pan of water analogy, thixotropy would result in the saucepan of pudding becoming less viscous and acting like plain water. Shear stress within the brain mass is understood to be the principal cause of DAI injury. With, or without thixotropy, a deficiency in conjugated sulphates has the potential to increase the severity of brain trauma injury via reduced fluid damping of applied mechanical force.

Rheopecty

There is a second time dependent shear stress related property known as rheopecty in which a fluid demonstrates an increase in viscosity under shear.  In the kitchen sink analogy this would result in the saucepan of water coming to resemble the pan full of thick pudding. This transformation of the fluid would occur within milliseconds. This property has clear benefit with regard to mitigating the effects of mechanical impact and is presently being exploited in the creation of protective equipment expressly designed to reduce impact stress.

The actual material characteristics of the conjugated sulphate described by Morley and Seneff is presently unknown. What is clear is that what they define as “structured water” has great potential to function as a means to inhibit shear stress within the brain mass and greatly reduce the potential for shear induced DAI which is recognized as a central aspect of mTBI, or concussion injury.

It is equally clear that any deficiency in the availability of this “structured water” has the corollary effect of potentially increasing the severity of traumatic brain injury.

 

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Note

The header image displays the illumination encountered on December 13th, 2015 at 0841 hours.

Posts in the PCS Sequence

PCS Thesis – Index
PCS Thesis – The Accident
PCS Thesis – Injury Modalities
PCS Thesis – UV Index