WSU SLP 6480 week 12 traumatic brain injury

traumatic brain injury (TBI)

damage to the brain that occurs as a result of an external and usually forceful event; falls, traffic accidents, sports accidents, being struck by an object, violent assaults; does NOT include damage to the brain caused by disease/stroke/etc

individuals most at risk for TBI

people younger than 4 years old and older than 75 years old; adolescent males, alcohol/drug users, ppl w lower socioeconomic status, law enforcement/military personnel, individuals who have experienced past TBI

closed head injuries

forms of trauma causing damage to the brain that do not break an individual’s skull open and penetrate the cerebral meninges surrounding the brain; skull remains intact

2 types of closed head TBIs

acceleration-deceleration injuries and impact-based injuries

acceleration-deceleration closed head injuries

occur when a person’s body is moving very fast through space and then comes to a very abrupt halt suddenly enough to cause the person’s brain to slam into and bounce around inside the skull with damaging levels of force; diffuse axonal shearing and coup-countercoup

impact-based TBI

injury to the brain that occurs as a result of an individual’s head being hit by another object

open head traumatic brain injury

injury that penetrates the skull into the brain; an object penetrates the skull into the brain; common cause is ballistic trauma

secondary mechanisms of damage in TBI

refer to negative health effects that occur indirectly as a result of TBI; increased intracranial pressure (headaches), cerebral edema (swelling), traumatic hydrocephalus (water on the brain)

traumatic hemorrhage

bleeding of blood vessels as a result of trauma - whenever blood hits neurons, the neurons die because they are suffocated; 3 types: intracerebral, subdural, epidural

intracerebral hemorrage

traumatic hemorrhage within the brain itself

subdural hemorrhage

hemorrhage that occurs between the dura mater and the arachnoid mater

epidural hemorrhage

hemorrhage that occurs between the dura mater and the skull, when a blood vessel bursts and creates a pool of blood between dura mater and skull

hematoma

gathering of blood outside of a blood vessel following a hemorrhage

subdural hematoma

occurs when blood vessels between the dura mater and the brain are broken and bleed out in that space in between

epidural hematoma

occurs when a blood vessel bursts between the dura mater and the skull, creates a pool of blood there

post-traumatic epilepsy (PTE)

a seizure condition that occurs consequent to a TBI; these seizures cause additional damage to the brain and significantly and negatively affect prognosis for recovery of lost functions; most common after open head TBI like gunshot wounds

50% of those with open head wounds

experience some degree of post-traumatic epilepsy

shaken baby syndrome

the physical violence of a caregiver shaking the child and a common cause of traumatic brain injury and death in children

diffuse axonal shearing

occurs when neuronal connections are broken and create microlesions across large areas of the brain as a result of the brain being warped inside the skull by high levels of g-force

coup-contrecoup

a two-step profile of damage from an acceleration-deceleration-style closed head injury

coup portion of damage

occurs when a person’s head is slung forward to hit an object; the head comes to an abrupt halt, which causes the frontal lobes of the brain to impact the anterior inside of the skull

contrecoup portion of damage

occurs when the head ricochets backward from the initial impact and makes a second impact, damaging another portion of the brain

increased intracranial pressure

when the amount of intracranial pressure (pressure within the skull that is exerted on the brain) rises above normal; possible side effect of TBI

cerebral edema

the swelling of the brain tissue that occurs following trauma to the brain; can cause increased intracranial pressure

traumatic hydrocephalus

when the brain is unable to reabsorb excess cerebrospinal fluid thereby leading to increased intracranial pressure (water on the brain)

polytrauma

describes the multiple causes of trauma experienced by military service members following exposure to an improvised explosive devices’ (IEDs) blast

blast-induced trauma

the signature traumatic brain injury experienced by military personnel in modern warfare via exposure to IEDs

primary-level damage (polytrauma)

result of the shock wave created by the IED explosion

secondary-level damage (polytrauma)

result of flying debris and bomb fragments

tertiary-level damage (polytrauma)

result of physical displacement of the body when impacted by the force of the wind associated w the shock wave, can cause open or closed head TBIs and further trauma to the body and brain

quaternary-level damage (polytrauma)

