Traumatic Brain Injury (TBI)

What is it?

1. An insult to the brain that is not degernerative or congenital( acquired). 
2. Caused by an external physical force that may produce a diminished or altered state of consiousness that causes an imporairment of cogitive abilities or phyiscal functioning. 
3. TBI is an injury

Epidemiology of TBI

1. 8-% have mild injuries--best chance for recovery. 
2. 15-19 and 75 and over populations have the highest incidence.
3. females typically have better recovery. 
4. Males 2x mroe likely to have TBI
5. mor common in low SES 
6. 0-4 also a vulnerable age group

Casuses of TBI

1. Transportation related 
2. falls
3. assults and abuse
4. alcohol use
5. war soldiers

Closed head injury

(Primary Mechanisms of Injury)

Penetrating head injury

(Primary Mechanisms of Injury)

**Coup & Contracoup

(Primary Mechanisms of Injury)

Where the contact of the brain within the cranium 

**

Diffused axonal shearing

(Primary Mechanisms of Injury)

meyalin sheath is taken away. the axon is very importnat in transimitting the neural impulses for neuro to neuron communication. 

Focal  contusions

(Primary Mechanisms of Injury)

Fancy word for bruises in a localized area with an increase in blood and fluid similar to a bruise on someones leg. 

Hemorrhage

(Secondary Damage after TBI)

Extra cerebral bleeding into the menengies. Intracerebral bleeding into the brain tissue. 

Cerebral edema

(Secondary Damage after TBI)

Swelling of the brain. Common around the primary cite of injury, but can be present throughout the brain. 

Intracranial Pressure

 (Secondary Damage after TBI)

increase of pressure within the skull do to accumulation of blood, verebral spinal fluid. 

• brian tissue is compressed and becomes displaced
• when arrive at ER this is the main focus to relieve pressure becuase the more pressure = more damage. 

Hypoxic-ischemic damage

(Secondary Damage after TBI)

Reduced oxgenation of the tissue and reduced blood flow. 

• Can result from increased cranial pressure
• Sometimes cardiopulminary can be injured, punctured lungs, heart issues may also cause this. 

Seizures

(Secondary Damage after TBI)

May occur within the first week and may be isolated events. Does not mean they will always have seizures

Late onset seizures, occur after the first week of injury. These can interfere with community reintegration and with therapy and employment. 

Life Expectancy

Morality after sever TBI is high in acute-post injury period

Short term: Primary cause of death is brain damage itself. Pnewmonia, mobility/spinal cor injuries, epilepsy, suicide, respiratory infections, diseases of circulatory system, nembolisms.

Long Term: age, males die more often than females, time sensitive (as time goes on less mortality), mobility (if abmbulatory more likely to survive). 

Complicated vs. Uncomplicated

(Mild TBI)

Complicated: where a person has a Glascocoma Scale of 13-15. Show some brain abnormailty on CT scan, complain of persistant cognitive and psychologic symptoms. 

Uncomplicated: no intercranial abnormality or skull fractures. Most mild TBI will not show up on CT or MRI scan. SPET may show some abnormality but isn't commonly used. 

Definition

(Mild TBI)

Traumatically induced physiological brain function

At least one of the following must co-occur:

1. loss of consiousness, 
2. loss of memory immediately before or after accident, 
3. alteration in mental state, or 
4. vocal neurological deficit that may or may not be transient. 

LOC

Loss of Consiousness

The loss of consiousness indicated severity of TBI

Pathoanatomy/physiology

(Mild TBI)

1. Normal strucutral neuorimaging studies.
2. Do not see as much sheering of axons--instead there is a twisting of axons and a stretching of axons. Gradually axons that are stretched and badly damaged will swell and seperate. 
3. S-100B: bio-chemical marker (neuroprotein) that has shown to be a reliable marker for brain damage. 

Neuro-psychological outcome

(Mild TBI)

1. Post-traumatic amnesia (PTA): if have greater than 30 minutes, is associated with worse ammediate outcome following a MTBI.
2. MTBI's don't typically have long lasting effects. 
3. 10-20% have incomplete recovery. 

