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Clinical Medicine III > Traumatic Brain Injury > Flashcards

Traumatic Brain Injury Flashcards

1
Q

Define traumatic brain injury (TBI)

A
  • brain dysfunction that results from external physical force
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2
Q

Define mild and moderate to severe TBI

A
  • Mild: majority kind also called concussions, symptoms generally self-limiting & temporary, less severe end of TBI but still ca involve complex pathophysiology
  • Moderate to severe: significantly worse outcomes
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3
Q

Set of symptoms of a TBI

A
  • altered mental status, physical function, behavioral/emotional problems (temporary or long lasting depending ons severity)
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4
Q

Complex symptoms of a TBI

A
  • also differences in clinical presentations/outcomes seen in individuals with apparent similar injuries
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5
Q

Categorization of TBI severity chart

A
  • Mild: normal imaging, loss of consciousness for 0-30 min., altered mental state up to 24 hrs, post traumatic amnesia for 0-1 day, Glasgow coma scale score of 13-15
  • Moderate: normal/abnormal imaging, loss of consciousness for >30min. & <24hrs, altered mental state for >24hrs, post traumatic amnesia for 1-7 days, Glasgow coma scale score of 9-12
  • Severe: normal/abnormal imaging, loss of consciousness for >24hrs, altered mental state for >24hrs, pot traumatic amnesia for >7days, Glasgow coma scale score of <9
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6
Q

Incidence of TBI

A
  • TBI occurrence peaks at 3 age ranges:
  • Early childhood (1-2 yrs): related to child abuse
  • Adolescent/early adulthood (15-24 yrs): related to risk-taking behaviors, sports concussion
  • Elderly: related to falls, often worse outcomes specially due to more susceptibility of tearing of bridging vessels over surface of brain & age related decline of CV autoregulation
  • Accounts for 1/3 of all injury related deaths inn US
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7
Q

What type of hemorrhage does an elderly TBI result in

A
  • stroke
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8
Q

Risk factors for mild TBI/concussion

A
  • Occur mostly during sports & recreational activities
  • Highest incidence in football, hockey, rugby, soccer, basketball
  • Bicycling: wearing a helmet reduces risk by 80%
  • Can occur in athletes on & off the field
  • Higher in female athletes than male athletes
  • Young age & level of play are risk factors
  • Pre-injury cognitive deficits, behavioral problems (ADHD) & migraine headaches could add to the risk & can sometimes complicate diagnosis
  • Single concussion can cause mild changes inn mental status like dizziness, brief headaches, feeling disoriented or confused for a short period of time
  • History of concussion
  • History of multiple concussions increase severity of symptoms & prolong recovery
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9
Q

Risk factors for severe TBI

A
  • Motor vehicle accident: ~60% of adults & 92% of children
  • Seatbelt & airbag reduce injury with significant decline in TBI mortality due to improved preventative measures like speed limits, seat belt laws, airbags, helmets as well as improved understanding of secondary injury process
  • Pedestrians injured by automobile: elderly are vulnerable due to slow gait, sensory impairments, frequently get stuck within crosswalks
  • Mortality from TBI in elderly is high with majority of deaths occurring at scene or emergency department
  • Gunshot wounds: associated with suicide or alcohol abuse
  • Military combat
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10
Q

What are the 2 types of TBI

A
  • Open
  • Closed
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11
Q

Describe an open TBI

A
  • penetrating lesions: fx, gunshots
  • meninges are breached
  • can cause damage to brain parenchyma, vascular damage
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12
Q

Describe a closed TBI

A
  • no skull fx or penetrating injury but brain experiences forceful contact on the inner side of hard bony skull
  • can lead to coup-contre-coup type injury
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13
Q

When would a closed TBI occur

A
  • Can occur without head hitting a hard surface: whiplash injuries
  • Diffuse axonal injuries (DAI): shearing/tearing of the brain’s long nerve fibers (axons) when the brain shifts & rotates inside the bony skull
  • Symptoms are worse if there is a rotational component or if brainstem structures are torn
  • Cause subdural/subarachnoid hemorrhage due to rupture of bridging veins draining to the sinuses
  • Contusions are hallmark of sever TBI but can occur without a contusion
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14
Q

Primary versus secondary injury for a TBI

A
  • Primary: result from forces exerted by impact on the brain (tissues are stretched, compressed, torn)
  • Secondary: changes that happen in brain overtime as a result of brain’s reaction to trauma (tissue, cellular, & biochemical levels); many TBI cases are not fatal immediately rather during days & wks after due to deterioration from secondary mechanisms
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15
Q

