Exam 2 MSD

Speech Assessment and Diagnosis for AOS

- Use speech sequential motion rates (SMRs) and imitation of complex multisyllabic words and sentences o Zip-zipper-zippering - AMRs as well - - Look for threshold at which patient succeeds or fails on tasks reflecting a continuum of speech programming demands (e.g., vowels, CV, CVC, AMRs, overlearned singing/speaking, words, etc.)

Etiologies of AOS

- Vascular lesions (e.g., stroke) most common cause of AOS; left hemisphere middle cerebral artery - Diffuse diseases rarely produce isolated AOS - Dementias, Dysarthria

Patient Compliants: AOS

- speech won't come out right - articulation problems (not respiration, phonation, or resonance) - speak slowly and carefully - long words difficult to pronounce

Hyperkinetic Dysarthria

Abnormal, rhythmic or irregular, rapid or slow, unpredictable involuntary movements - excess movements not the speed prominent effects on prosody Highly variable across types of this disorder category

Resonance of hypo and hyperkinetic dysarthria

Abnormalities not perceptually prominent - timing problems slow movement difficulty initiating reduced ROM

Tourette's syndrome is a prototypic example

Affects mostly males Co-occurs with obsessive-compulsive disorders, attention deficit hyperactivity disorders TS characterized by vocal tics: specific sounds are produced - Throat clearing - Grunting - Yelling-screaming - Barking - Snorting - Coughing - Echolalia (repetition of others' utterances) - Palilalia (repetition of own utterances) - Coprolalia (involuntary swearing) · TS is a disorder of disinhibition

CLusters of deviant dimensions of Ataxia : Articulatory inaccuracy Prosodic excess Phonatory-prosodic insufficiency

Articulatory inaccuracy • Irregular articulatory breakdowns • Distorted vowels—coordinate where the tongue is going Prosodic excess • Excess and equal stress, and • Prolonged phonemes and intervals: distinctive of ataxic dysarthria Phonatory-prosodic insufficiency

Differential Diagnosis: Ataxia and AOS

Ataxia: - Speech AMRs (rhythm)- Irregular - Rhythm is impaired - Sequencing of SMRs==Normal - Prosody==Highly variable - Islands of error-free speech==Unusual - Automatic & propositional speech= Equal - Perceived substitutions not frequent AOS - Speech AMRs (rhythm)==Regular - Rhythm is regular - Sequencing of SMRs==Abnormal - Prosody==Less variable prosody - Islands of error-free speech==Typical - Automatic & propositional speech==Automatic speech better than propositional speech - Perceived substitutions frequent

Principles of Treatment: General

Begin treatment knowing when it will end! Prognosis, prediction, planning based on treatment length ===Shared goals that are reasonable Remember external options: prostheses (VP insufficiency—palatal lifts—not good for gag reflexes because of hyperreactive gag), AAC, pacers (control speech rate—PD- make it as intrusive as possible)ß fade this as soon as possible etc. ==Amplifiers for reduced volume ==But, don't go there first

CN V and CN X(IX, XI) Flaccid

CN V: mandibular approximation CN X (IX, XI) - Hypernasality: slow speech rate - greater oral opening: bigger the oral opening the greater the likely the soundwaves will come out of the mouth

Acoustic and physiology of Ataxia: incoordination in breathing laryngeal musculature articulation

Incoordination in respiratory function (timing), making it difficult to inhale adequate amounts of air and expel in controlled fashion Incoordination of laryngeal musculature, affecting maintenance of constant tension... results in f0 and intensity variability (prosody) General articulatory timing control problems... affects VOT, initiation of utterances (prosody), nasality timing, etc.

