PSYC 301 Exam 4 Study Guide

1. Understand the 2 clinical components of consciousness (arousal

and awareness) and describe their neuronal and behavioural
(symptomatic) markers.
Awareness and arousal are clinical indicators of
consciousness

 Their relationship to consciousness can be

expressed linearly:

Wakefulness = a state of arousal

 Can be assessed by the presence of eye-opening and

brain-stem responses through the Glasgow Coma
Scale

 Neurobiological markers of wakefulness

o Passage of sensory information from brainstem

 cortex
o Conscious awake state = high energy demand,
electrical activity within corticothalamic
system

 Implicated brain regions: upper brainstem

(midbrain), thalamus, hypothalamus, brain stem,
cortex
o Reticular Thalamocortical Pathway necessary
for consciousness: brain stem  thalamus 
all over the cortex

 Relay of sensory information happens via

this pathway, therefore this pathway is
necessary for both arousal and awareness
PSYC 301 Exam 4 Study Guide

o Thalamus = relay station to cerebral cortex

for all sensory impulses except smell

 Registers conscious recognition of pain,

temperature, touch, pressure
Awareness = the ability of an individual to respond to
both external and internal stimuli in an integrated
manner

 Neurobiological markers of awareness

o Anatomical and functional connectivity of the
frontoparietal networks and the thalamus

*Unresponsive Wakefulness syndrome = vegetative state

Coma = most severe DOC

 Low arousal, low awareness

Other DOCs

 More arousal, less awareness

Sleep

 More awareness, less arousal

PSYC 301 Exam 4 Study Guide

2. Know the different DOC and the transition path between one
state to another in the process of recovery.
Disorders of Consciousness (DOC) are altered states of
prolonged pathologic consciousness

 Result from a withdrawal of excitatory synaptic

activity across the cerebrum as a result of
disfacilitation/ active inhibition of neocortical,
thalamic, and striatal neurons

 Neuron inactivation eventually leads to neuron

death
Sharp decrease in cerebral metabolic rate which results
from widespread disfacilitation

 Common denominator in all DOC following severe

brain trauma
Prognosis of DOCs gets better with movement through
stages
Coma

 State of unconsciousness characterized by a lack

of arousal and awareness

 Clinically: complete loss of spontaneous or

stimulus induced arousal

 No eye-opening; no sleep-wake cycles

 Neurologically: structural lesions usually involve

diffuse cortical or white matter damage or a
brainstem lesion

 Rehabilitation: survival of this stage is followed

by awakening and transition into a
Vegetative/Unresponsive Wakefulness state, or a
Minimally Conscious state within 2-4 weeks.
Vegetative/Unresponsive Wakefulness State (VS/UWS)

 High wakefulness/arousal, low awareness

 Clinically: unconscious, dissociative state of

wakefulness without awareness

 Eyes open spontaneously; sleep-wake cycles are

present

 Patients may be aroused externally by provocations

with no sign of conscious perception; act
spontaneously out of context
PSYC 301 Exam 4 Study Guide

 Neurologically: presence of wakefulness suggests

preserved brainstem functioning; lack of awareness
suggests underlying cortical dysfunction
o Sensory stimuli activate primary cortical
areas but not higher-order cortical areas
necessary for awareness

 Rehabilitation: with proper medical care, a

patient in this state can survive for many years
Minimally Conscious State (MCS)

 Wakefulness with partial awareness

 Clinically: characterized by a severe impairment

with evidence of wakefulness and partial
preservation of awareness

 There are purposeful behaviours – inconsistent but

reproducible command following; may exhibit visual
pursuit; emotional responses; gestures to
appropriate environmental stimuli; unable to
communicate their thoughts or feelings

 Neurologically: preservation of corticothalamic

connections
o May explain why patients retain capacity for
cognitive processing

 Rehabilitation: originally MCS patients were

categorized as VS but there was evidence that they
comparatively has meaningful improvement in
outcomes and the conditions were differentiated in
2002

