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12/19/2019

Head and

Head and Brain Injuries

Mehdi Shafieian Department of Biomedical Engineering Amirkabir University of Technology (Tehran Polytechnic)

29th International Course on Transport Planning and Safety December 2019

Traumatic Brain Injuries

Physical force causes nerve cells to stretch, tear and pull apart, therefore the brain is unable to relay messages Injury to brain cells affects processing: TBI in the thinking United States remembering seeing control & coordination mood

TBI in the world Causes of TBI ADULTS AGED 75 YEARS AND OLDER HAVE THE HIGHEST RATES OF TBI-RELATED HOSPITALIZATION AND DEATH

ANNUALLY, AN ESTIMATED THE YEARLY 10 MILLION PEOPLE SUFFER AGGREGATE A TBI EVENT WORLDWIDE INCIDENCE OF TBI HOSPITALIZATION ALMOST HALF A MILLION AND FATALITIES IS EMERGENCY DEPARTMENT VISITS ESTIMATED AT FOR TBI ARE MADE ANNUALLY BY 235 PER 100,000 CHILDREN AGED 0 TO 14 POPULATION

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Head Anatomy Skull Scalp Macroscopic Anatomy of Head and Brain Cerebrum Frontal lobe Microscopic Anatomy Arachnoid Temporal of Head and Brain Pia Mater Lobe Parietal Lobe Mechanisms of Occipital Lobe Criteria for Brain Injury Brain Stem

Spinal Cord

Solid Model of Head/Brain A bit more details Frontal Bone Based on CT and MRI 1 , 2 corpus callosum Parietal Parietal 3 ventricle Bone 4 fornix Bones 5 thalamus 6 pituitary gland 7 pons Temporal 8 Bone 9 10 cerebellum Sphenoid Occipital 11 midbrain Bone Bone

Dura and Brain Brain (Sagittal Section) Frontal Lobe Occipital Lobe

Lateral Ventricle

Midbrain

Cerebellum

Temporal Lobe Brain Stem

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Meninges and Superficial Cerebral Veins CSF Facts (Coronal Section) Superior Sagittal Sinus 1.The total volume of CSF is 125-150 ml. Scalp 2.Normal resting pressure of the CSF is between 150-180 mm H2O (11-13 mm Hg). Bridging Skull 3.Total production of CSF is about 400-500 ml/day (about .36 Veins Dura Mater ml/min) Pia Mater Note: Blood Pressure (Artery): 100 mm Hg = 13 kPa = 1.9 PSI CSF Pressure: 12 mm Hg = 1.6 kPa = 0.2 PSI Brain

Subarachnoid Space: Filled by CSF (11-13 mmHg)

CSF Functions Vasculature Contribution to Brain Material Properties

1. Protection: the CSF protects the brain from damage by "buffering" the brain. In other words, the CSF acts to cushion a blow to the head and lessen the impact. 2. Buoyancy: because the brain is immersed in fluid, the net weight of the brain is reduced from about 1,400 gm to about 50 gm. Therefore, pressure at the base of the brain is reduced. 3. Excretion of waste products: the one-way flow from the CSF to the blood takes potentially harmful metabolites, drugs and other substances away from the brain. 4. Endocrine medium for the brain: the CSF serves to transport hormones to other areas of the brain. Hormones released into the CSF can be carried to remote sites of the brain where they may act.

BBB (The Blood-Brain-Barrier) Brain is ANISOTROPIC Corona Radiata In the brain, the endothelial cells fit tightly together and substances cannot pass out of the bloodstream The BBB is semi-permeable; that is, it allows some materials to cross, but prevents others from crossing.

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Brain Facts

Weight of the human head? Weight of ? Microscopic Anatomy of Head and Brain

Axon - the long extension of a neuron that carries Neuron nerve impulses away from the body of the cell

Cell Body - the cell body of the neuron; it contains Axon Terminals - the hair-like ends of the axon the nucleus (also called the soma)

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Dendrites - the branching structure of a neuron Myelin Sheath - the fatty substance that surrounds that receives messages (attached to the cell body) and protects some nerve fibers

Node of Ranvier - one of the many gaps in the Nucleus - the organelle in the cell body of the myelin sheath neuron that contains the genetic material of the cell

Schwann's Cells - cells that produce myelin - they Neuron Facts are located within the myelin sheath.

How many neurons in an adult human brain?