Initial vascular changes related to a TBI

A
  • Lacerations or contusions at anterior poles, undersurface of temporal lobes, or unsurfaced of frontal lobes (primary injury)
  • Bleeding inside brain can result in decreased BP (hypotension) causing hypoperfusion -> ischemia -> infarction (primary injury)
  • Early hypotension = strong predictor of poor outcomes
  • Decreased blood O2 due to concomitant pulmonary insult
  • Can drastically increase mortality & morbidities
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16
Q

When do initial vascular changes occur

A
  • occurs between injury and transport to emergency department
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17
Q

What happens to the blood flow within 24hrs of a TBI

A
  • Blood flow can become normal & then go above normal level depending on secondary pathophysiology (secondary injury)
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18
Q

Describe a shearing injury from a TBI

A
  • Can cause gliding contusions
  • movement of cortical grey matter in relation to underlying white matter
  • Can rupture the penetrating vessels at the grey-white interface
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19
Q

What can a TBI cause in relation to superficial vessels in the brain

A
  • Can cause damage/rupture to superficial vessels causing hematomas
  • May or may not cause compression of brain tissue (important secondary injury)
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20
Q

What is the most critical secondary injury mechanism following a TBI

A
  • Increased intracranial pressure (ICP)
  • needs to be monitored & controlled
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21
Q

What can cause increased ICP following a TBI

A
  • Mass effects from hematoma putting pressure on brain
  • Cerebral edema from fluid accumulation intracellularly or in extracellular spaces due to additional 2ndy necrotic & inflammatory mechanisms
  • Hydrocephalus: blood accumulating in ventricles & putting pressure from inside
  • Increased CBF due to other metabolic reasons (accompanying seizures or pyrexia)
  • CSF outflow blockage
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22
Q

How does the brain normally maintain constant average CBF

A
  • by maintaining CPP (cerebral perfusion pressure) over a range of mean arterial pressure, MAP (50-150mmHg) using cerebral auto-regulatory mechanisms (that cause automatic vasoconstriction/vasodilation in cerebral arteries
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23
Q

What is the formula for auto-regulated CPP (cerebral perfusion pressure)

A
  • CPP = MAP - ICP
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24
Q

What happens to the CPP auto-regulation following a TBI

A
  • auto-regulation is disrupted
  • with rising ICP brain reacts by trying to maintain constant CPP by raising BP (MAP) & bring more blood in to brain which further increases ICP & thus decreases CPP -> vicious cycle starts with lead to additional ischemia/infarctions (secondary injury)
  • Emergency situation
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25
Q

Describe post traumatic aneurysms

A
  • due to weakening of cerebral arteries over days to years (average 3wks)
  • can develop in internal carotid artery inside the cavernous sinus if fx in basal skull/orbital
  • due to proximity of internal carotid artery to CNs 2, 3, 4, 5, 6 they may also be damaged later on leading to blindness, facial numbness, etc.
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26
Q

Parenchymal changes

A
  • primary triggers 2ndy which cause excitotoxicity & free radical formation
  • Excitotoxicity is common in diffuse brain injury glutamate rises to abnormal levels throughout the brain
  • Free radical damage to cell membrane can cause massive Ca2+ influx
  • Necrotic & apoptotic mechanisms can lead to cell death
  • Cerebral edema can also cause cell damage/death due to vasogenic, cytotoxic, or osmotic edema
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27
Q

Describe vasogenic, cytotoxic, and osmotic edema

A
  • Vasogenic: due to fluid leaking from disrupted BBB along endothelial linings
  • Cytotoxic: due to disruption of NA/K ion pump leading to water entry & retention
  • Osmotic: due to osmolar property changes b/w extra & intra cellular fluids causing water entry
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28
Q

Axonal damage due to TBI

A
  • From shearing due to coup-contre-coup forces along with rotational component (MVA, shaken baby syndrome)
  • Mostly affects white matter in areas including the brain stem, the corpus callosum, and the cerebral hemispheres
  • Most common in Diffuse Axonal Injuries (DAI)
  • Axonal segment can detach and trigger Wallerian degeneration
  • Retraction balls can be observed throughout the brain regardless of site of injury
  • Axon disconnections slowly developed over an extended time
  • Frequent cause of PVS and coma
  • Clinical picture worse than CT findings
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29
Q

