CSD 4270 Medical Speech Pathology Exam 2 Study Guide
"Reversible" forms of dementia
(10-15%) of Dementias are reversible Reversible or improves with treatment (most do not reverse to normal or some relapse) Causes: drugs, hydrocephalus, subdural hematoma, neoplasm, infections, inflammations, metabolic disturbances (Wilson's disease, B12 deficiency) Characteristics: shorter duration of symptoms, less severe dementia and more frequent use of prescription drugs
Direct Activation Pathway (Part of the UMN System)
(A.k.a. pyramidal or direct motor system) Directs skilled, discrete voluntary (consciously controlled) movements (speech) Facilitory Main launching area is primary motor cortex,premotor cortex, supplementary motor area Corticobulbar Tracts (control cranial nerves) Corticospinal tracts (control spinal nerves) Pathways originate in cortex of one hemisphere and terminate in the Cr. and spinal nuclei that innervate speech of the side of the body opposite the cerebral cortex of origin(e.g. left hemisphere stroke causes right sided paralysis) Also true for lower face (VII) and tongue (XII) Other cranial nerves receive bilateral input from DAP and IAP (i.e. serves protective function). Therefore, unilateral UMN lesions have minor effects on V, IX, X, XII.
signs of dysarthria
*May have the following: -Have "slurred" or "mumbled" speech that can be hard to understand. -Speak slowly. -Talk too fast. -Speak softly. -Not be able to move your tongue, lips, and jaw very well. Sound robotic or choppy. -Have changes in your voice. You may sound hoarse or breathy. Or, you may sound like you have a stuffy nose or are talking out of your nose.
subtypes of dysarthria
*based on how those valves are functioning and where the lesions and damages reside for which type of dysarthria is at play subdivided into categories: 1. flaccid 2. spastic (sounds like holding back a cry even though that is not how she feels) (tightness) 3. ataxic--cerebellar tumor/tumor from cerebellum; some articulatory imprecision/bad articulation 4. hypokinetic 5. hyperkinetic 6. unilateral upper motor neuron
purpose of mini mental state exam (MMSE)
*is a brief screening test originally developed to provide a quantitative assessment of cognitive performance
indirect strategies
*used for manipulating the environment of those with dementia are the use of external memory aids *posting relevant info where an individual with dementia can see and access the info helps to keep the affected individual oriented and calm Examples: -calendars that highlight the date -digital clocks that give the time of day -photos of family and loved ones -labeling cupboards, cabinets, and drawers in the kitchen and bathroom and other important locations in the house can also keep an individual with dementia functioning at higher levels for longer periods of time -playing music that is familiar and preferred by the affected individual also helps maintain orientation and reduce agitation -manipulating the communicative environment -turning off the TV/radio -closing the door or window to limit noise -closing the blinds to limit visual distractions
purpose of modified mini mental state exam (3MS)
*was developed to expand the usefulness of the MMSE by providing an expanded scoring system and additional subtests
Role of SLP
+ to recognize, appropraitely diagnose, and provide therapy for cognitive, communication, or swallowing deficits occurring as a result of dementia or dementia-producing illnesses +can teach behavirial or dietary modificiations to minimize swallowing difficulties +can also teach the patient to adapt to mild declines in language, speech, and cognition using compensatory strategies +regularly reevaluates the patient's chewing and swallow abilities as cognitive and motor deficits progress
ABCD testing strengths
+comprehensive assessment for investigating functioning of patients with dementia +quick to administer +now being administered to Parkinson's patients, stroke patients with and without aphasia, TBI, and depressed patients although no norms are available +manual is well written and easy to follow +easy scoring to learn and implement
ABCD Subtests
+mental status +story retelling immediate +following commands +comparative questions +word learning +repetition +object description +reading comprehension +generative naming semantic category +confrontation naming +concept definition +generative drawing +figure copying +story retelling delayed ---may be administered in isolation
Frontotemporal Dementia (FTD)
---is a category of degenerative diseases that are associated with the degeneration of the frontal and temporal lobes ---is the dgeneration of the frontal and temporal lobes ---this category of dementia includes Pick's disease, the primary progressive aphasias, and semantic dementia
reminiscnece therapy
---is a semicued conversation regarding past events or the affected individual's past experiences and activities that work to increase orientation and trigger recall of pleasant long-term or episodic memory ---SLP must focus on stimulating positive memories and evoking positive emotions ---emphasizing or discussing negative experiences and evoking negative emotions are NOT likely to pay off in a positive way
Errorless learning therapy
---is when the difficulty level of a task set well within the ability of the patient to maximize patient success and minimize patient failure ---researchers who have examined errorless learning approaches conclude that errorless learning therapies for anomia and memory deficits are effective in remediation of these deficits to some degree
Etiology of Spastic (stiff) Dysarthria (bilateral damage)
--60% of cases accounted for byvascular or degenerative etiologies) --Vascular (non-hemorrhagic) --Degenerative disease: Primary lateralsclerosis --Other causes: TBI, MS, Tumors
Dysarthria/Slurred Speech
--A collective name for a group of speechdisorders resulting from disturbances inmuscular control over the speech mechanismdue to damage of the central or peripheralnervous system. It designates problems inoral communication due to paralysis,weakness, or incoordination of the speechmusculature hypernasality are intact with everything --convert thought into linguistic code --is where you have difficulty speaking because the muscles you use for speech are weak --can be caused by conditions that damage your brain or nerves and some medicines --speech and language therapy can help (can happen with other speech and language problems) --common causes=extreme fatigue, intoxication, reading difficult text aloud, recent oral anesthesia, lack of teeth, concussion IMO sounds like a demon or Cookie Monster talking
direct activation pathway/ Pyramidal System, Direct Motor System
--Corticobulbar tracts --Corticospinal tracts Fibertracts originate in motor cortex and terminate in cranial nerve motor nuclei in brainstem (i.e. corticobulbar) or originate inmotor cortex and terminate in spinal nervemotor nuclei in spinal cord (i.e.,corticospinal)
Effects of Damage to the FCP/LMN
--Damage prevents normal activation of muscle fibers --Denervation - partial (paresis),complete (paralysis). All motor activities affected equally voluntary(smile) or automatic/reflexive (smile) Denervation can be unilateral or bilateral (affects the muscles supplied by the R or L cranial nerve). --Atrophy (shrinking or loss of bulk) ofmuscle tissue and tone (hypotonia) --Diminished reflexes (Hyporeflexia vs.are flexia). Why? --Excess or spontaneous motor activity on surface of skin (seen asfasciculations), can't see fibrillations
Systematic Review
--Mild and mild-moderate dementia may learn (relearn)facts and procedures using specific cognitive intervention strategies. (*not for mod-severe/severe). --SR is the most promising technique. --Intervention tasks should be functional and ecologically valid facts and procedures. -- Improvement on training items, but generalization and long term maintenance may be limited. --No improvement in overall cognitive fixing from training on specific tasks and information.
an important SLP principle in dysarthria
--Neurologic disease can affect motor speech processes in a manner that reflects... the localization & underlying pathophysiology of the neurologic disturbance. Dysarthrias are perceptually distinct. SLP's recognition of these perceptual characteristics can contribute to the localization and diagnosis of neurologic illness
Final Common pathway(a.k.a. Lower Motor Neuron-LMN)Structures and Functions
--Peripheral mechanism through which all motor activity is mediated. Other motor divisions of the CNS must act through it to influence movement. -- Final link to speech muscles of messages"written" and controlled elsewhere ("motor flunky"). --Carries out UMN commands for voluntary movements and postural adjustments. Stimulates muscle contraction and movement --Consists of cranial and spinal nerves --Mediates reflexes (e.g. gag) --The Motor Unit? Innervation ratio?
