II' Dynamic Neuropathology of Cerebral Injury

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II. Dynamic Neuropathology of Cerebral Injury
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Cerebral Energy

• A continuous supply of energy is important for
  maintaining several aspect of brain functioning,
  including
• membrane potentials and electrochemical
  gradients
• neurochemical processes responsible for synaptic
  transmission and
• integrity of intracellular structures and
  membranes.
• Energy is produced in the brain almost entirely
  from oxidative metabolism of glucose.
• Oxidative metabolism of glucose yields energy in
  the form of phosphate bonds, the most important
  of which is ATP (adenosine triphosphate).

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Cerebral Energy

• Under conditions of aerobic metabolism, not only
  is ATP produced, but CO2 is a resulting
  metabolite that facilitates vasodilation of
  cerebral vessels and increases cerebral blood
  flow.
• The energy status of any part of the brain is
  reflected by its content of ATP which demands
  more O2.
• Thus, increasing function results in increasing
  O2 requirements, while decreasing function
  reduces O2 demands.
• The brain can only store O2 for a few seconds and
  cannot store glucose.

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Cerebral Energy

• Therefore, an incessant supply of both glucose
  and O2 is essential for the continuing function
  of the brain.
• If the energy supply fails completely, rapid and
  dramatic events occur.
• After a few seconds neuronal function fails
• After a few minutes, permanent structural damage
  occurs.

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Hypoxemia

• Hypoxemia is an abnormal deficiency of O2 in the
  arterial blood.
• Hypoxemia can result from a variety of pulmonary
  conditions, such as chronic obstructive pulmonary
  disease (COPD), in which an inadequate amount of
  O2 makes it into the arterial blood.
• With inadequate arterial O2, the brain
  experiences a consequent inadequate level of
  cellular O2, a condition known as hypoxia.

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Hypoxemia

• With hypoxia at the cellular level of the brain,
  glucose can only be metabolized by less efficient
  anaerobic means.
• Anaerobic metabolism of glucose produces less ATP
  as well as metabolites other than CO2.
• Glucose only partially oxidized results in lactic
  acid, which accumulates in the blood and reduces
  the cells electron transport system.
• Lysosomes within the neuron cell bodies are
  sensitive to decreases in O2.

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Ischemia

• Ischemia refers to a reduced blood supply to the
  brain that deprives the neuronal tissue not only
  of O2 but of glucose as well.
• The effects of low O2 have been discussed
  (anaerobic metabolism), but low glucose levels
  (hypoglycemia) can contribute to mental
  confusion, dizziness, convulsions, and loss of
  consciousness.
• Tissue ischemia can damage the blood-brain
  barrierthe special mechanism that permits
  differential passage of certain materials from
  the blood into most parts of the brain.

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Ischemia

• This may result in brain edema and a rise in
  intracranial pressure (ICP).
• Ischemia may also cause a rapid depletion of ATP,
  paralyzing the membrane transport system, and
  allowing accumulation of toxic molecules.
• Increased tissue toxicity can also disrupt the
  blood-brain barrier, causing the capillary lumens
  to swell shut, further compounding tissue
  ischemia.

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Cerebral Blood Flow

• Blood flow, or perfusion, refers to the amount of
  blood that passes through a blood vessel in a
  given period of time.
• Blood flow is determined by (1) blood pressure
  and (2) resistance, the force of friction as the
  blood travels through blood vessels.
• The level of blood flow throughout the brain is
  carefully regulated to the metabolic needs of
  different parts of the brain.

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Cerebral Blood Flow

• Although the brain receives about 15 of the
  hearts total output, or about 800 ml/min of
  blood, the level of flow through the grey matter
  is much greater than that of the white matter.
• The difference in the level of flow reflects the
  greater metabolic activity and greater
  vascularity of the grey matter.
• Moreover, the level of flow also varies between
  different parts of the cerebral cortex, depending
  upon functional demands.

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Cerebral Blood Flow

• If PaO2 falls below 50 mm Hg, a distinct increase
  in cerebral blood flow takes place.
• If PaO2 falls to 30 mm Hg, cerebral blood flow is
  more than doubled.
• Raising PaO2 above 100 mm Hg causes only slight
  changes in cerebral blood flow.
• Point to Ponder What is the potential
  consequence of doubled blood flow of hypoxemic
  blood?