TRANSITIONAL PERIOD

 Acute Confusional State

o Transition from MCS  Full Consciousness

o Clinically: patients continue to experience a
transient period of disorientation and
agitation
PSYC 301 Exam 4 Study Guide

o Day to day fluctuation of behavioural

responses
o Irritability, distractibility, anterograde
amnesia, restlessness, emotional lability
(drastic fluctuation), impaired perception,
attentional abnormalities, disrupted sleep-
wake cycle
o Rehabilitation: return of behavioural
consistency despite situational stresses that
may indicate a resolution of this period

 In recovery from DOC, regaining of arousal

precedes awareness

3. Know other pathological conditions that are confused or

misdiagnosed as DOCs.
Brain Death

 Complete and irreversible loss of brain function

 Characterized by 3 clinical factors:

o Coma (with a known cause)
o Absence of brainstem reflexes
o Apnea (cessation of breathing)
Locked-in Syndrome/ Cognitive Motor Dissociation

 Rare; characterized by intact consciousness,

sensation, and cognition with anarthria and
quadriplegia (paralysis of limbs and facial
muscles)

 Patients unable to speak or react

PSYC 301 Exam 4 Study Guide

 Communicate through vertical eye movements and

blinking

 Caused by damage to the ventral pons and

corticospinal/corticotubular pathways which
communicate with brainstem

 Over time, some patients may regain control of the

fingers, toes, or head

 This atypical presentation, with lost speech and

motor control, places these patients at risk for
misdiagnosis as a DOC

 Interrupted transmission of efferent signals (CNS:

brain  body)

 In locked in syndrome, brain/cerebral metabolism

is more similar to healthy individuals than those
with DOC
o Implicated area: Medial Posterior Parietal
Cortex (PPC)

 Brain imaging can be used to detect hidden

consciousness
o Patients in MRIs and EEGs asked to imagine
playing tennis or walking around their house
as substitutes for yes/no answers
o Can reveal motor dissociation in 15-20% of
patients who seem unresponsive on behavioural
examinations and are misdiagnosed with a DOC
o Early detection of cognitive motor
dissociation (CMD)/ locked-in syndrome in ICU
predicts 1-year functional recovery
o Important discovery: asking a patient in CMD
if they were in pain and the answer was no
4. Be able to describe treatment intervention strategies
according to the meso-circuit model.
According to the mesocircuit hypothesis, disorders of
consciousness share a common pathophysiological mechanism

 Cortical, striatal, and thalamic neuronal death,

dysfunction or disconnection is responsible for
the decrease in cerebral synaptic activity (and
the deficits in arousal and awareness)

 Loss of excitatory output from central thalamus to

cortical areas has a causative role in DOC
PSYC 301 Exam 4 Study Guide

Main treatment goal is to maintain patient stability

while promoting and provoking arousal
Mesocircuit network has to work together cohesively in a
healthy brain
Pharmacological and non-pharmacological treatments

 Specific and local brain stimulation: transcranial

direct stimulation; transcranial magnetic
stimulation

 Central thalamic deep brain stimulation

 Low intensity focused ultrasound pulsation

Treatment methods can be used in a targeted, specific and
controlled way in a system context
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5. Know the Rancho Los Amigos Scale and the definition of each of
the 10 levels. What are the behavioural symptoms and quality
of consciousness at each level?
Rancho Level 1

 No response; total assistance

 Complete unconsciousness

 No awareness

 Coma

 Eyes closed

 Does not communicate, follow commands, or respond

to pain
Rancho Level 2

 Generalized response; total assistance

 Vegetative state

 Connection to higher brain = impaired

 Able to open eyes

 Periods of wakefulness

 Some return of sleep-wake cycle

 Awake but not aware of their surroundings

 No verbal communication

 Responses are not intentional or thought out

PSYC 301 Exam 4 Study Guide

o Responses are the same no matter the task

Rancho Level 3

 Localized response: total assistance

 Minimally conscious state

 Staring in direction of sound or voice

 Looking at pictures

 Grabbing toward tube or catheter

 Pulling away from pain

 No verbal communication

 May indicate yes/no nonverbally

 Responses remain inconsistent and delayed due to

fleeting attention and slowed ability to process
or make sense of what they see/hear

 Starting to recognize objects

 Decreased arousal

 Localizes to pain and pulls away

Rancho Levels 1-3: Waking Up
Rancho Level 4

 Confused and agitated; maximal assistance

 Still in a state of low arousal/sleepiness

o Outwardly seen as agitation/restlessness

 Agitation  hitting, foul language, yelling,

restlessness

 Short attention span – no day-to-day memory

 Confused; confabulation (distorted memories)

