BRAIN MOTION AND DEFORMATION DURING CLOSED HEAD INJURY IN THE PRESENCE OF CEREBROSPINAL FLUID

This paper presents a new analysis of the physics of closed head injury following brief, intense acceleration of the head. It focuses upon the buoyancy of the brain in cerebrospinal fluid, which protects against damage; the propagation of strain waves through the brain substance, which causes damage; and the concentration of strain in critical anatomic regions, which magnifies damage. Numerical methods are used to create animations or "movies" of brain motion and deformation. Initially, a 1 cm gap filled with cerebrospinal fluid (CSF) separates the brain from the skull. Whole head acceleration induces artificial gravity within the skull. The brain accelerates, because its density differs slightly from that of CSF, strikes the inner aspect of the skull, and then undergoes viscoelastic deformation. The computed pattern of brain motion correlates well with published high-speed photographic studies. The sites of greatest deformation correlate with sites of greatest pathological damage. This fresh biomechanical analysis allows one to visualize events within the skull during closed head injury and may inspire new approaches to prevention and treatment.

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A NEW BIOMECHANICAL HEAD INJURY CRITERION

Journal of Mechanics in Medicine and Biology ◽

10.1142/s021951940600200x ◽

2006 ◽

Vol 06 (04) ◽

pp. 349-371 ◽

Cited By ~ 4

Author(s):

CHARLES F. BABBS

Keyword(s):

Head Injury ◽

High Speed ◽

Compressive Strain ◽

Experimental Studies ◽

Closed Head Injury ◽

Lumped Parameter Model ◽

Viscoelastic Deformation ◽

Head Injury Criterion ◽

Closed Head ◽

The Brain

This paper presents a new analysis of the physics of closed head injury caused by intense acceleration of the head. At rest a 1 cm gap filled with cerebrospinal fluid (CSF) separates the adult human brain from the skull. During impact, whole head acceleration induces artificial gravity within the skull. Because its density differs slightly from that of CSF, the brain accelerates, strikes the inner aspect of the rigid skull, and undergoes viscoelastic deformation. Analytical methods for a lumped parameter model of the brain predict internal brain motions that correlate well with published high-speed photographic studies. The same methods predict a truncated hyperbolic strength-duration curve for impacts that produce a given critical compressive strain. A family of such curves exists for different critical strains. Each truncated hyperbolic curve defines a head injury criterion (HIC) or threshold for injury, which is little changed by small offsetting corrections for curvature of the brain and for viscous damping. Such curves predict results of experimental studies of closed head injury, known limits for safe versus dangerous falls, and the relative resistance of smaller versus larger animals to acceleration of the head. The underlying theory provides improved understanding of closed head injury and better guidance to designers of protective equipment and to those extrapolating research results from animals to man.

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Demonstration of massive traumatic brain swelling within 20 minutes after injury

Journal of Neurosurgery ◽

10.3171/jns.1977.46.2.0256 ◽

1977 ◽

Vol 46 (2) ◽

pp. 256-258 ◽

Cited By ~ 40

Author(s):

Arthur I. Kobrine ◽

Eugene Timmins ◽

Rodwan K. Rajjoub ◽

Hugo V. Rizzoli ◽

David O. Davis

Keyword(s):

Head Injury ◽

Closed Head Injury ◽

Brain Swelling ◽

Axial Tomography ◽

Content Type ◽

Closed Head ◽

Vascular Dilatation ◽

Computerized Axial Tomography ◽

The Brain ◽

Fine Print

✓ The authors documented by computerized axial tomography a case of massive brain swelling occurring within 20 minutes of a closed head injury. It is suggested that the cause of the brain swelling is acute vascular dilatation.

