Midterm Flashcards
Flaccid dysarthria
weakness; LMN; breathiness, hoarseness, diplophonia, reduced maximum vowel duration (weak vocal fold); vocal flutter, short phrases, audible insiration/stridor, weak cough ; reduced tone and reflexes; hypernasality; monopitch and monoloudness; harsh voice
Spastic dysarthria
spasticity; bilateral UMN; strained, harsh, strangled voice, grunt @ end of expiration; slow rate; increased tone and reflexes; slow rate, mild hypernasality; increased effort/fatigue
Ataxic dysarthria
incoordination; cerebellar control circuit; unsteadiness during vowel prolongation, sometimes alterations in loudness and pitch; irregular arctic breakdowns, increased errors w/ increased length, aud/visible groping for arctic posture, slow rate, sound prolongations, distorted substitutions & additions, syllable and word segmentation; irregular rate; scanning speech; harsh; dysmetria (over/under shoot)
Hypokinetic dysarthria
rigidity, reduced ROM, poor movement scaling; reduced dopamine in basal ganglia control circuit; breathiness (sometimes aphonia) or harsh, hoarseness, reduced volume, loudness decay, vocal flutter/rapid voice tremor, reduced max vowel prolongation; rapid, blurred rate; short rushes of speech parkinsonian
Unilateral UMN dysarthria
variable combinations of weakness, spasticity, incoordination; unilateral UMN ; imprecise consonants, slow AMRs, harsh voice, mild hyernasality, contralateral weakness of lower face, tongue; increased tone and reflexes; increased effort/fatigue
Apraxia of speech
impairment in planning, programming; left (dominant) hemisphere frontal cortex; usually co-morbid w/ nonfluenct aphasia; slow rate, prolonged speech segments, abnormal prosody, consonant and vowel distortions
Vocal flutter
rapid tremor like fluctuation in voice due to weakness and LMN CN X; common in ALS, hypo kinetic dysarthria
Hyperkinetic dysarthria
essential voice tremor (esp vowel prolongation), involuntary noises & movements; vocalizations, voice interruptions, variable or excessive volume, laryngeal myoclonus, voice: horse, strained, breathy, sometimes jaw tremor or chorea; may be irregular rate; pauses/stoppages
Myoclonus
slow, regular voice fluctuations during vowel prolongation; “slow tremor”; palatal-pharyngeal-laryngeal
Scanning prosody
robotic; mono rate and pitch
Chin fasciculations
LMN CN VII
Dysarthria
“accidental articulation”; neurologically based speech disorder due to CNS/PNS abnormality; movement or muscle abnormalities (weakness/paralysis, tone de or in, incoordination, speech, range, steadiness, accuracy)
Prevalence of various MSDs
Mixed most common (31%), hyperkinetic (21%), rest ~10% (apraxia, flaccid, spastic, hypokinetic, ataxic)
Motor Speech Disorders categorized by
age of onset, disease progression, lesion location, pathophysiology, and/or speech characteristics
UMN Dysarthria AKA & caused by
spastic dysarthria, pseudobulbar palsy; bilateral damage to UMN pathways (direct and indirect activation pathways)
UMN Direct pathway effects
loss of fine, skilled, rapid movement; contralateral weakness
UMN Indirect pathway effects
hyperactive reflexes; stretch reflexes (spasticity); clonus; increased muscle tone
Non-speech symptoms UMN Dysarthria
dysphagia; drooling; non-speech oral movements (reduced lip retraction, reduced DDK, weak, slow, reduced tongue ROM) ; emotional lability; hyperactive reflexes
Pesudobulbar or labile affect
emotional lability; pathological laughing or crying; reduced threshold for emotional responses
Most common spastic dysarthria etiology
stroke; multiple cerebral or single brainstem; corona radiate, internal capsule
Amyotrophic Lateral Sclerosis
progressive degeneration of UMNs and LMS; one presents first, eventually becomes mixed (flaccid-spastic) dysarthria
TBI
can cause bilateral pyramidal/extrapyramidal system damage; widespread cordial, subcortical and brainstem damage; linear & rotational movements; diffuse axonal injury (stretched/torn axons); lacerated brain tissue, blood vessel hemorrhages; mixed dysarthria frequent
Multiple Sclerosis
autoimmune disorder of myelin in CNS; often mixed ataxic-spastic dysarthria
Bilaterally innervated nerves