 Significant sleep disturbances  fatigue

 Goal = improving attention through the use of

familiar tasks such as:
o Brushing teeth
o Writing name
o Sorting objects by colour
o Simple activities they enjoy
PSYC 301 Exam 4 Study Guide

 Unable to attend to and recall new information

 Maximum assistance with familiar tasks

Rancho Level 5

 Confused; inappropriate; non-agitated; maximal

assistance

 Wakefulness with awareness

 Purposeful interactions with surroundings

 Difficult to complete various activities

accurately

 Post-Traumatic Amnesia – don’t have day to day

memory

 Better attention than previously but continues to

be highly distractable

 Still need assistance with basic and familiar

tasks

 Higher level cognitive processes not functioning

well yet
o Needs maximum supervision for safety

 May have vague understanding that things aren’t

right

 Potential for wandering off to try to get home

 May repeat action and get stuck on basic needs

 Disorientation, confusion

 Decreased awareness or understanding of injury

 Poor problem solving

 Maximum structure and step by step instructions

needed for basic tasks

 Decreased initiation

 Starting to demonstrate immediate memory, but

still poor recall
Rancho Level 6

 Confused but appropriate; moderate assistance

 Emerged from Post-Traumatic Amnesia (general day

to day memory)
PSYC 301 Exam 4 Study Guide

 Showing some recall of what is happening on a day

to day basis
o Orientation to the date, where they are, how
to get to different places

 Occasional assistance still needed

 Post Traumatic Cognitively Impaired State

o Result on ongoing impairments in: attention,
information processing, memory, executive
functioning

 May start and complete tasks with less assistance

but still need extra time to do so

 Able to hold simple social conversations RE

immediate needs and daily tasks

 Deficits related to specific injury to the brain

are able to be better evaluated  focal injuries

 Focal injury deficits:

o L/R weakness, comprehension, word-finding
problems

 Day to day recall improving but still limited

 Decreased problem-solving ability

 Can start to name deficits and recognize

disabilities
o Uninsightful as to how deficits impair return
to pre-injury activities

 Less assistance needed for familiar tasks

 Demonstrate lability (in behaviours)

Rancho Levels 5 & 6

 Marked improvement in ability to interact

 In Post-Traumatic Confusional state

 Severe cognitive limitations in new learning and

executive functioning

 Beginning to show problem areas specific to own

injury which can be addressed in individual
therapy

 Cognitive skills targeted at this level =

attention, orientation, memory, simple reasoning,
problem solving
PSYC 301 Exam 4 Study Guide

Rancho Level 7

 Automatic; appropriate; minimal assistance for

daily living skills

 Consistent day to day memory

 Higher brain functioning = improving

 Improved in wakefulness, awareness, perception,

attention, memory

 Limited recall of detailed, lengthy, complex

events

 Challenges in reasoning and executive functioning

 Routine self-care, set schedule

 Problems planning and organizing unfamiliar tasks

 May still need supervision due to poor safety

awareness and judgment

 Trouble understanding limitations from brain

injury

 May be showing deficits unique to focal injuries

o Physical limitations: speaking and
communication impairments
o Poor memory: executive functioning, challenges

 Less consistency in day = more evident deficits

 Superficial awareness, overestimates abilities,

concrete thinking, minimal awareness of errors,
needs assistance to identify errors
Rancho Level 8

 Purposeful; appropriate; stand-by assistance

 Readiness to explore returning to school/work

 May over/underestimate their abilities

 May need assistance or reminders to use

compensatory strategies

 Gaining independence but continuing to deal with

cognitive deficits

 Low frustration tolerance, irritability, self-

centeredness, depression, fatigue

 Awareness of and acknowledgement of impairments

PSYC 301 Exam 4 Study Guide

 Compensates for memory deficits

 Will complete familiar tasks with stand-by

assistance
Rancho Level 9

 Purposeful; appropriate; stand-by assistance on

request

 Goes through daily routine while being aware of

need for standby/occasional assistance

 Able to pay attention with distractions for up to

1 hour

 Able to switch between tasks

 Independently carrying out tasks with assistance

when requested

 Able to think about consequences to decisions

 Awareness of fatigue

 Estimates abilities

 Increased frustrations RE limitations

Rancho Level 10

 Purposeful; appropriate; modified independent

 Independent with everything within their physical

capabilities

 May sometimes require more time to complete an

activity

 Independently use compensatory strategies

 Able to transform back to work, school, etc.

