Neuroanatomy for Speech-Language Pathology and Audiology 2nd Ed. Matthew H Rouse

Chapter 11. The Neurology of Speech


We now turn to the neurology of speech. Speech is a complex motor act involving many muscles and nerves. The nervous system acts as a conductor coordinating a great orchestra of instruments that together produce human speech.



In this chapter, we will . . .

 Survey the motor speech system

 Examine different forms of dysarthria and apraxia of speech as they relate to motor pathways

 Review important sensory pathways for speech


1. The learner will outline the major components of the motor speech system.

2. The learner will connect different places of damage in the motor speech system to different forms of dysarthria.

3. The learner will identify places of damage associated with apraxia of speech.

4. The learner will describe the importance of the sensory system to speech.

5. The learner will describe the human response space and the communication disorders professional's role in expanding it.


 The Motor Speech System

 The Conceptual Level

 The Linguistic Planning Level

 The Motor Planning and Programming Levels

 The Motor Control Circuits

 The Direct Motor Pathway

 The Indirect Motor System

 The Final Common Pathway

 Multisystem Damage

 Sensory Pathways Important for Speech

 Ascending Sensory Pathways



 Summary of Learning Objectives

 Key Terms

 Draw It to Know It

 Questions for Deeper Reflection

 Case Study

 Suggested Projects



The motor system is a complex system involving a number of pathways and structures that make movement of both voluntary and involuntary muscles possible. The motor speech system is a subunit of the motor system, and an understanding of the motor system gives the student an understanding of the motor speech system as well as motor speech disorders.

The motor speech system is one possible language route. Humans can also express language through writing or through gestures, such as those used in American Sign Language (ASL). Speech is a dynamic motor process involving the coordination of respiration, phonation, resonance, and articulation in order to produce strings of speech sounds grouped together in words. The purpose of this chapter is to survey the neurology of the motor speech system and to discuss motor speech disorders.

 The Motor Speech System

A multilevel division of control is helpful in grasping the complexity of the motor speech system (FIGURE 11-1). These levels are as follows:

 The conceptual level

 The linguistic planning level

 The motor planning and programming levels

 The motor control circuits

 The direct motor pathway

 The indirect motor pathway

 The final common pathway

 The sensory system

The Conceptual Level

We all have ideas, thoughts, and feelings swimming around in our heads. This is our first-person perspective. These ideas, thoughts, and feelings are known only to us (i.e., they are private to us), unless of course we decide we would like to let someone into our first-person perspective through communication. When we make this decision to communicate, we then decide how to communicate. If we choose the route of producing language orally through speech, we then form an intention to express our ideas, thoughts, and feelings (BOX 11-1). Where do these thoughts swim and intentions reside? It is best thought of as being a whole-brain activity, involving the entire cerebral cortex, with the prefrontal cortex and limbic system taking primary roles in the process.

FIGURE 11-1 The motor speech system.

The Linguistic Planning Level

There are two parts of the planning level, linguistic planning and motor planning. Linguistic information, which includes content, form, and use, makes up the substance of our speech. Content or semantics is the meaning of our language. Form is the structure or grammar of language and includes phonology (sound system structure), morphology (word structure), and syntax (sentence structure). Lastly, language use involves all the pragmatic rules we use as we express language through speech.

Linguistic planning is nonmotor in nature. It involves taking one of our ideas, thoughts, or feelings and dressing it in language, what is called encoding. This planning engages the dominant language hemisphere, which is the left hemisphere in most people. Specifically, the dominant dorsal perisylvian region (i.e., the region around the lateral fissure) is highly engaged in linguistic planning.

BOX 11-1 Speech and Free Will

It has always been assumed that speech is a voluntary act of our free will. In other words, the typical order of events is that I create an intention to speak of my own volition, which then sets off a series of neural impulses to accomplish the very thing I intended to do.

In the 1980s, a researcher named Benjamin Libet produced a series of experiments that challenged this notion (Libet, Gleason, Wright, & Pearl, 1983; Libet, 1993). His research question was: What happens in the brain just before we make a voluntary, free-will action like speaking? Libet hooked his test subjects up to electroencephalography (EEG) equipment to detect the brain's electrical activity and to an electromyogram (EMG) on their finger (FIGURE 11-2). This way, he could measure the time it took from the generation of a neural impulse to when a subject actually moved his or her finger. In addition, a specialized clock was placed in front of the subjects so they could report the exact time they first had an intention to move their finger. In summary, Libet was attempting to measure three things:

1. The time at which a person formed an intention to move his or her finger

2. The time at which a neural impulse to move the finger was initiated

3. The time at which the finger actually moved

One would expect that the order of events would occur as follows: 1,2, 3. Instead, Libet found the order was 2, 1,3. In other words, the neural impulse came first, then the intention, and finally the action. It would appear that a so-called voluntary free act is not so free if neural impulses precede the conscious intention to act. If this is true, what do we do with the concept of free will? The brain seems to be doing all the choosing before I am consciously aware of it. Can I truly claim ownership of my acts, including my speech acts? There has been much criticism of Libet and his experiments in this arena (see Seifert, 2011). For example, some have criticized him for not considering other brain states that may be occurring before the intention was formed (a kind of deliberating stage).

Historically, there have been two views of free will, libertarianism and compatibilism. Libertarians define free will as a person's capacity for choosing otherwise, whereas compatibilists define it as acting without coercion. A libertarian would believe that free will and determinism are incompatible, whereas a compatibilist would believe that they are compatible. Typically, the discussion is centered around whether we have free will or not (i.e., a binary property), but

FIGURE 11-2 The Libet experiments attempted to demonstrate that the brain decides to initiate motor functions before a person consciously chooses to make any movements.


