DR.

ROMAN AL MAMUN

Lecturer and Autopsy Surgeon

Forensic Science and Toxicology

Anatomically it can be categorized into:

1. Scalp injury
2. Skull injury
3. Injury to meninges
4. Brain injuries
5. Facial injuries

Scalp injury
It is composed of 5 layers:
1. Skin
2. Connective tissue
3. Galea aponeurotica
4. Loose areolar tissue
5. Pericranium

Abrasions : brush abrasions are less common

Contusion : black eye, spectacle hematoma
Lacerations : split Lacerations ( incised looking lacerated
wound)
Incised wounds : clean cut margins, hair bulbs are cleanly cut

MLI : Infected wounds of scalp and may cause

thrombophlebitis of emissary vein.
Damage of axons and blood vessels
Stretching of axons with consequent disruption and loss of
function depending on strain.
M/E: wide spread white matter damage in the form of
ruptured axons and spheroids( circular or elongated
granular bodies containing cell organelles)
Dilatation of axons
Long standing duration: microglial reaction, myelin
degeneration,micro cavites, enlargement of ventricular system
d/t loss of white matter

e.g. punch drunk syndrome

Caused by diffuse neuronal damage brain stem with little or
no anatomical disturbance
More severe in deceleration injury.
No naked eye lesion on autopsy.
On histology microscopic hemorrhage may be found.
There is sudden loss of consciousness with tendency for
spontaneous recovery.
In less severe cases pt regains consciousness with signs of
cerebral irritation.
Recovery is often followed by retrograde amnesia, which
may extend from fortnight to month or more.
Post traumatic automatism may follow.

Can be confused with acute alcohol intoxication.

Extravasations of blood from traumatically ruptured blood

vessel into brain substance.
Generally involve crest of gyri but may extend as wedge
shaped lesion.
Cerebral hemorhage by small punctate or streak like
hemohages and mass focal destruction of tissue with or without
oedema
They enlarge with time, esp in persons with HTN, liver
cirrhosis or bleeding disorder.
After absorption of contusion golden brown area of gliosis
(blood cyst) is left.
Clinical manifestations vary with site and size of contused
area.
Brain contusions in infants differ from adults, they appear as
mild haemorrhagic tears in sub cortical white matter.

Can be caused by penetrating wound as well as by closed

head injury with high degree of shear strain.
These are accompanied by rupture of pia mater.
Usually surrounded by group of contusions.
Subarachnoid Hg commonly accompanies the lesion because
of rupture of pia mater.
Healing may be in form of adhesions b/w brain and dura
mater,which may result in post traumatic epilepsy.
Healing of laceration in cerebral ventricle may be in form of
large glial cysts k/a Porencephalic cysts, can be differentiated
from blood cysts by presence of blood pigments.
Most common cause of raised intracranial pressure.
m/b related to diffuse neuronal injury and concussion.
Autopsy findings: dura is stretched, brain bulges through
incision,gyri are pale and flattened,sulci are obliterated, cut
surface appears pale,ventricles are.
greatly reduced in size,herniation of hippocampal gyri,secondary
brain stem Hg and coning of intracellular tonsil.
Sports Injuries and Cognition
It has long been recognised that sports injuries, and particularly those
resulting from contact sports such as boxing, have the potential to cause
long term cognitive consequences when injuries involve the athlete’s
head.

Neuropsychologists are increasingly responsible for the diagnosis of

acute and chronic cognitive and emotional sequelae resulting from
sports-related head injuries.

In addition to cognitive fall out directly related to the head injury, a

growing body of literature details the long term consequences of
multiple head injuries sustained during sport activities, and in particular,
the increased risk of developing a neurodegenerative disease later in life.

A large proportion of what we know about sports related cognitive

presentation comes from the study of boxers. These included “punch
drunk” and “slug nutty”.

By the 1970’s, evidence from studies examining brains of boxers’

posthumously confirmed that chronic head trauma, such as that
experienced by boxers and other contact sport athletes, may lead to the
development of a unique neurodegenerative condition that presents
similarly but is distinct from other dementias such as that seen in
patients with Alzheimer’s disease and Parkinson’s disease.

Initially termed dementia pugilistica, the condition is now widely known

as chronic traumatic encephalopathy (CTE).

CTE is the most severe form of damage across a continuum of

conditions associated with sports injuries.