Post- Concussive Disorder

1. Concussion = MTBI
2. controversial diagnosis
3. Diagnoistic Criteria: History of head trauma with LOC preceding the symptoms by a period of up to 4 weeks. 
4. Need 3/6 symptoms and LOC: diziness/headaches, emotional changes, concentration complaints, memory, insomnia, decreased tolerance to alcohol, hypochondriac. 

Sport Related Concussion

Most occur without LOC--TF not concussion disorder

Definition: concussion is a trauma induced alteration in mental status that may or may not occur with LOC

How get/what is? acceleration and deceleration, low levels of axonal stretching that occur with concussion, limited cell death, decreased cerbral blood flow, impairment of neural transmission (disoriented), brief. 

Injury Severity Markers 

Sports related concussion

1. LOC=brief coma, eye typically closed, athlete is unresponsive to any type of stimuli, less than 1-2 min. brief=hard to id. 
2. confusion-impaired awareness? daxy starry eyed, forgets play prior or after event, clumsey movement. answer questions slowly?
3. amnesia-retrograde: dificulty with memory of event prior to the injury. anterograde: difficult with memory after injury. 

Outcome and Effects

(Sports related concussion)

1. tend to recover 2-14 days post ocncussion
2. cummulative effects: 

•  NFL athlete with 3 or more concucssions did more poorly on neuropsych tests than those with less than 3
• Amteur/highschool/univeristy athletes seem to have more of an effect with repeated consusion on neuropsych tests. 
• long lasting don't know

Cognitive Disturbances after TBI

1. attention/concentration: alterness levels tend to be reduced, unsustained attention is reduded, speech of processing slows down, pragmatic ability is lessend.
2. perception: dependent on attention, visual/perceptual issues. visual neglect/field cuts
3. memory and learning: big part. these are the most common complaints. severity of memoory loss will ary depending on severity of TBi. see amnesia but long term memory remains more intact that working memory. If have long term memory problems indicate increased severity. 
4. Exectuative Functions: target of what therapy for TBI focuses. Impaired resoning, insight, inability to moniotr and self-awareness, problem solving, planning
5. OVeral confusion, disorganization, impaired learning, limited insigt, and limited planning. 

Language Disturbances after TBI

1. linguistic characteristics: verbose, verbal disorganized, hard to follow story, fluency/recall problems, syntactic comp, erbal output may be repetitive, not very detailed.
2. discourse: disorganized becuase of memory problems
3. pragmaitcs: prosody probkems, topic selction, and tengential. 

Behavior and Personality Changes 

(TBI)

Difficult to adjust to for person and family.

Likely to see: aggresion, irratibility, emotiaonl volatility, impulsivity, deperession, lack of interest, reduced motivaiton

Factors Contributing to Outcome

1. Preinjury factors

• Age, social adjustment, neurological integrity, knowledge base

1. Postinjury Factors

• Early medical intervention, early rehab, long term supports, individual characteristics. 

TBI Care Continuum

1. trauma center and ER
2. neurosugery unit and acute hospitalization
3. nursing home and long-term care programs
4. acute rehab
5. tansitional living center
6. day treatment and outpaitent rehabilition
7. supervised indpendent living center and support services
8. vocational rehab

Rancho Los Amigos Hospital Levels of Cognitive Functioning

Based on responsiveness, purposeful activity, orientation, memory, self regualtion, spontaneity, independence. 

Early Stage: (RLA levels 2-3)

Middle Stage: (RLA levels 4-6)

Late Stage: (RLA levels 7, 8+) 

Glasgow Coma Scale

Medical rating system to measure the depth or quality of a brain injury. It allows medical personnel to grade the level of consciousness. Which helps plan their medical care and predict functional outcomes. The initital assessment is given in the ER. 

Scored on a scale ofo 3-15.

Less than 8= severe TBI

9-12 = moderate TBI

13-15 = Mild TBI

Assessment Issues of Cognitive-Language Disorders

Few instruments available. Those aren't always standardized. Sometimes use aphasia assessments.

Rating scales hard to track little movements-small progress not noticed

Dilemmas in assments: population, test instruments, interdiciplinary concerns, rating scales?