BOX 11-1 Speech and Free Will (continued)

perhaps it is better defined as a scalable property. In other words, free will is something of which we have more or less, depending on the constraints on us. Spence (2009) calls this the human response space. This is the space within a person can act, a space with constraints or walls around it. Some people have more space to act; others have less. What are some of these constraints? One example might be an anatomical restraint. A person who has a stroke might experience paralysis and thus might not be able to speak in the way that he or she wants. His or her response space has been narrowed by the stroke. Another example of a restraint is society. We might refrain from a certain action (e.g., eating one's grandmother) because society frowns on such an act. Other restraint categories include the physical environment, brain anatomy, neurochemistry, physiology, psychology, phenomenology (e.g., lack of'feeling emotion”), and genetics. Spence notes, "It is not the instant of the act but its context that seems to matter” (p. 395).

Perhaps it is time to reconsider what we mean by free will and move our attention away from the instant of action to the context of that action. Our patients with motor speech disorders (MSDs), like dysarthria and apraxia of speech (AOS), experience the restraint of their impaired neuroanatomy, which limits their ability to act as they desire. This is where speech-language pathologists (SLPs) and audiologists come in. Our job is to work hard in therapy with our patients and try to increase their human response space for communication.

The Motor Planning and Programming Levels

Motor Planning

The second part of planning is motor planning. Once phonological assembly (i.e., assigning correct phonemes in correct order) has taken place in the linguistic planning phase, the motor planning for phonemes takes place. Motor plans can be thought of as blueprints for actualizing phonemes. These blueprints are unrefined when we are babies, but as we grow and learn, they become more refined and precise and need only to be recalled in order to be executed (as opposed to being created anew each time). Neuroanatomically, the frontal lobe is important for motor planning, specifically Broca’s area (Brodmann areas [BAs] 44, 45), parts of the premotor cortex (BA 6), and the supplementary motor area.

Motor Programming

Motor plans are prerequisites for a motor program to be executed; without them, motor programs would be aimless. Programs have to do with the execution of phonemes in time and space. It takes many motor programs to accomplish a motor plan. An illustrative example is the Ford Motor Company. Ford has a planning division that designs cars, producing blueprints for them. Ford also has assembly plants with robotic machines that actually follow computer programs to make the car plans come into existence. Many different computer programs have to be executed to fulfill a car plan. It is similar with motor plans. Motor plans contain the specific, individual movements of the speech organs to produce speech sounds (i.e., motor programs).

Proper speech sound production requires that the speech organs move accurately and precisely in terms of articulatory target, timing, muscle tone, and force. Sensory information is also incorporated into the process to give feedback, allowing for midcourse corrections of the articulators. The neurological structures involved in programming include the cerebellum, basal ganglia, and supplementary motor area as well as other cortical areas, like Broca’s area.

Speech Issues Associated With the Motor Planning and Programming Levels

The umbrella term motor speech disorders (MSDs) includes two disorders, dysarthria and apraxia of speech (AOS). The different forms of dysarthria collectively make up 92% of MSD cases, while apraxia of speech accounts for the remaining 8% (Duffy, 2005). Duffy (2005) defines AOS as follows:

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 components of language. (p. 307)

When lesions occur to the structures vital to the motor planning and programming levels, AOS may result.

Duffy (2005) combines the motor planning and programming levels into what he calls the motor speech programmer (MSP), which anatomically is spread throughout the left hemisphere, particularly in the left perisylvian region. It is influenced by numerous other structures, such as the motor control circuits as well as the limbic system and the right hemisphere. The MSP relies heavily on the frontal lobe, particularly Broca’s area, and the supplementary motor area. Lesions in these areas can lead to AOS, but lesions to the insula or the basal ganglia can also lead to it.

The hallmark characteristic of AOS is searching and groping for articulatory placement when attempting to speak in the absence of any musculature abnormality. These patients know what they want to say, but they cannot “pull up” the appropriate motor plans and programs to execute saying the word. They are like a professional tennis player who suddenly “forgets” how to hit a forehand or backhand but retains his or her muscle strength and range of motion. The motor plans and programs, developed over years of practice, are absent or impaired even though the player’s muscles are intact.

In addition to searching and groping behavior, patients make more substitution errors than omissions, distortions, or additions. Errors also occur more in place rather than manner or voice. Consonants are more difficult to produce than vowels, and consonant clusters are more difficult than single consonants. These patients are more successful in producing sounds in the front of the mouth as compared to back sounds, probably because frontal sounds are highly visible and easier to mimic. Overall, people with AOS make inconsistent errors in articulation, differing from children with phonological disorders, who have discernable error patterns called phonological processes. One of the most amazing phenomena is the occasional periods of error-free speech. After struggling for many minutes, a patient might suddenly exclaim, “Oh damn it” as clear as a bell.

The Motor Control Circuits

There are two control circuits important to speech, the basal ganglia and the cerebellum. These circuits are important in motor programming of speech by coordinating, integrating, and refining the movements of the direct and indirect pathways, which will be discussed in a moment. These circuits can be thought of as fine tuners, just as tuning up a car makes it run smoother and more efficiently. Both these circuits could be discussed under the indirect motor pathway, but we will discuss them separately so they receive their due attention.

The Basal Ganglia Circuit

The basal ganglia are a collection of nuclei including the caudate nucleus, putamen, globus pallidus, substantia nigra, and subthalamic nucleus. This system is central to the indirect motor system, also known as the extrapyramidal system. The basal ganglia nuclei form various afferent and efferent loops connecting the cerebral cortex, premotor cortex, supplementary motor area, thalamus, and substantia nigra (FIGURE 11-3). In addition to these connections, the basal ganglia use several neurotransmitters to regulate motor functioning, including acetylcholine (ACh), dopamine, and gamma-aminobutyric acid (GABA). The purpose of these loops and neurotransmitters is specifically to regulate muscle tone and posture and to smooth or refine muscle contraction. They also seem to have a dampening effect on the motor signals sent from the cerebral cortex. Damage to the basal ganglia system results in dyskinesias and conditions like Parkinson disease and Huntington disease. In these conditions, we can witness the loss of this dampening effect as we observe tremors and other dyskinesias.

