Traumatic Brain Injury

Anatomical, Kinesiological, Physiological Background

I. Anatomical, Kinesiological, Physiological Background
A. Anatomical Background

• Frontal Lobe:
- Emotions
- Decision making
- Personality
- Memory formation
- Broca’s Area – Controls facial neurons, speech, and language comprehension.
Located on Left Frontal Lobe
 Broca’s Aphasia – Results in the ability to comprehend speech, but the
decreased motor ability (or inability) to speak and form words.

 Parietal Lobe:
- Spatial awareness and perception (Proprioception - Awareness of body/ body parts
in space and in relation to each other)
- Senses and integrates sensations
 Occipital Lobe:
- Processing
- Integration
- Interpretation
- Visual stimuli
  Temporal Lobe:
- Organization/Comprehension of language
- Information Retrieval (Memory and Memory Formation)
- Wernicke’s Area – Language comprehension. Located on the Left Temporal Lobe
 Wernicke’s Aphasia – language comprehension is inhibited. Words and
sentences are not clearly understood, and sentence formation may be
inhibited or non-sensical.
 Central Sulcus – Divides the Frontal Lobe from the Parietal Lobe
 Longitudinal Fissure – Divides the two Cerebral Hemispheres
 Longitudinal Fissure – Divides the two Cerebral Hemispheres
 Transverse Fissure – Separates the Cerebrum from the Cerebellum
 Sylvian/Lateral Fissure – Divides the Temporal Lobe from the Frontal and
Parietal Lobes

• Gyri – Elevated ridges “winding” around the brain.

• Sulci – Small grooves dividing the gyri
B. Physiological Background
 BRODMANN’S CLASSIFICATION SYSTEM

Table 10–1. Specialized Cortical Areas.

  Brodmann's Area Name Function Connections

Primary motor Voluntary muscle

Frontal Lobe 4 Contributes to corticospinal tract
cortex activation
Premotor
  6    
cortex
Sends projections to lateral gaze
Frontal eye
  8 Eye movements center (paramedium pontine
field
reticular formation)
Motor aspects of Projects to Wernicke's area via
  44, 45 Broca's area
speech arcuate fasciculus

Primary
Parietal Lobe 3, 1, 2 Somatosensory Input from VPL, VPM
sensory cortex

Striate Input from lateral geniculate

Occipital cortex = Processing of only
17
Lobe primary visual stimuli
visual cortex Projects to areas 18, 19

Extrastriate
= visual Processing of
  18, 19 Input from area 17
association visual stimuli
cortex
Primary
Temporal Processing of
41 auditory Input from medial geniculate
Lobe auditory stimuli
cortex
Associative
  42 auditory    
cortex
Inputs from auditory
Wernicke's Language association cortex, visual
  22
area comprehension association cortex, Broca's
area (via arcuate fasciculus)
Frontal Lobe

 Area 4 (primary motor area):

- Large pyramidal neurons (Betz's cells) and smaller neurons in this area give rise to
many (but not all) axons that descend as the corticospinal tract
- Lips, tongue, face, and hands are represented in order within a map-like homunculus
on the lower part of the convexity of the hemisphere
- body parts have a magnified size as projected onto the cortex, reflecting the large
amount of cortex devoted to fine finger control and buccolingual movements
- arm, trunk, and hip are then represented in order higher on the convexity; and the
foot, lower leg, and genitals are draped into the interhemispheric fissure

 Area 6 (the premotor area)

- contains a second motor map
- Includes the supplementary motor area.

 Prefrontal cortex
- extensive reciprocal connections with the dorsomedial and ventral anterior thalamus
and with the limbic system
- serves a set of "executive" functions:
 planning and initiating adaptive actions and inhibiting maladaptive
ones
 prioritizing and sequencing actions
 weaving elementary motor and sensory functions into a coherent,
goal-directed stream of behavior
 Damage may result to:
 apathy (in some cases motionless and mute)
 Disinhibition (uninhibition) and distractible
 loss of social graces and impaired judgment
Parietal Lobe

 Areas 3, 1, and 2 (primary sensory areas): in the postcentral gyrus

- receives somatosensory input from the ventral posterolateral (VPL) and ventral
posteromedial (VPM) nuclei in the thalamus

 remaining areas are sensory or multimodal association areas

 association area:
- receives inputs from multiple sensory modalities and integrates them

 areas 44 and 45 (Broca's area)

- Within the inferior frontal gyrus
- located anterior to the motor cortex controlling the lips and tongue
 important area for speech
Occipital Lobe

