TBI Flashcards
Traumatic Brain Injury
Any external mechanical force acting on the brain in which a temporary or permanent dysfunction is the result
Can be open/closed, focal/diffuse
3 initial phases of TBI
1) LOC/coma
2) Cognitive/bx abnormalities
3) Memory, sequencing time, inability to learn new info
4) Permanent cognitive sequelae
Timing of phases of TBI
LOC or cognitive/bx abnormalities can last a few days to one month post injury
6-12 month period following marked by rapid recovery of cognitive functions and subsequent plateau
Severe TBI
Altered/prolonged (>24 hours) loss of consciousness (coma), usually diffuse
Post-traumatic amnesia >7 days
Moderate TBI
Positive neuro imaging, skull fracture, intracerebral hemorrhage
Loss of consciousness: 30 min-24 hours
Altered consciousness: >24 hours
Post Traumatic Amnesia: >1 day, >7 days
Mild TBI
Negative neuro imaging, concussion, symptoms typically resolve
No loss of consciousness or LOC < 30 minutes
Altered consciousness for a few sec-24 hours
Post-traumatic amnesia 0-1 day
Common features: memory problems, photosensitivity, headache, irritability, cognitive inefficiency
Most common site of brain contusion in TBI
Due to bony prominences butting brain tissue in the cranial vaults are anterior temporal lobes and orbitofrontal regions
High rate of false negative errors in TBI may be caused by
Use of highly specific sign/symptom (contra lateral neglect)
How does Moderate-Severe TBI differ from anoxic brain injury?
Anoxic injury would be marked by slower recovery, poorer outcomes, and visual deficits complicating care/treatment
What might patients played on an SSRI or benzo post-TBI experience?
- Worsened gait/balance
- Cognitive sedating effects
- Increased disinhibition
What can single photon emission computed tomography (SPECT) provide?
May be used in diagnosis of head injury with no LOC/GSC/other imaging studies are normal
Glascow Coma Scale
Used to objectively describe the extent of impaired consciousness in all types of acute medical and trauma patients
Score from 3-15 (3 is worst, 15 is highest)
Ages 5+ (pediatric scale for youngers)
Correlated with mortality
Severe GSC
3-8
Moderate GSC
9-12
Mild GSC
13-15
Barriers with the GSC
- Langauge
- Hearing/speech
- intellectual/neurological deficits
- intubation
- pharmacological/paralysis
- orbital/cranial fracture
- spinal cord damage
- hypoxia-ischemic encephalopathy after cold exposure
What is a potential problem of the GSC in diagnosis mTBI?
Ceiling effect (questions are not difficult enough)
Coma
Complete unconsciousness, unable to be awakened, may not respond to sound, touch, pain, unable to communicate/see, unable to follow commands, show emotion, engage in purposeful bx
Vegetative State
Still unconscious but may awaken at times
Unresponsive wakefulness syndrome
Brief reaction to sounds, sights, touch
Cry, smile, and facial expressions (reflexes)
Automatically fx still controlled by brain
Minimally conscious state (MCS)
Regaining consciousness, some self-awareness
Engage in purposeful bx (inconsistent)
Follow simple commands
Makes intelligible verbalizations
Visually follows people in the room
Functional object use inconsistent
Emerged from MCS
Communication consistent
Use of 2 objects in purposeful manner
Yes/no responses
Follow instructions
Perform simple tasks
TBI factors in recommending that a patient not return to work
Age (over 50)
Education (less than HS)
Prior work hx (unable pre-injury)
TBI severity (severe)
Severe TBI in pediatrics
Children have poorer prognosis (worse with younger ages)
Continued neurobehavioral issues in children depend on age, severity, family resources, and support system
In the acute rehabilitation phase (discharge from inpatient to rehab unit), prognosis for functional outcome would depend on
the time to follow commands following the injury
Important in differentiating moderate and mild TBI
PTA and neuro imaging findings to accurately determine the severity of the injury
Annual TBI count in the U.S.