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Cerebral Blood Flow

• CO2 is a very potent stimulus of cerebral
  vasodilation, so variations in PaCO2 can cause
  profound changes in cerebral blood flow.
• Cerebral blood flow doubles when PaCO2 is
  increased from 40 to 80 mm Hg.
• Cerebral blood flow is halved when PaCO2 drops to
  20 mm Hg.
• Below 20 mm Hg, PaCO2 has very little effect on
  cerebral blood flow.
• The flow is probably so low because of tissue
  hypoxia.

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Cerebral Blood Flow

• In a variety of pathological situations, the
  response of cerebral blood flow circulation to
  either changes in PaO2 or PaCO2 levels may be
  profoundly altered.
• When there is a focal disorder, cerebral blood
  flow may fail to increase during low O2.
• Indeed, blood flow may be increased to the
  surrounding normal area at the expense of the
  fall in flow in the affected area.
• This is referred to as steal, where the normal
  surrounding areas of the brain are
  hyperperfused while the area in which there is
  some focal damage is actually hypoperfused.

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Pressure Regulation

• The brains mechanism for maintaining a constant
  flow of blood despite wide changes in arterial
  pressure is referred to as the autoregulator.
• Chemocoreceptors and baroreceptors in arterial
  walls cause them to constrict or dilate in
  response to changes in pressure or gas levels.
• When pressure is reduced, dilation occurs.
• When pressure is increased, constriction occurs,
  which over the long term can cause increased
  resistance and increased damage to the arterial
  lumen.

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Pressure Regulation

• Any factor which alters the ability of the
  cerebral vessels to constrict or dilate
  interferes with the autoregulator.
• The autoregulator can be impaired or even
  abolished by a wide variety of insults, such as
  ischemia, hypoxia, hypercapnia (?CO2), and brain
  trauma.
• At arterial systolic (top) pressures below 60 mm
  Hg, as in the case of hemorrhage, vasodilation
  still occurs but the mechanism is no longer
  sufficient to prevent blood flow from falling.

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Pressure Regulation

• At acute extreme rises in diastolic (bottom)
  blood pressure over 160 mm Hg, vasoconstriction
  fails and the cerebral vessels become distended.
• Cerebral blood flow increases, but in the areas
  of vessel distension, there may be breakdown of
  the blood-brain barrier with foci of cerebral
  edema.

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Reduced Blood Flow

• When cerebral blood flow is reduced, a
  progressive sequence of events can be
  demonstrated.
• Initially, electrical function and metabolism
  continue but impaired.
• From impairment of function follows complete
  failure of electrical activity.
• At certain critical reductions in blood flow,
  loss of cell homeostasis occurs.
• When blood flow is reduced to about 30-35 of
  normal values, responses to somatosensory
  information and cortical directives fail.

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Reduced Blood Flow

• Cell death becomes inevitable only at even lower
  levels of blood flow.
• At least in the short term, ischemic
  neurological dysfunction can be reversed by
  restoring blood flow.

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Intracranial Pressure

• There are four intracranial constituents
  contained within the noncompliant skull.
• These are the brain (neurons and neuroglia),
  cerebrospinal fluid (CSF), cerebral blood, and
  extracellular fluid.
• Glial and neural tissues account for about 70 of
  intracranial contents.
• CSF, cerebral blood, and extracellular fluid each
  account for another 10 of the total volume.
• Increased intracranial pressure (ICP) results
  from an addition to the volume of these
  intracranial constituents in excess of
  compensatory capacity.

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Intracranial Pressure

• CSF may be squeezed from the cranial subarachnoid
  space and ventricles into the spinal subarachnoid
  space.
• Cerebral venous blood may be expelled into the
  jugular veins or into the scalp via emissary
  veins.
• However, past these compensatory mechanisms, any
  increase in blood (e.g., hematoma), extracellular
  fluid (e.g., edema), brain tissue (e.g., tumor),
  or CSF (e.g., hydrocephalus) may induce an
  increase in ICP.
• The brain can handle some changes in ICP without
  affecting cerebral blood flow if the
  autoregulator is not impaired.