 Area 17: striate (primary visual) cortex

- Geniculocalcarine radiation relays visual input from the lateral geniculate to the
striate cortex
- Upper parts of the retina (lower parts of the visual field) are represented in upper
parts of area 17, and lower parts of the retina (upper parts of the visual field) are
represented in lower parts of area 17

 Areas 18 and 19: visual association areas

Temporal Lobe

 Heschl’s Gyrus: includes

- Area 41: primary auditory cortex
- Area 42: associative (secondary) auditory cortex
 receive input (via the auditory radiations) from the medial
geniculate
- The surrounding temporal cortex (area 22) is the auditory association cortex

 Wernicke's area:
 plays an important role in the comprehension of language
 Within the posterior part of area 22 (in the posterior third of the
superior temporal gyrus)

II. Definition

 Traumatic
Brain Injury is a
diagnosis that
can cause indirect
impairments
of the MSK system,
demonstrate
coordination
impairments
and problems with
dual- task control.
 The resultant
problems in
Motor Function of
TBI are numerous,
complex, and
difficult to delineate.
 It is an UPPER MOTOR NEURON LESION.
  A traumatic brain injury (TBI) is defined as “an alteration in brain function, or other
evidence of brain pathology, caused by an external force.”
 Brain tissue damage can be categorized as either:
 Primary Injury – due to direct trauma to the parenchyma
 Contact Injuries – results in contusions, lacerations, and intracerebral
hematomas
 This damage is generally focal in nature as the brain comes into
contact with bony protuberances on the inside surface of the skull or
damage from the penetrating object.
 Common areas of focal injury – anterior temporal poles, frontal poles,
lateral and temporal cortices, and orbital frontal cortices.
 Secondary Injury – results from a cascade of biochemical, cellular, and
molecular events that evolve over time due to the initial injury and injury-
related hypoxia, edema, and elevated intracranial pressure
 Processes develop over hours and days, and include glutamate
neurotoxicity, influx of calcium and other ions, free radical release,
cytokines, and inflammatory responses that can lead to cell death

 Mild TBI (mTBI) is A.K.A post-concussion injury

 Traumatic brain injury (TBI) is damage that impairs brain function resulting from external
physical force. The severity of brain injury varies widely, with the majority of injuries in
the mild category.
 Concussion is a subset of mild traumatic brain injury (mTBI) that is generally self-limited
and at the less-severe end of the brain injury spectrum but still involves a complex
pathophysiological process.
 Moderate to severe injuries have a significantly worse outcome.
 Altered state of consciousness is a hallmark of brain injury.
 Contusion is the hallmark of TBI

III. Etiology
 Falls – leading cause of TBI (32%) and 2 nd leading cause among persons age 65 and
older
 Motor Vehicle/traffic accidents – second leading cause of TBI (19%)
 Struck by/against events (18%)
 Assaults (10%)
 TBIs can come from open or closed head injury
 Open head injury, the meninges have been breached, leaving the brain
exposed
 Closed head injury occurs when there is no skull fracture or laceration of
the brain, but the soft tissue of the brain is forced into contact with the
hard, bony, outer covering of the brain, the skull.
 Suicide
 Risk Factors for prolonged recovery:
 Younger age
 Level of play
 Loss of consciousness for more than 1 minute
  Significance of cognitive symptoms
 Female gender
 depression
 Risk Factors for complicating diagnosis and management of a concussion
 Pre-injury mood, learning, attention-deficit disorders
 Migraine headaches
 Risk Factor for recurrent concussion
 History of concussion (longer recovery times with recurrence)
 Can come from open or closed head injury
 Close head injury – occurs when there is no skull fracture or laceration in the
brain
 Initial blow – point of impact (coup injury)
 Secondary blow – brain decelerates against the contralateral skull
(contre-coup)
IV. Epidemiology
 The TBI population is one of the most challenging that a physical therapist is likely to
encounter.
 Traumatic brain injury is the leading cause of injury related death and disability in the
United States
 Approximately 1.7 million people in the United States are admitted to emergency
departments with TBI each year
 Children, older adolescents/young adults (less than 25 years old), and older adults are
most at risk for experiencing TBI.
 Hospitalization and death as a result of TBI is most common in older adults (65 years old
and over).
 Between 1.6 and 3.8M sports related mTBIs occur annually in the US and ~12% of
military personnel reports symptoms consistent with blast related mTBI
 Incidence of vestibular-related symptoms after blast mTBI range from 24% to 83% and is
seen in the acute (1-3 days), sub-acute (3-30 days), and chronic (30-360 days) stage.
 Concussions occur in all sports, with the highest incidence in football, hockey, rugby,
soccer, and basketball. (Magee path pg. 1535)
 The reported incidence of concussion is higher in female athletes than in male
athletes despite similar playing rules in most sports.
 It is also highly likely that there is an increased risk for repeat concussion in the first 10
days after an initial concussion according to pathophysiologic studies.
 Sports and recreation-related emergency department visits for TBI among age ≤ 19
years increased to 62%.
 Widespread cause of head injury among young people is bicycling
 TBI peaks at 3 different age levels:
 1st peak – early childhood (1-2 years)
 Related to child abuse
 2nd peak – late adolescence and early adulthood (between 15 and 24 years)
 Related to risk taking behaviors
 sports concussion is more common
rd
 3 peak – elderly population
 related to falls
  ~60% of adults and ~92% of children are injured in a MVA.
 Headache – most common complaint following mTBI
 TBI is one of the leading cause of death and disability in children of all ages and
NONACCIDENTAL INJURY is the most common.
 Drowning is the 3rd leading cause of death in children aged 1-4 yrs

