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

Chapter 5. The Spinal Cord, Brainstem, Cranial Nerves, and Cerebellum

CHAPTER OUTLINE

CHAPTER PREVIEW

It is now time to embark on a journey through macroscopic structures (i.e., structures that can be observed with the naked eye). We will begin this leg of the journey at the bottom, with the spinal cord, and make our way up to the spinal nerves, brainstem, cranial nerves, and cerebellum.

IN THIS CHAPTER

In this chapter, we will . . .

 Survey the form and function of the spinal cord and discuss spinal cord injury

 Explore the structure and function of the brainstem

 Review select disorders of the brainstem

 Study the cranial nerves and their relationship to speech, swallowing, and hearing

 Survey the form and function of the cerebellum

 Introduction

 The Spinal Cord

 Spinal Cord Form

 Spinal Cord Function

 Select Disorders of the Spinal Cord

 Brainstem

 External Organization of the Brainstem

 Internal Organization of the Brainstem

 Select Disorders of the Brainstem

 The Cranial Nerves

 Cranial Nerve I: The Olfactory Nerve

 Cranial Nerve II: The Optic Nerve

 Cranial Nerve III: The Oculomotor Nerve

 Cranial Nerve IV: The Trochlear Nerve

 Cranial Nerve V: The Trigeminal Nerve

 Cranial Nerve VI: The Abducens Nerve

 Cranial Nerve VII: The Facial Nerve

 Cranial Nerve VIII: The

Vestibulocochlear (or Auditory) Nerve

 Cranial Nerve IX: The

Glossopharyngeal Nerve

 Cranial Nerve X: The Vagus Nerve

 Cranial Nerve XI: The Spinal Accessory Nerve

 Cranial Nerve XII: The Hypoglossal Nerve

 The Cerebellum

 Anatomy of the Cerebellum

 Cerebellar Function

 Select Disorders of the Cerebellum

 Conclusion

 Summary of Learning Objectives

 Key Terms

 Draw It to Know It

 Questions for Deeper Reflection

 Case Studies

 Suggested Projects

 References

LEARNING OBJECTIVES

 The learner will label a diagram of a cross-section of the spinal cord.

 The learner will label a diagram of the brainstem.

 The learner will be able to list all the cranial nerves (Roman numeral and name).

 The learner will list important cranial nerves for articulation, voice, swallowing, and hearing.

 The learner will describe the form and function of the cerebellum.

 Introduction

The spinal cord serves as a sort of communications superhighway for motor or efferent communication from the brain to the body and sensory or afferent communication from the body to the brain. The spinal cord extends from the bottom of the vertebral column up to the brainstem’s medulla. This chapter will begin by surveying the spinal cord’s form and function as well as spinal cord injury. We will continue the journey through the brain by also studying spinal nerves, the brainstem, cranial nerves, and the cerebellum.

 The Spinal Cord

Ranging from 17 to 18 inches (43-46 cm) in length and % to *Л inch (0.6-1.3 cm) in diameter, the spinal cord is a vital organ for interacting with our environment. Contained within it are both motor and sensory fibers that transmit information regarding our movement and sense experiences as well as our reflexes. The spinal cord is surrounded by the bony vertebral column and a three-layered membrane called the meninges (FIGURE 5-1). Within these membranes, there is the arachnoid space filled with cerebrospinal fluid, essentially wrapping the spinal cord in a watery cushion.

Spinal Cord Form

External Organization

Like the vertebral column, the spinal cord is organized into five regions. The neck area is the cervical region, the chest is the thoracic region, the lower back is the lumbar region, the pelvis is the sacral region, and the tailbone area is the coccygeal region (FIGURE 5-2).

Spinal nerves emerge from the spinal cord and innervate the body below the neck (FIGURE 5-3). They are organized by neuroanatomists using the same divisions used to organize the spinal cord (e.g., cervical spinal nerves). The spinal nerves carry afferent (sensory) and/or efferent (motor) information. There are two types of nerve fibers in spinal nerves, general somatic and general visceral. General somatic efferent (GSE) fibers carry motor information to skeletal muscles and general visceral efferent (GVE) fibers carry motor information to smooth muscle, the heart, and glands. General somatic afferent (GSA) fibers carry sensory information from the skin, and general visceral afferent (GVA) fibers carry sensory information from the lungs and digestive tract (FIGURE 5-4).

FIGURE 5-1 The vertebral column and spinal cord, which is surrounded by three layers: the dura mater, the arachnoid mater, and the pia mater.

FIGURE 5-2 The five regions of the vertebral column and spinal cord.

As the ventral rami leave the spinal cord and vertebral column, some of them form a network (except for the thoracic region) called a plexus. These networks then branch out and innervate certain parts of the body. Because innervation of limbs comes out of these networks, damage to one spinal root will not result in a totally paralyzed limb. The general motor or efferent functions of each spinal nerve plexus are presented in TABLE 5-1. For an example of a plexus, see FIGURE 5-5, which is an illustration of the cervical plexus. This plexus (C1-C4) is responsible for innervating some muscles of the neck. For example, the following neck muscles function to lower the larynx:

 Sternohyoid (laryngeal depressor innervated by cervical spinal nerves 1, 2, and 3)

 Thyrohyoid (laryngeal depressor innervated by cervical spinal nerve 1 and cranial nerve XII)

 Omohyoid (laryngeal depressor innervated by cervical spinal nerves 1, 2, and 3)

 Sternothyroid (laryngeal depressor innervated by cervical spinal nerves 1, 2, and 3)

FIGURE 5-3 Structure of a spinal nerve. A nerve consists of bundles of nerve fibers, various layers of connective tissue, and blood vessels.

FIGURE 5-4 Different types of spinal nerve fibers.

TABLE 5-1 The Spinal Nerves, Their Plexuses, and Some of Their Motor Functions

The phrenic nerve originates mainly from the fourth cervical spinal nerve but receives some help from the third and fifth cervical spinal nerves. This nerve innervates the diaphragm, which, along with other muscles, is crucial for supplying the air power for speech.

Beginning laterally, each spinal nerve has a dorsal ramus (branch) and a ventral branch (FIGURE 5-6A). The dorsal ramus carries motor and sensory information (GSE and GSA) to and from the dorsal or posterior part of the body; the ventral ramus carries the same type of information to and from the ventral or anterior part. Moving medially, these two branches meet outside the vertebral column to form the spinal nerve. Still outside the vertebral column, another branch joins the spinal nerve. This branch is called the ramus communicantis, and it contains motor and sensory visceral nerve fibers (GVE and GVA).

FIGURE 5-5 The cervical plexus.

Moving inside the vertebral column, the spinal nerve splits into a dorsal and a ventral root. The dorsal root is sensory, containing GVA and GSA fibers. In terms of general somatic sensation (GSA), each spinal nerve has an association with a specific skin region, known as a dermatome (from the Greek: derma = “skin”; tome comes from temnein, meaning “to cut”). The dermatomes of the human body are mapped in FIGURE 5-7. The ventral root is motor (GVE and GSE) (FIGURE 5-6B). Bulging from the dorsal root is the dorsal root ganglion, which contains the cell bodies of pseudounipolar neurons.

Internal Organization

A cross-section of the spinal cord is presented in Figure 5-6B. A gray butterfly-like figure in the midst of a white circle is apparent. The gray part is made up of neuron cell bodies, and the white consists of myelinated neuronal axons. We will examine the structure of the spinal cord’s white matter first and then consider the gray matter.

The spinal cord’s white matter is divided in half by the median fissure and the dorsal, lateral, and ventral white-matter regions or columns duplicated on each side of the spinal cord. Major ascending sensory and descending motor pathways or tracts course through these regions. These pathways are pictured in FIGURE 5-8, with the blue sections highlighting sensory pathways and red sections denoting motor systems.

FIGURE 5-6A A. Cross-section of the spinal cord showing spinal nerve connections.

FIGURE 5-6B B. Cross-section of the spinal cord showing GSA/GVA and GSE/GVE fiber input and output.

FIGURE 5-7 Dermatomes of the human body. Dermatomes are the sensory areas served by each of the spinal nerves.

FIGURE 5-8 Cross-section of the spinal cord at the cervical levels showing motor (in red) and sensory pathways (in blue).

The major descending motor pathways in the spinal cord’s white matter are as follows:

 Lateral corticospinal/corticobulbar tract;

This nerve tract originates in the motor cortex of the frontal lobe, decussates (i.e., changes sides) at the lower medulla-spinal cord juncture, and then inputs along the spinal cord at the ventral horns (FIGURE 5-9). That part of the tract from the cortex to the brainstem is called the corticobulbar tract (bulbar refers to the brainstem because of its bulbus appearance). Motor neurons in this tract arise in the cerebral cortex input into brainstem nuclei or the ventral horn of the spinal cord and are known as the upper motor neurons (UMNs). Motor neurons that leave the brainstem nuclei or the ventral horn of the spinal cord and connect to muscles are called the lower motor neurons (LMNs). Symptoms of UMN damage are different than those of LMN damage (BOX 5-1). Functionally, it is responsible for contralateral movement of the body and, in the case of the corticobulbar portion, contralateral movement of muscles in the head and some muscles in the neck. This tract is of major importance to speech production.

