Traumatic Brain Injury

Athira P M
Mohd Afsar
Dr. Jamuna Rajeswaran
Contents
• Definition
• Types
• Severity- measurement
• Causes
• Prognosis
Definition
of
An alteration in brain function, or other evidence of brain pathology, caused by
an external force…”
Brain Injury Association of America
atho, caused by an alteration in brain function, or of brain pathology, caused by an
external force…”
An alteration in brain function, or other evidence of brain pathology, caused by an external
force…”
Brain Injury Association of America

…”
Brain Injury Association of America
• Traumatic Brain Injury - A bolt or jolt to the head or a penetrating head injury
that disrupts the function of the brain

• Not all blows or jolts to the head result in a TBI. The severity of such an injury
may range from “mild” (a brief change in mental status or consciousness) to
“severe” (an extended period of unconsciousness or amnesia) after the injury.

• Post-injury individuals may experience various symptoms

• These symptoms can result in short- or long-term problems with functioning

Different classification.

• Classification Based on Mechanism:- To understand pathophysiology

and natural courses.

• Classification Based on Severity:- For clinical care of patients( most

commonly used classification.)

• Structurally based descriptions of TBI:- Aid in selection of patients

who may benefit from a specific therapy such as surgical
evacuation of hematoma
(Information from imaging studies.)
 Types of TBI

Primary Injury

Major classification

Secondary Injury
 Primary Injury
• Associated with structural changes resulting from mechanical forces
initially applied during injury as well as destabilization of cell
membrane.
• primary injury (occurs at time of application of force)
 Secondary Injury
• Systemic or local changes which increases tissue damages.

• Many secondary insults result from primary injuries.

• Some are caused by discreet systemic or local phenomena.

• secondary injury evolves over time subsequent to the primary injury

• Secondary injury mechanisms include:
Generation of free radicals
Excitotoxicity
Disturbance of ionic homeostasis.
Disruption of the blood brain barrier
Generation of Nitric oxide
Lipid peroxidation
Mitochondriacal dysfunction and energy failure
Secondary Haemorrhage
Axonal disruption
Apoptotic cell death
Ischemia
elevated intra cranial Pressure
 Closed/Blun
t

Mechanism Blast injury

Penetrating
injury
Closed/ Blunt Force
• Injury caused by direct force to head, acceleration, deceleration or
rotational forces.

• Common causes include

• falls
• Assualts
• Motor vehicle Collisions.
Closed or open depend on dura-integrity
closed open
• More common • Less common

• Dura intact • Dura disrupted

• Violent accelerations of brain tissue(coup or • Fracture of or force penetrating dura.

counter coup)
• Focal injury refers to an injury that is confined to a specific area of the
brain causing localized damage.

• Diffuse injuries are characterized by damage throughout the brain.

Blast Injuries
• Injury caused by over pressure waves generated from high grade
explosives.
• A large amount of thermal, Mechanical and electro magnetic energy
is transferred to the brain.
• Energy can come directly through the cranium or be transmitted
indirectly through oscillating pressures in fluid filled large blood
vessels.
• This may cause Damage to the blood brain barrier or gray-white
matter junction and can cause cerebral edema, axonal injury,
apoptosis, and tissue degeneration.
Penetrating Injury
• Injury induced by an object that penetrates the cranial vault.
• Common causes include;
• Gun shot wounds
• Shrapnel
• Knife wounds
 Mild TBI
Clinical Moderate TBI
classification
Severe TBI
GCS
• Glasgow Coma Scale (GCS) is a neurological scale which aims to give a
reliable and objective way of recording the conscious state of a
person for initial as well as subsequent assessment.

• The scale was published in 1974 by Graham Teasdale and Bryan J.

Jennett, professors of neurosurgery at the University of Glasgow's
Institute of Neurological Sciences at the city's 
Southern General Hospital.
Mild TBI
• GCS 13 to 15
• The majority of patients with cranial trauma fall in this group.
• Patients are awake, and may be confused but can communicate and
follow commands.
American Congress of Rehabilitation
Medicine definition of mTBI
• A traumatically induced physiological disruption of brain function, as
manifested by at least one of the following:
1. Any loss of consciousness;
2. Any loss of memory for events immediately before or after the accident;
3. Any alteration in mental state at the time of the accident (e.g. feeling dazed, disoriented,
or confused); and
4. Focal neurological deficit(s) that may or may not be transient; but where the severity of
the injury does not exceed the following:
 Loss of consciousness of approximately 30 min or less;
 After 30 minutes, an initial Glasgow Coma Scale (GCS) of 13-15; and
 Posttraumatic amnesia (PTA) not greater than 24 hrs.
• Katy, et al. (1993)
Moderate TBI
• GCS 9-12
• These patients are generally drowsy to obtunded but not comatose.
• They can open their eyes and localize painful stimuli.
• They are at high risk of clinical deterioration and must be monitored
carefully.
Severe TBI
• GCS 3-8
• These patients are obtunded to comatose.
• They do not follow commands
• May exhibit decerebrate or decorticate posturing.
• They have significant structural and metabolic brain dysfunction and
are at high risk of secondary brain injury and deterioration.
Measuring Severity/Level
of Consciousness
Glasgow Coma Scale:

