CODI 555  Motor Speech Disorders
Lecture 3:  Cortical Disorders:  Spastic Dysarthria & Apraxia of Speech

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 Direct Activation Pathway

•  Also known as upper motor neuron level
•  Consists of corticobulbar and corticospinal tracts
•  Originate in several areas of cerebral cortex
•  Axons converge at level of basal ganglia and thalamus to form internal capsule
•  Synapse on LMN of cranial(motor) and spinal nerves
•  Innervation of speech cranial nerves is primarily bilateral with exception of XII and VII (lower face)

 Functions of Direct Activation System

•  Generation of voluntary motor activity, especially consciously controlled skilled movements such as speech
•  Movements can be initiated/triggered through sensory stimuli or generated by cognitive activity
•  Effects of Damage to Direct Activation System
•  Loss or reduction of voluntary skilled movements
•  Muscle weakness though not as pronounced as with LMN lesions
•  Preserved reflexes - though may be reduced - hyporeflexia
•   Decreased muscle tone - hypotonicity
•  Babinski sign

 The Indirect Activation Pathway

•  Also considered as part of the Upper Motor Neuron level
•  Origin roughly same as DAP with final destination the LMNs
•  May involve multiple synapses before reaches LMN
•  Actual fiber tracts often intermingle with corticobulbar and corticospinal tracts
•  Major tracts include corticorubral, corticoreticular, reticulospinal, vestibulospinal & rubrospinal

 Function of Indirect Activation Pathway

•  Regulation of reflexes
•  Aids in maintaining posture and muscle tone
•  Controls movements supportive of voluntary movement

 Effects of Damage to Indirect Activation Pathway

•  Major effects are on muscle tone and reflexes
•  Increased muscle tone - spasticity (resistence to movement)
•  Results from loss of cortical controls on reticular system
•  Result is hyper excitable extensor muscles
•  Hyperactive stretch reflexes
•  Clonus - repetitive reflex contraction that occurs when muscle is kept under tension e.g. stretched by examiner

 Effects of Damage to Both UMN Pathways

•  Spasticity
•  Increased muscle stretch reflexes
•  Loss of skilled movement
•  Weakness

 Common Etiologies

•  Caused by damage to direct and indirect activation pathways bilaterally
•  Site of lesion could be in the cortex, corona radiata, internal capsule, basal ganglia, pons,& medulla
•  CVA in internal carotid, middle and posterior cerebral arteries and their branches
•  Lacunar infarcts and Binswanger’s subcortical encephalopathy
• TBI including trauma from intracranial surgery
• Degenerative diseases such as PLS & PSP
• Infectious and inflammatory diseases
• Tumors
• Demyelinating diseases such as multiple sclerosis
• Often accompanied by cognitive disturbances as seen in dementia, TBI, RHD & aphasia

  Speech Musculature Deficits

•  Loss or reduction in fine skilled movements
•  Spasticity - increased resistance to muscle stretch or movement
•  Hypertonicity
•  Hyperactive reflexes
•  Pathologic oral reflexes
•  Muscle weakness, reduced ROM and slowed movements

 Nonspeech Oral Mechanism Deficits

•  Dysphagia and drooling
•  Emotional or reflexive facial responses are slow to emerge but may become excessive
•  Direction and rhythm of movements are normal and regular
•  Rate is slow, range and force is reduced and tone is excessive

 Patient Perceptions & Complaints

•  Increased effort to speak
•  Fatigue when speaking
•  Swallowing-chewing difficulty
•  Difficulty controlling expressions of emotions especially crying and laughter
•  Nasal speech
•  Increased susceptibility to gagging when brushing teeth

 Deviant Speech Characteristics

• strained-strangled, harsh, monopitch, monloudness, intermittent voice arrests
• hypernasality, nasal air emissions
• slow-labored & imprecise articulation
• short phrases, excess/equal syllable stress
• antagnositic muscular contractions, reduced pressure generation,shallow inhalations, reduced exhalatory control, slow breaths

 Distinguishing Clusters

•  Prosodic Excess (excess & equal stress, slow rate)
•  Articulatory-resonatory incompetence (imprecise cons., distorted vowels, hypernasality)
•  Prosodic insufficiency (monopitch, monoloudness, reduced stress, short phrases)
•  Phonatory stenosis (low pitch, harshness, strained-strangled voice, pitch breaks, short phrases, slow rate)

