Ch. 13 Traumatic Head Injury and Rehabilitation

Psychology 4240 with Ragsdale at University of Central Florida

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By: Victoria Lake
Created: 2011-03-31
Size: 39 flashcards
Views: 5

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causes of traumatic head injury

motor vehicle accidents
sports (equestrian, gymnastics, cheerleading, football, lacrosse, ice hockey)
falls
violence
industrial accidents

risk factors for traumatic head injury

young (under age 30), single, male
young adult age 15-24
children and adolescents age 5-14
alcohol

traumatic brain injury (TBI)

a "bump" to the head becomes a TBI when the pathomechanism of head injuries relates to the physical forces placed on the neuron, specifically axon and cell body
shear and straining effects at the neuronal level

tensile strength

axon's resistance to longitudinal stress, measured by the minimal amount of stress required to to rupture the axon
shearing effects most noticeable at the junction of white and gray matter regions of the brain

retrograde degeneration

force that tears the axon to a point at which it may degenerate back to the cell body
may lead to cell death

anterograde degeneration

tear/rupture of the cell body leading to the degeneration of the axon fiber
may lead to "domino effect" of metabolic changes in the postsynaptic neuron and possible cell death

penetrating head injury (PHI)

occurs when a small object has lodged in the brain

extremely dangerous to the cortical integrity of the brain bc of location and extent of dmg and complications, including infection and hemorrhaging

closed head injury (CHI)

occurs bc of a rapid acceleration and deceleration, or both of the brain

acceleration

brain experiences significant physical force that propels it quickly from stationary to moving

deceleration

brain is already in motion, traveling at a certain speed, and then stops abruptly, sometimes simultaneously

impact injury

when physical forces acting on th brain tissue occur at the point of impact

countercoup injury

physical forces acting on the brain tissue occurring at the opposite pole of impact; brain "tears" away from skull
diffuse injury common and more likely in the frontal and temporal lobes bc of the uneven, "sandpaper-like" surface of the tentorial plates that hold those brain structures in place

Glasgow coma scale (GCS)

rapid, reliable measure of coma depth by assessing separate symptoms including language, consciousness and motor domains
scores range from 3 - 15, 3 being the deepest lvl of coma and 15 the mildest
some limitations due to eye swelling, drugs and endotracheal tube which prevents eye opening and verbal response

coma

a GCS score of 8 or less; patient cannot open eyes, make any recognizable sounds, and follow any commands
reliable measure of brain dmg and prognosis
comatose patients have sleep-wake cycles; it's not like being asleep
rated on a continuum, can be deep or light

edema

swelling of the brain
ICP often increases dramatically, causing diffuse dmg - severe and uncontrollable ICP is main COD in mod-severe head injury
surgeons routinely place intracranial monitoring catheters into ventricles or subarachnoid space

brain herniation

pathologic process associated with hematoma and increased ICP, which may result in displacement and deformation of the brain

transtentorial herniation

downward displacement of the parahippocampal gyrus and uncus of one (or both) temporal lobes through the tentorial hiatus

can place extreme pressure on brainstem, typically cutting off cranial nerve III (oculomotor nerve) and compromising integrity

subdural hematoma

a bleed btwn the dura and the arachnoid space
initial period of unconsciousness > prolonged interval of recovery in which bleed slowly enlarges, pushes brainstem laterally and downward > brain herniation, quickly deteriorating lvl of consciousness
symptoms: contralateral hemiparesis, ipsilateral pupil dilation, and changes in lvl of consciousness

extradural hematoma

bleed occurring btwn skull and dura; typically caused by bleeding of th large middle meningeal artery

epidural hematoma

bleed occurring btwn meninges and skull
cause most often related to rupture of an artery, but also as a result of dmg to meningeal vein or dural sinus

intracranial bleeding

collection of blood, typically clotted w/in the brain
difficult to treat, may require ER neurosurgery
appear in about 15% of fatal head injuries

linear skull fracture

relatively benign, resulting in a rather distinct, straight line

depressed skull fracture

more complicated; impact-driven skull fragments into the underlying dura and brain
location important; always creates possibility of infection, CSF leaks and bleeds as a result of rupture to the meningeal artery or large venous sinuses

post-traumatic epilepsy

seizures following a head injury, about 10% of CHI and 40% of PHI
onset can be delayed as much as 2 yrs
relate to the presence of scar tissue, specifically alterations in neuronal membrane function and its structure

concussion

mild head injury often entailing dizziness, fatigue, or headaches w/ no or only brief loss of consciousness

treatment of head injury

Airway: freeing the pharynx from blood and other obstructions (prevent anoxia)

Circulatory status: examine blood gases and pressure, initiate intravenous infusion

retrograde amnesia (post-traumatic amnesia)

loss of memory for the interval preceding the injury

anterograde amnesia (post-traumatic amnesia)

loss of memory for events after trauma or disease onset

diaschisis

passive process of uncovering working systems rather than an active process of repairing damaged systems (restitution)
complicated interplay and balance btwn excitatory and inhibitory functions

plasticity

behavioral or neural ability to reorganize after brain injury

immature nervous systems are much more plastic, therefore, children show less behavioral effect and recover faster from brain injury

axonal sprouting

regrowth of neurons that have been only partially damaged/severed

collateral sprouting

growth of nearby intact neurons

denervation supersensitivity

greater excitatory or inhibitory potential of remaining neurons in a lesioned area, in reaction to the neurotransmitters that act on them
mechanism appears to act via a proliferation of postsynaptic receptor sites

physical therapist (PT)

focus on motor control w/ the aim of improving physical functioning to the highest degree possible
defined by work with strength, balance, coordination, physical endurance, and range of motion
work primarily on muscles of the lower extremities

occupational therapist (OT)

focus on self-care activities, work activities and avocations
defined by function; work with sensory and perceptual-motor functioning, thinking, remembering, and problem solving
muscles of the upper extremities

speech therapist

provide therapy for patients experiencing a range of communication difficulties
focus on speech production, expressive language, hearing and understanding speech, reading, writing, and social use of language

therapeutic recreation

emphasize importance of recreational and leisure activities
helps in transfer of learning of skills acquired from OT and PT
helps in transition from hospital to home
skills gained from community outings include mobility: ramps, elevators, obstacles, etc. and daily living: money management, safety and nutritional awareness, etc.

cognitive remediation/retraining approach

stress retraining of an impaired skill through rebuilding axonal connections or finding compensatory strategies for the lost process
rests on theories of learning ad pedagogy

context-driven approach

training specific skills relevant to an individual's environment outside the hospital or laboratory setting

About this deck

By: Victoria Lake
Created: 2011-03-31
Size: 39 flashcards
Views: 5

About StudyBlue

“I have used this website for three exams, and I see a huge difference in my test results.”
Naj