Adult Motor Speech Disorders
Freed, Chapter 4: Flaccid Dysarthria
A. Definitions of Flaccid Dysarthria
o impairments of the lower motor neurons in the cranial or spinal nerves
o result of damage to the peripheral nervous system
o weakness in the speech or respiratory musculature
B. Neurological Basis of Flaccid Dysarthria
o caused by damage to lower motor neurons (PNS)
o LMNS are also known as the final common pathway because they are the last and only “road” that the neural impulses from the upper and motor neurons can travel along to reach the muscles
1. Cranial Nerves of Speech Production (6 total)
a. Trigeminal Nerve (V)
o Three main branches: ophthalmic, maxillary, and mandibular.
o Mandibular is most important for speech production.
s innervates the muscles that elevate and lower the jaw
s innervates the tensor veli palatine muscle in the velum, which helps elevate the velum
o Unilateral damage to CN V = jaw deviates toward affect side when it is open
s does not affect speech significantly because unaffected side can compensate.
o Bilateral damage to CN V = jaw cannot be raised sufficiently, (esp. problem for vowels, bilabials, linguadentals, or linguapalatals.)
s rate of speech often slowed by reduced ability to elevate the jaw
s hypernasality also may occur because of innervation to the velum
b. Facial Nerve (VII)
o Two major branches:
s cervicofacial branch innervates the lower face
s temporalfacial branch innervates the upper face
o If a lesion occurs above the point where the nerve branches it affects the whole face ipsilaterally, if it occurs below, it affects only that branch.
· Upper Motor Neuron Innervation of the Facial Nerve
s cervicofacial branch (lower face) receives unilateral UMN innervation from the contralateral side of the brain
s temporalfacial branch (upper face) receives bilateral UMN innervation
s Therefore: unilateral UMN of CN VII damage will result in contralateral weakness of the lower face.
c. Glossopharyngeal Nerve (IX)
o Innervates the stylopharyngeus and superior pharyngeal constrictor muscles
o Eliciting the gag reflex is one way to assess the function of this cranial nerve
d. Vagus Nerve (X)
· Pharyngeal Branch - innervates m. of pharynx & velum
s bilateral damage: moderate to severe hypernasality and distorted pressure consonants (b/c air is leaking through nasal cavity).
s unilateral damage: usually can be compensated for
· External Superior Laryngeal Nerve Branch - innervates the cricothyroid (pitch-change m.) of the larynx.
s bilateral damage: decreased loudness, increased breathiness, and notable difficulty in changing vocal pitch.
s unilateral damage: modest difficulty in varying pitch
· Recurrent Nerve Branch - innervates all other m. of larynx (phonatory m.)
s bilateral damage: paralyses both vocal folds; inhalatory stridor, breathy, hoarse voice quality
s unilateral damage: paralyses one vocal fold; breathy phonations, decreased vocal loudness
e. Accessory Nerve (XI) – not a “pure” CN; branches out from spinal cord
· positioned close to CN X (concomitant damage is typical)
· works in conjunction with CN X to innervate velum/pharynx/larynx
· innervates sternocleidomastoid & trapezius
f. Hypoglossal Nerve (XII)
· Provides innervations to all the intrinsic and most of the extrinsic m. of tongue.
s bilateral damage: overall weakness and slow movement and reduced ROM, bilateral atrophy; severe articulation problems
s unilateral damage: ipsilateral weakness; deviates to side of weakness, may atrophy on side of lesion; milder articulation problems
· CN XII receives unilateral, contralateral, innervation from the UMN
s Therefore damage to left UMN results in tongue deviation to right…
· Imprecise articulation is the primary characteristic of an individual with CN XII damage.
2. Spinal Nerves
o provide the motor innervation for the m. of respiration
o Phrenic nerve – provides motor innervation to the diaphragm. Damage to this nerve can paralyze the diaphragm and significantly weaken inhalation.
o Usually, damage must be wide spread (phrenic nerve is exception) to sig. impair respiration.
o Impaired respiration = decreased loudness, reduced subglottic air pressure, shortened phrases (which affects prosody), breathy or strained vocal quality towards the end of an utterance (speaking on residual air).
C. Etiologies of Flaccid Dysarthria
1. Physical Trauma
o iatrogenic, head/neck injury
2. Brainstem Stroke
o CN are so close together that small CVA can have big affect.