Assessment Issues of Cognitive-Language Disorders

(Processes vs. Function)

Processes: acknowledges that information is processed through different sequences. Analyzze the process and determine where the breakdown is. (traditional method approach)

Function: How does communication function in their life, how do they use langauge?

Assessment Issues of Cognitive-Language Disorders

Pre-onset factors & variables

Pre-onset factors: need information about this to be able to adequately assess where they came from, where they are, and where they are going as far as functionality and use of langauge. 

Assessment variables: rate of presentation is important becuase many TBI patients have processing problems. 

1. review of reasons to assess: track progress, give direction to tx, diagnosis, gather info to educate family.
2. Standardized instruments:

• Ross INofrmation Processing Assessment: orientation and processing. 1-5 scale; qualitative
• LATB: scale
• FARVERS (Functional assessment of verbal reasoning and executive strategies): laminated guide and asks the pt to find info on them or respond to the guide.

1. Nonstandardized instruments: systematic obersrvations in natural settings. 

Impairment level: use standardized test. 

Activity-Oriented assessment: observe function tasks in everyday life

Participation-Oriented assessment: interested in quality of life inventories. observation/interviews. 

use primarily nonstandardized testing, systemative preentation of certain stimuli. Tctile-rough, sound-lound. Alther amount of stimuli someone is getting and see how react. more response/consistent response is what you are looking for. 

SLP is respponsible for defining level of alertness for patient and ability to attend, responsiveness, receptive and expressive comm. Assess aduitory with bells, claping, music voice. Smells with perfumes, spice, soaps. Visual with family pictures, mirror. Tast with lemon, vinegar. 

Assessment at Levels VI, VII, and VIII

Assessment varies. At this stage can stand to have more of a standardized assessment, depending on severyity/type/communication needs of patient. 

Stage VI: SLP might want to focus on process and performance using functional ativites and look for where the breakdown occurs

Stage VII-VIII: SLP might use specific activities (grooming, meals). Appropriate for standardized assessment. 

Forms of Intervention

1. Facilitation of spontaneous recovery: the brain is recovering itself and we are helping things by providing stimulation and activities chosen to target deficits
2. Direct Retraining of Cognitive or Task Components: Targeted drill and practice
3. Retraining Functional-Inegrative Skills: skills that you practive behaviors not cognitive components. INtervention focuses on grooming, insetead of selective attention. 
4. Environmental Compensation: can be used at any stage. Adjustments amy be necessary to their environment. might need to adapt through educating people or modify environment so patient can funciton within their own space despite deficits. Ex: routines 
5. Personal Compensations: patients with residual cognitive deficits may be able to compensate for those deficits deliberately. Overt personal compensations like log books or asking speaker to slow down. This helps compensate for impaired memory.

Routine Based Intervention

Routine: central to TBI patients. Creates a behaviors chain: Bhavior->response->behavior->response. Implies normal activity of life. 

Supports: working with people in the environemnt who the patient is interacting with to ensure they are there and consistant. Long term the goal is to decrease supportd and make patient independent. 

Progression of intervention: follows sequence that can id what is successful and unsuccessful. 

Functional Approach Support

Theoretical: Vygotskyian theory. congnition in context=way we think related to the way we interact socially.

neuropsychological: learning comes from consequences. Learning means memory of last behaviors. consequences most apparent in function activities

Empirical: more data showing that not functional activities may have trouble genralizing

economic: decrease the inpatient time spent, more accomplished, less time. 

Dementia

Role of SLP

interrelationship bt cognition and langauge serves as the basis for effetice communication. A cognitive impairment can result in communication breakdown, requiring speech langauge intervention to improve functional ability. 

SLPs have a role in screening, assessment, and training caregier on effective ways to communicate with people who have memory impairments.

What is Dementia?

Syndrome that can be defined as the chornic, progressive deterioration of intellect, personalty memory, and communicative function resulting from central nervous system dysfunction. 

Some type of CNS neuropathology, and when the brain strats to atrophy, the person and what makes them that person begin to be altered. 