CNs EXCEPT CN VII facial (lower) CN XII hypoglossal
Contra laterally innervated nerves
CN VII, CN XII, spinal nerves
Unilateral (left) UMN lesion face
lower right face weak, both sides of forehead wrinkle
Mechanism of hyperactive stretch reflex (spasticity)
indirect activation pathway inhibits stretch reflex; daman to UMN releases this inhibition, resulting in hyperactive stretch reflex
Alpha motor neurons
LMN; innervate “extrafusal” muscle fibers, causes muscle fibers to shorten
Gamma motor neurons
innervate intrafusal muscle fibers (spindles); influenced by indirect activation pathway/basal ganglia/cerebellum; maintain muscle tone, stretch reflex; when fired, muscle spindle shortens
Stretch reflex
when muscle moved involuntarily, spindles contract, sensory neurons detect “stretch” SO alpha motor neurons fire to contract the muscle (back to original position)
Gamma motor neuron system
maintains normal tone by low-level alpha motor neuron firing; w/ UMN lesions, DISinhibited (overactive) so spasticity
Spasticity in orofacial system
depends on presence of muscle spindles (jaw=high spindle density, clear stretch reflex; face/lips=none, palate, pharynx, larynx- variable)
Management of spasticity
medical (botox, baclofen pumps); stretching (slow, passive stretch inhibits stretch reflex, fast stretch increases tone); vibration (may reduce tone); icing (short-term reduction of tone)
Unilateral UMN dysarthria
People experience speech system even though CN bilateral innervation; individual variation? bilateral innervation not enough?
Unilateral UMN Dysarthria Speech
imprecise consonants, irregular arctic breakdowns, harsh, reduced loudness, slow rate, hyper nasality, slow imprecise irregular AMRs; slurred/think speech that deteriorates w/ fatigue or stress
Unilateral UMN Dysarthria non-speech
unilateral lingual & lower facial weakness; hemiplegia, hemiparesis, sensory deficits (limb); hyperreflexia
Unilateral UMN Dysarthria etiology
stroke (90%)
Neuronal response to ischemia
lack of blood/O2; neurons become swollen (edema), shrink, die
Neuronal response to axonal injury
cell bodies swell, lose internal components
Neuronal response to wallian degeneration
axons separated from cell bodies will degenerate
Neuronal response to neurofibrillary degeneration
clumps of neural fibers from plaques or tangles, cell death
Nerve regeneration?
in PNS, axon may regenerate if cell body survives; NOT CNS
Neuronal response to muscle atrophy
district of nerve innervating muscle may result in wasting away of muscle
Neuronal response to diaschisis
abnormal function of healthy cells because of lack of input from diseased neurons
Demyelinization occurs in
MS, Guillain-Barre, leukodystrophy
Astrocytes
react to CNS injury by forming scars in neural tissue (process aka gliosis, astrocytosis, astrogliosis)
Degenerative disease
gradual decline in neuronal function; neurons may atrophy and disappear (Parkinson’s- substantial nigra, AD- neurofibrillary tangles); chronic, progressive, diffuse; can begin w/ focal impairment (e.g. speech); clinical difference on localization, progression rate
Inflammatory disease
infectious processes, subacute; meningitis- leptomeninges, CSF; encephalities- brain parenchyma
Toxic-metabolic disease
toxins result in altered neural function; e.g. vitamin deficiencies, biochemical disorders (genetic), drug toxicity, lead/mercury; Leads to edema, ischemia, demyelination; diffuse effects; acute, subacute, or chronic
Neoplastic disease (cancer)
-oma tumor of named organ; uncontrolled cell growth interrupts function of normal cells, mass lesions; focal chronic or progressive signs; CNS tumors rarely metastasize outside CNS
Traumatic disease
acute onset, improving course; PNS- focal or multifocal, CNS-TBI; penetrating vs closed head injury
Vascular disease
CVA; acute one, focal localization, course stabilizes/improves & progress due to edema
Motor plan preparation
left inferior frontal cortex (primary motor cortex) “brainstormer”; when damaged, poorly constructed motor plans and apraxia of speech
Motor plan selection
basal ganglia “gatekeeper”; when damaged, not enough or too much inhibition of cortical motor system and hyper/hypokinetic dysarthria; helps set stage for movement
