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Severe/Moderate Traumatic Brain Injury Flashcards

1
Q

Medical Definitions for Moderate/Severe Brain Injury:
Acquired Brain Injury

A

Open and Closed Head Injuries (Blunt Trauma)

Shaken Baby Syndrome Abuse

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2
Q

Medical Definitions for Moderate/Severe Brain Injury:
Non-Traumatic Brain Injury (Stroke)

A

Coup-Contra Coup Injury (Acceleration and Deceleration)

Diffuse Axonal Injury (DAI)

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3
Q

Medical Definitions for Moderate/Severe Brain Injury:
Anoxic Brain Injury

A

Complete Occulsion of Oxygen
15 seconds Loss of Consiousness
4 minutes

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4
Q

Medical Definitions for Moderate/Severe Brain Injury:
Hypoxic Brain Injury

A

Not sufficienct Oxygen Saturation (Altitude)
Suffocation

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5
Q

Leading Causes of TBI

A

Falls 40.5%
Motor Vehical Accident 14.3%

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6
Q

Traumatic Brain Injury Incidence

A

Higher incidence in Males at age 14-25

Males and Females increase starting at age 70 due to increased risk of falling

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7
Q

Brain Trauma:
Immediate Primary Damage

A

Scalp Laceration
Skull Fracture
Cerebral Contusions
Cerebral Lacerations
Intracranial Hemorrhage
Diffuse Axonal Injury

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8
Q

Brain Trauma:
Secondary Damage

A

Ischemia
Hypoxia
Cerebral Swelling
Infection

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9
Q

Results of a Brain Injury

A

Brain Injury (trauma)
results in 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 (ICP)

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10
Q

Definition Traumatic Brain Injury

A

An alteration in brain function, or other evidence of brain pathology, caused by an external force

External force is defined by blunt trauma, acceleration and or deceleration or shock wave injury

DON’T HAVE TO LOSE CONSCIOUSNESS TO HAVE A TBI

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11
Q

Primary Damage:
Diffuse Axonal Injury (DAI) = Shearing

A

Most common type of primary lesion
Unequal deceleration, acceleration, or rotational injuries

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12
Q

Diffuse Axonal Injury
Grade 1

A

Mildest form of DAI

Microscopic changes in the white matter of the Cerebral Cortex, Corpus Callosum, Brain Stem, and Cerebellum

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13
Q

Diffuse Axonal Injury
Grade 2

A

Moderate form of DAI

Grossly evident focal lesions isolated to the Corpus Callosum

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14
Q

Diffuse Axonal Injury
Grade 3

A

Severe from of DAI

Addiitonal and severe focal lesions on the brainstem itself

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15
Q

Diffuse Axonal Injury Outcomes

A

50% of people have a good recovery

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16
Q

How to take care of a DAI

A

Treat it like a Muscle Injury

Take a break and get sepcific training for recovery

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17
Q

Diffuse Axonal Injury MRI

A

Injury to the White Matter
Corpus Callosum, Cerebral Cortex, or Cerebellum

Diffuse = Widespread damage because of the shearing forces

Holes in the brain can heal with proper treatment

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18
Q

Primary Damage TBI:
Dural Hematomal

A

Penetrating Objects and Epidural Hematoma
- Skull fracture tearing Meningeal Artery Vessels

Subdural Hematoma
- Tears the Bridging veins in Superior Sagittal Sinus

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19
Q

Acute Subdural Hematoma

A

Midline shift and reduced/irregular shape of the Ventricles

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20
Q

Parimary Damage TBI:
Penetrating Injuries

A

Getting shot in the head man

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21
Q

Secondary Complications of Severe to Moderate TBI:
Cellular

a lot of things

A

Cerebral Edema
Cerebral Hypoxia and Ischemia
Cerebral Metabolic Impairment
Cerebral Vasospasm
Increased Intracerebral Pressure

Mitochondiral Dysfunction
Impairment of Glucose Metabolism
Increased Glutamate
Complement activation inflammation

ROS generation
Excitotoxicity
BBB Damage
Cell Death

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22
Q

Secondary Damage of modTBI:
Glutamate

A

Glutamate: Excitoxicity
Leads to CA++ entry into cells
Cerebral Edema
Cell Death

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23
Q

Secondary Complications of modTBI:
Cellular Excitotoxicity

A

Leads to Inflammation and Reactive Oxygen Species

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24
Q

Secondary Complications of modTBI:
Blood Brain Barrier

A

Neutrophils and activated Microglia crossing through the Blood Brain Barrier

Microglia cells are the immune cells of the CNS and play important roles in brain infections and inflammation.