Compressive damage due to TBI

A
  • increased ICP due to mass bleeding & edema can compress brain tissue
  • brain is surrounded by rigid skull so compression causes midline shift, increased pressure on important structures or brain tissue tries to push through openings or spaces known as herniation
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30
Q

Types of brain herniations

A
  • Trastentorial herniationof uncut: shifts the brainstem, pushes against the contralateral tentorium
  • Subfalcine herniation
  • Transforaminal herniation
  • Central herniation
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31
Q

Signs of Uncal herniation

A
  • Coma
  • Pupillary dilation
  • Hemiparesis
  • Decerebrate posturing
  • Hypertension, bradycardia
  • Abnormal breathing patterns
  • Posterior cerebral artery infarction
32
Q

Signs of Central herniation

A
  • Coma
  • Miosis
  • lateral gaze palsy
  • Decerebrate posturing
  • Hypertension, bradycardia
  • Abnormal breathing patterns
33
Q

Signs of Cerebellar/Tonsillar herniation

A
  • Hypertension, bradycardia
  • Abnormal breathing patterns
34
Q

Sign of Subfalcine/Cingulate herniation

A
  • Anterior cerebral artery infarction
35
Q

When treating TBI in acute settings any sign of a brain herniation that was not present before & developed recently should lead to what kind of referral

A
  • Immediate referral/consults
36
Q

Describe a headache

A
  • Most common complaint after TBI
  • Migraine headaches with or without aura may develop in hrs or wks after concussion
  • Migraine with aura might develop after first or additional blows in sports in adolescents/young adults (footballer’s migraine)
  • Cluster headaches can also develop in mild TBI
  • In moderate to severe TBI if headache appears later & person deteriorates neurologically after being lucid initially after injury then suspect increased ICP from hematoma (need to monitor & treat urgently)
37
Q

Clinical manifestations of a mild TBI/Concussion

A
  • Short-lived impairment of neurologic functions that resolve spontaneously
    Headache, dizziness, nausea
  • Cognitive problems - Disorientation, Irritable, distractible, memory problems and difficulty with reading
  • Fatigue and sleep disturbances/sleeping more than usual
  • Typically resolve in 7-10 days
  • Factors that may prolong recovery time are LOC for >1minute, significant cognitive problems, younger age, female gender and depression
  • Single concussion does not typically result in long-term deficits, but prediction is difficult
38
Q

Clinical manifestations of a moderate to severe TBI

A
  • Loss of consciousness from several minutes to hours, including coma and other disorders of consciousness
  • Persistent headache or headache that worsens or headache that keeps coming back with exertion
  • Repeated vomiting or nausea
  • Convulsions or seizures
  • Dilation of one or both pupils of the eyes
  • Inability to awaken from sleep
  • Agitation, combativeness, profound confusion or other behavioral problems
  • Weakness or numbness in fingers and toes
  • Loss of coordination
  • Slurred speech
39
Q

Clinical manifestations of disorders of consciousness

A
  • Can occur with diffuse or focal head injuries
  • Can be a result of diffuse bilateral cerebral hemisphere damage or smaller lesion that affects brainstem, wakefulness depends on intact reticular system
  • In acute settings GCS is used in rehab settings, Coma Recovery Scale Revised allows for more detailed assessment of responsiveness to various stimuli & basic functions during recovery; allows to track smaller changes in sensory & motor status within low levels of conscoiusness
40
Q

Signs at different levels of consciousness/disorders of consciousness

A
  • Coma: lowest level of consciousness, rarely lasts for more than 4 wks
  • Wakeful post comatose unawareness (AKA persistent vegetative state is lasts for >4 wks): might open their eyes, return of sleep-wake cycle but no tracking/fixing gaze, no purposeful movements or communication
  • Minimal conscious state: can track objects visually, inconsistent ability to follow commands, simple communications (yes/no gestures)
  • Once they can communicate consistently and follow instructions they overcome minimal conscious state
41
Q

Describe some cognitive & behavioral problems

A
  • After return to full consciousness pt can become disinhibited (inappropriate social & sexual behaviors, mood disturbances, involuntary laughing/crying)
  • Could become aggressive
  • Might progress to confused state characterized by disorientation, memory deficits, restless, sleep disturbances, delusions/hallucinations
  • Memory deficits: can have both retro- & anterograde amnesia (length of post traumatic amnesia is an indicator of TBI severity
  • Residual degrees of deficits in attention, problem solving, mental flexibility, poor speed/increased reaction time, language deficits may remain
42
Q