 Most Distinctive Speech Deviations

•  Strained-strangled voice quality
•  Slow speech rate
•  Slow and regular AMRs
•  Low pitch
•  Imprecise consonants, while the most deviant symptom, occur in almost all dysarthrias and therefore is not distinctive to spastic dysarthria

 Conceptual-Programming Level

•  Responsible for the design and plan of movement e.g. speech movements
•  Involves several areas of the cortex
•  Involves
•  Conceptualization
•  Spatial-temporal planning
•  Motor programming

 Motor Speech Programming

•  Muscles selected
•  Sequence of contraction/relaxation specified
•  Speed, strength and duration of excitation/inhibition specified
•  Contraction of speech muscles coordinated with other muscles
•  For over learned movement sequences, involves selecting, sequencing, activating and fine-tuning preprogrammed movement sequences (speech motor programs)

 Anatomical Structures & Functional Systems Involved

•  Cortical regions include premotor and supplementary motor areas of dominant hemisphere - Broca’s area specialized for speech motor programming
•  Somatosensory cortex, supramarginal gyrus and insula
•  Also dependent on:
•  Sensory feedback - especially auditory
•  Input form control circuits
•  Limbic system influence
•  Right hemisphere contributions
•  Reticular formation/thalamus

 Effects of Lesions to Conceptual/Programming Level

•  Conceptualization - dementia, confusion, disturbances of affect or thought
•  Spatial-temporal planning - aphasia
•  Motor speech programming - apraxia of speech

 Apraxia of Speech

•  Praxis - performance of an action or movement pattern
•  Apraxia - inability to perform volitional, purposeful movements in the absence of paralysis, sensory loss, comprehension deficit or ataxia
•  May result in inability to
•  Perform pretend actions
•  Use common objects
•  Respond to spoken commands
•  Produce a spontaneous movement pattern

 Type of Apraxia

•  Several different variations of apraxia have been described
•  3 are of importance to SLP
•  Oral apraxia
•  Limb apraxia
•  Apraxia of speech
•  Degree of impairment leads to variations in responses
•  Response absent
•  Haphazard, unrelated movement
•  Two or more gestures combined into one
•  Accurate response after several groping false starts

 Etiology of Apraxia of Speech

•  Unilateral left hemisphere damage
•  Usually includes posterior frontal lobe and/or subcortical areas closely associated with the area (basal ganglia and anterior limb of the internal capsule)
•  Most common etiologies are vascular lesions; also tumors & trauma
•  Rare to find AOS with degenerative disease
•  Common for AOS to co-exist with aphasia & dysarthria

 Patient Perceptions & Complaints

•  Often relate that they know the words to say, but they will not come out right
•  Some describe their problem as stuttering or mispronouncing words
•  Typically will not complain of chewing or swallowing problems unless there is co-occurring dysarthria

 Nonspeech Oral Mechanism Deficits

•  Can be normal
•  May show some mild right-side weakness of face and tongue, especially if AOS co-occurs with UUMN dysarthria
•  Nonverbal oral apraxic symptoms often apparent

 Deviant Speech Characteristics

•  General characteristics
•  Articulatory error characteristics
•  Prosodic characteristics
•  Others listed on pages 270-271 of text

 Most Distinctive Clinical Characteristics
 (According to Wertz, Lapointe, & Rosenbek)

•  Effortful, trial & error groping and attempts at self-correction
•  Dysprosody unrelieved by extended periods of normal rhythm, stress & intonation
•  Articulatory inconsistency on repeated productions of the same utterance
•  Obvious difficulty initiating utterances

Unilateral Upper Motor Neuron Dysarthria:  Common Etiologies

•  CVA- especially of left or right carotid or MCA
•  Lacunar infarcts in putamen, caudate, thalamus, pons, internal capsule, white matter
•  Also trauma if damage is focal & tumors if confined to one hemisphere

  Nonspeech Oral Mechanism Deficits

•  Lower facial weakness
•  Unilateral tongue weakness with deviation to affected side
•  Jaw usually OK - may have slight weakness
•  Mild dysphagia

 Unilateral UMN Dysarthria:   Patient Perceptions

•  Speech is slurred, thick, slow
•  Words don’t come out right
•  Drooling, heavy feeling on affected side
•  Chewing & swallowing problems
•  May comment on how much speech has improved

  Deviant Speech Characteristics

•  Overall mild-moderate dysarthria
•  Harshness, less often reduced loudness
•  Phonatory deficits occur most often with pts with concurrent dysphagia
•  Hypernasality - infrequent
•  Imprecise articulation, irregular articulatory breakdown, slow, imprecise and sometimes irregular AMRs
•  Slow rate