In recent years, traumatic brain injury (TBI) and chronic

traumatic encephalopathy (CTE) in contact sports participants
have received intense media,medical and scientific attention.

TBI is generally divided into acute and chronic.

Acute brain injury in sports-related trauma may lead to concussion,

subconcussion, haemorrhage or other structural brain damages.

The chronic consequence of TBI is CTE, a neurodegenerative condition,

in which progressive clinical symptoms often begin several years after
retiring from the sport with abnormal tau accumulation as the
histological hallmark.

The aim of this review is to give an overview of the short and long term
neurological consequences of sports-related TBI,including the
characteristic clinical and neuropathological findings.

The pathophysiology of TBI and the possible mechanisms leading to

progressive histological changes of CTE in later life years after the TBI
has ceased are discussed.

Common acute TBIs in sports are skull fracture, subdural and epidural
haematoma and ruptured vertebral artery with subarachnoid
haemorrhage.

Catastrophic brain injuries refer to severe brain trauma associated with

intracranial bleeding or cerebral contusions which may result in death
or long term neurological sequelae.

The most common cause of death in sports-related TBI is subdural

haematoma especially in boxers.

Approximately ten deaths occur each year in boxing,most of which

following knockout or technical knockout.

Most deaths are in lower weight classes in boxing.

Classification of TBI
• Mild (GCS 13-15)
• Moderate (GCS 9-12)
• Severe (GCS 3-8)

Pathophysiology:
 • TBIs are a result of dysfunction in neuronal
metabolism
• and the microscopic anatomy of the brain that occurs
in
• two distinct phases.
• Difuse axonal injury (DAI) is the hallmark injury of
TBI and occurs during an initial phase of neuronal
and parenchymal as the direct result of the traumatic
force.
• DAI is a result of a rotational forces, and is important
to distinguished from cortical contusions or other
hemorrhages due to linear acceleration/deceleration
injury
• A secondary delayed phase of the brain injury model
• includes inflammatory cascade activation, edema,
ischemia,
• efects of free radicals, excitatory amino acids, ion
release,
• and programmed cell death.
• Disruption of axonal neurofilament organization
occurs and impairs axonal transport leading to
axonal swelling, degeneration, and transection.
• Release of excitatory neurotransmitters
acetylcholine, glutamate and aspartate, and the
generation of free radicals may also contribute to
secondary injury.
Clinical Presentation of TBI in
Athletes:
• The clinical signs and symptoms of mTBIs may range
• from subtle mood changes to obvious loss of
consciousness.
• The onset of symptoms may be immediately
following the
• injury, or several minutes later.
• The signs of mTBI to be amnesia, behavior or
personality
• changes, confabulation, delayed verbal and motor
responses,
• disequilibrium, orientation, emotional labiality, loss of
consciousness,slurred/incoherent speech, or a vacant
stare.
• Symptoms of mTBI may include blurry/double vision,
confusion,dizziness, excessive drowsiness, sleep
difculties,
• feeling hazy, foggy, or groggy, headache, inability to
focus or
• concentrate, nausea, vomiting, and photo- or
phonophobia. Mood changes, emotional outburst,
and behavioral changes also may be the principle
manifesting symptoms of mTBI.
• Mild TBI should also be only a part of a broader
diferential diagnosis of the previously mentioned
signs and symptoms of other common sports-related
conditions such as poorly fitting helmet, dehydration,
migraine headache, heat exhaustion/stroke,
metabolic disturbances, and cardiac or other medical
conditions.
Sequelae of TBI in Sports
• The obvious immediate impact on the athlete is
dealing with the symptoms of a TBI including most
commonly headaches, but also poor sleep, excessive
drowsiness, poor concentration, and poorer cognitive
aptitude.
• Repeated mild TBIs occurring over an extended
period
• of time (i.e., months, years) may result in cumulative
neurological and cognitive deficits.
 • Professional football players with a history of three or
more TBIs were 5 times more likely to have mild
cognitive impairment.
• Professional boxers are well known to have a risk
• of significant cognitive decline and alterations in
brain
• function.
• Long term efects of repeated concussions include
chronic
• motor and neuropsychological deficits.
•
Prevention of TBI in Sports
• Helmets are primarily designed to reduce linear
accelerative/decelerative forces, not the rotational
forces which cause the DAI and in fact may increase
rotation forces experienced.
• Mouth guards have a definite role in preventing
dental and oro-facial injuries.
• The primary means in which rates of TBI incidence in
• sports will reduce is through rule changes to
minimize head
• impacts moving forward.
• Penalizing, fining, or suspending athletes who
intentionally impact another players head are means
to discourage brain trauma.

