TBI Rehab - Bernert Flashcards
1
Q
Incidence of brain injury annually
A
1.7 million people
2
Q
TBI is a contributing factor to _____% of all 1.injury related deaths in the US.
2. ______ patients have lifelong disability
A
- 30.5%
2. >3.1 million
3
Q
Total indirect and medical cost associated with TBI in 2010?
A
76.5 billion
4
Q
Top 5 causes of BI (in order with percentage)
A
- Falls 35.2%
- MVCs 17.3%
- Assault 10%
- Struck by/against 16.5%
- other
5
Q
_____ is the leading cause of TBI related death. Highest rates for which age group?
A
MVC; 20-24 yoa
6
Q
TBI Model systems:
- ___% male, ____% female
- Average age at injury?
- Describe the bimodal distribution
A
- 74% male, 26% female
- 40 yoa
- Ages 0-4 (falls) 15-19 (MVC) >65yoa (falls)
Increasing age increases probability of poor outcome (especially after 60)
Adults >74 yoa have highest rates of TBI related hospitalization and death
7
Q
with regard to survey sent to KYians in 2004:
1. what % had memory problems after injury?
2. depression
3. anxiety
need for professional services following injury?
A
- 24.2%
- 20.5%
- 23.3%
- 6%
8
Q
Seat belts reduce risk of serious injury by ___%, death by ____%
Helmets reduce risk of death in crash by ____% and head injury by ____%
A
50; 45%
42; 69%
9
Q
Define primary brain injury
A
disruption of brain tissue, directly caused by the event.
10
Q
5 types of primary brain injury
A
shear rotational percussion acceleration/deceleration penetrating
11
Q
describe pathophysiology behind primary injury
A
Impact depolarization (potassium release) leads to cortical disruption and vascular injury. Causes hemorrhage and axonal injury
12
Q
DAI:
- Dynamic stretch of ____
- Mechanical failure of _____
- Triggers for: ______
- INterrupts ____ transport
- ultimately leads to axonal ______. _____ formation
A
- axons
- microtubules
- progressive disassembly of the microtubules
- axonal transport
- axonal swelling and degeration (bulb formation)
13
Q
____ is the most common cause of immediate LOC and severe disability after TBI
A
Aiffuse axonal injury
14
Q
Define the 3 grades of DAI
A
- Scattered axonal retraction balls in parasagittal white matter of cerebral hemisphere. (brief LOC)
- Above plus focal lesions in the corpus callosum (coma of duration, recover process unclear)
- Grade 2 plus focal lesions in the dorsolateral rostral brain stem (immediate coma with posturing, incomplete recovery)
15
Q
Describe the 5 components associated with axonal swelling and degeneration (reversible cytoskeletal damage)
A
- secondary axotomy
- Ca Load/excess after stretch
- membrane depolarization
- transmitter release
- “retraction balls”
16
Q
8 types of secondary brain injury
A
Ischemia (Hypoxemia, Hypotension, IC Hypertension- Hypoperfusion) Cerebral Edema Herniation Hydrocephalus Infection Fever Hyperglycemia Seizures
17
Q
describe secondary brain injury on a molecular level
A
Excitotoxicity ( Glutamate release – injured membranes, depolarized neurons)
Neuronal Cell Necrosis & Apoptosis
Deaffferentation – Cell Dysfunction – Cell Death
18
Q
7 influences on head injury outcomes
A
Age
Drugs
Preexisting Disease
Psychosocial status- Family Functioning & Support
Genetic Makeup: Apolipoproteine E4 Allele
- Associated with poorer outcome and larger brain lesions
Education/ IQ-
Coping Style- Non productive coping (worry, , wishful thinking, self blame, substance use associated with postinjury anxiety and depression, lower psychosocial functioning
19
Q
In acute care brain injury ____ greatly
increases mortality and morbidity
A
Early Hypoxemia
20
Q
define hypoxemia.
What improves outcomes in TBI patients with hypoxemia
A
Apnea or Cyanosis in the field or Oxygen saturation (SaO2) < 90%/ Pa02< 60mm Hg
Intubation of unconscious and unresponsive TBI
patient improves outcome
21
Q
Hypotension in TBI patients: (2)
Define Hypotension
A
Doubles mortality, increased morbidity
one single episode of SBP <90mmHg in adults
22
Q
GCS in TBI patients: Perform after \_\_\_\_ and before \_\_\_\_ Mild TBI: Mod TBI: Severe TBI:
Should do ____ exams.
