1: Brain Injury Overview Flashcards
Primary injury defines and determines
Mechanism of primary injury
The primary injury defines the injury as either traumatic or non-traumatic ;
determine the severity of injury, informs surveillance data, and correlates the injury to an expected long-term outcome
The mechanism of injury is mechanical – for example, neurons damaged from a penetrating injury or from a stroke.
Examples of secondary injury
The release of excitatory amino acids Oxidative free-radical production Release of arachidonic acid metabolites Disruption of neurotransmitters Hypoxia Anemia Metabolic abnormalities Hydrocephalus Intracranial hypertension Hemorrhagic activity
Definition of Mild TBI
Can have either brief or no loss of consciousness and its presentation may demonstrate vomiting, lethargy, dizziness, and inability to recall what just happened
Can result in local neurological deficits that may or may not be transient
Most are not treated in the hospital or emergency department and therefore may not be diagnosed or under-diagnosed in studies
Definition of Moderate TBI
Will be marked by unconsciousness for any period of time up to 24 hours, will have neurological signs of brain trauma, including skull fractures with contusion or bleeding, and may have focal findings on an electroencephalograph (EEG)/computed tomography (CT) scan
Definition of Severe TBI
Marked by a period of loss of consciousness of 24 hours or greater
Risk of multiple TBI following 1st
After 1st TBI, 2nd is 3x more likely ; after 2nd, 3rd is 8x more likely
Rates of TBI 2001-2010
Rates are increasing, deaths are decreasing
TBI and death
TBI contributes to 30% of injury related deaths in US
incidence of mild TBI
75% of TBI are mild
TBI as chronic disease
TBI affects multiple organ systems can cause disease and accelerate disease
TBI as mortality/ morbidity
-Life expectancy is reduced by 7 years Increased risk of death: Aspiration pneumonia – 49X Seizures – 22X Septicemia – 12X Circulatory problems – 29X
neurological conditions associated with TBI
epilepsy, CTE, sleep disturbance, Alzheimer’s
neuroendocrine disorders associated with TBI
Dysfunction of the pituitary gland
Hypothroidism
Growth hormone deficiency/insufficiency
Gonadotropin deficiency
musculoskeletal dysfunctions associated with TBI
spasticity
gait dysfunction
post-injury fractures- at risk for heterotopic ossification
mTBI
aka concussion aka mild TBI
first identified in 16th century
1839 defined
1990’s - focus of increased study due to the prevalence of mTBI in military conflicts
75% of all TBI are mTBI and may be more due to underrepresentation
mTBI causes….
After the primary cause, the transfer of kinetic energy into brain tissues causes metabolic alterations or direct damage to physical structures:
- Diffuse axonal injury= most common
- Axonal shearing can disrupt neuronal communication
- Difficult to visualize with neuroimaging
- Massive release of the neurotransmitter glutamate
- High levels become toxic, impacting the amount of fuel available to the brain
- Constricted blood flow also impacts neurological function
mTBI symptoms and how long they last
most symptoms resolve in 2 weeks
-physical: headache, fatigue, light / noise sensitivity, seizure, impaired hearing, dizziness, nausea, blurred vision, poor sleep, neurological conditions
- cognition: inattention, diminished concentration, memory, impaired judgment, slowed processing, executive dysfunction
- behavioral: depression, anxiety, agitation, irritability, aggression, impulsivity
Fatigue and mTBI
Fatigue typically arises due to mental rather than physical overexertion and worsens memory and behavioral disturbances. Fatigue is exacerbated by sleep difficulties:
Difficulty falling asleep or waking through the night
Lack of restorative sleep
mTBI and vision
Blurred vision due to difficulty with subtle eye movements or motor control
Convergence insufficiency, in which eyes cannot focus effectively together
mTBI and balance
-most common inner ear disorder after mTBI is benign paroxysmal positional vertigo (BPPV), other causes of balance issues include:
Disorders of the inner ear, central nervous system, or musculoskeletal systems
Psychological issues
Orthostatic hypotension
Medication side effects
mTBI return to activity
REST and slow resumption of normal activities as long as symptoms do not recur
If symptoms recur, return to rest and then advance activity when symptoms have abated
mTBI headache
most common compmlaint after mTBI
primary reason to seek care
typically occurs with exertion
treated like a migraine (except in acute stage where it is a sign of danger)
- top/front of head
- hypersensitive to light/sound
- extracranial cause - trigeminal nucleus; occipital neuralgia ; cervicalgia
mTBI symptom management
sleep hygiene to improve sleep (meditation, education, sleeping pills)
physical therapy for dizziness / instability
educate/ treatment of headaches
psychological features and mTBI
can worsen or create symptoms
Persistent Post-Concussive Syndrome (or symptoms)
persistence of symptoms weeks to months after mTBI
common characteristics:
- Over age 40, Female, Traumatically injured, Low socioeconomic status, History of substance abuse, Positive mental health history, Pending litigation
15% of mTBIs
Tx = must see neuropsych for differential dx
then treatment is based on symptoms, positive light, resolution focused
second impact syndrome
RARE
after 1st mTBI, potential for fatal TBI if return to activity when neurologically unstable (neurochemical cascade)
Chronic traumatic encephalopathy (CTE)
rare and progressive degenerative condition in which diffuse axonal injury causes the release of Tau proteins and causes chronic inflammation. Researchers are still working to identify who is at risk for CTE after mTBI; most who have mTBI will not develop CTE
apoptosis and progression of chronic TBI
thought that cell death becomes earlier after TBI which causes progressive central nervous atrophy (suspected)
post-traumatic immune paralysis
right after TBI immune system is severely impaired – related to high prevalence of infections post TBI
PTA and TBI level
0-1 day - mild
1-7 days - moderate
7+ days - severe
GCS and TBI
13-15 - mild
9-12 - moderate
3-8 - severe
metabolic alterations and mTBI
direct physical damage to brain cells which leads to neurological function changes depending on location of injury
axonal shearing and mTBI
process where axons can be twisted and disconnected
aka DAI
cannot be seen on MRI
mTBI and glutamate
massive release of this neurotransmitter - this is dangerous as it deregulates use of ATP
brain starved for fuel
decreased energy
frontal release and mTBI
damage to frontal areas of brain can result in disinhibition and lability
occipital neuralgia
migraine like headache caused by mTBI
pain in back of head worsens with tension
connections in upper spinal cord and trigeminal nucleus - can radiate pain to forehead and behind eyes
cervicalgia
simple neck pain associated with mTBI and can cause headache and chronic pain syndromes
nystagmus
involuntary eye movement - hallmark of BPPV