 Eye Opening (1-4)

 Spontaneous -4
 To speech -3
 To pain -2
 None -1

 Verbal Response (1-5)

 Oriented -5
 Confused conversation -4
 Inappropriate Words -3
 Incomprehensible Sounds -2
 None -1

 Best Motor Response (1-6)

 Obeys commands -6
 Localizes Pain -5
 Withdrawal -4
 Abnormal flexion(Decorticate) -3
 Extension(Decerebrate) -2
 None -1
Injury severity
Mild Moderate Severe

Altered or LOC<30 minutes LOC<6 hours with abnormal LOC>6 hours with abnormal CT
with normal CT and/or MRI CT and/or MRI and/or MRI

GCS 13-15 GCS 9-12 GCS<9

PTA<24 hours PTA<7 days PTA>7days

 EDH
SDH

Structural IVH
Lesions in TBI TSAH/SAH
TAI
Contusion
Epidural hematoma (EDH)
• An extradural collection of blood.
• Often associated with a skull fracture.
• Typically has arterial origin.
• Margins of the hematoma do not cross the skull suture lines and
often appear convex on imaging studies.

• If an EDH is evacuated in a timely fashion to reverse mass effect or if

the hematoma is small in size, patient outcomes are usually good.
Epidural hematoma
Subdural hematoma (SDH)
• A collection of blood in the subdural phase.
• SDHs may be chronic or acute, and they are caused by venous
bleeding from cortical bridging veins.
• Bleeding may extend over the entire hemisphere.

• Acute SDHs are significantly associated with seizures.

• Acute SDHs are also associated with significant alteration of cerebral
blood flow and metabolism of the underlying hemisphere and
generally have a worse outcome than EDHs
Intra ventricular hemorrhage (IVH)
• Bleeding in to the ventricular system after trauma.
• May be associated with acute hydrocephalous and is a risk factor for
development of delayed hydrocephalous.
• IVH is typically seen in conjunction with TSAH.
Traumatic subarachnoid hemorrhage (TSAH
or SAH)
• Hemorrhage in the sub arachnoid space that is not associated with
the significant mass effect.
• Often accompanies other types of traumatic hemorrhages.
• The presence of TSH has been associated with an increased risk of
unfavorable 6 month outcome in patients with moderate to severe
TBI.
Traumatic axonal injury (TAI)/ Diffuse
axonal injury( DAI)
• Injuries to axonal connections triggered by inertial forces.
• Predominantly acceleration-deceleration, with subsequent structural and metabolic
consequences of mechanical deformation.
• Results from a tearing of nerve bundles and/or stretching of blood vessels.
• Frontal & Temporal lobes are most susceptible.
• Disorganization
• Impaired memory
• Problems related to attention

• https://www.youtube.com/watch?v=UbGDFT6cVNg
Contusion
• Parenchymal hemorrhage, typically in frontal or temporal lobes.
• Bruises that cause swelling and bleeding resulting in tissue damage
• Frontal & Temporal lobes
• Abnormal sensations
• Behavior impairment
• Problems related to vision
• Memory impairment

• Can be;-

• Coup Injury

• Counter Coup Injury

• COUP
• Results from direct transmission of force to brain tissue underlying the region
of impact .

