MODULE 1 ○ Interpret visual fields

MOOC: TRAUMATIC BRAIN INJURY ● Temporal lobe

→ Acquired brain injury; a multitude of injuries w/c may include: ○ Memory formation,
● Hypoxia, brain tumors, epilepsy, surgical resection, ○ Role in emotion and language
infections, and traumatic brain injury ● Cerebellum – “the little brain”
→ Injury to the brain from external forces ● Brian stem – sends signals
→ Impacting on an object or by the head stopping suddenly ● Corpus callosum – white matter tract
→ Spectrum of mild or concussive like injury ○ Connects the two hemispheres
→ Multitude of s/x and recovery patterns (do not always align ○ To allow communication
with the injury severity) ● Hippocampus & amygdala – memory and emotions
→ Public health and socioeconomic problem (silent epidemic) ○ Amygdala – lots of fear processing
● 69 million every year ● Midrain & brainstem
→ Many individuals do not seek attention for minor TBIs ○ Breathing
→ Major cause of death ○ Heart rate
→ Can cause life-long disability (common in adults) ○ Motor functions
● Impaired attention ● Hypothalamus & pituitary gland
● Psychological health issues (including depression) ○ Forms the HPA axis
→ Higher in males than for females ○ Responsible of hormones (sex and growth)
Peaks for Traumatic Brain Injury ○ Desire to eat
● Young children – falls CELLS THAT MAKE UP THE BRAIN
● Adolescents – vehicle accidents/risk taking behavior The brain has two main cell types: (1) nerve cells & (2) glia
● Elderly – falls Neurons:
Traumatic brain injury (TBI) can be mild (concussion) through to ● Dendrites: (input zone) messages are received
severe. There are a variety of different ways, or modes, in which ● Axon hillock: where the action potential travels
TBI can occur. The mode of injury, and rates of TBI differ with ○ Electrical signals will move down the axon and
age. For example, in the very young and those aged over 65 to the axon terminals, where a chemical also
years falls are the leading cause of TBI. This information is known as a neurotransmitter will be released.
depicted in the infographic below. Glia
→ Supporting cells
● Myelin: [Link]. Oligodendrocytes
○ Fatty white substance
○ Produce myelins that wraps around the axons
and this provides insulation for those electrical
signals
○ Allows the signal to travel further and faster
● Microglia: immune cells of the brain
○ Protects the brain from disease and damage
● Astrocytes: supporting cells
○ Help bring nutrients from the blood into the
brain to help feed the cells
○ Provides stability to blood-brain barrier
BIOMECHANICS OF TRAUMATIC BRAIN INJURY
Whatever the cause of the trauma the resulting head injury
presents as one of two general types:
Introduction to the Brain: Structure & Function 1. Open head injury
STRUCTURES & PROTECTIVE LAYERS 2. Closed head injury
● Skull – (6-7) millimeters ; primary protective layer OPEN/PENETRATING HEAD INJURY
● Meninges >> An object enters the brain causing damage to a specific area
○ Dura – outermost layer tough & thick >> Dura mater is breached – w/c exposes the brain to the
○ Arachnoid mater – spongy external environment
○ Pia mater – innermost layer >>> Increases the risk of infection
● Brainstem → Spinal Cord Example:
Brain: ● Bullet/ shrapnel
● Soft tissue; 1.5 kilos (average ● Bone fragments from a skull fracture
● Sulic, grooves >> Rare; 1-2% of all TBIs
CLOSED HEAD INJURY
“Folds allow more brain in a smaller region” >> More common
Right hemisphere: >> Dura mater is not breached
● Frontal lobe – higher decision making/problem solving/ >> Can involve the skull fracture but there’s no penetration in
order thinking the brain
○ Emotional regulation and personality Example:
● Parietal lobe – ● Head blows
○ Interpreting sensory information ● Severe acceleration/deceleration/rotational
● Occipital lobe ○ Rotational – rapid twisting of the head

