TBI Intro Pt 1 Flashcards
define a TBI
an injury that disrupts the normal function of the brain. It can be caused by a bump, blow, or jolt to the head or a penetrating head injury
what populations are more at risk for a TBI?
- Children and older adults
- ages 0-3, 15-24 and over 65
- Men > Women 2:1
- Other:
- racial and ethnic minorities
- service members and veterans
- homeless
- incarcareted individuals
- domestic abuse survivors
- rural area dwellers
Causes of TBI
- MVA
- Falls
- Acts of violence
- Sports
Most common causes of TBI based on age
- Children
- falls and abuse
- Adolescents and young adults
- falls, assult, MVA
- Older Adults
- overwhelmingly fall related
2 main categories for brain injuries
Traumatic Brain Injury
Acquired Brain Injury
Mechanisms for Brain injuries
- TBI
- open head injury
- closed head injury
- deceleration injury
- hemorrhage/hematoma
- ABI
- chemical/toxic
- hypoxia
- tumor
- infection
difference between open and closed injury
- Open
- results from penetrating types of wounds
- skull → fractured or displaced
- meninges are compromised
- Closed
- impact to the head but skull isn’t frx
- only cortical neuronal tissue is damaged
- meninges are intact
pathophysiology of primary brain damage from a TBI?
primary brain damage resulting from mechanical issue at time of trauma
can be a focal or diffuse injury
difference between a focal and diffuse injury?
- focal → localized to area under site of impact or site opposite to site of impact
- contusions, lacerations, hemorrhage and/or hematoma
- coup-contracoup injury
- diffuse → diffuse axonal injury (DIA)
Focal Injuries
- Epidural hematomas (EDH)
- Subdural hematomas (SDH)
- Subarachnoid hemorrhage (SAH)
- Intracerebral hemorrage (ICH)
- Contusions
- Coup-contrecoup injuries
describe epidural hematomas
occur between dura mater and skull
- often seen after blow to the side of the head or severe trauma from an MVA
- brief LOC → snap back then rapidly deteriorate
- craniotomies and hematoma evac may be required
describe subdural hematomas
rupture to the cortical bridging veins
- develops betwen the dura and arachnoid
- blood leaks slowly over several hours or weeks
- seen in elderly after falls w/blow to head
- symptoms can be similar to those of CVA
- small clots may be reabsorbed by body, larger ones require surgerical removal
describe SAH
hemorrhage between arachnoid and brain tissue
- most life threatening!
- 1/3 of pts will survive w/good recovery
- 1/3 will survive with disability
- 1/3 will die
- common sequale → vasospasm
describe ICH
hemorrhage within brain tissue itself
- causes → head injury, HTN, AVM
- stroke-like presentation
Coup vs Contrecoup contusions
both are brusing on the surface of brain sustained at time of impact
- coup lesion → same side as impact
- contrecoup → opposite side of brain trauma, a result of deceleration
describe Coup-Contrecoup Injuries
blows to the head cause the brain to “bounce” off of irregular boney prominences on the inside of skull
most common structure invovled:
- anterior poles
- underside of temporal lobe
- underside of frontal lobe
describe DAI
acceleration, deceleration, rotational forces (most common causes MVA)
results in widespread shearing and retraction of damaged axons as well as traumatic micro bleeds
T/F: DIA have a good prognosis?
FALSE
poor prognosis
what is the cause of secondary brain damage during a TBI?
physiological response to initial injury
hypoxic/ischemic injury
swelling/edema
electrolyte imbalance and mass release of damaging neurotransmitters → metabolic cascade → apoptosis
list some causes of non-traumatic brain injuries (aka ABI)
- stroke
- infectious disease
- seizure
- electric shock
- tumor
- toxic exposure
- metabolic disorder
- neurotoxic poisoning
- lack of O2
- drug OD
list some vulnerable areas to anoxic/hypoxic injuries
- hippocampus
- cerebellum
- BG
subtypes of blast injuries that result in TBIs
- Primary → direct effect of blast overpressure on organs
- direct transcranial blast wave propagation
- kinetic energy through vasculature
- increase CSF or venous pressure
- Secondary → shrapnel injury
- Tertiary → direct blow to head
what is a concussion?
a force from a bump, blow or jolt to the head
sustained either directly or indirectly to the body that disrupts normal brain functioning
these forces results in various directional forces inside the skull which initiate a complex pathophysiologic process that alters neurometabolism
symptoms of a concussion
- dizziness
- disorientation
- difficulty concentrating
- sleep distrubances
- nausea
- HA
- loss of balance
- blurred vision and light sensitivity
acute management of a TBI
- Diagnostic imaging
- MRI, CT, PET, EEG
- Medication management
- decrease BP, ICP and intracranial bleeding
- antiseizure
- decrease infection rate, and body temp
- Surgical management
- secondary complications
- ICP management
- seizure reduction or prophylaxis
- dysautonomia
- trauma managment
List secondary complications to a TBI
- Increased ICP
- Post traumatic seizures
- dysautonomia
- heterotophic ossification
- other
what is normal vs abnormal ICP?
- normal = 5-10 mmHg
- abnormal = >20 mmHg
list some activities that increase ICP
- full supine or trendelenburg
- cervical flexion
- percussion and vibration
- valsalva
- coughing , sneezing, holding breath, etc
- exertional activities
- quick elevating HOB
- supine → sit
S/S of increased ICP
- decreased responsiveness
- impaired consciousness
- severe HA
- vomiting
- irritability
- papilledema
- increased BP and decreased HR
treatment for increased ICP
- careful monitoring
- pharmacological agents
- ventricular peritoneal shunting if permanent correction is needed
what are post traumatic seizures?
discrete clinical event reflecting temporary, physiologic brain dysfunction, characterized by excessive hypersynchronous cortical neuron D/C
what is dysautonomia?
anything that goes awry in our autonomic system
PAID is common
what is PAID?
