MSD Exam 2

Unilateral Upper Motor Neuron Dysarthria

"Unilateral upper motor neuron dysarthria is a distinguishable motor speech disorder that is associated with damage to the upper motor neurons that carry impulses to the cranial and spinal nerves that supply the speech muscles. It is primarily a disorder of articulation" Causes damage to BOTH: Pyramidal tract AND Extrapyramidal tract (Unilaterally)

AOC Diagnosis key tasks:

***Sequential motion rate (SMR) NOT AMR!!!! - unless severe Pts with mild to moderate apraxia can be normal on the alternating motion rate (AMR) Only requires one movement sequence with one place of articulatory contact The SMRs will show deficits because it requires the sequencing of multiple articulatory positions at multiple places of articulation. ***Conversational Speech and Reading Looking at speech initiation and prosody ***Other tasks from the Oral Mech/Speech Exam Repeating words of increasing length (Fan-fancy-fantastic) Multiple trials of same target Voluntary vs. involuntary movements - for differential diagnosis Doing error pattern analysis

Etiologies of Spastic Dysarthria

- Anything that may produce bilateral damage to the UMN pathways - Stroke, trauma, toxins, diseases, Peripheral Lateral Sclerosis - Children may display spastic dysarthria due to - Cerebral palsy, trauma - Multiple Sclerosis - Damage to myelin sheath covering axons - Brainstem tumors

What is the primary function of the cerebellum?

- Helps time the components of movement - scale the size of muscle actions - coordinate sequences of muscle contractions for skilled motor behavior - Accomplished by processing sensory information from all over body and integrating that information into execution of movement.

LISTEN FOR_____ in hypokinetic dysarthria

- Rapid (& regular) AMRs - Very often associated with reduced range of articulatory motion - Imprecise ("blurred') consonants - Rapid (and blurred) AMRs are not uncommon in hypokinetic dysarthria & not expected in any other MSD type - Palilalia - Galloping (a rhythmic cadence) sometimes heard in hypokinetic dysarthria, even when task instructions are understood. Galloping is uncommon in other MSD types - Breathiness (mild) - Hoarseness (mild) - Reduced loudness ? Vocal flutter MAYBE but not the same as flaccid **Listen to samples of vocal fold paralysis to compare

Hyperkinetic dysarthria is characterized by

- variable articulatory imprecision, vocal harshness, and prosodic abnormalities. - damage to the extrapyramidal system - lesions in the basal ganglia (important in the planning and programming of learned movements)

Etiologies of Ataxic Dysarthria

-Friedrich's ataxia -Cerebral Palsy (ataxia) -Stroke (cerebellar artery; anterior inferior cerebellar artery) -Tumors -Vascular damage -Drug Toxicity (exposure to chemicals; medicines (Dilantin, Lead, mercury poisoning; alcohol) -Malnutrition (E or B12 deficiency) - Autosomal dominant cerebellar ataxia of late onset - idiopathic sporadic late-onset cerebellar ataxia - Olivopontocerebellar degeneration, - TBI Cerebellar peduncles vulnerable, tumors

General characteristics of UUMN dysarthria

-Hemiplegia/hemiparesis -Initial hypotonia, but may resolve toward spasticity -Lower face and tongue weakness (contralateral) -Often co-occurs with aphasia/AOS Articulation -Imprecise consonant production -Slow AMRs and imprecise and irregular AMRs -Irregular articulatory breakdowns (less common) Phonation -Harsh vocal quality -Strained-strangled vocal quality (uncommon) Resonance -Hypernasality -Mild and likely related to weakness Prosody and Respiration -Rarely impaired

Ataxic Dysarthria

A dysarthria associated with damage to the cerebellar system and characterized by speech errors relating primarily to timing, giving equal stress to each syllable; articulation problems are typically characterized by intermittent errors ranging from mild to severe; vocal quality can be harsh, with monotonous pitch and volume; prosody may range from reduced to unnatural stress. Ataxic dysathria is a disorder of sensorimotor control for speech production that results from damage to the cerebellum or its input and output pathways. The dragging and blurred quality of ataxic dysarthria speech has sometimes been likened to "drunken speech."

What is the motor speech planner (programmer)?

A network of interacting cortical areas that obtain abstract cognitive-linguistic phonemic goals and translate these goals into a code for motor plans of speech. This is where the motor commands for the production of temporally ordered syllables, words and particular rates and patterns of stress and rhythm including the spatial location of the target movement live.

Dopamine

A neurotransmitter associated with inhibitory effects Tends to slow neural activity within the striatum Produced by special neurons in the substantia nigra *** there will not be enough of this in Parkinson's and too much of this in hyperkinetic Conditions producing excessive dopamine = excitatory effect on movement

Ataxic dysarthria is not

A problem of weakness Accompanied by excess movements that interfere Associated with increased rate on AMRs Associated with groping movements Associated with difficulty sequencing volitional utterances Regular in rhythm/volume

Where in the CNS might a single stroke cause a spastic dysarthria? Why?

A single brainstem stroke can produce spastic dysarthria, whereas a single cerebral hemisphere stroke usually does not.* In the brainstem the right and left UMN pathways are in proximity to one another thus, a single infarct in the vertebrobasilar arterial distribution is sufficient to produce the bilateral UMN damage associated with spastic dysarthria.

To distinguish flaccid from hypokinetic when you have breathiness and hoarseness

AMR - if increased speed hypokinetic if slow it's flaccid glottal coup and cough - this would not be weak in hypo kinetic dysarthria Ahh will be longer in hypo kinetic and shorter in flaccid

AOS vs. Ataxia

AOS CAN BE CONFUSED WITH ATAXIA BECAUSE BOTH ARE ARTICULATION AND PROSODY BASED The puh puh puh will be easier than the kuh kuh kuh in people with apraxia of speech because they have more difficulty with more complex sounds In ataxia the person will have difficulty across all of the sounds equally Look for inconsistency, if you cannot find any its more likely ataxia Look at production of voluntary versus non-voluntary productions in apraxia they will do better with non-voluntary tasks (e.g. bye) while ataxia will have equal difficulty with both

Apraxia of speech

AOS is a neurologic speech disorder that reflects an impaired capacity to plan (or program) sensorimotor commands necessary for directing movements that result in phonetically and prosodically normal speech. It can occur in the absence of physiologic disturbances associated with the dysarthrias and in the absence of disturbance in any component of language. Groping movements is a hallmark Inconsistency in pronunciations is KEY Movement sequencing errors are often very inconsistent, even on repeated attempts at the same movement.

Which two subsystems of speech are usually affected most in cases of ataxic dysarthria?

Articulation and Prosody

Which two subsystems are usually affected most in apraxia of speech?

Articulation and prosody

Unilateral upper motor dysarthria is primarily a disorder of what (e.g., respiration, phonation)? Why?

Articulation because of weakness of the articulators contralateral to the side of the lesion.

Flaccid Dysarthria Characteristics

Atrophy, fasciculations Hypotonia, hypoactive gag reflex Phonatory (e.g., hoarse-breathy phonation) Resonatory (e.g., hypernasality) Slow-labored articulation Caused by - disease of the neuromuscular junction - execution/muscle level disorder - lower motor neuron damage

Why does unilateral damage to the upper motor neurons result in less severe symptoms in comparison to bilateral upper motor neuron damage?