 Anterior (or ventral) corticospinal tract; This tract originates in the motor and premotor areas of the frontal lobe and then courses ipsilateral down the spinal cord, inputting at the ventral horn. It controls the trunk muscles.

 Rubrospinal tract; The rubrospinal tract begins in the midbrain, where it decussates and courses down the brainstem and spinal cord until inputting in the ventral horn of the spinal cord. In terms of function, it modulates flexor tone in the upper extremities. Flexor tone is the amount of tension present in muscles when a joint is flexed.

 Vestibulospinal tract; This tract originates in the medulla and courses down the spinal cord ipsilateral until inputting into the ventral horn. Functionally, this tract controls extensor tone, which is the amount of tension present in muscles when a joint is extended.

 Reticulospinal tract: This tract is made of a medial (pontine) tract and a lateral (medullary) tract. It originates where the brainstem’s pons and medulla meet, an area known as the reticular formation, and then descends and terminates at various levels of the spinal cord. It is involved in muscle tone in the trunk muscles as well as the proximal limbs and overall helps to control a person’s posture and facilitate gait (walking).

 Tectospinal tract: Also known as the colliculospinal tract, the tectospinal tract connects the midbrain (specifically, the superior colliculus of the midbrain) to the cervical regions of the spinal cord. Functionally, it coordinates the movement of the head and neck with the eyes.

Sensory tracts are divided into parts by the neurons that make up the tract. For example, first-order neurons carry sensory signals from the sense receptors to the central nervous system. Second-order neurons decussate from one side of the central nervous system to the other side and input into the thalamus. Third-order neurons route sensory information to the appropriate sensory perception processing area in the cerebral cortex (fourth-order neurons).

FIGURE 5-9 The lateral corticospinal/corticobulbar tract.

This major descending motor pathway mediates volitional motor activity.

The major ascending sensory tracts are as follows:

■ Dorsal columns: As their name implies, the dorsal columns reside in the dorsal area of the spinal cord. The first-order neuron begins in the sensory receptors and courses through the dorsal root ganglia and synapses with the dorsal horn of the spinal cord. The second-order neuron arises from the dorsal horn, decussates, and then travels to the thalamus, which projects a third-order neuron to the somatosensory cortex

BOX 5-1 Upper Motor Neuron Damage Versus Lower Motor Damage

The concept of upper motor neurons (UMNs) and lower motor neurons (LMNs) is not an anatomical notion; rather, it is a neuropathological concept that helps explain the symptoms of chronic UMN versus LMN damage. When the UMNs are initially damaged by a lesion via a stroke, the patient experiences flaccid paralysis, loss of muscle tone (hypotonia), and loss of reflexes (areflexia). As the condition becomes chronic, these symptoms change into the classic signs of UMN damage: spastic weakness (paresis), too much muscle tone (hypertonia), exaggerated reflexes (hyperreflexia), and involuntary muscular contractions and relaxations (clonus). LMN damage is the opposite of chronic UMN damage and resembles acute UMN damage with flaccid paralysis and areflexia. In addition, patients experience muscle wasting (atrophy) and muscle twitches (fasciculations).

(FIGURE 5-10). These columns consist of two bundles, the fasciculus gracilis (the slender bundle) and the fasciculus cuneatus (the wedge-shaped bundle). The dorsal columns relay fine and discriminative touch, pressure, and proprioceptive sensory information to the brainstem, then the thalamus, and finally the sensory cortex for final processing. Proprioception can be thought of as the body’s eyes for itself. In other words, through various receptors throughout the body, the brain has a sense of where its various parts are in space at any given time.

 Spinothalamic tracts: There are two spinothalamic tracts, the ventral and the lateral. The lateral tract lies in the lateral portion of the spinal cord and the ventral tract in the ventral portion. Its first-order neuron begins at the sensory receptors and passes through the dorsal root ganglia and synapses with the dorsal horns of the spinal cord. Its second-order neuron then ascends from the dorsal horn to the thalamus. The tract’s third- order neuron leaves the thalamus and projects to the somatosensory cortex. Functionally, this tract sends the following sensory information to the somatosensory cortex: pain, temperature, and crude touch. The ventral tract has the same basic route as the lateral tract but is responsible for light touch (e.g., touching the skin with a cotton ball).

 Spinocerebellar tracts: There are two spinocerebellar tracts, the ventral tract and the dorsal tract. Both lie on the lateral edge of the spinal cord, but as the names imply, one is dorsal in location and the other is more ventral. They are two-neuron tracts that originate in peripheral sense receptors. They then course through the dorsal root ganglions and input into the dorsal horn. From there, the dorsal tract ipsilaterally ascends to input in the cerebellum, while the ventral tract decussates and inputs into the cerebellum (second-order neuron). The spinocerebellar tracts convey proprioceptive information about the body to the cerebellum.

FIGURE 5-10 The dorsal column-medial lemniscus pathway.

The descending and ascending tracts of the spinal cord are summarized in TABLE 5-2.

Now we will consider the spinal cord’s gray matter. The gray matter consists of the dorsal horn at the top of the butterfly’s upper wing and the ventral horn at the bottom. It is at these horns that the spinal nerve roots connect. Each spinal nerve passes through a notch between the vertebrae. Motor information leaves the spinal cord’s ventral root and courses to skeletal muscles and viscera, whereas sensory information enters the spinal cord through the dorsal root via its spinal nerve. Beginning above the first cervical vertebra (C1), this arrangement of dorsal and ventral roots repeats itself 31 times down the length of the spinal cord.

As discussed earlier, the content of the spinal cord white matter is various ascending and descending neural tracts. The dorsal gray matter is divided into six layers and is involved in sensory information (e.g., touch), whereas the ventral gray matter is involved in motor information through different types of LMNs. These neurons are classified by the type of muscle they innervate:

 Alpha motor neurons innervate extrafusal muscle fibers. These muscle fibers are what contract a muscle.

 Gamma motor neurons innervate intrafusal muscle spindles. These muscle fibers, which involve both a motor and a sensory neuron, form stretch receptors called muscle spindles. This mechanism is important for proprioception and reflexes.

The motor neuron plus the muscle fiber it innervates are called a motor unit.

Spinal Cord Function

As mentioned in the introduction, motor and sensory information passes up and down the spinal cord between the body and the brain. The major motor and sensory tracts and their functions have already been outlined. There is one last important topic to cover—reflexes. Reflexes are lightning-quick responses to stimuli controlled at the level of the spinal cord and spinal nerves. Instead of sending a signal all the way to the cerebral cortex and back down the spinal cord, the signal is sent to the spinal cord, which in turn responds and sends a signal back to the muscle. This signaling process is called the reflex arc, but how does it work? Muscles contain spindles, structures that detect the amount of stretch in a muscle. When a muscle is stretched (e.g., the physician’s reflex hammer hitting the patellar tendon), information is sent via sensory neurons to the dorsal roots of the spinal gray matter. This information is then sent to motor neurons via an intercalated neuron, a neuron that makes connections between two neurons. A motor message is then sent through the ventral root for the muscle to contract (or, in essence, oppose the stretching, which is called the stretch reflex). This process is illustrated in FIGURE 5-11. Reflex messages do eventually make it to the cerebral cortex for perceptual processing (e.g., pain). Damage along this pathway can cause reflexes to be diminished or completely absent.

TABLE 5-2 Mlajor Descending and Ascending Pathways in the Spinal Cord

Type

Tract

Origin

Decussation

Ending

Function

Descending Motor Tracts

Lateral corticobulbar

Primary motor cortex (BA4)

Medulla-spinal cord juncture

Brainstem

Movement of contralateral head region

Lateral corticospinal

Primary motor cortex (BA4)

Medulla-spinal cord juncture

Spinal cord

Movement of contralateral limbs

Rubrospinal

Midbrain

Midbrain

Cervical spinal cord

Flexor tone

Anterior corticospinal

Primary (BA4) and premotor (BA6) cortex

None

Cervical and thoracic spinal cord

Trunk muscles

Vestibulospinal

Pons and medulla

None

Throughout whole spinal cord

Extensor tone and spinal reflexes

Reticulospinal

Pons and medulla

None

Throughout whole spinal cord

Posture and gait

Tectospinal

Midbrain

Midbrain

Cervical spinal cord

Coordination of head and eye movements

Ascending Sensory Tracts

Dorsal column

Spinal cord

Medulla

Primary sensory cortex via thalamus

Fine touch, vibratory sense, proprioception

Spinothalamic

Spinal cord

Spinal cord

Primary sensory cortex via thalamus

Crude touch, pain, pressure, temperature

Spinocerebellar

Spinal cord

None

Cerebellum

Proprioception

Select Disorders of the Spinal Cord

Spinal Cord Injury

What Is It?

Spinal cord injury (SCI) involves traumatic damage to the spinal cord in which it is partially or completely severed or crushed (BOX 5-2). There are about 17,500 new cases of SCI each year and approximately 285,000 people currently living with SCI in the United States.

Causes

In the United States, vehicle crashes account for approximately 38% of SCIs, followed by falls (30%) and violence (13.5%). Males account for over 81% of SCIs, and 63% of cases involve non-Hispanic whites (National Spinal Cord Injury Statistical Center [NSCISC], 2017).

Signs and Symptoms

Damage from this type of injury can result in paresis (incomplete) or plegia (complete) depending on what level of the spinal cord is damaged (FIGURE 5-12).