Spastic Dysarthria Review
--Results from bilateral damage to the direct and indirect activation pathways (UMN's) --Combined effects of spasticity and weakness on speed, range and force of movement account for most of the deviant speech characteristics --Clinical signs are weakness, loss of skilled movements, spasticity, hyperactive reflexes and pathologic reflexes (e.g. sucking, jawjerk) --Slow and regular speech AMR's (Alternating movement rate) --Dysphagia and pseudobulbar affect arecommon --Prosodic excess (excess and equal stress), articulatory-resonatory incompetence, prosodic insufficiency, and phonatory stenosis (strained-strangled quality)
Dementia Patient Video From Recorded Lecture Symptoms
--Tendency to repeat phrases --Tendency to have a degree of emptiness to overall speech --Lacks factual material > does a good job of camouflaging and minimizing her deficits --Vagueness to picture description --Had a degree of distraction from original task that she was asked to do which was describing the picture
management of dementia patients
--The SLP has a critical role in the management of dementia patients in relation to diagnosis, monitoring development of the syndrome, identifying most effective means of communicating with the dementia patient, assessing efficacy of pharmacological and other therapies, and counseling the family. --Early therapeutic intervention in the disease is important so that families can get information about how to maximize communicative performance. --Caregiver education is a critical step in therapy. Clinical experience has demonstrated improvement in interpersonal relations between the caregiver and the patient when the caregiver understands the nature of the linguistic and intellectual problems experienced by the patient. --In the early stages of dementia, families are generally ignorant of neuropathology and its consequences and frequently misinterpret the behaviors of the affected individual. When apathy, depression, confusion, forgetfulness, and other features of early dementia are explainable, caregivers become more objective and less likely to feel angry toward the affected individual. --In addition to educating the family about communication deficits of their loved one, clinicians should explore the efficacy of various techniques for improving the communicative function of the patient. --One aspect of exploration should be evaluation of the communicative skills of the caregiver. Many caregivers have sensory deficits and communication habits detrimental to effective communication. --To improve communication with the patient with dementia, the caregiver generally needs instruction about the process of communication. Caregivers are often unaware of variables under their control when communicating with the dementia patient, variables such as: 1. the topic 2. amount of new information 3. amount of redundancy 4. speaking rate 5. number of conversants 6. complexity of syntax 7. word choice
indirect activation pathway/ Extrapyramidal System, Indirect Motor System "milk run"
--Tracts originate in motor cortex and synapse with other structures (basal ganglia before terminating in CR. andSP. N. motor nuclei in brainstem and spinal cord. Note: The direct (pyramidal) and indirect(extrapyramidal) motor systems together form"the upper motor neuron" system (UMN).
Management of Motor Speech Disorders
--What is the overarching goal of management? *To maximize the effectiveness, efficiency and naturalness of communication --How do we achieve this goal? --Do we treat everyone with a motor speech disorder? Medical diagnosis and prognosis? Disability and Handicap? Patient Motivation and needs Associated Problems Health Care System (access, insurance coverage?) --Focus of Treatment understand the neuropathology strength training makes little to no difference a plan for when treatment is going to end --How long do you treat? --Factors influencing duration of treatment: Predicting course of recovery Severity of deficits Specific goals and techniques of management Patient's motivation and communication needs Duration of hospitalization Patients ability to travel for outpatient services Health care coverage
Dementia
--a major neurocognitive disorder --is one of the most common syndromes that SLP encounters when working outside of the pediatric population --an acquired global loss of brain function with a slow insidious onset caused by a variety of diseases --NOT a single entity --an umbrella generic term that encompasses many subtypes --no consensus on classification of dementia but some prefer to subtype according to where brain pathology resides i.e. cortical, subcortical, mixed --an acquired persistent compromise in intellectual function with impairments in at least 3 of the following spheres of mental activity: 1) language memory 2) visuospatial skills 3) personality 4) cognition
Flaccid Dysarthria
--a motor speech disorder resulting from flaccid weakness or paralysis of musculature used to produce speech --results from damage to peripherial nervous system (cranial or spinal nerves) or lower motor neuron system --affects respiration, phonation, resonance, and articulation depending on which nerves are damaged --nasopharyngeal vowel damaged --breathy and wetness in his secretions --wet cough --weak jaw and drooling --injury or malfunction of one or more of the cranial or spinal nerves --offending lesion is always between the brainstem or spinal cord and the muscles of speech --can have unilateral or bilateral nerve damage and can affect overall speech affect --isolated or damage to group of nerves can have an effect --distortion in articulations --reduced tone --diminished reflexes Clinical Characteristics: -weakness: paralysis or paresis -hypotonia -diminished reflexes -atrophy -visible fasicuculations + invisible fibrillations
Mini-Mental State Examination (MMSE)
--also known as the Folstein test --takes about 10 minutes to administer --the most commonly used screen and is used with a variety of disorders, not just dementia --no training is required to administer
environmental manipulations
--are meant to keep the individual with dementia safe, calm, oriented with the environment being altered to keep the individual with dementia safe and welcomed Examples: 1. Remove all firearms and weapons from the house 2. Minimize the number of mirrors in the house which some individuals with dementia find to be agitating 3. Lock up poisonous substances 4. Use nightlights 5. Place decals on glass doors to keep the individual with dementia from walking into or through the glass 6. Utilize nonslip mats in the bathrooms 7. Post signs on doors identifying which room is which (eg bathroom, bedroom) 8. Keep the keys to the car secured to prevent the individual from driving if it is deemed dangerous for them to do so 9. Have an identification bracelet made with the individual's name and home address
trigeneral nerves
--facial sensation and sensation of the oral cavity (teeth, hard palate, tongue, gums, lips) --when dentist injects, they are blocking a nerve in this region --really important for chewing/mastication and opening and closing the jaw
hyperkinesias/hyperkinesis
--hyperactivitiy --opposite of hypokinesia --is a state of excessive restlessness
Pick's Disease
--is a dementia resulting from progressive degeneration of and damage to the frontal and temporal lobes changes in personality, behaviorial abnormalities, antisocial and inappropriate behavior, memory loss --is a progressive terminal illness that is characterized by early behavioral, emotional, and personality changes in the absence of significant language deficits
lacunar state/lacunar syndrome
--is the result of multiple subcortical thrombotic ischemic strokes occurring in small and deep blood vessels that supply blood flow to the brain stem, basal ganglia, and other subcortical structures --a form of vascular dementia
Pseudobulbar
--pathological laughing and crying (PLC)--often associated with Alzheimer's, ALS, MS, Parkinson's stroke, TBI --inappropriate involuntary laughing and crying due to a nervous system disorder --an involuntary and uncontrollable reaction and episode of laughter and crying that is disproportionate to an event. --the crying or laughing may start as a response to a situation, such as a sad movie, but the feelings are more intense and last longer than expected. --they're difficult or impossible to stop.
fasiculations/ muscle twitch
--shakiness to voice --a brief and spontaneous contractions or twitch in a muscle affecting a small number of muscle fibers often causing a flicker of movement under the skin --can be a symptom of disease of the motor neurons --lower motor damage bumpy tongue=atrophy
Geriatric Depression Scale (GDS)
--takes 10 minutes to administer --used to assess the presence of depression in older adults --the presence of dementia can confound results so the possibility and presence of dementia needs to be assessed separately so that SLP can differentiate whether the results are from dementia or depression
Global Deterioration Scale (GDS)
--takes about 2 minutes to administer --used to rate level of dementia with a 7 stage scale and to track detorioriation over time
Alzheimer's Disease Assessment Scale (ADAS)
--takes about 45 minutes to administer --this scale is designed to evaluate the cognitive and noncognitive manifestations of Alzheimer's disease
Dependence Scale
--takes about 5 minutes to administer --this rating scale is designed to assess the level of dependence of the individual with dementia --is generally to assess the need for institutionalization
atrophy
--the wasting away of a body organ or tissue; any progressive decline or failure; (v.) to waste away --can have diminished reflex --shrinking or loss of bulk --bumpy tongue when having fasiculations
Neuromuscular Deficits associated with Flaccid Dysarthria
-Direction is normal -Tone is reduced (hypotonia) -Range is reduced due to movement -Rhythm is regular no sign of dysrhythmia -Rate is slow/normal (bilateral vs.unilateral?) -Force is weak
symptoms of dementia Cognitive changes