Postural Disturbances

Loss of postural reflexes - involuntary flexion head, neck, trunk, arms stooped over

Communication Oriented Treatment

Modify the communication interaction GOALS: increase functional communication - reducing the handicap with specific environments

Prosodic Char. of hypo and hyper kinetic dysarthria

Monopitch and monoloudness Reduced variation in syllable duration Continuous voicing Syllable reduction Indistinct syllable boundaries due to imprecise articulation

Etiology of PD

PD most frequent cause of hypokinetic dysarthria PD patients may have more than just hypokinetic dysarthria--> hyperkinetic due to increase in medications

CN X: Flaccid - phonation, prosody

Phonation: - push-pull-pitch goes up - hold breath then exhale - hard glottal attack - head turning- see the vocal fold paralysis-- need the vocal fold to medialize, physically twists the larynx and bring the vocal folds closer together Prosody: - pitch ranges exercises - constrastive stress - chunking into syntactic units

Effects of Cerebellar Damage

inability to stand or sit without swaying or falling, gait disturbances, nystagmus and ocular movement abnormalities -- flocculonodular lesion of the caudal vermis are associated with gait ataxia lesion in lateral and paravermial cerebellar hemispheres are associated with intention tremor and incoordination of voluntary movements - dysmetria - dyssynergy - DDK abnormal timing and velocity Incoordination and hypotonia Ataxic dysarthria: damage in vermis or cerebellar hemispheres bilaterally or to cerebellar output pathways in the brainstem

Cluster of deviant dimensions: hypokinetic dysarthria

VOice: hoarse, rough, tremulous and breathy Articulation: imprecise consonants -- spriantization; fricatives undershoot - rate abnormalities: syllable rep. shortened sylllables Prosodic insufficiency: monopitch, loudness, reduced stress Palilalia: compulsive reiteration of utterances in context of increasing rate and decreased loudness

Rigidity

increased in muscle tone with passive stretch -slowness of movement - stiffness and tightness - resistance throughout range of movement - rigidity present during passive stretch - Result of excessive drive to alpha MN, because cortical output not inhibited by BG

Hyperkinesia: movement symptoms

involuntary movements and abnormal voluntary movements Chorea Other movement abnormalities: - akinesia - dystonia - bradykinesia - hypokinesia - motor incoordination Oculomotor deficits: diplopia - buffero spasm

Control Circuits: Structures

located: posterior , inferior aspect of the brain

General Clinicial Char. for Hyperkinetic dysarthria

abnormal involuntary movements "hyper" refers to the abnormal movement, NOT excessive speed of movement AKA dyskinesia

Respiration of hypo and hyperkinetic dysarthria

alternations to normal agonist- antagonist relationships of respiratory muscles (results in rigidity) -- paradoxical respiratory movements

Dysmetria DDK

aren't able to judge how much movement is needed -fragmentation of rapid alternating muscle movements - disrupted rhythm of fine motor movements - errors in speed of component parts of a movement

Strategies for TX: hyperkinesia

behavioral strategies (early in disease) slow rate, respiratory support External memory (or cognitive) aids AAC Communication partner training

ballism

circular movement

Impact of cognitive changes on communication interactions may include: hyperkinesia

cognitive slowing memory changes processing delays attention deficits cognitive rigidity

Etiologies of Ataxic Dysarthria

degenerative diseases - fredrich's ataxia -- heredity (recessive) both parents have to have the gene - Olivopontocerebellar atrophy (OPCA)-- heredity (dominant) Vascular Disorders -- vertebrobasilar system-- stroke affecting this region Neoplastic disorders -- acoustic neuromas can affect cerebellum, as well as cranial nerves Trauma/ TBI-punch drunk (slurred speech) Toxic/metabolic conditions: chronic alcohol abuse; possibly related to nutritional deficiency (slurred speech) --- toxins such as mercury, glue-- seizure medications

Clinicial Characteristic of Ataxic Dysarthria

difficulties standing and walking - ataxic gait, broad, and unstable stance Nystagmus: rapid oscillation of eyes Impaired check and excessive rebound: feedback systems isn't doing well in their limbs

Dysmetria Dyssynergia

disruption of the movements decreased smooth performance of elements of movements - not in the appropriate space and the correct time --> time spend in contact is greater - errors in speed of the component -- breakdown of multi-joint movements into its constituent parts -- the motor acts decomposes into a series of fragmented individual movements so that smooth movements become erratic and irregular -- halting imprecise, jerky, poorly coordinated movements lacking in speed and smoothness intention or kinetic tremor (3 Hz (2-5 Hz)) - tremor is usually at its worst before end of a goal directed movement is reached

