MOTOR SPEECH DISORDERS

ANUSHA REDDY SALLARAMAYJNIHH, SRC

MOTOR SPEECH DISORDERS

Definition :

• Disorders of speech results from neurological impairment.

(or)

• A collection of communication disorders involving:

1) the retrieval and activation of motor plans for speech (apraxia)

2) the execution of movements for speech production (dysarthria)

(speech = movement)

Types of motor speech disorders:

• The two main types of motor speech disorders are Dysarthria and Apraxia. 

Dysarthria

Definition: A group of speech disorders

resulting from disturbances in muscular control-weakness, slowness, or incoordination- of the speech mechanism due to damage to the central or peripheral nervous system or both.

Dysarthria site of lesion:

•Upper motor Neuron (UMN) -Cerebellum, basal ganglia, substantia nigra, and pseudobulbar palsy) 

•Lower motor neuron (LMN) -cranial nerves V, VII, IX, X, XI, XII - all involved with movements of speech

Dysarthria etiology

•Degenerative (ALS)

•Inflammatory (Meningitis, encephalitis)

•Toxic/Metabolic (kidney liver disease, vitamin deficiency) 

•Neoplastic (tumor)

•Traumatic (closed head injury)

•Vascular disease (CVA)

TYPES OF DYSARTHRIA

• Ataxic• Spastic • Flaccid • Hyperkinetic• Hypokinetic • Unilateral UMN • Mixed

Darley, Aronson, & Brown (1975, 1969) have developed a perceptual classification system of dysarthrias :

• Pitch• Loudness• Voice quality• Respiration• Prosody• Articulation

Types of Dysarthria, Their Associated Lesion Loci, and the Neuromuscular

Deficits

Dysarthria type Lesion locus Distinctive neurologic deficit

Flaccid Lower motor neurons(cranial and spinal nerves)

Weakness

Spastic Upper motor neurons (bilateral)

Spasticity

Ataxic Cerebellum(cerebellar control circuit)

Incoordination

Hypokinetic Basal ganglia control circuit Rigidity, reduced range ofmovement

Hyperkinetic Basal ganglia control circuit Involuntary movements

Unilateral upper motor neuron

Upper motor neuron (unilateral)

Weakness, (?)incoordination, (?) spasticity

Mixed Two or more of the above Two or more of the above

Flaccid Dysarthria

• Site of Lesion - Peripheral nervous system or lower motor neuron system.

• Neuromuscular Symptoms– Weakness– Lack of normal muscle tone

• Perceptual Characteristics– Hypernasality– Imprecise consonant productions– Breathiness of voice– Nasal emission

Spastic Dysarthria• Site of lesion - Pyramidal and

extrapyramidal systems• Neuromuscular Symptoms

– Muscular weakness– Greater than normal muscular tone

• Perceptual Characteristics– Imprecise consonants– Harsh voice quality– Hypernasality– Strained-strangled voice quality

Ataxic Dysarthria• Site of lesion - Cerebellum• Neuromuscular Symptoms

– Inaccuracy of movement and Slowness of movement.

• Perceptual Characteristics– Imprecise consonants– Irregular articulatory breakdowns– Prolonged phonemes– Prolonged intervals– Slow rate

Hypokinetic Dysarthria• Site of Lesion - Subcortical Structures

involving Basal Ganglia• Neuromuscular Symptoms

– Slow movements– Movements limited in extent (limited range

of movement)

• Perceptual Characteristics– Articulatory mechanism - Impaired because

of reduced range of motion involving the lips, tongue, and jaw. Disturbance may range from mildly imprecise to total unintelligibility.

Hyperkinetic Dysarthrias• Site of Lesion - Subcortical Structures

involving Basal Ganglia• Neuromuscular Symptoms

– Quick, unsustained, involuntary movements

• Perceptual Characteristics associated with Gilles de la Tourette's syndrome– Emission of grunts as a result spontaneous

contractions of the respiratory and phonatory muscles

– Barking noises– Echolalia– Coprolalia: obscene language without

provocation or reason.

Mixed Dysarthrias• Amyotrophic Lateral Sclerosis

– Site of Lesion - Progressive degeneration of the upper & lower neuron system. Most cases appears without a known cause

– Neuromuscular Symptom• Impairs the function (weakness and paralysis) of

all the muscles used in speech production

– Perceptual Characteristics• Slow rate• Shortness of phrase• Imprecision of consonants• Hypernasality• Harshness

Apraxia of Speech

• “Disorders of the execution of learned movement which cannot be accounted for either by weakness, in coordination, or sensory loss, or by incomprehension or inattention to command”.

• Although it can affect any component of speech production, it is primarily a disturbance of articulation and prosody.