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Intracranial Pressure

• However, if the autoregulator is impaired because
  of some pathological condition (see slide 28),
  much smaller increases in ICP can be tolerated
  before the sufficient reduction in cerebral blood
  flow may produce neurological dysfunction.
• In multiple trauma, hypotension from other organ
  injuries may further narrow the difference
  between mean arterial pressure and ICP.
• In other words, since raised ICP is common in
  brain trauma and since trauma impairs the
  autoregulator, it should not be surprising that
  ischemic brain damage is also found.

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Brain and Water Edema

• The brain has a high water content 80 in grey
  matter and 70 in white matter, where the fat
  content is higher.
• The majority of brain water is intracellular, but
  extracellular fluid volume makes up as much as
  10 of the intracranial space.
• Brain water is derived from the blood and
  ultimately returns to it by reentry at the venous
  ends of the capillaries.
• Relatively little brain water passes through the
  CSF, but this route may be more important when
  edema is present.

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Brain and Water Edema

• Edema refers to an increase in tissue fluid
  content that results in increased tissue volume.
• Two different forms of cerebral edema are
  recognized vasogenic and cytotoxic edema.
• Vasogenic edema is the most common cause of brain
  edema and results from disruption of the
  blood-brain barrier.
• Fluid is allowed to flow out of the cerebral
  vessels into the extracellular space.
• In other words, the origin or genesis of the
  edema is in the vessel (vaso).
• This form of edema largely affects the white
  matter and is the most common kind of edema
  encountered after HI.

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Brain and Water Edema

• Cytotoxic edema, on the other hand, is
  intracellular swelling of neurons and glia in
  grey matter, with a concomitant reduction of
  brain extracellular space.
• It occurs in hypoxia, after cardiac arrest, or
  asphyxia because the ATP dependent
  sodium-potassium pump allows sodium and water to
  accumulate within the cells.
• In other words, the cell (cyto) becomes toxic
  from the accumulation of sodium and water within
  the cell.

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Morphological and Neurochemical Changes

• The most characteristic morphological change in
  the brains of AD patients is the formation of
  neurofibrillary tangles.
• Neurofibrillary tangles are an intracellular
  abnormality, involving the cytoplasm of nerve
  cells.

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Neurofibrillary Tangles

• Neurofibrillary tangles consist of paired
  filaments twisted around one another in a helical
  fashion that course throughout the cytoplasm.

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Neurofibrillary Tangles

• In Alzheimer's disease, neurofibrillary tangles
  are generally found in the neurons of the
  cerebral cortex and are most common in the
  temporal lobe structures, such as the hippocampus
  and amygdala.
• Spared cortical areas are seen in dark blue.

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Neuritic Plaques

• Neuritic or senile plaques are extracellular
  abnormalities.
• They consist of a dense central core of amyloid,
  surrounded by a halo and a ring of abnormal
  neurites (degenerated axon terminals and
  preterminals).

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Neuritic Plaques

• They are found in the same brain centers as FTS,
  especially in the outer half the cortex where the
  number of neuronal connections is greatest.

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Neuritic Plaques

• A slide showing NFTs (in black) and senile
  plaques (in brown).
• Neurons containing NFT eventually die.

31
Granulovacular Degeneration (GVD)

• GVD is a descriptive term that refers to the
  presence of fluid-filled space and granular
  debris within nerve cells.
• Like NFTs and neuritic plaques, GVD has a
  predilection for the hippocampal formation, and
  are significantly related to the presence of
  dementia

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Lewy Bodies

• Lewy bodies are structures located within the
  cytoplasm of neurons that characteristically have
  a circular and dense protein core surrounded by a
  peripheral halo.
• They have often been likened to a sunflower--a
  dense central core of circular shaped structures
  with a rim of radiating filaments.

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Lewy Bodies

• These kind of Lewy bodies are usually found in
  brainstem locations, such as the substantia nigra
  and the locus ceruleus , and may appear singlely
  or multiply within a neuron.
• In other locations, such as the cerebral cortex,
  they are often more elongated, and usually
  lacking the peripheral halo around the central
  core.