Because most of the cranial nerves serving the speech muscles (except lower face and tongue) receive bilateral innervation from the upper motor neuron, the speech deficits seen after unilateral upper motor neuron damage almost always are less severe than those occurring after bilateral damage

Why is it appropriate to describe hyperkinetic dysarthria as actually being a collection of separate dysarthrias?

Because this dysarthria can be caused by many different disorders with different presentations of impairments.

Cerebellum communicates with the rest of the CNS through

CEREBELLAR PEDUNCLES 3 neural bundles The neurons that course through these 3 cerebellar pathways are called cerebellar control circuits (not upper motor neurons) They transmit neural impulses but do not synapse with lower motor neurons These neurons either synapse directly with upper motor neurons or interneurons in the brainstem and spinal cord

Striatum is

Caudate nucleus, Putamen, Made up of same type of neurons in the BG

Key Assessment tasks for ataxic dysarthira

Conversational speech and reading Evokes errors of articulation (imprecise consonants, irregular breakdowns, prolonged phonemes, distorted vowels,), prosody (excess & equal stress, monopitch, prolonged, slowed & variable rate), respiration, phonation Alternate motion rate (AMR) May be irregular and uncoordinated (irregular amplitude and duration), fluctuating loudness, slowed & variable rate Prolonged vowel May hear excess loudness or variable loudness, respiratory support generally adequate, vocal quality may be slightly harsh

direct action pathway of BG

Direct pathway EXCITES active motor movement. If this is impaired you will see HYPOkinetic dysarthria because there will be greater inhibition and less excitation of movement.

Hyperkinetic Dysarthria

Dysarthria in which involuntary movements are present... muscle tone is abnormal ranging from hypotonic to hypertonic, and, in some cases, fluctuating between the two. It includes various subclassifications, all of which are marked by disorders of loudness, rate, and inappropriate interruption of phonation. (Nicolosi et al., 1983, p.80) Hyperkinetic dysarthria is characterized by variable articulatory imprecision, vocal harshness, and prosodic abnormalities. It is associated with damage to the extrapyramidal system, more specifically, lesions in the basal ganglia and the major pathways, which are important in the planning and programming of learned movements (Zraick & LaPointe, 1997, p.251)

Ataxic Dysarthria - Prosody

Equal and excess stress - sounds like a robot Prolonged phonemes (not as long as spastic dysarthria) Prolonged intervals between phonemes Monopitch Monoloudness Slow rate

Hyperkinetic dysarthria prolonged AHH

Essential voice tremor involuntary noises/vocalization voice interruptions variable or excess loudness variations Laryngeal myoclonus (slow tremor)

Differential diagnosis of dysarthria's based on oral mech and speech

Flaccid Atrophy, fasciculations Hypotonia, hypoactive gag reflex Phonatory (e.g., breathy voice) if 10 Resonatory (e.g., hypernasality) if 10 Spastic Pathologic oral reflexes, hyperactive gag reflex Dysphagia, drooling Slow rate, slow and regular AMRs Strained voice Ataxic Normal oral mech not uncommon Dysmetric movements Irregular artic breakdown in speech and AMR Unsteadiness (mild) harsh vocal quality voice tremor (phonation) Exaggerated movements - can lead to loudness Intermitten hyponasality Hypokinetic Facial masking Tremors Reduced range of motion Monopitch, monoloudness, reduced stress Rapid AMRs Hyperkinetic Abnormal, involuntary movements Involuntary movements UUMN Unilateral right or left central facial or lingual weakness without atrophy of fasciculations Imprecise articulation, probably milder than other MSDs AOS Substitutions difficulty with complex sounds Equal stress is often placed on all syllables (Monotone, monoloudness) Difficulty initiating speech (silent pauses, + groping) Frequent revisions and restarts

A young farmer was hit by a falling piece of heavy farm machinery. He sustained complex skull base, bilateral petrous ridge, and bilateral carotid canal fractures. The accident caused bilateral otorrhea, cranial nerve 5 palsy, and bilateral cranial nerve 7 palsies. EMG and nerve conduction studies demonstrated near-complete paralysis of both cranial nerves 7, with some fibrillation potentials. Surgical management of cranial nerve 7 palsies was deferred in the hope that spontaneous regeneration would occur. The patient initially had significant difficulties with chewing and speech, primarily because he was unable to open his jaw. When seen for speech examination about 1 month after onset, his restricted jaw movement had cleared and he no longer had any chewing or swallowing complaints. He admitted, however, that liquids would sometimes escape his mouth. He recognized that his speech difficulty was related to his facial weakness, but he did not feel people were having significant difficulty understanding him. His mouth and lips would get dry easily, and he frequently needed to protrude his tongue to moisten his lips. Oral mechanism examination was normal except for bilateral facial paralysis. He was completely unable to make any isolated lip movements toward retraction or rounding. Attempts to puff his cheeks resulted in flutter of the lips as a result of air escape. He could not approximate his lips with his jaw closed. All bilabial and labiodental sounds were distorted. He had mild distortion of anterior lingual fricatives and affricates that the clinician felt was secondary to facial weakness. There was mild distortion of /r/ in phonemic environments requiring lip rounding. He achieved some lip approximation for bilabial sounds, and bilabials and labiodentals were distorted rather than omitted. Speech intelligibility was remarkably adequate in the evaluation setting, although it was felt that it would be mildly reduced in some phonetic environments or under adverse environmental conditions.

Flaccid It was concluded that the patient had a flaccid dysarthria that was consistent with his bilateral cranial nerve 7 paralyses. Key signs: bilateral facial paralysis., weakness in oral mech (weak retraction and rounding), air escaping, distortions of anterior lingual fricatives and affricates CN 5 signs: none CN 7 signs: lips weak, liquid escaping mouth, weak labial sounds Bilateral facial weakness can cause articulatory imprecision for phonemes requiring facial movement. When a single cranial nerve is damaged, even if bilaterally, considerable compensation is possible if paralysis is not complete and other cranial nerves are functioning normally. The specific speech deficits encountered in flaccid dysarthria depend on the specific cranial nerves that are involved. In this case, all of the patient's speech distortions could be explained by his bilateral facial weakness.

A 45-year-old man presented with a 3-month history of dysphagia, which had begun with a choking episode that was followed by continuing difficulty swallowing solid food. Speech difficulty, which he described as "slurring" and "difficulty with pronunciation," began about 1 month later. Neurologic examination was normal with the exception of possible palatal and tongue weakness. EMG failed to find evidence of neuromuscular junction disease but did find an abnormality of the hypoglossal nerve or its nuclei. MRI failed to find evidence of abnormality in the brainstem or posterior fossa. A video swallow study was normal. ENT examination was normal. During speech evaluation, he complained of a dull, aching pain in his ears, tongue, jaw, and gums, which he attributed to increased effort to chew food completely before swallowing. He noted mild chewing difficulty and a tendency to put food to the left in his mouth. He was able to initiate a swallow but often gagged and had to bring food back up and swallow again. He did not drool during the day, but his pillow was frequently wet when he awoke in the morning. During the examination, he cleared his throat frequently. Jaw strength was normal. Lip rounding was equivocally weak. The tongue was moderately weak bilaterally. Tongue protrusion and lateralization were limited (2,3); there were equivocal right side tongue fasciculations. The palate elevated more extensively toward the right. There was a trace of nasal emission during pressure sound production. Cough and glottal coup were normal. Speech was characterized by imprecise articulation, primarily for lingual consonants (0,1), and by hypernasality with occasional audible nasal emission (1). Voice quality was hoarse-breathy (0,1). He was able to sustain a vowel for 25 seconds. Speech AMRs for "puh" and "tuh" were normal, but "kuh" was slow (1). There was no significant deterioration of speech during stress testing.