Motor Command transmission
UMN system: motor cortex to brainstem “middle manager”; when damaged, reduced transmission of motor commands/failed inhibition of stretch reflex and spastic dysarthria
Motor execution
“worker bee” LMN System: Brainstem to muscles; when damaged, failure to contract muscles and flaccid dysarthria
Motor correction/coordination
Cerebellar control circuit “clean up crew” error corrector; when damaged, failure to correct for irregularities and ataxic dysarthria; makes sure movement goes all right
CNS speech motor system
Control circuits (basal ganglia, cerebellum) and UMN system (direct and indirect activation pathways)
PNS Motor Speech System
Final Common Pathway- LMN System
Direct activation pathway
Sends motor commands from motor cortex to LMN system via corticbulbar tract (CN nuclei) or Corticospinal tract (spinal nerves); AKA pyramidal tract; facilitates skilled, discrete movements;
Indirect activation pathway
Helps regulate muscle tone, reflexes; AKA Extrapyramidal tract; inhibits activity of direct path, maintains posture, tone, regulates reflexes, stable frame for skilled movements
Damage to UMN leads to
contralateral limb weakness, loss of skilled moments or slowness, spastic muscle tone
Corticobulbar tract
*Most important in speech/dysarthria; primary motor cortex –> corona radiata/internal capsule –>partial decussation and synapse on CN nuclei; mostly bilateral activation of LMN; unilateral damage to one side of cortex=minor speech difficulties
LMN System affected indirectly through
reticular formation, red nucleus, vestibular nuclei, basal ganglia, cerebellum
Damage to UMN results in spasticity by
releasing inhibition of the indirect activation pathway, resulting in hyperactive stretch reflex
Damage to UMN results in (symptoms)
Damage to direct AND indirect pathways: muscular weakness on contralateral limb, jaw tongue, loss skilled movements, spastic muscle tone
LMN system (peripheral speech control)
Final Common Pathway- peripheral mediation of ALL motor activity, last link in neural chain to movement; mediated via alpha motor neurons that innervate muscles
Peripheral speech control
CN innervate muscles of phonation, resonance, articulation; spinal nerves involved in respiration; muscle ipsilaterally LMN innervated; damage=flaccid/reduced tone on affected side
CN V Trigeminal
origin: pons; function: jaw movment; face, mouth, jaw sensation
CN VII Facial
origin: pons; function: facial movement; hyoid elevation; stapedius reflex; salivation; lacrimation; taste
CN IX Glossopharyngeal
origin: medulla; function: pharyngeal movement, pharynx and tongue sensation, taste
CN IX Glossopharyngeal
origin: medulla; function: pharyngeal movement, pharynx and tongue sensation, taste
CN X Vagus
Origin: medulla; Function: pharyngeal, palatal, and laryngeal movement; pharyngeal sensation; control of visceral organs
CN XI Accessory
origin: medulla, spinal cord; function: shoulder and neck movement
CN XII Hypoglossal
origin: medulla; function: tongue movement
Spinal nerves for speech control
innervate diaphragm, intercostal muscles (rib expansion), abdominals; damage=reduces respiratory support; innervation widely distributed BUT SN3-5 damage can paralyze diaphragm
Basal ganglia function
sets background for intentional moment- regulates tone, suppresses extraneous movements; involved in selection of movements, early acquisition of learned, skilled movements
Basal ganglia mechanism
inhibiting or release of inhibition (disinhibiting) activity of motor cortex; dopamine and BAGA inhibit, acetylcholine excites; regulates inhibition output of basal ganglia to thalamus which contains exciting output to motor cortex
Basal ganglia lesion to striatum
hyperkinetic; reduced actitation in striatum, too LITTLE inhibition from globes plaids to cortex, uncontrollable involuntary movements
Basal ganglia lesion to substantia nigra
damages dopamine cells- hypo kinetic; not enough inhibition from substantial nigra to striatum, overactive sub thalamic nucleus, too much inhibition from globes plaids to thalamus and back to cortex; inability to move
Cerebellum functions
