PATHOPHYSIOLOGY

1. Acceleration- Decelaration Injuries

• are caused when a moving head hits a relatively fixed object, such as the ground or a windshield,
or sustains a high-speed change from acceleration to deceleration.
• This can lead to coup or contrecoup brain contusions against the skull.
• Coup injuries – (pronounced coo) are present on the brain directly below the site of the impact.
The surface bruises, cuts, contusions, or other marks can help to pinpoint the location. Trauma
can range from relatively mild to severe including bruising, brain swelling, and hemorrhaging of
the brain.
• Contrecoup injuries – (pronounced “contra coo”) injuries affect the side of the brain opposite
from where the impact occurred. They are often overlooked or misdiagnosed because of their
location. Contrecoup occurs when a force or blow causes the brain to strike the side of the skull
opposite from the point of impact. These injuries often occur in motor vehicle rollover
accidents and motorcycle crashes. If not identified, they pose long-term risks for victims.
• Why Infant are susceptible to Acceleration and Deceleration Injuries?
-The young infant is particularly susceptible to acceleration deceleration injuries, because there is less
restraint of motion in the neck owing to musculoskeletal development.
• Therefore, acceleration–deceleration injury in infancy may result in greater differential
displacement of the skull and cranial contents potentially causing shearing injury. The direction
of acceleration injuries may be translational (linear) or rotational (angular).
• Most TBIs are a result of a combination of both translational and rotational injuries.

2. Translational Injury
• In translational injury, the head in motion strikes a stationary object and responds with lateral
displacement of both the skull and the brain.
The injury that results from the initial impact of the skull on the brain is known as coup
The lesion that occurs in the direction opposite to the initial force is termed contrecoup
*Contrecoup occurs because the brain decelerates against the bony structures of the skull.

3. Rotational Injury
• Rotational injury occurs when the skull rotates as the brain remains stationary. The effect is
angular forces on the brain, surface contusions, lacerations, and shearing trauma.
• Rotational injury can result in either focal or diffuse brain damage. These injuries can occur with
MVA involving whiplash with rotation.
4. Impression Injuries
• Impression injuries occur when a solid object, such as a rock or a blunt object, impacts a
stationary head.
• Impression injuries produce skull fracture and a focal lesion at the site of the impact.
• The presence of a skull fracture is associated with an increased risk of intracranial injury;
however, the absence of a skull fracture does not reliably exclude a significant intracranial injury.
CLINICAL PRESENTATION

 Primary brain damage from trauma- is a direct result of the forces that occur to the head at the
time of initial impact.
1. Concussion
- is a complex pathophysiologic process affecting the brain, and is characterized by headache,
altered awareness and cognitive function, and impaired balance immediately following trauma.
-Concussion can be seen without obvious pathologic changes to the brain; however, it may also
be seen with mild diffuse white matter lesions or neurochemical injury.
 - Following concussion, a child may exhibit clinging behavior, disturbances in sleep, irritability,
delayed response to others or in understanding, sensitivity to light, nausea, or more distractibility
than usual. These behavior changes can last a few days to a few months.
2. Contusion
-is a bruising or hemorrhage of the crests or gyri in the cerebral hemispheres. Contusion can be
seen following a crush injury or blunt trauma, or during an inertial load injury, such as
acceleration–deceleration of the brain within the skull.
- occur most commonly in the frontal and temporal lobes of the brain because of bony
irregularities in the cranial vault.
3. Skull Fractures
- are seen in both closed and open head injuries and compound head injuries.
- Linear comminuted fractures result from an impact with low-velocity objects, and depressed
fractures generally result from an impact with higher velocity objects.
- Linear fractures can produce contusions, hemorrhage, and cranial nerve damage. Depressed
skull fractures of greater than 5 mm are considered significant. Depressed fractures can produce
herniation syndromes, contusions, lacerations, and cranial nerve damage.
4. Intracranial Hemorrhages
- can occur with or without immediate loss of consciousness or skull fracture.
-Two types of intracranial hemorrhage frequently seen following pediatric TBI are extradural and
intradural hematomas. Signs of an intracranial hemorrhage may not appear initially on clinical
examination.
-The rate of blood collection and the location of the hematoma are related to severity and
outcome. Intracranial hemorrhage is a common cause of clinical deterioration and death in those
who experience a lucid interval immediately after injury.
5. Extradural Hematomas
-Extradural or epidural hematomas develop because of the tearing of an artery in the brain,
primarily the middle meningeal artery and its branches.
-In children, epidural hematomas usually follow skull fracture or bending of the skull into the
brain. With unilateral epidural hematoma, there is often herniation of the temporal lobe.
-Coma may ensue and cardiorespiratory arrest is possible. Other signs and symptoms include
confusion, headache, nausea, vomiting, and confusion.
6. Intradural Hematomas
-Intradural hematomas include subdural and intracerebral hematomas. Acute subdural hematomas
occur secondary to injury of veins in the subdural space causing blood to accumulate as a space-
occupying lesion.
7. Diffuse Axonal Injury
-is a microscopic phenomenon, not commonly visible on computed tomography (CT) scan, due to
acceleration–deceleration motion that causes shearing damage to white brain matter.
-DAI is seen following rotational injury within the cranial vault. The shearing trauma results in
diffuse disturbance of cellular structures following TBI.
-DAI is associated with much of the significant brain damage seen in TBI, including sudden loss
of consciousness, extensor rigidity of bilateral extremities, decorticate or decerebate posturing,
and autonomic dysfunction.