inhalation of toxic gases, smoke, or dust, any burns sustained to the body, any trauma created by the blast that is not attributable to primary, secondary or tertiary mechanisms

barotrauma (polytrauma)

trauma after exposure to intense levels of pressure following an explosion, can affect the brain, eyes, & air-filled & fluid-filled organs in the abdomen

concussion

a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces; athletes are at risk of suffering multiple concussions because their symptoms might be unrecognized or the symptoms’ significance might be unknown

chronic traumatic encephalopathy (CTE)

a degenerative disease of the brain caused by repeated head trauma (such as repeated concussions in sports or repeated exposure to IED blasts); manifests as dementia, confusion, memory loss, headache, depression, and excessive aggression within months or years of brain damage

neurometabolic cascade

a wave of detrimental neurochemical changes to the brain that causes widespread neuronal and cognitive dysfunction following concussion; includes ionic flux, glucose hypermetabolism, & glucose hypometabolism

ionic flux

the widespread & unregulated release of ions through damaged cell membranes in the brain following concussion that pushes the brain far from homeostasis

glucose hypermetabolism

a period of rapid burning of glucose in the brain prompted by ionic flux that is an attempt to return the brain to homeostasis

glucose hypometabolism

a period of too little glucose in the brain to maintain normal energy levels that leads to a lack of energy, an energy crisis, that can persist for many days & cause cognitive deficits

TBI motor deficits

possibly include swallowing disorders, motor speech disorders, spastic bilateral paralysis or paresis, spastic contralateral hemiplegia ataxia

TBI cognitive deficits

possibly include personality changes, impaired arousal, orientation, attention, memory, problem solving, & inferencing, impulsivity, emotional lability, lack of motivation, underestimation of their deficits

photophobia

oversensitivity to light; common deficit following TBI

phonophobia

oversensitivity to sound; common TBI deficit

coma

period of unconsciousness lasting more than six hours during which the unconscious individual can’t be awakened & is unresponsive to sensory stimuli

vegetative state

when a person is minimally responsive to stimuli but lacking consciousness; labeled as persistent if lasts longer than 4 weeks

post-traumatic amnesia

a combination of retrograde & anterograde memory losses that present in individuals following TBI

minimally conscious state

when, following brain damage or coma, individuals show inconsistent but distinct behavioral signs of consciousness

personality changes following TBI

can result in inappropriate sexual advances, inappropriate statements at inappropriate times (pragmatic deficits), loss of awareness of social & cultural conventions, and milder alterations like changes in food & music preference

language deficits following TBI

are often present and can be dwarfed by deficits in arousal or cognition; individuals w generalized damage across large portions of the brain usually display some level of receptive & expressive deficit; individuals w open head TBI w focal damage it’s possible to have more specific deficits in the context of far fewer cognitive deficits than seen in closed head TBI

assessment of TBI deficits

formal assessments that test level of arousal, orientation, agitation, long-term memory, visual memory, immediate recall, & short-term recall; varies depending on individual’s age, education level, & severity of deficits; mirrors procedures used for aphasia & RHD

goals for TBI treatment

reflect the person’s deficits as identified in assessment; depends on the deficits’ severity, level, & impact on functioning, & the patient’s overall prognosis & stage of recovery

TBI treatment practices for arousal

sensory stimulation therapy, which includes visual stimulation, auditory stimulation, oral stimulation, olfactory stimulation, cutaneous stimulation, & gustatory stimulation

TBI treatment practices for working memory

instructions and utterances that are short, using functional tasks in the context of activities of daily living, avoiding speaking fast, emphasizing important words or phrases, increasing automaticity of responses, & breaking down complex tasks into individual components

3 primary social communication themes for treating TBI patients

cognitive, social competence, pragmatics

more TBI treatment practices

spaced retrieval training, internal memory strategies, external memory strategies, clients may benefit from participation in group-based treatment that targets pragmatic aspects of communication & that provides opportunities to practice newly learned strategies & skills

spaced retrieval training

involves presenting information and cuing the patient to recall the information over increasingly greater intervals of time

internal memory strategies

cognitive acts that increase the likelihood of retaining information over the short term and long term to compensate for memory deficits

external memory strategies

material devices used to allow compensation for memory deficits