Size of the Cell body 15 m

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Gray Matter, White Matter Glial Cells Functions

Astrocyte (Astroglia) Star-shaped cells that provide physical and nutritional support for neurons: 1) clean up brain "debris"; 2) transport nutrients to neurons; 3) hold neurons in place; 4) digest parts of dead neurons; 5) regulate content of extracellular space Microglia like , microglia digest parts of dead neurons. OligodendrogliaNumber of provideneurons the insulation compared (myelin) to to glialneurons cells? in the . Satellite Cells provide physical support to neurons in the peripheral nervous system. Schwann Cells Provide the insulation (myelin) to neurons in the peripheral nervous system. Oligodendrocyte

Macroscopic Anatomy of Head and Brain Microscopic Anatomy of Head and Brain Mechanisms of Traumatic Brain Injury Criteria for Brain Injury

TBI Brain Injuries

Severity depends on amount of Primary and Secondary brain injury Main cause of Secondary injury = hypoxia TBI ranges from mild to severe: Categories: Open or Closed degree of force Forces: multiple trauma Shearing and Compression neurological complications speed of assistance

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Severity of Brain Injuries Mild TBI

41 yr old Mike Hill graded on: Attacked from behind length of unconsciousness Full recovery after removal length of amnesia No infection Both caused by sudden trauma and nerve cell tearing Left hospital one week after Brain cannot maintain functioning and shuts down either: removal fully (unconsciousness) or partially (dazed) Mild TBI refers to loss of consciousness for 30 mins or less

Mild TBI Concussion vs Coma

Unconscious Concussion: May be defined as Amnesia Any of these brief unconsciousness. Altered consciousness Indicate Mild TBI neurological deficits Coma: May be defined as unconsciousness.

MBI can result in life changing consequences

Coma can result from: Glasgow Coma Scale diffuse axonal injury The Glasgow Coma Scale (GCS) is the most common AIS Scales for Brain Injury neurological scoring system used to describe the level of AIS 3: Brain contusion (open) consciousness in a person following a traumatic brain injury. brainstem injury AIS 4: Subdural , small AIS 5: Diffuse axonal injury It is based on 3 functions: AIS 6: Brain stem transection Eye opening bilateral hemispheric damage Verbal response Motor response

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Severe TBI Severe TBI

Best Eye Best Verbal Best Motor TBI is a process, not an event! Response Response Response 1. No eye opening 1. No verbal 1. No motor Secondary injury can be more damaging than primary injury. 2. Eye opening to response response pain 2. Incomprehensible 2. Extension to pain Main cause of Secondary injury: hypoxia 3. Eye opening to sounds 3. Flexion to pain verbal 3. Inappropriate 4. Withdrawal from command words pain 4. Eye opening 4. Confused words 5. Localizing to pain spontaneously 5. Appropriate 6. Obeys verbal responses commands Head trauma associated with a Glasgow Coma

Brain Injury: Major Mechanisms Types of Brain Injury

Direct contusion from skull deformation and/or fracture Contusion from internal movements Focal brain injury: a lesion causing local damage which can be seen by the naked eye. Indirect contusion or contrecoup Reduced blood flow Tissue stress and strain Diffuse brain injury : is associated with global disruption of brain tissue usually and is invisible. Edema and Interstitial Pressure

Focal injuries Diffuse Injuries

Subdural hematoma (SDH) Concussion The most common mechanism :tearing of veins that bridge the . The mortality rate is greater than 30 %. The most common head injury diagnosis, involves immediate loss of Epidural hematoma (EDH) consciousness following injury. 95 % recover at the end of 1 month. It occurs as a result of trauma to the skull and the underlying meningeal vessels and may not be associated with brain injury. Contusions Diffuse axonal injury (DAI) It consists of heterogeneous areas of necrosis, pulping, infarction, hemorrhage and edema. Mechanical disruption of many axons in the cerebral hemispheres and Generally occurs at the site of impact (coup: blow) and at remote sites from the impact (contrecoup: can be more significant) subcortical white matter. Involves immediate loss of consciousness lasting Intracerebral (ICH) for days to weeks. 55% are likely to have died at the end of 1 month. Homogeneous collections of blood within the cerebral parenchyma. Most commonly caused by sudden acceleration/deceleration of the head. Other causes are penetrating wounds and blows to the head.

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Proposed In Vivo Injury Mechanisms Mechanism 1: Focal Brain Contusion

A brain contusion is defined by cell death accompanied by hemorrhage (leakage of blood). The soft brain tissue is vulnerable to contusion in head trauma. The contusion often occurs at a site distant from the point of Pressure causes a change in Deformation causes extension, impact www.pathology.vcu.edu tissue volume, thereby causing shear and/ or compression of damage tissue, causing primary damage

Coup - Contrecoup Injury Impact Location and Contusion 83% 7% 10%

79% 14% 7%

50% 10% 40%

LifeArt: Williams & Wilkins http://www.lifeart.com

Mechanism 2: Increase in ICP Mechanism 2: Increase in ICP

Intracranial Contents: Important Point: The intracranial vault is a fixed volume since 80% brain tissue 10% blood bone does not expand! 10%

An increase in the volume of any of these intracranial contents ICP greater than 20mmHg, there is a high chance of Injury. causes increased intracranial pressure: 1.The brain can swell (edema) 2.Excess blood can accumulate due to hemorrhage 3.Cerebrospinal fluid can accumulate due to blockage of outflow

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Mechanism 2: Increase in ICP Mechanism 2: Increase in ICP

Important Point: There is only one way out of the intracranial vault Herniation: When the brain is squeezed through the foramen magnum, the brainstem is compressed. This would cause the patient to stop breathing and die.