FIGURE 5-11 The reflex arc.

BOX 5-2 Christopher Reeve and Spinal Cord Injury

Christopher Reeve (1952-2004) was an American actor best known for playing Superman in the Superman movies of the 1970s and 1980s. On May 27, 1995, he was thrown from a horse, and the injuries he sustained resulted in quadriplegia. He required a wheelchair and a portable ventilator to help him breathe. After his injury, Reeve became an activist for people with SCI. He also advocated for stem cell research, believing that a cure for SCI could result from this research. He died on October 10, 2004, due to cardiac arrest following an adverse reaction to an antibiotic he was taking to treat a pressure ulcer.

The term complete refers to complete loss of sensation or movement, and incomplete denotes partial loss of movement or sensation. Approximately 59% of cases are either complete or incomplete quadriplegia; the remaining 41% are complete or incomplete paraplegia (NSCISC, 2017).

Assessment and Treatment

Diagnosis of SCI is made through a neurological exam along with neuroimaging. Treatment can include surgery, steroid treatment, and rehabilitation. Treatment revolves around steroids to reduce swelling in and around the spinal cord, surgery to remove any bone fragments and to stabilize the spine, and rehabilitation (FIGURE 5-13). The prognosis varies from patient to patient, but the majority of cases involve some lasting impairment in movement and/or sensation.

Myelitis

What Is It?

Myelitis is a general term for inflammation of the spinal cord. If the inflammation is to only the gray matter of the spinal cord, the condition is called poliomyelitis. If it is confined to the white matter, it is called leukomyelitis. If the inflammation involves both the white and the gray matter, it is called transverse myelitis. If the inflammation extends to the meninges, it is called meningomyelitis. Poliomyelitis or polio is probably the most well-known form of myelitis because of the great epidemics of the 20th century that left many people paralyzed below the waist, including one of our presidents, Franklin D. Roosevelt (BOX 5-3).

Causes

Myelitis can be caused by a variety of factors, including immune system disorders, viruses, bacteria, fungi, parasites, and toxic agents (e.g., lead). Sometimes the cause is unknown and is referred to as idiopathic myelitis.

The Spinal Cord 105

FIGURE 5-12 Levels of spinal cord injury and the results.

FIGURE 5-13 A spinal cord injury patient wearing a halo ring brace to stabilize the spinal cord.

BOX 5-3 Franklin Delano Roosevelt and Polio

Franklin D. Roosevelt (1882-1945) was the 32nd president of the United States, a position he held for an unprecedented 12 years. At about the age of 40, Roosevelt contracted polio while on vacation in Canada. Because of his illness, he was paralyzed from the waist down. Roosevelt was careful to hide his disability and was rarely photographed in a wheelchair. In fact, only two known photographs exist depicting him in one. Roosevelt served as president during a crucial time in our nation's history. He helped pull the country out of the Great Depression and guided the United States through World War II.

Signs and Symptoms

The primary sign of the disease is rapid loss of motor and/or sensory abilities in the legs and possibly the loss of reflexes. If it is the poliomyelitis form, motor abilities will be affected, but not sensory. In the leukomyelitis variety, motor abilities are preserved but sensory abilities are impaired or lost. In the transverse form, both motor and sensory abilities are impaired. Some specific symptoms patients experience include weakness, pain, dysesthesia, and bowel and bladder issues.

Assessment and Treatment

Myelitis is usually diagnosed through a combination of blood tests and spinal tap to discern the cause of the inflammation. If the cause is bacterial or parasitic, antibiotics will be employed. Fungal infections will be treated with antifungal medications. Viruses are difficult to treat after infection, but vaccines can prevent myelitis. Poliomyelitis has all but been eradicated in the United States due to a vaccine developed in the 1950s, but it does still unfortunately occur in other places around the world (Victor & Ropper, 2001).

BOX 5-4 My Experience With Peripheral Neuropathy

When I was in my early 30s, I read a Time magazine article about diabetes. The article contained a list of diabetic symptoms, and as I scanned the list I realized that I had almost all the symptoms (e.g., dry mouth, frequent bathroom trips). My wife told my sister-in-law, who is a nurse, about this and she asked that I stop by her emergency department to have my blood checked. I did and she got a 600 reading on my blood sugar test (normal is around 100). I saw my physician shortly after, who diagnosed me with type 2 diabetes and immediately put me on medication. One of the symptoms I had been experiencing was strange sensation (dysesthesia; Greek for "impaired sensation”) in my feet. There were times when my feet hurt or burned. Sometimes I could not wear socks or have the blankets on my feet. My doctor told me this was the beginning of peripheral neuropathy. Apparently, the extra sugar in my blood was breaking down small capillaries in my feet, which was affecting sensory nerve endings in my feet. He was unsure whether it would get better or not because it depended on how long I had had diabetes and the damage that had been done. Fortunately, most of the neuropathy has disappeared because my diabetes is now under control.

Peripheral Neuropathy

What Is It?

Peripheral neuropathy is an inflammation of the peripheral nervous system that results in degeneration of the spinal nerves.

Causes

This condition can have a variety of causes, including toxic poisoning (e.g., alcohol abuse), infections, metabolic disorders (e.g., diabetes), and nutritional issues, such as the lack of vitamin B1 in beriberi. A good causal example is diabetes, a condition that causes excessive sugars in the blood. This excess sugar degenerates small capillaries in the extremities, causing nerve fibers to die. As nerve fibers die, people lose sensation in their fingers and hands, and with this loss of sensation are susceptible to wounds that will not heal because of the diabetes.

Signs and Symptoms

Sensory impairment or loss is the main symptom of peripheral neuropathy, but people can lose motor function as well. In the case of sensory impairment, patients might experience burning, prickling, and eventual numbness.

Assessment and Treatment

Peripheral neuropathy is diagnosed through clinical presentation and laboratory tests. For example, in diabetes, a blood test will determine the presence or absence of the disease, and sensory testing of the feet will tell the extent of the neuropathy if diabetes is indeed present. Treatment can consist of treating the underlying disease process. In the case of diabetes, the use of oral medications or insulin can control the disease and prevent the neuropathy from worsening. In some cases, neuropathies can be reversed if the disease is treated early enough (BOX 5-4).

► Brainstem

At the superior end of the spinal cord is the brainstem (FIGURE 5-14) . It contains both ascending (sensory) and descending (motor) tracts as well as nuclei that make up major centers for sensory and motor function. Life functions, such as breathing, heart rate, blood pressure, and digestion, are found in it, as are centers for wakefulness and alertness. It also has nuclei for most of the cranial nerves.

FIGURE 5-14 An illustration of the brainstem and its three main parts: the medulla, pons, and midbrain.

© Oguz Aral/ShutterStock.

External Organization of the Brainstem The Medulla

The lowest part of the brainstem is a 1-inch-long (2.5-cm-long) structure called the medulla. The medulla’s lower boundary is the spinal cord, and the pons forms the upper boundary (FIGURE 5-15). The medulla is ventral (or anterior) to the cerebellum and is connected to it by the inferior cerebellar peduncle (Latin for “stalk”). Between the upper medulla and the cerebellum is the bottom of the fourth ventricle. On the medulla’s anterior surface are the pyramids, which contain descending motor tracts, and the olive. Inside the olive is the inferior olivary nucleus that integrates signals from the spinal cord and the cerebellum for the purpose of coordinating motor movements and learning. Many of the tracts discussed earlier this chapter run through the medulla, including the corticospinal, spinocerebellar, spinothalamic, and dorsal columns tracts. Roughly 80% of motor tracts cross, or decussate, at the level of the lower medulla (FIGURE 5-16).

FIGURE 5-15 A. Anterior view of the brainstem. B. Lateral view of the brainstem. C. Posterior view of the brainstem.

In neuroanatomy, a nucleus is a cluster of specialized neurons that serve a specific purpose in the nervous system, and the medulla contains many such nuclei (Figure 5-16). For example, cranial nerve IX, X, XI, and XII nuclei arise from the medulla, while cranial nerve V and VIII nuclei dip down into the medulla from the pons. Various autonomic nervous system nuclei are located in the medulla, including cardiac, vasoconstrictor, gastrointestinal motility, respiratory, and swallowing centers. In addition, several reflexes are mediated at this level, including coughing, vomiting, and gagging by the nucleus of solitarius and swallowing by the nucleus ambiguous.

The Pons

The pons (Latin for “bridge”) lies superior to the medulla, anterior to the cerebellum, and inferior to the midbrain (Figure 5-15). It is about an inch (2.5 cm) in length and is bulbous in shape. The cerebellum is connected to the pons by the middle cerebellar peduncles, and between the two structures lies the fourth ventricle (FIGURE 5-17).

FIGURE 5-16 Cross-sections of the various levels of the medulla. A. The upper medulla. B. The middle medulla. C. The lower medulla.

Overall, the pons acts as a bridge, relaying neural tracts between the cerebral cortex, cerebellum, and lower structures like the medulla and spinal cord. Some of these tracts include corticobulbar and corticospinal tracts. The pons contains nuclei that help regulate respiration, swallowing, hearing, eye movements, and facial expression and sensation. There are also a number of cranial nerve nuclei in the pons, including nuclei for cranial nerves V, VI, VII, and VIII (Saladin, 2007; Zemlin, 1998). The superior olivary nucleus and lateral lemniscus (Greek for “ribbon”) are found in the pons, both of which play an important relay function for auditory information.

