RS3330

Clinical Sciences in Medical &

Neurological Conditions
Traumatic Brain Injury (Part A) -
(head injury, brain damage, cerebral lesion, closed
head injury, head trauma, mild brain injury)

Presenter: Dr Hoe Lee

 Objectives
• To be able to describe the aetiology,
symptomology and medical investigations for
various Traumatic Brain Injuries (TBI)
• To be able to discuss the progression of and
stages of TBI, recommended medical
treatment used in the treatment of the
symptoms of TBI.
• To be able to identify the impact of the
symptoms of TBI has on a person’s daily
functioning and quality of life during the
acute, rehabilitation and recovery stages.
Brain anatomy

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Brain functions
 Acquired Brain Injury and Traumatic Brian Injury
An acquired brain injury (ABI) is an injury caused to the brain since birth
(not related to congenital defect or degenerative disease).
• many possible causes, including a fall, a road accident, tumour,
stroke, infection, substance abuse, toxic exposure etc.

Traumatic brain injury (TBI) causes substantial disability and mortality.

• It occurs when a sudden trauma damages the brain and disrupts
normal brain function.
• It can be a structural injury and/or physiological disruption of brain
function as a result of an external force
• It may have profound physical, psychological, cognitive, emotional,
and social effects.
• TBI is also characterized as a “silent epidemic” because of its potential
for negative outcomes, affecting all ages.

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 What’s the difference between and ABI
and a TBI?
Traumatic brain injury (TBI) Acquired brain injury (ABI)

Caused by a blow to the head, or a Some are considered “non-

missile intruding into the head. traumatic” (The cells and tissues
are damaged by toxic substances,
Caused by the head being moved lack of oxygen, pressure, direct
rapidly e.g. in car crashes, in Shaken infection or stroke).
Baby Syndrome
By definition it includes TBI, an
Usually some loss of consciousness umbrella term includes TBI.
Brain tissue can be damaged

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Aetiology – how does it happen?
 Causes are numerous:
◦ Sporting injuries, injuries causing bleeding into the
brain tissues and structures
◦ Car accidents, car vs pedestrian
◦ Assault and war injuries
◦ Near drowning
◦ Tumours
◦ Infections
◦ Medical mishap
◦ Stroke
◦ Alcohol and drug abuse
◦ Bungee jumping – if the rope breaks!
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 Closed Head injury
• Most common

• Skull and /or membranes not

• broken or penetrated

• Damage is due to brain moving inside skull

• Often results in diffuse brain injury

• Focal lesions, bruising eg contrecoup injuries in car

accidents

• Effects depend on what areas of the brain is affected

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 Open Head injury
• Skull and membranes are disrupted, fractured, or
penetrated and/or exposed
• Pieces of bone or CSF or other material (eg
gravel) may enter the brain tissues + infections.
• Considerable localised damage likely to occur

CSF = cerebrospinal
fluid – the fluid that
surrounds, nourishes,
supports the brain
and spinal cord.
Common Injured Sites and the
corresponding signs & symptoms
 Frontal lobe
 Impaired executive & motor abilities
 Temporal lobe
 Impaired ability to consolidate new information into memory
 Parietal lobe
 Difficulty with language comprehension
 Difficulty comprehending visual stimuli
 Occipital lobe
 Deficits in visual abilities
 Axonal injury
 Slowed thinking
 Difficulty accomplishing tasks
 Mix-of-3 disabilities?
In what proportion
(short-term and long-term effect)
Physical disabilities

TBI

Emotional and Cognitive disabilities

behavioral disabilities
 TBI: Insidious Signs & Symptoms
 TBI is indicated by new onset or worsening of at least one of the
following clinical signs, immediately following the event

 Signs and symptoms after a brain injury may include:

 Headache or a sensation of pressure in the head (most common symptom
of TBI)
 Loss of or alteration of consciousness; confusion
 Blurred eyesight or other vision problems (such as dilated or uneven
pupils);
 Dizziness (feeling off-balance or the sensation of spinning)
 Ringing in the ears (Tinnitus)
 Nausea or vomiting Q1: Is medical attention required if S/S
 Slurred speech
evolve over time following a TBI?
 Delayed response to questions
 Memory loss
 Fatigue
 Mood swings
 Clumsiness in motor activities 12
 Some signs/symptoms may not appear for hours or
days:
Trouble concentrating
Continued or persistent memory loss
Irritability and other personality changes
Sensitivity to light and noise
Sleep problems
Mood swings; stress; anxiety or depression
Disorders of taste and smell
Q2: Why there is a delayed appearance of sign and symptoms?
Mechanism of TBI:
Acceleration/Deceleration mechanism

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Q3. Which is “Coup” injury and which is “contrecoup” injury?
Diffused Axonal Injury
DAI
Brain injury NOT just at the moment of impact.