AOS disturbance in

disturbance in programming of speech movements muscles capable of normal function -- no movement disorder

Speech system affected: PD

disturbed respiratory function; yielding poor support for speech - normal vegetative support - LVST helps with this Laryngeal dysfunction resulting in pitch, loudness, and vocal quality disturbances - reduced monopitch - respiration no during laryngeal system to produce variation disruption articulation produces articulation and rate deficit prosody and flattened throughout because of reduction

PD degenerative disease

idiopathic = unknown post encephalic may experience dementia/cognitive impairment and depression nerve cell loss in substancia nigra results in decreased dopamine in striatum - imbalance between dopamine and Ach for clinicial signs - responds to dopaminergic drugs - side effects: dystonia and dyskinesia -- hyperkinetic (unintended movements) - on and off effects with dosage cycle: very individual

Articulation of hypo and hyperkinetic dysarthria

imprecise articulation as a result of undershoot (failure to reach articulatory target)

Dystonia: Distinguishing features

imprecision and irregular articulatory breakdowns, inappropriate variability of loudness and rate, strained harshness, transient breathiness and audible inspiration Highly varied depending on locus of expression and individual variation

Distinguishing Char. hypo and hyper kinetic dysarthria

monopitch monoloudness decreased loudness reduced stress variable rate short rushes of speech increased rate repeated phonemes silences

Treatment AOS Motor Learning

motor learns Conditions of Practice: lots of trails - Mass or Distributed Drill Knowledge of Results Influence of rate

Motor Speech and Communication: hyperkinetic

motor speech and communication Dysphagia cognition

Hyperkinesia: characterized by

movement disorders communication deficits Dysphagia Cognitive decline Personality changes

Etiologies: Hyper - Toxic-metabolic conditions

neuroleptic and antipsychotic drugs that block dopamine receptors

Speech Pathology of Hypo and Hyper kinetic dysarthria: non speech

nonspeech: expressionless facies: unblinking, unsmiling, lack of animation reduced chest (abdominal movements during respiration) infrequent swallow: drooling

Nonspeech: dystonia Speech:

nonspeech: drooling, chewing, and swallowing problems dystonic movements are slower than choreiform movements speech: rate of abnormal movement is slow vowel prolongations to observe movement s

Myoclonus

normal and abnormal movement of the faucial pillar

Planning planning for speech tasks place in motor association areas

o Premotor o Broca's Area o Supplementary Motor Area o Prefrontal and Parietal Association Areas—lesions can result with symptoms as apraxia of speech o Caudate Circuit of the Basal Ganglia o Wernicke's Area supertemporal gyrus

Cortical Area involved in AOS

o Premotor areas (6) and Broca's area (44 & 45) § Where do these areas connect? Diffuse all around the brain (long and short association fibers o Supplementary motor areas (medial aspect of frontal lobe- area6 o parietal lobe somatosensory cortex (3,1 & 2) and supramarginal gyrus (40) o insula o basal ganglia (especially striatum: caudate & putamen)

Cerebellum: pathway

o Same organization in the brain except grooves are very deep—foolia ----Makes for a lot of processing o Cortico (cortex)-ponto (pons)-cerebello (cerebellar)-thalamo (thalamus)-cortico pathways ----Right premotor cortex projects to pons and cross over to the superior peduncle to enters left cerebellum—processes and out the left superior peduncle goes to the right thalamus up to the right premotor cortex ----Right motor cortex "consults with" left cerebellar cortex o Influence of cerebellum is on SAME side of the body -----Left cerebellum consults with right premotor cortex which controls left side of the body Left cerebellum influences left side of the body -----Because of the double crossing

Chorea

rapid, involuntary, random, purposeless movements of a body part - sometimes voluntarily modified to make movement look intentional