Rancho Levels 9 & 10

 Gradually increases independence w amount of

instruction and structure

 Assistance decreasing over time

6. Using what we learned about DOCs, try to speculate about the

neuronal change and recovery supporting these different
stages.
Rancho Level 1

 No arousal or awareness
PSYC 301 Exam 4 Study Guide

 Sensory information not passing through from

brainstem to cortex

 Impaired connection between frontoparietal network

and thalamus
Rancho Level 2

 Arousal, low awareness

 Increase in arousal suggests activation of brain

stem  thalamus  cortex pathway for sensory
information
o Reticular thalamocortical pathway
Rancho Level 3

 Arousal and awareness

 Return of awareness suggests connectivity of

frontoparietal networks to thalamus
Rancho Levels 4-6

 Gradual improvements in arousal and awareness

Rancho Levels 7-10

 Improved mesocircuit functioning as arousal and

awareness return to normal
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7. Describe experience effects that are maladaptive for
behavioural outcome after brain damage (Kerr, Cheng, & Jones,
2011).
Use of compensatory processes (i.e. use of a “good limb”)
may delay and prolong recovery

 Increased neural plasticity after injury may cause

compensatory processes to become stronger than
damaged processes
8. Describe manipulations of experience that drive functionally
beneficial neural plasticity (Kerr, Cheng, & Jones, 2011).
If done early enough in the treatment process, skilled
motor learning can have lasting and impactful
rehabilitative effects
Experiences continuously change the nervous system and
can enable behavioural flexibility
9. Describe reasons why rehabilitative training effects can be
expected to vary with age, training duration, and timing
(Kerr, Cheng, & Jones, 2011).
PSYC 301 Exam 4 Study Guide

Age

 Neuroplasticity associated with behavioural change

varies with age

 With higher age, it takes longer to occur and

occurs at a lessened magnitude

 Decreased synaptic potentiation, synaptogenesis

and cortical map reorganization
Training Duration

 Repeated practice enhances the likelihood that the

skill will be well established and enduring
Timing

 Early vulnerable period following insult –

excessive exercise can impede recovery and
exacerbate damage

 2 weeks after = optimal

 Skilled motor rehabilitation is most effective

when initiated early, but not immediately, after
insult
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10. What is chronic traumatic encephalopathy and how is it
related to TBI?
CTE = a form of dementia
Brain degeneration caused by several/reoccurring TBIs
Correlated with early onset neurodegenerative diseases
Can only be diagnosed at autopsy
Common in contact sports like Football – e.g., Aaron
Hernandez
Symptoms

 Behavioural problems

 Mood problems

 Problems with thinking

11. What is the role of neuroplasticity in brain recovery? How is
it similar and how is it different from developmental
plasticity during brain development?
After a TBI there are new plasticity waves that would not
otherwise occur
PSYC 301 Exam 4 Study Guide

 This capacity for neuroplasticity in adulthood is

not possible in normal development

Similar pattern to developmental plasticity: growth 

peak  pruning
12. What are the major physiological processes that take place
following TBI as part of the healing process?
Cell dysfunction

 Cell death

 Edema (swelling due to trapped fluid in tissue)

 Metabolic depression

 Axonal growth inhibition

Cell genesis

 Injury  spontaneous recovery

 Gliogenesis

 Neurogenesis

 Angiogenesis (development of new blood vessels)

Adaptive plasticity

 Axonal sprouting

 Synaptogenesis

 Functional plasticity

 Receptor function

 Cell signalling

 Network relearning

 Generation of new cells and new neurons invited

new neuroplasticity (fire together, wire together)
o Usually do not have the capacity for this
level of neuroplasticity in the adult brain
o High level of neuroplasticity = necessary to
regain functions and abilities that were lost
Therapies