With severe TBI & increasing compression/herniation at low levels of consciousness (low GCS scores), postural changes & changes in vital signs may be seen such as

A
  • Decorticate posturing/rigidity: sustained posturing of UE in flexion and LE in extension
  • Decerebrate posturing/rigidity: worse condition, sustained posturing of UE/LE and trunk on full extension
  • Compression of brainstem vital centers can elicit abnormal pulse rate, respiratory rate, BP changes, excessive sweating, salivation
43
Q

Causes of decorticate and decerebrate posturing

A
  • Decorticate: due to compression of cortical connections to the red nucleus, resulting in disinhibited rubrospinal activity
  • Decerebrate: due to further compression of cortical connections to reticular/vestibular nuclei, resulting in disinhibited reticulospinal/vestibulospinal activity
44
Q

The anatomical divide between decorticate and decerebrate posturing is generally thought to be where

A
  • at the intercollicular line at the level of the red nucleus
45
Q

Describe Cheyne-Strokes breathing

A
  • rhythmic pattern of alternating rapid breathing with momentary stopping, bilateral hemispheric or midbrain lesions
  • associated with severe TBI and sign of poor prognosis
46
Q

Describe Hyperventilation

A
  • ‘over breathing’ where blood CO2 decreases causing respiratory alkalosis
  • pontine/midbrain lesions
  • associated with severe TBI and sign of poor prognosis
47
Q

Describe apneustic and ataxic breathing

A
  • Apneustic: prolonged pause at the end of inspiration; mid to lower pons lesions
  • Ataxic: irregular rate & depth of breathing; medullary lesions
  • Associated with severe TBI and sign of poor prognosis
48
Q

Motor deficits related to TBI

A
  • Depends on area of brain injured
  • Hemispheric lesions can involve one limb or cause hemiplegia, cerebellar lesions can cause ataxia, basal ganglia lesion can cause tremors/bradykinesia
  • Flaccidity can gradually be replaced by spasticity
  • Movement disorders can occur immediately due to acute trauma or can develop later
49
Q

Describe Kernohan’s notch phenomenon due to transtentorial herniation

A
  • if cerebral peduncles are compressed against contralateral tentorium: false localizing signs, resulting in ipsilateral hemiplegia
50
Q

What does a completely normal eye exam/pupillary reaction suggests for a TBI

A
  • suggests lesion is above midbrain
51
Q

How can a TBI damage CN III, IV, VI

A
  • compression or stretching from cerebral herniation or crushing injuries distorting the skull
52
Q

How can a TBI damage CN VIII

A
  • transverse fracture of temporal bone, pressure waves from blast can damage hair cells
53
Q

How can a TBI damage CN IX, X, XI, XII

A
  • all pass through foramen at base of skull
  • fracture or projectile injuries to base of skull
54
Q

Pain manifestations resulting from a TBI

A
  • Head & neck pain common with whiplash
  • Sleep disturbances
  • Can contribute to behavioral problems like anxiety or depression
  • Neuropathic pain due to abnormal processing by the somatosensory system
  • Thalamic pain from injury to thalamus, initially numbness & tingling, later can develop into chronic pain
  • Painful leg & moving toes syndrome: rare; deep burning pain in leg followed involuntary movement in toes
  • Can cause fibromyalgia later due to central sensitization of pain
55
Q

Describe heterotopic ossification

A
  • abnormal bone growth in periarticular soft tissue (muscles, tendons)
  • Pathogenesis is unknown
  • Can be associated with trauma, immobility or spasticity following injury
  • Onset about 4-12 wks after injury
  • First detected as tenderness, swelling, pain with movements, loss of ROM, later can be palpated as mass
56
Q

Describe second impact syndrome (with successive concussions)

A
  • Effect of a 2nd concussion before the brain has a chance to recover fully results in worse clinical presentation
  • Existence of this condition is still controversial but human & animal studies support post-concussion vulnerability of brain
  • 2nd injury can cause rapid/severe disruption of cerebral autoregulation, LOC and progressive disability or death if not monitored & treated
  • Suspected to occur mainly in sport related death of adolescents
57
Q

Describe chronic traumatic encephalopathy (CTE)