Two types of Microglia M1 and M2

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25
Neuroprotective and Neurotoxic Microglia
Neurotoxic Microglia Can increase after 10-12 days Continue to have symptoms, but there is a larger difference between the Pre and Post of the 10-12 day mark Neuroprotective Microglia Peak at 1 day post TBI and decrease over the next 7 days
26
Microglial Activity in a TBI
Even after 30 days, there is a possiblity of increasing damage, from Microglial Activity Severity of the damage depends on the secondary injury by the fluctuating Microglia Especially the M1 (Neurotoxic) microglia
27
Similarities with mTBI and Repetitive injuries and Severe TBI
Mild Repetitive TBI - Variable chronic cognitive and/or neuropsychiatric impairment, assocaited with PTSD - Dementia Pugilistica, chronic traumatic encephalopathy, pugilistic parkinsonism Severe TBI - Alzheimer Disease - Total or partial functional recovery, often with variable chornic cognitive and/or neuropsychiatric impairment
28
Recovery after a Traumatic Brain Injury
Recovery after TBI takes place in the 2 years after the Injury In some patients, further improvement is seen even as late as 5-10 years after injury
29
Brain Areas involved in TBI: Midbrain Structures
1. Prefrontal Cortex (Decreased) - Working Memory - Self-Control - Decision Making 2. Amygdala (Increased) - Emotional regulation - Fear response 3. Hippocampus (Decreased) - Learning Memory
30
Motor Areas Affected in TBI
Brainstem, Mid Brain Cerebellum, Cortex, Basal Ganglia
31
Neuro-Cognitive Effects in TBI
Memory (STM & LTM) Judgement (Safety) Language (Aphasia) Sleep-Wake Cycle/Arousal (Mid-Brain)
32
Behavioral Effects of TBI
Impulsive, Irrational Behaviors out of context Personality Changes
33
Outcomes of Moderate to Severe TBI: Motor Outcomes
1. Hemiparesis - Synergistic versus primary weakness 2. Ataxia - Cerebellar 3. Signs of Hypertonia - Clonus, Spasticity, Rigidity - Contractures 4. Syndergistic Movement 5. Tremors
34
Outcomes of Moderate to Severe TBI: Arousal/Attention
1. Attentional 2. Arousal 3. Coma Status
35
Outcomes of Moderate to Severe TBI: Autonomic Nervous System
1. Sleep Wake Cycle
36
Reticular Activating System: 3 Systems of Control
1. Waking - Increasing Thalamic input (Sensory) - Arousal - Attention and activation of appropriate responses 2. Sleeping - Reduction in Sensory Information - Atonia (not activating movement) 3. Fight or Flight - Autonomic Nervous System - Hypothalamus - Circadian Rhythm
37
Reticular Formation
The reticular formation functions as an integration, relay, and coordination center Due to the expansive network of tracts and the interconnected structure
38
Other Functions of the Reticular Formation
Circadiain Rhythm Sleep-Wake Cycles Coordination of Somatic Movement CV and Respiratory Control Pain Modulation Habituation
39
Reticular Formation: Associations
Associated with the Cranial Nerve Motor Nuclei of the Trigeminal, Facial, Glossopharyngeal, Vagus, and Hypoglossal nerves to coordinate the complex task of Respiration
40
Reticular Formation: Brainstem
Brainstem is a complex area of neurons and nuclei that are necessary for survival Forms a network of brain systems that govern many essential functions of the CNS and PNS Ascending brainstem sensory systems to the reticular foramtion influence the entire cortex
41
Sleep Dysfunction Melatonin in TBI
Sleep Dysfunction Melatonin is reduced in TBI
42
Pathophysiology of Post-TBI Sleep Dysfunction
1. Primary Injury - Sheer Force - Stretching 2. Secondary Injury - Oxidative Stress - Neuroinflammation - Excitotoxicity - Apoptosis - Neurodegeneration
43
What lobe is vulnerable to TBI?
TBI vulnerability is in the Frontal Temporal Lobe
44
How is nighttime Melatonin affected by TBI?
REDUCED (41% of TBIs)
45
What assists with sleep in Post-TBI Sleep Dysfunction?
The Hypothalamus Suprchiasmistic Nucleus (SCN) produces hormones that regulate rhythm
46
Disruption of Melatonin in a TBI
Long pathways are susceptible in TBI Disrupts these long pathways and it is thought to disrupt to melatonin
47
Memory Disruptions in TBI
Short Term in Moderate and Mild TBI In severe TBI, LTM is disrupted. Connections involved hippocampus and cortex (Prefrontal)
