Traumatic Brain Injury (TBI)
Definition
Traumatic Brain Injury (TBI) is a disruption in the normal function of the brain that can be caused
by a blow, bump or jolt to the head, the head suddenly and violently hitting an object or when an object
pierces the skull and enters brain tissue.
(Agarwal N., et al, 2020)
Anatomy
Cerebrum:
●
largest part of the brain
●
functions: interpreting touch, vision and hearing, as well as speech, reasoning, emotions, learning,
and fine control of movement
Cerebellum:
●
located under the cerebrum
●
function: coordinate muscle movements, maintain posture, and balance
Brainstem:
●
acts as a relay center connecting the cerebrum and cerebellum to the spinal cord
●
performs automatic functions: breathing, heart rate, body temperature, wake and sleep cycles,
digestion, sneezing, coughing, vomiting, and swallowing
(Rut T., et al., 2023)
●
The cerebrum is divided into two halves: the right and left hemispheres
●
Joined by a bundle of fibers called the corpus callosum that transmits messages from one side to
the other
●
Each hemisphere controls the opposite side of the body
●
In general, the left hemisphere controls speech, comprehension, arithmetic, and writing
●
The right hemisphere controls creativity, spatial ability, artistic, and musical skills
●
The left hemisphere is dominant in hand use and language in about 92% of people
Each lobe (4) may be divided into areas that serve very specific functions
Frontal lobe
●
Personality, behavior, emotions
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Judgment, planning, problem solving
●
Speech: speaking and writing (Broca’s area)
●
Body movement (motor strip)
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Intelligence, concentration, self awareness
Parietal lobe
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Interprets language, words
●
Sense of touch, pain, temperature (sensory strip)
●
Interprets signals from vision, hearing, motor, sensory and memory
●
Spatial and visual perception
Occipital lobe
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Interprets vision (color, light, movement)
Temporal lobe
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Understanding language (Wernicke’s area)
●
Memory
●
Hearing
●
Sequencing and organization
(Khoi T., et al., 2023)
Etiology & Epidemiology
●
Trauma is the leading cause of death in people ages 1 to 44, and more than one-half of these
deaths are due to brain trauma. Traumatic brain injury ( TBI ) is arguably the primary cause of
neurologic mortality and morbidity in the United States.
●
Age distribution is bimodal.
○
Peak ages: 0 to 5 years, with second peak in the elderly (age 65 and older); older group
has a higher mortality rate.
●
Male to female ratio → 2.5:1.
○
●
Mortality in males is three to four times higher than in females.
The single most common cause of death and injury in automobile accidents is ejection of the
occupant from the vehicle (Spitz and Fisher, 1991).
●
Violence/assault is the second most common cause of TBI in young adults.
(K. Hackenberg, et al., 2016)
Pathophysiology (Mechanism)
Primary Injury - Direct disruption of the brain parenchyma from the shear forces of the impact. It occurs
immediately (minutes to hours after the impact) and is not amenable to medical intervention.
Primary injury includes the following:
●
Contusions: Bruising of the cortical tissue
●
Diffuse Axonal Injury (DAI)
○
Immediate disruption of the axons due to acceleration–deceleration and rotational forces
that cause shearing upon impact.
○
There is also evidence of a secondary axotomy due to increased axolemmal permeability,
calcium influx, and cytoskeletal abnormalities that propagate after the injury.
○
Clinically, the coupling of the injury to these structures leads to the picture of white
matter punctate petechial hemorrhages characteristic of DAI.
●
Impact depolarization: Massive surge in extracellular potassium and glutamate release
(excitatory) occurs after severe head injury and leads to excitotoxicity (secondary injury).
(Capizzi A, et al, 2020)
Secondary Injury
●
Cascade of biochemical, cellular, and molecular events, which include both endogenous cerebral
damage as well as extracerebral damage that comes with trauma. Mechanisms of secondary injury
include the following:
●
Ischemia, excitotoxicity, energy failure, and resultant apoptosis
○
Excitotoxicity is the process by which neuronal damage occurs due to a massive surge in
neurotransmitters.