3. Myasthenia Gravis
o Antibodies damage acetylcholine receptor sites (neurotransmitter that triggers muscle contraction) at the neuromuscular junction (where LMN meets m. tissue).
o Rapid fatigue; weakness; hypernasality; decreased loudness; breathy voice quality; decreased articulatory imprecision during prolonged speaking tasks
o Stress-tests (e.g. count to 100)
4. Gullain Barré Syndrome
o Progressive inflammatory loss of the myelin sheath around axons (demyelination). Rapid progression, usually occurs in the PNS
o Demyelination of CN cause flaccid dysarthria and dysphagia
o Typical recovery takes weeks to months
5. Polio
o viral disease that attacks cell bodies of the LMN, most frequently attacks the spinal nerves (resulting in isolated respiratory weakness). On rare occasions it can affect the CN’s.
o labored inhalation; short phrases; speaking on residual air, decreased loudness.
6. Other Causes of Flaccid Dysarthria
o Tumors
o Muscular Dystrophy (progressive degeneration of m. tissue)
o Progressive Bulbar Palsy (can affect LMN and UMN)
D. Speech Characteristics of Flaccid Dysarthria
1. Resonance
o hypernasality is the most prominent characteristic of flaccid dysarthtria
o Bilateral damage to pharyngeal branch of vagus (CN X), which innervates velum
s Nasal emissions (due to VPI)
s Weak pressure consonants (decreased intraoral pressue)
s Shortened phrases (wasted air through nasal cavity)
2. Articulation
o imprecise consonant production is the second most prominent characteristic of flaccid dysarthria
o Bilateral damage to facial (CN VII)
s significant effect on bilabial, labiodental and lip rounding
o Bilateral damage to hypoglossal (CN XII)
s misarticulation of phonemes requiring tongue elevation
o Bilateral damage to trigeminal (V)
s Difficulty elevating jaw and approximating articulators
3. Phonation
o Damage to the recurrent branch of the vagus (X)
s phonatory incompetence (incomplete adduction of vocal folds) – a valuable diagnostic sign of flaccid dysarthria
s breathy voice quality
s audible inhalation stridor
the combined presence of hypernasality and phonatory incompetence (breathy voice) is the strongest confirmatory sign that flaccid dysarthria is the correct diagnosis
4. Respiration
o may or may not be a component of flaccid dysarthria
o reduced loudness; shortened phrases; strained vocal quality
5. A Problem of Respiration and Phonation?
o How can we determine if the problem is one of air wastage because of poor laryngeal valving or reduced vital capacity from weakened respiration?
o Listen to cough and a glottal stop (uh-oh).
s Poor respiration = breathy cough; sharp glottal stop
s Poor laryngeal closure (or both): breathy cough; weak glottal stop
6. Prosody
o Weakened laryngeal m. result in monopitch and monoloudness
s not diagnostic markers
E. Key Evaluation Tasks for Flaccid Dysarthria
1. Conversational speech and reading
2. AMRs
3. Prolonged vowel
4. Speech stress test (for MG)
F. Treatment of Flaccid Dysarthria
o No definitive research studies have shown that strengthening tasks make significant contributions to the recovery of speech production
1. Damage to the Trigeminal Cranial Nerve (V)
a. Jaw Muscle Strengthening
b. Jaw Sling
2. Damage to the Facial Cranial Nerve (VII)
a. Lip Strengthening Exercises Using Button and String
b. Lip Puckering
c. Holding a Smile
3. Damage to the Vagus Cranial Nerve (X)
a. Treatments for Resonance Deficits
1. Surgical and Prosthetic Treatments
· pharyngeal flap
· Teflon injection
· palatal lift
2. Velar Strengthening Exercises
3. Modification of Speech
· Increase Loudness
· Reduce Rate of Speech
s (gives slow-moving velum more time to close)
· More Open-Position Mouth During Speech
b. Treatments for Phonation Deficits
· Pushing and pulling procedures
· Holding breath
· Hard glottal attack
· Head turning and sideways pressure on the larynx
c. Treatments for Prosodic Deficits
· Pitch range exercises
· Intonation profiles
· Contrastive stress drills
· Chunking utterances into syntactic units
4. Damage to the Hypoglossal Cranial Nerve (XII)
a. Strengthening Exercises
· Tongue strengthening
b. Traditional Articulation Therapy
· Intelligibility drills
· Phonetic placement
· Exaggerating consonants
· Minimal contrast drills
c. Treatments for Respiratory Weakness in Flaccid Dysarthria
· Correct posture
· Compensatory devices
· Speaking immediately on exhalation
· Cueing for complete inhalation
Chapter 5: Spastic Dysarthria
A. Definitions of Spastic Dysarthria
o bilateral damage to UMN
o imprecise articulation; monotone; monoloud; poor prosody; reduced ROM; speech is slow, effortful, words are prolonged
o increased muscle tone w/ concomitant weakness
B. Neurological Basis of Spastic Dysarthria
o Specifically, spastic dysarthria is caused by bilateral damage to both the pyramidal and extrapyramidal neural pathways that serve the speech mechanism.