Foramen Magnum (the small opening at the base of the skull) Robbins and Cotran. Pathologic Basis of Disease. 7th ed.: Elselvier; 2005.

Causes of Increase in ICP: Causes of Increase in ICP: Epidural Hematoma

sportmedi.ru http://openi.nlm.nih.gov

Causes of Increase in ICP: Causes of Increase in ICP: Brain Swelling Brain Swelling

findlaw.doereport.com drugline.org

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Causes of Increase in ICP: Mechanism 3: Diffuse Axonal Injury Brain Swelling Occurs in almost 50% cases of TBI.

The damage occurs in a more widespread area than in focal brain injury.

Shearing of axons in the white matter tracts is the main cause.

drugline.org

Mechanism 3: Diffuse Axonal Injury Mechanism 3: Diffuse Axonal Injury

DAI is one of the major causes of unconsciousness and persistent vegetative state (PVS) after head trauma.

Over 90% of patients with severe DAI never regain consciousness (and if they do so, they remain significantly impaired)

trialexhibitsinc.com

Question: Do the occupants sustain injuries?

Criteria for Brain Injury

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Mechanical Quantities Need to Translate to Injury

Brain Injury Criteria WSTC The Wayne State Tolerance Curve Wayne State Tolerance Curve Gadd Severity Index HIC Angular Acceleration Velocity GAMBIT HIP

Head Injury Criteria (HIC)

2.5 Gadd s Line : TA2.5 = 1000 1 t2 SI = a(t) 2.5 dt HIC (t2 t1) adt t1 (t2 t1) Injury: SI > 1000

Gadd s Line: Risk of Injury 5% for AIS 4 and above. t2 - t1

HIC > 1000 serious brain injury

NHTSA Signal Processing Software: http://www-nrd.nhtsa.dot.gov/software/signal-analysis/downloads.html

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HIC Revision Relationship Between HIC and Injury HIC time interval (1972) was 36ms

Skull Yes Fracture No

In 2000 revision, maximum critical time reduced from 36 to 15 ms 0 1000 2000 3000 HIC

Vascular Yes Brain Damage No

Relationship Between Results: HIC Variability due to Impact Location HIC and Injury

Low injury risk HIC < 750

Moderate injury risk 750 < HIC < 1000

High injury risk HIC > 1000

What is wrong with HIC? Rotational Acceleration and Brain Trauma

Only considers linear acceleration. It does not consider Injury type Rotation Direction Mass

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Thresholds for DAI in Monkey Monkey Head Translation/ Rotation and in Human Accelerations exceeding 10 krad/s2 combined with an angular velocity of 100 rad/s or higher gives a risk of DAI in the adult.

Proposed Rotational Brain Injury Tolerances: Proposed Threshold for SDH & Concussion Human An angular acceleration exceeding 175 krad/s2 combined with an impuls time exceeding 5ms, would produce SDH in the rhesus 1,000 monkey. DAI (Severe) more than 99% probability of concussion was estimated for >75 100 krad/s2, when the impulse duration exceeds 6.5ms.

SDH 10

1,000 10,000 100,000

Rotational Acceleration (rad/s2)

GAMBIT Criteria GAMBIT Criteria Generalized Acceleration Model for Brain Injury Tolerance Based on instantaneous values of resultant translational and rotational accelerations Does not account for time dependency Weighs effects of the two forms of motion similar to principal shear stress theory Inadequate validation General form of GAMBIT equation:

1 m n s G(t) a(t) /ac (t) / c Injury 2 * n = m = s = 2.5 ac = 250 g ac = 25,000 rad/s

* values from Kramer and Appel field accident database, 1990

GAMBIT Gmax

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Rotational Injury Inconclusive HIP : Head Impact Power

Lately developed Coefficients for different directions could be chosen

Solution ? Computational (Finite Element Models)

Questions?

Head and Brain Injuries

Mehdi Shafieian Department of Biomedical Engineering Amirkabir University of Technology (Tehran Polytechnic)

29th International Course on Transport Planning and Safety December 2019

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