error control/input and output; monitors motor output to muscles by input from somatosensory cortex & some from brainstem
Cerebellum mechanism
cortex sends “efferent copy” to cerebellum as motor command sent to brainstem; spinocerebellar tracts bring sensory info on body position/movement; cerebellum compares efferent (intended) copy w/ sensory info from actual movements and sends corrective feedback to cortex or brainstem if they don’t match
Effectiveness as treatment target
getting message across; adjustment to disability
Efficiency as treatment target
getting message across in reasonable time; compensation for impairment
Naturalness as treatment target
how did message sound? restoration of impaired function ; “cosmetic”; unilateral UMN dysarthria, unilateral VF paresis
Compensation treatments
speech strategies (slow rate, over arctic); prosthetic devices (AAC, palatal lift, amplification, pacing board); speech & gesture; modification of physical environment
Adjustment treatments
reduce need for lost function (planning for progressive speech loss, changing career/lifestyle) **as SLP, ID factors that limit communication and shape pragmatic decisions
Treatment goals
relate symptoms to functional components and pathophysiology; target pathophysiology when possible then functional components
Principles of motor learning in speech treatment
drill, specificity of training, practice schedules, speed v accuracy
5 components of speech
respiration, phonation, articulation, resonance, prosody
Motor speech exam
history, structural/functional exam, acoustic motor speech exam, testing connected speech, nonverbal oral apraxia, apraxia of speech, stress testing (MG), assessment of intelligibility, comprehensibility, efficiency
Motor Speech Exam- CN VII
symmetry, involuntary movements, fasciculations? lip movements, puffing cheeks, ROM, affect
Motor Speech Exam- CN V
jaw hang low, involuntary movements, opening mouth/resist pressure to close, clench teeth/resist close, speech movements
Motor Speech Exam- CN XII
symmetry of tonge, wet, fascinations, protrusion/pressure, side to side movement, ROM
Motor Speech Exam- CN X
palate hang, symmetry, ahhh, airflow on mirror from nares, resonance
Motor Speech Exam- CN X and Spinal nerves
cough, glottal coup, respiration
Reflexes
gag (asymmetric?); jaw jerk (if present w/ chin tap, maybe UMN disease); sucking (w/ stroke upper lip, UMN disease); snout 9tip of nose??); palmomental (elevation of ipsilateral chin w/ hand stroking, UMN)
Acoustic Motor Speech Exam
/a/ phonation/resonation; /u/ resonance/nasal flutter, velopharyngeal closure (w/ nasal occlusion); DDK AMR pppp kkkk tttttt, SMR pu tu ku; connected speech (passage/convo)
nonverbal oral apraxia testing
difference between command vs imitation responses; reflex (imitate) sometimes intact when volitional impaired
Motor Speech Exam indicators of Apraxia of Speech
distorted arctic, substitutions, omissions, blocking, groping; AMR better than SMR; automatic better than volitional; mono > multi syllabic words
Stress testing
fatigue; LMN present, test for Myasthenia Gravis; deterioration of vocal quality, resonance, arctic, w/ subsequent recovery
Intelligibility testing
single word, phoneme, sentence, conversation (% words intelligible); intelligibility= # words correct/total words vs efficient intelligible words/time
Flaccid dysarthria mechanism
muscular weakness & reduced tone caused by damage to final common pathway; neuronal nuclei, axons, neuromuscular junction, muscle fibers may be affected
Flaccid dysarthria etiology
degenerative disease (40%) surgical trauma (20%) stroke (10%)
Flaccid dysarthria characteristics
neuromuscular weakness, hypotonia, hyporeflexia, muscle atrophy, fasciculation/fibrillations
Flaccid dysarthria (dysphonia)
larynx; CN X Vagus pharyngeal branch (pharyngeal, superior laryngeal- internal and external (cricothyroid, pitch and adduction), recurrent laryngeal (adduction/abduction); muscles of larynx, pharynx, soft palate), CN V Trigeminal, CN VII Facial, CN XII Hypoglossal
Vagus CN X: Recurrent Laryngeal Nerve
laryngeal adduction & abduction; aspiration, dysphagia, stridor, unilateral VF paralysis; breathy, reduced volume, decreased pitch, shortened phrase
