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104 Terms
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CN V: Trigeminal Nerve
chewing, motor control of mastication muscles
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CN VII: Facial Nerve
production of saliva, facial muscles such as orbicularis oris for mouth closure
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CN IX: Glossopharyngeal Nerve
pharyngeal phase of swallow, lifts up throat
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CN X: Vagus Nerve
closure of the nasal pathway pharyngeal portion of swallow closure of the vocal folds
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CN XII: Hypoglossal Nerve
tongue muscles for oral and oral prep phase of swallow, moves the bolus
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Oral Prep Phase (Buccal Phase)
i. VOLUNTARY PROCESS ii. Mastication 1. Labial seal and salivation are two important processes, the tongue is helping form the bolus along with the saliva 2. We need sensory feedback for the correct positioning of the bolus on the teeth, prevents tongue injury during chewing 3. Tension in the buccal area prevents food from falling into gap between mandible and teeth 4. Rotary movement by jaw and tongue continues until bolus is formed iii. Bolus formation 1. After chewing, the tongue will form the bolus 2. Tongue will contract to push the bolus against the soft palate and into the oropharynx
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Oral Transport Phase
i. Once bolus formation is complete, the tongue will be the primary mover of it to the pharynx ii. Sensory receptors in the oropharynx are stimulated and a reflex (involuntary) known as the pharyngeal swallow reflex is triggered iii. The tongue will elevate, the sides and the tip pressed against the alveolar ridge iv. This process lasts for 1-1.5 seconds v. NEED VOLUNTARY AND INVOLUNTARY portions of the swallow for it to work
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Pharyngeal Phase
i. Complete closure of the velopharyngeal port to prevent material from moving upward into nasal cavity ii. Hyoid and larynx move superior and anterior 1. Elevation opens airway 2. Forward movement opens upper esophageal sphincter iii. Closure of VFs to prevent food or liquid penetration 1. Laryngeal vestibule closes, where the true and false vfs contract, arytenoids move in a downwards, forward, and inward direction (narrows opening), larynx is elevated and pulled forward, epiglottis inverts iv. Top to bottom contractions of pharyngeal constrictor muscles begin v. Opening of cricopharyngeal sphincter to allow material to pass from pharynx to epiglottis
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Esophageal Phase
i. This phase begins when the bolus passes through the cricopharyngeal muscle ii. Esophageal propulsion begins through muscles contractions along the esophagus (peristalsis) ((also propelled by pressure changes)) iii. Proximal to distal (anterograde) sequence of contractions that propel material distally toward the digestive system iv. Lower esophageal sphincter relaxes so the bolus can enter the stomach v. This process as a whole can take 8-20 seconds, and it normally takes two peristaltic waves to clear the esophagus vi. Once the bolus has entered the stomach, the swallowing process is finished and digestion begins
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What is a bolus?
the combination of saliva and masticated food that will be traveling through the swallow
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List several clinical signs of dysphagia
choking and coughing while or after eating food sticking in the throat or vallecula regurgitation pain while swallowing drooling weight loss and nutritional deficiencies recurrent (aspiration) pneumonia
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Videofluoroscopy
also known as modified barium swallow exposes the client to radiation visualizes all phases of the swallow x-ray video
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Fiberoptic Endoscopic Evaluation of Swallowing (FEES)
dyed food is swallowed by client fiberoptic camera is introduced through the nose cannot see the pharyngeal phase, just the results also cannot evaluate the full function of the esophageal phase
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List the components of a bedside swallow exam
i. No instruments to see if instrumental assessment is necessary ii. Make sure dentures are worn if needed iii. Observe feeding history, respiration patterns, mental and neurological status, cough, and voice quality iv. Sit the patient upright 90 degrees v. Two-ounce water screening test (high specificity, low sensitivity) vi. Feed different textures vii. Meal observation viii. Note any difficulty chewing, swallowing coughing, or breathing
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What medical complications can occur due to untreated dysphagia?