Pathophysiology of sports-related
TBI: Biophysical mechanisms in risk sports
Rapid acceleration and deceleration forces on the brain,
either linear or rotational, are the primary mechanism in
which concussion and subconcussion occur.
Rotational acceleration such as blows to the head by hook
punches in boxing results in concussion more frequently
than linear acceleration caused by straight head blows
and head contacts in other sports such as American
football.
When subjected to rapid acceleration, deceleration and
rotational
forces, the brain and all its components including
neurons, glial
cells and blood vessels are stretched, which may disrupt
their normal functions.
Axons that span long distances fromthe cell bodies are
particularly susceptible to stretching,whichmay lead to
difuse axonal injury,a basis for the symptoms
experienced in concussion.
Neurobiology and neurometabolic
cascade:
A neurometabolic cascade of concussion sets into motion
immediately following the biomechanical injury to the
brain, with rapid release of neurotransmitters, efflux of
K+ and influx of Na+, causing an increase in intra-axonal
calcium concentrations, which activates protease calpain
and triggers calpain-mediated proteolysis of the
cytoskeletal proteins, a process that can potentially lead
to irreversible
axonal pathology:
1). An increase in intra-axonal calcium also stimulates
glutamate release
and glutamate-mediated activation of N-methyl-D-
aspartate
receptors causing depolarization of neurons.
To restore the ionic balance, glucose consumption is
increased, which depletes the energy stores, leading to
events of impaired oxidative metabolism, glycolysis with
lactate production resulting in acidosis and cerebral
oedema.
Progressive microtubule disassembly is evident at the
time of acute TBI impairing axonal transport.
Axonal swellings occur and axons become disconnected
at the location of the injury, which most commonly occur
in
the deep gyri at the grey and white matter interface.
Difusion tensor imaging has found a correlation between
white matter abnormalities after mild TBI and the severity
of postconcussive cognitive problems.

Biomarkers
Cerebrospinal fuid
Several cerebrospinal fluid (CSF) biomarkers of TBI have
been
established.
The levels of total tau protein and neurofilament light
polypeptide (NFL) are raised reaching peak levels
4–10 days after TBI.
Total tau protein levels are elevated in lumbar CSF in
boxers 4–10 days after a bout and in boxers who have not
been knockout.
The level of total tau protein levels normalize within the
8–12 weeks providing the boxers have not been subjected
to further bouts.
Blood:
Blood biomarkers have been studied but no reliable
markers of TBI.
Levels of total tau and S100-B in the blood are increased
in professional ice-hockey players following concussion
and returned to pre-concussion baseline levels during
rehabilitation,suggesting acute axonal and astroglial
injury associated with the concussion.

Boxers exhibiting cognitive, behavioral, or motor abnormalities were

well known to lay persons, sportswriters, and others within the boxing
community and were referred to by various terms, such as “punch
drunk,” “goofy,” and “slug-nutty”2,3; later, the more formal term
dementia pugilistica was introduce.
Chronic traumatic encephalopathy (CTE):
Chronic traumatic encephalopathy (CTE):

CTE is a neurodegenerative disorder which has been noted in athletes

who have sustained chronic cerebral trauma.

The symptoms typically become evident years after the individual has
stopped engaging in the sport/activity and manifests as mild confusion,
ataxia (lack of voluntary muscle co-ordination) and features associated
with Parkinson’s disease such as tremors, rigidity and motor slowing.
As the disease progresses, changes in cognition become more evident
and are characterised by poor memory, attention, processing speed and
executive functions such as decision making, planning, organising and
prioritising.

Personality and behaviour changes also become evident and often take
the form of impulsivity, rage/aggression, and childish or inappropriate
behaviour.

CTE is associated with several structural, chemical and pathological

changes in the brain. The image below illustrates some of the structural
changes evident post-mortem in a patient with CTE.
Over the last several decades, clinical and neuropathologic evidence of
CTE has emerged in association with various sports, including American
football, professional wrestling, professional hockey, and soccer, as well
as other activities associated with repetitive mild head trauma, such as
physical abuse, epileptic seizures, and head Banging.
Although the incidence and prevalence of CTE is currently unclear, it
probably varies by sport, position, duration of exposure, and age at the
time of initial or subsequent head trauma, and with additional
variables, such as genetic predisposition.