48
What does Memory Involve?
Memory not only involves persons/events - Identification of Objects - Use of Objects (Apraxia) - Finding their way back to their room or rehab (spatial cognition) Relearning of Mobility, Transfers, Assistive Devices
49
Memory Loss in TBI Loss of Synaptic Signaling
The Hippocampus retrieves, stores, and recalls memory and interacts with the Pre-frontal cortex Both the Hippocampus and Cortex work together for Spatial Info (Naviation) and Non-Spatial (Identification)
50
Memories in Moderate to Severe TBI
Memories become harder to retrieve or store Rehabilitation works with Physical Activity to assist in Memory Formation
51
Parts of the Brain involved in Memory: TBI
1. Prefrontal Cortex - Working Memory 2. Amygdala - Emotional Memory 3. Hippocampus - Episodic Memory 4. Cerebellum - Procedural Memory
52
Exercise and BDNF
BDNF helps increase Long Term Potentiation, Synaptic Plasticity, and Neurogenesis
53
Injury and Repairs: BDNF and Orexin-A Primary Injury
Shearing and Tesnile Effects -> Traumatic Axonal Injury and Neuronal Disconnection
54
Injury and Repairs: BDNF and Orexin-A Secondary Injury
Neuronal and Vascular Damage -> Proteolytic pathways, Excitotoxicity, Oxygen-free radicals, Apoptosis, Inflammatory processes, and ischemia
55
Injury and Repairs: BDNF and Orexin-A Repair
Increases in BDNF and Neurotrophic Factors -> Reconnection through fiber sprouting and synaptogenesis
56
Exercise and the Reduction of Inflammatory Cytokines
Exercise leads to: Decreased Proinflammatory Cytokines Increased Antinflammatory Cytokines Decreased Neurotoxic activation of Microglia Increased Neuroprotective activation of Microglia
57
TBI Pathology: Primary Injury
Focal brain ontusion Vascular and Blood-Brain Barrier Rupture Hemorrhage Neuronal and Axonal Injury Release of Cytokines, Chemokines, and damage associated molecular patterns
58
TBI Pathology: Secondary Injury
Excitotoxicity Oxidative Stress Inflammation Programmed Cell Death Demyelination Autoimmunity Neurodegeneration
59
TBI Pathology: Neurological Deficits
Loss of Neurological Function Cognitive Decline Psychological Alterations Chronic Disability
60
TBI Combination of Primary & Secondary Injury
Secondary injury can continue for years Microglial and Astrocyte activation contribute to Pro-inflammatory elements and Neuronal Death
61
What kind of Issues are seen in a Moderate to Severe TBI
Physical, Cognitive, Neurocognitive, and Behavioral Issues
62
2 Stages of Moderate to Severe TBI
Initial Trauma Hematoma, Hemorrhage, Diffuse Axonal Injury Cellular Response Can last for weeks, months, years
63
Cranial Pressure after Severe TBI
Increased Cranial Pressure can lead to Edema, Hemorrhage or Hematoma This can lead to brain herniation and requires monitoring
64
What is Increased Cranial Pressure after Severe TBI correlated with?
ICP is correlated with lower outcomes and higher mortality Linked to Acute Hydrocephalus
65
Increased Cranial Pressure after Severe TBI: Acute Hydrocephalus
Blood begins to accumlate in the Ventricles and requires External Ventricular Drain
66
Increased Cranial Pressure after Severe TBI: Normal Pressure Ranges
Normal Pressure: 7-15 mm Hg
67
Increased Cranial Pressure after Severe TBI: When to be concerned
LOSS OF CONSCIOUSNESS Pupillary Changes HEADACHE
68
"GET-UP Trial" - Post TBI: The Focus
Focus on Early Mobilization Assess whether a patient is allowed to mobilize early after a burr hole craniotomy for cSDH would lead to better outcomes
69
"GET-UP Trial" - Post TBI: Significance
Provided evidence that early mobilization after a craniotomy can be a safe and beneficial practice
70
Hydrocephalus with TBI
Ventricular Catheter Intracerebral Monitor pressure from Hydrocephalus Brain Bolt Monitor Brain Oxygenation
71
TBI - Epidueral Hematoma
TBI often leads to Epidural Hematomal skull flap with Burr Hole or Hydrocephalus - External Ventricular Drain
72
Medical Considerations for Epidural Hematoma
Ventilation Constant ICP monitoring Nasogastric Tube Compression Leggings Foley Catheter Central Line IV Catheter for Meds & Drawing Blood Pulse Oximeter and BP/HR monitors
73
PT with EVD