Diagnositic Critera

Dementia

1. Presence of multiple cognitive deficits including  both: evidence of short and long term memory impairment & at least one of the following: aphasia, apraxia, agnoisa, impaired executive functioning. 
2. Distrubances in 1 and 2 result in significant problems with employment
3. does not occur exclusively with delirium

Casues of Dementia

1. Irreversible Dementias

• Primary degenerative diseases: Alzheimer's Parkinsons
• Vascular: multi infarct dementia (tiny strokes)

1. Reversible dementia: vitamin deficiencies, metabloic disorders.

Causes of Non reversible Dementias

Dementia of the Alzheimer's type (DAT)

1. gradual onset and progressive cognitive deterioration
2. cognitive deficits not due to

• other CNS etiologies (parkinsons)
• systematic condistions (kidney or heart problems)
• sustance-induced conditions

1. cognitive deficits are not due to axis 1 disorder (schizo or major depressive disorder)

This is a diagnosis of exclusion. 

DAT (dementia alzheimer's type)

Alzheimers (AD) most common cause of dementia

Typically beings in the perirhina, hippocampus (memory), temproal lobes, and basal forebrain.

Frontal lobe is important in episodic memory see change in this. As disease progresses posteriorly to the parietal and temporal, semantic memory will be affected. 

DAT Neuropathology Specifics

1. Neurofibrillary tangles: fibers are twisted in neurons and consist of the protein A68 and it is twisted into perifilimients
2. Senile Plaques (amaloid plawues): accumulation of these plawues between the neurons in the brain of AD people. Amaloid is a protein that is typically produced in the normal brain. Beta-Amaloid is a ragments of a protein that comes from another protein Amaloid precurser. In a normal brain the fragments happen, but are broken down-in AD brain not broken down and stay in brain.
3. diffuse loss of neurons: AD patients have brains that are about 10% smaller. Lose most in medial temporal. And also in tempral and frontal lobes, hippocampus, amygdala, and some brainstem nuclei. Sulci are wider in AD and shrinkage of the gyri. Ventricles are enlagred and NT change so there is less communication
4. Why? unclear and unknown.

Risk factors for AD

1. age. every decade after 50 # of people with AD doubles.

2. family history

3. 3 genes related to early onset

4. less education = more likely to develop

5. history of head trauma.

6. being female-we live longer

7. older/younger age of mother

8. 2 copies of the type 4 allele of apoliprprotein E- cholesterol repairing protein

9. exercise and diet-increased omega 3 help ward off AD. 

average duraiton is 8 years

rapid decline linked to:

early onset (40s/50s)

preence of delusions or hallucinations

presence of extrapyramidal signs-some kind of damage to the basal ganglia. 

Medications for AD

Aricept

exelon

razadyne

Mild AD-General Characteristics

Mental Status: disoriented for time

Motor Function: good. 

Memory: impaired working memory (what did I have for lunch?) impaired declarative and some semenatic and episodic memory. 

Intellect: problem-solving deficit

Olfaction: affected (perihrinal area)

Visuospation: mildly affected

Toileting: unaffected

Mild AD- Linguistic Characteristics

Form: intact

Content: affected-> shrinking vocab, less to say, referencing errors, lack of cohesion, repetitious, retention of social phrases

Use: affected-> comprehends but forgets, insensitive to contexual effects, lexical access difficulties, repeats, tangential, misses humor, less able to define. 

Complaint is word finding, finding objects, difficulty writing email, open ended sentences. 

mental status: disoriented for time and place

mortor function: ambulatory but increased restlesses

memory: impaired workin gand declaritive memory

intellect: obvious deficits

olfaction: affected

visuospatial: viusal-perceptual and constructive deficits evident

toileting: may be incontinent

Moderate AD- Linguistic Characteristics

Form: intact

Content: makedly affected-> decreased output, reference errors, empty langauge, tangential, still use social phrases. 

use: markedly affected-> dysnoia, comprehension of wirtten and spoken langauge, insensitve to context humor, concrete, can read aloud, and comprehend at word level 

*a lot like mild just more impaired

Severe AD-general characteristics

Mental status: disoriented for time, place, and person

Motor function: impaired, may have rigidity, may be non ambulatory

memory: global failure of working and declaritive memory systems

intellect: devastated

olfactionL affected

visuospatial: makedly affected

Toileting: incontinent of bladder and bowel

form: still intact

content: bizarre and meaningless

use: virtual inability to use langauge for purpose

*little if any effection verbal comm. May also have difficulty comprehending spoken or written lanaguage. May still have reflexive use of soaical phrases. 