Recurrent pneumonia
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What are the four treatment methods for dysphagia?
diet modifications postural adjustments environmental modifications training of swallowing maneuvers muscle strengthening other
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What is important to keep in mind with diet modification
texture, temperature, taste
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Outline the stages of the NDD (national dysphagia diet)
NDD I -> pureed foods, such as veggies, fruits, and meats NDD II -> mechanically altered foods, mashed fruits or veggies, soft or ground meats with gravy NDD III -> advanced foods, soft-solids like meat, fruit, or veggies that are easy to cut or mash, avoid crackers, nuts, and other snacks NDD IV -> regular foods, all foods allowed
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What are some NDD liquids?
honey, nectar, pudding, overall should be a thin consistency
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What are the five postural adjustments?
sit up chin down chin up head rotation head tilt
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Postural Adjustment Sit up
avoid aspiration, good advice for anyone
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Postural Adjustment Chin-down
Tongue base closer to posterior pharyngeal wall Keep bolus in oral cavity until voluntary movement
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Postural Adjustment Chin-up
use gravity to help bolus move through the oral cavity
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Postural Adjustment Head Rotation
Turn head to the damaged side to force the bolus to go through the stronger side of the pharynx
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Postural Adjustment Head Tilt
Use gravity to help keep food on stronger side during oral phases
put tongue tip in between teeth and do a dry swallowM
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Muscle Strengthening Shaker
1. Lay on a flat surface 2. Raise your head (look at your toes) 3. Either hold there for a time or lift and relax multiple times in a sequence
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Muscle Strengthening Laryngeal Elevation
lift larynx and hold (glide up a scale and hold a high note)
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Muscle Strengthening Lingual Isometrics
tongue strengthening against resistance
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Other Methods of Dysphagia tx
respiratory swallow training (exhale, swallow, exhale) transcutaneous electrical stimulation
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Where is Broca's area?
left frontal lobe, inferior frontal gyrus
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Where is Wernicke's area?
left temporal lobe, superior temporal gyrus
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Where is the arcuate fasciculus?
it runs from Wernicke's to Broca's area, superior to the lateral sylvian fissure in the left hemisphere
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What is aphasia?
an acquired selective impairment of language modalities and functions resulting from a focal brain lesion in the language-dominant hemisphere it affects a person's communicative and social functioning, quality of life, and the quality of life of caregivers/family members
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Speech Production Errors Paraphasia
something is wrong with what is being produced
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Speech Production Errors Semantic Paraphasia
using the wrong word, often related to the intended word semantically
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Speech Production Errors Phonological Paraphasia
some of the phonemes are not produced correctly
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Speech Production Errors Perseveration
try to move on to a new task, keep answering the previous task
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Speech Production Errors Neologism
creation of a new word, maybe a combination of other words
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Speech Production Errors Jargon
incomprehensible language, frequent distortions, semantic erroes, and new words (neologism)
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Speech Production Errors Circumlocution
talking around the topic, can be used if a person cannot find the word
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Speech Production Errors Echolalia
repetition of words or phrases produced by another person
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Speech Production Errors Stereotypy
one word is used frequently, does not make sense
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Broca's Aphasia
Lesion location: Broca’s Area Output: nonfluent, slow, pauses, mostly just content words Comprehension: mostly intact Repetition: poor Writing: nonfluent, matches speech (typically not cursive)
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Wernicke's Aphasia
Lesion location: Wernicke's Area Output: fluent, relatively effortless, but with paraphasias, jargon, and circumlocutions Comprehension: impaired Repetition: poor Writing: fluent, matches speech (cursive, effortless and fast)
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Global Aphasia
Lesion location: large area of the MCA region Output: nonfluent, may be limited to a stereotype or two Comprehension: poor, even yes/no difficulty Repetition: poor Writing: poor or absent
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Conduction Aphasia
Lesion location: arcuate fasciculus Output: fluent with paraphasias Comprehension: good Repetition: poor (often dramatically compared to fluent output) Writing: fluent with paraphasias
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Anomic Aphasia
Lesion location: not clearly localized Output: fluent, problems with word finding may result in long pauses, nonspecific words, and circumlocutions Comprehension: good Repetition: good Writing: probably good (although with anomia)
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Transcortical Motor Aphasia
Lesion location: anterior superior frontal lobe (Broca's intact, although isolated) Output: nonfluent Comprehension: okay Repetition: good Writing: nonfluent
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Transcortical Sensory Aphasia
Lesion location: upper parietal lobe, isolating the perisylvian area Output: fluent Comprehension: poor Repetition: good Writing: fluent
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Transcortical Mixed Aphasia
Lesion location: areas surrounding the perisylvian area, complete isolation of speech area Output: poor Comprehension: poor Repetition: good Writing: probably poor
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What must the clinician decide on based on the outcome of an evaluation for the treatment of specific language modalities and cases?