●
Secondary cerebral swelling (brain swelling and brain edema):
○
Brain swelling occurs early on after acute head injury (within 24 hours) due to an
increase in cerebral blood volume (intravascular blood). Identified on CT as collapse of
ventricular system and loss of cerebrospinal fluid (CSF) cisterns around the midbrain.
○
Brain edema occurs later after head injury (in comparison to brain swelling) due to an
increase in brain volume secondary to increased brain water content ⇒ extravascular
fluid. There are two types of brain edema:
○
○
Vasogenic edema:
■
Due to outpouring of protein-rich fluid through damaged vessels
■
Related to cerebral contusion
Cytogenic edema:
(Woo J, et al, 2020)
■
Found in relation to hypoxic and ischemic brain damage
■
Due to failing of the cells’ energy supply system
Focal Injury
●
Localized injury in the brain occurring immediately after the injury and easily visualized by CT
or MRI
●
●
Cerebral contusions:
○
Occurs when the brain impacts the inner table of the skull
○
Occurs usually in the inferior frontal lobe and anterior portion of the temporal lobe
Focal ischemia occurs secondary to vasospasms after a traumatic subarachnoid hemorrhage
(SAH) or from physical compression of the arteries.
Focal hemorrhages:
●
Epidural hematoma (EDH): Occurs commonly (90%) with a skull fracture in the temporal bone
crossing the vascular territory of the middle meningeal artery (60%–90%) or veins (middle
meningeal vein, diploic veins, or venous sinus; 10%–40%). Hematoma expansion is slowed by
the tight adherence of the dura to the skull. Clinically presented with a lucid interval (50%) prior
to rapid deterioration. Biconvex acute hemorrhagic mass seen on head CT
●
Subdural hematoma (SDH): Occurs in 30% of severe head trauma. They result from shearing of
the bridging veins between the pia-arachnoid and the dura. They are usually larger in the elderly
due to generalized loss of brain parenchyma.
●
○
High density, crescentic, extracerebral masses seen on head CT
○
Acute SDH: Immediately symptomatic lesions
○
Subacute SDH: Those between 3 days and 3 weeks
○
Chronic SDH: Lesions >3 weeks
SAH: These are closely associated with ruptured cerebral aneurysms and arteriovenous
malformations (AVMs) creating blood around the cisterns, although they could also result from
leakage from an intraparenchymal hemorrhage and trauma. CT findings demonstrate blood within
the cisterns around the brainstem and the subarachnoid space within 24 hours. CT sensitivity
decreases to 30% 2 weeks after the initial bleed.
(Verduzco M, et al, 2020)
Diffuse Injury
●
Widespread cerebral injury
●
DAI is unique to TBI. Its classification is based on severity
○
Grade I: Widespread white matter/axonal damage but no focal abnormalities on imaging
○
Grade II: Widespread white matter/axonal damage, and focal findings (most common in
the corpus callosum)
○
●
Grade III: Damage involving the brainstem
It is the leading cause of morbidity including impairments in cognition, behavior, arousal, and
coma in TBI. The severity of impairments depends on the magnitude, duration, and direction of
angular acceleration
●
of the initial impact.
●
It is initiated at the time of the injury by axonal shearing from acceleration–deceleration rotational
forces, followed by pathophysiologic changes that persist long after the injury. Axonal injury is
the most common cause of unconsciousness during and following the first 24 hours of injury.
●
Damage is seen most often in the corpus callosum and other midline structures: the parasagittal
white matter, the interventricular septum, the walls of the third ventricle, and the brainstem
(midbrain and pons).
●
Pathophysiology:
○
Excitotoxicity: After impact, release of excitotoxic neurotransmitters (glutamate) causes
calcium influx and a series of events (oxygen-free radical release, lipid peroxidation,
mitochondrial failure, and DNA damage) that ultimately lead to nerve cell death.