Flaccid Dysarthria due to neoplasm Key features: fasciculations on the right side, nasal emission, palatal and tongue weakness, hoarse-breathy, low vowel sustain time, AMR kuh slow another sign of palatal weakness, lingual consonant imprecise weakness of CN 12 most likely bilateral. tongue weakness and weakness with lingual consonants, swallowing difficulty weakness of CN 10 most likely bilateral. Nasal emissions, palatal tongue weakness There was no significant deterioration of speech during stress testing, as might be encountered in MG. Finally, I hear no evidence to suggest the presence of a spastic component to his dysarthria The apparent involvement of more than one cranial nerve does not always place the lesion inside the skull, even when muscle disease and neuromuscular junction disease are not present. Neurologic signs and symptoms do not always mean the patient has primary nervous system disease. Although cranial nerves were affected, the neoplasm, in this case, was nonneurologic.

A 40-year-old millwright presented with an 8-month history of voice difficulty. His dysphonia began after anterior-approach cervical disk surgery. He had been unable to return to work because coworkers were unable to hear him in the noisy work environment. He occasionally coughed and choked after swallowing and had to clear his throat frequently. Speech and oral mechanism examination were normal except for markedly breathy-hoarse voice, moderately decreased loudness, and short phrases. He could sustain "ah" and "z" for only 2 seconds but sustained "s" for 12 seconds. His cough and glottal coup were markedly weak. There was no palatal asymmetry; the palate was mobile; and the gag reflex was normal. Subsequent laryngeal examination identified a right vocal fold paralysis (paramedian position) and agreed it was probably secondary to surgical trauma. Teflon injection (rarely used currently) of the right vocal fold resulted in normal conversational loudness, ability to sustain "ah" for 14 seconds, /s/ for 12 seconds, and /z/ for 10 seconds. The patient remained unable to shout. He was, however, pleased with his voice improvement and returned to work as a millwright, although with some fatigue in his voice by the end of the workday.

Flaccid dysarthria Suspect CN 10 involvement due to surgical LMN lesion of VF (same side) and difficulty swallowing. Key signs: Decreased loudness and short phrases a sign of weakness seen in flaccid, dysphonia - VF weakness/paralysis, cough and coup both weak Flaccid dysarthrias can be caused by surgical trauma. The degree of impairment perceptually does not always predict the impact of the problem on a person's day-to-day functioning (in this case, ability to work). Some speech deficits can be managed effectively with medical intervention. (but hopefully not w/ teflon since that shit probably causes cancer)

A 37-year-old man presented with a 2-month history of speech difficulty, problems with "tongue control," and headache and neck pain. He described his speech as "slurred" and complained of excess saliva accumulation and difficulty moving food with his tongue. Oral mechanism examination identified a bilaterally atrophic tongue but no fasciculations. He was barely able to move his tongue in any direction, and tongue strength was rated −4 bilaterally. Saliva pooled in his mouth. Phonation and resonance were normal, as were AMRs for "puh" and "tuh," but those for "kuh" were equivocally slowed and mildly imprecise. Lingual sounds were distorted. Nonlingual sounds, rate, and prosody were normal. Jaw and facial movements during speech were exaggerated in apparent compensation for his lingual weakness. Intelligibility was good. Neurologic examination was otherwise normal except for mild weakness of neck flexor muscles. Radiographs showed destruction of the interior portion of the clivus (the bony part of the posterior fossa anterior to the foramen magnum) and an associated nasopharyngeal soft tissue mass. Magnetic resonance imaging (MRI) and computed tomography (CT) scans identified a tumor mass in the anterior rim of the foramen magnum bilaterally. The patient underwent neurosurgery for radical subtotal removal of a chordoma tumor of the clivus. Postoperatively, articulatory imprecision was mildly worse, but no other speech deficits developed. He underwent radiation therapy, and his speech gradually improved, though not to normal. Lingual atrophy and weakness persisted. He did well, but 2 years later developed headache, nausea, vomiting, and double vision. There was evidence of tumor recurrence, but further radiation therapy or surgery was not advised because of risks and unlikely benefit.

Flaccid dysarthria Suspect CN 12 involvement based on lingual weakness, non-lingual sounds being normal, neck flexor muscle weakness, pooling saliva, difficulty with ROM of the tongue resulting in difficulty moving food, tongue atrophy What is the likely underlying pathophysiology? LMN lesion resulting in weakness of the tongue What is the likely localization? CN 12 based on labial weakness and neck flexor muscles Are there any discrepancies between the suspected neurologic disorder(s) and your MSD diagnosis? Exaggeration of jaw and facial movements during speech could suggest ataxic component What other tasks would you want to complete? Ask the patient if they were compensating by moving jaw and face excessively Flaccid dysarthria can be caused by damage to a single cranial nerve, unilaterally or bilaterally. Speech intelligibility can be remarkably preserved in isolated bilateral tongue weakness.

A 44-year-old woman presented with an 8-month history of speech difficulty that she thought was caused by ongoing stress. Neurologic examination was normal, and her neurologist wondered whether her complaint was stress related. Speech pathology consultation was requested. During speech evaluation the patient said her speech deteriorated when she was tired or under stress and that it frequently changed while she was coaching volleyball. She described it as "slurred, almost like my mouth freezes ... almost sounds like it goes nasal." She vaguely described alteration of chewing and swallowing at such times but denied choking or drooling. The speech problem would persist until she rested. Speech was initially normal. After 6 minutes of continuous reading aloud, she developed mild sibilant distortions, equivocal hoarseness, and intermittent vocal flutter. Speech AMRs were normal. She did not become hypernasal, but inconsistent nasal airflow was detected on a mirror held at the nares during repetition of nonnasal sounds and phrases. After another 4.5 minutes of reading, she began to interdentalize /s/ and /z/, distort affricates, and mildly distort /r/. Oral mechanism examination immediately after stress testing demonstrated only equivocal lingual weakness. She became upset and cried when her speech changed, making it difficult to separate the effects of her emotional response from weakness. Speech returned to normal after 30 seconds of rest. She was asked to return the following day at 5 pm, following volleyball practice. Although speech was initially normal, it deteriorated quickly and significantly, but its character was the same as that noted the day before. In addition, pitch breaks and some fluttering of the cheeks during speech were apparent.

Flaccid dysarthria nasal airflow suggests CN 10 involvement Suspect Myasthenia gravis based on stress testing showing she returns to normal after rest, weakness during stress, and during activities What is the likely underlying pathophysiology? caused by LMN lesion, suspect mysatia gravis based on stress testing. What is the likely localization? CN 12 causing lingual weakness, CN 10 causing hypernasality, CN 7 because of drooling indicating facial weakness Are there any discrepancies between the suspected neurologic disorder(s) and your MSD diagnosis? Pitch breaks seems more spastic suggests resistance to movement. What other tasks would you want to complete? Check for reflexes (suck, snout) to rule out spastic component.