mild and severe may benefit from communication tips and modifications
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What are examples of language aphasia treatments?
global aphasia auditory comprehension reading comprehension speech production writing functional communication
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When should a clinician focus especially on functional communication?
when a patient has a low number of appointments
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Global Aphasia Treatmnet
Treatment of Aphasia Perseveration Program (TAPP) -> involves imposing delays, increase awareness to improve inhibition of perseverative responses
Voluntary Control of Involuntary Utterances -> take what is already being said, make it the right answer, vary the questions, order, responses required, to obtain propositional and volitional control over it
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What are some goals to keep in mind when treating global aphasia?
tx focus: consistent yes/no response simple gestures small set of "communicative intentions" improve auditory comprehension for one-step commands improve patient's writing of daily life word improve patient's drawing
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Where should you start with treatment for auditory comprehension deficits?
Where your patient can at least get it right thirty percent of the time, levels of single word vs. sentence vs. discourse
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Auditory Comprehension Treatment
i. picture identification: can build up to multiple words ii. answering yes/no questions (questions can vary on many level: general knowledge, sentence length, semantic or phonemic discriminations, syntactic analysis, semantic information iii. following spoken directions (hierarchy of complexity) iv. sentence verification (e.g., based on clinician-provided picture descriptions) v. task-switching vi. answering questions about discourse samples (play sample recording, then ask questions) vii. may need to adjust: topic familiarity, sample length, redundancy, cohesion, coherence, salience, directness (not implied), speech rate
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Reading Comprehension Treatment
i. reading comprehension requires word comprehension, syntactic analysis, semantic mapping ii. initial question: how much of a priority is reading for the patient? iii. starting point: single-word vs. discourse comprehension? iv. surface dyslexia vs deep dyslexia v. flash cards, retraining grapheme to phoneme correspondence, comprehension drills vi. adjust difficulty as needed as in treatments for auditory comprehension deficits
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Speech Production Treatments
i. repetition drills ii. confrontation naming iii. sentence completion iv. semantic feature analysis (SFA) v. phonologic components analysis (PCA) vi. response elaboration treatment (RET) vii. verb network strengthening treatment (VNeST) viii. helm elicited language program for syntax stimulation (HELPSS) ix. melodic intonation therapy (MIT) x. script training
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Confrontation Naming Treatment
i. present stimulus (object, picture, etc.) ii. use cueing hierarchies to facilitate (semantic, phonological) iii. examples that seems to work for multiple aphasia types: first sound, sentence completion, rhyme, function, and superordinate
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Semantic Feature Analysis (SFA)
i. assisted analysis of the meaning of the word ii. frequent association of the word’s sound with the word’s meaning
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Response Elaboration Treatment (RET)
i. a loose training technique designed for aphasia patients in order to increase the length and information content of verbal responses ii. how it works... 1. clinician elicits spontaneous response from client using picture stimuli 2. clinician models and reinforce initial response 3. expand and elaborate response through scaffolding 4. reinforces client's attempts at elaboration 5. repeats and expands the client's utterance 6. models and the expansion by scaffolding the client's response iii. overall idea is to have less structured treatment to increase creative language use (more content words)
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Melodic Intonation Therapy
i. for a person with severe auditory comprehension and limited telegraphic speech output (Broca's/Global aphasia) ii. uses rhythm and melody to facilitate verbal production (right hemisphere) iii. rhythm and melody gradually faded down to that of typical speech iv. DO NOT USE POPULAR SONGS
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Script Training
i. the client and the clinician work together to create scripts. ii. a script is a predictable sequence of sentences 1. can be a story that the person with aphasia tells (monologue). 2. can also be between two people, such as ordering food in a restaurant. 3. try to select scripts where words/sentences are easy to predict. 4. examples: getting to know you, talking about your feelings, story of your stroke, retelling a personal event, etc.