The Cerebellar Circuit

The cerebellar circuit could also be subsumed under the indirect motor pathway (i.e., extrapyramidal system), but it will be discussed separately to highlight the cerebellum’s contribution to speech production. As discussed previously, the cerebellum rests posterior to the pons and inferior to the temporal lobe. The cerebellum can be divided into two hemispheres, the right cerebellar hemisphere and the left cerebellar hemisphere. Each hemisphere has three lobes: the flocculonodular, anterior, and posterior. Of these three, the posterior lobe plays the most important role in speech production. Specifically, it automatically incorporates feedback “for coordinating skilled, sequential voluntary muscle activity” (Duffy, 2005, p. 54). This type of movement is obviously crucial in speech production. The cerebellum also has a number of afferent and efferent tracts that run to and from it (FIGURE 11-4). Afferent tracts greatly outnumber efferent ones, which demonstrates how important sensory feedback (e.g., proprioception of the speech muscles) is to coordinated motor function like speech.

Functionally, the cerebellum plays a role in a motor feedback loop between the cerebellum and the premotor cortex (BA 6) and the precentral gyrus (BA 4). When the primary motor strip (BA 4) sends a motor signal through the direct motor system, the signal is most likely unrefined and needs the refining effect of the cerebellum. A copy of this message travels to the cerebellum via the corticopontine-cerebellar tract. The cerebellum then compares this information with the proprioception and kinesthetic information it receives from muscles and joints and coordinates muscle activity so that it is smooth and precise. Thus, the cerebellum makes an important contribution to the diadochokinesia (i.e., precise, rapid, alternating movements) necessary for speech. Disruptions in this ability lead to ataxia, a lack of order and coordination between muscles, and adiadochokinesia, an inability to perform rapid, alternating movements. Diadochokinesia can be tested in speech by having a patient say “pa-ta-ka” as rapidly and accurately as possible. Cerebellar damage can lead to a dysarthria called ataxic dysarthria that is characterized by harsh voice, monopitch, loud voice, imprecise consonants, and irregular breakdown in articulation. Often, patients with ataxic dysarthria sound drunk to the listener; as a result, listeners are not always empathetic regarding the patient’s disorder and may even accuse him or her of being intoxicated.

FIGURE 11 -3 The basal ganglia control circuit.

FIGURE 11-4 The cerebellar control circuit.

The Direct Motor Pathway

The direct motor pathway is also known as the pyramidal system. This system is made up of two motor pathways, the lateral corticobulbar tract and the lateral corticospinal tract, and one medial motor pathway, the anterior corticospinal tract (TABLE 11-1 ). The lateral corticobulbar tract will be the focus in this section because it controls the movement of the speech muscles. The cortico portion of this name refers to the cerebral cortex, and the bulbar part refers to the brainstem because it is bulbous (i.e., “bulging”). This tract controls the muscles of the neck and face, including those important for speech and swallowing.

The pyramidal system receives its name from the primary type of cell in this system, pyramidal neurons. The neurons’ cell bodies are in the shape of pyramids, hence their name (FIGURE 11-5). Betz cells, the largest type of pyramidal cell, are found only in the fifth layer of the cerebral cortex and the lateral corticospinal and lateral corticobulbar tracts of the pyramidal system; they occur nowhere else in the nervous system. The Betz cell bodies are located in the cerebral cortex, and their axons course down through the lateral corticospinal tract and synapse directly to the ventral horn cells of the spinal cord, which then synapse directly with muscles. The lateral corticobulbar tract follows the same pattern as the lateral corticospinal tract, except it synapses with cranial nerve nuclei in the brainstem rather than the spinal cord. Overall, pyramidal cells are crucial for the modulation of the pyramidal system as well as the nervous system overall (Spruston, 2009).

TABLE 11-1 The Motor Pathways







Lateral motor pathways

Lateral corticobulbar

Primary motor cortex (BA 4)

Medulla/spinal cord juncture


Movement of contralateral head region


Lateral corticospinal

Primary motor cortex (BA 4)

Medulla/spinal cord juncture

Spinal cord

Movement of contralateral limbs





Cervical spinal cord

Flexor tone

Medial motor pathways

Anterior corticospinal

Primary (BA 4) and premotor (BA 6) cortex


Cervical and thoracic spinal cord

Movement of trunk muscles



Pons and medulla


Throughout whole spinal cord

Extensor tone and spinal reflexes



Pons and medulla


Throughout whole spinal cord

Posture and gait





Cervical spinal cord

Coordination of head and eye movements

The pyramidal system is a voluntary motor system that controls gross motor movement. In other words, it controls those actions we consciously make (e.g., I will now stick out my tongue), but in an unrefined way. The refinement comes through the basal ganglia and cerebellar control circuits. The tracts that make up this system are very direct, like an express train (FIGURE 11-6). They begin in the primary motor cortex (BA 4), which lies on the frontal lobe’s postcentral gyrus, and in the premotor cortex (BA 6). When mapped out, a homunculus (Latin for “little person”) can be generated from the primary motor cortex’s motor areas. Exaggerated parts of the homunculus illustrate that more motor fibers are associated with that area than others are, primarily because that body part (e.g., hand or mouth) performs fine motor activity and needs more motor fibers to make this type of activity happen. A similar homunculus can be created for the primary sensory cortex. Many of the same structures (e.g., hands and mouth) are enlarged, indicating a larger number of sensory fibers going to those structures. This illustrates the importance of sensory feedback to motor activities.

FIGURE 11-6 The direct motor system. Note the directness of this pathway and the decussation at the level of the medulla.

The pyramidal tracts then descend through the corona radiata and into the internal capsule. Because tracts like the corticobulbar and corticospinal run through the internal capsule, even small lesions from strokes can cause catastrophic motor problems. The pyramidal tracts travel to the brainstem where they decussate (i.e., cross over) to the other side at the medulla and spinal cord juncture. This decussation is responsible for what is called contralateral innervation, meaning that the right side of the brain controls the left side of the body, and the left side of the brain controls the right side of the body. In the case of the lateral corticobulbar tract, once it has decussated at the medulla, it leaves the brainstem as a cranial nerve that then innervates various muscles in the head and neck. The cranial nerves that are important to speech include V, VII, IX, X, and XII.