○
Hypoxia occurs.
○
Apoptosis: Programmed cell death defined by cell shrinkage, nuclear condensation, and
intranucleosomal
●
DNA fragmentation with dissolution of the cell membrane. It has both intracellular (cytochrome
C, apoptosis-inducing factor [AIF]) and extracellular (tumor necrosis factor [TNF]) triggers.
Imaging:
●
MRI is more sensitive than CT in revealing DAI, but because axonal injury occasionally has a
delayed onset and may or may not be accompanied by edema, diagnostic imaging may not always
be reliable.
●
There are now functional MRI studies that can further elucidate dysfunction more clearly than
static imaging.
(Gutierrez M, et al, 2020)
Missile/Fragments
●
Deficits are focal and correspond to the area of injury caused by a bullet/fragment, stab wounds,
motor vehicle injury, or occupational injury (e.g., nail).
●
If the brain is penetrated at the lower levels of the brainstem, death is instantaneous from
respiratory and cardiac arrest. 80% of patients with through-and-through injuries die at once or
within a few minutes.
●
Mortality rate of patients who are initially comatose from a gunshot wound to the head is 88%,
more than two times the mortality rate of closed head injury (CHI).
●
Focal or focal and generalized seizures occur in the early phase of the injury in 15% to 20% of
cases. Risk of long-term posttraumatic epilepsy (PTE) is higher in penetrating head injuries
compared to nonpenetrating injuries.
(Dixon KJ, et al, 2020)
Signs and Symptoms / Clinical Manifestations
(Centers for Disease Control and Prevention)
Diagnosis / Special Tests
GLASGOW COMA SCALE
●
The GCS is a simple scale for assessing the depth of coma. Lower GCS scores are associated with
worse outcomes based on the best GCS within the first 24 hours. Using the highest GCS score
within the first few hours after the injury is preferred, as this reduces the likelihood of using
excessively low, very early scores (often before cardiopulmonary resuscitation [CPR]) and
confounding factors such as decreased arousal due to use of sedatives or paralytic agents.
●
●
●
Severity of TBI
○
Severe TBI (coma): GCS score 3 to 8
○
Moderate TBI: GCS score 9 to 12
○
Mild TBI: GCS score 13 to 15
Total GCS score is obtained from adding the scores of all three categories.
○
Highest score = 15
○
Lowest score = 3
○
GCS score <8: Patient is said to be comatose. The lower the score, the deeper the coma.
Of the three items in GCS, best motor response, particularly 2 weeks postinjury, is the best acute
predictor of outcome. The verbal response was the second-best acute predictor of outcome.
●
Jennett (1979): Relationship between best GCS score (within the first 24 hours; Table 2–1) and
outcome as measured on the Glasgow Outcome Scale (GOS):
○
GCS score 3 to 4: Death or VS in 87% of patients
○
GCS score 5 to 7: Death or VS in 53% and moderate or good recovery in 34%
○
GCS score 8 to 10: Moderate or good recovery in 68%
○
GCS score 11: Moderate or good recovery in 87%
○
These data are often missing, as patients arrive paralyzed and intubated.
(Unterberg A, et al., 2020)
GLASGOW OUTCOME SCALE
(Wilson L, et al., 2020)
GALVESTON ORIENTATION AND AMNESIA TEST (GOAT)
●
Galveston Orientation and Amnesia Test (GOAT)—developed by Harvey Levin and colleagues, it
is a standard technique for assessing PTA. It is a brief, structured interview that quantifies the
patient’s orientation and recall of recent events.
●
Assesses orientation to person, place, time; recall of the circumstances of the hospitalization; and
the last preinjury and first postinjury memories
●
The end of PTA can be defined as the date when the patient scores 75 or higher in the GOAT for 2
consecutive days. The period of PTA is defined as the number of days beginning at the end of the
coma to the time the patient attains the first of two successive GOAT scores ≥75 (Ellenberg et al.,
1996).