Change in GCS > ___ is significant prognosticator
A
After resuscitation, before administering paralytics. 13-15: mild 9-12 moderate 3-8 severe Serial exams >2 change is significant
23
Q
Hyperventilation prior to ICP monitoring
Reserved for
A
transtentorial herniation
HPV to pC02 = 30-35 mmHg
20 breaths per minute for adults
24
Q
ICP management in acute phase BI
ICP:
CPP:
A
Medical Management:
Keep ICP < 20
Keep CPP > 60
25
```
Nutrition in TBI
Begin within:
By day 7 ______% of Basal energy expediture in non-paralyzed patient.
____ % in peds
_____% in multitrauma
____% in paralyzed pateint
```
```
72 hours
140% non-paralyzed
160% peds
250% multitrauma (15-20% of calories = protein)
100%
```
26
Define post TBI seizures (timewise)
Immediate seizure – first 24 h
Early Seizure – first 7 days
Late seizure – after 7 days
Routine Seizure Prophylaxis
1 week
Prevention of Early Seizures
Phenytoin versus Depakote
27
6 prognostic indicators of TBI
```
Initial Glasgow Coma Scale
Age
Presence of prior brain injury
Injury severity
Duration of Coma
Duration of Post-traumatic Amnesia
```
28
```
Initial GCS best if within 24h of resuscitation:
Prognostic precentages:
GCS 3-4:
5-7:
8-10:
11 and greater:
```
```
GCS 3-4 – death or Vegetative State 87%
GCS 5-7 – Death or Vegetative State 53%
Moderate recovery 34%
GCS 8-10 – moderate or good recovery 68%
GCS – 11 moderate or good recovery 87%
```
29
With regard to age and TBI
_____ do better.
if > ______: worse outcomes
% good outcome vs mortality in >60 years and <40 years.
Children/ young Adults
Age > 40 worse outcome
> 60 years good outcome 2 %/ mortality 79%
< 40 years good outcome 38%/ mortality 33%
Controlled for severity
30
If coma lasts > ______: rarely good recovery
Coma > 2 weeks – rarely good recovery
31
Definition of Post traumatic amnesia
Disorientation to time, place and person, confusion, diminished memory and reduced capabilities for attending and responding to environmental cues
Almost always recall name
Episodic Memory not stored
Basic Orientation Information not stored
Assessment with Goat
32
What is the post-TBI PTA O-log
10 questions
0-30 points possible
Each item is scored from 0 to 3
3=spontaneous and correct response
2=spontaneous response is lacking, but correct response with a logical cue (e.g. to identify place, cue “This is a place where doctors and nurses work”)
1=spontaneous and cued responses are incorrect, but correct response when provided if given choices to recognize (e.g. to identify the month, provide three months from which to choose)
0=spontaneous, logical cue and recognition cue approaches don’t cause a correct response
Domain specific scores can be generated – place (3 items), time (5 items), situation (2 items)
Scoresheet provides a graph to plot serial assessments over time
33
PTA emergence tested by
| Considered "emerged" when:
GOAT - long list of orientation questions
Clearance: GOAT Score> 75 on (2) 3 occasions
on consecutive days
34
TBI scale according to PTA length of time:
___ mild
___ Moderate
___ Severe
___ Very severe and recovery will take months
___ Very severe and recovery will take years
___ Very severe and recovery could be life long disability.
Up to 1 hour - The injury is very mild in severity and full recovery is expected. The patient may experience a few minor post-concussive symptoms (e.g. headaches, dizziness).
1 – 24 hours - The injury is moderate in severity and full recovery is expected. The patient may experience some minor post-concussive symptoms (e.g. headaches, dizziness).
1 – 7 days - The injury is severe, and recovery may take weeks to months. The patient may be able to return to work, but may be less capable than before the injury.
1 – 2 weeks - The injury is very severe, and recovery is likely to take many months. The patient is likely to experience long-lasting cognitive effects such as decreased verbal and non-verbal intelligence as well as decreased performance on visual tests. Patients should, however, still be able to return to work.