Upper Motor Neuron Damage Versus Lower Motor Neuron Damage

Neuroscientists have made a useful distinction in the pyramidal system (and the extrapyramidal system to be discussed next), calling the part that courses from the cortex to the brainstem the upper tract, or upper motor neurons (UMNs), and calling the part that leaves the brainstem as a cranial nerve the lower tract, or lower motor neurons (LMNs). UMNs are housed entirely within the central nervous system (CNS) and control LMNs. LMNs are housed in the peripheral nervous system (PNS). UMNs also include both the direct and indirect motor pathways (i.e., pyramidal and extrapyramidal). We will mainly discuss the UMNs here and provide a lengthier discussion on the LMNs under “The Final Common Pathway.”

The distinction between UMNs and LMNs is helpful because UMN damage differs from LMN damage (TABLE 11-2). Damage to the UMNs results in spastic muscles due to overactive muscle tone (hypertonia) and reflexes (hyperreflexia), whereas damage to the LMNs results in the opposite—flaccid muscles due to lack of muscle tone (hypotonia) and reflexes (hyporeflexia). Clonus, a jerky resistance when putting a limb into extension, is present in UMN damage, but not in LMN damage.

TABLE 11-2 Symptoms of Upper Versus Lower Motor Neuron Damage

Upper Motor Neuron Damage

Lower Motor Neuron Damage

Spastic muscles due to:

■ Hypertonia

■ Hyperreflexia


No fasciculations

Positive Babinski sign

No atrophy

Flaccid muscles due to:

■ Hypotonia

■ Hyporeflexia

No clonus


No Babinski sign

Marked atrophy

Clonus, which involves larger movements, can be contrasted to fasciculations, which are small spontaneous twitches. There are no fasciculations in UMN damage, but it is evidenced in LMN damage. A Babinski sign is elicited when scratching the bottom of the foot. A normal (negative) Babinski sign occurs when the toes curl and withdraw from the scratching. An abnormal (positive) Babinski sign occurs when the big toe moves back and the toes spread out, which is what occurs in UMN damage. In LMN damage, there is no Babinski sign at all (i.e., the toes do nothing when the bottom of the foot is scratched). Finally, atrophy refers to muscle shrinking and wasting; this is seen in LMN damage, but not in UMN damage.

Why does LMN damage differ symptomatically from UMN damage? Reflexes are mediated at the level of the brainstem or spinal cord, depending on which reflex is being discussed. In UMN damage, the reflex arc is left intact, but in LMN damage, this arc is interrupted. Remember that reflexes occur along the route of cranial and spinal nerves, the very structures that make up the LMNs. When the LMNs are damaged and the reflex arc is interrupted, reflexes will be absent (hyporeflexia, no Babinski sign) and muscles will shrink due to lack of tonal stimulation (hypotonia, marked atrophy). LMN fasciculations occur because of spontaneous depolarization of the LMNs, leading to contraction, not of the whole muscle, but of individual muscle fibers.

Speech Issues Associated With Pyramidal System Damage

Dysarthria is speech that is slurred and/or uncoordinated due to CNS or PNS problems that affect one or more of the following: respiration, phonation, resonance, and articulation. There are seven types of dysarthria; of these, three are associated with pyramidal system damage (TABLE 11-3). Spastic dysarthria is due to bilateral UMN damage and results in stiff, rigid muscles. Speech is characterized by a harsh/strained voice, monopitch intonation, hypernasality, slow speech rate, and imprecise consonants. When there is unilateral UMN damage, the condition is called unilateral UMN dysarthria, a milder form of dysarthria that affects only one side of the face and mouth. It usually has minimal impact on speech because the person still has one functional side of the face and mouth. The third type of dysarthria associated with pyramidal system damage is flaccid dysarthria. It is caused by LMN damage and results in speech that is breathy in voice, monopitch, and hypernasal and that uses short phrases and imprecise consonants.

TABLE 11-3 Types of Dysarthria

Dysarthria Type

Place of Damage



Bilateral upper motor neuron

Bilateral spasticity and weakness

Unilateral upper motor neuron

Unilateral upper motor neuron

Unilateral spasticity and weakness


Lower motor neuron

Hypotonia and weakness


Basal ganglia and its connections

Extra and abnormal movements


Basal ganglia and its connections

Reduced movement and range of motion


Cerebellum and its connections

Incoordination of muscles


Variable; any mix of the above places of damage

Variable; depends on what type of dysarthria mix

Adapted from: Manasco, M. H. (2017). Introduction to neurogenic communication disorders. Burlington, MA: Jones & Bartlett Learning.

The Indirect Motor System

The indirect motor system is also known as the extra- pyramidal system. Whereas the pyramidal system controls voluntary motor movement, the extrapy- ramidal system controls involuntary movements involved in posture, muscle tone, and reflexes, as well as the coordination or modulation of movements.

There are several tracts involved in the extrapy- ramidal system (FIGURE 11-7). Two that originate in the cortex are the corticoreticular and corticorubral tracts. The corticoreticular tract begins at the premotor (BA 6), motor (BA 4), and sensory cortices (BAs 1, 2, 3) and inputs into the reticular formation of the brainstem, which projects to various other structures like the cerebellum and cranial nerve nuclei. The cor- ticorubral tract also arises from the cortex but inputs into the midbrain’s red nucleus.