CLINICAL SIGNS AND SYMPTOMS OF CTE:

Whereas concussion and postconcussion syndrome represent
temporary states of neuronal and axonal derangement, CTE is a
neurodegenerative disease that occurs years or decades after recovery
from the acute or postacute effects of head trauma.
The exact relationship between concussion and CTE is not entirely clear,
although repetitive axonal perturbation may initiate a series of
metabolic, ionic, membrane,and cytoskeletal disturbances, which
trigger the pathologic cascade that leads to CTE in susceptible
individuals.
The onset of CTE is often in midlife, usually after athletes have retired
from their sport.
In some individuals, the early manifestations of CTE affect behavior; in
particular, individuals with neuropathologically documented CTE have
been described by family and friends as being more irritable, angry, or
apathetic or as having a shorter fuse.
Increased suicidality seems to be a particularly
salient symptom of CTE.
In other cases, cognitive difficulties may be the first signs to
emerge, with poor episodic memory and executive functioning being
two of the most common cognitive dysfunctions reported.
Later in the disease, movement (eg, parkinsonism),speech, and ocular
abnormalities may emerge in the context of declining cognition and
worsening comportment.
A minority of cases with neuropathologically documented CTE
developed dementia before death; the relative infrequency of
dementia in individuals with CTE may be due in part to many individuals
with CTE having committed suicide or died from accidents or drug
overdose at an early age.
NEUROPATHOLOGY OF CTE
Gross Pathology
Neuropathologic studies of athletes with a history of repeated mild
head injuries have produced several consistent findings that, together,
make CTE a distinctive disorder.
On gross examination, there is often anterior cavum septi pellucidi and,
usually, posterior fenestrations.
These changes may be caused by the force of the head impact
Being transmitted through the ventricular system, thereby affecting the
integrity of the intervening tissue.
Enlargement of the lateral and third ventricles is also commonly
seen in CTE; the third ventricle may be disproportionately widened.
Additional gross features include atrophy of the frontal and temporal
cortices and of the medial temporal lobe, thinning of the hypothalamic
floor, shrinkage of the mammillary bodies, pallor of the substantia nigra,
and hippocampal sclerosis. Atrophy of the cerebrum, diencephalon,
basal ganglia, brainstem, and cerebellum mayresult in an overall
reduction in brain mass.
Microscopic Neuropathology:
Microscopically, CTE is characterized by an abundance of neurofibrillary inclusions
in the form of neurofibrillary tangles (NFTs), neuropil threads (NTs), and glial
tangles (GTs).
Although CTE shares many microscopic similarities with Alzheimer disease (AD)
and other tauopathies, it has several distinguishing features.
Although the precise pathologic mechanisms that tie repeated mild head injuries
to NFT formation are not known, they may involve a series of diffuse axonal
injuries (DAI) set in motion by the initial trauma and aggravated by subsequent
mild traumatic injuries.
Beta-amyloid (Ab) deposits are found in 40% to 45% of individuals with CTE, in
contrast to the extensive Ab deposits that characterize nearly all cases of AD.

CLINICAL IMPLICATIONS:
CTE is a Potential Late Effect of Repeated Head Injuries
CTE is not thought to be a long-term sequela after a specific head trauma.
Rather, its clinical symptoms emerge later in life, usually after athletes retire from
their sport.
Like most other neurodegenerative diseases that cause dementia, CTE has an
insidious onset and gradual course.
CTE in athletes, the mean age at onset is 42.8 years.
On average, onset occurs approximately 8 years after retirement ,although
approximately one-third of athletes were reportedly symptomatic at the
time of retirement.
Clinical dementia may occur late in the course of the disease.
Diagnosis of CTE:
Currently, the clinical diagnosis of CTE is difficult because there are no
consensus diagnostic criteria or large-scale longitudinal
clinicopathologic correlation studies.
The differential diagnosis of CTE often includes AD and frontotemporal
dementia (FTD), depending on the age at onset and the presenting
problem.
When the age at onset is earlier (eg, 40s or 50s) and the patient
presents with behavioral dysregulation or apathy, it may be difficult to
rule out FTD.
Although a history of remote head trauma may be suggestive of CTE,
head trauma has been implicated as a risk factor of AD, Parkinson
disease, ALS, and other neurodegenerative diseases.
Therefore, without neuropathologic confirmation, currently, a clinical
diagnosis of CTE cannot be made with a high degree of confidence.
Furthermore, the clinical phenotype of CTE may be confounded by
alcohol or other drug abuse.
Magnetic resonance spectroscopy may be capable of detecting changes
in glutamate/glutamine, N-acetyl aspartate, and myo-inositol,
molecular abnormalities that may serve as markers of brain damage
caused by head injuries.
Further,measuring tau and phospho-tau in cerebrospinal fluid may yield
diagnostically useful markers of CTE.