o These two pathways work in parallel and it is rare to only have damage to one pathway
1. Role of Upper Motor Neurons in Spastic Dysarthria
a. Pyramidal Neural Pathway – direct pathway from cortex to LMNs. Responsible for transmitting neural impulses for discrete skilled movements to the LMN, which then send them to the muscles
o damage to the parts of the pyramidal system serving the speech mechanism will result in weakness and slowness in the speech musculature.
b. Extrapyramidal Neural Pathway – indirect pathway from cortex to LMNs. Responsible for maintaining posture, regulating reflexes, and monitoring muscle tone.
o damage to the extrapyramidal system can result in weakness, increased muscle tone (spasticity), and abnormal muscle reflexes.
2. Significance of Bilateral Damage
o For spastic dysarthria to occur, the damage must be bilateral and affect both the pyramidal and extrapyramidal pathways.
o The symptoms are a combination of what would be expected if each system were damaged individually: weakness, slow movements, spasticity, and abnormal reflexes.
o The spasticity will be most noticeable in the laryngeal muscles (hyperadduction of the vocal folds)
C. Etiologies of Spastic Dysarthria
1. Stroke (must be bilateral)
o a single stroke if it occurs in the brainstem
o a stroke in each hemisphere (sometimes a single stroke can appear to cause spastic dysarthria if an unidentified preexisting condition has caused damage in the other hemisphere.)
2. Amyotrophic Lateral Sclerosis
o Progressive degeneration of LMN and UMN
o May start with UMN and therefore spastic dysarthria (eventually both UMN and LMN and a mixed dysarthria)
3. Traumatic Head Injury
4. Multiple Sclerosis
o immunologic disorder that causes destruction of the myelin sheath
o spastic dysarthria is a possibility (as are many other types of dysarthria)
5. Other Causes of Spastic Dysarthria
o brainstem tumor
o cerebral anoxia
o viral or bacterial infections
D. Speech Characteristics of Spastic Dysarthria
1. Articulation
o imprecise consonants; abnormally short VOT; incomplete articulatory contact; incomplete consonant clusters.
o vowel distortion
2. Phonation
o harsh vocal quality (perceptually: “friction-of-air”)
o strained-strangled vocal quality (perceptually: air forced through constriction)
o low pitch
3. Resonance
o hypernasality that’s not as severe as the hypernasality in flaccid dysarthria
4. Prosody
o monopitch intonation in connected or conversational speech
o monoloudness
o short phrases
o slow rate of speech
strained-strangled vocal quality and monopitch are two of the most distinguishing speech errors of spastic dysarthria, but they do not consistently occur in all cases of spastic dysarthria
5. Respiration
o not really a problem; the bigger issue is the hyperadduction of the vocal folds.
6. Additional Characteristic of Spastic Dysarthria
o pseudobulbar affect – uncontrollable crying or laughing that can accompany damage to the UMNs of the brainstem (independent of the emotions actually felt by the patient)
o drooling, although it can occur in several other dysarthrias, appears most prominently in spastic dysarthria.