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Treatments for Writing
can usually give to OT, often a less important goal for us than speech i. Anagram and Copy Treatment ii. Copy and Recall Treatment
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Treatments focused on Functional Communication
i. PACE (promoting aphasics’ communicative effectiveness) 1. convey information to a partner (info unknown to the partner), with the clinician modeling behaviors he/she would like the PWA to use. 2. emphasizes that communication requires sender and receiver. 3. provides practice with comprehension and production. ii. supported communication training for conversation partners iii. life participation approach to aphasia (LPAA) 1. focus on functional activities of daily living and participation in life
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Benefits of Group Aphasia Treatment
i. economical, efficient ii. provides support network iii. share techniques, strategies iv. provide opportunities for communication practice with a variety of communication partners in a supported environment
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Group Aphasia Treatment Disadvantages
i. requires homogenous grouping of patients so everyone experiences success (can’t couple severe with mild – frustrating for both) ii. scheduling issues iii. billing/third party payment issues
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List the neurologic processes of speech and language production with their corresponding disorder
i. Conceptualization; dementia/cognitive impairments ii. Symbolization; aphasia iii. Motor Speech Planning; apraxia iv. Motor Speech Execution; dysarthria
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What represents the issue with the "musical score" in the orchestra analogy?
apraxia
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What represents the issue with the "musicians playing instruments" in the orchestra analogy?
dysarthria
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What does motor speech execution involve functionally?
the direct activation pathway (precentral gyrus, supplemental motor area, primary motor area) the indirect activation pathway (basal ganglia and cerebellar control circuit) the final common pathway (lower motor neuron in peripheral nervous system)
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Apraxia of Speech
i. impairment at the level of motor speech planning and programming ii. often co-occurs with Broca and is hard to differentiate iii. may display as difficulty transitioning between sounds, transposition of phonemes, increasing difficulty with increasing complexity of words, slow/inconsistent rate of speech, and trial or groping behaviors of articulators iv. its developmental form is developmental or childhood apraxia of speech
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What are some speech characteristics of apraxia of speech?
i. Prosodic and segmental abnormalities 1. Distortions and distorted substitutions 2. Slow or inconsistent rate of speech 3. Syllable segregations and/or segmentations 4. Transpositions of phoneme/syllables (metathetic errors) 5. Increased difficulty with increased phonetic complexity (not specific to AOS) ii. Abnormal Speech gestures 1. Trail-groping movements of articulators, as if searching for the correct positions
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Dysarthria
i. impairment at the level of motor speech execution (control and/or performance) ii. deficits in various parameters of neuromuscular movement for any part of the speech subsystems 1. range of motion 2. force 3. tone 4. speech (rate) 5. accuracy (direction) 6. rhythm
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Functional Motor Speech System
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Direct Action Pathways
influences the excitation of the motor cortex, increasing motor activity corticobulbar and corticospinal tracts, primary motor cortex, UMN to LMN
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Indirect Action Pathways
decreases activity of the cortical motor neurons and suppresses extemporaneous movement has modulating loops, including the thalamus, basal ganglia, and cerebellum control centers important for regulating reflexes, posture, and TONE
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Final Common Pathway
lower motor neuron system of PNS impairments can result in atrophy, flaccid dysarthria
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What are examples of treatment for apraxia of speech?