 Secondary brain damage from trauma

-evolves as a result of the pathophysiologic changes initiated by the primary trauma.
1. Cerebral Edema
-Perhaps the most frequently occurring cause of secondary injuries is cerebral edema. Unchecked
cerebral edema accompanied by an increase in intracranial pressure (ICP) can lead to multiple
cerebral infarctions, brain herniation, brainstem necrosis, and irreversible coma.
 - Controlling brain swelling is often difficult, and may require the use of a combination of the
following techniques: narcotic sedation, diuretics, barbiturates, systemic neuromuscular paralysis,
or hyperventilation
2. Intracranial Pressure
-When a mass, such as a hematoma or cerebral edema, is present following TBI, ICP increases in
response to the pressure exerted on the brain. Initial increases in ICP are accommodated by the
mechanisms of the ventricular system. However, when the compensatory mechanisms are no
longer effective, ICP rises.
-In infancy, increases in ICP will cause bulging of the fontanels and separation of the sutures. In
children older than 5 years of age, as ICP rises, the contents of the cranial vault are forced
downward through the foramen magnum. This causes brainstem compression and may lead to
drowsiness, difficulty breathing, and even cardiorespiratory arrest.
-Prolonged increased ICP may lead to the development of posttraumatic hydrocephalus
presenting with incontinence, spasticity, poor appetite, and seizure activity.
3. Herniation Syndromes
-result from displacement of the brain by an expanding lesion and cerebral edema. Depending on
the location of the lesion, herniation can cause obstructive hydrocephalus, brain shift past
midline, or brainstem compression.
- Herniation can lead to neurologic deterioration of a grave nature, with resultant decreasing
levels of consciousness, altered respiration, hypertonicity, hemiparesis, and decorticate posturing.
4. Hypoxic–Ischemic Injury
- The supply of oxygen and nutrients to the brain is dependent on adequate cerebral perfusion.
Alterations in cerebral perfusion, raised ICP, or lack of oxygen to the brain may result in
hypoxic– ischemic brain damage.
- Ischemia frequently occurs in the tissue surrounding cerebral contusions or hematomas and
ultimately leads to further brain damage. Severe hypoxic injury and diffuse axonal injuries are
most likely to cause severe disabilities, including prolonged postcoma unawareness.
5. Neurochemical Events
-When trauma occurs to the brain, there is a disruption of the blood–brain barrier and a release of
excitatory neurotransmitters and oxygen-free radicals into the blood system.
-Oxygen-free radicals have an extremely toxic effect on the brain and are damaging to cell
membranes and vessel walls. The damage from oxygen-free radicals causes internal disruption of
neuronal functioning and further brain damage.
3. Other consequences from brain damage
• Hydrocephalus
• Seizures
• Infections
• Dysautonomia
• Endocrine Disorders
PHYSICAL EXAMINATION:
1. MEDICAL HISTORY
- Onset and mechanism of injury (including time frames)
- Diagnostic test results (CT scan, MRI, radiographs)
- Medical precautions (weight bearing or ROM precautions)
- Vital signs
- Autonomic nervous system function (history of orthostatic hypertension or dysautonomia).
2. Social History and Living Environment
- Family and support system
- Educational/prevocational status
3. Cognitive/Behavioral Status
- Level of arousal
- Orientation
- Attention
- Behaviour/ Affect
4. Basic Sensorimotor Status
- Hearing/ auditory
- Vision, perception, and visuospatial ability
- Sensation (light touch, vibration, pain, temperature)