●
Most important, attempts at more involved neuropsychological assessment usually prove
unproductive until the patient consistently obtains scores of 70 or greater. Once a score of 70 is
achieved, neuropsychological test data usually are reliable for further rehabilitation and post
dismissal planning.
(DeLisa et al., 2005)
Orientation Log (O–Log)
●
Orientation Log (O–Log): Developed by Jackson, Novack, and Dowler as an alternative
assessment of PTA
●
The O–Log was developed because of some of the problems related to the GOAT, including
unequal weighting of scored items, difficulty verifying some responses, and a lack of relevancy.
The O–Log focuses on orientation to place, time, and circumstance and consists of 10 items
scored 0 to 3.
●
Components:
●
○
Place: Type of place, name, and city
○
Time: Month, date, year, day of week, and time of day
○
Circumstance: Event that made the person require care and the deficits that have resulted.
Items are scored 0 to 3:3 = spontaneous/free recall; 2 = logical cuing; 1 = multiple choice,
phonemic cuing; 0 = unable/incorrect/inappropriate.
●
Two consecutive scores of 25 and higher indicate the person is out of PTA.
Rancho Los Amigos Levels of Cognitive Function Scale (Rancho or LCFS)
(Boase K, et al., 2021)
Functional Independence Measure
Prognosis (Prediction)
Pharmacological Management
Pharmacologic interventions:
●
Elimination of unnecessary medicines (e.g., benzodiazepines, H-2 blockers, dopamine blockers,
pain medications, etc.) and selection of agents with fewest adverse effects on cognitive and
neurologic recovery
●
Addition of agents to potentially enhance specific cognitive and physical functions
●
In patients emerging out of coma or VS, the recovery process may be (theoretically) hastened
through the use of pharmacotherapy.
●
Agents frequently used include:
○
Dextroamphetamine
○
Dopamine agonists
○
Amantadine—increases EXOGENOUS dopamine; watch for seizures and nephrotoxicity
○
Bromocriptine—increases ENDOGENOUS dopamine; watch for hypotension
○
Levadopa/carbidopa—increases EXOGENOUS dopamine
○
Methylphenidate—blocks reuptake of dopamine and norepinephrine
○
Modafinil—stimulates dopamine, histamine, serotonin, norepinephrine, and orexin
○
Acetylcholinesterase inhibitors
○
Antidepressants (tricyclic antidepressants [TCAs], selective serotonin reuptake inhibitors
[SSRIs], and selective serotonin and norepinephrine reuptake inhibitors)
Note: The efficacy of pharmacologic therapy to enhance cognitive function has not been proven.
(Nelson LD, et al., 2020)
Physical Therapy Management
Just as two people are not exactly alike, no two brain injuries are exactly alike. Therefore,
approach to neurological rehabilitation and physiotherapy post-traumatic brain injury should observe
neuroplasticity, motor learning, and motor control principles as well as the patient-centred approach with
an individual’s goals setting and choice of treatment procedures.
Specific Measurable Achievable Relevant Timed goals and patient’s involvement in goal setting
allows the clear orientation of the rehabilitation process and enhances individual speciality targets and
plans to contribute to the overall rehabilitation outcome. Patient’s goals for rehabilitation vary according
to the stage of recovery and their condition.
Ranchos Los Amigos Levels I, II and III: Decreased or Low-Level Response Levels of Recovery
a. Objectives of Care
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Physical function and level of alertness are increased.
●
Risk of secondary impairments is reduced.
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Motor control is improved.
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Effects of tone are managed.
●
Postural control is improved.
●
Tolerance of activities and positions is increased.
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Joint integrity and mobility are improved or remain functional.
●
Family and caregivers are educated on patient’s diagnosis, physical therapy interventions, goals
and outcomes.