E. Spastic Dysarthria vs. Flaccid Dysarthria
1. Check medical reports for UMN vs. LMN lesion
2. Hypernasality in spastic dysarthria is not as severe, may be more variable and intermittent than in flaccid dysarthria
3. In spastic dysarthria, phonation is likely harsh, tight or strained-strangled, in flaccid it’s more likely breathy.
4. Pseudobulbar affect and drooling and associated more with spastic dysarthria
F. Key Evaluation Tasks for Spastic Dysarthria
1. Conversational speech and reading
2. AMRs
3. Prolonged vowel
G. Treatment of Spastic Dysarthria
1. Treatment of Phonation Deficits
a. Head and Neck Relaxation
b. Easy Onset of Phonation
c. Yawn-Sigh Exercises
2. Treatment of Articulation Deficits
a. Stretching Exercises
o Reducing hypertonicity in the tongue and lips through stretching may result in increased speed and ROM.
o Little research has examined the effectiveness of stretching as a treatment for spastic dysarthria
o In some patients, active stretching may increase hypertonicity. The clinician should carefully monitor muscle tone
· Tongue stretching exercises
· Lip stretching exercises
3. Traditional Articulation Treatments
· Intelligibility drills
· Phonetic placement
· Exaggerating consonants
· Minimal contrast drills
4. Treatment of Prosody Deficits
o Regain vocal tract flexibility
· Pitch range exercises
· Intonation profiles
· Contrastive stress drills
· Chunking utterances into syntactic units
5. Treatment of Resonance Deficits
a. Surgical and Prosthetic Treatments (same as flaccid dysarthria)
· Decreasing velar hypertonicity (desensitizing for palatal lift)
b. Exercise-Based Treatments for Hypernasality
· Visual feedback (mirror for nasal emissions)
· Increased loudness
Chapter 6: Unilateral Upper Motor Neuron Dysarthria
A. Definitions of Unilateral Upper Motor Neuron Dysarthria
o Primarily a disorder of articulation
o Almost always mild in severity, often transient, usually too mild to impair speech permanently, but the effects can be persistent
o Weakness in the lower face, lips, and tongue contralateral to the lesion.
o Weakness in extremities ipsilateral to the lesion.
B. Neurological Basis of Unilateral Upper Motor Neuron Dysarthria
o Most of the CN serving the speech muscles receive bilateral innervation from the UMNs, so the deficits are less severe
· innervation from the unaffected hemisphere is not a perfect replacement – bilaterally innervated speech structures can still be affected.
o The cervicofacial branch of the facial nerve (VII) receives only unilateral innervation from the UMNs. Therefore, the most significant effect of UUMN dysarthria is on the lower face and tongue contralateral to the lesion.
· movements are slow, have reduced ROM, tongue deviates to the opposite side from the lesion when protruded, lower facial droop may be evident
C. Etiologies of Unilateral Upper Motor Neuron Dysarthria
o Left hemisphere UUMN damage often co-occurs with aphasia or apraxia of speech
o Right hemisphere UUMN damage often co-occurs with the cognitive and visual deficits associated with right hemisphere damage
1. Stroke
o especially those affecting the internal capsule (point where many descending UMN are compacted closely)
2. Tumors
3. Traumatic Head Injury
D. Speech Characteristics of Unilateral Upper Motor Neuron Dysarthria
o Often a short-term disorder for many mildly impaired patients, with recovery occurring over a period of days or weeks
1. Articulation
o principally a disorder of articulation
o irregular articulatory breakdowns
o slow AMRs
2. Phonation
o mild to moderate harsh vocal quality may be present
3. Resonance
o possibly hypernasal (only 11% in one study)
4. Prosody and Respiration
o rarely impaired
E. Key Evaluation Tasks for Unilateral Upper Motor Neuron Dysarthria
1. Consult medical records
2. Conversational speech and reading
3. Alternate Motion Rates (AMRs)
4. Prolonged vowel
F. Treatment of Unilateral Upper Motor Neuron Dysarthria
o Treatment of dysarthria is typically low priority when the patient has aphasia, apraxia or cognitive deficits.
· Intelligibility drills
· Phonetic placement
· Exaggerating consonants
· Minimal contrast drills
1. Oral Motor Exercises
o Self-help oral strengthening exercises that the patient can work on independently
Chapter 8: Hypokinetic Dysarthria
A. Definitions of Hypokinetic Dysarthria
o reduced vocal loudness with concomitant harsh-hoarse quality, slow speaking rate with intermittent bursts of rapid fire articulation, excessive and overly long pauses, prolonged syllables, monoloudness, and reduced phonation time.
B. Neurological Basis of Hypokinetic Dysarthria
o only dysarthria where increased rate of speech may be one of the symptoms
o only dysarthria in which the vast majority of cases share the same etiological factor (parkinsonism)
o cause by dysfunction in the basal ganglia or by damage to the basal ganglia’s neural connections to other parts of the CNS.
o hypokinetic mean “less motion”, describes decreased range and frequency of motion (not muscle tonicity). Individuals with parkinsonism are usually hypertonic.