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Classification of TBI by time of onset

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 TBI classification by time of onset
• Two principle categories, primary and secondary.
• Primary damage occurs at the moment of injury
and results mainly from contact or inertial forces.
– Primary injuries include fractures, focal injuries,
diffuse injuries, and penetrating injuries. These
injuries often occur simultaneously, but one type of
injury usually more predominant than the other.

• Secondary damage produced by processes

initiated at the time of injury but manifested
hours to days after injury include ischemia,
swelling (edema), and alterations of endogenous
neurochemical mechanisms.
 Primary Damage (Acute)
Damage that occurs at the time of actual impact. There are many
types of Primary Damage that may occur. These include:

1. Skull Fracture- breaking of skull bone

2. Contusion/Bruise- discoloration and/or swelling at the location
of actual impact or at the point or points where the force of
the blow has driven the brain against the skull’s bony ridges
3. Haematoma/Blood Clot- swelling or mass of blood between
the skull and the brain or inside the brain itself
4. Laceration- tearing of brain tissue and/or blood vessels, caused
by forceful rotation of the brain across the skull’s bony ridges
5. Nerve Damage (Diffuse Axonal Injury)- shearing or tearing of
white matter in connecting nerve fibers in the brain; can cause
unconsciousness and/or coma
Immediate change- tissue damage, swelling, bleeding

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Heamatoma shifts brain tissue, compresses and
changes shape of nearby structures

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 Penetrating injuries
• Penetrating injuries are primary injuries that
are directly related to the ballistic forces that
generate extensive damage to tissue by direct
missile damage or by the shock and cavitation
waves caused by the missile etc.

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Classification of TBI by time of onset

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 Diffuse brain injuries/
Diffused axonal injury (DAI)
•Common injury is the axonal pathologic
condition
•Diffuse injuries not only those severe injuries
that result in vegetative or highly dysfunctional
outcomes but also those mild brain injuries of
the concussive type
•There are, however, substantial microscopic
changes to the axons, but this damage cannot
been seen on CT scan.
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 DAI
• A characteristic of DAI is functional
cerebral failure ranging from confusion
without amnesia to unconsciousness
and death
• The axonal damage is diverse, because the
mechanical load that produces the injury
varies in amount, location, and severity

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 Secondary Damage (< one week)
1. Ischemia – not enough blood flow to the brain due to blood vessel
constriction or blockage
2. Hypoxia – not enough oxygen in the brain
3. Hypotension – low blood pressure
4. Edema – swelling, inflammation
5. Increased intracranial pressure – due to inflammation – if this
becomes excessive, it ends up with brain herniation – parts of the
brain bulging out of holes in the skull
6. Hypercapnia – too much carbon dioxide in blood
7. Acidosis – blood becomes acidic which indicates a disease state
8. Excitotoxicity – excess release of neurotransmitters that over excite
neurons leading to cell death
9. Further breakdown of the Blood-Brain-Barrier (BBB) – immune
system invades the brain and destroys neurons and other cells.
10. Reactive gliosis
11. Oxidative stress
Classification of TBI by location of injury

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 Focal TBI, Diffuse TBI
• Location of injury is determined by neuroradiology
techniques.
• Injuries classified as focal are those detected with
computed tomography (CT) scanning, magnetic
resonance imaging (MRI), or single proton emission
tomography (PET) scanning and include surface
contusions and lacerations and intracranial hematomas.
• Diffuse injuries, those that can only be determined
microscopically, include concussions and diffuse axonal
injuries (DAI).
• Cellular events are also occurring after the initial insult
and include cell dysfunction, receptor dysfunction, free-
radical formation, inflammatory events, and calcium-
mediated damage.
Figure 1. The relationship among
injury onset, location of injury, and
cellular pathophysiologic events
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 Focal contusion
• Contusions occur at the crest of gyri, where
the brain encounters the rough and irregular
surfaces of the skull during the deceleration or
contact phase of a force
• The distribution is typically in the frontal
poles, the orbital surfaces of the frontal lobes,
the temporal poles, the lateral and inferior
surfaces of the temporal lobes, and the cortex
above and below the Sylvian fissure

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 Focal contusion
• The more severe contusions are found most often
in the frontal and temporal lobes
• Histologically, there is widespread interruption of
the blood–brain barrier (BBB), especially
pronounced at the area of the contusion, which
allows passage of neurotoxic components to
enter brain tissue
• Regional swelling and vasogenic edema thought
to be related to the BBB breakdown also
accompany these injuries
Contusion

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CT scan intracerebral haemorrhage

Blood clot building

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Meninges of the brain
 Intracranial Haemorrhage (ICH)
顱內出血
• The dural and arachnoid membranes and
their associated blood vessels are readily
torn by impact and by fractured bone
fragments.
• The process of haemorrhage results in
the formation of a localised accumulation
of blood, or haematoma.

