Physiological Psychology Lecture #7 Flashcards
Traumatic Brain Injury
“When a sudden, external, physical assault damages the brain”.
In the U.S.:
- 27,000 are hospitalized.
- 52,000 die from their injury.
Causes of traumatic brain injury
In adolescence and young adults:
- Motor vehicle collisions.
In older adults:
- Falls
TBI Sex and Age Breakdown
- Most common age: 15-24
- More common in men than women (at age 15-24), becomes more even as age progresses.
Closed Brain Injury
Non-penetrating injury to the brain-no break to the skull. Injury can result from:
- Rapid forward and backward movement of brain in the skull–tearing and bruising of brain tissue and blood vessels.
Coup
point of impact
Countercoup
Injury of opposite side
Diffuse Axonal Injury
Car crash, falls, sports, shaken baby syndrome.
Penetrating Brain Injury
Penetrating or open head injuries where there is a break in the skull. Injury results from:
- Penetrating objects, and skull bone fragments damaging brain tissue and blood vessels = deprivation of normal blood supply and accumulation of blood.
- Cognitive impairment tend to be more focal.
Ischemia
Deprivation of normal blood supply
Hemorrhage
Accumulation of blood.
Diffuse Axonal Injury (DAI)
“The shearing (tearing) of the brain’s long connected nerve fibers (axons) that happens when the brain is injured as it shifts and rotates inside the bony skull”.
- Damage to white matter.
- Changes are microscopic.
- Can lead to disorders of consciousness (persistent vegetative state, coma).
- Difficult to see on CT scan or MRI
- Can occur without other visible damage.
Grade 1 Axonal Injury
Mildest form of DAI
- Microscopic changes in the white matter of the cerebral cortex, corpus callosum, brain stem, and cerebellum.
Grade 2 Axonal Injury
Moderate form of DAI (diffuse axonal injury)
- Grossly evident focal lesions isolated to the corpus callosum.
Grade 3 Axonal Injury
Severe form of DAI
- Additional and severe focal lesions on the brainstem itself.
Primary Injury
- Skull lacerations
- Skull fractures
- Contusions
- Cerebral lacerations
- Intercranial hemorrhage
- Diffise axonal injury
Primary Injury
- Skull lacerations
- Skull fractures
- Contusions
- Cerebral lacerations
- Intracranial hemorrhage
- Diffuse axonal injury
Secondary Injury
Due to:
- Increased intracranial pressure.
- Hypoxia
- Hypotension
- Hypothermia
- Electrolyte disturbance (Na, Ca, K)
- Toxic amino acids
- Oxygen radicals.
Chronic Traumatic Encephalopathy (CTE)
- Produces neurodegeneration due to repeated head trauma.
- Prevalence in athletes who participate in contact sports.
- Mood and cognitive impairment can appear years after the injury occurred.
- Characteristic deficits include: dysexecutive functioning and mood liability.
How can CTEs be confirmed postmotem?
Examination of brain tissue:
- Abnormal tau protein accumulation (similar to Alzheimer’s disease)
- Reduced brain volume (in corpus callosum and limbic system).
- Ventricular enlargement.
True/False Individual will remember what happened/occurred after TBI
False
Mild TBI
<30 minutes unconscious
- 13-15 Glasgow coma scale
- <24hrs post-traumatic amnesia
Moderate TBI
30 min-24hours unconscious
9-12 Glasgow coma scale
1-7 days post-traumatic amnesia
Severe TBI
> 24hrs unconscious
3-8 Glasgow coma scale
7days post traumatic amnesia
Limitations to Glasgow Coma Scale
- Substance use.
- Administered drugs
- Intubation
- Injury to eye
- Hemiplegia
- Language
Post-Traumatic Amnesia
state of confusion and disorientation that occurs immediately after TBI–part of healing process.
- Brain is unable to form continuous day to day memories–memory is the slowest part of conscious mint to recover.
Post-Traumatic Amnesia Behaviorally can present with:
- Confused and disoriented
- Agitation and aggression
- Inability to recognize loved ones
- Childlike/clingy behaaviors
-Confabulations - Can be difficult to remember family members
- Goal is support re-orientation and sense of safety
- Do not ask they to recall the injury–they cannot do this.
Rancho Los Amigos Scale Revised (RLAS-R)
IV: Confused/Agitated: Maximal Assistance
Dose Response Relationship
Most well-designed studies, using a representative, non-clinically referred study sample show:
- Cognitive changes after TBI resolve within weeks to about 3 months at most spontaneously without treatment while changes tend to persist for less than or equal to 2 years following moderate to severe TBI
Non-Injury Risk Facotrs that Can Influence TBI Outcomes
- pre-injury psychiatric status and conduct issues/incarceration
- age at injury
- level of education
- stable employment 6 months pre-injury (best predictor of return to employment post injury.
- marital status
- other non-neurological injuries sustained–physical injuries can prevent return to meaningful activities.