The Midbrain

The midbrain lies inferior to the diencephalon and superior to the pons (Figure 5-15). Its ventral portion consists of two cerebral peduncles; the dorsal consists of the tectum (Latin for “roof-like”). Each peduncle has a dorsal part called the tegmentum (Latin for “covering”) and a ventral piece called the crus cerebri (Latin for “leg of the brain”), which are fibers that link the pons with the cerebral hemispheres. Between these is a layer of dark gray matter called the substantia nigra (Latin for “black substance”) where the neurotransmitter dopamine is produced (FIGURE 5-18). Dopamine plays an important role in addiction and movement. Destruction of dopamine-producing cells can cause progressive neurological movement disorders, like Parkinson disease. The tectum contains the paired superior and inferior colliculi (Latin for “little hills”). The inferior colliculi are the auditory center of the midbrain and are important in moving the eyes and/or head toward the source of a sound and our startle response to a loud noise. This area may play a role in disorders like posttraumatic stress disorder (PTSD) (Davis, Falls, & Gewirtz, 2000). The superior colliculi are the visual center of the midbrain, receiving input from the retinas and the primary visual cortex. Sandwiched between the superior and inferior colliculi is a small endocrine gland that Rene Descartes thought was the seat of the soul named the pineal gland (Latin for “pine cone”). It produces a hormone called melatonin, which helps regulate sleep and circadian rhythms.

FIGURE 5-17 Cross-sections of the upper and lower pons. A. Upper pons. B. Lower pons.

FIGURE 5-18 Cross-sections of the midbrain. A. Upper midbrain. B. Lower midbrain.

Internal Organization of the Brainstem

Tegmental Regions

The tegmentum is the core of the brainstem, which is continuous throughout the medulla, pons, and midbrain. The nontegmental areas are not continuous and lie near the surface of the brainstem. The tegmental areas include the reticular formation, inferior olivary complex, and red nucleus.

Reticular Formation

As mentioned, in neuroanatomy, a nucleus is a group of neuron cell bodies that relay and integrate neural signals. It also plays a role in the reflex arc. The nuclei of the reticular formation are scattered throughout the tegmentum (Figure 5-17B). These nuclei receive axon collaterals from special sensory systems (e.g., hearing, vision) and project axons throughout the brain, including the brainstem, cerebellum, diencephalon, and cerebral hemispheres. The reticular formation regulates many aspects of human experience, including consciousness, the sleep-wake cycle, cardiovascular functions, and respiration.

Inferior Olivary Nucleus

The inferior olivary nucleus (not to be confused with the superior olivary nuclei related to hearing) is a bulge on the medulla (Figure 5-16). It receives axons from the cerebral cortex and after processing the information sends it to the cerebellum. Its connection to the cerebellum suggests it plays a role in the control and coordination of motor movements.

Red Nucleus

The red nucleus is a paired structure located in the tegmentum of the midbrain next to the substantia nigra (Figure 5-18). Its name comes from the fact that it is pink due to the presence of iron. It receives connections from the cerebral cortex, and its axons give rise to the rubrospinal tract that descends the brainstem and inputs into the spinal cord’s ventral horn cells. This tract modulates flexor tone in the upper extremities and probably participates in activities such as a baby’s ability to crawl and arm swinging in walking.

Nontegmental Regions

As mentioned earlier, nontegmental areas of the brainstem are found at or near the brainstem’s surface rather than deep in the tegmentum. Three non- tegmental areas will be briefly discussed: the tectum, cerebral peduncles, and ventral pons.

Tectum

The tectum is the roof of the midbrain. Dorsally, it has two hills: the superior colliculi and the inferior colliculi. The superior colliculi are connected to vision and the inferior colliculi to hearing. The inferior colliculi’s axons carry auditory information to the thalamus’s auditory center, the medial geniculate body, which then is projected to the cerebral cortex’s auditory areas.

Cerebral Peduncles

The cerebral peduncles, or crus cerebri, are bulges on the ventral side of the midbrain. The lateral corticospinal and corticobulbar tracts run through these bulges, the lateral corticobulbar tract being important for speech production. Between the peduncles and the tegmentum is the substantia nigra, which produces dopamine. The substantia nigra has a close connection to the basal ganglia, an important structure in speech production.

Ventral Pons

The corticopontine fibers originate from the motor cortex, pass through the cerebral peduncles, and input into ventral pons nuclei. Projections from the ventral pons then course to the cerebellum. Because of the pontine nuclei’s close connection to the cerebellum, it is thought this connection plays a role in motor movement error correction. Error correction is an important aspect of learning new motor skills (think of learning tennis). This would be an important skill for learning to speak both a first and a second language.

Select Disorders of the Brainstem

The Medulla

One disorder that can result from medullar damage is Wallenberg syndrome (also called lateral medullary syndrome). It is typically caused by a stroke involving one of the arteries that supplies blood to the medulla. Patients with this condition experience contralateral loss of pain and temperature in the body, ipsilateral loss of pain and temperature in the face, vertigo, ataxia, paralysis of the ipsilateral palate and vocal cord, and dysphagia. One additional symptom is frequent and violent hiccups that can last for weeks and make speaking, eating, and sleeping difficult. Treatment for Wallenberg syndrome is generally centered on relieving symptoms, rehabilitation, and counseling patients in adjusting to life with the syndrome. The prognosis varies from patient to patient, with some making a complete recovery, whereas others may have ongoing disability and/or handicap.

The Pons

Damage to the ventral pons can result in coma and/ or locked-in syndrome (LIS). LIS is characterized by quadriplegia and cranial nerve paralysis except for eye movements. Basically, the person is locked inside his or her body, unable to move, but is cognitively intact. The person cannot speak or swallow, and somatosensory abilities may or may not remain intact. Treatment involves support and rehabilitation, especially establishing a system for communication. The prognosis is poor for patients with LIS; 90% of those with the condition die within 4 months of onset.

The memoir The Diving Bell and the Butterfly by Jean-Dominique Bauby (1998), as well as the film of the same title, familiarized the general public with this condition. Bauby did not recover from LIS and died about a year and a half after his stroke. Though extremely rare, there have been documented cases of people with LIS having spontaneous, full recoveries. A British woman named Kate Allatt suffered a brainstem stroke around the age of 40 years and was diagnosed with LIS, but made a complete recovery (British Broadcasting Corporation [BBC], 2012). Another British woman, Kerry Pink, also reportedly recovered from the syndrome (BBC, 2010).

The Midbrain

Midbrain damage can result in Weber or Benedikt syndrome. Weber syndrome is characterized by contralateral hemiplegia and ipsilateral oculomotor paralysis with ptosis. The hemiparesis affects the lower face muscles and tongue. Benedikt syndrome is similar to Weber syndrome but results in contralateral hemiparesis and ataxic tremor.

► The Cranial Nerves

When we were learning about spinal nerves, we learned that they carry four different kinds of fibers—general somatic afferent (GSA), general somatic efferent (GSE), general visceral afferent (GVA), or general visceral efferent (GVE). There are 12 cranial nerves that carry some of these same types of fibers. However, some cranial nerves also carry special somatic and special visceral fibers for a total of seven possible fibers. Special senses refer to our special sense organs, like the eyes or ears. More specifically, special somatic afferent (SSA) fibers conduct visual and auditory information from the eyes and inner ear to the appropriate cerebral cortex area. (Note: There are no special somatic efferent [SSE] fibers.) Special visceral efferent (SVE) fibers control glands in the head and neck, and special visceral afferent (SVA) fibers relay special sense information like smell and taste.

As mentioned, there are 12 pairs of cranial nerves that control sensory, special sensory, motor, and visceral (or parasympathetic) functions of the head and neck. Most, except cranial nerves I and II, originate from the brainstem (FIGURE 5-19). Not all the cranial nerves play a role in speech and hearing, so critical attention should be directed toward six cranial nerves: V, VII, VIII, IX, X, and XII. All the cranial nerves are presented in TABLE 5-3, along with a mnemonic that has helped many students remember them.

Cranial Nerve I: The Olfactory Nerve

The olfactory nerve (I) is an SVA that mediates our sense of olfaction (Latin for “to smell”). This nerve is not considered a true cranial nerve because it does not arise from the brainstem and because it does not interface with the thalamus. It is, however, included with the other cranial nerves, being the shortest of all of them.

Bipolar olfactory receptor cells (first-order neurons) imbedded in the nasal cavity’s epithelium pass upward through the cribriform plate of the ethmoid bone and input into mitral cells (second-order neurons) in the olfactory bulb (FIGURE 5-20). The bulb then projects as the olfactory tract to third-order neurons in the cerebral cortex. This tract divides into two branches, a lateral branch and a medial branch. The medial branch projects through the anterior commissure, a white matter tract connecting the temporal lobes, and connects to the olfactory bulb on the other side. The lateral branch projects to the olfactory cortex of the temporal lobe of cerebral cortex. This area then sends fibers to the limbic system (amygdala) as well as to the hippocampus. The fact that smell can have strong connections to both emotion and memory are explained by these two connections.