A
  • Thought to be caused by multiple repeated concussive blows over a lifetime
  • Etiology is unclear
  • Progressive degenerative condition
  • Deterioration in cognition & behavior
  • Post-mortem analysis reveals evidence of degeneration, deposition of protein Tau
  • First noted in boxers, now footballers
58
Q

What do you need to do before concluding CTE (chronic traumatic encephalopathy)

A
  • Need to examine full clinical hx
  • Chronic substance abuse, genetic predisposition & other chronic health conditions could also contribute to signs of CTE
59
Q

Diagnosis of a TBI in an acute/ICU setting

A
  • Pupillary response & oculomotor signs: valuable in knowing depth of LOC & localizing brainstem damage
  • Sluggish or unreactive pupillary response may indicate increased ICP = severe TBI
  • Pupillary size > 1mm difference = abnormal
  • Gaze palsies: lesion of oculomotor nerves on one side, tonic downward gaze = compression of thalamus, ocular bobbing = pontine lesion
60
Q

Diagnostic imaging for a TBI

A
  • CT: primary image modality; reveals presence of hemorrhage, brain swelling, infarction; used to rule out need for surgical intervention
  • MRI: complementary to CT; can detect small hemorrhages, shear injuries
  • Proton magnetic resonance spectroscopy: can be used quantitatively to monitor metabolic recovery
  • Electrophysiologic tests: evoked potentials; tests integrity of sensory circuits; can be used to document changes for prognosis
61
Q

Diagnosis for a TBI in a sports/outpatient setting

A
  • Sideline assessment tools: SCAT-5 (sport concussion assessment tool) is becoming standard regulation in sports
  • SCAT-5 includes a battery of tests, GCS for mental status, Maddock’s score, symptom checklist, cognitive tests, balance & coordination tests, also includes a cervical spine exam
62
Q

Diagnosis for a TBI in a school setting

A
  • Neurophysiological tests: more sensitive for subtle cognitive impairments than clinical signs
  • Immediate post concussion assessment & cognitive testing: proprietary tool - normative data is available
63
Q

Treatment for a mild TBI (concussion)

A
  • 80-90% of sports concussion recover fully in 7-10 days
  • Concussed brain is less responsive to usual neural activation & if premature cognitive & physical activity is forced before complete recovery, it can be vulnerable to prolonged dysfunction (need rest)
  • Avoid repeat concussion during first 7-10 days
  • Individual with concussion should be immediately removed from play & not be allowed to play same day
  • 24-48 hrs of both relative physical & cognitive rest before beginning progression
  • Stay in each stage for 24 hrs & if symptoms recur stop activity until symptoms stop & start the previous asymptomatic stage
64
Q

Stages of the consensus statement for management of sports related concussion (return to sport)

A

1) Symptom limited activity: daily activity that doesn’t provoke symptoms
2) Light aerobic exercise: walking/slow to medium pace, no resistance training
3) Sport specific exercise: running/skating drills, no head impact
4) Non-contact training drills: harder training drills, may start progressive resistance training
5) Full-contact practice: following medical clearance, participate in normal training activities
6) Return to sport: normal game play

65
Q

Stages of return to activity for a mild TBI

A

1) Initial rest
2) Prepare to return to activity
3) Increase your activity
4) Gradually resume daily activities
5) Full return to activity
- start after a brief period of rest during the acute phase after injury (24-48 hrs)
- If new or worsening symptoms are experienced at any stage go back to the previous stage for at least 24 hrs

66
Q

Stages of return to school for a mild TBI

A

1) Physical & cognitive rest
2) Start with light cognitive activity & when light cognitive activity is tolerated
3) Back to school part time: max accommodations
4) Part time school: moderate accommodations
5) Full time school: minimal accommodations
6) Full time school
- Immediately after concussion the student should rest 24-48 hrs & not participate in any sport or academic activities

67
Q

Prehospital management of a severe TBI

A
  • Efficient transport, rapid triage, resuscitation
  • Survival & medical stability are the goal: vital signs
  • If hypoxia: clearing upper airway & then intubation & ventilation if indicated
  • If hypotension: administering fluids
  • If Hypotension & hypoxia should be avoided to prevent/minimize secondary injury
68
Q

Emergency department management of a severe TBI

A
  • Determination of type of head injury (CT)
  • Continued control of hypoxia & hypotension
  • Monitoring for increase in ICP & other factors responsible for secondary injury
  • Determination of need for surgical intervention
69
Q