 Protectants

 Neuro-activators

 Growth promoters
PSYC 301 Exam 4 Study Guide

 Cell therapy

 Cortical stimulation

 Want to leverage the natural processes and harness

neuroplasticity to train the body and brain to
regain function
First stage in recovery: Spontaneous Reorganization

 Acute and immediate recovery of the local damaged

brain tissue
o Subacute recovery and chronic recovery involve
the renewal and stabilization of functional
brain networks that may be infected as well

 Enhanced neuroplasticity
o Activation of learning networks which are
usually active only during development, to
facilitate relearning

 Early recruitment of contralesional homologous

brain regions or perilesional regions to
compensate for the lost function

 Spontaneous recovery plateaus after 3 months (in

stroke) to 6 months (TBI) after injury

 Upregulation of proteins involved in neural growth

and guidance
o Many of which mimic events during neural
development, occur over a relatively narrow
window of time after injury
Second stage in recovery: Training-induced Recovery

 Training can induce plastic changes in the brain

to promote longer term improvement

 A shift from greater neural dynamics and

flexibility during early stages of recovery to
increasing efficiency and decreasing malleability
during later stages of recovery
13. How can neuroplasticity be directed and leveraged in brain
recovery? How can it “go wrong”? What are its limitations?
The plasticity that occurs spontaneously may largely
reflect the development of compensatory motor patterns
rather than true recovery of the original kinematic
patterns

 Composition of the motor cortex is changed (in

regard to proportion) due to compensation
PSYC 301 Exam 4 Study Guide

Spontaneous reorganization without additional training

may lead to compensation rather than recovery
Compensatory functions can be helpful in the short term
but damaging in the long term and impeding to recovery
Rehabilitation is about supporting not replacing the
damaged system
Neuroplasticity can have negative consequences resulting
from maladaptive changes

 Early contralateral homologous region recruitment

may be a compensatory adaptation early on but may
become maladaptive over time

 Spontaneous reorganization of circuitry may

interfere with regaining of function
o Learned non-use may result from a failure to
reassociate the function to the relevant brain
region during recovery

 Solution: restraining the healthy limb

Limitations

 Cortical plasticity sems to be possible only if

subcortical connectivity is preserved
o Studies in stroke and TBI suggest that
extensive white matter damage may result in
severe permanent deficits

 Spontaneous plasticity with no directed training

may have negative consequences resulting from
maladaptive changes

 Revealing the molecular mechanisms behind the

recovery cascade is crucial for optimizing timing
and dose of training to leverage and not hamper
the neuroplasticity boost that follows brain
injury
14. What are the static and dynamic protective factors and how do
they contribute to recovery from TBI?
Static Protective Factors

 Cannot be modified

 Age
o Once believed there was a negative correlation
between age and potential of recovery
o Because of their ongoing development, younger
children actually show attenuated recovery
PSYC 301 Exam 4 Study Guide

patterns compared to older children and young

adults

 Sex/gender
o According to CDC, men are three times more
likely to die from a TBI than women
o Progesterone = protective factor

 Hypothesized to improve outcome in

females by helping to reduce inflammation
and apoptosis within the hippocampus in
the acute and post-acute period following
an injury

 Intelligence and education level

o Brain damage, especially to the temporal and
frontal areas frequently disrupts intellectual
and cognitive abilities (frontal lobes =
executive functions)
o Access to services is not equal
o Cognitive reserve effect: preinjury
intellectual and cognitive abilities are
predictive for recovery trajectory (return to
baseline and fewer long-term cognitive
deficits)

 Based on age, privilege, access

 Psychiatric history
o Many suffer from psychiatric disorders after
sustaining a TBI
o Preinjury psychiatric history is an important
variable in postinjury emotional adjustment
and recovery of function following brain
trauma
o Past psychiatric disorders = negative effect
on recovery
o Correlation between preinjury psychiatric
disorders and novel psychiatric disorders
following a TBI
Dynamic protective factors

 Can be potentially modified with intervention

 SES
o One of the most significant predictors of
recovery following TBI
PSYC 301 Exam 4 Study Guide

o May impact recovery indirectly through access

to appropriate follow-up medical care,
adequate rehabilitation services, and
educational training programs
o May also be related to reduced stress levels
in families with relatively more economic
resources