Definition of Concussion:

 Literally “To Shake Violently”.

 “…a traumatically induced alteration in
mental status, often manifested as
confusion or amnesia that is not
necessarily associated with loss of
consciousness”.

The 4th International Conference on Concussion in

Sport in 2012 (ICCS) defined:
“A concussion as a complex process induced by
biomechanical trauma, with the following common
clinical, pathologic, and biomechanical features.”
Concussion is frequently referred as mild TBI in the literature
and the two terms are used interchangeably.
A concussion is defined as ‘a complex pathophysiological
process affecting the brain, induced by biomechanical forces
either by a direct or indirect blow resulting in an impulsive force
transmitted to the head.’

Pathophysiology of Concussion
Trauma displaces the brain within the skull;
compresses neural tissue; accelerates, decelerates,
and rotates the brain within the hard casing of the
skull; and causes a coup as well as a contre-coup
injury.
Cortical pathways are disrupted, as seen on
difusion tensor tractography, especially with
frontal lobe connections; damage to the
brainstem’s reticular activating pathways alters
consciousness.
Pathologic changes include neuronal swelling and
axonal disruption.
Biochemical abnormalities include a sterile
inflammatory response and metabolic changes.
Injury to the young brain may also be related to
elasticity of the skull sutures and the presence of
vulnerable unmyelinated fibers in white matter
tracts.
Difuse axonal injury involves mechanical
disruption of the axon’s cytoskeleton and axonal
transport as well as axonal
swelling,proteolysis,disconnection and reorganiza-
tion. Disruption of neural membranes afects ion
channels, leading to potassium efflux, the release
of glutamate, higher energy (ATP and glucose)
consumption, increased lactate, increased Na-K
pump activity, suppressed nerve activity,
decreased blood flow, a hypometabolic state, and
eventual cell death.
Mitochondrial dysfunction and demyelination are
also involved in difuse axonal injury.

Grades of Concussion:
 There are diferent grades or degrees of severity but
it is important to note that concussions are not black
and white they are more of a GREY MATTER!
 Grade 1 (mild) –No LOC, symptoms last less
than 15min
 Grade 2 (moderate) – No LOC, symptoms
last longer than 15min
 Grade 3 (severe) – LOC, symptoms last
greater than 15 min (often days or weeks)
Concussion Types
• Simple
– Symptoms resolve over 7 – 10 days
– Limit physical activity
– No neuropsychiatric testing required
– Rest until all symptoms resolve and then graded
program of exertion before return to sport.

• Complex
– Persistent symptoms even with exertion, specific
sequelae, LOC> 1 min, prolonged cognitive
deficit.
– Neuropsychiatric testing indicated.
– Multidisciplinary approach.

Clinical Signs of Concussion

• Vacant stare
 • Delayed verbal and motor response
• Inability to focus attention
• Disorientation
• Slurred or incoherent speech
• Gross observable incoordination
• Emotional disturbances
• Memory deficits
• Any Loss of Consciousness

Concussion Symptoms:
• Early
– Headache
– Dizziness
– Confusion
– Tinnitus
– Nausea
– Vomiting
– Loss of balance

• Late
– Memory Disturbances
– Poor Concentration
 – Irritability
– Sleep disturbances
– Fatigue
– Personality changes

Concussion Evaluation
• Begins with basic life support:
– Airway, Breathing and Circulation.
• Determine if there is any loss of consciousness:
– If LOC exists the athlete must be suspected to
have a cervical spine injury and treated
appropriately.
• If the athlete can be moved to the sideline a
neurologic exam should be performed.
• Evaluate long and short term memory:
– Assess memory using sport specific questions;
orientation questions have poor yield for
assessing memory.
• Assess for retrograde and antegrade amnesia
 • Monitor frequently

• Preparticipation Exam
– Baseline evaluation for cognitive screen and
symptom score.
– Sport Concussion Evaluation Tool (SCAT)
– ImPact .