-Memory loss, which is usually noticed by someone else -Difficulty communicating or finding words -Difficulty with visual and spatial abilities, such as getting lost while driving -Difficulty reasoning or problem-solving -Difficulty handling complex tasks -Difficulty with planning and organizing -Difficulty with coordination and motor functions -Confusion and disorientation
Symptoms of dementia Psychological changes
-Personality changes -Depression -Anxiety -Inappropriate behavior -Paranoia -Agitation -Hallucinations
risk factors that can NOT be changed w/ dementia
-age -family history -Down Syndrome
complications with dementia
-death -Poor nutrition -Pneumonia -Inability to perform -self-care tasks -Personal safety challenges
risk factors you CAN change w/ dementia
-diet and exercise -excessive alcohol use -cardiovascular risk factors -Depression -Diabetes -Smoking -Air pollution -Head trauma -Sleep disturbances -Vitamin and nutritional deficiencies -Medications that can worsen memory
latest/final stage of dementia
-difficulty initiating conversation -no meaningful speech
Symptoms of mid-stage Alzheimer's
-disorientation -short term memory loss continues to worsen -attention deficits -more dramatic personality changes -visuospatial deficits -visuoconstructive deficits -wanderlust -general confusion -bladder incontinence -sleep disturbances -sundowner syndrome
risk factors of DAT
-family history -Down Syndrome -family history of Down Syndrome(10-23% likelihood for those with parents and siblings of someone with DAT, early onset, 14-50 years, increased risk factor for siblings up to 40%) -depression -hypertension -head trauma -little exercise
Brainstem CVA- JC- Anarthria
-is speechlessness due to a severe loss of neuromuscular control over the speech musculature -is the most severe form of dsyarthria -language and cognition may be intact -but the neuromuscular disorder prevents speech -anarthric patients are motivated to speak but are unable Video Case Illustration-Multiple Cranial Nerve Involvement Multiple "Valves" Impaired (i.e.,articulatory, laryngeal, velopharyngeal)
Symptoms of late stage Alzheimer's
-lack of motor function -bedridden -incontinence -unresponsiveness -severe to profound memory deficits -severe to profound cognitive deficits -dysphagia -mutism -fluent but empty speech
latest stage of dementia
-motor problems (later) -weight loss -complete incontinence
ABCD testing weaknesses
-norming sample was limited questionable generalization to other populations -no inter-intrajudge reliability -words on stimulus cards are small -four of the subtests (concept definition, object description, figure copying, and generative drawing) -4 of the subjects require subjective analysis
GDS stage 5
-patient cannot survive without some assistance from others due to disorientation to time and place -patient has knowledge of major facts about themselves -patient may clothe self inappropriately
GDS stage 4
-patient has decreased knowledge of current and recent events -patient has difficulty remembering personal knowledge -patient has difficulty of orientation of where they are -patient denies symptoms -patient does not recognize familiar people
GDS stage 6
-patient is unaware of recent events and their surroundings -patient can distinguish familiar people from unfamiliar people -patient demonstrates personality and emotional changes (delusional behavior, obsessive behavior, anxiety)
GDS stage 7
-patient loses verbal ability (often there is no speech at all) -patient loses basic psychomotor skills (ability to walk)-the brain appears no longer able to tell the body what to do
GDS stage 3
-patients gets lost -other people notice a change in the patient -patient has word and name finding deficits (anomia) -pateints retain little info during oral reading -patient misplaces valued objects -patient demonstrates concentration difficulties during clinical testing
moderate to severe dementia
-picking at teeth -persistent desire and agitation to scratching and itching -cannot remember names -forgets that they have eaten and had a meal -gets irritated/that indifference
symptoms of early stage Alzheimer's
-short term memory loss -word finding deficits (anomia) -receptive language deficits -personality changes
2 major types of dementia
1) Alzheimer's disease (AD) 2) Multi-infarct dementia (MID)
Counsel caregivers and family members of fam member with dementia to (suggestions for caregivers):
1) Approach the patient slowly, as they become apprehensive about sudden events. 2) Establish eye contact before speaking 3) Supplement verbal expression with gestures, smile, posture and other cues. 4) Speak clearly and directly. 5) Avoid complex conversation material. 6) Speak in short simple sentences. 7) Specify your referents when you speak; minimize the use of pronouns 8) Ask yes/no questions, not open-ended questions. 9) redundant; restate important information. 10) Keep topics familiar and observable 11) Use touch 12) Structure the living environment, establish a routine 13) Always say good-bye or give other departing signals.
2 major causes of dementia
1) DAT=Dementia of alzheimer's type=75%-85% of all dementias 2) Multi-infarct dementia (MID)=atherosclerosis thromboembolic causes; abrupt onset and stepwise decline > the type of pathology of repeated CVAs and strokes and could have focal deficits have less control of their emotions
The Upper Motor Neuron
1) Direct Activation pathway (pyramidal tracts) 2) Indirect Activation pathway (extrapyramidal tracts)
Acoustic & Physiological Testing
1) Endoscopic (nasendoscopy, nasalance, aerodynamics)2) 2) EMG (electromyography) 3) Spectrographic analysis depends on where you work and variability of these tools
types of subcortical dementias
1) Huntington's disease 2) Parkinson's disease
Standardized Tests
1) Intelligibility Testing (AIDS single word vs. sentence level) 2) Multiple word intelligibility test (MWIT)
Approaches to Management (3) (cognitive or psychiatric problems)
1) Medical Management Pharmacologic=some can be well managed with drugs; injecting Botox to larynx Surgical=removal of the tumor that is giving speech and motor problem 2) Prosthetic Management Mechanical and electronic prosthetic devices to improve speech: temporary or permanent have a prosthesis palatal lift prosthesis of raising the teeth of separating nose from mouth 3) Behavioral Management Goal: maximize communication by whatever means will produce the most rapid, effective, and natural results
ABCD Subtests: There are 14 subtests.
1) Mental Status - orientation to person, place, and time 2) Story Retelling Immediate - recall verbal info in the form of a story 3) Following Commands - perform one, two, and three step commands 4) Comparative Questions - assess auditory comprehension 5) Word Learning - assess free recall, cued recall, and recognition of 16 words 6) Repetition - repeat nonmeaningful phrases controlled for length 7) Object Description - generate meaningful descriptors of a common object 8) Reading Comprehension - at the word level and sentence level 9) Generative Naming Semantic Category - name items in a category 10) Confrontation Naming - name pictured objects 11) Concept Definition - i.e. give defn. of a hammer 12) Generative Drawing - generate accurate drawings of named objects (i.e. kite) 13) Figure Copying - copy a figure (not as effortful as previous) 14) Story Retelling Delayed - effect of delay on the recall of verbal info (1st story)
rating scales commonly administered to those with dementia include the following
1) Mini-Mental State Examination (MMSE) 2) Alzheimer's Disease Assessment Scale (ADAS) 3) Dependence Scale 4) Global Deterioration Scale (GDS) 5) Geriatric Depression Scale (GDS)
dysarthria
1) Neurogenic 2) Abnormal neuromuscular control may affect speech movements Speed Range Strength Timing Accuracy Respiration, phonation, resonance, articulation and prosody.
2 primary variants of Lewy Body Disease
1) Parkinson's disease 2) dementia with Lewy Bodies both are the result of the formation of Lewy bodies in the brain
Flaccid Dysarthria Perceptual Clusters (you will be asked these attributes and label the attributes and clusters)
1) Phonatory Incompetence -breathiness -breathy voice -short phrases/repeated phrases -audible inspiration/inhalation -nasal emission 2) Resonatory Incompetence -hypernasality in speech -imprecise consonants (neopharyngeal valve is leaky) -nasal emission -short phrases 3) Phonatory-Prosodic Insufficiency -harsh voice -monoloudness -monopitch You can have all 3 going on at the same time !
neuropathology of Pick's disease
1) Pick bodies 2) ballooned neurons
Perceptual Clusters of Spastic Dysarthria (SD)
1) Prosodic Excess -excess and equal stress -slow rate 2) Articulatory-Resonatory Incompetence -imprecise consonants -distorted vowels -hypernasality 3) Prosodic Insufficiency -monopitch -monoloudness -reduced stress 4) Phonatory Stenosis -low pitch -harshness -strained-strangled voice -pitch breaks -short phrases -slow rate (most pervasive and perceptually salient feature of SD) *Tend to be distinctive or more severely impaired in SD
To reduce hostility and emotional outbursts in dementia patients (suggestions for caregivers):
1) Teach family members to identify and eliminate antecedents 2) Reduce excessive difficult demands on patient 3) Redirect patient
Prosthetic Management
1) Velopharyngeal Incompetence 2) Palatal Lift Prosthesis
SLP needs to get individual's history including
1) a complete list of medications currently being used 2) a description by the affected individual of problems they are having and how it is affecting the individual's life 3) a description by the family of the problems they see the affected individual is having 4) a social, educational, and medical history of the patient, especially including an exploration of risk factors such as family history of dementia, personal history of depression, and personal history of TBI
assessment of dementia can often include the following:
1) a detailed case history, review of medical history and interviews with the family and patient 2) rating scales such as the Mini-Mental State Exam-are used to assess an individual's level of function on certain abilities through observation 3) other rating scales include the Alzheimer's Disease Assessment Scale, Global Deterioration Scale, Dependence Scale and Geriatric Depression Scale 4) comprehensive, formal test, such as the Arizona Battery for Communication Disorders of Dementia can be given to warrant therapy