• COUNTER COUP INJURY

• Result from the indirect forces acting in a region contralateral to the region of
impact.
Types and causes continued
• Hemorrhage
• Bleeding into brain tissue
• Infarction (stroke)
• Occipital/Temporal lobes
• Occur when an artery is compressed by the swelling of surrounding tissues,
restricting blood flow and its essential nutrients
• Hematoma (SDH)
• Bleeding over the surface of the brain exerts pressure and may need to be
surgically drained
Skull Fracture
• Skull fractures may occur after trauma because of blunt or
penetrating injury.
• They may involve the convexity or the skull base and may be open or
closed depending on the presence of a overlying scalp laceration.
• Large depressed skull fractures may needs to be surgically elevated.
• Depressed skull fractures are associated with an increased risk of
seizures.
Causes
• MVA, bicycle, etc. - more than 50%
• Falls - 25%
• Violence- 20%
• Homicides, assault
• Rotational forces, sports, Acceleration & deceleration

• Men more than women

• Bimodal Age Distribution of TBI
• 15 - 24 years old and 75+ years
Prognostic Factors
• Duration of coma
• Severity of coma immediate post-injury
• Duration of post-traumatic amnesia
• Location and size of injury
• Severity of injuries to other body systems
To Remember:
• More severe the injury, the longer the recovery period
• Recovery from diffuse damage takes longer than from localized damage
• Need for surgery does not necessarily indicate a worse prognosis.
• Initial improvement may be due to reduction in swelling (edema)
• Damaged neurons begin functioning again
• Plasticity - undamaged areas of the brain may assume the functions of nearby
damaged areas
Persons with a history of TBI compared to persons without a
history had significantly higher levels of:

• Seizures
• Mental health problems
• Alcohol problems
• Drug abuse problems

• The risk of these conditions increased significantly with severity of injury

Diagnosis
 History of TBI
 Length of unconsciousness, post traumatic amnesia
 Physical examination
 Imaging
 CT (Computed Tomography)
 or MRI (magnetic resonance imaging)
 Neuropsychological Assessment
Concussion

• Altered mental state occurring after trauma. Which may or may not include brief loss of
consciousness.
• Symptoms reflect a functional disturbance rather than structural injury.

• Concussions are usually caused by a blow to the head. Violently shaking the head and
upper body also can cause concussions.

• Concussions are particularly common if you play a contact sport, such as football. Most
people usually recover fully after a concussion.
• Post traumatic amnesia:-Impaired recall of events surrounding the
injury.

• Retrograde amnesia:-Impaired recollection of events immediately preceding

the injury.

• Anterograde amnesia:-deficits in forming new memories after the injuries.

Post concussion disorder/syndrome
• Post concussive symptoms that persist for 3 or more months post
injury.
• Symptoms are variable and not unique to this diagnosis.
• Depression, Dizziness, Drowsinss
• Excess sleep, Fatigue, Feel “in a fog”
• Feel slowed down, Head ache, irritability.
• Memory problems, Nausea, Nervousness
• Numbness/tingling, poor balance, Poor concentration
• Ringing in ears, Sadness, Sensitivity to light.
• Sensitivity to light, Trouble falling asleep, Vomiting.
Common Mild TBI/Postconcussive
Symptoms
e • Depression
• Headache • Anxiety
• Poor concentration • Dizziness
• Memory difficulty • Light sensitivity
• Irritability • Sound sensitivity
• Fatigue
Motor and Sensory Deficits

• Slowed motor response (often due to processing delay vs. motor

deficit)

• Paralysis, disturbed balance and coordination, ataxia, tremors,

parkinsonism, bradykinesia, and weakness

• Distorted pain, touch, temperature and positional information

Common Behavioral Complaints

• Restlessness • Paranoid Ideation

• Agitation • Hypomania
• Confabulation
• Combativeness
• Irritability
• Emotional Lability
• Impulsivity
• Confusion • Egocentricity
• Hallucinations • Emotional Liability
• Disorientation
Common Behavioral Complaints
continued

• Impaired Judgment • Aggressiveness

• Impatience • Apathy
• Depression • Immaturity
• Hypersexuality • Disinhibition
• Hyposexuality • Loss of interest
• Dependency • Anxiety
• Silliness
Common Neuropsychological Complaints
• Disordered consciousness • General intellectual deficits
• Disorientation • Deficits in processing/sequencing information
• Memory deficits • Illogical thoughts
• Decreased abstraction • Perseveration
• Decreased learning ability • Confabulation
• Language/communication deficits • Difficulty with generalization
• Poor judgment • Poor attention
• Poor quality control • Fatigue
• Inability to make decisions • Reduced motor speed/poor hand eye
• Poor initiative coordination
• Poor depth perception • Visual neglect
• Dizziness
 Ft. Carson: Post-Deployment Data (n = 907)

90%
80% Acute (right after mTBI)

70% Post-Deployment
60%
50%
40%
30%
20%
10%
0%
Headache Dizziness Balance Irritability Memory
Problems Problems
Terrio, H., Brenner, L.A., Ivins, B., Cho, J.M., Helmick, K.,Schwab, K., Scally, K., Bretthauser, R., Warden, D. Traumatic Brain Injury Screening: Preliminary Findings Regarding
Prevalence and Sequelae in a US Army Brigade Combat Team. Journal of Head Trauma Rehabilitation. 2009
Neuro-psychological Sequelae of TBI
• CHANGES IN PERSONALITY