Treatment for a severe TBI in an ICU/acute care setting

A
  • Continued monitoring of ICP: invasive catheters (risk of infection but allowing monitoring & drainage of CSF) or non-invasive (doppler waveform)
  • ICP monitoring recommended for severe TBI and abnormal CT
  • If ICP increases decompressive craniotomy can be done to remove hematoma & counter effects of ICP
  • CSF volume can also be reduced pharmacologically: mannitol; progesterone promising agent to reduce cerebral edema
70
Q

Roles of physical therapy in acute care setting for severe TBI

A
  • Monitoring of CN function
  • Monitoring reflexes & voluntary motor behavior
  • Positioning
  • ROM exercises
  • Maintaining head of bed at 30 degrees would avoid aspirations and also helps with venous drainage to avoid increase in ICP
  • Pulmonary management: percussion, vibration to keep airway clear with caution, need to monitor vital signs and blood gas numbers, may be contraindicated with increased ICP
  • Functional mobility training as indicated and tolerated: early mobilization is found to show better outcomes, need to monitor chest tubes, NG tubes, ICP monitor, arterial lines as they may be compromised during movements
  • Passive verticalization of unconscious/minimally conscious patients also found to improve awareness
  • Need to decide on appropriate w/c seating for non-ambulatory pts
71
Q

Roles of physical therapy in an in-patient/out-patient setting

A
  • Spasticity management using pharmacological agents: baclofen, diazepam, side effects, weakness & lethargy
  • Functional skills management using task-oriented training (per task analysis)
  • Aggressive behavior can be controlled by agents like carbamazepine
  • Cognitive & behavioral management per the Rancho Los Amigos LOCF Scale
72
Q

Levels of assistance

A
  • Level I - No response: Total Assistance
  • Level II - Generalized nonpurposeful/stereotyped response: Total Assistance
  • Level III - Localized Response: Total Assistance
  • Level IV - Confused/Agitated: Maximal Assistance
  • Level V - Confused, Inappropriate, Non-Agitated: Maximal Assistance
  • Level VI - Confused, Appropriate: Moderate Assistance
  • Level VII - Automatic, Appropriate: Minimal Assistance for Daily Living Skills
  • Level VIII - Purposeful, Appropriate: Stand-By Assistance
  • Level IX - Purposeful, Appropriate: Stand-By Assistance on Request
  • Level X - Purposeful, Appropriate: Modified Independent
73
Q

Rehab management/Implications for physical therapy

A
  • Goals are to restore functional mobility, self-care abilities, cognitive abilities, return to community with employment & recreational activities
  • Complex patients need interdisciplinary approach to improve both cognitive & physical abilities: medical, nursing, PT, OT, SLP, social worker, etc.
74
Q

What types of patients are more difficult to integrate into society (patients with higher physical skills & lower cognitive or patients with higher cognitive & lower physical skills

A
  • Patients with higher physical skills and lower cognitive are more difficult to integrate into society
75
Q

Roles in outpatient setting as indicated for rehab management

A
  • Motor problems: spasticity, hemiplegia often persists for months with severe TBI, HO, need to optimize function
  • Balance problems: postural imbalance
  • Vestibular problems: dizziness, motion sensitivity, balance problems due to VOR impairment - avoid overstimulating the vestibular and visual systems, can use settling techniques like putting weight on shoulders, pressing down on top of head, can use habituation exercises, also can use gaze stabilization exercises
  • Cognitive problems: successful re-integration into community needs ability to learn to cope with the multiple demands of work, school and recreational activities, needs high level executive functions for managing time and information – teach coping skills using checklists and reminder devices
  • Rate of recovery will vary a lot depending on movement disorders, sensory dysfunctions and cognitive deficits and other comorbidities that would determine prognostic outcomes
76
Q

Highly recommended outcome measures for TBI

A
  • Coma Recovery Scale - R
  • Agitated Behavior Scale
  • Moss Attention Rating Scale
  • Rancho LOCF
  • HiMAT
77
Q

Factors that affect outcomes of TBI/Prognosis

A
  • Injury severity : depth and duration of decreased responsiveness, duration of amnesia, loss of pupillary reflexes, hematomas, DAI, cerebral compression, epilepsy within 7 days, all indicate poor prognosis
  • Pre-injury factors: hx of substance abuse, low educational level, psychiatric disorders can limit success
  • Post-injury factors: access to appropriate care, intense therapy after emergence from vegetative state, family support and education can also be key factors for recovery

Clinical Medicine III (20 decks)

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