2 – 12 weeks - The injury is very severe, and recovery is likely to take a year or more. The patient is likely to exhibit permanent deficits in memory and cognitive function, and the patient is unlikely to to able to return to work.
12+ weeks - injury is very severe and accompanied by significant disabilities that will require long-term rehabilitation and management. The patient is unlikely to be able to return to work.
35
Describe the rancho levels
Level I: No response to pain, touch, sound or sight. Level II: Generalized reflex response to pain. Level III: Localized response. Blinks to strong light, turns toward/away from sound, responds to physical discomfort, inconsistent response to commands. Level IV: Confused/Agitated. Alert, very active, aggressive or bizarre behaviors, performs motor activities but behavior is non-purposeful, extremely short attention span. Level V: Confused/Non-agitated. Gross attention to environment, highly distractible, requires continual redirection, difficulty learning new tasks, agitated by too much stimulation. May engage in social conversation but with inappropriate verbalizations. Level VI: Confused/Appropriate. Inconsistent orientation to time and place, retention span/recent memory impaired, begins to recall past, consistently follows simple directions, goal-directed behavior with assistance. Level VII: Automatic/Appropriate. Performs daily routine in highly familiar environment in a non-confused but automatic robot-like manner. Skills noticeably deteriorate in unfamiliar environment. Lacks realistic planning for own future. Level VIII: Purposeful/Appropriate. Level IX: Purposeful, Appropriate: Stand-By Assistance on Request. Level X: Purposeful, Appropriate: Modified Independent.
36
3 Criteria for DOC
Coma
Vegetative State - eye opening
Minimally Conscious State - voluntary behavior
Once form of communcation has emerged -- emerged
37
Define coma (6)
Loss of spontaneous or stimulus-induced arousal
No sleep-wake cycle
No purposeful motor activity
No response to command
No receptive or expressive language ability
No awareness
38
Define vegetative state: (8)
```
1 No purposeful motor activity
2No response to command
3No receptive or expressive language ability
4No awareness
5Sleep-wake cycle
6Spontaneous or stimulus-induced arousal
7Postures or withdraws to noxious stimulus
8Occasional non-purposeful movement
```
39
Define Minimally conscious state (7)
1 Minimal but definite awareness
2 Simple command-following
3 Intelligible Verbalization
4 Recognizable Yes/ No responses -Unreliable-
5 Purposeful Behavior
6 Sleep-wake cycle
7 Spontaneous or stimulus-induced arousal, movement or emotional responses
40
emergence from minimally conscious state:
Recovery of interactive Communication
| Reliable and consistent Communication or Object use
41
4 routes of brain plasticity:
Reversal of Diaschisis/ Activation of cellular repair
CNS Reorganization
Dendritic and axonal sprouting- functional plasticity
Vicariation- anatomic plasticity
42
5 impairments of brain injury
Medical Impairment
Physical Impairment
Cognitive Impairment
Emotional Impairment
Behavioral Impairment
43
6 neurologic complications of brain injury in rehab
Hydrocephalus
Hygroma (subdural CSF)
Infection (Meningitis, Abscess, Empyema)
Posttraumatic Seizures (generalized, partial)
Abnormal muscle activity
Spasticity-excessive resistance to passive stretch
Movement Disorders
44
4 types of movement disorders seen in brain injury
Dystonia –tonic muscle activity maintaining fixed posture
Tremor
Myoclonus
Parkinsonism
45
Posttraumatic Seizures (generalized, partial)
1. _____ % of hospitalized patients with non-penetrating TBI (late)
2. ____ % of patients with severe non-penetrating TBI (17 % Rehab)
3 ____ %of patients with penetrating TBI
1. 4-7
2. 11
3. 35-50
46
Risk factors for post-traumatic seizures: 11
| Highest risk within _____
```
1 Glasgow Coma Scale score of <10
2 Cortical Contusions (Bil Parietal:66%)
3 Depressed Skull Fractures (3-70%)
4 Epidural Hematoma
5 Intracerebral Hematoma (25-30%)
6 Dural Penetration (33-66%)
7 Prolonged length of coma
8 Prolonged Length of PTA
9Early Posttraumatic Seizure: 25 %
10 Alcohol Abuse
11 Dural Tearing