• CHANGES IN COGNITION

• INCREASED RATES OF PSYCHIATRIC ILLNESS

(There are certain brain regions which are highly vulnerable to injury and account for the high
rate of challenging behavior and probably the increased rates of psychiatric illness that are
associated with TBI. These include the frontal cortex and sub-frontal white matter, the
deeper midline structures including the basal ganglia, the rostral brainstem, and the temporal
lobes including the hippocampi)
• There is evidence that neurotransmitters with important roles in
maintaining cognitive and behavioral homeostasis are altered in TBI.

• For example, there is significant dysfunction of catecholaminergic systems

associated with TBI. There is also evidence of altered central cholinergic tone
following trauma.

• The cholinergic system plays an important role in many cognitive domains,

particularly memory and attention (24) and may play a role in the genesis of
mood disorders, particularly depression (25).

• The serotonergic system is activated in TBI, with increased levels of serotonin

particularly evident in areas of significant tissue damage and in association
with lowered regional cerebral glucose utilization (10,26-28).
• Survivors and family/caregivers frequently describe alterations in
emotional and behavioral regulation as “changes in personality.

• exaggeration of pre-injury traits, or fundamental changes in response

patterns.
• impulsivity. This may be manifest in verbal utterances, physical actions, snap
decisions, and poor judgment flowing from the failure to fully consider the
implications of a given action.
• Irritability: Survivors may be described as more irritable or more easily
angered. (Although a particular cue might be perceived as a legitimate aggravation, the response is
characteristically out of proportion to the precipitating stimulus. Responses can range from verbal outbursts
to dangerous aggressive and assaultive behavior.)
• Affective instability. Survivors and family/caregivers frequently
describe exaggerated displays of emotional expression, out of
proportion to both the precipitating stimulus and the pre-injury
range of response to similar stimuli. Cues that previously elicited
momentary sadness now precipitate weeping or crying.
• Apathy
• lack of awareness of these changes: The injured individual may be
unable to appreciate that his or her behavior is different.
• The literature suggests that lack of awareness of illness is not simply a
function of global cognitive deficits, but perhaps is more related to frontal-
executive dysfunction
• Five major frontal-subcortical circuits have been identified, of which three
have significant roles in non-motor forms of behavior. Each of these three
circuits can affect motivated behavior, though in somewhat different ways.
• Damage to the dorsolateral prefrontal cortex and its circuitry impairs executive
functions such as working memory, decision making, problem solving and mental
flexibility.

• Damage to the orbitofrontal cortex and related nodal points impairs intuitive
reflexive social behaviors and the capacity to self-monitor and self-correct in real time
within a social context.

• Damage to anterior cingulate and related circuitry impairs motivated and reward-
related behaviors
• TBI results in an increased relative risk of developing various psychiatric disorders,
including;
• mood and anxiety disorders
• substance abuse
• psychotic syndromes

Kopenen et al (76) studied 60 individuals 30 years after their TBI and found that almost half (48%)
developed a new Axis I psychiatric disorder after their injury. The most common diagnoses were
depression, substance abuse, and anxiety disorders. Rates of lifetime and current depression (26%;
10%), panic disorder (8%; 6%), and psychotic disorders (8%; 8%)

After TBI, the most frequent diagnoses were major depression and anxiety disorders (i.e., post-
traumatic stress disorder (PTSD), obsessive-compulsive disorder and panic disorder).(Hibbard et al )

Individuals with TBI report a variety of symptoms in different domains (discouragement, frustration,
fatigue, anxiety, etc.). Not all of these symptoms will rise to the level of a disorder( if it is interfere with
social or occupational function or quality of life, are legitimately considered disorders)

significant impairments in memory and executive function meet the DSM-IV definition of dementia
TBI increases the risk of a progressive dementing disorder such as Alzheimer’s disease later on.
• Behavioral change could be caused by the meaning of the accident or
injury, being a reaction to a loss of self-esteem due to disfiguring
injury, loss of mobility, or unemployment.