 Family and social support

o Research in children/adults suggests improved
family functioning and increased social
support facilitate protective factors
following a TBI

 Nutrition
o The brain is highly metabolic, especially
during the process of repair following acute
injury
o Many animal models support the idea that
adequate nutrition is an important protective
factor that may help facilitate positive
recovery following a TBI
o Human studies are inconsistent regarding the
role of nutrition within TBI recovery

 Exercise
o In health animals and humans, exercise
increases neurogenesis in the hippocampus and
supports learning and memory
o Exercise is related to decreases in neuronal
apoptosis following a TBI
o A brief period of rest followed by regular
noncontact activities including (low intensity
aerobic) exercise is associated with better
recovery
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15. What is a traumatic brain injury and how are they classified
into mild, moderate, or severe? What are the main criteria for
each classification?

TBI  caused by a blow to the head or violent movement

of head

 Classified by initial length of loss of

consciousness and post traumatic memory loss
Mild
PSYC 301 Exam 4 Study Guide

 When patient initially loses consciousness for 15

minutes or less

 If they have any memory loss about trauma event,

feel dazed, disoriented, confused = concussion
Moderate

 Loss of consciousness for 15 minutes – a few hours

 Followed by several days/weeks of confusion

Severe

 Loss of consciousness 6 hours or longer after

injury
16. What is the Glasgow Coma Scale and how is it used to assess
TBI level?
The Glasgow Coma Scale measures the level of alertness as
well as eye response, verbal response, and motor response
Measured on a scale of 3 (deep coma) to 15 (fully awake)

 13 – 15 = Mild TBI

 9 – 12 = Moderate TBI

 8 or less = Severe
17. What are the common behavioral, cognitive, and emotional
symptoms following TBI?
Difficulty coordinating balance and walking
Blurred vision
Headaches
Trouble speaking and swallowing
Lack of bowel and bladder control
Motor impairments
Seizures
Vision problems
Changes in sensory perception, sleep patterns, sexual
function
Personality changes
Trouble communicating; difficulty forming sentences or
choosing vocabulary
Memory impairment, forgetfulness
Depressed
PSYC 301 Exam 4 Study Guide

Disoriented
Mood swings
May act inappropriately
Struggle with reason, logic
Poor concentration, limited attention span
18. What is a neuropsychological assessment after TBI and how
does it contribute to the recovery process?
Neuropsychological assessment evaluates basic hand-eye
coordination, higher level thinking, cognitive skills for
everyday life
Measures a patient’s understanding of where they are,
what new things they are able to learn, what happened to
them, and how their memory was affected

 Also measures basic language and intelligence

skill, perception, complex planning, abstract
thinking, understanding and obeying rules,
initiating appropriate behaviour, inhibiting
inappropriate behaviour
Also focuses on psychological and personal interpersonal
thoughts, behaviours, and skills
Helps the team oof doctors and therapists to develop an
effective plan of care for rehabilitation
19. In class, we referred to 3 main neuronal processes that occur
following a TBI. In this video, the following medical terms
are mentioned and explained: axonal shearing, brain
herniation, cerebral atrophy, and hematoma. To which of the
processes/phases we discussed would you relate these
phenomena?
Axonal shearing

 When the brains axons (main forms of

communication) are stretched to the point of
breaking causing damaged brain cells to die

 Cell death
Brain herniation

 Rising pressure inside the brain causing parts to

shift out of place

 Metabolic depression
Cerebral atrophy
PSYC 301 Exam 4 Study Guide

 Loss of nerve cells in the brain and the

connection between them; can be focused or global

 Axonal growth inhibition

Hematoma

 Pool of blood or bruise inside the skull which can

increase pressure inside the brain

 Edema
All types of cell dysfunction
20. How do the treatment and rehabilitation programs described at
the end of the video relate to the main stages/principles of
recovery we discussed in class (spontaneous reorganization and
training-induced recovery)?
In the early weeks of treatment the priority is
stabilizing
Afterwards patients can move through a rehabilitation
centre, and then to an outpatient centre when they are
well enough
After stabilization and minimizing damage, the focus
shifts to relarning the basics and improving attention
span, memory, and self care