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ROMAN AL MAMUN
Scalp injury
It is composed of 5 layers:
1. Skin
2. Connective tissue
3. Galea aponeurotica
4. Loose areolar tissue
5. Pericranium
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.
Common acute TBIs in sports are skull fracture, subdural and epidural
haematoma and ruptured vertebral artery with subarachnoid
haemorrhage.
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.
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.
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:
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.
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.
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.
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.