The other four extrapyramidal tracts, which originate in the brainstem, are the rubrospinal, vestibulospinal, reticulospinal, and tectospinal tracts. The rubrospinal tract arises from the midbrain’s red nucleus and inputs along the cervical spinal cord. It influences flexor tone in the limbs. Its involvement in speech is uncertain, but damage to it has led to cases of myoclonus in speech muscles. The vestibulospinal tract originates at the vestibular nucleus (where the medulla and pons meet) and inputs into motor neurons throughout the spinal cord. Functionally, it regulates muscle tone to maintain balance and posture. Like the rubrospinal tract, the vestibulospinal tract’s function in relation to speech, if any, is unknown. The reticulospinal tract begins in the reticular formation and ends at motor neurons in the spinal cord. This tract has connections to cranial nerve nuclei and plays a role in certain reflexes, like swallowing. The tectospinal tract originates from the tectum (“roof”) of the midbrain and ends in the cervical spinal cord. It functions to coordinate head posture with eye movements and does not appear to play any meaningful role in speech.

In addition to the functional difference with the pyramidal system, the extrapyramidal system is different anatomically in that it is made up of many short tracts that are very indirect, much like a commuter train that makes numerous stops along its route. These stops include the basal ganglia, cerebellum, and thalamus (pictured in Figures 11-3 and 11-4), as well as their final destination at either brainstem cranial nerve nuclei or the ventral horn cells of the spinal cord.

Damage to the extrapyramidal system causes a loss of coordination and modulation, leading to dyskinesias, or movement disorders. Some common dyskinesias include tremors (rhythmic shaking), chorea (quick movements of the hands and feet), athetosis (slow writhing movements of extremities), dystonia (distorted posture), and clonus (large muscle contractions). All of these conditions are involuntary in nature.

FIGURE 11-7 The indirect motor system. Note the many stops this pathway makes, leading it to be called an indirect pathway.

In terms of speech problems, either hyperkinetic or hypokinetic dysarthria is possible in extrapyrami- dal system damage, depending on where in the system the damage takes place. Hyperkinetic dysarthria (hyper = too much; kinesis = movement) is usually due to damage in the basal ganglia and is associated with conditions like Huntington disease, a progressive, hereditary disorder. The speech of patients with this form of dysarthria is characterized by a harsh voice, monopitch, loud voice level, imprecise consonants, and distorted vowels. These symptoms are due to the constant involuntary motion from which these patients suffer. Hypokinetic dysarthria (hypo = too little; kinesis = movement) is typically due to problems in the substantia nigra, specifically with dopamine production. Dopamine is an important neurotransmitter for the smoothing and regulation of motor behavior. High levels of dopamine can lead to abnormally increased motor behaviors and impulsivity; low levels lead to stiff, rigid, and slow movements. Parkinson disease is characterized by low levels of dopamine. Patients with Parkinson disease suffer from hypokinetic dysarthria, which involves breathy voice, monopitch, reduced syllable stress, variable speech rate, and imprecise consonants.

The Final Common Pathway

Alpha and Gamma Motor Neurons

The final common pathway (FCP) was briefly introduced in the discussion of the LMN system. It is called the final common pathway because it is the last leg of the journey for all motor signals. Speech is a voluntary motor activity that occurs through the contraction of skeletal muscles. We will begin to discuss the FCP by examining its relationship to skeletal muscles.

Skeletal muscles are made up of many individual muscle fibers. Some of these fibers are extrafusal and others are intrafusal. Extrafusal fibers are innervated by alpha motor neurons that contract these fibers, facilitating muscle movement, whereas intrafusal fibers are innervated by gamma motor neurons and are involved in proprioception. The motor neuron and the fibers it innervates are known as motor units. Both alpha and gamma motor neurons are part of the LMN system. Alpha motor neurons are influenced more by the direct motor system, whereas the indirect motor system has more influence on gamma motor neurons. We will focus on alpha motor neurons and their involvement in speech muscle contraction.

The alpha motor neuron axon leaves the brainstem as part of a cranial nerve and courses to a muscle. The axon divides into many terminal branches. Because of this branching, an axon might innervate many muscle fibers. In addition, each muscle fiber may be innervated by multiple alpha motor neurons. This arrangement allows for greater control of contraction. Motor units vary in size depending on the number of fibers an axon innervates. Muscles involved in fine motor activity (e.g., speech) have fewer fibers per axon (e.g., 15:1), whereas gross motor movement involves larger ratios of fibers per axon (e.g., 500:1).

Alpha and gamma motor neurons have a relationship in maintaining muscle tone. Normal, healthy muscles are neither too tight nor too floppy. They constantly receive some level of neurological stimulation to keep them in a state of readiness; thus, muscles are never completely relaxed. The gamma motor system firing causes intrafusal fibers to contract, which is detected by sensors in these fibers. The intrafusal fibers send sensory signals back to the brainstem and to alpha motor neurons, which in turn send motor signals to extrafusal fibers to shorten and match the length of the intrafusal fibers. The result is that instead of being completely relaxed, the indirect motor system keeps muscles stimulated and prepared for voluntary movements, such as those that occur in speech.

The FCP and Speech

The FCP for speech includes the cranial and spinal nerves involved in phonation, resonance, and articulation as well as spinal nerves involved in respiration. Respiration, phonation, resonance, and articulation are the four main subsystems of speech, and the contributions of each of these subsystems are as follows:

 Respiration provides the power for speech.

 Phonation provides the raw sound for speech.

 Resonance provides the tonal qualities for speech.

 Articulation provides the speech sounds for speech.

We will briefly look at the neurological control of each of these subsystems with their relevant cranial and spinal nerves.

Neurological Control of Respiration

Several neurons in the pons and medulla regulate respiration, which is ultimately controlled by the autonomic nervous system (FIGURE 11-8). The ponto- medullary respiratory center is the CNS area responsible for automatic breathing, and damage to it can lead to respiratory arrest, asphyxiation, and death.

FIGURE 11-8 Neurological control of respiration.

This control center has three groups. The dorsal respiratory group (DRG) is found in the dorsomedial portion of the medulla and is responsible for respiratory rhythm and inspiration (i.e., breathing in). It is driven by the apneustic (Greek for “not breathing”) center and inhibited by the pneumotaxic (Greek for “breathing arrangement”) center, both of which are in the pons and are collectively called the pontine respiratory group (PRG). The ventral respiratory group (VRG) is located in the ventrolateral area of the medulla and is responsible for inspiration and expiration during forced breathing (e.g., breathing during exercise). Lesions in this system can produce irregular breathing patterns, sometimes found in dysarthric patients. For example, Cheyne-Stokes respiration is a common phenomenon in which breathing switches back and forth from hyperventilation to hypoventilation. Another example is ataxic breathing where respiration is irregular and uncoordinated with speech.