Trauma to the nose can lead to the cribriform plate shifting and shearing off olfactory neurons, leaving a person with anosmia, which is a loss of smell. Trauma to the nose can also lead to cerebral spinal rhinor- rhea (Greek for “nose flow”), in which cerebrospinal fluid leaks through the nose. This rare condition can occur through a basal skull fracture (i.e., fracture to bones on the bottom of the skull) that leads to bone fragments puncturing the meninges, the three-layer membrane that surrounds the brain and spinal cord. This kind of damage can create a route for infection leading to a condition called meningitis, an infection in the meninges (Seikel, King, & Drumright, 2010). Lastly, temporal lobe epilepsy can lead to olfactory hallucinations, which often involve unpleasant smells (Monkhouse, 2006).

Cranial Nerve II: The Optic Nerve

Like the olfactory nerve, the optic nerve (II) does not originate off the brainstem, but unlike the olfactory nerve, it does connect with the thalamus. Overall, the optic nerve is an SSA fiber tract that conducts visual information to visual centers of the brain. Though not involved in speech and hearing, it is obviously involved in decoding the graphemes associated with written language.

This tract begins with the photoreceptor rod (night vision) and cone (daylight and color) cells of the retina (first-order neurons) and then projects to bipolar neurons (second-order neurons) that enhance visual contrast. These neurons then connect with an inner layer of ganglion cells whose axons form the optic nerve (third-order neurons) that projects to the lateral geniculate body of the thalamus (FIGURE 5-21). The projections from the nasal regions of the optic nerve cross (known as the optic chiasm), while the temporal regions remain uncrossed (FIGURE 5-22). Fourth-order neurons project from the thalamus via the geniculocalcarine tract (also known as the optic radiations) to the visual cortex in the occipital lobe.

FIGURE 5-19 The cranial nerves.

TABLE 5-3 The Cranial Nerves

Mnemonic

Number

Name

Origination

Function

Dysfunction

Speech/Hearing Importance

On

1

Olfactory

Olfactory bulb

Sensory

SVA: smell

Anosmia

None

Old

II

Optic

Thalamus

Sensory

SSA: vision

Visual disturbances;

visual loss

None

(language in terms of reading/ writing)

Olympus

III

Oculomotor

Midbrain

Motor

GSE: eyeball movement; controls eyelids

GVE: pupil constrictor

Loss of pupillary light reflex; papilledema; ptosis

None

Towering

IV

Trochlear

Midbrain

Motor

GSE: eyeball movement

Diplopia; nystagmus

None

Tops

V

Trigeminal

Pons

Motor

SVE: chewing muscles

Sensory

GSA: touch, pain, temperature, vibration for face, mouth, anterior two-thirds of tongue

Loss of sensations (see Function column); difficulty chewing, abnormal jaw-jerk reflex

Speech/chewing

A

VI

Abducens

Pons

Motor

GSE: eyeball movement

Strabismus; nystagmus

None

Fin

VII

Facial

Pons

Motor

SVE: face muscles

GVE: salivary glands

Sensory

GSA: sense at auricle's concha; behind auricle

SVA: taste in anterior two-thirds of tongue

Facial paresis or plegia; loss of taste

Speech

And

VIII

Auditory

(vestibulocochlear)

Pons/medulla

Sensory

SSA: hearing and balance

Hearing loss; balance issues

Hearing

German

IX

Glossopharyngeal

Pons/ medulla

Motor

SVE: pharyngeal movement

GVE: parotid gland

Sensory

GVA: middle ear; pharynx, posterior one- third of tongue

SVA: taste on posterior one-third of tongue

GSA: tactile sensation on external and middle ear

Absent gag; impaired or absent swallow; loss of taste; loss of pharyngeal movement

Speech

 

Viewed

X

Vagus

Medulla

Motor

SVE: pharyngeal and laryngeal muscles

GVE: viscera of the thoracic and abdominal cavities

Sensory

GSA: tactile sensation to external ear canal

GVA: pain sense from mucous membranes of pharynx, larynx, esophagus, trachea, and thoracic and abdominal viscera

SVA: taste from epiglottis/pharynx

Absent gag; impaired or absent swallow; loss of velar movement; loss of voice

Speech/voice/ resonance

 

Some

XI

Spinal accessory

Medulla

Motor

SVE: neck and shoulder muscles

Droopy shoulder, movement of neck

None

 

Hops

XII

Hypoglossal

Medulla

Motor

GSE: tongue muscles

Loss of tongue movement;

tongue fasciculation,

tongue atrophy

Speech

 

Abbreviations:

GSA, general somatic afferent; GSE, general somatic efferent; GVA, general visceral afferent; GVE, general visceral efferent; SSA, special somatic afferent; SVA, special visceral afferent; SVE, special visceral efferent.

Data from Monkhouse, S. (2006). High-yield neuroanatomy (5th ed.). Philadelphia, PA: Wolters Kluwer; Bhatnagar, S. C. (2013). Cranial nerves: Functional anatomy. Cambridge, UK: Cambridge University Press; Gould, D. J. & Brueckner-Collins, J. K. (2016).

Neuroscience for the study of communicative disorders (4th ed.). Philadelphia, PA: Wolters Kluwer.

FIGURE 5-20 A. Olfactory receptor cells in the lining of the nasal cavity and the olfactory bulb. B. Enlarged view of the olfactory receptor cells.

FIGURE 5-21 Neurons of the retina. A. The eye. B. Cellular components on the retina.

Damage to the optic system will result in different types of problems, depending on where the damage is in the system (FIGURE 5-23). Some level of blindness is one possibility, and hemianopsia (Greek for “half seeing”) is another. For example, if the left optic nerve is damaged, a person would suffer from monocular blindness. This condition would result not in a total loss of vision in the left visual field, but only a small fraction of this field outside the binocular field. If the lesion is further down the optic nerve at the optic chiasm, the subject would lose both temporal visual fields (bitemporal hemianopsia), whereas a lesion behind the optic chiasm but before the thalamus would result in loss of the left temporal and right nasal fields (homonymous hemianopsia).

FIGURE 5-22 The visual pathway.

Cranial Nerve III: The Oculomotor Nerve

The oculomotor nerve (III) is a motor nerve made up of GSE and GVE fibers. The nerve arises from the midbrain, courses through the red nucleus to the cerebral peduncles, and then exits as inferior and superior branches. The GSE component innervates the following muscles that control the eyeball’s movement up and out, inward, and down and out (FIGURE 5-24):

 Superior levator palpebrae (elevates upper eyelids)—superior branch

 Superior rectus muscle (elevates, adducts, and rotates eyeballs inward)—superior branch

 Medial rectus muscle (adduction of the eyeballs)— inferior branch

■ Inferior rectus muscle (depresses, adducts, and rotates eyeballs inward)—inferior branch

FIGURE 5-23 The visual pathway and the effect of lesions at different levels of the pathway. Damage at A would result in monocular blindness. Damage at B would result in heteronymous bitemporal hemianopsia. Damage at C would result in homonymous right hemianopsia.

FIGURE 5-24 Muscles of the eye with their cranial nerve innervation.

The GVE fibers of the nerve constrict the pupils and also help to focus the eyes.

Damage to oculomotor nerve GVE fibers leaves the pupil dilated and unable to focus. Damage to the GSE fibers would result in ptosis (Greek for “falling”) or droopy upper eyelids, strabismus (Greek for “to squint”) or crossed vision, and diplopia (Greek for “double eyes”) or double vision.

Cranial Nerve IV: The Trochlear Nerve

Cranial nerve IV is called the trochlear (Greek for “pulley”) nerve, and it is another eyeball muscle nerve containing GSE fibers. It arises from a midbrain nucleus called the trochlear nucleus and innervates the superior oblique muscle that is responsible for turning the eyeball down and out (Figure 5-24). Damage to this nerve results in difficulty moving the eyes downward, which can make walking down stairs difficult, and diplopia.

Cranial Nerve V: The Trigeminal Nerve

The trigeminal nerve (V) originates from the lateral surface of the pons and it splits into three branches: the ophthalmic, maxillary, and mandibular (FIGURE 5-25). The trigeminal is both an SVE and a GSA nerve.

In terms of motor (SVE) function, the mandibular branch innervates muscles that lower the mandible (mylohyoid and anterior belly of the digastric), raise the mandible (temporalis, masseter, and medial pterygoid), and protrude the mandible (lateral pterygoid muscle). The opening and closing movements of the mandible are important in sound production and chewing. The trigeminal nerve controls the tensor tympani, a muscle of the middle ear that connects the wall of the middle ear to the malleus. When this muscle contracts, it stiffens the ossicular chain of the middle ear. This protective reflex guards against intense low-frequency sounds, particularly the sound of one’s own voice and chewing. The trigeminal also dilates the eustachian tube, thus helping to equalize pressure between the middle ear and the environment.

FIGURE 5-25 The trigeminal nerve (V).

As far as sensory function, the ophthalmic branch relays sensation from the upper face back to the brainstem and cerebral cortex. The maxillary branch carries sensory information from the nose, mouth, lower face, auditory meatus, and meninges. Finally, the sensory portion of the mandibular branch relays sensation from the lateral side of the head and scalp, lower jaw, anterior two-thirds of the tongue, and mucous membranes of the mouth. This branch also carries proprioceptive information from the muscles of chewing to the brainstem. This sensory feedback information is important for jaw opening and closing during speech and chewing.