11 Principles of Dementia Syndromes
1) degenerative disorders (cortical + subcortical) Ex: AD, Pick's disease (frontotemporal dementia=atrophy), Lewy body (with and without PD), HC< PSP 2) vascular disorders Ex: MID, mixed cortical + subcortical 3) myelinoclastic disorders Ex: MS, demyelinating 4) traumatic conditions Ex: subdural hematoma, dementia pugilistica 5) neoplastic dementias Ex: glioma, meningioma 6) hydrocephalic dementias 7) inflammatory conditions Ex: systemic lupus erythematosis 8) infection-related dementias Ex: syphillis, postencephaltitic dementia syndrome. AIDS, CJ disease (Prion Disease-Mad Cow) 9) toxic conditions Ex: alcohol related, metals, psychotropics, antihypertensive drugs, anticonvulsant agents, drug abuse 10) metabolic disorders Ex: uremia/kidney failure, cardiopulmonary failure, endocrine disorders 11) psychiatric disorders Ex: depression, mania, schizophrenia
4 major functional and anatomic divisions of the speech motor system
1) direct activation pathway 2) indirect activation pathway 3) final common pathway 4) control circuits
plan the following:
1) discuss anatomy and function of each division as it relates to speech motor control 2) what happens when each division becomes damages
types of indirect therapies
1) life history videos 2) environmental manipulations *purpose=are strategies that focus on modifying or manipulating the physical or communicative environment
neuropathology of Alzheimer's disease
1) neurofibrillary tangles 2) amyloid plaques 3) granulovacuolar degeneration
GDS 7 Stages
1) no cognitive decline: "Normal" 2) very mild cognitive decline: "forgetfulness" 3) mild cogntive decline: "early confusional" 4) moderate cogntive decline: "late confusional" 5) moderately severe decline: "early dementia" 6) severe cogntive decline: ""middle dementia" 7) very severe cogntive decline: "late dementia"
etiologies/causes of dementia include
1) polypharmacy 2) depression 3) lack of sleep
purpose of Arizona Battery for Communication Disorders (ABCD)
1) provides a comprehensive evolution of the linguistic communication processes of language 2) provides info about verbal episodic and semantic memory, mental status, figure copying and drawing abilities 3) once testing is completed, the clinician will have an idea of the patients abilities to read, name, describe, define, repeal, answer comparative questions, follow commands, retell a story, recall and recognize words, copy figures and draw 4) comprehensively assess the functional linguistic communication skills of individuals diagnosed with mild and moderate AD
6 possible scenarios to account for the relationship between dementia and depression
1) the treatment used to reduce depression increases risk for dementia specifically electroshock therapy 2) the risk factors for depression and dementia are the same 3) depression is an early sign of dementia 4) depression is a reaction to the early cognitive changes experienced by those with dementia 5) the presence of depression reveals an already present dementia syndrome that the person was able to compensate for and hide prior to developing depression 6) the presence of depression actually increases the risk of developing dementia
medical management of cognitive deficits in dementia
1) therapy should focus on strengthening abilities and knowledge bases that are capable of improving 2) therapy should reduce demands on impaired cognitive abilities while increasing use of intact cognitive abilities 3) therapy should provide stimuli that evoke positive memories and positive emotion not negative
types of mixed dementias
1) vascular dementia 2) multi-infarct dementia 3) cortical multi-infarct dementia
DSM 4 describes deficits in at least one of the following:
1) verbal expression or verbal and written receptive language skills 2) recognition and identification of objects 3) ability to execuete motor activities (assuming normal motor skills, normal sensory function, and comprehension of the task) 4) abstract thinking, judgment, and execution of complex tasks *also stipulates that these deficits must affect the individual's ability to execute activities of daily living (ADLs)
risk factors certain factors increase an individual's likelihood of developing Alzheimer's disease
1) women are more likely than men to develop Alzheimer's disease 2) a family history of individuals who developed Alzheimer's disease 3) a history of depression 4) past head trauma 5) individuals with less education are at a higher risk
progressive dementias
1. AD 2. vascular dementia 3. Lewy body dementia 4. Mixed dementia 5. frontotemporal dementia
2 medications now universally prescribed to individuals with Alzheimer's disease
1. Aricept/donepezil +helps with early and moderate stages of Alzheimer's disease 2. Namenda/ memantine +helps with moderate and late stages of AD --can reduce the behavioral and psychological symptoms associated with Alzheimer's
Clinical Findings "pseudobulbar palsy"
1. Dysphagia 2. Drooling 3. Pseudobulbar laughing and crying 4. Nonspeech AMR's, slow and reducedin range, rhythm regular 5. Pathologic oral reflexes common -sucking, snout, and jaw jerk reflexes
5 Essential Components of Motor Speech Examination
1. History (onset, progressive, stable, medicaldiagnosis)--when did this occur? 2. Oral mechanism examination (neuro-based) 3. Assess Perceptual characteristics (reading passage, speech AMRs, sustained vowel), 4. Results of standardized intelligibility tests(AIDS, MWIT) 5. Acoustic and physiologic analyses(endoscopy etc.)
other disorders linked to dementia
1. Huntington's disease 2. TBI 3. Parkinson's disease 4. Creutzfeldt-Jakob disease
Patient Symptoms and Complaints
1. Speech is slow and effortful 2. Nasal speech 3. Swallowing complaints 4. Drooling 5. Difficulty controlling emotion
(suggestions for caregivers) Generally, teach the client to exploit strengths and compensate for weaknesses. For example:
1. Teach client to write down instructions when memory begins to fail. 2. Teach client to ignore merely annoying problems (word-finding problems) and to concentrate on problems of consequence.
cranial nerves most involved in speech in the pons
1. Trigeminal (V) < most oral sensation > jaw muscles 2. Facial (VII) < taste, ant. 2/3 tongue and palate > lip and facial muscles 3. Glossopharyngeal (IX) < taste, post. 1/3 tongue > lip and facial muscles
cranial nerves most involved in speech in the medulla
1. Vagus (X) < taste, pharynx and larynx > palatal, pharyngeal and laryngeal muscles 2. Hypoglossal (XII) > tongue muscles 3. Accessory (XI) < taste, pharynx > laryngeal muscles
hallmark features of Alzheimer's
1. amyloid plaques 2. neurofibrillary tangles
neuropathology of DAT
1. cerebral atrophy (loss of neurons)-most brain atrophy takes place in the mid frontal areas of the brain, gyri of the parietal-temporal association areas of the cerebral cortex and the hippocampus) 2. ventricular dilation (loss of brain mass) 3. twisted neurofibrillary tangles 4. granulovacuaolar degeneration (degenration of nerve cells)
11 Principle Dementia Syndromes
1. degenerative disorders 2. vascular disorders 3. myelinoclastic disorder 4. traumatic conditions 5. neoplastic dementias 6. hydrocephalic dementias 7. inflammatory conditions 8. infection-related dementias 9. toxic conditions 10. metabolic disorders 11. psychiatric disorders
(suggestions for caregivers) Environmental controls for helping individuals with dementia:
1. establish a simple routine 2. design various reminders-alarm, written instructions, staff reminders, self-monitoring devices, signs that remind activities and their times 3. teach the client to write down a list of what to do each day 4. keep phone numbers and possessions in a particular and invariable place 5. keep a checklist of things to do before leaving the house 6. carry a card with names, addresses, and phone numbers of caregivers 7. wear a bracelet that contains identifying info addresses, and phone numbers of caregivers
types of direct therapies
1. reminiscence therapy 2. errorless learning therapy 3. spaced retrieval training (SRT)=increase the space 4) memory prostheses 5) Montessori Approach *purpose=are individual or group therapy sessions that target deficits
Appropriate code-switching behavior to speak to someone with dementia to increase comprehension and attention it is important to do the following
1. should be subtle 2. speak slower though not abnormally so 3. use shorter sentences 4. augment what you are saying with appropriate gestures and facial expressions and possibly write out any words not readily understood 5. avoid abstract topics and focus on more concrete topics 6. use frequently used words and avoid less frequently used words or jargon 7. repeat important points often and rephrase important info if not understood 8. give the individual with dementia plenty of time to both respond and process what has been said 9. avoid teasing and sarcasm (can lead to confusion)
the purpose of assessing communication and cognition deficits as a result of dementia is the following
1. to document that there are changes 2. to establish strengths 3. to delineate deficits 4. to set goals and therapy strategies 5. to counsel the family and caregivers
time limit of ABCD
45-90 minutes to administer
Epidemiology of dementia
5.4 million Americans suffer from dementia (2010)(increasing numbers as general population ages). 25 million worldwide (one new case every 7 seconds). 6 to 20% of people in nursing homes may have dementia In over 65 population in all settings, the prevalence of dementia may be as high as 25%. After age 65, the prevalence of dementia doubles every five years. The number of very old (i.e., over 85 yrs) is the fastest growing cohort of the elderly. At least 30 billion dollars a year spent in health care dollars on problems associated with dementia. By 2050, 11 to 16 million Americans (>65 yrs) will have dementia! 3rd most common disorder on SLP caseloads...