Apraxia: Also known as...• Apraxia• Dyspraxia• Verbal Apraxia of Speech (VAS)• Childhood Apraxia of Speech(CAS)• Developmental Apraxia.

Causes :• Genetic Disorder• Stroke• TBI• Unknown

• Localization - Apraxia results from a unilateral, left hemisphere lesion involving the third frontal convolution, Broca's area. There is a possibility of apraxia following more posterior, probably parietal lesions.

Early Possible Indicators• Decreased babbling/cooing in infancy• Late acquisition of first words• Avoidance of first words (grunts/points)• One syllable words favored beyond age 2

Limited consonant/vowel repertoire noted (compared to developmental expectations)

• Open mouth posturing prominent.

Speech Characteristics• Articulation Process

– Common characteristic is the patient's groping to find the correct articulatory postures and sequences.

– Facial grimaces, moments of silence, and phonated movements of articulators are common occurrences.

– Consonant phonemes are involved more often than vowel phonemes

– Articulation errors are inconsistent and highly variable, not referable to specific muscle dysfunction

– Articulatory errors are primarily substitutions, additions, repetitions, and prolongations-essentially complications of the act of articulation.

• Prosody Process– Durational relationships of vowels and consonants are

distorted– Rate of production is slow– Alterations of the intonation

Apraxia 23

1.Koskia, L., M. Iacobonia, and J.C. Mazziottaa, Deconstructing apraxia: understanding disorders of intentional movement after stroke. Current Opinion in Neurology, 2002. 15: p. 71-77.

Controversial: Ideational may be a severe form of ideomotor apraxia

Apraxia 24

Motor Engram

Paralyzed hand

Apraxic Hand

Therefore

Apraxia 25

Motor Engram

Paralyzed hand

Therefore

No engram here

Apraxia 26

Motor Engram

Paralyzed hand

Therefore

No engram here

Ipsilateral side must need the left-side engram

Apraxia 27

Motor engram damaged

Paralyzed hand

Ideational ApraxiaIdeomotor Apraxia

No imitation

Motor engram okay

Diffuse damage

Can imitate

Confused motor sequences

Apraxia 28

Ideomotor Apraxia(Unilateral ideomotorapraxia)

Inaccurate pantomime of skilled movements on both sidesof body in response to verbal demand:

Incorrect but recognizable movement Partial movement = abridgement of target move Distorted movement Use of body part as object Incorrect orientation of arm, hand, or fingers for movement Substitution of verbal responseInaccurate imitation of pantomimed skilled movements onboth sides Evidenced by types of errors aboveInaccurate performance of skilled movements using objects Movement not appropriate for object Partial movement (abridgement) Incorrect orientation of arms, hands, limbs Incorrect orientation of object in space Use of body part as object

Ideational Apraxia Inaccurate sequencing of individual steps within a goal-directed sequence Confusion of sequential order of steps Omission of one or more steps Substitution of incorrect actions for one or more of the

actions in a series Inability to use a tool to act on another objectRelatively preserved performance of individuals actionswithin the series on verbal commandRelatively preserved imitation of individual actions withinthe series

Lesions:Primarily parietal,with possibleextension to frontal.Also, supplementalmotor cortex offrontal, possible tocorpus callosum,insular cortex andadjacent white matter,basal ganglia (caudatenucleus & lenticularnuclei)

Lesions:Frontal lobe, extensionto parietal & temporalLateral surface oftemporal lobeParietal lobe

Apraxia 29

Paralyzed ApraxicLanguage OK

Apraxia 30

Heilman, M. Kenneth, John Coyle, Edward Gonyea & Norman Geshwind. (1973). Apraxia and agraphia in a left hander. Brain, 96, 21-28.

• “. . .Account for the presence of agraphia in the hand opposite a hemisphere which still serves speech, following a lesion in the hemisphere ipsilateral to that hand.”

• Apraxia & agraphia on the right• Case 1: Callosal lesion = right

sided agraphia and apraxia• Left hander with Right

Dominance for both handedness and speech.

• Left hand writing requires no callosal activity

SPEECH

Skilled Engrams

Motor Control

Motor Control

Apraxia 31

Heilman, M. Kenneth, John Coyle, Edward Gonyea & Norman Geshwind. (1973). Apraxia and agraphia in a left hander. Brain, 96, 21-28.

• They discuss the Poeck & Kerschensteiner (1971) case

• Patient is Right Dominant for both speech and motor skills but writes with the right hand.

• So left hemisphere controls right hand via the corpus callosum

• Callosal lesion =• apraxic & agraphic with right

hand• Left paresis? Damage to

callosum at site?• Why not second lesion on left

parietal? No other Gerstmann symptoms

SPEECH

Skilled Engrams

Motor Control

Motor Control

Paresis