Cranial Nerve VI: The Abducens Nerve

So far, we have seen that the oculomotor (III) and trochlear (IV) nerves control movement of the eyeball. There is a final and third nerve that contributes to this movement called the abducens (Latin for “to pull away from”) nerve (VI). This is a GSE nerve like the oculomotor nerve. Its nucleus is found in the dorsal part of the pons, which projects through the point where the pons and medulla meet. It courses to the orbit and innervates one muscle—the lateral rectus muscle, which moves the eyeballs laterally (Figure 5-24). If injured, the eyeballs will deviate inward, leading to diplopia

Cranial Nerve VII: The Facial Nerve

The facial nerve (VII) has motor (SVE), sensory (GSA), special sensory (SVA), and parasympathetic (GVE) functions, but only the motor aspect has relevance for speech production. The facial nerves originate from the cerebellopontine angle and have two branches, the intracranial and extracranial (FIGURE 5-26). The intracranial branch is involved in sensory, special sensory, and parasympathetic functions. These functions include sensory information behind the auricle and in the auricle’s concha (GSA), taste on the anterior two- thirds of the tongue (SVA), and gland secretion (GVE; lacrimal, sublingual, and submandibular glands). The extracranial branch (SVE) innervates all the facial muscles that are crucial in speech production and the oral preparatory and oral stages of swallowing. These muscles include the following:

 Orbicularis oris (constricts oral opening)

 Risorius (retracts lip corners)

 Buccinator (moves food onto molars for grinding)

 Levator labii superioris (elevates upper lip)

 Zygomatic minor (elevates upper lip)

 Levator labii superioris alaeque nasi (elevates upper lip)

 Levator anguli oris (draws mouth corner up)

 Zygomatic major (elevates and retracts mouth angle)

 Depressor labii inferioris (pulls lips down and out)

 Depressor anguli oris (depresses mouth corners)

 Mentalis (pulls lower lip out)

 Platysma (depresses mandible)

FIGURE 5-26 The facial nerve (VII).

Additionally, the facial nerve innervates the posterior belly of the digastric muscle (depresses mandible and elevates the hyoid bone), the stylohyoid muscle (elevates the hyoid bone), and the stapedius muscle (dampens vibrations on the stapes) of the middle ear.

The SVE fibers originate out of the facial motor nucleus in the pons (FIGURE 5-27). This nucleus is divided in such a way that the lower face muscles (i.e., speech muscles) receive only contralateral innervation, whereas the upper face muscles receive bilateral innervation. If there is unilateral damage to the left cerebral cortex (i.e., a UMN lesion), then the result is deficits (e.g., weakness) in the right lower face muscles, with the upper right face muscles unaffected because they receive bilateral innervation. Thus, a person with this kind of damage could still wrinkle the right forehead and close the right eye, but the right side of the lower face would droop. If the damage is to the LMNs, then the whole ipsilateral side of the face is paralyzed (upper and lower face muscles). An example of an LMN disorder is Bell palsy (FIGURE 5-28 and BOX 5-5).

FIGURE 5-27 Effects of upper and lower motor neuron lesions on cranial nerve VII and its motor control of the upper and lower face muscles.

FIGURE 5-28 A woman with Bell's palsy, a lower motor neuron disorder that affects all the facial muscles on one side of the face. Note the drooping on the left side of her face.

FIGURE 5-29 The spiral ganglion of the auditory pathway.

BOX 5-5 Bell's Palsy

The term palsy is a Middle English word that came from the Latin word paralysis. It refers to paralysis, weakness, or even uncontrolled movements (e.g., shaking). The condition known as Bell's palsy (also known as seventh nerve palsy or idiopathic facial paralysis) is named after the 19th-century Scottish surgeon Charles Bell, who first described the condition in which one side of the face is weakened or paralyzed due to dysfunction of cranial nerve VII, the facial nerve (Figure 5-28). The cause of the condition is unknown, but it might occur after a viral infection that leaves the facial nerve inflamed and swollen. Stress may be another trigger for the condition. The symptoms of the condition include rapid onset of facial weakness on one side of the face, facial drooping, drooling, hyperacusis (sensitivity to loud sounds), changes to taste, and headache. In most cases, these symptoms last 4 to 6 months and then resolve. A small number of people may have the symptoms for life. Assessment of the condition is made through the patient's clinical presentation and through ruling out other conditions, like stroke. Treatment revolves around corticosteroids to decrease swelling, antiviral drugs in cases where a viral cause is suspected, and physical therapy to prevent facial muscles from atrophying.

Cranial Nerve VIII: The Vestibulocochlear (or Auditory) Nerve

The main cranial nerve of hearing is the auditory nerve (VIII). It is also known as the vestibulocochlear nerve, a more accurate name that describes its SSA branches, one for hearing and one for balance.

The cochlear branch begins with the spiral ganglion, a collection of neuron somas that are first-order neurons. These neurons receive auditory information from the hair cells inside the organ of Corti (FIGURE 5-29). Their axons form the cochlear nerve, which joins the vestibular branch to become the vestibulocochlear nerve. The vestibulocochlear nerve courses to the border of the pons and medulla and inputs into the cochlear nucleus. Auditory information is then relayed via a second neuron to the superior olivary complex in the pons. A third neuron continues the relay from the superior olivary complex to the inferior colliculus of the midbrain and a fourth from the inferior colliculus to the medial geniculate body of the thalamus. A final neuron projects from the thalamus to the auditory cortex, where the auditory information is decoded.

The vestibular branch has a more complicated pathway that begins with the vestibular ganglion picking up vestibular information from the semicircular canals. The axons of this ganglion form the vestibular branch, which interfaces with the cochlear branch and becomes the vestibulocochlear nerve. The vestibular nerves input in the vestibular nucleus near where the pons and medulla meet. From there, neurons project to the spinal cord, cerebellum, thalamus, and cortex.

Damage to cranial nerve VIII is associated with problems in equilibrium and hearing. In terms of impaired vestibular function, patients might experience balance issues and/or dizziness. Symptoms of auditory impairment could include various levels of hearing loss in addition to ringing in the ear, which is called tinnitus.

FIGURE 5-30 The glossopharyngeal nerve (IX).

Cranial Nerve IX: The Glossopharyngeal Nerve

The glossopharyngeal nerve originates at the medulla, and, like the facial nerve, it has both motor and sensory functions (FIGURE 5-30). In terms of motor function, it has GVE and SVE fibers, and for sensory it has GVA and SVA as well as GSA fibers. Only its SVE and GVA functions are notable for speech. Its SVE component innervates the stylopharyngeus muscle, a muscle that helps to elevate the pharynx and larynx. Elevation of the larynx is an important function in swallowing and may play a role in phonation. In terms of GVA function, the glossopharyngeal nerve relays touch, pain, and temperature information from the pharynx and tongue back to the brainstem and the sensory areas of the cerebral cortex. This function provides important feedback information for the motor function of these structures. This nerve mediates the gag reflex that involves a reflex contraction of the pharyngeal constrictor that helps to evacuate foreign materials in the throat and assists in vomiting.

Cranial Nerve X: The Vagus Nerve

The vagus nerve originates from the medulla and has three main branches: pharyngeal, superior laryngeal, and recurrent laryngeal. It has both motor (GVE, SVE) and sensory (GSA, GVA, and SVA) functions. Relevant for speech are its motor (SVE) functions (FIGURE 5-31).

FIGURE 5-31 The vagus nerve (X).

The pharyngeal branch enters the pharynx, where it connects with branches from the glossopharyngeal and superior laryngeal nerves. From there, it distributes fibers to the pharyngeal and palatal muscles, with the exception of the stylopharyngeus (innervated by IX) and the tensor veli palatini (innervated by V). The muscles this branch innervates include the following:

 Superior pharyngeal constrictor (narrows pharyngeal diameter)

 Middle pharyngeal constrictor (narrows pharyngeal diameter)

 Inferior pharyngeal constrictor (narrows pharyngeal diameter)

 Salpingopharyngeus (elevates lateral pharyngeal wall)

 Levator veli palatini (elevates velum)

 Musculus uvulae (shortens velum)

 Palatoglossus (lowers velum)

 Palatopharyngeus (lowers velum)

These connections mean that the pharyngeal branch controls pharyngeal constriction as well as palatal elevation through its SVE fibers. Palatal elevation is a key feature in speech and swallowing, and this mechanism is known as the velopharyngeal mechanism. For speech, the palate elevates, allowing for the production of non-nasal sounds and lowers for the production of nasal sounds. Children born with cleft palate will commonly have trouble with the velopharyngeal mechanism due to musculature weakness. When the palate does not seal off the nasal cavity sufficiently, it is known as velopharyngeal insufficiency.