Epidemiology of Dementia
5.4 million Americans suffer from dementia (2010)(increasing numbers as general population ages). 25 million worldwide (one new case every 7 seconds). 6 to 20% of people in nursing homes may have dementia In over 65 population in all settings, the prevalence of dementia may be as high as 25%. Epidemiology of Dementia (cont.) After age 65, the prevalence of dementia doubles every five years. The number of very old (i.e., over 85 yrs) is the fastest growing cohort of the elderly. At least 30 billion dollars a year spent in health care dollars on problems associated with dementia. By 2050, 11 to 16 million Americans (>65 yrs) will have dementia! 3rd most common disorder on SLP caseloads...Epidemiology of Dementia (cont.) After age 65, the prevalence of dementia doubles every five years. The number of very old (i.e., over 85 yrs) is the fastest growing cohort of the elderly. At least 30 billion dollars a year spent in health care dollars on problems associated with dementia. By 2050, 11 to 16 million Americans (>65 yrs) will have dementia! 3rd most common dis
glutumate
90% glutumate with neurons excitatory neurotransmitter key role in processing, storage, and retrieval (too much of this term-33neurotransmitter)=overexcites and becomes too toxic (think of a toxic energy draining friend)
Damage to Direct Activation Pathway
A loss or reduction in it's ability to facilitate fine, discrete movements Initially reduced tone and weakness, but eventually leads to increased tone and spasticity Positive Babinski sign---occurs when stimulation of the lateral plantar aspect of the foot leads to extension (dorsiflexion or upward movement) of the big toe (hallux Pathological oral reflexes...suck, snout. damage to bilateral
control circuits (basal ganglia and cerebellum)
A. basal ganglia control circuit B. cerebellar control circuit Unlike direct and indirect activation pathways, control circuits do not have direct contact with LMN's They coordinate, integrate and help control the diverse activities of the many structure pathways involved in motor performance (i.e.integrate activities of direct and indirect pathways) Integration is completed by the basal ganglia control circuit and the cerebellar control circuit
The Indirect Activation Pathway
A.k.a. extrapyramidal or indirect motorsystem Multiple synapses from its origin in cerebral cortex and its destination in the FCP The "milk" run (local route), whereas DAP(pyramidal tract) is the "express" run. Primary function is motor control to regulate reflexes and maintain posture and tone. Ensures that specific speech movements occur without constant or variablei nterference with their speed, range anddirection. Effect seems to be inhibitory, whereasthe direct activation system seems tobe facilitory In speech, the IAS probably inhibitsinterference with the movements ofspecific muscles so that appropriatespeed, range, and direction ofmovement can be maintained
Epidemiology of Dementia (cont.)
After age 65, the prevalence of dementia doubles every five years. The number of very old (i.e., over 85 yrs) is the fastest growing cohort of the elderly. At least 30 billion dollars a year spent in health care dollars on problems associated with dementia. By 2050, 11 to 16 million Americans (>65 yrs) will have dementia! 3rd most common disorder on SLP caseloads
Basic Principle of Dysarthria Treatment
Always treat first order subsystems before targeting third order subsystems. The first order subsystems provide the foundation for third order subsystems, and must be optimized first.
cellular damage leads to
Alzheimer's disease
Etiologies of Flaccid Dysarthria
Any process that damages the motor unit: Trauma (34%) (mostly surgical) Neuropathies of undetermined origin (viral?)(27%) Degenerative Disease (6%) Neuromuscular junction disease (MG 6% Vascular causes (5%) Infectious processes (3%) Demylinating Disease (1%) primary cause=trauma to the nerve or surgical and iatrogenic trauma iatrogenic=relating to illness caused by medical examination or treatment.
possible experimental drug treatments for AD
Aricept Razadyne Exelon="acetylcholinesterase inhibitors" Namenda Namzaric (combo of Aricept and Namenda) *the disease=progressive; does not kill disease; does NOT cure disease but IS a delay Alzheimer=neurodegenerative recent use of antitoxidants 1. free radical mechanisms 2. Gingko Biloba and Vitamin E
Spastic Dysarthria (excessive tone/increased tone)
Bilateral damage to the direct and indirect activation pathways of the CNS Can affect any or all of the phonatory, resonatory, articulatory and respiratory components of speech Speech characteristics reflect a combination of weakness and spasticity...slow movement and reduced range and force can be unilateral or bilateral damage to the upper motor neuron
RLN (Recurrent Laryngeal Nerve)
Branches off the vagus nerve (cranial nerve X) and has an indirect course through the neck. It supplies innervation to all of the intrinsic muscles of the larynx, except for the cricothyroid muscles, as well as sensation to the larynx below the level of the vocal cords
Cranial Nerves of Speech
CR. N. IX, X, XI 1) Accessory 2) Vagus CR. N. X The Vagus- The Wandering Nerve 3) Glossopharyngeal 4) CR. N. XII Hypoglossal N. Innervates all intrinsic andextrinsic muscles of the tongue
the neurologic process of speech production
Cognitive-Linguistic - thoughts organized and converted in verbal symbols that abide by rules of language Motor Speech Programming- verbal message must be organized for execution... selection and organization of sensorimotor programs to activate speech muscles at appropriate coarticulated times, durations & intensities. Neuromuscular Execution- CNS & PNS must execute the speech motor programs by innervating the speech muscles in a manner that reflects the goals of the program... neural transmission, muscle contrxn, & movement of articulators.
Final Common Pathway (FCP)
Cranial nerves and spinal nerves that exit brainstem and spinal cord A.k.a. lower motor neuron (LMN) - i.e.motor nucleus, nerve, neuromuscular JXN, muscle).
Clinical Characteristics of UMN Damage and Spastic Paralysis
Damage to Direct Activation Pathways: Loss or reduction in its ability to facilitatefine, discrete movements Initially reduced tone and weakness, buteventually increased tone and spasticity Reflexes diminished initially, but morepronounced overtime Positive Babinski sign Pathologic oral reflexes (suck, snout, jaw) Damage to Indirect Activation Pathways: Loss of inhibitory role in motorcontrol...positive signs (overactivity) Increased muscle tone Spasticity Hyperactive reflexes NOTE: Selective damage to only DAP or IAPis uncommon. Thus patients with spasticparalysis show... Spasticity Weakness Reduced range of movement Slowness of movement Excessive or biased muscle tone producesperceptual features Laryngeal valve-biased towardhyperadduction VP valve - biased toward reduced VP closure
Dementia: NOT a single entity
Dementia is an umbrella (generic) term that encompasses many distinct subtypes. No consensus on classification of dementia (but some prefer to subtype according to where brain pathology resides i.e. cortical and subcortical, mixed)
Multi-Infarct Dementia (MID)
Dementia is the result of bilateral, repeated CVA's (thromboembolic). Previously known as "hardening of the arteries" History of hypertension-atherosclerosis Multiple diffuse cortical and subcortical infarcts (lacunar - cavities created by ischemic events) Abrupt onset - stepwise deterioration -fluctuating course
Summary of the UMN input into the MotorNuclei of the Cranial Nerves involved in Speech
Fact 1: Cranial Nerves V, VII, (upper face),IX, X, XI receive Bilateral UMN input This means that each cranial nerve motornucleus (in the brainstem) receives bilateral(two) messages from the cortex (launchingpad). So the left cranial nerve motor nucleuswould receive a message from both the rightand left sides of the brain. And, the rightcranial nerve motor nucleus would receive amessage from both the right and left sides ofthe brain. For example, let's consider the Trigeminal Nerve (V). Inthe diagram, the Right motor nucleus of the Trigeminalnerve resides in the pons of the brainstem, and suppliesthe muscles of mastication (via the Trigeminal) on theRight side of the face (jaw). It is important to note, thatthe right motor nucleus receives UMN input from both theleft and right hemispheres of the brain. There is also aleft motor nucleus for the Trigeminal N. that is the pons ofthe brainstem. The left motor nucleus and trigeminalnerve supply the muscles of mastication on the left side ofthe face. The left motor nucleus also receives bilateralinput from the UMN as well. So both motor nuclei (i.e.the left and the right) receive two messages from the brain. There is redundancy built into the nervous system.This bilateral UMN input into the motor nuclei is true for the other cranial nerves (i.e. V, VII-upper face, IX, X, XI. Fact 2: Cranial Nerves VII-lower face and XII receive unilateral UMN input. For these two nerves the input from the UMN into the motor nucleus is unilateral and comes from hemisphere opposite (contralateral) the motor nucleus. In the case of these nerves, the motor nucleus receives only one message and it originates from the opposite hemisphere Let's consider the right XIIth Cr. Nerve, which supplies the muscles on the right-side of the tongue. The right motor nucleus of the XIIth Cr.N. receives the command to move only from a message originating from the left hemisphere of the brain. In this case, the input from the UMN is said to be unilateral (and more specifically, contralateral). This unilateral UMN input is also true for theVIIth cranial nerve. However, the VIIth Cr.Nerve motor nucleus is organized into two parts - the upper and lower face. The motor nucleus that supplies the upper face receives bilateral UMN input (i.e. two messages), whereas the part of the motor nucleus that supplies the lower face receives only unilateral UMN input (i.e. only one message from the side of the brain opposite the motor nucleus).
advantages of GDS
GDS describes the course of progressive dementia through the final stages of the disease giving the clinician an enhanced ability to track the course of dementia in each patient
Background Information
GV - 21 year old male Grade 10 education Former cement finisher Previous history of alcohol abuse
Examination of Motor Speech Disorders
Goals of Examination: 1) Problem Description Describe the features which characterize the speech disorder 2) Specify Severity 3) Differential Diagnosis: the process of narrowing the diagnostic possibilities and arriving at a specific diagnosis Determining what it is not - often a process of exclusion i.e. not aphasia, not dementia, not psychogenic, not apraxia Determining what it is? What type of dysarthria? (i.e.relate perceptual features to possible neurological explanation). Dissect the speech problem into components (treatment implications) Establish lesion localization and disease process (classic features vs. anomalous features of a specific neuro disease)
Most Deviant Speech Characteristics Encountered in Flaccid Dysarthria
Hypernasality (most distinctive in FD than anyother dysarthria subtype) (X) Imprecise Consonants (V, VII, X, XII) Breathiness (very distinctive in FD) (X) Monopitch (X) Nasal Air Emission (very distinctive in FD) (X) Audible Inspiration (X) Harsh Vocal Quality Short phrases (very distinctive in FD, X, spinalrespiratory) Monoloudness (X, Spinal respiratory)
Effects of Lesions to CranialNerves on Speech (cont.)