Some spinal nerves support speech by innervating muscles of respiration. LMNs that innervate respiration are found in the cervical and thoracic spinal cord. The diaphragm is the main muscle of inspiration, and it increases the vertical dimensions of the thoracic cavity when contracted. It is innervated by cervical nerves C3, C4, and C5, which combine to form the phrenic nerves. Each phrenic nerve innervates one-half of the diaphragm. The external intercostal muscles contract to pull the ribs up, thus increasing the horizontal dimensions of the thoracic cavity. The internal intercostal muscles assist the external intercostals, but also appear to be involved in expiration. These muscles are innervated by thoracic spinal nerves T2 through T11.

Neurological Control of Phonation

The vagus nerve (cranial nerve X) is a crucial nerve for proper phonatory function. Lateral corticobulbar fibers arise from the primary motor cortex (BA 4) and input into the nucleus ambiguous (NA) in the brainstem (FIGURE 11-9). The vagus nerve projects from the NA and splits into two branches, the superior laryngeal nerve (SLN) and the recurrent laryngeal nerve (RLN). The RLN innervates all the intrinsic laryngeal muscles with the exception of the cricothyroid muscle, which is innervated by the SLN.

Unilateral UMN damage to the vagus nerve has little effect on the voice other than possible vocal harshness. Bilateral UMN lesions can paralyze both vocal cords in a paramedian position due to spasticity and lead to a more significant strained-strangle phonation. LMN lesions of the vagus nerve cause paresis or paralysis of the larynx. For example, unilateral damage to the RLN leads to unilateral vocal fold

FIGURE 11-9 Neurological control of phonation.

paralysis and a breathy or hoarse voice. Bilateral LMN lesions cause severe deficits in phonation due to bilateral vocal fold paralysis. The voice will be very breathy. Damage to the SLN is less catastrophic than is damage to the RLN, causing damage to pitch control in light of the cricothyroid being an important muscle in raising and lowering vocal pitch.

Neurological Control of Resonance and Articulation

Neurological control of articulation and resonance is a complicated process controlled by at least five cranial nerves: the trigeminal (V), facial (VII), glossopharyngeal (IX), vagus (X), and hypoglossal (XII). The pathway for motor control arises in the primary motor cortex (BA 4), projects as the lateral corticobulbar tract to various brainstem nuclei, and then continues as cranial nerves V, VII, IX, X, and XII to the various articulatory muscles.

The trigeminal nerve controls the opening and closing of the mandible. In elevating or closing the mandible, it controls the masseter, temporalis, and medial pterygoid muscles (FIGURE 11-10). For depressing or opening the mandible, it innervates the anterior digas- tricus and mylohyoid muscles. It also supplies the lateral pterygoid, tensor veli palatini, and tensor tympani muscles. LMN lesions can produce paresis or paralysis of the mandibular muscles on the same side as the lesion. Unilateral lesions have minimal impact on speech, but bilateral lesions can lead to significant problems in which patients cannot raise the mandible, which prevents other articulators from hitting their articulatory targets. Vowel distortions may also be present. Because the trigeminal nerve receives bilateral UMN input, there is no real effect with unilateral UMN damage. Bilateral UMN damage can limit jaw movement and thus affect articulation of vowels and labial and lingual consonants.

The facial nerve controls the muscles of the face, including muscles that purse, open, raise, lower, and retract the lips (Figure 11-10). For example, orbicularis oris is a crucial muscle for lip rounding that is important for the /w/ sound, a labial sound, among others. The facial nerve also innervates two mandibular openers, the posterior digastricus and the platysma. Unilateral UMN lesions lead to paresis or paralysis of the contralateral lower two-thirds of the face muscles, but have little effect on speech (FIGURE 11-11). Bilateral UMN lesions will have more serious consequences, affecting all the face muscles and labial and labiodental sounds. Unilateral LMN lesions result in ipsilateral paresis or paralysis of the upper and lower face muscles. Fasciculations and atrophy of the speech muscles are also present. Speech will be affected only mildly, if at all, as compared to bilateral LMN damage, which involves significant difficulty producing labial and labiodental sounds.

The stylopharyngeus muscle is innervated by the glossopharyngeal nerve. This muscle plays a role in elevating and opening the pharynx, so it may play some role in resonance but is more relevant for swallowing. It also mediates the gag reflex. LMN damage will not affect speech, but it may lead to a loss of pharyngeal sensation, diminished gag, and decreased pharyngeal elevation during swallowing.

The vagus nerve’s role in phonation has already been discussed, but this nerve also innervates muscles of the soft palate (or velum) with the exception of the tensor veli palatini and the three pharyngeal constrictor muscles. The vagus nerve functions with the assistance of the spinal accessory nerve (cranial nerve XI). Unilateral UMN damage has little effect on resonance because of the nerve’s bilateral innervation, but bilateral UMN damage will lead to hypernasality due to a faulty, spastic velar mechanism. Like unilateral UMN damage, unilateral LMN damage has little effect on speech. Patients demonstrate a droopy palate ipsilateral to the lesion and a mild hypernasality. Bilateral UMN damage results in complete palatal drooping and severe hypernasality.

FIGURE 11-10 The muscles of the jaw and face. These muscles are innervated by the facial nerve (cranial nerve VII).

FIGURE 11-11 Upper motor neuron and lower motor neuron damage involving the facial nerve (cranial nerve VII).