A 76-year-old man presented with a 10- to 11-week history of speech and swallowing difficulty. A swallowing study conducted elsewhere was normal. An ear, nose, and throat (ENT) examination was normal. His local physician thought the patient might have amyotrophic lateral sclerosis. He was referred for speech and neurology consultations. Speech examination the next day was difficult because of the patient's immature affect, anxiety, and difficulty following directions. He reported that his swallowing problem was present upon awakening one morning and that his speech difficulty appeared a day or two later. He had greater difficulty swallowing food than liquids, but he did have nasal regurgitation when swallowing water. He thought his problems were worsening. Oral mechanism examination revealed left ptosis and difficulty closing both eyes completely. His face was moderately weak bilaterally. There were no lingual fasciculations or atrophy, but the tongue was −2,3 weak bilaterally. Palatal movement gradually decreased over repetitions of "ah ah ah ..." There was consistent nasal air escape during speech. There was some reduction in speed and range of motion during alternating retraction and pursing of the lips. Cough and glottal coup were weak. Speech examination was difficult because of his anxiety and difficulty following directions, but the following characteristics were apparent: hypernasality, weak pressure consonants, imprecise articulation (2), and reduced rate (0,1). Prolonged "ah" was breathy (0,1), and inhalatory stridor was apparent after maximum vowel prolongation. He prolonged "ah" for 20 seconds initially, but over multiple trials this decreased to 12 seconds. It was difficult to get him to persist in speaking for stress testing, but hypernasality and weak pressure consonants became more pronounced over time.

Flaccid dysarthria Implicating, at the least, cranial nerves 10, 7, and 12, bilaterally. There is no evidence of a spastic dysarthria or other CNS-based dysarthria. There is some deterioration of speech during stress testing, raising suspicions about neuromuscular junction disease such as mystia gravis CN 10 - difficulty swallowing food than liquids, nasal regurgitation when swallowing water. Cough and glottal coup were weak. Consistent nasal air escape during speech. inhalatory stridor was apparent after maximum vowel prolongation. CN 7 - left ptosis and difficulty closing both eyes completely, reduction in speed and range of motion during alternating retraction and pursing of the lips CN 12 - the tongue was −2,3 weak bilaterally. Careful perceptual evaluation of speech often is more enlightening than anatomic examination of speech structures.

A 62-year-old woman presented with an 8- to 10-year history of mild swallowing difficulties and a 2- to 3-year history of speech problems. Her history was significant only for radiation treatment to the face for acne at age 13. Clinical neurologic examination was normal with the exception of bilateral weakness in the face, tongue, and sternocleidomastoid muscles. Speech pathology evaluation revealed normal jaw movement and strength. The lower face was lacking in tone, but lip retraction and rounding were grossly normal. The tongue was full and symmetric, without atrophy or fasciculations, but it was mild to moderately weak bilaterally. Lateral lingual AMRs were slow. Palatal movement was symmetric, and cough and glottal coup were normal. There were no pathologic oral reflexes. The patient's speech was characterized by an equivocally slowed rate and imprecise articulation, particularly for anterior lingual fricatives, liquids, and bilabial sounds. There was some fluttering of the cheeks during production of bilabials. She had some exaggerated lip movements during speech that were judged to be compensatory. Voice quality was normal. Speech AMRs and sequential motion rates were normal. Speech intelligibility was normal.

Flaccid dysarthria Suspect CN 7 involvement due to bilateral weakness in the face and sternocleidomastoid muscles, equivocally slowed rate and imprecise articulation, particularly for anterior lingual fricatives, liquids, and bilabial sounds, and fluttering of the cheeks during production of bilabials. "mild flaccid dysarthria whose deviant speech characteristics are consistent with facial and lingual weakness." Flaccid dysarthria can develop in response to radiation-induced cranial nerve weakness. Such effects can be delayed for many years after radiation treatment. Speech evaluation can help rule out certain neurologic diagnostic possibilities. In this case, it was pos- sible to state that there was no evidence of any CNS-based dysarthria and that the speech deficit reflected LMN involvement alone. Speech therapy for dysarthria is not always necessary. In this case, the patient was com- pensating well and had no difficulty with intelligibility or efficiency of verbal communication. Her primary desire was to establish the etiology of her mild speech and swallowing difficulty.

The ONLY dysarthria assessment

Frenchay Dysarthria Assessment 2 Edition (FDA-2)

STARSS and Cerebellar control circuit

Helps regulate muscle Tone (hypotonia) Scales the size (amplitude) of movements Accuracy & Range of movements Helps coordinate timing between muscle movements (Speed) Helps maintain muscular Steadiness For speech: allows smooth, coordinated flow of movement from one articulatory position to the next Impact on speech is widespread - only area notimpacted is strength

UUMN dysarthria is characterized by....

Hemiplegia/hemiparesis (paralysis or slight paralysis of one side of the body) Initial hypotonia, but may resolve toward spasticity Lower face and tongue weakness (contralaterally) on the right side if they have a left side lesion Often co-occurs with aphasia/AOS The primary issue is ARTICULATION, not very severe

A 73-year-old woman presented with a 10-year history of voice difficulty that was present upon awakening one day. The problem progressed for a while but had been stable for several years. She had had speech therapy, without benefit. The neurologic evaluation identified the presence of a head tremor, postural upper extremity tremor, and "spastic speech." A cause for these abnormal movements was not identified during a complete neurologic workup. During the speech examination, the patient noted that her voice problem began during a period of considerable psychological stress (her adopted son was having difficulty with drugs and was in the process of attempting to locate his biologic parents). She felt her voice was worse when she was anxious or spoke in a group and that it was mildly improved when she had a glass of wine. Her voice was characterized by a tremor that consistently interrupted her voice and slowed her speech rate. Prolonged "ah" contained consistent, somewhat irregular and strained voice interruptions. At higher pitches, voice interruptions were absent but a voice tremor became apparent. Tremor fluctuations were not apparent during prolongation of voiceless fricatives.

Hyperkinetic dysarthria Adductor spasmodic dysphonia of essential voice tremor, moderate to marked in severity. Key features: tremor (lack if the ability to inhibit excess movement), slow speech rate, strained and irregular voice interrupptions, voiceless fricatives do not require VF so that explains why she doesn't have tremor during prolonged fricatives - and not due to respiration Botox injection was provided. Her voice improved significantly after several weeks of a weak-breathy dysphonia and mild swallowing difficulty. She noted a marked reduction in the physical effort to speak and was pleased with her voice quality. Voice quality was indeed markedly improved, although evidence of mild voice tremor persisted, but without voice interruptions. Adductor SD can develop in association with essential voice tremor. Voice tremor may be accompanied by tremor elsewhere in the body. The onset of SD is often associated with psychological stress, even when examination reveals an organic basis for the problem. The relationship between psychological stress and SD is unclear, but the presence of stress at the time of onset does not rule out the possibility of neurogenic etiology.