Hypoglossal (CR. N. XII) Weakness, atrophy, and fasciculations of the tongue on the side of the lesion Intrinsic muscles of the tongue- flatten, narrow, elongate, tip and sides upward... unilateral or bilateral damage. Extrinsic m. of tongue protrude and draw tongue up and back, retract and depress tongue Unilateral weakness causes tongue to deviate to the side of the weakness i.e., lesion upon protrusion
Glossopharyngeal Nerve (Cr.N. IX).
Innervates stylopharyngeus muscle(helps elevate larynx during swallow) Sensory fibers carry taste and pressure for posterior one-third of tongue- gag-reflex (sensory). Works in concert with vagus, making independent function difficult to determine
So, what happens if we haveUMN damage...
Let's deal with unilateral UMN damage. Forinstance, what if I have a stroke in the lefthemisphere of the brain. Because eachmotor nucleus (for Cr. Nerves V, VII-upperface, IX, X, XI) receives bilateral messages(input) from the UMN, there will be nodiscernible effect on the function of thosenerves (i.e. no functional effect). The reasonis that the right hemisphere can still relay themessage to the motor nucleus, and themovement can be accomplished. Because of the redundancy built into thenervous system for the Cr. Nerves, one needsto experience bilateral UMN damage to havea negative functional effect on Cr. Nerves V,VII-upper face, IX, X, XI. Therefore, I would need to have bilateral strokes, or a tumor that somehow affected both the left and rightUMN pathways, in order for me to have obvious effect on the muscles supplied by these nerves.
normative data
MMSE has been extensively normed over 100K and found to be valid and reliable in different various populations including normal vs dementia, normal vs Alzherimer's, dementia vs depression and others is a screening tool adjusted therefore it has not been found to be suitable for differentiating discreet levels of impairment normed scales adjusted for age and education have been found to have increased sensitivity the 3MS has been normed in limited populations and shown to be more sensitive to change in the patient
MMSE
MMSE is commonly used by health professionals to quickly determine a patient's cognitive status is also used extensively as a research tool MMSE may be more useful for screenings and/or research within specific populations or across large groups due to well-establised normative data 3MS may be more useful for measuring change in individual patients due to the expanded scoring system and increased sensitivity
ALS (Lou Gehrig's) spastic-flaccid
Note pseudobulbar laughing with tightness in voice and nasality ALS patients usually have a mixed dysarthria characterized by defective articulation, slow laborious speech, imprecise consonant production, marked hypernasality with nasal emission of air during speech and harshness
Spastic Dysarthria (JF)
Note voicing of voiceless consonants --sounds like Cookie Monster
Spastic-flaccid CB
Note: velopharyngeal incompetence with hypernasality and nasal air emission
Hyperkinetic Dysarthria
Numerous subtypes, usually classified based on the nature of the underlying involuntary movement (e.g. chorea, dystonia, tics, palatopharynolaryngeal myoclonus, etc) Results from dysfunction of basal ganglia control circuit, but also may be related to involvement of cerebellar control circuit or other parts of the extrapyramidal system Speech characteristics reflect the effects of abnormal rhythmic, or irregular and unpredictable, rapid or slow involuntary movements The most common abnormal movements include myoclonus, tics, chorea, athetosis, dyskinesia, dystonia, spasm, and tremor. The jaw, face and tongue are frequently affect, usually in combination - sometimes involuntary movements are action induced and occur only during speech (e.g. SD) Slow and irregular AMR's
Case Study: Assessment Procedures
Oral Motor Examination Assessment for Intelligibility Test (single word format) Phonetic contrast error profile Nasometry (nasalance) Aeromechanical Assessment of Velopharyngeal Function Flexible endoscopic evaluation of VPFXN Optometric assessment Restorative dental work Family counseling arranged --Diagnosis: Severe Spastic Dysarthria Perceptual features/clusters --Main Goal: Increase intelligibility --Specific Goals: Reduce speaking rate Reduce distortion of vowel production Improve aspiration of plosives and affricates Improve voiced vs. voiceless contrasts for all phonemes Improve inclusion of final consonants Reduce hypernasality and nasal air emission
FCP/LMN for Speech consists of:
Paired Cranial nerves that supply muscles of: -phonation -resonance -articulation -prosody 6 Paired Cranial Nerves most involved in speech: Trigeminal (Cr. N. V) Facial (Cr. N. VII) Glossopharyngeal (Cr. N. IX) Vagus (Cr. N. X) Accessory (Cr. N. XI) Hypoglossal (Cr. N. XII) Many paired spinal nerves that supply muscles of respiration
Speech Pathology Involvement (Intensive Rehab Center)
Provided Epson computer with voice output and gestures Oral communication and writing Oral communication - "intelligibility fair for familiar listeners, connected speech poor for unfamiliar listeners and contexts"Referred to you (SLP) for management: what do you do next?
ABCD scoring system
Raw Score=total correct on each test Summary=standardized score that allows comparison Construct=average of summary score related to 5 constructs measured on ABCD Total Overall=sum of average construct summary scores Construct Scores=mental status, episodic memory, linguistic expression, linguistic comprehension, visuospatial construction *summarized into Normal, Mild AD, and Moderate AD scores
Other "Types" of Dysarthria
Reflect damage to different site(s)/locations within the Central Nervous System (CNS) Ataxic Dysarthria (Cerebellar C.C.) Hypokinetic Dysarthria (Parkinson's; substantianigra) Hyperkinetic Dysarthria (Extrapyramidal, BasalGanglia, or Cerebellar C.C.'s) Unilateral Upper Motor Neuron Dysarthria (Unilateral UMN stroke/damage).