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 Four types of ICH:
1. Epidural (Extradural) haemorrhage (EDH)硬膜外出血

– A blow to the temple often fractures the thin

temporal bone and tears the middle meningeal
artery as it passes upwards within a groove
between the inner skull table and the dura. In 15% of
cases no fracture is identified.

– Arterial bleeding strips the dura off the inner skull

table to form a haematoma which acts as a space-
occupying lesion (SOL). This accumulation can be
immediate or delayed.

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– EDH is easily overlooked, as mild concussion is
followed by a lucid interval before neurological
symptoms and coma develop many hours later when
the enlarging haematoma begins to exert pressure on
the brain.

– Amenable, responsive to surgical decompression in

early stages.

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2. Subdural haemorrhage (SDH)
硬腦膜下出 血, 硬腦膜下血腫
– More common than EDH.

– Not usually associated with skull fracture.

Sudden jarring or rotation of the head (often
a trivial blow or fall) causes movement of the
brain relative to the dura.

– This shears and tears the small veins which

bridge across the gap between the dura and
the arachnoid mater of the brain.
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– The leaking blood accumulates over several hours and
usually tracks extensively as a thin film over the surface
of the brain.

– SDH is especially common in the elderly (brain atrophy

widens the gap), children (shaking injury as part of the
child abuse syndrome) and alcoholics (frequent
unprotected falls and prolonged bleeding times).

– A small, self-limiting SDH may remain asymptomatic

and be an incidental finding at autopsy.

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3. Subarachnoid haemorrhage (SAH )
蛛網膜下腔 出血:

• May be natural, due to rupture of a dilated

blood vessel (an aneurysm), or traumatic.
SAH is highly irritant to the brain-stem and is
usually rapidly fatal.

• Traumatic SAH is usually associated with

contusion or laceration to the brain surface.

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4. Intracerebral haemorrhage 腦內出血:

– May be spontaneous, due to unexpected

rupture of a small blood vessel (arteriole)
which has been weakened by the effects
long-standing high blood pressure.

– Rupture is likely to occur at a time of stress

or excitement when the blood pressure is
acutely elevated.

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– May be traumatic, due to extension of
haemorrhage from surface contusions deep into
the substance of the brain.

– Traumatic intracerebral haemorrhage may also be

the result of rupture of small blood vessels deep
within the brain due to shearing stress.

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Classification of TBI by cellular pathophysiology
changes after the accident

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 Cell pathophysiology
• Four pathophysiologic events within the cell
are responsible for the severity of injury to
axons.
– primary (instantaneous) axotomy
– transient ion fluxes
– fluid perturbations and cell swelling
– transport block leading to secondary (delayed)
axotomy

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 Complications of TBI
• Posttraumatic seizures: Frequently occur after moderate or
severe TBI
• Hydrocephalus
• Deep vein thrombosis
• Heterotopic ossification
• Spasticity
• Gastrointestinal and genitourinary complications: Among the
most common sequelae in patients with TBI
• Gait abnormalities
• Agitation
• Chronic traumatic encephalopathy (CTE) - is a degenerative
disease found in people who have suffered repeated blows to
the head
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 Complications
• Long-term physical, cognitive, and behavioral
impairments that most commonly limit a patient's
reintegration into the community and his/her return to
employment. They may include the following:
– Insomnia
– Cognitive decline
– Posttraumatic headache: Tension-type headaches are the
most common form, but exacerbations of migraine-like
headaches are also frequent
– Post-traumatic depression: Depression after TBI is further
associated with cognitive decline, anxiety disorders,
substance abuse, dysregulation of emotional expression, and
aggressive outbursts
 Chronic Cognitive Problems
• Attention and concentration problems
– Although some chronic problems can remain, especially in moderate
to severe injury, in the first few months, rapid recovery is the rule
• New learning and memory deficits
– Cognitive functioning usually reaches a plateau within the first 2 yrs
• Executive control dysfunction
• Compensatory cognitive therapy
– May be helpful if environment or social situation has changed and a
decline in function is noted
Q. Executive function is a set of mental skills that help you get things done. These skills are
controlled by which area of the brain?
Q. In what EF helps you?
Q. When EF is not working, what abilities can be affected?
 Emotional & Behavioral Problems
 Difficulty handling frustration
 Increased irritability
 Increased anger
 Immature behavior
 Obsessive eating
 Inappropriate sexual behavior
 Poorly controlled spending
 Self-centeredness
 Social isolation
 Increased divorce & exhaustion of financial resources
 Severity Factors
• Extent & severity of TBI after an initial event depends on
factors to include:
– Magnitude of direct or indirect forces applied to the head
– Direction of the force
– Subsequent direction, duration and amplitude of angular
accelerations to which the brain is subjected