the overall focus is to rehab speech movements (not postures or non-speech oral mvmts) i. Sound Production Treatment ii. Visual feedback iii. Rate/Rhythm treatments 1. metrical pacing treatment
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Flaccid Dysarthria
i. Final common pathway damage ii. Variability of nerves involved iii. Cranial nerves, spinal if severe, or diaphragm (c3 -c5) iv. Impairment of motor execution results in hypotonia, hyporeflexia, decreased voluntary movement, involuntary movement (fasciculations and fibrillations) v. Low tone, reduced force, speed can be reduced or normal, ROM reduced, often normal ACCURACY and RHYTHM vi. Common speech characteristics: breathiness, imprecise consonants, hypernasality, short phrases, audible inspiration (no full adduction of VFs)
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Spastic Dysarthria
i. Bilateral DAP and IAP damage (UMN or LMN, basal ganglia or cerebellum) ii. Unilateral will have different pattern iii. Can happen in ALS, also with strokes iv. Impairment in motor execution, results in spasticity, hypertonia/excessive tone, reduced force, speech and ROM, normal accuracy and rhythm v. Common speech characteristics: harsh phonatory quality (strangled), monopitch and monoloudness, slow speech rate, slow and regular AMRs vi. Pseudobulbar (emotional excitability)
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Ataxic Dysarthria
i. Cerebellar control circuit damage ii. Impairment in motor control leads to ataxia (jerky movment), can have gait problems, impaired check and excessive rebound, under/overshoot, dysdiachokinesis iii. Normal to excessive ROM and force, reduced tone and speed, inaccurate direction, irregular rhythm (problems with coordinating space and time) iv. Common speech characteristics: sound drunk or slurred, excessive variations in volume and pitch, inconsistent sound errors, slow rate, irregular speech AMRs (everything went wrong)
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Hypokinetic Dysarthria
i. Basal ganglia control circuit damage ii. TOO MUCH INHIBITION (lack of dopamine) iii. Typically associated with Parkinson’s iv. Symptoms 1. Rigidity 2. Resistance spread more evenly 3. Bradykinesia (reduced movement, range) 4. Akinesia (freezing or lack of movment) 5. Masked facies 6. Festination (involuntary gait quickening) 7. Resting tremor v. Reduced ROM and force, excessive tone (rigidity), excessive speed for repetitive movements but slow for individual movements, normal accuracy and rhythm vi. Common speech characteristics: monopitch, reduced stress, monoloudness, inappropriate silences, short rushes of speech, sort and breathy voice, repeated phonemes
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Hyperkinetic Dysarthria
i. Basal ganglia control circuit damage ii. Abnormal and involuntary iii. Damage to inhibitory components results in extra movements, may also be a result of increase in dopamine (excitatory) and decrease in acetylcholine (inhibitory) iv. May affect jaw, face, tongue, palate, larynx, or respiratory system 1. Usually a combination of structures 2. isolated effects are also possible v. reduced intelligibility estimated in around 27% of cases 1. appearance and discomfort of Hyperkinesias themselves may impact verbal and nonverbal communication 2. etiologies: Tourette’s, Huntington’s, vocal tremor 3. Hyperkinesias: dystonia, chorea, athetosis, myoclonus, stereotypies
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Hyperkinesias Dystonia
involuntary muscle contraction, causes repetitive or twisting movements
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Hyperkinesias Chorea
jerky, involuntary movements
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Hyperkinesias Athetosis
abnormal muscle contractions cause involuntary writhing movements
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Hyperkinesias Myoclonus
involuntary, lightning-fast muscle twitches, brief and sudden jerks
i. Unilateral DAP and IAP damage ii. No highly distinctive perceptual features iii. Diagnosis typically made by considering a variety of perceptual features and knowledge from case history, etc. 1.Typically involves unilateral central face and tongue weakness, stroke etiology, moderate or greater articulatory imprecision, sometimes mild irregular articulatory breakdowns, slow rate, slow/irregular AMRs, harsh or strained or hoarse-breathy dysphonia, and reduced loudness (no distinctive perceptual features)
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List the four areas of treatment for motor speech disorders (dysarthria)
Behavioral Prosthetic Pharmacological Augmentative and/or Alternative Communication