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Lewy Bodies

• They are distinctive neuronal inclusions, thought
  to be the result of altered neurofilament
  metabolism and/or transport due to neuronal
  damage and subsequent degeneration, causing an
  accumulation of altered cytoskeletal elements.
• F. H. Lewy first described Lewy bodies in 1912.

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Lewy Bodies

• They were first linked to idiopathic Parkinson's
  disease, but more recently, it has been noted
  that Lewy bodies may be seen in several different
  neurodegenerative processes, including diffuse
  Lewy body disease, Alzheimer's disease, and
  idiopathic Parkinson's disease.

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Picks Bodies

• Ultrastructuraly, Pick bodies consist mostly of
  bundles of disorganized straight filaments, which
  may be mixed with coiled fibrils.
• PB are homogeneous and smooth-edged, and the
  large majority are round or ovoid, although some
  are occasionally flame-shaped.

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Picks Bodies

• In addition to Pick bodies, the cerebral cortex
  in Pick's disease may contain neurons with
  distended cytoplasm called "ballooned cells" or
  "Pick cells.
• In Picks disease, there is extensive neuron loss
  and gliosis concentrated in the outer third of
  the cerebral cortex.
• Some authorities believe Pick cells represent
  deafferented neurons.

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Picks Bodies

• In Picks disease the frontal and temporal lobes
  are most affected with brain cells in these areas
  found to be abnormal and swollen.
• When these typical features are not seen on post
  mortem examination but the same areas of the
  brain are affected by cell death, the case may be
  described as Picks syndrome or frontotemporal
  dementia.

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III. Structural Neuropathology of Cerebral Injury
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Categories of Brain Injury

• CHI to the brain results in two categories of
  brain injury, primary and secondary.
• Primary injury occur immediately following impact
  and is related to instantaneous events directly
  caused by the blow.
• The resultant tissue disruption is usually
  permanent, and does not respond to pharmacologic
  or physiologic manipulations.
• It frequently constitutes the limiting factor for
  the most idea recovery.
• Extensive primary injury presupposes a poor
  outcome, regardless of medical and rehabilitative
  therapy.

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Categories of Brain Injury

• Secondary injury occurs as a result of
  epiphenomena causally related to the primary
  injury.
• Impact disruption of large dural or cortical
  vessels often lead to epidural or subdural
  hematomas.
• Disruption of capillaries or disturbance of
  vascular endothelial membranes during the
  original impact may lead to vasogenic cerebral
  edema.
• As both hematoma and edema constitute mass
  effect, they raise intracranial pressure and may
  result in brain shift and cerebral hypoperfusion.
  
• Brain herniations represent shift of the normal
  brain through or across regions to another site
  due to mass effect.

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Schematic of Brain Injury
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Herniation

• The cranial cavity is partitioned by the
  tentorium cerebelli and falx cerebri.
• When a part of the brain is compressed by an
  extrinsic lesion, such as a subdural hematoma, or
  is expanded because of a contusion or other
  intrinsic pathology, it is displaced (herniates)
  from one cranial compartment to another.

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Herniation

• Three major herniations can occur, either alone
  or in combination.
• Subfalcial herniation is displacement of the
  cingulate gyrus from one hemisphere to the other,
  under the falx cerebri.

The left cingulate gyrus has herniated under the
falx.
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Herniation

shift of the uncus into the suprasellar cistern
as well as a subfalcine shift to the right.
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Herniation

• Acute foramen magnum herniation clinically can be
  catastrophic as the brains extrudes through the
  foramen magnum.
• Increased pressure within the posterior fossa
  will result in herniation of the cerebellar
  tonsils into the foramen magnum and compression
  of the medulla.

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Secondary Injury

• Hypoperfusion and herniation lead to further
  brain damage in the form of pressure necrosis and
  infarction, often remote from the site of the
  primary injury.
• Secondary lesions, unlike primary ones, are
  potentially avoidable if they are caught quickly
  and amenable to treatment, such as surgical
  evacuation of hematoma and edema therapy.

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Skull-Brain Interface

• The frontal lobes sit in the anterior fossa of
  the cranial cavity region of the skull.
• The anterior lateral aspects of the frontal bone
  swing around each of the frontal lobes,
  encapsulating them.