• Other factors influencing the nature and severity of a TBI

might include:
– Age, sex, body size and weight, comorbidities, alcohol use,
genetics, and previous brain injuries
 TBI Definition/Severity
American Congress of Rehabilitation Medicine
Diagnostic Features
 Mild TBI:
 Traumatically induced disruption of brain function that results in loss of
consciousness of less than 30 minutes’ duration
 Or in an alteration of consciousness manifested by an incomplete memory of
the event
 Or being dazed and confused
 More difficult to diagnose

 Moderate TBI:
 Usually loss of consciousness from an hour to a day
 Confusion from days to weeks
 Mental or physical deficits that can last months or become permanent.

 Severe TBI:
 Significant closed head injury
 Impact: speech, sensory, vision and cognitive deficits including difficulties
with attention, memory, concentration & impulsiveness
 Different measures of severity in TBI
• Severity is usually based on various clinical factors,
including duration or length of LOC, coma scaling, or
imaging.
• Glasgow Coma Scale (GCS): A 3- to 15-point scale used to
assess a patient's level of consciousness and neurologic
functioning ; scoring is based on best motor response, best
verbal response, and eye opening (e.g., eyes open to pain, open
to command)
• Duration of loss of consciousness: Classified as mild
(mental status change or loss of consciousness [LOC] < 30
min), moderate (mental status change or LOC 30 min to 6
hrs), or severe (mental status change or LOC >6 hrs)
• Posttraumatic amnesia (PTA): The time elapsed from
injury to the moment when patients can demonstrate
continuous memory of what is happening around them
 Glasgow Coma Scale

Mile (GSC ≥ 12) Moderate (GSC 9-11) Severe (GCS < 8)

Dysfunctions Dysfunctions Dysfunctions

Teasdale et al Lancet 1974; ii: 81-4

 TBI Level of Severity
Mild Moderate Severe
frequently mixed,
blast+ complex, blast+
Primary Damage/Injury predominately blast,
acceleration/decelerati acceleration/decelerati
mechanism: non-penetrating
on, typically non- on + penetration
penetrating
Loss/alteration > 30 minutes, < 24
< 30 minutes > 24 hours
of consciousness: hours
Amnesia: <24 hours > 24 hours, < 7 days > 7 days
GCS 13-15 9-12 <9
positive, lasting
Imaging negative transient changes
abnormalities

Post Traumatic Stress

Polytrauma, such as
Comorbidity: Disorder, overlapping PTSD, other injuries
multiple organ injuries
symptoms

Transient
death, significant
neuropsychiatric
mild-to-moderate, neurological and
deficits, mostly full-
typically chronic, neuropsychiatric
recovery, long term
Outcome: neurological and deficits, sever, chronic
neuropsychiatric
neuropsychiatric physical and
especially after
abnormalities neuropsychiatric
repeated injuries are
disabilities
frequent
 Outcome measures
• Commonly used are Glasgow Outcome Scale (GOS) with or without
extended scores, Disability Rating Scale (DRS), Functional
Independence Measure (FIM), Community Integration Questionnaire
(CIQ), and the Functional Status Examination (FSE).
– Glasgow Outcome Scale/GOS Extended (GOS, GOSE): GOS defines
5 categories of possible outcomes after a brain injury
– Disability Rating Scale (DRS): Measures general functional changes over
the course of recovery after TBI
– The Functional Independence Measure (FIM): An 18-item scale used
to assess the patient's level of independence in mobility, self-care, and
cognition
– Community Integration Questionnaire (CIQ): Consists of 15 items
relevant to home integration (H), social integration (S), and productive
activities (P). It provides subtotals for each of these, as well as for
community integration overall
– The Functional Status Examination (FSE): A structured interview
designed to evaluate change in activities of everyday life as a function of
an event or illness, including traumatic brain injury. The measure covers
physical, social, and psychological domains.
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Disability Rating Scale (DRS)

Each of the areas of functioning is

rated on a scale of 0 to either 3 or
5, with the highest scores
representing the higher level of
disability. The maximum score is
29 (extreme vegetative state); a
person without disability would
score zero.
Functional Independence Measure

score ranges from 18 (lowest) to 126 (highest)

level of independence
Outcome after illness and health status can be considered at many different levels.
The place of any assessment method should be considered in the context of the ICF
system proposed by the World Health Organization (2001). It is clear that no single
method of assessment can cover all levels of interest. Different assessments have
merits in different contexts, and the choice of assessment needs to be related to the
question to be answered.

Health condition

(disorder or disease)

Body Functions Activity Participation

& Structure

Environmental Personal
Factors Factors
Contextual factors
 THANK YOU
FOR
YOUR ATTENTION!

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