The larynx, which contains the vocal folds, is the voice-producing organ. As air passes upward during expiration, it vibrates the vocal folds, which in turn produce sound or voice. The vocal folds are controlled by the intrinsic laryngeal muscles, which are innervated by the superior and recurrent laryngeal branches of the vagus nerve. These muscles are responsible for the adduction, abduction, tension, and relaxation of the vocal cords, thus playing a critical role in speech production. They include the following:

 Lateral cricoarytenoid (adducts vocal folds)

 Transverse arytenoids (adduct vocal folds)

 Oblique arytenoids (adduct vocal folds)

 Posterior cricoarytenoid (abducts vocal folds)

 Cricothyroid muscle (tenses vocal folds)

 Thyrovocalis (tenses vocal folds)

 Thyromuscularis (relaxes vocal folds)

As mentioned, cranial nerve X contains two branches, the superior laryngeal nerve and the recurrent laryngeal nerve. The recurrent laryngeal nerve (RLN) controls all the intrinsic laryngeal muscles through its SVE fibers (except the cricothyroid muscle). This branch is called “recurrent” because it courses down under the aorta and then back up to the larynx. Damage to the RLN, especially bilateral damage, can be catastrophic for voice production. The superior laryngeal nerve’s external branch controls the cricothyroid muscle, which is crucial for pitch control. Its internal branch relays sensory information from the thyrohyoid membrane, a broad layer of tissue that runs from the hyoid bone down to the thyroid cartilage.

The vagus nerve’s afferent functions include taste from the epiglottis and pharynx (SVA) and tactile sensation from the external ear canal (GSA). In addition, it conveys pain information from the mucous membranes of the following:

 Pharynx

 Larynx

 Trachea

 Esophagus

 Thoracic viscera

 Abdominal viscera

Cranial Nerve XI: The Spinal Accessory Nerve

The accessory nerve (XI), which begins at the medulla, is sometimes referred to as the spinal accessory nerve. It is motor in nature (SVE) and has two portions, the cranial and the spinal (FIGURE 5-32). The cranial portion joins the vagus nerve and becomes indistinguishable from it, thus possibly playing a role in pharyngeal and laryngeal function. It is debated whether this function is the work of the vagus nerve alone or a combination of the vagus and the accessory nerve; thus it is unknown whether the accessory nerve plays any role in speech. For the purposes of this text, we will assume it does not have a speech function. The spinal portion innervates the sternocleidomastoid and trapezius muscles of the neck.

Cranial Nerve XII: The Hypoglossal Nerve

Lastly, cranial nerve XII, the hypoglossal nerve (FIGURE 5-33), originates at the bottom of the medulla and controls the muscles of the tongue. It is a GSE nerve. The tongue is crucial for chewing, swallowing, and speech and damage to it can cause significant issues with these functions. It is the prime organ of articulation and consists of both intrinsic and extrinsic muscles.

Intrinsic tongue muscles enable precise tongue movements, like the ones needed for articulation. These include the following:

 Superior longitudinal (elevates, retracts, and deviates tongue tip)

 Inferior longitudinal (depresses tongue tip; retracts and deviates tongue)

 Transverse (narrows the tongue)

 Vertical (pulls tongue down to mouth floor)

FIGURE 5-32 The accessory nerve (XI).

The extrinsic tongue muscles work to move the tongue as a whole unit. This group of muscles includes the following:

 Genioglossus (retracts, protrudes, and depresses tongue)

 Hyoglossus (pulls tongue sides down)

 Styloglossus (draws tongue up and back)

 Chondroglossus (depresses tongue)

The palatoglossus is also an extrinsic tongue muscle but is controlled by cranial nerve X.

► The Cerebellum

Anatomy of the Cerebellum

Macroscopic Anatomy

The cerebellum (Latin for “little brain”) lies inferior to the cerebral hemispheres and posterior to the pons (FIGURE 5-34). It looks like a piece of cauliflower in that it has numerous wrinkles, called folia, that give the cerebellum enormous surface area like the cerebral cortex. The cerebellum also has lobes similar to the cerebral cortex. The cerebellum’s lobes include the anterior, posterior, and flocculonodular (Latin for “small mass”) lobes (FIGURE 5-35). It also has two hemispheres like the cerebral cortex, a right hemisphere and a left hemisphere. The two hemispheres are separated by a mound of tissue called the vermis.

FIGURE 5-33 The hypoglossal nerve (XII).

FIGURE 5-34 The cerebellum shown in isolation. A. Posterior view of the cerebellum. B. Sagittal section of the cerebellum.

FIGURE 5-35 The cerebellum shown in relation to the rest of the brain.

Each hemisphere is made up of a central core of white matter and a surface of gray matter. Three large bundles of fibers called peduncles connect the cerebellum with the spinal cord, brainstem, and cerebral hemispheres. There are three of these bundles—the inferior, middle, and superior cerebellar peduncles. The inferior and middle cerebellar peduncles carry mainly afferent information, whereas the superior peduncle carries primarily motor information.

Microscopic Anatomy

The cerebellum has about 80% of the total neurons in the brain, some 69 billion neurons compared to about 18 billion in the cerebral cortex (Azevado et al., 2009). Cerebellar neurons are arranged in three layers: the molecular layer, the Purkinje cell layer, and the granular layer (FIGURE 5-36). The molecular layer consists of the dendrites from Purkinje neurons, a class of large GABA- ergic cells located only in the cerebellum. This layer also contains two other cells—stellate cells and basket cells—that provide inhibitory communication to Purkinje cells. The somas of Purkinje cells lie in the second Purkinje layer. The axons of these neurons project the neurotransmitter GABA to inhibit cerebellar nuclei deep in the cerebellum. This inhibitory control facilitates the cerebellum’s motor coordination function. The granular layer contains the Purkinje cells’ axons as well as granule cells, which use glutamate to excite the Purkinje, basket, stellate, and Golgi cells. Golgi cells have an inhibitory role on granule cells. This layer also has mossy fibers, which are one of the major afferent inputs into the cerebellum and are part of two tracts—the spinocerebellar and the pontocerebellar. They excite granule cells.

There are four major cerebellar pathways. The vestibulocerebellar pathway helps in overall body posture and balance as well as coordination of eye movements with body posture. The vermal spinocerebellar pathway maintains muscle tone and posture over trunk muscles and muscles in the pectoral and pelvic girdles. The paravermal spinocerebellar pathway maintains posture and muscle tone over distal limb muscles (e.g., hands, feet, lower arms and legs). Finally, the pontocerebellar pathway is responsible for planning, initiating, and timing motor activity that is volitional in nature. These pathways are summarized in TABLE 5-4.

Cerebellar Function

Motor Function

Functionally, the cerebellum is like a second brain, monitoring sensory input from a wide array of sensory sources and integrating this feedback into motor movement. It monitors head and body position at rest as well as muscle tension and spinal cord activity. The cerebellum participates in the planning, monitoring, and correction of motor movement using all the sensory input it collects. This structure is also involved in our learning of motor skills. Cerebellar control is ipsilateral as compared to the cerebral cortex, where the majority of control is contralateral in nature.

FIGURE 5-36 Cellular layers of the cerebellum.

TABLE 5-4 Major Cerebellar Pathways

Pathway Name

Function

Vestibulocerebellar

Overall body posture and balance; coordination of eye movements

Vermal spinocerebellar

Trunk and girdle muscle tone and posture

Paravermal

spinocerebellar

Distal muscle group tone and posture

Pontocerebellar

Planning, initiating, and timing of volitional motor activity

Because speech is a motor process, it makes sense that the cerebellum would play an important role in speech production. It has long been known that a stroke in the cerebellum can lead to a type of dysarthria called ataxic dysarthria. Patients with this condition sound like they are intoxicated because their breathing and voice quality are irregular, articulation overshoots and undershoots place targets, and their speech rate is slow. In addition to this kind of motor coordination, the cerebellum may play a role in motor planning and a disorder of motor planning, apraxia of speech. This role is theorized because some of the symptoms of ataxic dysarthria and apraxia of speech overlap (e.g., speech timing, slowness of speech) (Marien et al., 2014).

The motor functions of the cerebellum can be tested through a variety of methods. The finger-nose- finger method involves a person touching the examiner’s finger, then his or her own nose, and then the examiner’s finger again. The observer is looking for accuracy and smoothness of movement. Another test is diadochokinesia ability, which is a person’s ability to make rapid, alternating movements with either the fingers or the mouth. For the mouth, the speech-language pathologist will ask the patient to say “pa-ta-ka” as fast as possible. Uncoordinated, sloppy movement may indicate cerebellar damage.

TABLE 5-5 Symptoms of Cerebellar Damage

Symptom

Description

Ataxia

Discoordinated, clumsy movements

Dysmetria

Over- or undershooting touching a mark

Dysdiadochokinesia

Inability to perform rapid, alternating movements of hand or mouth

Nystagmus

Fast, involuntary eye movements either side to side or up and down

Ataxic dysarthria

Slurred or scanning (broken into syllables) speech

Hypotonia

Reduced muscle tone and reflexes; muscle tire

Linguistic Function

Growing evidence points to the cerebellum having an important modulating role in nonmotor, linguistic functions. Neuroimaging studies as well as cases of cerebellar-induced aphasia have contributed to the idea of a “linguistic cerebellum” (Maiden & Manto, 2015). Theorized language functions include assistance in the following: perception of speech/language, verbal working memory, verbal fluency, grammar processing, writing, and reading (Maiden et al., 2014).

Select Disorders of the Cerebellum

All cerebellar disorders are motor in nature (although, as mentioned, there are some cases of possible cerebellar-induced aphasia; see Maiden et al., 2014, for more information). The symptoms of these disorders are shown in TABLE 5-5. Four specific syndromes are discussed in the following sections.