Tics:

rapid, sterortyped coordinated or patterned movements that are under partial voluntary control (may be voluntary suppressed temporarily) simple tic-difficulty to distinguish from myoclonus Complex are well coordinated movements

Speech : hypo and hyperkinetic dysarthria

reduced ROM reduced rate or rapid accelerating rate (festination) - speech AMRs may become blurred ---- accelerating Rate ---- decreased ROM overtime

hypokinesia akinesia and effects of PD

reduced movement absence of movement Masked facies arm swing during walk reduced micographia festination-- rapid short shuffle

Damage to BG

reduces movement (hypokinetic) Failure to inhibit involuntary movement (hyperkinetic) imbalance of NT associated with BG malfunction especially dopamine - usually produced in adequate quantities in substancia nigra and transmitted to striatum where its function is inhibitory

PHonation hypokinetic dysarthria

reduction of pitch and loudness variability breathiness related to vocal fold bowing slow initiation phonation evidence of continuous voicing

Trauma and infection in hypo and hyper kinetic

repeated head injury "punch drunk" viral encephalitis

Speaker Oriented Treatment

restore or compensate, reduce impairment - Goal: increase intelligibility, reduce disability Then work on Efficiency, naturalness, and quality of communication - Goal: recruit the patient about the process, increase ecological communication, reducing handicap

Cognitive slowing may result in: hyperkinesia

short phrases/sentences Difficulty with: - conversation initiation - topic maintenance -complex directions - abstract language - new learning - problem solving

Akinesia (Bradykinesia)

slowness of movement (Reduced ROM) Delays in beginning of movement (initiation of movement) slowness of movement once begins Difficult to stop movement decreased amplitude and speed intermittent freezing or immobility

Etiologies: hyperkinesia Vascular Infectious neoplasm

streptococcal throat infections rheumatic fever of BG or thalamus

Speech char: hyperkinetic

sustained vowels to observe fluctuations in articulatory Clusters: - most prominent= prosodic excess - prolonged intervals, inappropriate silences, prolonged phonemes, excess and equal stress) - also exhibit prosodic insufficiency and variable rate - moment to moment variability loss of functional speech by end stages of HD

Apraxia of Speech

the inability to accurately produce volitional speech movements independent of dysarthria, aphasia, and other non- verbal apraxia's - people are more believing that there is an independent between aphasia and apraxia - some people believe they can't occur without each other

Vascular Disturbances in hypo and hyper kinetic

toxic metabolic conditions - antipsychotic meds: block dopamine receptors - heavy metals and chemical exposure

Pathology of hypokinetic dysarthria

tremor of jaw and lips at rest or during sustained postures appears tight and immobile muscle size, strength and symmetry may be normal AMR's slow or rapid, restricted range of movement getting smaller and smaller Overall lack of vigor and animation

Hyperkinetic Dysarthria

variable rate, prolonged intervals, and inappropriate silences, reduced pitch variability, irregular and imprecise articulation, phonatory deviations and sudden forced inspiration or expiration May be present in any or all of the levels of speech (e.g. respiratory, phonatory, articulatory, resonatory levels) with effects on prosody and rate

Anatomy and Phyisology of AOS

widespread left cerebral hemisphere involved in MSP - Linguistic input to MSP from left perisylvian area (temporoparietal cortex and posterior portions of frontal lobe) and basal ganglia and thalamus - Overlap between these linguistic areas and MSP; therefore, damage to perisylvian zone often results in co-occurrence of AOS and aphasia - MSP transforms abstract phonemes to a neural code, which is to be executed by the motor system

Basal Ganglia Structures

§ Putamen § Caudate nucleus § Globus Pallidus § Thalamus § Substantia Nigra § Subthalamic nuclei

