States of Consciousness Flashcards

1
Q

What is the Rancho Los Amigos Scale?

A

The Rancho Los Amigos Scale
- monitor changing conditions in a patient recovering from a disorder of consciousness
- assessment levels of the scale describe patient’s cognitive function with regards to arousal levels, behavioural responses, and task performance

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2
Q

Rancho Los Amigos Level 1

A

No response, total assistance → coma

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3
Q

Rancho Los Amigos Level 2

A

Generalized response, total assistance → vegetative state

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4
Q

Rancho Los Amigos Level 3

A

Localised response, total assistance → minimally conscious state
staring in direction; grabbing; nonverbal

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5
Q

Rancho Los Amigos Level 4

A

Confused and agitated, maximal assistance → low arousal and sleepiness
hitting, foul language, confabulation

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6
Q

Rancho Los Amigos Level 5

A

Confused, inappropriate, and non-agitated, maximal assistance → post-traumatic confusional state
purposeful interactions; post traumatic amnesia

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7
Q

Rancho Los Amigos Level 6

A

Confused, appropriate, moderate assistance → post traumatic cognitively impaired state
emerged from post-traumatic amnesia; focal injuries better evaluated

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8
Q

Rancho Los Amigos Level 7

A

Automatic and appropriate, minimal assistance → higher brain function improving
improvements in memory, awareness, perception; planning still difficult; low safety awareness

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9
Q

Rancho Los Amigos Level 8

A

Purposeful and appropriate, stand-by assistance → explore returning to work/school
continued cognitive deficits

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10
Q

Rancho Los Amigos Level 9

A

Purposeful and appropriate, stand-by on request → increased independence
tasks; consequences; accurate ability estimation; increased frustration

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11
Q

Rancho Los Amigos Level 10

A

Purposeful and appropriate, modified independent → physical independence
compensatory strategies

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12
Q

What are the two clinical components of consciousness

A

Arousal (wakefulness)
Awareness (subjective experience)

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13
Q

Arousal - neuronal and behavioural markers

A

neuronal - sensory info passed from brainstem to cortex; high energy demand; electrical activity in corticothalamic system; cerebral cortex active
behavioural - eye-opening; brainstem responses; sensory impulses received

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14
Q

Awareness - neuronal and behavioural markers

A

neuronal - connectivity of frontoparietal networks and thalamus
behavioural - ability to respond to both external and internal stimuli

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15
Q

Disorders of Consciousness - meaning; three categories plus transitional state

A

DoC: altered states of pathologic consciousness
- withdrawal of excitatory synaptic activity across cerebrum
- widespread disfacilitation; sharp reduction in cerebral metabolic rate
Coma, VS, MCS; Acute confusional state

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16
Q

Coma

A

lack of arousal and awareness; no spontaneous or stimulus induced arousal, eye-opening, or sleep-wake cycles

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17
Q

Vegetative State

A

wakefulness without awareness; spontaneous eye-opening, sleep-wake cycles, external arousal with no signs of conscious perception

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18
Q

Minimally Conscious State

A

wakefulness with partial awareness; non-verbal, inconsistent but reproducible command following

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19
Q

Acute Confusional State

A

transient period between MCS and full consciousness; fluctuation of behavioural responses

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20
Q

disfacilitation

A

active inhibition

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21
Q

Two possible misdiagnoses of DoC

A

Brain death
Locked-in syndrome

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22
Q

Brain Death

A

complete and irreversible loss of brain function

23
Q

Locked-in Syndrome

A

cognitive motor dissociation: intact consciousness, sensation, and cognition; limb and facial muscle paralysis
- ascending (sensory/afferent) signals intact
- descending (motor/efferent) transmission interrupted

24
Q

TBI - definition; classification

A

Traumatic brain injury caused by blow to head or violent movement of head

Mild - loss of consciousness for 15 min or less; predominantly blast, non-penetrating; includes concussion

Moderate - loss of consciousness for 15 min to a few hours, followed by a few days/weeks of confusion; blast + acceleration/deceleration, typically non-penetrating

Severe - loss of consciousness for 6 hours or longer (after injury or period of clarity); complex, blast + acceleration/deceleration + penetration; includes coma, VS, and MCS

25
Q

Glasgow Coma Scale - purpose; three categories assessed; result classification

A

Objectively describes extent of impaired consciousness
Assesses eye opening, verbal response, and motor response
3 (deep coma) - 15 (fully awake)
Mild TBI 13+; Moderate TBI 7-12; Severe TBI 3-6

26
Q

Common diagnostic tests used to identify brain damage

A

Rancho Los Amigos scale
JFK coma scale
Standard diagnostic tests (x-ray, CT, MRI)
Neuropsychological assessment

27
Q

JFK coma scale (5 categories)

A

hearing, vision, movement, communication, arousal

28
Q

Neuropsychological assessment - what is assessed; how does it contribute to recovery process

A

Hand-eye coordination and cognitive skills (psychological, personal, and interpersonal thoughts, behaviours, and skills)