1. Characteristics of Parkinsonism
a. Tremor – most common in fingers/hands; resting tremor
b. Bradykinesia – movements are slow, labored, and limited in range
c. Akinesia – difficulty initiating movements; trouble stopping a movement once it is started.
d. Muscular Rigidity – constant resistance to passive movement (state of greater-than-normal contraction); “lead pipe resistance”; “cogwheel resistance.”
e. Disturbances of Postural Reflexes – struggles with balance and movement
(depression, dysphagia and hypokinetic dysarthria are other characteristics)
2. Etiology of Parkinsonism
o Basal Ganglia (striatum (caudate nucleus + putamen) and globus pallidus)
o part of neural pathway that smoothes and refines planned movements
o Parkinsonism is caused by a reduction of dopamine in the striatum. Result is that there is relatively too much acetylcholine.
s Dopamine is an inhibitory neurotransmitter
s Acetylcholine is an excitatory neurotransmitter
3. Pharmacologic Treatments for Parkinsonism
o Replace dopamine in the striatum
s l-dopa, a chemical that that cross blood-brain barrier and be converted to dopamine in the brain
o Decrease acetylcholine in the striatum
s anticholinergic drugs deplete acetylcholine
s often used in conjunction with l-dopa
o Speech disturbances are helped the least by pharmacological treatments
o None of the treatments are cures
o Range of side-effects
o All eventually become ineffective
C. Etiologies of Hypokinetic Dysarthria
1. Idiopathic Parkinson’s Disease
o Most frequent cause of hypokinetic dysarthria
o Disease is the result of the progressive degeneration of dopamine producing neurons in the substantia nigra.
s additional symptoms include dementia
2. Neuroleptic-Induced Parkinsonism
o Negative side effect of using antipsychotic (neuroleptic) drugs
s increase the amount of acetylcholine in the basal ganglia
s symptoms usually disappear within weeks of discounting use of the drugs, but then psychotic symptoms return too…
s l-dopa cannot be used in conjunction b/c it increases psychotic symptoms
3. Postencephalitic Parkinsonism
o Cause by viral encephalitis (the effects of the infection are concentrated in the basal ganglia, which reduces dopamine)
s can affect children
4. Traumatic Head Injury
o Damage to the substantia nigra or basal ganglia, frequently from cumulative effects of repeated blows to the head (i.e. boxing)
s punch drunk encephalopathy (memory deficits, slow movements, dysarthria)
s cerebral anoxia
5. Toxic Metal Poisoning
o long-term exposure to manganese
6. Stroke
o No credible evidence for PD caused by a stroke
o However, on rare occasions, a single stroke can affect the basal ganglia and cause the sudden onset of parkinsonian symptoms
D. Speech Characteristics of Hypokinetic Dysarthria
1. Prosody
o monopitch
o monoloudness
o reduced stress
monopitch, monoloudness and reduced stress are the three most prominent speech characteristics of hypokinetic dysarthria.
o inappropriate silences (akinesia)
o increased rate of speech (related to the difficulties some individuals with parkinsonism have in stopping a voluntary movement once it is started)
o short rushes of speech (more common than a constant increase in speech rate)
s significant individual differences in speech rate abnormailites (slow to fast)
2. Articulation
o Imprecise consonants characterized by reduced ROM
o repeated phonemes (especially at the beginning of an utterance)
o palilalia (compulsive, increasingly rapid repetition of a word or phrase)
3. Phonation
o harsh, breathy, rough or tremulous voice quality (not the most noticeable aspect)
o low pitch
s significant individual differences (low or high pitch is possible)
4. Respiration
o breathing rates that are faster than normal
o paradoxical movements of the muscles of exhalation and inhalation
s shallow breath support; poorly controlled exhalations of air for speech; short breathing cycles
5. Resonance
o nothing significant, mild hypernasality is sometimes noted.