Number that result in hospitalization
Number that suffer chronic disability
2 million
500,000
80,000
Men
2x as frequent
4x more likely that TBI will be fatal
Bi-modal distribution of TBI
Increases from childhood and peaks at 15-25
Falls afterward
Rises again in later states of life
Top 4 causes of TBI by percentage
50% MVA
21% falls
12% violence
10% sports
TBI Risk factors
Increased age
Arteriosclerosis
Alcoholism
Premorbid personality
Marital discord
Poor interpersonal relationships
Problems at work/school
Financial instability
Mechanism of TBI
Mechanical forces applied to the skull is then transmitted to the brain
Damage can be focal or diffuse
Intracerebral hemorrhage
Bleeding into the brain tissue
Ischemic infarct
blood supply to part of the brain is interrupted or reduced, preventing brain tissue from getting oxygen and nutrients
Motion from brain inside the skull may lead to
Diffuse injury
Stretch/shearing of the axons
Secondary processing of TBI
Hypoxia (lack of oxygen)
Anemia (lack of blood)
Metabolic abnormalities
Hydrocephalus (build up of CSF in brain ventricles)
Intracranial hypertension
Fat embolism
Free radicals
Result from the release of excitatory amino acids
Subsequent release of arachidonic acid metabolites
Leads to disruption of neurotransmitters in the synapse
Subarachnoid Hemorrhage
Bleeding in the space surrounding the brain
Most often occurs when a weaker area in the blood vessel on the surface of the brain bursts and leaks
Blood builds up around the brain and inside the skull, increasing pressure on the brain
Nuchal rigidity
Nuchal rigidity
Neck stiffness, common symptom of subarachnoid hemorrhage
Subdural hematoma
Collection of blood forming on the surface of the brain
Blood presses against brain and damages tissue
Can be life-threatening
Can occur in older individuals after minor head injuries
Worsening headache pain within 72 hours, decreased GCS, vomiting, trouble following commands, midline shift, hyper dense crescent-shaped abnormalities on CT
Diffuse Axonal Injury
Shearing/tearing of the axons
Occurs when brain is injured as it shifts/rotates inside the skull
May cause coma
Often diffuse
Commonly marked by decreased mental efficiency, complex reasoning ability, and ability to perform mental arithmetic
Intracranial Pressure
Common signs/symptoms:
Heached
Altered mental status (irritability, depressed alertness/attention)
Nausea/vomiting
Likely the cause of decompensation of a patient following TBI within 72 hours of injury
Hydrocephalus
Abnormal build up of CSF in the ventricles
Causes ventricles to widen and put pressure on brain tissue
Commonly affects the posterior region
Symptoms: headache, nausea, vomiting, cognitive impairment, papilledema (visual), decreased vision
Children with early onset hydrocephalus typically perform better on ___ than ____.
VIQ (VCI + WMI)
PIQ (PSI + PRI)
Normal Pressure Hydrocephalus
Abnormal buildup of CSF in ventricles, occurs if the normal flow of CSF in the brain or spinal cord is blocked
Similar to hydrocephalus causing enlargement of the ventricles which put pressure on the brain
Occurs slowly and worsens over time, pressure usually isn’t dangerously high
Classic indications: dementia, mental decline, gait difficulties, urinary incontienence
Primary treatment: shunting
Way to distinguish NPH from subcortical dementia
Incontinence
Congenital Hydrocephalus
Extensive accumulation of CSF within the ventricles due to an imbalance between synthesis and absorption of CSF
One of the most common abnormalities of CNS
Most common cause: Lennox-Gastaut Syndrome
TBI impact on glutamate pathways
CSF increased glutamate
Glutamate antagonists may be beneficial
TBI impact on cholinergic neuronal activity
Reduction in cholinergic neuronal activity within hippcampal and neocortical areas
Dysfunction of septohippocampal cholinergic pathways, resulting in post-traumatic cognitive and bx deficits
TBI impact on ascending biogenic amine pathway
Circulating levels of catecholamine (directly correlates with TBI severity)
Increased serotonergic sodium metabolites in CSF
Dysregulation of mesolimbic/mesocortical dopaminergic pathways give rise to manic/hypo manic symptoms
Related mood disorders
Anxiety, depression, psychoses, apathy
** functioning impairment is related to anxiety/depression, but less so if the imaging is positive
Related cognitive problems
Delirium, dementia, amnestic disorder, intellectual impairment
Impairment of arousal, attention, concentration, memory, language, exec Fx, memory loss
Related behavioral problems
Frontal/temporal lobe syndromes, aggressive disorders, personality change
Physiological impacts
Sleep disturbance, headache, dizziness, fatigue
General pharmacological TBI treatment
Antiepileptic medications used in inpatient units to manage bx post-severe TBI
Side effect: drowsiness/sedation
Mood disorders secondary to TBI
Depression/mania most common
Persistent dysphoria (feelings of loss, demoralization, discouragement)
Fatigue, irritability, SI, anhedonia, disinterest, and insomnia (seen in the majority of pts 6-24 months or longer after TBI)
Psychological impairments correlated with severity
Risk factors: poor premorbid Fx, psychiatric hx
Mechanism: disruption of biogenic amine containing neurons as they pass through the basal ganglia or frontal-subcortical white matter
Left dorsolateral frontal and left basal ganglia associated with increased probability of MDD
Mood Disorder Treatment Secondary to TBI
Antidepressants, psychostiumlants
SSRIs - typically safe, useful for comorbid MDD, mood lability, and impulsivity (no evidence that they treat TBI)
Sertraline and citalopram are preferred based on beneficial effects, limited side effects, and short half-life
Tricyclics and monoamine oxidase inhibitors are not preferred due to anticholinergic side effects and drug/food interactions
Psychostim/some domainergicss can be beneficial
Methylphenidate performs similar to sertraline (and improved neuropsychological performance)
Mania/Hypomania