●
Care is coordinated among all team members.
b. Appropriate Interventions and Rationale of Each Action
●
●
●
PROM
○
Improve joint mobility and integrity
○
Reduce risk of secondary impairments
○
Provide sensory stimulation
Proper positioning
○
Prevent indirect impairments such as contractures, decubiti, pneumonia and DVT
○
Prevent skin breakdown and contractures
○
Improve pulmonary hygiene and circulation
Postural drainage , percussion, vibration and positioning
○
Prevent pulmonary complications
○
Improve pulmonary function
○
●
●
Contraindication: increased ICP
Sensory stimulation
○
Increase level of arousal
○
Elicit movement in individuals in a coma or persistent vegetative state
○
Sensory systems are systematically stimulated
■
Auditory
■
Olfactory
■
Gustatory
■
Visual
■
Tactile
■
Kinesthetic
■
Vestibular
Early transition to sitting postures
○
Promote functional training in early levels of recovery
○
Improve overall level of alertness
○
Head should be properly supported
○
Use of tilt table allows early weight bearing through the lower extremities
c. Relevant health teaching(s) to patient & family
●
Stages of recovery and what can be expected of the future
●
ROM exercises
●
Positioning
●
Sensory stimulation
●
Possible outcomes
Ranchos Los Amigos Level IV: The Confused-Agitated Level of recovery
a. Objectives of Care
●
Patient’s endurance, joint mobility and integrity are improved.
●
Tolerance of activities is increased.
●
Prevent agitated outbursts and assist patient to control his/her own behavior
b. Appropriate Interventions and Rationale of Each Action
●
Special considerations
○
Consistency
■
Help decrease confusion of the patient
■
See the patient by the same person, at the same time and in the same place
everyday
○
○
Expect no carryover
■
Teaching new skills is unrealistic
■
Utilize charts or graphs
■
Help patient progress each day
■
Without such aids, patients will have no recall of previous day’s performance.
Model calm behavior
■
○
Expect egocentricity
■
○
○
Assist patient in perceiving and reflecting the demeanor of the caregiver
Patient cannot be expected to see another’s point of view
Flexibility/Options
■
Allows patient to feel that he/she has some control over the situation.
■
Be prepared with numerous activities
■
Provide safe choices.
Safety
■
Patients may be kept on a locked unit of the hospital
■
Keep patient and those interacting with him/her safe
■
One-to-one supervision and assistance throughout the day
c. Relevant health teaching(s) to patient & family
●
Level of the patient’s recovery and control of his/her behavior
●
Assurance that entering this level is a good sign and aggressive behaviors are short-lived
●
Use of previously mentioned strategies in interacting with their loved one
●
Consistency is observed for everyone.
Ranchos Los Amigos Levels V and VI: Confused-Inappropriate and Confused Appropriate Levels of
Recovery
a. Objectives of Care
●
Gait, mobility and balance are improved.
●
Motor and functional control, strength and endurance are increased.
●
Maximize functional recovery.
●
Prepare patient and family for discharge to home and community.
b. Appropriate Interventions and Rationale of Each Action
●
Compensatory approach
○
●
Restorative approach
○
●
●
●
Improve functional skills by compensating for lost ability
Restore “normal” use of affected areas
Locomotor training with body weight support and treadmill
○
Allows for repetitive training throughout a complete gait cycle
○
Improve walking ability
Constraint-induced (CI) movement therapy
○
Promote use of most affected UE for up to 90% of waking hours
○
Reduce use of least affected UE
Developmental postures
○
Facilitate and help restore movement and functional mobility
c. Relevant health teaching(s) to patient & family
●
Emphasize safety awareness education
●
Proper body mechanics
○
●
Avoid risking injury to patient or themselves
Assist patient with strengthening exercises and PROM
Ranchos Los Amigos Levels VII and VIII: Appropriate Response Levels of Recovery
a. Objectives of Care
●
Ability to perform physical tasks related to ADL skills, community and work reintegration and
leisure activities is increased.