A 67-year-old man presented with complaints of gradually progressive dizziness, visual difficulties, slurred speech, and mild swallowing difficulty. He had had a mild stroke and subsequent left carotid endarterectomy 8 years previously, but his speech and visual difficulties did not emerge until 2 years later. The neurologic examination was normal except for speech. Concern was raised about motor neuron disease. He was referred for EMG, MRI, and ENT and speech consultations. During the speech evaluation he reported having mild difficulty with speech after his stroke, with subsequent improvement, but then worsening in recent years, characterized by voice difficulty and occasional problems with pronunciation. He did not have swallowing difficulties during meals but did have problems controlling saliva. The oral mechanism examination was normal with the exception of some quick myoclonic-like movements of the tongue and 2- to 4-Hz myoclonic movements of the palate at rest and during phonation. A hoarse-rough voice quality, sporadic voice breaks, and inconsistent, imprecise articulation of lingual fricatives and affricates characterized his speech. Speech AMRs and SMRs were normal in rate and rhythm. Vowel prolongation was variable but consistent with the rate of the palatal myoclonus. EMG and ENT evaluations were normal. MRI showed old lacunar strokes in the thalami and right caudate nucleus but no lesion in the brainstem or cerebellum. His speech difficulties were thought to be related to an undetectable brainstem stroke, but a degenerative neurologic disorder could not be ruled out. Clonazepam was prescribed in the hope that it would help the myoclonus. He returned for neurologic reassessment 1 year later with worsening of symptoms. He had been unable to tolerate the side effects of Clonazepam and had discontinued it. Examination revealed palatal myoclonus and mild gait unsteadiness. MRI now showed clear evidence of hypertrophic olivary degeneration. He was not seen for speech reassessment. It was concluded that he had a neurodegenerative disorder that, at the present time, could not be more clearly defined.

Hyperkinetic dysarthria based on hoarse-rough voice quality, sporadic voice breaks, and inconsistent imprecise articulation of lingual fricatives and affricates, myoclonus (slow tremor), inconsistent vowel prolongation, unwanted movements of the tongue during oral mech What is the likely underlying pathophysiology? Basal ganglia control circuit impairment resulting in palatal myoclonus and difficulty with lingual constants due to lack of inhibition of excess movements during speech, due to chemical imbalance of increased dopamine and decreased acetylcholine "palato-laryngeal and perhaps lingual myoclonus suggestive of dysfunction in the brainstem or cerebellum". What is the likely localization? Basal ganglia, dysfunction in the brainstem or cerebellum Are there any discrepancies between the suspected neurologic disorder(s) and your MSD diagnosis? Speech AMRs and SMRs were normal in rate and rhythm, vison and gain issues suggest cerebellar involvement What other tasks would you want to complete? Nothing? Palatal-laryngeal myoclonus is a well-localized disorder. Its presence in this case predicted the MRI abnormality that eventually emerged. Although uncommon, PM can be the result of degenerative neurologic disease. Changes in speech and the results of the oral mechanism examination can be among the first signs of neurologic disease.

A 51-year-old man presented for an opinion about his neurologic deficit. His difficulties began 3 years previously, over a period of 10 days, when he had had several suspected myocardial infarctions. His symptoms at that time included speech difficulty and problems with gait. Neurologic examination showed a loss of facial expression, generalized loss of associated movements, generalized bradykinesia, and generalized rigidity, greater on the left than right side. During the speech examination, the patient stated, "I can't talk in long sentences; I repeat myself; bad volume; out of breath fast." He had had three periods of speech therapy, benefiting only temporarily from each. Examination revealed facial masking; reduced range of movement of the jaw, lips, and tongue; and perhaps mild left tongue weakness. The connected speech was characterized by imprecise articulation, the accelerated rate within utterances, monopitch and monoloudness, and a breathy-harsh-strained voice quality. During conversation he exhibited numerous phoneme and syllable repetitions and fairly frequent word and phrase repetitions, usually with associated accelerated rate, consistent with palilalia. At times his repetitions appeared voluntary, based on his perception that he had not been understood, but at other times they seemed involuntary. Speech AMRs were markedly imprecise and blurred. Intelligibility was significantly reduced but improved with slowing of rate, which was facilitated by hand tapping.

Hypokinetic Dysarthria Key signs: Facial masking, bradykinesia, generalized rigidity, palilalia, the accelerated rate within utterances, monopitch and monoloudness, and a breathy-harsh-strained voice quality, improvement when asking him to slow down and tap hands What is the likely underlying pathophysiology? BG lesion or imbalance resulting in little dopamine and too much acetylcholine, impacting the BG ability to excite movement What is the likely localization? BG lesion Are there any discrepancies between the suspected neurologic disorder(s) and your MSD diagnosis? mild left tongue weakness, more difficulty with left side What other tasks would you want to complete? Look carefully at facial symmetry to rule out UUMN Hypokinetic dysarthria and palilalia can result from cerebral ischemia and stroke. It can be among the most debilitating deficits stemming from basal ganglia disease. Although neuroimaging evidence suggested only a unilateral lesion, the dysarthria and associated neurologic findings were strongly suggestive of bilateral involvement.

Hyperkinesia

Impairs indirect pathway Can't inhibit excess movements Effect: Greater excitation Result: Excess movement (many sub-types of hyperkinetic mvmt disorders Hyperkinetic dysarthria

Ataxic Dysarthria - Articulation

Imprecise consonant articulation Distorted vowels (slurred quality) Irregular articulatory breakdown imprecise consonant and vowel productions that can vary from utterance to utterance. primarily in multisyllabic words hyperkinetic and ataxic are only dysarthrias that have irregular breakdown (with other dysarthrias, errors are consistent during speech)

damage to extrapyramidal tracts results in _______________________

Increased muscle tone (hypertonia) Spasticity Clonus (involuntary, rhythmic, muscular contractions and relaxations) Decorticate or decerebrate posture Hyperreflexia Damage to BOTH pyramidal tract and extrapyramidal tract BILATERALLY results in spastic dysarthria

indirect action pathway of BG

Indirect pathway inhibits other possible movements. If this path is impaired you will see HYPERkinetic dysarthria because there will be less inhibition of excess movement and therefore more UNWANTED movements.

Describe the functions of the basal ganglia.

Inhibits cortical neuronal firing and excess movement. This supports the inhibition of unwanted/unneeded movements. Basal Ganglia control circuit: Cortical areas make a rough plan of movement BG smoothes and refines that movement Thalamus makes further refinements Neural impulses for planned movement sent back up to the cortex Motor cortex sends the refined movement to the muscles

MIXED DYSARTHRIA

Is a combination of two or more of the pure dysarthria types This can change over time - someone might evolve from mixes spastic/flaccid to flaccid/spastic the more predominant one is listed first e.g. Ataxic-flaccid mixed dysarthria Spastic and flaccid mix is the most common

The motor speech planner (programmer) receives input from what other parts of the brain?