V. Pathophysiology

Motor Struck by/ rapid

Vehicle FALLS
Blast against acceleration
waves from Accident events or
an deceleration
explosion forces

external
forces that
cause brain Assaults
tissue to
make direct TBI
Early Sensory
Task- Mobility Stimulation
Oriented
Approac
h
ROM Motor
relearning
Proper
strategies
Positioning
both in bed Stretching
and
wheelchair Aerobic and
Endurance
Conditioning,
Resistance
Training, ES

 Traumatic Brain Injury is a heterogenous injury, with a wide variety of pathophysiological

mechanism.
 The brain damage results from external forces that cause brain tissue to make direct
contact with an object, rapid acceleration or deceleration forces (leads to Wallerian-type
axonal degeneration), or blast waves from an explosion.
  PRIMARY INJURY
 PREDOMINANT MOI in Severe to Moderate TBI: Diffuse Axonal Injury
Common in High speed MVAs and can be seen in some sports related TBIs
 Common areas – Parasagittal white matter of the cerebral cortex, corpus
callosum, and the pontine-mesencephalic junction adjacent to the superior
cerebellar peduncles.
 Result of forces exerted on the brain at impact
 BLAST INJURY
 Considered a signature injury of the U.S. military conflicts in the Middle East.
 There appear to be three mechanisms by which primary blast brain injury may occur:
 Direct transcranial blast wave propagation
 The transfer of kinetic energy from the blast wave through the
vasculature, which triggers pressure oscillations in the blood vessels
leading to the brain
 Elevations in cerebrospinal fluid (CSF) or venous pressure caused by
compression of the thorax and abdomen and by propagation of a shock
wave through the blood vessels or CSF.
 SECONDARY INJURY
 Secondary processes develop over hours and days, and include glutamate
neurotoxicity, influx of calcium and other ions, free radical release, cytokines, and
inflammatory responses that can lead to cell death
 The release of glutamate and other excitatory neurotransmitters exacerbates ion-
channel leakage and contributes to brain swelling and raised ICP.
 Hypoxic-ischemic injury results from a lack of oxygenated blood flow to the brain
tissue.
 It can be caused by systemic hypotension, anoxia, or damage to specific vascular
territories of the brain. Because the rigid skull surrounds the brain, swelling,
abnormal brain fluid dynamics, or hematoma can result in elevated ICP. Hematomas
are usually classified according to their site (epidural, subdural, or intracerebral).
 Severely increased ICP typically results in herniation of the brain, requiring prompt
emergency treatment.
 Common types of herniations are uncal, central, and tonsillar