Paroxysmal Autonomic Instability and Dystonia
(sympathetic storming, GCS 3-8)
diagnosed via clincial observation and managed by “riding out the storm” and managing symptoms
symptoms of dysautonomia
- alterations in level of consciousness
- increased posturing
- dystonia
- HTN
- hyperthermia
- tachycardia
- tachypnea
- diaphoresis
- agitation
Heterotrophic Ossification in TBI
- occurs in 10-20% of TBIs
- increased risk if TBI is polytrauma w/fractures near joint lines
- most common in large joints of the body
- unknown cause but is associated with trauma, immobility, and hypertonicity
- onset ~ 4-12 weeks after brain injury
clinical presentation of hetertrophic ossification
- initial signs are:
- loss of ROM (HARD END FEEL)
- pain in joint area
- local erthyema
- pain w/movement
- swelling and warm to touch
- severe HO may result in vascular and/or nerve compression
treatment for heterotropic ossification
- PROM and stretching
- to maintain ROM and prevent further complications from HO (not to fix it)
- Medication
- didronel → preventative
- anti-inflammatory agents for symptom management
- surgical excision (>1.5 years after injury)
describe the clinical manifestation of TBI
- altered level of consciousness/impaired arousal
- cognitive and behavioral impairments
- neuromuscular impairments:
- impaired balance
- abnormal tone
- Autonomic Dysfunction
- Sensory abnormalities → loss of sensation and pain
- cranial nerve damage
- vestibular deficits
- secondary complications
clinical presentation of a TBI impacting the frontal lobe
Problems with:
- initiation
- problem solving
- judgement
- inhibition of behavior
- planning/anticipation
- self-monitoring
- motor planning
- personality/emotions
- insight
- organization
- attention/concentration
- mental flexibility
- Speaking (expressive language)
clinical presentation of TBI impacting temporal lobe
problems with
- memory
- hearing
- understanding language (receptive language)
- organization and sequencing
clinical presentation of TBI impacting brain stem
problems with:
- breathing
- heart rate
- arousal/consciousness
- sleep/wake functions
- attention/concentration
clinical presentation of TBI impacting parietal lobe
problems with:
- sense of touch
- differentiation
- size, shape, color
- spatial perception
- visual perception
clinical presentation of TBI impacting the cerebellum
problems with:
- balance
- coordination
- skilled motor activity
what types of cognitive deficits are present following a TBI?
- Arousal dysfunction
- Disorientation
- Poor attention span
- Loss of memory
- Poor organization and reasoning skills
- Inability to control emotional responses
- Learning difficulties
TBI pts may be referred to as __________ pts
Walkie-Talkie
- may be able to walk independently w/o AD negotiating barriers but might not recall their name or family members
- confabulation (fill in w/fabricated stories)
- more problematic for functional independence
what are the 5 categories of attention?
- focused
- sustained
- selective
- alternating
- divided
list S/S of impaired attention
unable to
- engage on relevant or functional info
- sustain attention to task
- switch to new task
- resist distraction
- multitask
- manipulate mental info while maintaining overarching goal in mind
list memory deficits that may be present in TBI
- retrograde and/or anterograde amnesia
- posttraumatic amnesia
- short-term > long-term memory deficits
- declarative and procedural memory often both difficult
executive function deficits following TBI
- volition/planning
- problem solving
- insight
- social pragmatics
- self-regulation
language deficits following TBI
- generally non-aphasic in nature and related to cog impairment
- common deficits:
- disorganized and tangential oral and written communication
- imprecise language
- word-retrieval difficulty
- disinhibited lanuage
behavorial issues following TBI
*most enduring and socially disabiling of impairments after TBI
- sexual disinhibition
- apathy
- aggressive disinhibition
- hyperactive, restless
- low frustration tolerance
- depression
- evaluation and management considerations
behavioral issues are prominent in pts classified as what Rancho level(s)?
IV and V
frontal lobe syndromes are also known as ______
dysexecutive syndrome
what are the 2 types of frontal lobe syndrome?
- Orbitofrontal Lobe Syndrome → disinhibited
- Frontal Convexity Syndrome → apathetic
describe the Orbitofrontal Lobe Syndrome
Disinhibited
- impulse behavior (pseudopsychopathic)
- inappropriate jocular affect, euphoria
- emotional liability
- Poor judgement and insight
- Distractability
describe Frontal Convexity Syndrome
Apathetic
- indifferent
- psychomotor retardation
- motor perseveration and impersistence
- stimulus-bound behaviour
- motor programming deficits
- poor word list generation
list motor and sensory deficits that may occur following a TBI
- Strength deficits
- focal lesions → hemiparesia/plegia
- diffuse injuries → MC or coordination deficits
- tone abnormalities
- flaccidity, rigidity or hypertonicity
- brain-stem injury → posturing
- primitive and tonic reflexes may reemerge
- sensory deficits
- proprioceptive and kinesthetic deficits most common
compare the 2 types of posturing
- decorticate → above red nucleus
- LE extension and UE flexion
- decerebrate → below red nucleus
- UE and LE extension
how common is it to have vestibular dysfunction following a TBI?
as many as 50% report signs of dizzines and imbalance
could be due to:
- injury to vestibulocochlear nerve
- injury to vestibulocerebellum
- damage to brainstem or cortex involving vestibular pathways
list other causes of vestibular dysfunction that may arise following a TBI
- trauma/falls → labyrinthine concussion = related to development of BPPV
- Perilymph fistula is associated with blast injuries
- with flexion/extension type injuries may have cervigogenic component