• Finally, changes in environment such as living situation, change in

caregivers, or change in routine or flow of daily life can have an
enormous impact on the behavior and adaptation of an individual
with brain injury or other neuropsychiatric illness.
Neuropsychological Assessment in TBI
• Assessment of Cognitive Functions
• Assessment of Mood and Emotions
• Assessment of Behavior and Personality
• Assessment of Socio-adaptive functioning
• Assessment of Quality of Life
Assessment of Mood and Emotions
• Beck’s Depression Inventory – II
• Beck Anxiety
• Hamilton depress
• Hamilton’s Anxiety
• Apathy Evaluation Scale
Assessment of Behavior and Personality
• Predominantly through History from significant others
• Compare with the pre morbid level
Assessment of Quality of life
• WHO QOL Scale
• QOLIBRI: Quality of Life after Brain Injury
• Compare with the pre morbid level
BATTERIES DEVELOPED IN INDIA
• PGI BATTERY OF BRAIN DYSFUNCTION (PGIBBD)
• AIIMS COMPREHENSIVE NEUROPSYCHOLOGICAL BATTERY IN HINDI
• NIMHANS NEUROPSYCHOLOGY BATTERY
NIMHANS NEUROPSYCHOLOGY
BATTERY
 NIMHANS
NIMHANS
neuropsychologi Neuropsychology
cal Battery (Dr. Battery (Kavitha et
Mukundan, al., 1987
1979)
NIMHANS NIMHANS
neuropsychology neuropsychol
battery for ogical battery
children (Kar et., for adults
al 2004) (Rao, 2004)
NIMHANS
neuropsychologic
al Battery for
elderly (Dr.
Ravikesh Tripati,
2013)
• Standardised on 540 community sample
• Norms for Indian adults between ages 16-65
• Normative data given for age, gender and
education
Domain Function Test
Finger tapping test
Motor Speed
Speed Digit symbol
Mental Speed
Substitution Test

Focused Attention
Color Trails
Attention Sustained
Digit Vigilance
Attention
Finger Tapping Test
• Measures the speed with which index finger of each hand can tap
• Prefrontal cortex
• Premotor cortex
• Basal ganglia and cerebellum

Digit Symbol Substitution Test

• Mental speed
• Visuomotor coordination
• Motor persistence
• Sustained attention
• Response speed
Color Trails 1 & 2
• Orbito frontal cortex
• Attention
• Cognitive shifting in CT 2
• Digit Vigilance
• Sustained Attention
Domain Function Test
Controlled Oral
Verbal Fluency Word Association
Test
Category Fluency Animal names test
Design Fluency Design Fluency Test
Executive Functions N Back Test
Working memory
Planning Tower of London
test
Set Shifting
Wisconsin card
Response sorting Test
inhibition Stroop Test
Fluency Wisconsoin Card Sorting Test
• Phonemic fluency(Controlled oral • Ability to adapt to responses in a
word association ) changing environment
• Category fluency (Animal names • Bilateral dorsolateral prefrontal
test) areas
• Design fluency
Verbal N Back Test Stroop Test
• Working memory • Response inhibition
• Prefrontal areas • Ease with which a perceptual set
• Broca’s area can be shifted
• Left dorsolateral prefrontal • Bilateral superior medial
cortex prefrontal areas
Spatial Span • Anterior cingulate cortex
• Visual Working memory
Domain Function Test
Comprehension Verbal comprehension Token test

Auditory verbal
Learning and memory Verbal
Learning Test

Visuo -spatial
Construction Visual Complex Figure Test
Learning and memory
Auditory Verbal Learning Test
• Learning and memory
• Anterior temporal cortex
• Amygdala
• Hippocampus
• Prefrontal cortex
Complex Figure Test
• Visuo constructive ability and visual learning and memory
• Right parietal structure
• Right Temporal
Bender Gestalt Test

Apraxia
Disorder of skilled movement in the absence of impaired
motor functions or paralysis
Ideomotor apraxia Construction
Ideational apraxia
apraxia

• Mimicking • Inability to • Difficulty in

simple motor perform sequential drawing, copying
commands motor acts and building
 Agnosia
inability for
recognizing familiar
objects in the
absence of sensory
deficit

Object agnosia Color agnosia Finger agnosia

Body schema disturbances- dissociation with respect to one’s

body as compared to object in the external space
Neuro Psychological Interventions for TBI
• It is important to point out that there are two broad factors that contribute to the
neurobehavioral sequelae of TBI:

• The injury induced changes in personality

• The increased rate of psychiatric disorders.
• increased irritability or lowered frustration tolerance.

• Cognitive rehabilitation
• Neuro feed back training. (EEG bio feedback)
 References
• Zollman, Felise S. Manual of Traumatic Brain Injury Management. 2nd
ed., Demos Medical Pub., 2011.