Consequences of Concussions:
• Immediate
• Cognitive impairment (attention, memory,
slowed reaction time)
• Somatic problems: Sensitivity to light, dizziness,
headaches, etc.

• Life Threatening
• Second Impact Syndrome

• Long term
• Post concussive syndrome (cognitive
impairment, personality changes, language
difculties, etc.)
 • Concussion in Younger Athletes
• Although most (80–90%) concussions resolve within
7– 10 days, the recovery process can be longer and
more complicated in children and adolescents.
• Furthermore, younger athletes have a higher risk of
severe symptoms and cognitive decline.
• This age diference in recovery and prognosis is
probably related to the ongoing development of a
child’s brain.
• The primary senses, motor skills, and language are
well developed by age ten.
• Frontal lobe maturation, however, goes on during the
teenage years and even into the early 20s; these
brain functions include
abstraction,reasoning,judgment, insight, and
emotional control.

Postconcussive syndrome:
Postconcussive syndrome (PCS) is a clinical entity
referred to as the presence of persistent neurological
symptoms lasting for more than 3 months and is
observed in 40–80% of individuals exposed to mild TBI.
About 10–15% of individuals experience persistent
symptoms after 1 year.
PCS and SIS symptoms, most commonly, headache,
dizziness, impaired attention,poor memory, executive
dysfunction, irritability and depression.
CPCS is a clinical entity of chronic TBI, which is probably
distinct from CTE, and the onset of neurological
symptoms begins rapidly after the head trauma and
persists but rarely progresses.
The term post-concussion syndrome was developed to describe a
persistent groggy state experienced by some athletes following a
concussion.

While symptoms most often persist for several weeks, they can occur for
months or up to a year. The most common physical symptoms are
headache and dizziness, while the cognitive symptoms are those
described under concussions.

Post-concussion syndrome has been identified as a risk factor for later

development of neurodegenerative disorders.

Post Concussive Syndrome:

 Develops in 2-15% of patients with Mild TBI
 A Cluster of Symptoms
 Physical
 Cognitive
 Emotional/Behavioral Symptoms

 Multiple Symptoms
 Poor Memory and Concentration
 Irritability
 Headaches or Neck Pain
 Fatigue
  Depression
 Anxiety
 Dizziness
 Increased Sensitivity to Light and Sound.

Diagnosis
• Deficits
• Clinical exam and impression
• Often not sensitive
• Neuropsychological testing,
• Best test
• Not available on sidelines
• Neuroimaging
• Currently not sensitive and/or not available
• CT, MRI, fMRI, SPECT, PET
Second impact syndrome:
The term second impact syndrome (SIS) is a rare but widely feared
complication of TBI among athletes.

SIS refers to ‘an athlete who has sustained an initial head injury,most
often a concussion, sustains a second head injury before the symptoms
associated with the first have fully cleared’.

The second head injury is typically only a minor blow to the head, but
within minutes, the athlete collapses into a coma.
It is postulated that severe cerebrovascular engorgement and cerebral
oedema ensue following the second impact leading to brain herniation.

Like juvenile head trauma syndrome, SIS is also more common in

children and adolescents with a mean age of 17.9 (range:10–24),
predominantly male, and 71% occurred in American football players,
usually at the high school level, 14% in boxing, and few cases were
reported in karate, skiing and ice hockey.

Return to play
 Must be determined by a health care professional
 Usually no exercise for 24 hours after symptoms
disappear
 No risk of contact for twice the time of the symptoms
plus 24 hours
 LOC is automatic 3 weeks but if symptoms persist
could be longer still!
 If the space available for the spinal cord is reduced
because of a narrow canal, an athlete is at greater
risk
 Cord compression can be anticipated when the
diameter of the midsagittal cervical spinal canal is 10
mm or less
 Cervical spine injuries can be classified as either
catastrophic or noncatastrophic
 The initial evaluation follows the ABCDE sequence of
trauma care
 Distinct regional diferences exist between the upper
cervical spine and the lower cervical spine
 The occipit and the first two vertebrae make up the
upper cervical spine
 The atlas (C1) is a bony ring that articulates with the
occipital condyles
 The axis (C2) has a true vertebral body, from which
the odontoid process, or dens, projects.
 The major stabilizing force at this joint is the
transverse atlantal ligament (TAL).
 TAL crosses posterior to the dens and attaches to C1
on both sides; this prevents anterior translation of
the atlas on the axis.