Evaluates multiple aspects of mind to develop effective care plan

29
Q

Common behavioural, cognitive, and emotional symptoms following TBI

A

behavioural - sleep pattern changes, personality changes, trouble communicating, inappropriate action

cognitive - balance, walking, headache, trouble speaking and/or swallowing, lack of bowel/bladder control, motor impariment, seizure, vision problems, sensory perception changes, poor concentration, memory impairments, difficulty forming sentences/choosing vocabulary

emotional - depression, mood swings

30
Q

Main goals of treatment and rehabilitation programs

A

early weeks - stabilizing physical condition, preventing complications, addressing medical issues
follow-up - regular appointments, outpatient therapy, or rehabilitation facility
rehabilitation - relearn basic skills, independence; safety → awareness → stretching/strengthening/balance → date, time, location, memory

31
Q

Signs and symptoms of TBI (CPPB)

A

Cognitive - thinking, attention, memory, decision-making

Perceptual - sensory and spatial/temporal orientation problems

Physical - headache, fatigue; consciousness issues

Behavioural - irritability; changes in affect

32
Q

TBI assessment using amnesia length

A

Mild <24 hrs
Moderate >24 hrs, <7 days
Severe >7 days

33
Q

TBI assessment using imaging

A

Mild - negative
Moderate - transient changes
Severe - positive, lasting abnormalities

34
Q

Chronic Traumatic Encephalopathy

A

Repeated head traumas can cause gradual brain degeneration; mild TBIs
Eg., Aaron Hernandez

35
Q

What are the (3) major neuro-physiological processes that take place following TBI as part of the healing process?

A

Cell dysfunction - cell death, decrease in cortical inhibitory pathways

Cell genesis - neuronal and nonneuronal cells recruited to replace damaged cells

Adaptive plasticity - systems remodeling, relearning and cortical changes for recovery

36
Q

How can neuroplasticity be directed and leveraged in brain recovery? How can it “go wrong” (what are its limitations)?

A

Training induced recovery to avoid compensation
- subcortical connectivity must be preserved (extensive white matter damage may lead to permanent deficits)
- directed training must occur (avoid maladaptive changes)
- molecular mechanisms must be revealed

37
Q

Static protective mechanisms promoting recovery from TBI

A

Factors that cannot be modified

  • age
    (young children - reduced recovery patterns; older people - slower recovery)
  • sex/gender
    (men 3x more likely to die from TBI)
  • cognitive reserve
    (intelligence and education level pre-injury - return to baseline)
  • psychiatric history
    (disorders common after TBI - PTSD, depression, anxiety, etc.)
38
Q

Dynamic protective mechanisms promoting recovery from TBI

A

Factors that can potentially be modified through intervention

  • leveraging socioeconomic status (SES - can also be considered static)
    (access to care, reduced stress levels with economic resources)
  • family and social support
    (increased well being)
  • nutrition
  • exercise
    (increases neurogenesis in hippocampus; decreases in neuronal apoptosis) not too soon after injury (2 weeks)
39
Q

Axonal shearing

A

Axons in brain are stretched to point of breaking; damaged cells die and release toxins that spread to neighbouring cells

40
Q

Brain herniation

A

rising pressure inside brain or hematoma; parts are shifted out of place

41
Q

Cerebral atrophy

A

loss of nerve cells and connections between them in the brain

42
Q

Edema

A

swelling inside the skull;
brain cells are squeezed, interrupting blood flow and oxygen to brain tissue

43
Q

Hematoma

A

pool of blood or bruise inside skull caused by damaged blood vessels; can increase pressure inside skull

44
Q

Hemorrhage

A

internal or external bleeding caused by damage to a blood vessel

45
Q

Intracranial pressure (ICP) monitoring

A

monitoring of pressure inside skull using threaded catheter or sensor

46
Q

Shock

A

body response triggered by loss of blood to brain;
can indirectly injure brain tissue

47
Q

Sympathetic storming

A

elevated stress response;
thought to be a sign of returning activity to sympathetic or protective nervous system

48
Q

What is the typical course of cognition rehabilitation (and how may it differ between mild, moderate, and severe TBI)?

A

Early weeks:
- stabilizing physical condition
- preventing complications
- addressing medical issues

Follow-up:
mild - regular follow-up appointments
moderate - outpatient therapy, testing, monitoring
severe - rehabilitation facility; continuing outpatient therapy

49
Q

Principles that need to be considered and balanced in the rehabilitation process following TBI?

A

Spontaneous reorganization - first stage in recovery
- renewal and stabilization of functional brain networks; enhanced neuroplasticity
- may lead to compensation rather than recovery without training (learned non-use)

Training-induced recovery - second stage in recovery
- longer-term improvement
- shift neuroplasticity towards healing injured system

50
Q

angiogenesis

A

new blood vessels

51
Q

synaptogenesis

A

new synapses (points of contact between neurons)

52
Q

neurogenesis

A

neurons de novo (anew)

53
Q

Self-taught compensatory strategies -
how are they different from rehabilitative interventions?

A

Reliance on uninjured areas to compensate for loss of injured area function; can prevent healing of injured area by rewiring networks (can shape neuroplasticity), rather than rebuilding loss

54
Q

How does experience interact with the post-stroke CNS environment to promote restorative plasticity?

A

Regenerative and degenerative responses are influenced bidirectionally (contribute to and are influenced by behaviour); behavioural interventions can improve functional outcome