There are two sets of tongue muscles, the intrinsic tongue muscles that control fine motor movement and the extrinsic tongue muscles that control gross motor function (FIGURE 11-12). The hypoglossal nerve controls all of these muscles with the exception of one extrinsic tongue muscle, the palatoglossus muscle. Thus, this nerve and the muscles it supplies are crucial for speech. The brainstem nucleus of the hypoglossal nerves receives bilateral UMN innervation with the exception of the genioglossus muscle, which receives only contralateral UMN input. Patients with unilateral UMN damage to this nerve have some paresis on the contralateral side of the tongue. The tongue deviates on protrusion, but there is only a mild impact on articulation. Bilateral UMN damage results in bilateral tongue weakness and more significant articulatory problems. Unilateral LMN lesions result in weakness (with the tongue deviating toward the side of lesion), atrophy, and fasciculations ipsilateral to the lesion and mild articulatory problems. Bilateral LMN lesions do not result in tongue deviation due to bilateral weakness but are consistent with more significant speech issues.

FIGURE 11-12 The extrinsic tongue muscles. The intrinsic tongue muscles make up the tongue itself and are not visible in this view.

 Multisystem Damage

As discussed in this section, damage to one system leads to one or two types of dysarthria, whereas damage to another system leads to one or two other types of dysarthria. What happens when multiple systems are damaged, such as in the case of amyotrophic lateral sclerosis (ALS)? People with conditions like ALS will have mixed dysarthria, which is a mixture of two or more of the pure dysarthrias discussed earlier. For example, both the UMN and LMN systems are damaged in ALS, causing patients to have characteristics of both spastic and flaccid dysarthria. This flaccid-spastic subtype accounts for about 42% of mixed dysarthria cases (Duffy, 2013). Sometimes one form of dysarthria will characterize the beginning of the disease process and then the other form will appear as the disease progresses. Other conditions, such as traumatic brain injury or multiple strokes, can lead to mixed dysarthria. Many patients with dysarthria have the mixed form, because neurological injury often involves more than one neurological system component. Duffy (2013) found that mixed dysarthria accounted for nearly one-third of all dysarthric conditions.

 Sensory Pathways Important for Speech

Ascending Sensory Pathways

Descending neural pathways are motor in nature, whereas ascending neural pathways are sensory. Three major ascending sensory pathways relay sensory information like touch, pressure, temperature, and proprioception to various brain structures (TABLE 11-4). The first and most important of these to speech is the dorsal column medial lemniscal pathway, which is made up of two bundles, the fasciculus gracilis (slender bundle) and the fasciculus cuneatus (wedgeshaped bundle) (FIGURE 11-13). Sense receptors in the skin and muscles send sensory signals to the dorsal root ganglion of the spinal nerve or the ganglia of sensory cranial nerves in the brainstem. Neurons in the spinal cord or brainstem then carry the signal through the thalamus to the postcentral gyrus of the parietal lobe. The sensory functions of this pathway include fine touch (as is found in the hands and mouth), vibratory sense, and proprioception. This sensory feedback is important to the speech process, and heightened awareness of it is often targeted in stuttering therapy.

The second tract is the spinothalamic tract, which follows the same course as the dorsal column but has final connections in the cingulate and insular cortices as well as the postcentral gyrus. The spinothalamic tract is the primary route for pain information as well as temperature, pressure, and crude touch.

TABLE 11-4 Ascending Sensory Tracts


Site of Origin

Site of Ending


Dorsal column

Spinal cord

Primary sensory cortex via thalamus

Fine touch, vibratory sense, proprioception


Spinal cord

Primary sensory cortex via thalamus

Crude touch, pain, pressure, temperature


Spinal cord



FIGURE 11-13 The dorsal column medial lemniscal pathway.

The third tract is the spinocerebellar tract. This tract has the same origin as the previous two, but its final input is in the cerebellum. Its function is to relay proprioceptive information from the arms, legs, and trunk of the body to the cerebellum, where it is then processed. The cerebellum is an important neural structure for our balance, and it uses proprioceptive information from the body to help us maintain our balance.


It is a common assumption that the brain uses only our sense of hearing as a source of feedback for how our motor speech system is performing. For example, if we mispronounce a word (as we all tend to do at times), we hear the error and make the appropriate corrections in order to say the word correctly. Auditory feedback is not the only sensory system the brain uses to monitor speech, however; if it were, how would a person who is deaf ever learn to speak? Some people who are deaf have speech that is as good as any hearing person’s. How is this possible? The answer is that the brain also uses somatosensory information to achieve the precision needed in speech (Nasir & Ostry, 2006). Specifically, the brain uses kinesthesia, which is the brain’s awareness of the position and movement of the articulators through sense organs imbedded in muscles called proprioceptors. Proprioception is the body’s eyes for itself or the brain’s ability to know where the different parts of the body (arms, legs) are in space at a given time. Kinesthesia and joint position sense are the two components of proprioception (Konradsen, 2002).

Deemphasizing auditory feedback and emphasizing kinesthetic feedback has been a standard tool for decades in treating stuttering. This approach was illustrated in the Academy Award-winning film The King’s Speech, which was about the British king George VI, who stuttered. In the film, the speech-language pathologist (SLP), Lionel Logue, placed headphones on King George with music playing. King George then went on to read from Hamlet as the music played in his ear. Mr. Logue recorded the king’s speech and when it was played later in the film, the king was perfectly fluent. How did this happen? King George was deprived of auditory feedback, which is thought to be flawed in those who stutter, and relied solely on the kinesthetic feedback from his mouth. This proves to be a more reliable form of feedback for those who stutter, and SLPs have taken advantage of this insight in stuttering therapy. Often, delayed auditory feedback, rather than music, is used with people who stutter. In this therapeutic technique, the person who stutters wears headphones connected to a system (or a smartphone with an app) that sends auditory feedback back to him or her, but in a delayed fashion. Because it is delayed, it is of no use to the person because it does not match up with what is currently happening with the articulators. Delayed auditory feedback thus forces the person to depend on kinesthetic feedback rather than auditory feedback and helps to produce improved fluency.