Differential Diagnosis: Dysarthria and AOS

Dysarthria: - alterations of strength, tone, range, and steadiness of movement-- observed when you observe the oral mech - components of speech: all components of speech may be affected - aphasia: frequently not associated with aphasia -variability: speech consistent- automaticity, stimulus modality, linguistic variable - error types: predominantly distortions and simplifications - Groping: rarely observed - Neuromuscular o No changes in the physical system - but errors in speech production - Components of speech o Predominately articulation - Aphasia o Frequently (always) associated with aphasia - Variability o Speech is variable § Automatic= okay § Propositional (say somethings) and repetition influenced by multiple factors - Error types o Perceived substitutions, additions, repetitions, prolongations, and complications of targeted sounds - Groping o Groping highly prevalent ASO - no changes in the physical system ---only speech production - articulation - associated with aphasia - speech is variable= automatic, propositional and repetition influenced by multiple factors - errors: perceived substitution, additions, repetitions, prolongations, and complications of targeted sounds - groping: highly prevalent - AMR: consistent SMR-- rarely consistent

Distinguishing Cluster: hyperkinetic

Hypernasality, strained harshness, transient breathiness, articulatory distortions and irregular articulatory breakdowns, loudness variations, and sudden forced inspiration and expiration

Speech char. Ataxia

Impaired coordination of movement patterns (across muscles) vs. individual muscles Articulatory and prosodic breakdowns Inaccurate movements Slow movements Hypotonia Irregular speech AMRs are a distinguishing characteristic of ataxic dysarthria ---> SMRs are arrhythmic in both ataxia and apraxia

AOS by definition

- AOS is, by definition a Motor Speech Disorder - The essential nature and characteristics of AOS must be consistent with the models of speech production and with known pathology at the motor planning/programming levels - Phonological, lexical and syntactic errors should not be lumped under the AOS umbrella. Not supported by data. - There are frequently concomitant errors at phonetic, syntactic, phonologic, and lexical levels of speech production. o This happens because the responsible anatomical areas are in very close proximity and because many pathologies are not strictly localizable. § NOT AOS!

Other aspects of AOS

- Automatic-reactive speech may be better than volitional-purposive speech - Articulation may be better with both auditory & visual stimulation than either one alone - Mirror work has no effect on single word accuracy - Imitation is better than spontaneous speech - Accuracy may increase on consecutive attempts - Motivational/inspirational instruction do effect accuracy of production

Ataxia Dysarthria

- Damage to cerebellar control circuit - connections with the cerebellum, thalamic, pontine, and basal ganglia pathways - Affects mostly (but not exclusively) articulation and prosody o Require fine coordination of muscle movements - Incoordination and reduced muscle tone o Slowness and inaccuracy in the force (strength), range, timing, and direction of speech movements (slightly different direction that is not as precise or accurate) - Different from Apraxia—because the direction of the speech movement is totally off intended movement - Breakdown primarily in motor organization and control (not neuromuscular execution) o Receive a plan that is not coordinated well - Motor activity is poorly controlled and coordinated o Moderate to severe decreases in tone will affect execution

other treatment factors for dysarthria

- Don't forget counseling for patient and family - Early intervention—advance their recovery farther if we didn't intervene - Know the medical plus the speech diagnoses - Physiologic support first then other interventions—working on posture for better speech - Learn about motor learning - Flexibility is often the key!!!

Nonspeech oral mechanism: Hyperkinesia

- Drooling, chewing, and swallowing difficulties - Easily observed choreiform movements

AOS and Dysarthria are different

- Dysarthria should be evident in both speech and nonspeech movements - AOS is only present in speech o Not seen in nonspeech movements

Flaccid Dysarthria Treatment

- Evidence for usefulness of strengthening exercises (oral motor exercises) is limited/suspect/week/doo-doo o EBP says NO - Flaccid Dysarthria - some rational to improve the muscle fibers on the impacted side - doesn't say anything about the speech production - making lips stronger doesn't make a person more intelligible - Goal of treatment is improving speech production, thus work directly on speech production—accuracy

Non verbal oral Apraxia

- Inability to imitate or follow commands to perform volitional movements of speech structures - Can occur independently from AOS - Table 3-2 for nonspeech oral mechanism tasks....sequencing is important o Open and close mouth and lips o Stick out tongue \