Hypokinetic Dysarthria
Results from damage to the basal ganglia control circuit (substantia nigra). Most often due to Parkinson's disease, a degenerative condition associated with depletion of dopamine (neurotransmitter) Clinical signs include limb, jaw, tongue tremor, facial masking Speech problems are most evident in voice, articulation, and prosody Reflect the effects of rigidity, reduced force and range of movements, slow individual and sometimes fast repetitive movements Rapid, "blurred" speech AMR's Prosodic insufficiency - monopitch, monoloudness, reduced stress Short rushes of speech, increased overall rate(variable), imprecise articulation, repeated phonemes, inappropriate silences, reduced loudness
Ataxic Dysarthria
Results from damage to the cerebellar control circuit (C.C.) Speech patterns (articulatory and prosody)reflect incoordination and reduce muscle tone. Inaccuracy in force, range, timing, and direction of speech movements produce"drunken" quality; slow & dysmetric(irregular) speech and nonspeech AMR's. Telescoping of syllables and prolonged phonemes Articulatory inaccuracy (irregular articulatory breakdown, distorted vowels), prosodic excess, andphonatory-prosodic insufficiency are prominent speech clusters
Unilateral Upper Motor Neuron Dysarthria
Results from unilateral damage to the UMN pathway (usually stroke) Primarily manifests in articulation problems but phonation and prosody may be affected Disordered speech reflects effects of weakness and perhaps incoordination of tongue and lower face movements (imprecise articulation and irregular articulatory breakdown are primary perceptual characteristics) UUMN dysarthria is only mild to moderate in severity and recovery is often quite good
Review of DAP and IAP (partsof the UMN system)
Review of DAP and IAP (partsof the UMN system) Direct Activation Pathway Directs skilled, discrete voluntary movements(speech) Facilitatory Corticobulbar and corticospinal tracts Pathways originate in cortex of one hemisphereand terminate in the Cr. and spinal nuclei that innervate speech muscles on the side of the body opposite the cerebral cortex of origin Muscles of lower face and lesser extent tongue Other cranial nerves receive bilateral input fromDAP and IAP (i.e. serves protective function)Review of DAP and IAP (parts of the UMN system) Indirect Activation Pathway Regulates reflexes and maintains posture, tone and associated activities that provide a framework for skilled movements Inhibitory Originates in cortex and terminates in brainstem,but it's course is the milk run with connections(stops) to basal ganglia, cerebellum, reticularformation, red nucleus
DS palatal lift
Spastic-flaccid dysarthria with VPI and use of palatal lift
Oral Mechanism Exam: Salient Neuromuscular Features that Influence Speech Production
Speed Range Strength Steadiness Tone Accuracy
Huntington's disease is divided into 5 stages
Stages 1 AND 2: characterized by the motor symptoms of chorea, emotional problems, difficulty concentrating, memory problems, difficulties with executive functioning as well as concerns regarding sleeping and swallowing Stages 2,3,4: are characterized by chorea and hyperkinesias that begin to interfere with speech production. Training the individual on an AAC device during these stages helps prepare the individual for the full loss of verbal and written expression caused by motor deficits Stage 5: is when individuals are nonambulatory, dependent on others, at high risk for aspiration, and often uses AAC devices to communicate
Medical History
TBI secondary to MVA on July 3, 1989 (passenger on motorcycle without helmet, alcohol related). Neuroimaging results unavailable "Vegetative state" for 3 mos. 8 mos. post onset, medically stable, transferred for intensive rehab Intensive rehabilitation for 7.5 months Returned home 15 mos. Post onset; residing at home with mother, step father (head injured) and younger brother Family dynamic "extremely stressed." Cognitive skills grossly intact
Effects of Lesions to Cranial Nerves on Speech
Trigeminal (CR. N. V) Unilateral Damage: no effect Bilateral Damage: (Imprecise Articulation) Bilabial (p, b) Labiodental (f, v) Linguadental (th) Lingual-alveolar (t, d, s, z,) Distorted vowels, glides, liquids Slow rate Facial (CR. N. VII) Unilateral Damage: mild articulation distortions (bilabial and labiodentals, anterior lingual fricatives and affricates) Bilateral damage: same pattern as above but +++, vowel distortions Slow rate (compensatory or primary?) Glossopharyngeal (CR. N. IX) Runs with CR. N. X therefore indeterminate effect on speech Dysphagia - pharyngeal elevation? Vagus (CR. N. X) Intramedullary Lesions (damage nerve in the brainstem) Extramedullary (damage trunk of nerve as leaves brainstem) Extracranial (damage after it exits the skull) Intracranial affect more nerves and bilateral usually Extracranial (more often unilateral and isolated branch) Damage reflects branches. Vagus cont. Above pharyngeal branch (hypernasality, imprecise consonants, nasal emission, short phrases) Below pharyngeal branch Superior branch only (poor pitch elevation,hoarseness) Recurrent Branch only (breathiness, hoarseness, reduced loudness, short phrases, audible inspiration, limited pitch range, diplophonia
The Exception
Unilateral UMN damage is sufficient to cause functional weakness in the case of CR. N. VII(lower face) and XII (tongue). Why? Because these Cr. Nerves receive only unilateral input from the UMN (a single message that originates from the hemisphere opposite the motor nucleus). Therefore, the result of unilateral UMN damage is weakness (paresis)to the lower side of the face opposite the hemisphere of damage, or weakness of the½ of the tongue contralateral to the side ofUMN damage. To be specific, left UMN (hemisphere)damage can cause right lower facial weakness, because of the unilateralinput to the VIIth nerve motor nucleus(lower face). Also, left UMN damage can cause right tongue weakness,because of the unilateral input of theXIIth nerve motor nucleus (tongue).
Effects of Damage to IAP: Generallyreferred to as UMN damage
Usually in combination with damage to the direct activation system (pyramidaltract) Lesions affect muscle tone and reflexes Depending upon location of the lesion(how high in the central nervous systemi.e. cerebrum or brainstem) can contribute to different types of problems
nerve
a group of myelinated axons if we have enough of these axons we will get weakness in the muscle
parasthesia
a sensory abnormality usually characterized by sensation of pins and needles, tingling, or burning on the skin as well as general body aches
delirium
a sudden disturbance in consciousness or a change in cognitive ability that fluctuates through the course of a day with an onset is a result of a general medical condition
scoring procedures
a total score is derived from a presribed point system on the MMSE protocol the score can be compared to norms developed for specific populations MMSE cutoff score for normal vs not normal is generally considered to be 23/30 3MS cutoff score for normal vs not normal is generally considered 77/100
vascular dementia clinical features
abrupt onset; stepwise progression evidence of multiple ischemic lesions hemorrhagic events and white matter lesions required for diagnosis present focal neurologic signs score of 7 or greater on Hachinski Ischemia Scores (HIS) attention-worse performance than Alzheimer's disease episodic memory impairment-better performance on immediate and delayed verbal memory measures compared to persons with Alzheimer's gait alterations-present early and more common personality changes-more likely; tend to occur earlier in the course
Pick's Disease
affects women more than men average age of onset=between 50-70 years can present as early in life as age 20 or 30 typical life span=2 to 10 years after diagnosis far rarer than Alzheimer's and can often go undiagnosed or misdiagnosed
Clinical Dementia Rating Scale
an assessment tool looking at the following -memory -orientation -judgment/problem solving -community affairs -home hobbies -personal self care is scored on mild, moderate, severe rating scale
Pseudodementia
an outdated term once used to indicate cognitive changes and deficits brought on by depression was used ot indicate the cognitive changes and deficits brought on by depression
life history videos
are custom-made personal videos that are composed by the SLP or the family of the individual with dementia to provide an audiovisual presentation of relevant personal facts such as relationships and past events to increase orientation and decrease confusion
memory protheses
are external memory aids to augment the memory capacity of those with memory deficits such as memory books, wallets, calendars, smart phones, and personal digital assistants
ABCD screening tasks
are included to help the clinician identify probs such as speech deficits, visual perception problems, visual agnosia, illiteracy, depression, apraxia speech discrimination-are the words same or different visual perception and literacy-read a sentence visual field-circle all the As on the page visual agnosia-show objects and have patient tell what they are
stages of DAT (heterogeneous disorder)
begins with mild symptoms which intensifies over years 58% of people with DAT have significant behaviorial symptomatology including: -delusions -agitation/internal agitation (picking and scratching themselves repeatedly) -diurnal rhythm disturbances (sleep) -motor restlessness -violence -emotional lability (uncontrolled laughing or crying, heightened irritability or temper, rapid/exaggerated changes in mood) -suspiciousness -does not recognize when someone is taking away a belonging of theirs -hallucinations (seeing someone after their passing away but negatively)-altered sense of reality or make up a scenario; can verbalize that person is dead but still sees them; hearing voices or music * can be the worst part of the dementia*
bilateral
both sides
normal brain
can see small ventricles + bark of the brain
oral mechanism with cold mirror testing
cannot articulate s and turning the voice on and sounds like a v or f sounds like z sound voice will start coming on s and e are both oral and no nasality should be perceptible or perceived > has nasal air emission seen with cold mirror fogging
neurogenic
caused by/controlled by or arising in the nervous system forming, originating in, or controlled by nervous tissue
oxidative stress
cells begin to die and leads to disease (heart disease), aging
free radicals leads to
cellular damage attack the mitochondriaglutumate
the 3 amigos damage comes to all 3
cranials 9, 10, 11 accessory, vagus, glossopharyngeal
Latin roots of dementia
de=out of mens=one's mind
types of long-term memory (LTM)
declarative memory=explicit memories that can be consciously recalled such as facts/semantic memory and personal events/episodic memory non-declarative memory/procedural memory=type of implicit memory that allows us to carry out commonly learning tasks without consciously thinking about them procedural memory=less impaired in dementia "how to" memory=how to ride a bike, wash dishes, tie a shoe, etc
hypotonia
decreased or lost muscle tone
DSM 5 Criteria "Major Neurocognitive Disorder"
deficits in at least 1 of the following areas: --learning and memory --language --execuetive function (making it challenging for them to complete simple tasks) --complex attention --perceptual motor skills --social-cognitive Must interfere with independence NOT delirium
types of cortical dementias
definition: damage to parts of the brain in the cerebral cortex 1) Alzheimer's 2) Frontotemporal Dementia
more on dysarthria (from Rosalea CSD 1010 class)
definition: slowness, weakness, and or incoordination of the muscles for speech of the pathways for neurological speech could affect respiratory pulmonary system, phonatory system, resonating system, articulatory system vocal folds affected=breathy voice, strange voice, characteristic of Parkinson's disease
projection pathways
descending pathways from going to the higher centers to the lower lower regions to higher regions of CNS=ascending pathways *descending and ascending pathways ARE opposites!
mutated Tau protein
destroys microtubules=neurofibrillary tangles
Global Deterioration Scale (GDS)
developed by Dr. Barry Reisberg, Steven Ferris, Thomas Crook is one of the most widely used dementia assessments used to assess disease severity it separates progressive dementia into 6 distinctive stages in addition to 1 stage for the "unaffected" population has been studied extensively has been proven to be reliable and valid for the assessment of dementia is NOT always used specifically by SLPs but clincians should aware of it
Pseudobulbar palsy
due to an upper motor lesion caused by bilateral disturbance of the corticobulbar tracts characterized by dysarthria, dysphagia, facial and tongue weakness, and emotional lability
stages of DAT
early (mild) 1-3 years mild (moderate) 5-7 years late (severe) 2-5 years die within 10 years with the Alzheimer's disease
Hallmark of Pick's Disease
early behaviorial abnormalities affected individuals often present a lack of social inhibition and say things inappropriate to social situations
bradykinesia
extreme slowness in movement and speed progressive hesitations/halts as movements are continued
tracts/pathways
groups of nerve fibers that run together in the brain and spinal cord fibertracts within the CNS are categorized according to the areas they connect A. Commissural Fiber tracts - connect similar (homologous) areas in each hemisphere: 1. Corpus Callosum 2. Anterior Commissure 3. Posterior Commissure B. "Projection Fibertracts"- fibers which connect higher and lower centers in the CNS E.g. Corticobulbar, thalamocortical, corticospinal C. Association Fibertracts - tracts which join locations within the same hemisphere e.g. Arcuate fasciculus (joins Broca's area to Wernicke's area).