Linguistic input to the MSP comes from the left hemisphere's perisylvian area, including the temporoparietal cortex, parts of the frontal lobe, the insula and parts of the basal ganglia and thalamus.

damage to pyramidal tract results in _____________________

Loss of fine, skilled movement Hypotonia Weakness Slow movements Hyporeflexia Damage to BOTH pyramidal tract and extrapyramidal tract BILATERALLY results in spastic dysarthria

A 68-year-old man presented stating, "I don't know what's the matter with me. If you have a cure, I'd be delighted." Over a 1-year period, he had developed impotence, occasional stumbling and falling, dysphagia with aspiration of liquids, and occasional laryngeal stridor. He had recently developed urinary urgency and clumsiness in his hand. A neurologic examination revealed axial rigidity, orthostatic hypotension, reduced upward gaze, and dysarthria. An EMG revealed a mild, predominantly motor peripheral neuropathy. Autonomic reflex testing identified a generalized autonomic neuropathy. Laryngeal examination revealed left vocal fold paresis. During the speech examination, he noted a 1-year history of a "higher and weaker" voice and a sense that his speech was "clumsy." He was choking on liquids and having occasional "laryngospasms" during sleep. He was no longer able to play the trumpet or flute because of respiratory fatigue; he stated, "I get out of breath for no good reason." Finally, he complained that his lips were "tight and being stretched across my mouth." Examination revealed a left lower facial droop, equivocal bilateral reduction in tongue strength, a weak cough and glottal coup, and inhalatory laryngeal stridor at phrase boundaries during speech and when inhaling rapidly. His speech was characterized by accelerated rate, monopitch and monoloudness, imprecise articulation, and reduced loudness. Pitch was mildly elevated. Vowel prolongation was strained-harsh and unsteady. Vocal flutter was sometimes evident. Speech AMRs were irregular and occasionally accelerated and "blurred."

Mixed dysarthria - Hypokinetic-Flaccid Dysarthria - Hypokinetic component is most prominent. - His mildly irregular AMRs and vocal unsteadiness suggest an ataxic component. - The subtle strained component to his voice could represent a mild spastic component, although there are no other features of spasticity. Key sign of hypokinetic: Accelerated rate, monopitch and monoloudness, and reduced loudness all key signs of hypokinetic, rigidity Key signs flaccid: His laryngeal stridor suggests posterior cricoarytenoid weakness, and his vocal flutter may reflect weakness of laryngeal adductors. Dysphasia, left VF pariesis, stridor suggests flaccid w/ CN 10 involved A number of dysarthria types may be perceptually evident in mixed dysarthria. This patient had unequivocal hypokinetic and flaccid dysarthria, probable ataxic dysarthria, and possible spastic dysarthria. All of these types were compatible with the diagnosis of MSA or Shy-Drager syndrome.

Hypokenetic dysarthria is....

Only dysarthria associated with increased rate of speech Only dysarthria where majority of cases share etiology (Parkinsonism) Caused by damage to BG or BG connections to CNS Hypokinetic = less motion With regard to Parkinson's = decreased range and frequency of movement Mostly associated with Parkinson's disease

Cranial nerves of speech system

Phonation is mainly CN X/10 (vagus) not CN 9 (glosso) ***Testing CN X phonation - you can do the gag reflex but not everyone has a gag reflex so you would need to test further in another way. You could test CN 10 by "ahhh" or "coup" or using a mirror to look at VF. You need to test the VOCAL FOLD function - quality of the sound will tell you this. Respiration is primarily spinal nerves and CN 11 Prosody is primarily CN 10 vagus Articulation is primarily CN 7 Facial ***CN 7 test - smile CN 9 is not primary CN for any of the speech systems. Has some laryngeal involvement but not much with speech

Corticocerebellar control circuit

Planned motor impulses sent from cortex to cerebellum via middle peduncle Cerebellum coordinates and refines these preliminary speech movements according to sensory info about articulator positions, conditions, prior practice on skilled target movements Coordinated motor impulses sent to thalamus for additional refinement, forwarded to motor cortex, then impulses to the appropriate muscles for speech

Summary of most evident speech errors in hyperkinetic dysarthria

Prolonged intervals between syllables and words Variable speech rate Inappropriate silences Excess loudness variations Prolonged phonemes Rapid, brief inhalations and exhalations of air Vocal stoppages Intermittent breathy voice quality

speech characteristics of hypokinetic dysarthria

Prosody - Monopitch - Reduced stress - Monoloudness - Inappropriate pauses - Short rushes of speech Articulation - Imprecise consonants - Repeated phonemes - Palilalia / "stutter" like Phonation - Harsh or breathy voice - Low pitch Respiration - Faster breathing rates - Incoordination of muscles for breathing - Shallow breath support - Poorly controlled exhalation of air for speech * maybe mild hypernasality

Rigidity VS Spastic

Rigidity is all the time resistance to movement - overall stiffness (seen in hypokinetic dysarthria) Spastic can change tends to increase at the onset of movement and with increased velocity (seen in spastic dysarthria)

UUMN STARSS

SR Strength and ROM

Spastic/UMN damage starss

STRS Strength (weakness) Tone (increased; spasticity) Range of motion (reduced d/t weakness) Speed (slow)

AOS defining characteristics

Slowed rate of speech production (temporal) Increased time to produce individual sounds Increased time to transition between sounds Increased intervals between syllables and words Inability to increase rate without sacrificing articulation Articulation: Substitutions more than other types of errors (voiceless for voiced sounds, other) Placement the most frequent substitution error (followed by manner, then voicing...) More difficulty with the later developing sounds (fricatives/affricates more than stops) Consonant clusters more difficult than singletons More difficulty with complex sounds (multi syllabic, affricates, fricatives) Initial position of words are most problematic Phonemes that are the least frequently occurring are most problematic More problems with nonsense rather than meaningful and/or real words More problems with multisyllabic words than single syllables Increased errors with increased phonetic and linguistic complexity The farther the distance between the points of articulatory contact the greater the difficulty (puh puh vs. puh kuh) Voluntary or novel production more difficult than automatic, reactive production Errors are inconsistent - they might not make that error all the time, it's consistently inconsistent Labial and alveolar sounds are the easiest ('visible' sounds easier than harder to see sounds) Prosody: Rate of connected speech is slow Equal stress is often placed on all syllables (Monotone, monoloudness) Difficulty initiating speech (silent pauses, + groping) Frequent revisions and restarts Normal variations of pitch and loudness may be reduced Subtle difficulty with respiration But only on voluntary tasks (take a deep breath) Resonance is seldom a significant problem Can see inconsistent repetitive movements, but these remain within normal limits Seldom isolated deficits of phonation: can see a delay in phonation associated with grouping for articulation position

What are the characteristics of Parkinsonism?

