MSD Quiz 2 Review
Hypokinetic Dysarthria
Cause:
Damage to basil ganglia that reduces production of dopamine from the basil
ganglia control circuit
 Overactive indirect pathway
Anatomy Review:
Control Circuit: Basal Ganglia
 Function: Motor relay nuclei responsible for smooth, precise muscle
activity
1.) Regulate duration of an action
2.) Determine whether another action is of enough importance and
value to interrupt the existing action
3.) Choose when to terminate the current action
4.) Movement scaling (w/ cerebellar circuit)
 Structures:
Structure
Basil Ganglia
Motor cortex
Substantia Nigra
Striatum
Globus Palatus externus
Function
Starting and stopping movements
Plans what movement will happen
Dopamine origin, trigger basal
ganglia
-Receives motor plan from cortex
-Formulates motor plan
-Stops excess movement
-Tells Substantia nigra to turn on or
off dopamine production
-Sends GABA
-Determines if thalamus is on or off
Globus Palatus Internus
Thalamus
-receives stop signal from striatum
-Controls thalamus activation
Carries out motor plan if activated
Stop and Go Commands:
 Glutamate= Excitatory
 GABA= Inhibitory
 Dopamine= Controls activation of pathways
Pathways: Direct and Indirect
 Direct Pathway: Activated with HIGH dopamine BLOCKS inhibition
o High dopamine production triggers direct activation
o Motor plan travels from motor cortex to the striatum
o Striatum formulates motor plan and surpresses the globus
palatus
o Globus palatus is inhibited allowing the thalamus to activate
 Indirect Pathway: activated with LOW dopamine and STOPS the
thalamus
o Subthlamic nucleus DOES NOT send dopamine to basal ganglia
o Globus palatus is active and sends signal to thalamus to STOP
motor plan/movement
 Overactive Direct pathway= UNINTENTIAL MOVEMENTS
 Overactive Indirect pathway= MOVEMENT SIZE/DURATION REDUCED
Clinical Characteristics: Reduced
 Unilateral Tremor (pill rolling)
 Rigidity of muscles/joints
 Hypokinesia- Reduced volitional movement
o Reduced gesturing
o Micrographia
o Gait and arm swing
 Bradykinesia (slowness of movement)
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 Facial masking
 Postural instability
Speech Characteristics:
 Dysphonia
o Rigid variant: Hoarseness/breathiness/monopitch
o Tremor Variant: Vocal tremor, breathiness
 Monopitch/loudness
 Reduced stress
 Variable rate with short rushes
 Consonant/vowel imprecision
 Reduced ROM of articulators
 Neurogenic stuttering
Etiologies:
 Parkinsons=most common (overactive indirect activation)
 Parkinson plus disorders: starts off as hypokinetic then other
symptoms emerge
 Vascular parkinsons
 Toxicity
 Infection
Treatment:
 Levadopa: supplements dopamine produced by body
 Deep Brain Stimulation (DBS): Electrode in basal ganglia which
stimulates direct/indirect pathways
o Can increase risk in dysphagia
 Respiration: EMST (Loudness, breath control) IMST)
 Speech: LVST (Cognitive awareness of loudness/speech rate, increase
breath support/loudness/rate control
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Hyperkinetic Dysarthria:
Cause:
Difficulties due to excessive movement
Overactive DIRECT pathway
Clinical Characteristics:
 EXCESS in any of the 4 speech systems
 Hyperkinesis:
o Dyskinesias: any abnormal involuntary body movement
o Myoclonus: Single or repetitive brief involuntary jerks of a body
part (random twitch) due to damage in basal ganglia
o Tics: Rapid movements under partial voluntary control
o Chorea: Involuntary rapid random movements during sustained
posture or rest
o Bllismus: Abrupt contractions of extremities (wild flailing)
o Athetosis: Slow writhing movements that flow into one another
o Dystonia: Abnomrla posture from excessive contraction of
aganost and antagonist muscles
o Spasm: Abnormal muscle contraction
o Tremor: Most common involuntary movement
Speech characteristics:
Speech System
Respiratory
Phonatory
Resonance
Articulation
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Characteristic
-Excessive loudness variations due
to sudden inhale/exhalation
-Reduced phrase length
-Harsh or strained vocal quality
-Breathiness
-Sudden voice breaks
(hyperadduction)
Mild, intermittent hypernasality
-Irregular articulatory breakdowns
-Prolonged phonemes
-Variable rate
Prosody
Equal/excess stress
Reduced prosodic contour
Etiologies:
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Undetermined
Toxic/metabolic
Infections
Tumors
Genetic disorders
Related Disorders:
 Tourettes:
 Chorea
o Caused by Huntington’s
o Involuntary inspiration/exhalation, harsh quality, hypernasality,
imprecision form excess movement, prosodic excess, prolonged
intervals, inappropriate silences
 Dystonia: spasmodic dysphonia
o Most evident at rest
o Clusters of deviant speech characteristics
o Adductor: part/whole word repetitions, hypernasality, strained
and effortful
o Abductor: Voice interruptions by brief breathy aphonic speech
triggered by voiceless consonants