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 ● Violent movements
● Assaults
● Sporting accident
>> Can occur with or without an impact to the head
>> Skull fractures may or may not occur
>> Resulting brain injury can range from mild to severe
>> Injury severity is traditionally diagnosed by assessing a
combination of clinical sx, including the duration of loss of
consciousness, depth of coma (GCS), post-traumatic amnesia, → A contusion is the result of direct damage to the neurons, glial
and brain imaging results cells, and blood vessels exposed to the compression forces
→ Lacerations
MILD MODERATE SEVERE ● Another type of focal injury
● Involve tearing of the brain tissue, as the brain rotates
Loss of consciousness secs/min 1-2 hours > 24 hours across the rough ridges inside the skull
● Could also be caused during an open head injury, by an
Post--traumatic < 1hr 1-24 hours > 24 hours
object penetrating the brain
amnesia
● Swelling/edema, toxic molecules from damaged cells
Imaging results Normal Abnormal Abnormal (secondary brain injury)
→ Bleeding/Hemorrhaging
● Third type of focal injury occurs in the brain or between
PRIMARY VS. SECONDARY INJURY
the brain resulting in accumulation of blood called as
PRIMARY INJURY
“intracranial hematoma”
>> Initial damage that occurs at the time of the head injury
● Types of hematomas:
>> Results directly from mechanical forces affecting the brain
○ Epidural hematoma
tissue, s/a blows [Link] acceleration and deceleration forces
■ Blood clot forms underneath the skull
>> Direct result of injury
but outside of the dura and the brain
>> Classified into two sections: focal and diffuse injury
○ Subdural hematoma
>> Cannot be altered once occurred, however its severity can be
■ Between the brain and the dura
controlled by preventive and safety measures s/a wearing of
○ Intracerebral hematoma
helmets or seat belts
■ Within the brain tissue itself, following
FOCAL INJURY DIFFUSE INJURY a rupture of blood vessels within the
brain
→ Localized tissue damage in the → Spread throughout the brain
brain → Predominantly affects the long
DIFFUSE BRAIN INJURY
→ A.k.a. contusion/lesion axons that comprise the brain’s >> Caused by rotational and linear acceleration-deceleration
white matter forces
>> Entails widely distributed damage to axons
→ Easy to identify w/ standard → Difficult to detect
>> “DIffuse axonal injury”
imaging technique
>> Damage to the very fine blood vessels causing microbleeds
→ May be surgically removed throughout the brain
>> The damage to the axons, or diffuse axonal injury, is caused
by shearing forces that are generated within the brain tissue
SECONDARY INJURY
when certain segments of the brain move at a faster rate than
>> Follows the primary injury (secs) and can continue for
others
months
>> Gray and white matter interface as well as the long white
>> Series of steps of cellular, chemical, tissue, and blood vessel
matter projections are the most susceptible to this kind of injury
changes in the brain that contribute to further damage of brain
→ Global edema
tissue
● Secondary injury event following diffuse brain injury
>> The type and extent of secondary insults that arise depend
● Leads to increased intracranial pressure w/c can cause
on the type and severity of the primary injury
further damage to neurons
>> Potentially treatable
MODULE 2
FOCAL BRAIN INJURY
INTRODUCTION – SPECTRUM OF TBI SEVERITY
→ Produced by collision forces of the brain
How do we measure TBI severity?
→ Impacting on the skull and resulting in compression of the
tissue underneath the cranium
There are three main ways in which we measure how severe a
→ The force of collision can also tear blood vessels causing
TBI is:
bleeding into the brain
● Depth of coma, measured by the Glasgow Coma Scale
→ Coup & Contre coup
(GCS)
● Length of post-traumatic amnesia (PTA)
● Length of Loss of consciousness (LOC)
It is important to note that each of the measures has advantages
and disadvantages, and often medical and rehabilitation
specialists will take into account all three, if they are known.

→ Concussions are belittled and not often given attention

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→ Moderate to severe injury more obvious and significant
changes can easily be identified within the brain
Glasgow Coma Scale (GCS)
→ Assesses level of consciousness based on three behaviors:
1. Eye opening: for example, is the person able to open
their eyes when asked, or in response to pain?
2. Verbal response: for example, can the person say
where they are, what day/time it is? Can they speak
but are unable to provide coherent responses?
3. Motor response: for example, can the person move
when asked to, or in response to pain?
→ Mild impairment of consciousness: 14-15
→ Moderate impairment of consciousness: 9-13
→ Severe impairment of consciousness: 3-8
POST TRAUMATIC AMNESIA (PTA)
PTA measures the length of time following TBI in which the
person is incapable of learning new information, and remains
confused and disoriented.
● Mild: PTA less than an hour
● Moderate: PTA less than a day
● Severe: PTA longer than a day
● Very Severe: PTA longer than a week
What is a Concussion?

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