Bruce Willis
had been recently diagnosed with frontotemporal dementia + primary progressive aphasia (neurodegenerative)
MWIT (multiple word intelligibility tool)
helps clinicians identify the extent of errors provides direction of treatment designed with 19 phonetic contrasts in mind larynx can be a problem and if the contrast is not made about larynx being a problem then they could have intelligibility issues phonetic contrasts in error (looks at glottal-null, voiced-voiceless, alveolar palatal fricative, nasal stop, miscellanous)
! test questions hint droppers in class lectures !
hypoglossal and tongue and unilateral the cranial nerves like what nerve type is this number associated with Flaccid Dysarthria Perceptual Clusters (you will be asked these attributes and label the attributes and clusters) with a video example
Montessori approach
includes the breaking down of complex tasks into an individual component tasks for practice into hierarchical order of difficulty
Alzheimer's disease clinical features (Dementia with Lewy Bodies and Parkinson's Disease clinical features)
insidious onset; gradual progression histopathology--Hallmark: neurofibrilliary tangles and neuritic plaques composed of beta-amyloid extrapyramidal signs and Parkinsonian features-rare but possible visuospatial impairments AND execuetive function impairments-better than dementia with Lewy bodies and Parkinson's disease infrequent visual hallucinations and fluctuations in consciousness
Alzheimer's disease clinical features (with that of vascular dementia clinical features)
insidious onset; gradual progression neuroimaging finding-evidence of hypoperfusion of the medial temporal lobe areas, including the hippocampus, entorhinal and perirhinal cortices and parahippocampal gyrus no evidence of a CVA event focal neurologic signs-usually absent score of 4 or lower on Hachinski Ischemia Scores (HIS) attention-better performance than vascular dementia episodic memory impairment-cardinal, early-appearing, severe deficit on delayed verbal memory measures gait alterations-may present later not as common personality changes-less likely than in vascular demential tend to present in the middle to late stages
Dementia with Lewy Bodies and Parkinson's Disease clinical features
insidious onset; relatively rapid progression histopathology--Hallmark: abnormal intracellular inclusion bodies called Lewy bodies composed of alpha-synuclein protein extrapyramidal signs and Parkinsonian features-present (tremors, rigidity, bradykinesia) visuospatial impairments AND execuetive function impairments-worse than Alzheimer's disease visual hallunications and fluctuations in consciousness-present early and more common
purpose of FAS verbal fluency measure
is a generative naming test is used to assess the ability to name items within a category
Huntington's disease (HD)
is a subcortical dementia that is a progressive terminal illness characterized by distinctive, involuntary, erratic body movements -can also cause changes in personality, cognition, language, and emotions
Unilateral Upper Motor Neuron Dysarthria (UUMN)
is considered a milder form of spastic dysarthria. It's also one of the most common types of dysarthria. often caused by a stroke involves damage to the upper motor neurons, which control movement
amyloid plaques- alzheimers
is responsible for the accumulation of amyloid in plaques
spaced retrieval training
is the presentation of new or previously known information to those with memory deficits that they must recall over increasingly greater intervals of time
ADLs/Activities of Daily Living
is used for the activities that are performed for self-care and hygiene [washing hair, taking a shower, brushing teeth and hair, taking care of hair, hands, nails]
uremia
kidney failure
ALS mixed UMN and LMN oral motor exam and flex exam video example
lateralized no obvious lower motor weakness no symmetry slightly weaker left side fasiculations on tongue cannot raise tongue without bringing in his jaw protrusion/lateralized against resistance bilateral weakness bubbling in the middle of esophagus hypo adduction/hypo-closure cannot see true vocal folds > does not really open up
Orientation MMSE test
looks at: 1. time 2. location 3. date
Brain of Alzheimer's
loss of and shrinkage of sulcis dramatic shrinkage of the brain
1 of the hallmarks of dementia
memory loss
DSM 5 Defintion
memory loss + deficits in at least 1 of the following deficits: --verbal expression --recognition + identification of objects --ability to execute motor activities --abstract thinking, judgment, + execution of complex tasks *deficits must affect ADLs
early stages of DAT
memory loss is just the beginning! -subtle memory problems -impaired visuospatial skills (not recognizing items/belongings) -patients get lost and disoriented in familiar places/situations -going to new places=problematic -reasoning problems, poor judgment -disorientation, especially in new places -mood changes, depression, some indifference, different tone, anxiety, sleep issues
comprehensive evaluation of functioning for Arizona Battery for Communication Disorders (ABCD) assessment
mental status story retell (immediate) following commands comparative questions word learning repetition object description reading comprehension generative naming (semantic category) confrontation naming concept definition generative drawing figure copying story retelling (delayed)
stenosis
narrowing of the airway
Polypharmacy
negative side effects including unexpected drug interactions of taking many prescription drugs at once
GDS stage 1
no complaints of memory deficits
scoring procedures of FAS verbal fluency measure
no credit is given for the recitation of proper names, numbers, derivations or previously produced words becuz the verbal fluency task is open ended a total possible score cannot be specified
Denervation
no electrical impulses partial=paresis complete=paralysis can be unilateral or bilateral
materials and time required for administering FAS verbal fluency measure
no materials are needed and the subjects are asked to name as many words as possible that begin with each of the 3 letters in 1 minute/each letter gets 1 minute 1. F 2. A 3. S these are the easiest letters which is why it is chosen healthy elderly n=39.5 about 13 words/letter mild AD n=15.9 about 5 words/letter moderate AD=4.89 1.5 words/letter
Sundowner (Sundowning) Syndrome
oftentimes individuals during the middle stage of this disease or other dementia may present as only mildly impaired during the daytime but then their cognitive and emotional state changes for the rose at night once the sun has set leading to greater disorientation, confusion, and behaviorial difficulties
unilateral
one-sided
nerve
peripheral structures are a collection of nerve fibers/axons bound together by connective tissue the term is reserved for groups of fibers that run together in the PNS (ie cranial and spinal nerves)
weakness unilateral or bilateral
protrude to the weak side
auditory-perceptual assessment
rating of deviant speech characteristics Three speech stimuli... Reading Passage Sustained Vowel Speech AMRs(including sequencedAMRs)
Tau Proteins in Alzheimer's Disease
seems to be responsible for the neurofibrillary tangles
nasophrayngeal port
separates nose from the mouth/oral cavity
AMR
sequenced amr example=putika
GDS stage 2
subjective complaints including: patients forgets where they placed a familiar object, forgets names known previously
mild cognitive impairment
subtle cognitive changes that are often prediagnostic signs of dementia and usually manifest as decreased ability to concentrate, decreased word finding abilities, decreased short term memory, and difficulty following detail heavy conversations of writings
neuropathology of Huntington's disease
the production of the mutant Huntington by the HD gene role--creates degenration of the basal ganglia, hippocampus, substantia nigra, and Purkinje cells of the pons
Neuroanantomy
the study of the structure and organization of the nervous system
12 cranial nerve
the tongue
10th cranial nerve
the vagus has 3 branches multiple divisions: 1. pharyngeal nerve branch 2. superior laryngeal nerve branch (internal and external) 3. recurrent laryngeal nerve branch
(suggestions for caregivers) When condition deteriorates
then shift management focus to family and caregivers
administration
these screening tools include verbal questions and simple task requests generally completed in less than 10 minutes MMSE includes 11 items 3MS adds 4 items, changes some content, adjusts the question order, suggests standardized testing procedures , and expands the scoring system materials needed include the testing protocol, pencil, paper, a watch
the SLP should be able to do the following
to recognize, diagnose, and provide treatment for cognitive, communicative, and swallowing deficits as a result of dementia or dementia-producing illnesses
Antioxidants purpose
tries to stabilize by donating electron in order to prevent these events from happening
sagittal median section of the head and neck
valves control flow; the head is thrown backward into complete extension which explains the relations between the lower jaw and the hyoid bone
normative data of FAS verbal fluency measure
was provided on a group of 31 healthy elderly, 21 mild AD, 37 moderate AD, 16 non-fluent aphasia, 15 fluent aphasic patients