E. Key Evaluation Tasks for Hypokinetic Dysarthria
1. Conversational Speech
2. AMRs
3. Prolonged Vowel
F. Treatment of Hypokinetic Dysarthria
o typically treatment is pharmacological
1. Articulation
a. Rate Reduction (allows the articulators more time to reach the target positions)
· Pacing boards
· Hand or finger tapping
· Alphabet boards (also gives visual cue to partner)
· Delayed auditory feedback
· Reciting syllables to a metronome
b. Stretching Exercises
o Clinician needs to monitor muscle tone – may trigger hypertonicity
· Tongue stretching exercises
· Lip stretching exercises
· Jaw stretching exercises
c. Traditional Articulation Treatments
· Intelligibility drills
· Phonetic placement
· Exaggerating consonants
· Minimal contrast drills
2. Phonation
· Pushing and pulling procedures (overcome reduced ROM)
· Hard glottal attack
· Voice amplifiers
· Instrumental biofeedback (feedback on pitch, loudness, rate)
3. Respiration
· Speak immediately on exhalation; Slow and controlled exhalation
· Cues to inhale completely
· Stop phonation early
· Optimal breath group
4. Prosody
· Intonation profiles
· Contrastive stress drills
· Chunking utterances into syntactic units
Chapter 9: Hyperkinetic Dysarthria
A. Definitions of Hyperkinetic Dysarthria
o also a disorder of the basal ganglia
o characterized by excessive involuntary movements of various body parts
o Hyperkinetic dysarthria is actually a group of various motor speech disorders (each associated with one of the hyperkinetic movement disorders)
hyperkinetic dysarthria is unique among the other dysarthrias in that a clinician can often make an accurate diagnosis by just observing the individual’s uncontrolled movements.
B. Neurological Basis of Hyperkinetic Dysarthria
o many are associated with damage to basal ganglia or basal ganglia control circuit (plays an important role in “smoothing out” movement plans.)
o others are idiopathic
1. What causes Hyperkinetic Movement?
o too much dopamine or too little acetylcholine in the basal ganglia
o true cause of hyperkinetic movement is more complicated than just a few neurotransmitters
C. Etiologies of Hyperkinetic Dysarthria
1. Chorea – characterized by relatively quick, unpredictable, coordinated movement of the limbs, head, face, mouth and neck; sometimes having a dancelike quality.
a. Sydenham’s Chorea (St. Vitus dance)
o Closely associated to rheumatic fever, rare disorder that affects children 5 – 15
s usually clears in 3 to 4 months without treatment
b. Huntington’s Disease
o progressive disorder cause by the gradual degeneration of neurons in the basal ganglia and cerebral cortex.
s inherited disorder
s dementia, personality changes, impaired problem solving abilities, word-finding difficulties choreic movements
c. Stroke
o hemichorea (involuntary movements occur contralateral to lesion)
o stroke to subthalamic nucleus can cause hemiballism
s wild, violent involuntary movements of the limbs contralateral to the lesion.
d. Tardive Dyskinesia
o choreic movements of the face, mouth and neck caused by taking certain neuroleptic drugs over a period of months or years
s stopping the medications does not reverse the condition
e. Other causes of Chorea
o cerebral anoxia
o carbon monoxide poisoning
o rare cases of pregnancy and oral contraceptives
2. Myoclonus – distinguished by brief contractions of a single muscle or body part. These contractions may occur singly, in a repeating irregular pattern, or rhythmically. Unlike tics, myoclonic contractions cannot be consciously suppressed.
s may occur with kidney failure, epilepsy, cerebral anoxia, strokes, TBI, Alzheimer, Creutzfeldt-Jakob disease
s speech is affected only in the most severe cases
o Hemifacial spasm: facial muscles on one side of the face are affected
o Palatopharyngolaryngeal myoclonus: a rare result of brainstem strokes, cerebellar lesions, encephalitis, and tumors.
s results in fairly rhythmic contractions of soft palate that can open and close eustachian tube and result in really annoying constant ear popping
3. Tic Disorders – motor or vocal behaviors that can be controlled voluntarily until the compulsive desire to perform the behavior becomes overwhelming. Motor tics include eyeblinks, shoulder shrugs, and head jerks. Vocal tics include grunting, humming, and barking noises.
o Gilles de la Tourette Syndrome
o coprolalia- compulsive utterance of obscene words
4. Essential (or Organic) Tremor – an idiopathic, benign, action tremor that usually affects the hands, arms, or head. Essential tremor results in essential voice tremor when is affects the vocal folds.