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Skull-Brain Interface

• Arising medially in the anterior cranial fossa is
  the crista galli, a bony protuberance originating
  from the ethmoid bone.
• It partially separates the anterior ventral
  aspect of both frontal lobes and provides an
  anchor for the falx cerebri.

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Skull-Brain Interface

• The middle cranial fossa that bounds the temporal
  lobes is formed by the temporal bone, laterally,
  and the greater wing of the sphenoid bone,
  anteriorly and medially.
• The sphenoid wing and ethmoid bone are quite
  irregular, jagged, and rough in some locations.

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Skull-Brain Interface

• With cerebral trauma, it is quite common for
  contusions (bruising) to occur in cerebral
  regions adjacent to these skull regions where
  there is the greatest brain-bone interface.
• The most common neuropathological consequence is
  damage to the hippocampus and other medial
  temporal lobe limbic structures, resulting in
  post-traumatic memory disorder and emotional
  behavior changes.

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Skull-Brain Interface

• Superficial bruising of dural crests are
  frequently found in frontal and temporal regions
  regardless of the site or direction of initial
  impact.

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Primary Impact Damage

• CHI typically gives rise to contusions and
  lacerations on or within the surface of the
  brain.
• Strictly speaking, lacerations are lesions that
  break the pia mater, while contusions leave the
  pia mater intact.
• Lacerations are usually found on the superficial
  crests of the gyri of the cerebral hemispheres,
  but they may penetrate the whole thickness of the
  cortex and extend into the subcortical white
  matter.

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Primary Impact Damage

• Lacerations are hemorrhagic lesions which may
  lead to edema and necrosis within the brain.
• They usually heal and leave yellow-brown atrophic
  scars that are easily recognized on autopsy.

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Primary Impact Damage

• The lesions seen here are the result of extensive
  blunt force trauma to the head in a vehicular
  accident.
• Mainly the gyri are affected with hemorrhage from
  contusions and lacerations.

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Primary Impact Damage

• Potential sites for cerebral contusion following
  CHI include
• Site of impact
• Sites diametrically opposite site of impact
• Frontal and temporal lobe crests and
• Surface lesions of the upper borders of the
  hemispheres.
• Primary brain injuries can be caused by both
  acceleration dependent and non-acceleration
  dependent factors.
• The majority of CHIs involve acceleration
  dependent mechanisms.

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Acceleration Dependent Factors

• There are two common types of acceleration
  translational acceleration and angular
  acceleration.
• Translational acceleration results when the
  resulting pathway of force applied to a ridge
  body passes through the bodys center of gravity,
  the body will assume linear acceleration along
  the direction of the force.
• If the resulting force pathway does not pass
  through the bodys center of gravity, the body
  rotates around its own center of gravity.
• This is called angular acceleration.

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Acceleration Dependent Factors

• Pure angular acceleration only exists if the body
  is simultaneously acted upon by two opposing
  forces of equal magnitude directed at opposite
  sides of the center of gravity.
• If a single linear force does not pass through
  the center of gravity, two pathways will result.
• The one passing through the center of gravity
  will produce translational acceleration.
• The one passing perpendicular to the center of
  gravity will cause angular acceleration.
• In other words, the body spins around its own
  center of gravity while at the same time
  traveling linearly.

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Acceleration Dependent Forces
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Acceleration Dependent Forces

• Most impact forces are unpaired and produce
  combined rotational and linear motions.
• The observed cranial movement is always a
  combination of both translation and rotation.
• Some degree of rotation always occurs around the
  foramen magnum, because of the how the head is
  attached to the cervical spine.
• The traumatized brain always includes inseparable
  markings of both translational and rotational
  trauma.

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Translational Trauma

• Pure translational trauma is exemplified by a
  sharply dealt blow to the occiput of a stationary
  but movable head.
• The head will rapidly accelerate forward.
• Because of inertia, the brain will lag behind
  until it is pushed forward by the advancing
  skull.
• This lagging results in differential movements of
  the brain and a skull.
• The delicate cortex is rubbed against rough
  surfaces of the dura-lined skull base.