Speech AOS

- Lots of phoneme level errors - Inconsistent errors -HALLMARK of AOS - Errors may vary as complexity of articulatory output varies - Errors increase with word length - Imitative performance is poor- - Patient is aware of errors, yet cannot anticipate or correct them - When patient tries to monitor speech to anticipate errors prosodic deficits result - Oral nonverbal apraxia is often, but not always seen in conjunction with AOS

Nonverbal oral Mechanisms

- May be no evidence of weakness; gag reflex and chewing/ swallowing may be normal - Lesions are usually large enough, that there may be concomitant unilateral corticobulbar damage (with weakness, etc.).....dysarthria - Possible sensory deficits

Treatment of AOS: other treatment

- Phonetic placement: manipulate articulators - Phonetic derivation: use intact non-speech gestures to elicit target speech sounds - Imitation/integral stimulation: watch, listen, simultaneously produce, delay to produce - Contrastive stress drill: change stress, rate, rhythm, intonation - putting stress on different words in the sentence o MIT - Melodic Intonation Therapy - Increase speed; increase contextual complexity - Family counseling/education - Total communication - AAC

Programming breakdown takes place in:

- Programming for speech take place in: o Basal Ganglia (caudate and putamen) o Lateral cerebellum o Supplementary motor areas o Premotor cortex o Primary motor cortex o Frontolimbic system

BG functions

- Regulates muscle tone - Regulates movements that support goal-directed movements - Controls postural adjustments during skilled movements - Adjusts movements to the environment - Assists in the learning of new movements o Change the way they are making movements o Compensate for that lots of repetition needs to happen

Athetosis

- Relatively slow hyperkinesia - Inability to maintain a body part in a single position because of superimposed slow, writhing, purposeless movements, that tend to flow into one another o Typically not considered an adult onset dysarthria - Repeated writhing movements slowly shifting from one set of muscles to the next; - If bilateral damage the bulbar musculature involved, else typically restricted to extremities o Unilateral you see it in the limbs - Athetosis is a major category of cerebral palsy

Dystonia

- Relatively slow hyperkinesia - Involuntary abnormal postures resulting from excessive co-contraction of antagonistic muscles o Need agonist antagonist muscles -

Treatment that do not work AOS

- Response delay intervals of 0, 3, & 6 sec. do not influence accuracy - For most patients binaural masking has no positive effect - Delayed auditory feedback (DAF) may have a negative effect on articulatory accuracy - Auditory discrimination is better than verbal production - Oral perception and sensation may be impaired

Programming

- Speech "programming" is "...a set of muscle commands that are structured before a movement sequence begins which can be delivered without reference to external feedback" (Marsden, 1984; p228) - Programs specify muscle: tone, movement direction, force, range, rate and mechanical stiffness of joints.

Sydenham's Chorea (acquired pediatric chorea)

Childhood onset (typically between 5 and 15 years old) - Girls more frequently affected than boys Disease (infection) that damages BG Fast, involuntary, irregular, and aimless involuntary movements of the limbs, body,, and muscles of the face. Movements are uncoordinated with weak muscles, imprecise speech, reduced ability to concentrate (focus attention), and emotional challenges. Recovery is quick in most children (1-2 months), but can last longer Disease reoccurs in about a third of cases Correlated with later disorders o Autism o Tics o Obsessive-compulsive disorder o ADHD

Cerebellar Function

Coordination of skilled voluntary muscle activity and tone - involved in all kinds of movement - alpha and gamma neurons ---- helps them what to do Knows what a movement should be (know the temporal spatial function) - monitors results based on feedback - influences subsequent cortical motor output based on that feedback - smooths the coordination of movements

Tasks for SPeech for Ataxic Dysarthria

DDK tasks AMRS - apraxia: grouping and incorrect targeting early on and able to get the target -- rhythm is irregular - Ataxia: never gets to the target SMRs - Apraxia: sequencing errors - Ataxia: able to get to the right position rhythm error

Hypokinetic and Hyperkientic Dysarthria

Damaged Basal Ganglia control circuit - Hypokinetic -- reduction/ depletion in neurotransmitter dopamine - hyperkinetic -- disease of BG and related portions of extrapyramidal system