Sorry this is so long!! Parkinson's= hypokinetic Posture - involuntary flexion of the head, trunk, and arms Rigidity - slowness of movement and feeling of stiffness or tightness Tremor - in limbs, mouth, jaw static or resting tremor is most apparent when the body part is relaxed, and it tends to decrease during voluntary movement. Pill-rolling movement between the thumb and forefinger Cogwheel rigidity - resistance of the limbs to passive stretch has a jerky character Bradykinesia - problems with movement planning, initiation, and execution. Reduced speed with which muscles can be activated, characterized by delays or false starts at the beginning of movement and slowness of movement once begun. Movement may also be difficult to stop. Repetitive movements decreased in speed "freezing" or immobility (akinesia) when there is desire to move Rapid shuffling steps (festination) Difficulty estimating movement displacements and poor temporal discrimination of auditory, tactile, and visual stimuli Reduced range of movement Lack of facial expression Monopitch Reduced stress Monoloudness Imprecise consonants Inappropriate silences Short rushes of speech Harsh voice quality Breathy voice (continuous) Low pitch Variable rate Increased rate in segments Increase of rate overall Repeated phonemes

A 71-year-old woman presented to the ear, nose, and throat (ENT) department with a 3-month history of "lost voice." The prior medical history was unremarkable. The only abnormality on ENT examination was decreased tongue mobility. "Neurologic dysphonia" and possible "LMN disease" were suspected. Speech pathology and neurology consultations were arranged. During speech evaluation, the patient recalled that her progressing speech difficulty had been present for about 15 months. She complained that her voice was strained, speech was slow, and speaking effortful. She occasionally choked on liquids and had infrequent nasal regurgitation. She had not had to modify her diet, nor had she lost weight. She denied change or difficulty controlling emotional expression, drooling, and problems with memory or other cognitive skills. Speech AMRs of the jaw, lower face, and tongue were slow but regular. Jaw and lower face strength were normal; the left side of the tongue was equivocally weak. There was a slight droop at the right corner of the mouth and a subtle "snarl" of the left upper lip at rest. The palate was symmetric and moved little during vowel prolongation but moved normally during elicited gag. Her cough was normal. A strained-harsh-groaning voice quality (2), reduced rate (1,2), hypernasality (1,2), imprecise articulation (1), and monopitch and monoloudness (1,2) characterized connected speech. Lip and jaw movements were slightly exaggerated during speech, possibly reflecting compensatory efforts to maintain intelligibility. Speech AMRs were slow (2,3). "Ah" was strained (3) and sustained for only 6 seconds. Neurologic examination noted brisk muscle stretch reflexes. No fasciculations were detected.

Spastic dysarthria pseudobulbar palsy with spastic dysarthria, moderately severe. No clear evidence of a flaccid (LMN) component. Speech characteristics are strongly suggestive of bilateral UMN dysfunction affecting the bulbar musculature. key signs spastic; strained, speech was slow, and speaking effortful. choked on liquids and had infrequent nasal regurgitation, monopitch, monoloudness, effortful speech, brisk stretch muscle reflexes, snarl at rest Spastic dysarthria can occur in the absence of other significant neurologic deficits and can progress without significant clinical findings in the limbs. Spastic dysarthria is frequently accompanied by dysphagia. Dysarthria affecting the bulbar muscles, in the absence of limb findings, is some- times misinterpreted as LMN disease (frequently MG).

Difficulty with swallowing is more likely due to

Spastic dysarthria - drooling and laryngeal function more impaired Pocketing food might be more flaccid

Spasticity VS Rigidity

Spasticity: increase at onset of movement and high velocity / changes Rigidity: all the time resistance to movement, limited movement / reduced ROM / increased muscle tone

Etiologies of UUMN dysarthria

Stroke Cortical, subcortical, brainstem Tumors TBI

Neurological basis of hyperkinetic dysarthria

The cause of excessive movement in hyperkinetic dysarthria not fully understood Assumption is that it is related to chemical imbalance: Conditions producing excessive dopamine = excitatory effect on movement Conditions producing too little acetylcholine = excitatory effect on movement

Pathways to and from cerebellum

The middle peduncle sends the plan itself (afferent) Inferior peduncle sends sensory information (afferent) Superior peduncle sends programming info (efferent)

What nervous systems tracts must be damaged before spastic dysarthria can occur?

UMN. Both the pyramidal and extra pyramidal tracts. Bilateral upper motor lesions cause Spastic Dysarthria.

A 57-year-old man was seen in the outpatient clinic for evaluation of residual symptoms stemming from a stroke about 3 years earlier. The neurologic examination revealed dysarthria and left hemiparesis. The neurologist concluded that the patient had a "pure motor hemiparesis, almost like a capsular infarct." Speech evaluation revealed mild left lower face and tongue weakness. Mildly imprecise articulation and imprecise AMRs characterized speech. Articulatory precision improved noticeably with a moderate slowing of speech rate. Phonation and resonance were normal

UUMN dysarthria Mild nature of articulation imprecision, left face only weakness (suggests right side stroke), and with slowing precision improving suggests UUMN because the effects are mild as we would expect in unilateral upper motor neuron lesions UMN dysarthria can result from lesions on the right or left side of the brain. It sometimes persists long after the spontaneous recovery period. Persistent UUMN dysarthria is usually mild, and clinicians and patients frequently conclude that therapy is unnecessary.

A 55-year-old right-handed man was hospitalized with a 4-day history of progressive right-sided weakness and dysarthria. Neurologic evaluation revealed dysarthria, right hemiparesis, and mild sensory loss in the right face and upper limb. CT identified an infarct in the posterior limb of the left internal capsule. Speech evaluation 2 weeks later revealed right central facial weakness. Speech was characterized by imprecise articulation, harsh voice quality, and slow speech AMRs. Intelligibility was moderately reduced. There was no evidence of aphasia or any other cognitive disturbance.

UUMN dysarthria One side of the face being weak and hemiparesis is key, imprecise articulation, slow AMRS are signs of lingual weakness What is the likely underlying pathophysiology? Impairment in the UMN on the left side of the body resulting facial and lingual weakness What is the likely localization? UMN lesion impacting synapse with CN 7 and 12 due to damage in extra pyramidal and pyramidal tracts Are there any discrepancies between the suspected neurologic disorder(s) and your MSD diagnosis? No What other tasks would you want to complete? Would listen to sustained ahh for any pitch breaks or strain suggestive of resolving towards spastic component of UUMN dysarthria UUMN dysarthria commonly affects articulation and sometimes voice quality and frequently seems predominantly explained by UMN weakness. Can be associated with moderate reductions of speech intelligibility. The internal capsule is a common site for lesions that cause UUMN dysarthria. Isolated internal capsule lesions in the dominant hemisphere are rarely if ever, associated with aphasia or other cognitive disturbances.

A 70-year-old right-handed man was hospitalized because of a sudden inability to express himself and right face and upper extremity weakness. CT identified an area of decreased attenuation in the left frontal lobe consistent with recent stroke. Speech and language evaluation 3 days after onset revealed mild to moderate aphasia. Spoken communication was functional. Right face and tongue weakness was apparent. There was no apraxia of speech. The patient's speech was characterized by imprecise articulation, reduced loudness, and hoarseness. Intelligibility was normal. The patient began speech-language therapy. Within 1 week his dysarthria had resolved, and the only evidence of aphasia was infrequent word-finding difficulties.

UUMN dysarthria Key signs: one-sided weakness, quick recovery, left frontal lobe stroke damage - aphasia, normal intelligibility UUMN dysarthria associated with dominant hemisphere lesions is frequently associated with aphasia. In this case, the dysarthria and aphasia were about equal in severity at onset. UUMN dysarthria frequently resolves rapidly and completely (in this case, within 1 week after onset). The frontal lobe is most often implicated when UUMN dysarthria is the result of a cortical lesion.

Divisions of the cerebellum

Vestibulocerebellum Spinocerebellum Cerebrocerebellum

Describe how the substantia nigra and the striatum are involved in the cause of Parkinsonism.