Treatment:
 Bite blocks/sensory tricks (oromandibular dystonia)
 Myoclonus: slow speech rate
 Vocal tremor: shortening voice duration in connected
speech/adjusting pitch
 Deep brain stimulation (DBS)
 Botox injections for dystonia’s
 Meds
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Unilateral UMN Dysarthira
UMN Cause: Damage to UMN pathways
Dx by anatomy and NOT physiologic changes
 Damage to right hemisphere: cooccurring w/ aprosodia and cognitive
deficits
 Damage to left hemisphere: co-occurs with aphasia/apraxia
Characteristics of pathways:
 Direct Activation damage:
o Weakness
o Hemiplegia
o Unilateral lower face/tongue weakness
o Abnormal reflexes
 Indirect activation damage:
o Increased muscle tone
o Clonus
o Hyperreflexia
UMN Clinical Characteristics:
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Quick resolution even without treatment
Symptoms similar to stroke
Contralateral lower facial weakness
Contralateral lingual weakness
Jaw is ok
Velopharyngeal function ok
Some contralateral VF weakness
High likelihood of dysphagia
Upper Face characteristics:
 V,IX,X,VII
 UMNs bilaterally innervate LMNs of the jaw, velum, pharynx/larynx
 More mild deficits in these speech structures
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Lower Face characteristics:
 XII
 UMNs contralaterally innervates LMNs for tongue/lower face
 More deficits to speech
Speech characteristics:
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Consonant imprecision- tongue/lip weakness
Irregular articulatory breakdowns- Inconsistent info provided
Slow/imprecise AMRs- tongue/lip weakness
Slow rate
Monopitch/monoloudness/mild hypernasality- Damage to
palate/larynx
Etiology:
 Vascular stroke- remember because it is unilateral damage!
o Frontal lobe near motor strip
 Lacunar stroke- impacts the internal capsule (white matter bringing
info to brainstem)
 TBI, Tumor resection, MS UNILATERAL damage in/around motor
strip
Mixed Dysarthria:
Cause: When one or more systems are affected creating combined effects of
one or more subtypes
 More common than a single dysarthria dx
 Multiple lesion sites or one diffuse lesion
Etiologies:
 Degenerative Disease is the most common
ALS- Amyotrophic lateral sclerosis  Flaccis-spastic
 All 4 pathways will be affected over time
 Symptoms occur based on which area is impacted first
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o Spinal nerves: weakness, hyporeflexia, hypotonia, atrophy
o Cranial Nerves: Flaccid dysarthria, dysphagia, reduced gag,
lingual fasciulations
o Corticospinal: weakness and spasticity, hyperreflexia, muscle
cramps
o Corticobulbar: Spastic dysarthria, hyperactive gag, slow
movements, dysphagia, pseudobulbar affect
 Speech characteristics:
o Imprecise consonants
o Hypernasality
o Harshness
o Slow rate
o Monopitch
o Short phrases
o Distorted vowels
o Vocal flutter- flaccid/spastic issues in larynx and palate
Friedrichs Ataxia ARAXIC-SPASTIC
 Starts in cerebellumbrainstem/spinal cord
 Speech characteristics:
o Harshness, breathiness, strained strangled vocal quality
o Audible inspiration
o Monopitch, pitch breaks, fluctuations pitch, inappropriate pitch
level
Parksinsonisms:
 Ataxic/spastic almost always involved
Name
Progressive
Supranuclear Palsy
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Characteristics
Dysarthria
-Damage in or around Hypokinetic/spastic/ataxic
basal ganglia extending
to
brainstem/cerebellum
-Wont respond to
Parkinson’s meds
-Restriction of vertical
eye movement
-Dysarthria/dysphagia
are early signs
Multiple system
-Basal ganglia into
atrophy-A
brainstem
-More autonomic
troubles
-no tremor
-respiratory
incoordination
-sleep apnea
MSA-P
-Leads into brainstem
(parkinsonism)
-Faster progression
-More severe more
quickly
-wont respond to
Levadopa
MSA-C (CEREBELLAR) -Early parkinsons w/
MASSIVE shift into
cerebellar involvement
Corticobasal
-more rare than
Degeneration
parkinsons
-Simultaneous
degeneration of cortex
and basal ganglia
-PPA common
-Apraxia common
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-spastic-ataxichypokinetic
-hypokinetic-ataxic
-ataxic-spastic
Hypokinetic w/ spastic or
ataxic or both
Ataxic w/ spastic or
hypokinetic or both
Hypokinetic, spastic,
ataxic
MS SPASTIC-ATAXIC:
 Most common demyelinating disease
 Occurs in brainstem, cerebellum, cerebral hemispheres, spinal cord
(anywhere in CNS)
 Common complaints:
o Vision troubles
o Chronic feeling of tiredness/weakness in limbs
o Gait disturbance
o Sensory disturbances
TBI-MAINLY SPASTIC-ATAXIC
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Occurs in 1/3 of TBI patients
Severity based on location and severity of injury
Spastic=most common
Mixed because of diffuse nature of injury
Congruent w/ motor deficits
Multiple TBI’s= Chronic traumatic encephalopathy
o Cause parkinsonisms
o Hypokinetic mixtures
Guide to Dysarthrias and etiologies
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