o Essential voice tremor = tremulous, quavering vocal quality
o Distinguishing parkinsonism tremor from essential tremor:
s essential tremor is faster than parkinsonism tremor
s essential tremor = action tremor; parkinsonism tremor = resting tremor
s individuals with essential tremor have no neurological symptoms
5. Dystonia – characterized by sustained, involuntary contractions of muscles in one or more body parts; these contraction often come and go in a waxing and waning pattern. Dystonic movements are usually slower and more prolonged than those seen in chorea.
o Dystonia is categorized according to the number of affected body parts:
s Focal dystonia: present in only one part of the body (i.e. tongue, arm, hand)
s Segmental dystonia: 2+ body parts (i.e. Meige’s syndrome)
s Generalized dystonia: all four limbs and the torso or neck
s Hemidystonia: 2+ body parts on the same side of the body
o Primary dystonias: The following disorders are disorders w/ dystonia as the primary symptom…
a. Spasmodic Torticollis
o Dystonic contractions of neck muscles resulting in involuntary turning of the head.
s speech is slow in rate, mildly reduced in intelligibility, and lower in pitch for many females.
b. Chronic Drug-Induced Dystonia (or Tardive Dystonia)
o also caused by antipsychotic drugs; dystonic contractions occur near the mouth and face
s grimacing, sustained tongue protrusions and so forth.
c. Meige’s Syndrome
o rare idiopathic disease characterized by repetitive eyeblinking and abnormal facial movements that can affect the jaw, tongue, mouth and neck
s when sufficiently strong, they can often cause hyperkinetic dysarthria
d. Spasmodic Dysphonia
o Involuntary vocal fold movements during phonation; vocal folds are involuntarily closed tightly during phonation
s voice can have continuously strained and effortful quality or intermittent jerky and tight quality
s involuntary laryngeal contractions like laughing and crying are often NOT affected
D. Speech Characteristics of Hyperkinetic Dysarthria of Chorea
o Choreic movements may affect any number of muscle groups at any given time
s due to variability and unpredictability, listed errors may seem contradictory
1. Prosody (most affected area)
o prolonged intervals between syllables and words
o variable rate
o monopitch; monoloundess
o inappropriate silences
2. Articulation
o imprecise consonants
o distorted vowels
o prolonged phonemes
s caused by choreic movements that force the individual to hold a position longer than normal
3. Phonation
o harsh vocal quality
o excess loudness variations
o breathy vocal quality
o voice breaks
o strained-strangled vocal quality
s caused by intermittent, involuntary hyperadduction of the vocal folds during speech
4. Respiration
o unexpected inhalations and exhalations of air
5. Resonance
o hypernasality is occasionally a problem (usually intermittent)
o brief moments of hyponasality also possible
6. Summary of Distinctive Errors in Chorea
o Most evident speech errors in individuals with Chorea:
s prolonged intervals between syllables and words
s variable rate of speech
s inappropriate silences
s excessive loudness variations
s prolonged phonemes
s rapid, brief inhalations or exhalations of air
E. Speech Characteristics of Hyperkinetic Dysarthria of Dystonia
1. Articulation (most prominent)
o imprecise consonants
o distorted vowels
o irregular articulatory breakdowns
o prolonged phonemes
2. Prosody
o monopitch; monoloudness
o inappropriate silences
o shorts phrases
3. Phonation
o harsh vocal quality
o strained-strangled quality
o excessive loudness variation
4. Respiration
o not common in dystonia
s however, it’s possible that excessive loudness variation is the result of patients compensating for the effects of dystonia on respiration…
5. Resonance
o hypernasility possible but not common
in general, the speech errors in individuals with chorea tend to primarily reflect errors of prosody and those in individuals with dystonia tend to primarily reflect errors of articulation
F. Key Evaluation Tasks for Hyperkinetic Dysarthria
1. Vowel prolongation
2. AMRs
3. Conversational speech and reading
4. **Careful observation of the associated involuntary movements
G. Treatment of Hyperkinetic Dysarthria
1. Sensory Tricks
o idiosyncratic movements or actions that help the affected individual release the contraction (e.g. a light touch to the affected body part)
s lose their effectiveness after long-term use
2. Relaxation therapy and related treatments
o many hyperkinetic movements are worse with stress
s mental imagery, etc.
3. Bite blocks
o good for focal dystonic jaw movements; voluntary contraction of jaw from the bite reduces the involuntary contractions
4. Easy onset of phonation
5. Most common treatment is pharmacological | 