When neurons in the substantia nigra are destroyed, dopamine supply to the striatum is reduced and its role in the basal ganglia control circuit is diminished. Since the basal ganglia control circuit connects motor areas of the cerebral cortex for inhibiting cortical output that's in excess of what's required to accomplish movement goals, this damping effect is excessive in hypokinetic dysarthria.

Spastic dysarthria prolonged AHHH

Will be long (no shortness) Look for strained sounding quality Grunt at end of expiration may be present

Ataxic dysarthria prolonged AHHH

Will sound unsteady - this includes mild alterations in pitch and loudness ** this can be found in hyperkinetic dysarthria so look for AMRs if they can slow down their AMR that wouldn't be ataxic (lack of cerebellar control) if they can slow down AMR that suggests hyperkinetic. UNWANTED movement would be another sign of hyperkinetic

Parkinson's is caused by _____

a reduction of dopamine causing profound disruptions in striatum because of the neurochemical imbalance Results in to much excitatory neurotransmitter (Acetylcholine) acting on the neurons

Middle and inferior peduncle in cerebellum sends...

afferent info (into the cerebellum)

Hypokinetic dysarthria prolonged AHHH

breathiness vocal flutter or rapid voice tremor Reduced maximum vowel duration (less weak compared to flaccid examples) *Loudness decay (reduced loudness across all utterances) *Occasional aphonia ****Need to rule out respiration through the use of a spirometer

Ataxic Dysarthria is caused by

damage to cerebellum or neural pathways that connect cerebellum to CNS

Superior peduncle in cerebellum sends...

efferent info (out to the rest of the body)

Confirmatory Signs of Flaccid Dysarthria

fasciculations atrophy hyporeflexia NOT hyperreflexia this would be UMN sign

Hypokinetic

fast but small movements Associated with impaired direct pathway Can't excite action Effect: Greater inhibition Result: Reduced movement Hypokinetic dysarthria

Besides prosody and articulation ataxic dysarthria can cause

harsh vocal quality voice tremor (phonation) Exaggerated movements - can lead to loudness Paradoxical movement - limited sub-glottic air available for speech which causes the person to speak on residual air which can lead to increased rate of speech decreased loudness and a harsh voice Intermittent hyponasality due to timing errors between muscles of velum and other muscles of articulation (Seldom)

A 49-year-old woman presented with a 1-year history of movement difficulties, including speech. Her problems began suddenly with a severe headache and "drunken" speech. Within days she noticed some twitching of the right facial muscles and shaking and twitching in her hands. A medical workup shortly after onset suggested a diagnosis of myoclonic epilepsy of cortical origin. During the speech examination, she complained of slurred speech. She noted a feeling of "tightness" in her face and neck intermittently when speaking. The oral mechanism examination was normal at rest, but myoclonic movements of the tongue were present during protrusion and lateral movements. There was no palatal or pharyngeal myoclonus. Jaw and perioral myoclonus was more apparent during sustained phonation than when her mouth was open without phonation. Traces of nasal emission were apparent during pressure-sound production. Some dystonic-like perioral movements were also apparent during speech. Her speech was characterized by reduced rate and imprecise articulation, with difficulty achieving bilabial closure during connected speech, apparently secondary to dystonic lip contractions. Voice quality was strained-hoarse with monopitch and monoloudness. Prosody was characterized by excess and equal stress. Prolonged "ah" was unsteady. Speech AMRs were regular when produced at a rate of 1 per second but markedly irregular when she attempted to maximize the rate. Intelligibility was reduced.

hyperkinetic dysarthria of action myoclonus (AM). Drunken speech = not always ataxic Key signs: monopitch, monoloudness, dystonic lip contractions, excess and equal stress, unsteadiness, irregular when increasing rate of AMRs, tightness in her face (rigidity), twitching of facial muscles Some dystonic perioral movements during speech that make it difficult for her to achieve bilabial closure. Speech clearly worsens during attempts to increase speech rate, and she has consciously reduced her rate because of this." Suspicion was raised about accompanying ataxic and spastic components to her dysarthria, although it was thought that her scanning prosody and strained voice could be secondary to efforts to compensate for her hyperkinetic dysarthria. The neurologic evaluation indicated the presence of ataxia in the limbs, hyperreflexia, and action-induced myoclonus of the trunk, extremities, and face. A complete workup confirmed a diagnosis of myoclonic epilepsy of cortical origin. The etiology was unclear, but an undiagnosed viral illness was thought to be the most likely cause. Some movement disorders are speech-specific. AM can cause dysarthria, one in which manifestations are noticeably exacerbated by increased speaking rate. In some cases, the myoclonus is associated with dystonic-like movements.

Hypokinetic dysarthria

is a perceptually distinguishable motor speech disorder associated with basal ganglia control circuit pathology. Its characteristics are most evident in voice, articulation, and prosody. Its deviant speech characteristics reflect the effects of rigidity, reduced force and range of movement, and slow but sometimes fast repetitive movements of speech (Duffy, 1995 p. 166) We get fast bursts of movement but overall it's decreased movement Hypokinetic dysarthria is characterized by reduced loudness with concomitant harsh-hoarse quality, slow speaking rate with intermittent bursts of rapid fire articulation, excessive and overly long pauses, prolonged syllabus, monoloudness, and reduced phonation time. (Dworkin, 1991 p. 9)

Impairment in articulation in flaccid dysarthria

is imprecise consonant production

Cerebellum issues are

motor programming issues

Aceytlcholine

neurotransmitter associated with voluntary muscle control and excitation of muscle firing ***there is not enough of this in hyperkinetic Conditions producing too little acetylcholine = excitatory effect on movement

Why is it impossible for a single hemisphere stroke to cause spastic dysarthria?

the UMN pathways on the left and right are not in proximity to one another, therefore lesions in both the left and right hemispheres are required to produce the bilateral UMN damage

The basal ganglia is

the gatekeeper of movement It inhibits movement that are not wanted and initiates moments that are wanted

Pathophysiology is

the underlying impairment (e.g. laryngeal system) - most broad would be LMN - specific would be CN 10 Vagus on the laryngeal branch that is contributing to VF weakness

To distinguish ataxic from hypokinetic

they will be able to slow down if hypo, not if ataxic

Describe a behavioral and other (surgical, pharmacological) treatment approach for hyperkinetic dysarthria.

• Botox injections are used in managing jaw opening or closing for mandibular dystonias, for lingual dystonias that cause involuntary tongue protrusion, and for the levator and/or tensor veli palatini muscle to treat palatal myoclonus/tremor • Bite blocks are used on patients with oromandibular dystonias or other hyperkinesias affecting jaw or tongue movement to inhibit or limit adventitious jaw or tongue movements during speech, resulting in improvement in articulation and rate. • Sensory tricks - patients with focal dystonias of the jaw, tongue, or face can discover sensory tricks/postural adjustments that inhibit adventitious movements and facilitate speech.

Describe two rate control treatment tasks for individuals with increased rate of speech/hypokinetic dysarthria

• Delayed auditory feedback - person's speech is delayed and feedback through headphones earphones. Varying intervals are set to slow speech rate • Alphabet supplementation - speaker points to the first letter of each spoken word on an alphabet board • Hand tapping - person taps hand in pace with each syllable