Vagus CN X: Pharyngeal branch
muscles of pharynx, velum, palatoglossus (palatal elevation); asymmetric velum at rest- deviation to strong side, decreased gag reflex; hyper nasal, decreased phrase length, imprecise pressure consonants
Trigeminal CN V mandibular branch
muscles of jaw, soft palate; lesion- slow/limited ROM for jaw, jaw deviated to weak side, inability to elevate jaw (imprecise bilabial and lingual arctic, slow rate of speech)
CN VII motor branch
muscles of facial expression, speech production;bell’s palsy, hypotonicity, distortion labial consonants
CN XII Hypoglossal
receives taste, tactile info; innervates intrinsic and extrinsic muscles of tongue; lesion- tongue movement and tone, atrophy, shrunken tongue, fasciculations, deviation to weak side,imprecise lingual and velar consonants ; mostly contralateral innervation from UMN
Fibrillations
invisible spontaneous muscles contractions due to slow repetitive action potentials
Spinal nerve damage
respiratory muscles, shoulder/neck to compensate for breathing, short phrases, decreased loudness, prosodic abnormality (monopitch/loud)
Hyopkinetic dysarthria features
muscle rigidity, reduced foce & ROM, resting tremor
Hypokinetic dysarthria mechanism
loss of dopamine cells in substantia nigra- OVER inhibits motor context (so less movement)
Hyperkinesia mechanism
damage to striatum (putamen/caudate) in basal ganglia causes UNDERinibition of motor cortex
Basal Ganglia circuitry
Morot cortex –> striatum input, output globus pallidus –> thalamus, cortex; little loops: striatum to Globus Paladus to Substantia Nigra to Globus Paladus; Striatum to Substantia Nigra back to Striatum
Hypokinetic dysarthria etiology
degenerative disease (~90%)
Hypokinetic dysarthria medications
neuroleptic med (blocking effect on dopamine receptors)
Hypokinetic dysarthria motor characteristics
reduced, slow (bradykinesia) movement; rigid tone; difficulty initiating, resting tremor, reduced postural reflexes, irregular gait, masked facies
Hypokinetic dysarthria speech characteristics
reduced movement, imprecise consonants, repetition of syllables, short phrase and short “rushes of speech”, rapid rate, harsh, breathy
Parkinson’s disease treatment (med)
med: L-dopa dopamine replacement, levodopa- induced dyskinesia; ;
Deep Brain Stimulation for PD
reduces rigidity, increases movement aplitude, reduces L-Dopa dosage; new speech problems (harsh, reduced fluency)
Parkinson’s disease treatment (surgical)
surgical ablation- pallidotomy, thalamotomy (Globus pallidus, ventral lateral nucleus of thalamus), Subthalamotoy (subthalamic nucleus all symptoms);today- deep brain stimulation (globes pallidus, thalamus (VL), STN; nigral cell transsplantation- to striatum to replace dopaminergic cells (mixed outcomes)
Parkinson’s disease treatment (behavioral)
rate based (Delayed auditory feedback, pacing boards, hand tapping) or aptitude-based (LVST) (intensive, high effort- PT OT Big)or pitch-limiting voice treatment
Intra-cerebellar mechanism
Input goes from deep nuclei –> mossy & climbing fibers; if mossy & climbing match, Purkinje fires to cancel the correction of the movement; output goes from deep cerebellar nuclei to thalamus
Mossy fibers
intended movement
Climbing fibers
actual movement; primes deep cerebellar nucleus for correction by activating purkinje cell
Ataxic dysarthria etiology
degenerative disease (45%), vascular (11%), demyelinating disease (10%)
Ataxic dysarthria characteristics
dysmetria (over/undershoot); decomposition of movement; halting, imprecise, poorly coordinated, lacking in speed and fluidity; stumble over/slur words, difficulty coordinating breathing, slow rate improves intelligibility
Motor characteristics of ataxia
broad stance/gait, unstable trunk, excessive rebound, intention/terminal tremor, hypotonia, nystagmus, oculodysmetria, normal strength of oral structures but irregular AMRs
Speech characteristics of ataxia
imprecise consonants, irregular arctic breakdowns, distorted vowels, excess/equal stress, slow rate, prolonged sounds, harsh, mono pitch and loud, explosive loudness, respiratory incoordination