While in bed, the elevation of bed and patient position must not change Before mobilizing, EVD must be clamped with Nurse Monitor CPP, ICP, HR, BP, and O2 saturation
74
Importance of Cerebral Perfusion Pressure
Amont of pressure for blood perfusion for overall brain function >60 Intracranial Pressure <20
75
Medical Defintion of Consciousness: Loss of Consciousness
Duration: Several minutes to hours to days
76
Medical Defintion of Consciousness: Coma
Complete paralysis of cerebral function: state of unresponsiveness Eyes closed, no resopnse to painful, auditory or tactile stimulation
77
Medical Defintion of Consciousness: Persistent Vegetative State
Reduced responsiveness with no evidence cerebral cortical function Diffuse hypoxia, axonal white matter impact
78
Symptoms of TBI: Physical
LOC unable to arouse Convulsions or seizures Dilation of Pupils Inability to awaken Weakness, Ataxia, Tremors
79
Symptoms of TBI: Cognition
Attention Memory Orientation Judgment/Safety Awareness
80
Symptoms of TBI: Behavioral
Profound Confusion Agitation Combativeness Personality Change Amnesia (Loss of Memory)
81
TBI Assessments: ICU
Glasgow or LOC - Neuro - CN - Movement
82
TBI Assessments: Acute
Glasgow or LOC - Physiological - Neuro - Movement - Function - Amnesia - Rancho Levels
83
TBI Assessments: Rehab
Rancho Levels - Neuro - Movement - Function: FGA - Memory - Safety/Judgement - Spatial Oreintation - Disability Rating Scale
84
Attention and Orientation - TBI: Arousability
Tactile Sound Pain
85
Attention and Orientation - TBI: Attention
Visual Attention Auditory Attention Follows Commands
86
Attention and Orientation - TBI: Orientation
Self, Place, and time Orientation in Room
87
Severity of TBI: Glasgow Coma Scale GOLD STANDARD
Mild: 13-15 Moderate: 9-12 Severe: <9
88
Severity of TBI: Post Traumatic Amnesia
Mild: <1 day Moderate: >1 to <7 days Severe: > 7 days
89
Severity of TBI: Loss of Consciousness
Mild: 0-30 min Moderate: >30 min to <24 hours Severe >24 hours
90
Glasgow Coma Scale Areas of Examination
Eye Opening Verbal Response Motor Response
91
Severe Brain Injury What GCS Score?
GCS below 8
92
Severe Brain Injury
Prolonged unconsious state or coma lasts days, weeks, months
93
Subgroups of Severe Brian Injury
Coma Vegetative State Persistent Vegetative State Minimal Responsive State Locked-In Syndrome
94
Rancho Cognitive Functioning Levels 1-5
Level 1 No reponse, deep sleep Level 2 Generalized reponse, inconsistent reaction not direct Level 3 Localized response, inconsisent reaction direct Level 4 Confused/Agitated, confused Level 5 Confused-Inappropriate, innacurate response
95
Rancho Cognitive Functioning Levels 6-10
Level 6: Confused-Appropriate, confused Level 7: Automatic-Approriate, minimal confusion Level 8: Purposeful-Appropriate, functioning memory Level 9: Purposeful-Appropriate, stand-by assistance Level 10: Purposeful-Appropriate, requries more time
96
Motoric Issues in TBI
Motor Planning and Execution Affected (Pre-Frontal Lobe) Weakness and Possible contractures Spasticity/Hypertonia Coordination (Cerebellar and Basal Ganglia) Balance Disorders Syndergistic Patterns Postural Malalignment
97
Cognitive Assessment in Mod to Severe TBI
Arousability: Coming in room, sound Alertness: Eyes open, orient to sound, Visual Orientation: Self, Place, Time (Cues?) Verbal Direction: 1 step, 2 step, Complex Memory: Recent / Past events, Spatial, ID, Procedural Judgement: Functional judgement - Transfers, Gait
98
Agitated Behavior Scale (ABS)
Common items from the ABS that occur in the Acute Phase in persons with Moderate to Severe TBI
99
Agitated Behavior Scale (ABS) Early Issues
Violent or Explosive Anger Resistant to care Pulling at tubes Sudden changes in mood Impulsivity and lack of judgement
100
Considerations for Functional Assessment
Bed Mobility: Memory, safety, impulsiveness, procedure Transfers: Motor loss, visual capability, impulsivity Upright Stability: Postural alignment, dizziness, orientation, fatigue Gait: Assistive device, fatigue, ocular disturabances, environmental stimulation
101
Environmental Consideration for TBI
Light Source Background Noise People in Room Extraneous Movement

529 Neuro (12 decks)

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