```
2 years post TBI
47
7 CT findings that would make you consider seizure ppx
Biparietal contusions (66%)
o Dural penetration with bone and metal fragments (63.5%)
o Multiple intracranial operations (36.5%)
o Multiple subcortical contusions (33.4%)
o Subdural hematoma with evacuation (27.8%)
o Midline shift greater than 5mm (25.8%)
o Multiple or bilateral cortical contusions (25%)
48
4 MSK comlications of TBI
Contractures
Shortening of muscle length
(fascia, nerves, blood vessels, skin)
Heterotopic Ossifications
Ankylosis
Muscle weakness and atrophy
49
Risk of HO in TBI:
| Which body locations? (in order)
20%:
Increasing with severity,duration of immobility, duration of coma
Increasing with presence of spasticity, fractures
Hips, Elbows, Shoulders, Knees
50
4 cardiovascular complications of TBI
```
Dysautonomia (HTN, Tachycardia, Tachypnea,Fever, Diaphoresis, pupillary dilation, Dystonia or extensor posturing)
Cardiac arrhythmia, Myocardial Damage
Postural Hypotension
Hypovolemia
Disordered sympathetic response
```
Thrombogenesis- Thromboembolism (11-50%)
51
Dysautonomia associated with: (5)
```
Higher risk of critical illness neuropathy
Higher risk of Heterotopic Ossicfication
Prolonged dysphagia
Prolonged PTA
Longer hospital admissions, ICU stays
```
52
8 types of respiratory complications in TBI
Trauma (PTX, HTX, Flail chest)- respiratory failure 43%
Respiratory insufficiency – Tracheostomy 39%
Decreased Inspiratory Drive- Hypoventilation
Pooling of Secretions
Weakness
Atelectasis
Mucus Plugs
Pneumonia (incl. Aspiration Pneumonia) up to 60%
53
11 GI complications in TBI
“Feeding Difficulty” s/p PEG
Gastroesophageal Reflux
Delayed Gastric emptying
Aspiration
Gastritis/Erosions/Ulcers
Constipation
Abnormal Absorption
Diarrhea (Sorbitol, Lactose intolerance, TF,Infection)
Hypermetabolism- Depletion of nutritional stores
Hyperglycemia
Liver/ Pancreas Dysfunction
54
4 GU complications in TBI
```
Urinary Incontinence (62 % in first 6 weeks)
Primarily uninhibited overactive bladder
```
Timed Voiding Program
Urinary Retention (9.5%)
Urinary Tract Infection (38%)
55
5 endocrine complications in TBI
```
Hyperglycemia
Diabetes Insipidus
SIADH
Cerebral Salt Wasting
Pituitary Dysfunction
```
56
____ after TBI is usually preserved.
| What 8 factors are impaired instead
Language:
```
Pragmatics/ Social Communication is commonly impaired
Comprehension of indirect language
Use of indirect language
Situational appropriateness
Organization and structure
Information processing
Self Perception
Unable to process facial affect
```
57
Dorsolateral Prefrontal Cortex (5) functions
| Injury would present as: (5)
```
1 Problem solving,
2 Working memory,
3 planning,
4 strategy,
5 initiation
```
Injury: Apathy, personality changes, abulia, impaired executive function, poor working memory for verbal (left) or spatial information (right)
58
Ventromedial Prefrontal Cortex/ Orbitofrontal Cortex
functions: (5)
If impaired: (3)
```
Emotion Systems (Insula, Amygdala)- affect, impulses, motivation, social drive
Injury: Poor judgment, inappropriate weighing of values, aggression and more
```
59
Most common excitatory neurotransmitter:
Too much = ____
Involved with:
Glutamate
Toxic
in formation and storage of memory/ synaptic plasticity
60
Most common inhibitory neurotransmitter
| if increased?
gaba - 25% of cortical neurons
Treats Insomnia, Pain, Anxiety (agitation, other)
Glycin- less common- inhibitory
61
5 neurotransmitter systems that can be targeted during TBI therapy
```
Dopamine
Norepinephrine
Serotonin
Acetylcholine
Histamine
```
62
4 Dopamine pathways and what is controlled by each?
Mesocortical Pathway- ventral tegmentum to Prefrontal cortex
- attention, working memory, Initiation, executive function
Mesolimbic Pathway- ventral tegmentum to Nucleus accumbens, amygdala, hippocampus
Memory, Motivation, Pleasure, Reward, Emotional Response
Nigrostriatal Pathway- Projection to caudate and Putamen
Motor Control, Movement
Tuberoinfundibular Pathway- hypothalamus (arcuate- portal veins of pituitary
Maternal behavior)
63
Norepi pathway:
effect:
Involved in:
Originating in
Locus Ceruleus
Lateral tegmental area (pons/medulla)
Basal Forebrain (Nucleus basalis a.o.)