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Translational Trauma

• A not so pure example of translational trauma
  occurs when the accelerating head hits some
  unyielding surface, like a windshield.
• The skull decelerates to a sudden halt, but the
  brain continues to plunge forward at its
  accustomed velocity until it too is stopped by
  the frontal skull.
• This site of initial brain impact with the skull,
  termed the impact pole, causes the coup lesion.
• The exact sequence of events reverses direction,
  and the brain lags behind the skull moving in the
  opposite direction.

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Translational Trauma

• The resulting injury at the antipole, at the site
  directly opposite the impact pole, is called the
  contrecoup lesion.
• The deceleration process, in both directions,
  often takes several oscillations before the brain
  achieves zero velocity.
• The repeated slamming of the brain at the impact
  pole and antipole results in contusive coup and
  contrecoup lesions.
• The brain also pulls away from the skull at the
  antipole, causing greater tissue displacement and
  greater contrecoup injury.
• Moreover, the brain-skull interface will undergo
  several pendular swings, as the head rotates
  around its vertical axis.

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Translational Trauma

• The cortex rubs repeatedly against the sharp
  dural edges of the falx, the sphenoid ridge, and
  the jagged floor of the anterior cranial fossa.
• As a result, severe lacerations are often seen on
  the orbital frontal cortices and the tips of the
  frontal and temporal lobes (see slide 18).
• With translational trauma the force applied to
  the skull is distributed over an appreciable area
  of the brain.

65
Rotational Trauma

• Rotational trauma depends on shearing strainthe
  displacement of one point relative to another as
  a consequence of the stress per unit area.

66
Rotational Trauma

• During angular acceleration of the head, the
  brain will initially remain stationary while the
  skull rotates.
• Eventually, the brain is dragged along by
  friction forces over the bony prominences of the
  anterior and middle fossa floors.
• The brain matter dragged over their prominences
  is subjected to parallel shearing, causing
  cortical contusions.
• The location of these surface shearing sites
  corresponds to the basal frontal and temporal
  lobes, the cingulate gyrus, the temporal poles,
  and the frontal poles.
• The inferior surface of the occipital lobes
  usually escapes injury.

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Rotational Trauma

• The neurons and glia suffer damage with even
  slight distortion of shape.
• Cell to cell and cell to axon shearing leads to
  multiple tearing of neural elements throughout
  the deep portions of the brain.

68
Rotational Trauma

• Instead of cortical lesions, intracranial
  hemorrhages, or raised intracranial pressure,
  there is diffuse white matter lesions in the form
  of axon retraction balls from widespread axonal
  transection.

69
Rotational Trauma

• Shearing lesions have a predilection for the
  grey-white matter junctions around the basal
  ganglia, the ventricles, the superior cerebellar
  peduncles, the corpus callosum, and the fiber
  tracts of the brainstem.

70
Non-Acceleration Dependent Factors

• Clinical head injuries not involving acceleration
  of the skull are rare.
• A typical example is the car mechanic lying in
  the grease pit when the car falls on his
  supported head.
• A less pure example is the individual whose
  head is hit directly on the vertex by a falling
  object.
• In both cases, there is no head movement, and the
  energy is usually diffuse causing extensive
  fractures but little brain injury.

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Impression Trauma

• If an object falls on the vertex of the head, the
  initial loading of forces results in inward
  bending of the skull at a relatively small impact
  point.
• When the loading is exhausted, the elasticity of
  the skull forces it to recover its initial
  configuration.

72
Impression Trauma

• The inertia of the skull causes it to overshoot
  its initial contour, like a spring suddenly
  released from a compressed state.
• When the overshoot occurs, the brain is pulled
  away from the skull, and the tissue is displaced
  creating a coup lesion at the point of impact.

73
Ellipsoidal Deformation

• In the case of a fronto-occipital impact of the
  supported head, the impact will momentarily
  convert the ellipsoidal skull into a sphere, by
  lengthening the bitemporal axis and shortening
  the fronto-occipital axis.
• Portions of the brain located along the collision
  axis will move to the center because of the
  shortening of the axis.

74
Ellipsoidal Deformation

• Those portions parallel to the vertical axis will
  move away from the center.
• Thus, destructive shearing strains will occur in
  and around the center of the brain.
• The ventricular walls and part of the corpus
  callosum abutting against the lateral ventricles
  may be particularly vulnerable to this type of
  central shearing.