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Cytokine production in the brain following closed head injury: dexanabinol (HU-211) is a novel TNF-α inhibitor and an effective neuroprotectant

Journal of Neuroimmunology ◽

10.1016/s0165-5728(96)00181-6 ◽

1997 ◽

Vol 72 (2) ◽

pp. 169-177 ◽

Cited By ~ 235

Author(s):

E Shohami ◽

R Gallily ◽

R Mechoulam ◽

R Bass ◽

T Ben-Hur

Keyword(s):

Head Injury ◽

Cytokine Production ◽

Closed Head Injury ◽

Tnf Α ◽

Closed Head ◽

The Brain

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44. Pathomorphological Studies on the Brain of so-called “Closed Head Injury” (1st Report)

Neurologia medico-chirurgica ◽

10.2176/nmc.6.87 ◽

1964 ◽

Vol 6 (0) ◽

pp. 87-87

Author(s):

Michio INUI ◽

Masatoshi MOROOKA ◽

Yohsuke ARAI

Keyword(s):

Head Injury ◽

Closed Head Injury ◽

Closed Head ◽

The Brain

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Quantitative analysis of magnetization transfer images of the brain: Effect of closed head injury, age and sex on white matter

Magnetic Resonance in Medicine ◽

10.1002/(sici)1522-2594(199910)42:4<803::aid-mrm24>3.0.co;2-f ◽

1999 ◽

Vol 42 (4) ◽

pp. 803-806 ◽

Cited By ~ 27

Author(s):

P.A.M. Hofman ◽

G.J. Kemerink ◽

J. Jolles ◽

J.T. Wilmink

Keyword(s):

Quantitative Analysis ◽

White Matter ◽

Head Injury ◽

Magnetization Transfer ◽

Closed Head Injury ◽

Closed Head ◽

The Brain ◽

Age And Sex

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Oxidative Stress in Closed-Head Injury: Brain Antioxidant Capacity as an Indicator of Functional Outcome

Journal of Cerebral Blood Flow & Metabolism ◽

10.1097/00004647-199710000-00002 ◽

1997 ◽

Vol 17 (10) ◽

pp. 1007-1019 ◽

Cited By ~ 168

Author(s):

Esther Shohami ◽

Elie Beit-Yannai ◽

Michal Horowitz ◽

Ron Kohen

Keyword(s):

Head Injury ◽

Antioxidant Capacity ◽

Defense Mechanisms ◽

Antioxidant Properties ◽

Closed Head Injury ◽

Iron Chelator ◽

Experimental Models ◽

Closed Head ◽

Total Tissue ◽

The Brain

It has been suggested that reactive oxygen species (ROS) play a role in the pathophysiology of brain damage. A number of therapeutic approaches, based on scavenging these radicals, have been attempted both in experimental models and in the clinical setting. In an experimental rat and mouse model of closed-head injury (CHI), we have studied the total tissue nonenzymatic antioxidant capacity to combat ROS. A major mechanism for neutralizing ROS uses endogenous low-molecular weight antioxidants (LMWA). This review deals with the source and nature of ROS in the brain, along with the endogenous defense mechanisms that fight ROS. Special emphasis is placed on LMWA such as ascorbate, urate, tocopherol, lipoic acid, and histidine-related compounds. A novel electrochemical method, using cyclic voltammetry for the determination of total tissue LMWA, is described. The temporal changes in brain LMWA after CHI, as part of the response of the tissue to high ROS levels, and the correlation between the ability of the brain to elevate LMWA and clinical outcome are addressed. We relate to the beneficial effects observed in heat-acclimated rats and the detrimental effects of injury found in apolipoprotein E-deficient mice. Finally, we summarize the effects of cerebroprotective pharmacological agents including the iron chelator desferal, superoxide dismutase, a stable radical from the nitroxide family, and HU-211, a nonpsychotoropic cannabinoid with antioxidant properties. We conclude that ROS play a key role in the pathophysiology of brain injury, and that their neutralization by endogenous or exogenous antioxidants has a protective effect. It is suggested, therefore, that the brain responds to ROS by increasing LMWA, and that the degree of this response is correlated with clinical recovery. The greater the response, the more favorable the outcome.

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