Projections to entire Forebrain & Cerebral Cortex
Projections to Thalamus, Cerebellum, Pons, Medulla
Effect on Thalamus: Excitatory
Involved in: Arousal, Alertness & Memory, Mood, Elevation
Sleep-Wake Cycle,
Sympathetic Function e.g. BP Control
64
Methylphenidate mechanism
- Increase presynaptic release of dopamine and norepinephrine
- Weak reuptake inhibitor; (cognitive disorders, fatigue,depression)
65
dextromethorphan mechanism
Increase presynaptic release of Norepinephrine and Dopamine
| -Weak reuptake inhibitor
66
amantadine mechanism
dopamine: enhanced release & reuptake inhibition
- NMDA antagonist
- May increase Circulation of Norepinephrine
67
bromocriptine mechanism
-dopamine agonist, glutamate release inhibitor
L-Dopa
- Dopamine Precursor
68
antipsychotics mechansim:
Blocks: ____
Conventional med:
Causes:
D2 receptors
Haldol
block experience of pleasure, lack of motivation, reduced interest, reduced joy (mesolimbic); worsening cognition (mesocortical), tardive dyskinesia (nigrostriatal), sexual dysfunction, weight gain, hyperprolactinemia)
69
4 most used atypical antipsychotics:
mechanism:
Caution in:
Use ___ first
```
Risperdone, Quetiapine, Olanzapine, Ziprasidone
Transiently occupy dopamine receptor D2
Caution in acute/ subacute phase
LAST LINE (trial of AEDs first)
```
70
4 Pharmacological Interventions for TBI
for
Attention, Information Processing, working memory
Ritalin
Adderall
Amantadine
Donepezil
71
cholinergic pathways for
attention:
Memory and learning
Nucleus Meynert (Nucleus Basalis)
Projects to entire Cortex
Attention
Medial Septal Nuclei/ Nucleus of the diagonal Band
Project to hippocampal formation
Memory & Learning
Donepezil
72
serotonin pathway:
Produced in Raphe Nuclei in Midbrain, Pons & Medulla
| Send Serotonin to entire forebrain incl.cortex, thalamus, and basal ganglia as well as cerebellum, medulla & SC
73
serotonin effects:
Mood/ Elevation
| Pain Modulation
74
cholinergic agents for Memory, Attention
Donepezil
Rivastigmine
Physostigmine
75
Top 4 for: Depression/ Mood dysregulation
| Role in agitation, anxiety, sleep, pain
Citalopram
Sertraline
Desipramine (tricyclic)
Fluoxetine
76
"multitasking" drug for Sleep, nausea, depression, anxiolytic, appetite
Mirtazapine (Tetracyclic-central alpha-/ Serotonin antagonist- increased release of norepinephrine and serotonin, H1 antagonist)
77
histamine pathway
| effects: (6)
Neurons located in posterior hypothalamus
in tuberomamillary nucleus & scattered in midbrain
Projects to all regions of the brain
Nociception, Satiation, Control of pituitary hormone release, cognitive functions, arousal, attention
78
explain H1, H2, H3 histamine receptors and function
H1 block interferes with wake-promoting actions- sedation, drowsiness, sleep
H2 receptors may not be directly linked to wakefulness
H3 receptors presynaptic autoreceptor in the brain- turns off Histamin release
79
3 drugs for sleep in TBI
Trazodone (SSRI)
Melatonin
Ambien (preferential omega 1 GABA A receptor agonist)
Some concern with neuroplasticity
80
Neuromodulation:
| Agitation occurs in up to ___% of moderate to severe TBI
33-50
70% agitation for average of 32 days
81
```
Definitions:
Agitation:
Aggression-
Akathisia-
Disinhibition-
Emotional Lability
```
1. Excess of behavior without something else going on to cause it. Agitated Behavior score>22
2. damaging to the individual threatening or intimidating actions or gestures
3. motor restlessness
4. verbal or physical; hurtful, inappropriate, poor judgement
5. speaks for itself
82
4 setbacks of presence of agitation:
Limits Functional gains
Poorer cognitive function
Disruptive and dangerous to staff and family
Increased burden of care, LOS , 1:1
83
2 agitation scales
Agitated Behavior scale
| Overt Agitation Severity Scale
84
14 types of behaviors with agitation scale
1. Short attention span, easy distractibility, inability to concentrate.
2. Impulsive, impatient, low tolerance for pain or frustration.
3. Uncooperative, resistant to care, demanding.
4. Violent and or threatening violence toward people or property.
5. Explosive and/or unpredictable anger.
6. Rocking, rubbing, moaning or other self-stimulating behavior.
7. Pulling at tubes, restraints, etc.
8. Wandering from treatment areas.
9. Restlessness, pacing, excessive movement.
10. Repetitive behaviors, motor and/or verbal.
11. Rapid, loud or excessive talking.
12. Sudden changes of mood.
13. Easily initiated or excessive crying and/or laughter.
14. Self-abusiveness, physical and/or verbal.
85
describe scoring system of agitation scale:
Agitated Behavior scale
14 different behaviors rated of 1-4
Score >21- agitated (14-56)
For clinical purposes, consider any scores 21 or below : within normal limits
from 22 through 28 : mild occurrence;
29 through 35 : moderate;
more than 35 : severe.
86
12 DDx of agitation
```
Infection
Metabolic/ Endocrine
Seizure
Renal or hepatic insufficiency
Medication withdrawal/ side effect
Pain
Environmental
Other: Stones, Appendicitis, Pressure sore, dehydration, constipation
```
87
6 things to order in setting of agitation without ruling out other ddx
CBC, CMP, UA, EEG, CT head, Medication levels
88
7 ways to treat agitation non-pharm
```
Reduce environmental stimuli
Minimize Irritants
Evaluate Medications
Scheduled Toilet program
Regulate Sleep
Nutrition
Monitor for pain
```
Avoid Antipsychotics if possible
Avoid Benzodiazepines if possible
89
1. agitation is a disruption of what 3 transmitters
2. Exposure to confrontational situation-: (2)
3 Violent behavior associated with
4 Agitated patients have low levels of
5. _____ often cause delirium
```
1 dopamine, serotonin and acetylcholine
2 increases dopamine and decreased serotonin
3 decreased serotonin
4 serotonin
5 Anticholinergic agents
```
90
Best pharm agent for agitation to start/
BBs
91
3 AEDs good for BI agitation
Carbamazepine- Anger, Agitation
Valproic Acid – less sedation- no difference in neuropsych testing
Lamotrigine (Case Report)
92
four post-TBI agitation antidepressants
```
Antidepressants
Sertraline
Buspirone
Amitriptyline
Trazodone
```
93
last resort for agitation treatment:
| why bad?
Haldol and Risperdal
Both delay motor recovery
Impair acquisition of spatial learning
Impair memory
94
9 side effects of Haldol/olanzipine
```
impaired cognitive performance (not olanzipine)
Dystonia
Motor restlessness
Tardive dyskinesia
Dry Mouth
Blurred vision
Confusion
Constipation
Urinary retention
```
95
4 unwanted SEs of olanzipine
Diabetes
HL
Obesity
Hypersalivation
96
7 medications that impede brain recovery
```
Typical antipsychotics
Benzodiazepines
Strongly anticholinergic medications
Phenytoin
Alpha 2 agonists
High – dose opiates
Alcohol and other substances of abuse
```
97
14 reasons why amantadine is the wonder drug
```
Indirect Dopamine Agonist (reuptake inhibitor, facilitates synthesis, may increase postsynaptic dopamine receptor density
N-methyl-D-Aspartate receptor Antagonist
Potential anti-inflammatory effect
Increases expression of neurotrophic factors
May be neuroprotective
May improve rate of functional recovery
May improve executive function
May improve arousal
May improve attention
Has been used for Aphasia
Has shown to improve aggression
```