► Conclusion

The motor and sensory systems important for speech have been surveyed, as have AOS and the types of dysarthria associated with damage to the motor systems. Spastic, unilateral UMN, and flaccid dysarthria result from pyramidal system damage, whereas hypokinetic dysarthria and hyperkinetic dysarthria are a consequence of extrapyramidal system damage. The sixth dysarthria type, ataxic, is due to impairment in the cerebellar system. A seventh type, mixed dysarthria, results from diffuse brain damage that impacts multiple speech systems. ALS is one example of a condition that leads to this type of dysarthria. As the disease progresses, the patient will eventually deteriorate to the point of having anarthria, which means no speech at all.


The following were the main learning objectives of this chapter. The information that should have been learned is below each learning objective.

1. The learner will outline the major components of the motor speech system.

 The conceptual level: Includes the ideas, thoughts, and feelings in our minds.

 The motor planning level: Involves phonological assembly and motor planning for phonemes.

 The motor programming level: Involves the actual execution of phonemes in time and space.

 The motor control circuits: Include the basal ganglia and cerebellar circuits, which are important in motor programming of speech by coordinating, integrating, and refining the movements of the direct and indirect pathways.

 The direct motor pathway: A voluntary motor system that controls gross motor movement; also known as the pyramidal system.

 The indirect motor pathway: Controls involuntary movements involved in posture, muscle tone, and reflexes, as well as the coordination or modulation of movements; also known as the extrapyramidal system.

 The final common pathway: the last leg of the journey for all motor signals, which occurs through the lower motor neurons (LMNs).

2. The learner will connect different places of damage in the motor speech system to different forms of dysarthria.

 Spastic dysarthria: bilateral upper motor neuron (UMN) damage

 Unilateral UMN dysarthria: unilateral UMN damage

 Flaccid dysarthria: LMN damage

 Hyperkinetic dysarthria: basal ganglia, extra- pyramidal system

 Hypokinetic dysarthria: substantia nigra, extrapyramidal system

 Ataxic dysarthria: cerebellar circuit

 Mixed dysarthria: multisystem damage

3. The learner will identify places of damage associated with apraxia of speech.

 Apraxia of speech: Can be caused by lesions to the perisylvian region, insula, or basal ganglia.

4. The learner will describe the importance of the sensory system to speech.

 Both kinesthesia and proprioception are used in the speech system to provide the brain with information regarding where the articulators are and to make last-minute adjustments and corrections.

5. The learner will describe the human response space and the communication disorders professional’s role in expanding it.

 Speech is thought to be an act of our free will.

 Free will may be better thought of as a scalable property—you have more or less of it.

 Patients with motor speech disorders, like dysarthria and apraxia of speech, experience the restraint of their impaired neuroanatomy, which limits their ability to act as they desire.



Ataxic dysarthria


Babinski sign

Cerebellar circuit



Contralateral innervation


Dorsal column medial lemniscal pathway




Extrapyramidal system

Flaccid dysarthria Hyperkinetic dysarthria Hypokinetic dysarthria Kinesthesia

Lower motor neurons (LMNs)

Mixed dysarthria

Motor speech disorders


Motor units Proprioception Pyramidal neurons Pyramidal system Spastic dysarthria Tremors

Unilateral upper motor neuron dysarthria

Upper motor neurons (UMNs)

1. Draw the flowchart of the motor speech system found in Figure 11-1 from memory.

2. Given the following figure (FIGURE 11-14) roughly draw the pyramidal and extrapyrami- dal pathways.

FIGURE 11-14 Unlabeled coronal section of the brain and brainstem.


1. List the basic levels of the motor speech system beginning with the conceptual level.

2. Compare and contrast UMN damage to LMN damage.

3. Write out the names of the seven types of dysarthria along with where damage occurs in the motor speech system to cause each. Use Table 11-3 as a guide.


William is a 70-year-old male with a 6-year history of stiffness and difficulty transferring from chairs and bed to standing. He reports “difficulty talking”. The neurologist’s report states that William demonstrates diminished arm swinging and shuffling steps while walking. He also demonstrates tremors in both hands with the tremors being more pronounced on the right.

Overall movements are slow (bradykinesia). His facial expression is masked.

1. What neurological condition do you think the neurologist diagnosed William as having? Why do you think this?

2. What kind of dysarthria does William most likely have?


1. Write a five- to six-page paper surveying the seven types of dysarthria.

2. Search the scholarly literature and locate two or three recent articles (i.e., from the last 3 years) regarding apraxia of speech. Share what you found with your class.

3. Read the Libet studies found in the References and summarize his experimental design. Do you see any flaws in it?

4. Write a three- to four-page paper on the concept of free will.


Duffy, J. R. (2005). Motor speech disorders: Substrates, differential diagnosis, and management (2nd ed.). St. Louis, MO: Mosby.

Duffy, J. R. (2013). Motor speech disorders: Substrates, differential diagnosis, and management (3rd ed.). St. Louis, MO: Mosby.

Konradsen, L. (2002). Factors contributing to chronic ankle instability: Kinesthesia and joint position sense. Journal of Athletic Training, 37(4), 381-385.

Libet, B. (1993). Unconscious cerebral initiative and the role of conscious will in voluntary action. In B. W Libet (Ed.), Neurophysiology of consciousness (pp. 269-306). Boston, MA: Birkhauser.

Libet, B., Gleason, C. A., Wright, E. W., & Pearl, D. K. (1983). Time of conscious intention to act in relation to onset of cerebral

activity (readiness-potential). The unconscious initiation of a freely voluntary act. Brain, 106(3), 623-642.

Nasir, S. M., & Ostry, D. J. (2006). Somatosensory precision in speech production. Current Biology, 16(19), 1918-1923.

Seifert, J. (2011). In defense of free will: A critique of Benjamin Libet. The Review of Metaphysics, 65, 377-407.

Spence, S. A. (2009). The actor’s brain: Exploring the cognitive neuroscience of free will. New York, NY: Oxford University Press.

Spruston, N. (2009). Pyramidal neuron. Scholarpedia, 4(5), 6130. Retrieved from /Pyramidal_neuron

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