●
Skills in judgment, problem solving, planning self-awareness, health and wellness, and social
interaction are emphasized.
b. Appropriate Interventions and Rationale of Each Action
●
Advanced activities such as community, social and daily living skills
○
To approximate demands of the real world
○
Reintegrate him/herself into the community l
c. Relevant health teaching(s) to patient & family
●
Patients learns how to best compensate for residual impairments or disabilities
●
Contact local support groups
●
Community resources to assist in transition to home and community
●
Wellness and prevention
○
Aerobic exercise program
■
Improve exercise capacity
■
Improve psychosocial abilities
Special Considerations
a. Abnormal Tone
●
●
Clinical features of spasticity
○
Brisk deep tendon reflexes
○
Involuntary flexor and extensor spasms
○
Babinski sign
○
Velocity dependent increase in stretch reflexes
Interventions
○
○
Spasticity management
■
Stretching and strengthening with adjunctive modalities and functional retraining
■
PROM and selective strengthening of antagonist muscles
■
Positioning
●
Keep whole body in proper alignment
●
Maintain head and neck in neutral position
Hypertonia management
■
Serial casting
●
Often used for plantarflexor or biceps contractures from increased tone
or prolonged shortening
●
Precise ROM measurements should be taken between each casting
●
Presence of risk of skin breakdown or patient hurting him/herself with
the cast
■
Cryotherapy
■
Air splints
b. Rehabilitation Technology
●
Use of adaptive equipment to increase social participation and independence
●
Environmental control units
●
Pocket computers
●
Wheelchairs
●
Seating systems
●
Virtual reality technology
(Temkin NR, et al., 2021)
Some of the PT interventions commonly used for MS management include:
1. Range of motion exercises - lowers muscular stiffness, aids in reducing contractures and
spasticity, and helps to preserve and increase joint mobility.
2. Strengthening exercises - may promote total functional capability and independence by reducing
weakness and boosting endurance.
3. Electrical stimulation therapy - can be used to lessen pain, stiffness, and enhance muscular
function. In certain circumstances, it may also aid with bowel and bladder function.
4. Proper bed positioning - maintaining alignment and avoiding bed sores (pressure ulcers), foot
drop, and contractures require that a patient be properly positioned in bed.
References
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Feb;87(2):203-14; quiz 215-6. German. doi: 10.1007/s00115-015-0051-3. PMID: 26810405.
2. Capizzi A, Woo J, Verduzco-Gutierrez M. Traumatic Brain Injury: An Overview of
Epidemiology, Pathophysiology, and Medical Management. Med Clin North Am. 2020
Mar;104(2):213-238. doi: 10.1016/j.mcna.2019.11.001. PMID: 32035565.
3. Dixon KJ. Pathophysiology of Traumatic Brain Injury. Phys Med Rehabil Clin N Am. 2017
May;28(2):215-225. doi: 10.1016/j.pmr.2016.12.001. Epub 2017 Mar 2. PMID: 28390509.
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Teasdale G, Manley GT. A Manual for the Glasgow Outcome Scale-Extended Interview. J
Neurotrauma. 2021 Sep 1;38(17):2435-2446. doi: 10.1089/neu.2020.7527. Epub 2021 Apr 6.
PMID: 33740873; PMCID: PMC8390784.
5. Braddom, Randall. Physical Medicine & Rehabilitation. 3rd ed. pp. 1137-1145.
6. Braddom, Randall. Physical Medicine & Rehabilitation. 4th ed. pp. 1133-1150.
7. DeLisa, Joel. DeLisa’s Physical Medicine & Rehabilitation: Principles and Practice. 5th ed. pp.
575-592.
8. Lindsay, Kenneth et al. (2011) Neurology and Neurosurgery Illustrated. 5th ed. pp. 218-225, 242,
280-281, 296-297, 308, 490-491, 504-506
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