- Range of Motion
- Strength
- Muscle tone
- Abnormal movement patterns, posture, reflexes, pathologic reflexes, deep tendon reflexes)
- Balance and balance strategies (sitting and standing)
- Praxis and coordination
- Speed of movement
- Endurance
5. Functional Status
- Bed/floor mobility
- Transfers/transitions
- Sitting and standing skills (static and dynamic)
- Ambulation on level surfaces (supports needed)
- Stair ascension/descension (supports needed)
- Ambulation outside/rough terrain (supports needed)
- Advanced gross motor skills/sports • Generalization of functional abilities
- Skin integrity
- Respiratory status
- Bowel and bladder status
- Dysphagia status
- Medications
- Cultural issues
- Discharge environment
- Memory
- Language/communication (productive and receptive)
- Executive functions
- Neuropsychological or psychological assessments
Subjective Examination: Patient History
1. Medical History
- The PT should thoroughly review the child’s past medical/surgical and current condition before
initiating the physical examination. Information should be gathered regarding the mechanism of
the injury, severity of damage, and significant changes in the clinical picture over time.
- The child’s history of prior concussions or other cognitive issues should be noted. Particular
attention should be given to reports from CT scans, magnetic resonance imaging (MRI) scans,
radiographs, and other diagnostic tests.
2. Social History and Living Environment
3. Systems Review
Objective Examination: Tests and Measures
-Children who sustain TBI may experience a complex array of deficits in body structures and
functions in physical abilities, emotional development, and cognitive/behavioral functioning.
1. Cognitive/Behavioral Status
2. Level of Arousal (ALOSC)
3. Attention
4. Behavior/ Affect
 5. Behavior Management
6. Memory
7. Language
8. Executive Function
9. Sensorimotor Status
-abnormal muscle tone
-Muscle spasticity
-Ataxia
10. Muscle Performance Impairment
-Strength loss
-Impaired Endurance
-Range of Motion loss
- Balance and Postural Control Loss
- Sensory Deficits ( Hearing, Vision, Visuospatial skills)
11. Orthopedic Complications
-Heterotopic Ossification
-Fractures
12. Functional Measures
- Alberta Infant Motor scale (AIMS)- useful in noting gross motor function in children 0 to 18
months old.
- Peabody Developmental Motor Scale- useful in assessment of function in toddlers and
preschoolers.
- WeeFIM (Functional Independence Measure) - useful for assessing and tracking the
development of functional independence in children with disabilities, including TBI, between the
ages of 6 months and 7 years. The adult FIM can be used with older children. It measures six
domains of function: self-care, sphincter control, mobility, locomotion, communication, and
social cognition.
- The Bruininks–Oseretsky Test of Motor Proficiency- used to assess gross and fine motor
functioning.
- The Gross Motor Function Measure (GMFM) - evaluate changes in motor performance over
time. Commonly use in Cerebral Palsy Patient
- the Acquired Brain InjuryChallenge Assessment (ABI-CA)- demonstrates challenges in gross
motor activities that are beyond what the GMFM examines and can be used in older children
- The PEDI- It measures both capability and performance in the domains of self-care, mobility, and
social function.
- The ABI-specific PEDI subscales -used to measure functional change in children with TBI.
- the Caregiver Assistance Self-Care subscale-
- 2-minute walk test and the shuttle walk–run tests - helpful in evaluating children with higher
functional levels specifically for endurance during gait.