Huntington's Disease or Chorea

Degenerative, slowly progressive - hereditary, autosomal dominant, neurodegenerative Onset typically 30-50 years of age Death 10-20 years from onset HD affects approximately 5.7 per 100,000 people in North America, Europe, and Australia HD affects approximately 0.4 per 100,000 people in Asia Degeneration of caudate and putamen Chorea plus dementia, psychosis, depression

Functions of BG

Regulates muscle tone Regulates movement that support Goal directed movement (arms swinging) Controls postural adjustments during skilled movements (stablized shoulder during writing) Adjust movement to the environment Assist in learning new movements

Parkinson's Disease

Rigidity reduced force and range of movement, slow individual movements sometimes fast repetitive movements - different from spastic tone--- caused by lack of inhibition of alpha motor neurons-- consistently contracting Decreased mobility and range of movement - medications not as responsive to speech problems Less dopamine available Problems with maintenance of proper background tone and supportive neuromuscular activity for fast discrete speech movements

Effects of BG Damage: Reduced mobility or hypokinesia

Too little movement overactivity in the STN and in the output from the GPi and SN leading to excessive inhibition of thalamic neurons that project to the SMA Increase muscle tone no velocity dependent and present throughout the range of motion- resistence to movement (rigidity) - movements are slow and stiff and may be initiated or stopped with difficulty-- reduced range of movement is underlying many of deviant speech char. hypokinetic rigid syndrome often result from loss of dopaminergic neurons in the SN

Effects of BG Damage: Involuntary movements, or hyperkinesia

Too much movement decreased activity in the STN can lead to hyperkinetic movement disorder excessive can result from excessive activity in dopaminergic nerve fibers reducing the circuit damping effect of cortical released of unwanted competing motor program-- resulting in involuntary programs vary in locus speed regularity and predictabilty -- unpredictable muscle tone and movement underlie many deviant speech char.

TRAP

Tremor Rigidity Akinesia Postural Disturbances

Anatomy and physiology of Ataxia Dysarthria

o Two cerebellar hemispheres, each connected to the opposite thalamus and cerebral hemisphere; each hemisphere provides input to control the ipsilateral side of the body (double crossing) o Cortico-ponto-cerebello-thalamo-cortical loop o Cerebellum receives input from widespread cerebral cortex (sensory and motor), brainstem and spinal cord o Purkinje cells send inhibitory output to deep nuclei of cerebellum; deep nuclei send excitatory output (via superior or inferior cerebellar peduncles) to thalamus, brainstem and spinal cord—DO NOT MEMORIZE o Involved in coordination of skilled voluntary muscle activity and tone o Knows what movement should be; monitors results based on feedback, and influences subsequent cortical motor output based on that feedback; smooths the coordination of movement o In general, ataxic dysarthria most commonly associated with bilateral or generalized cerebellar disease § Damage effecting both sides of the cerebellum and they are more diffuse

Social Interaction Disturbances: Hyperkinetic

oculomotor deficits may impact consistent eye contact, person with HD may not recognized nonverbal signs Facial chorea (grimacing) may result in a mismatch intended of facial expressions leading to communication partner confusion/misinterpretation Difficulty interpreting facial expressions of communication partners

Nonspeech Ataxic Dysarthria

oral mechanism exam often normal nonspeech AMRs of jaw, lips, tongue may be irregular : - look at smoothness of movement: not smooth and regular ---- problem with rhythmic disruption in speech - not speech specific -- ataxia both oral motor and speech effected -- if you dont see the nonspeech symptoms -- apraxia

Tremor

oscillations around forced point 4-7 hz decreased during voluntary movements pin rolling movements

Etiologies: Tardive Dyskinesia

prolonged use of neuroleptic drugs, especially those used to treat schizophrenia Orolingual chorea: when they are not eating they have eating movements Chewing, lip smacking tongue protrusion Discontinue drugs often improves symptoms -- extended use may result in permanent damage

Dystonia: clusters

prosodic disturbances (e.g. monopitch, monoloudness, short phrases, reduced stress)