75
Concussion

• On of the continuing puzzles in head injury is
  the pathological basis for the phenomenon of
  concussion.
• The person becomes briefly unconscious after a
  blow to the head, recovers consciousness, and
  goes on to make an apparently perfect recovery.
• The pathogenesis is unknown (probably chemical
  and physiological abnormality).
• There is no gross or microscopic abnormality.
• Loss of consciousness implies interference with
  the function of the reticular system in the
  brainstem.

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Concussion

• Features of concussion that also suggest
  brainstem dysfunction are changes in blood
  pressure, pulse rate, and respiration.
• Concussion is thought to result from minor
  structural and biochemical changes of brainstem
  nuclei.

77
Post-Traumatic Complications

• Residual disability or new developing
  complications (e.g., seizure disorder
  hydrocephalus) may be related to impact damage,
  to various early secondary pathological
  processes, or to later events, such as scarring
  or adhesions of brain tissue or blockage of CSF
  pathways.
• Some of the post-traumatic complications are
  caused by diffuse (widespread) injury other by
  focal (limited) injury.
• The most severe form of diffuse damage is the
  chronic or persistive vegetative state, affecting
  about 5 of head injury survivors.

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Post-Traumatic Complications

• In cases where there is extensive neocortical
  necrosis, the cause is not so much the severity
  of the injury, but a consequence of resuscitation
  following cardio-respiratory arrest.
• In cases where there is extensive subcortical
  white matter shearing, the cause is the severity
  of the initial impact damage.
• In either case, the cortex has been rendered
  functionally inactive by widespread severe
  destruction of brain tissue.

79
Post-Traumatic Complications

• Focal injuries, such as contusions or hematomas
  will often leave residual focal neurological
  deficits such as hemiplegia (paralysis of one
  half side of the body), hemiparesis (weakness of
  one half side of the body) hemianopsia (loss of
  one half of the visual field), aphasia (disorders
  of language, both receptive and expressive).
• Cranial nerve abnormalities often arise when
  cranial nerves are damaged when the skull is
  fractured or when the brain is thrown about
  during acceleration/deceleration injury.

80
Post-Traumatic Complications

• Some common occurrences are damage to the
  olfactory (CN I) nerve after basilar skull
  fracture, resulting is anosmia, a partial or
  total loss of the sense of smell.
• Damage to the optic nerve (CN II) may lead to
  transient loss of vision.
• Damage to the facial (CN VII) nerve after
  temporal bone fracture may produce facial
  paralysis and
• Damage to the vestibulocochlear nerve (CN VIII)
  after basilar fracture in which otorrhea or
  hematotympanum is present, may affect hearing as
  well as vestibular function.

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Post-Traumatic Complications

• There is a definite risk of developing a chronic,
  recurring seizure disorder after significant head
  trauma.
• The following factors significantly raise the
  probability of developing post-traumatic
  epilepsy
• 1. depressed skull fracture with dural tear
  (gt50)
• 2. penetrating wounds (gt50)
• 3. Amnesia of gt than 24 hours
• 4. Time after injury that first seizure occurs
  a. Immediate (little chance of becoming chronic)
  b. 1st week (33) and c. 1st 8th week (70).

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Post-Traumatic Complications

• Seizures can first appear many years after an
  accident.
• They are usually focal and more difficult to
  treat than idiopathic epilepsy.
• Post-traumatic epilepsy is a chronic disorder,
  with only a 40 cure rate after 5 years.
• Post-traumatic syndrome (PTS) is the most common
  and probably most complex sequelae of HI.
• The basic elements of the syndromes are headache,
  dizziness, difficulty concentrating, and a host
  of vague behavioral symptoms such as anxiety,
  depression, and nervous instability.

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Post-Traumatic Complications

• This syndrome is more common with slight trauma
  than serious.
• The syndrome usually lasts a few weeks to a few
  months, with symptoms gradually disappearing only
  to be exacerbated by strenuous physical activity,
  emotional stress, or the use of alcohol.
• Patients in highly physical or stressful jobs
  should be warned that symptoms might recur when
  they return to work.
• Rest and symptomatic treatment are usually
  required.