VI. Clinical Manifestation

 Blast-Related Bran Injury
 Edema
 Contusion
 Diffuse Axonal Injury (DAI)
 Hematomas
 Haemorrhage
 Dyautonomia
 Post-traumatic seizures
 Mild TBI experiences:
 Neurocognitive deficits
 postural control and balance impairments
  blurred vision, nausea, light sensitivity, sleep disturbance, ringing in the ears
 (appearance of s/sx may be delayed by several hours)
 Cognitive Deficits
 Depressive reactions
 Diminished or altered state of consciousness regardless of the severity
 Impairment of cognition and physical function (temporary or permanent)
 Amnesia
 Dystonia (c lesion to contralateral basal ganglia or thalamus)
 Symptoms associated c concussion: typically resolves in 7-10 days
 Headache, disorientation, nausea
 Irritable/distractible
 Difficulty in reading and memory
 Fatigue and disruption of sleep patterns
 Footballer’s migraine – Syndrome that may trigger multiple times after additional
mTBI.
 Moderate TBI:
 Haemorrhage or contusion
 Epidural hematoma
 Facial Asymmetry
 Pain, CN damage, Motor deficits
VII. Sequelae
 Traumatic brain injury is associated with a wide spectrum of neuromuscular,
cognitive, and behavioral impairments that can lead to limitations in activity,
restrictions in social participation, and diminished quality of life.
VIII. Prognosis
 Low initial scores on the GCS, particularly motor score and pupillary reactivity, have
been identified by a number of studies as a predictor of poor recovery in patients with
moderate to severe TBI. Other factors associated with poor outcomes are age, race,
and lower education level. Petechial hemorrhages, subarachnoid bleed, obliteration
of 3rd ventricle or basal cisterns, midline shift, and subdural hematoma findings on
initial CT scan are also predictive of poor outcomes.
 Duration of post-traumatic amnesia (PTA), the length of time between the injury and
the time at which the patient is able to consistently remember ongoing events, is also
an important factor in predicting recovery.
 Patients with PTA less than 48.5 days are likely to have higher Functional
Independence Measure (FIM) scores at discharge from inpatient rehabilitation;
patients with PTA less than 27 days are likely to be employed; patients with PTA less
than 34 days are likely to have a good overall recovery (as measured by the GOS);
and those with PTA less than 53 days are likely to be living without assistance.
 Severe traumatic brain injury (TBI) accompanied by extensive disability and
multisystem involvement, a prognosis or prediction of level of improvement can be
determined only at various increments during the course of rehabilitation. Knowledge
of recovery patterns (stage of disorder) is sometimes useful to guide decision
making.
 Most individuals with mTBI fully recover in ~3 months. However, up to 10%-20% of
people with mTBI experience postconcussive syndrome and have deficits months
to years after the initial injury.

IX. Medical Assessment

MRI CT SCAN

 CT is the primary imaging modality for the initial diagnosis and management of the
person with brain injury
 The GCS is used to determine the severity of the brain injury. A complete
neurological examination is also done. Additional information about the extent of the
injury is obtained through x-ray films and neuroimaging studies such as CT and MRI.
  Subdural bolt and a fiberoptic catheter
 Glasgow Coma Scale – Gold Standard used to document level of
coma/consciousness
 Galveston Orientation and Amnesia Test or Orientation Log– for the assessment of
Post-traumatic amnesia

X. Medical Treatment
 The patient with a brain injury is treated across a wide continuum of care, which includes
the ICU, acute hospitalization, rehabilitation centers, community re-entry programs,
outpatient therapy, schools, vocational rehabilitation, and assisted living centers.
 Interdisciplinary team (aside from PT) includes:
o Patient and Family, Physician, Speech-Language Pathologist, Occupational
Therapist, Rehab nurse, Case Manager/ Team coordinator, Social Worker,
Neuropsychologist, Respiratory care practitioner, Respiratory Therapist,
Recreational Therapist
 Early Medical Management
o Starts at the scene of the accident
o Early Resuscitation
o Intubation
o Sedating Medication, Osmotherapy, Surgical Decompression, Barbiturates

XI. PT Assessment
• Arousal, attention, and cognition
• Integument integrity
• Sensory integrity
• Motor function
• Range of motion
• Reflex integrity
• Ventilation and respiration/gas
exchange
XII. PT Treatment
1. Moderate to Severe TBI (Acute Stage)
a. Proper Positioning both in bed and wheelchair
i. Head – kept in neutral
ii. Hips and knees – Slightly flexed
iii. Repositioning every 2 hrs
b. ROM
c. Stretching
d. Early Mobility
e. Sensory Stimulation

2. Moderate to Severe TBI (Active Rehab)

a. Motor Relearning Strategies
b. Restorative vs. Compensatory based interventions
c. Restorative intervention and Neural Plasticity
d. Task-Oriented approach
e. Locomotor Training with Body Weight Support
f. Constraint-Induced Therapy
g. Aerobic and Endurance Conditioning, Resistance Training, Electrical Stimulation
h. Dual-Task Performance
i. Patient/Family/Caregiver Education, Behavioral Factors, Community Re-entry
Programs
3. Mild TBI

a. Return to Play
b. Vestibular, Balance, and Dual Task
c. Stretching, Strengthening, and manual therapy modalities – for post-traumatic
headache or TMD
d. Patient education – includes ROM, isometric strengthening, proper sleep
posture, vestibular positional changes, gaze stabilization exercises, balance
exercises, and aerobic exercise
References:
Snell's Essential of Anatomy and Physiology 9th Ed.
Waxmann's Clinical Neuroanatomy 26th Ed.
O'Sullivan's Physical Rehabilitation 6th Ed.
Goodman's Pathology Implications for the Physical Therapist 4th Ed.
Braddom's Physical Medicine and Rehabilitation 5th Ed.

Prepared by:
Castillo, Arren Fria P.
Hernandez, Niña Angelica R.