Pick's Disease (Frontotemporal Dementia) 

Starts earlier: 40-60 years

Very rare

lots of atrophy in frontotemporal lobe. Parietal lobe spared. includes inferior motor areas=can have motor problems

Cognitie impairment: usually some personality changes; can lose tact; poor judgement; recent/working memory tends to decline quickly, impulsive

Linguistic impairment: more difficulty with form than content. communication more affected than memory. echolalia, audiotry agnosia (interp of senses), anomia

Can look like primary progressive aphaisa. 

laps bt language and memory problems can be several years. word recall first thing to go. 

etiology: related to repeated strokes. 

deficits depend on where strokes are. Typically the strokes are distributed throughout the brain and can ahve a variety of symptoms. 

stepwise decline

cognitive disorders 

linguistic impairment

parkinson's disease

Patients in the later stages can demonstrate aphasia or apraxia

HIV assoc. dementia

Cognitive-linguistic impairments: more motor problems because cerebellum becomes involved—coordination of movements. Aphasia develops, muteism towards the end

sensory stores-have direst intervation with the environment and have a high capacity. it contains more info that will be filtered into cognitive processing. 

This is a playback system. Incoming info sustained long enough for mroe processing. 

iconic (visual store): visual information-it decays within half a second

Echoic: transient auditory store holding relatively unprocessed input information and decays within 2 seconds. Ex: asked a question say what, but then answer before get a response. 

2 characteristics: (1) limited capacity-only about 7 digits. (2) fragility of storage- if something is said, any kind of distraction will help you forget. 

recency effects-if you give a patient a list of items to list and recall, the items at the end of the list will be easier to recall

Double dissociation-see evidence bt distinction of short term and long term memory. 

Baddeley and Hitch proposed this. 

memory in consicience awareness and the ations of the conscience awake perosn. 

Replace STM with working memory

Articulatory phonological loop: makes it possible for the sub vocal rehersal of things hear. 

visuospatial sketch pad: subvisual rehersal as we think of what something might look like. 

central executive-helps focus attention on what is important and helps to encode information, retrieve information for long term stores and helps plan and help solve problems 

prefrontal regions of frontal lobes are ESSENTIAL for working memory. PFCortext extensiely connected with sensory processing. 

articulatory phonological loop: (broca's area, inferior parietal, inferior temporal cortex). 

Visual spacial sketch pade: occipitoparietal cortex. 

1. fact memory
2. facutal information that can be declared
3. explicit memory
4. cn be consiously reclled like facts
5. requires consience control, not automatic, more effort than non-declaritive. 

1. conceptual knowledge is represented
2. concepts are constructs we form about the world bsed on our experiences
3. not limited to words-can also include nonlinguistic concepts

Episodic memory (declarative LTM)

semantic memory + context

1. system that receies and stores info about a temporally dated episode/event and temporal-spatial relations among them
2. play golf=semantic, remembering the event is episodic. 
3. chrologic memory
4. helps recall past events
5. emotional events stay with us longer. 

memory for words, referents, and meaning, spelling, and pronunciation

some believe this is a subsystem of semantic memory. 

Neural subtrates of declarative memory

(3)

1. cortex-factual knowlwedge is fairly well distributed through out the brain (typically L hemisphere and dominant for word recall. the occipital is more activated for visual memory). 
2. parahippocampal region-includes the amygdala (anterior to the hippocampus) very important in emotional processing. amygdala modulates declarative memory based on emotions
3. hippocampus-extremely important in memory especially with episodicmemory. affected by stress. glucochoticoids are in our bodies when under stress get a burst of sugar/energy release. this is good in short term but long term will attack hippocampal system. 

motor skills

cognitive skills

priming

motor procedures that are learned an the processes that support them

performance of an action

neural substrates: cerebrellum, motor cortex, basal ganglia