Cerebellar Hemispheral Syndrome

Cerebellar hemispheral syndrome can be caused by stroke, tumor, and multiple sclerosis. The syndrome primarily affects the ipsilateral limbs, causing tremor, dysmetria, and dysdiadochokinesia. Patients also experience the Holmes rebound phenomenon, which can be elicited by the patient holding out one of his or her arms while the examiner tries to push down on it. The rebound phenomenon occurs when the examiner lets go of the patient’s arm, which then bounces up significantly.

Vermal Syndrome

Vermal syndrome is due to damage to the vermis. Common causes include stroke, tumor, multiple sclerosis, and other degenerative disorders. The condition primarily affects the trunk muscles, causing unsteadiness, tremor, postural issues, and gait ataxia. Gait ataxia involves the patient walking with a wide base (i.e., the feet wide apart), which gives the sense of extra stability.

Friedreich Ataxia

Friedreich ataxia is an inherited, progressive neurological disorder that follows an autosomal recessive inheritance pattern. Symptoms begin between the ages of 8 and 14 years and can include progressive muscle weakness in the limbs, loss of coordination, dysmetria, dysarthria, curvature of the spine, and vision and hearing issues. Most patients have cardiac issues (chronic myocarditis); as a result, the median age of death is 35 years.

Cerebellar Agenesis

Can a person live without a cerebellum? The answer is yes, and the rare condition is known as primary cerebellar agenesis. Yu, Jiang, Sun, and Zhang (2014) present a case of a 24-year-old woman who was admitted to the hospital with a 1-month history of dizziness and nausea. Her mother reported that she began to walk at age 7 years and speak at 6 years. Doctors at the hospital performed a computed tomography scan and discovered that she did not have a cerebellum. cerebrospinal fluid filled the space where the cerebellum should have been. The woman was remarkably functional despite this significant loss of 10% of the brain’s volume and 50% of the brain’s neurons, demonstrating how the brain rewires itself and compensates for losses. Though primary cerebellar agenesis is rare, other cases have been reported in the literature (Boyd, 2010; Glickstein, 1994).

► Conclusion

Following the course of this chapter is akin to tracing a tree up its trunk and through its branches. The spinal cord is the trunk that transitions into the brainstem and cerebellum. From the brainstem, branches called cranial nerves extend away from the brainstem and connect to head and neck structures. These nerves play a role in linking the cerebrum to the body by relaying either motor, sensory, special sensory, or parasympathetic information or some combination of the four. Many of these nerves are of concern to the speech-language pathologist and audiologist because they relay information related to articulation, voice, hearing, and swallowing.

SUMMARY OF LEARNING OBJECTIVES

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

3. The learner will be able to list all the cranial nerves (Roman numeral and name).

On

I Olfactory

Old

II

Optic

Olympus

III

Oculomotor

Towering

IV

Trochlear

Tops

V

Trigeminal

A

VI

Abducens

Fin

VII

Facial

And

VIII

Auditory

German

IX

Glossopharyngeal

Viewed

X

Vagus

Some

XI

Spinal accessory

Hops

XII

Hypoglossal

4. The learner will list important cranial nerves for articulation, voice, swallowing, and hearing.

• Articulation: Cranial nerves involved in speaking include V, VII, X, XI, and XII.

 Voice: Cranial nerves for voice include V, VII, X, and XII.

 Swallowing: Cranial nerves V, VII, X, XI, and XII are used for the oral preparatory and oral phases of the normal swallow. The pharyngeal phase of the swallow depends on another set of muscles to move food and liquid through the pharynx. These muscles are controlled by cranial nerves IX, X, and XI.

 Hearing: Cranial nerves V, VII, and VIII are involved in hearing.

5. The learner will describe the form and function of the cerebellum.

 The cerebellum is located inferior to the cerebral hemispheres and posterior to the pons.

 It has lobes similar to the cerebral cortex. The cerebellum’s lobes are the anterior, posterior, and flocculonodular (Latin for “small mass”) lobes.

 The cerebellum also has two hemispheres like the cerebral cortex, a right hemisphere and a left hemisphere.

 It monitors head and body position at rest as well as muscle tension and spinal cord activity.

 It participates in the planning, monitoring, and correction of motor movement using all the sensory input it collects.

 It is involved in our learning of motor skills.

 The cerebellum may have an important role in assisting in language functions.

KEY TERMS

Alpha motor neurons Anosmia

Anterior (ventral) corticospinal tract

Benedikt syndrome

Cerebellar hemispheral syndrome

Cerebellar peduncle Cerebral peduncles Cerebral spinal rhinorrhea Crus cerebri

Dermatome

Diplopia

Dorsal columns

Friedreich ataxia Gait ataxia

Gamma motor neurons

General somatic afferent (GSA) fibers

General somatic efferent (GSE) fibers

General visceral afferent (GVA) fibers

General visceral efferent (GVE) fibers

Holmes rebound phenomenon

Inferior colliculi

Lateral corticospinal/ corticobulbar tract

Locked-in syndrome (LIS) Medulla

Midbrain Motor unit Myelitis Palsy Peripheral neuropathy Phrenic nerve Pineal gland Plexus Pons

Primary cerebellar agenesis

Proprioception Ptosis

Red nucleus Reflex arc Reticulospinal tract

Rubrospinal tract

Spinal cord injury (SCI)

Tectum

Special somatic afferent (SSA)

Spinocerebellar tracts

Tegmentum

fibers

Spinothalamic tracts

Vermal syndrome

Special visceral afferent (SVA)

Strabismus

Vestibulospinal tract

fibers

Substantia nigra

Wallenberg syndrome

Special visceral efferent (SVE)

Superior colliculi

Weber syndrome

fibers

Tectospinal tract

 

DRAW IT TO KNOW IT

1. Sketch a cross-section of the spinal cord along with its spinal nerve (see Figure 5-6). Label all the important structures.

2. Sketch a cross-section of the spinal cord and label all the motor and sensory tracts (see Figure 5-8).

3. Sketch the brainstem and label the midbrain, pons, and medulla.

QUESTIONS FOR DEEPER REFLECTION

1. Describe the functions of the brainstem.

2. List and describe disorders that can occur in brainstem injury.

3. List the cranial nerves involved in each of the following: speech, voice, swallowing, hearing.

4. List the functions of the cerebellum.

CASE STUDIES

A 50-year-old man experienced a sudden loss of muscle function in the left side of his face. In addition, he experienced pain behind his left ear and some changes in taste. Stroke was ruled out as the remainder of his motor function was preserved, and he was diagnosed with Bell’s palsy. Given his symptoms, please explain the following:

1. What cranial nerve VII muscle fibers are responsible for the loss of muscle function on the left side of his face, pain behind his ear, and the changes in his taste? Look at Table 5-3 if you need help.

2. Is this condition a lower motor neuron or upper motor neuron issue? Please explain why you think so.

SUGGESTED PROJECTS

1. Take one of the disorders in this chapter and write two to three pages about it including the following sections: cause, signs and symptoms, diagnosis, treatment, and speech/swallowing/hearing issues.

Mary is a 47-year-old-female who was diagnosed with Stage IV breast cancer about a year ago. She is status post chemotherapy and bilateral mastectomy and is currently completing radiation therapy to the chest. Recently, she has been experiencing difficulty moving her tongue, which is affecting chewing, swallowing, and speech. Upon investigation, the left side of her tongue appears paralyzed. An MRI revealed a lesion at the base of her skill that appears to be affecting one of her cranial nerves. Which cranial nerve do you think is being affected and why?

2. Create a digital movie using your smartphone, teaching the class about reflexes and the reflex arc. Include reflexes important in communication disorders.

REFERENCES

Azevedo, F. A., Carvalho, L. R., Grinberg, L. T., Farfel, J. M., Ferretti, R. E., & Leite, R. E., . . . Herculano-Houzel, S. (2009). Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain. Journal of Comparative Neurology, 513(5), 532-541.

Bauby, J. D. (1998). The diving bell and the butterfly. New York, NY: Vintage Books.

Boyd, C. A. (2010). Cerebellar agenesis revisited. Brain, 133, 941-944.

British Broadcasting Corporation. (2010). “I recovered from locked-in syndrome.” Retrieved from http://www.bbc.com /news/health-10985836

British Broadcasting Corporation. (2012). Womans recovery from “locked-in” syndrome. Retrieved from http://www.bbc.com /news/health-17363584

Davis, M., Falls, W A., & Gewirtz, J. (2000). Neural systems involved in fear inhibition: Extinction and conditioned inhibition. In M. Myslobodsky & I. Weiner (Eds.), Contemporary issues in modeling psychopathology (pp. 113-142). Norwell, MA: Kluwer Academic.

Glickstein, M. (1994). Cerebellar agenesis. Brain, 117, 1209-1212.

Marien, P., Ackermann, H., Adamaszek, M., Barwood, C. H., Beaton, A., & Desmond, J., . . . Leggio, M. (2014). Language and the cerebellum: An ongoing enigma. The Cerebellum, 13(3), 386-410.

Marien, P., & Manto, M. (Eds.). (2015). The linguistic cerebellum. Waltham, MA: Academic Press.

Monkhouse, S. (2006). Cranial nerves: Functional anatomy. Cambridge, UK: Cambridge University Press.

National Spinal Cord Injury Statistical Center (NSCISC). (2017). Spinal cord injury facts and figures at a glance. Birmingham, AL: University of Alabama at Birmingham. Retrieved from https:// www.nscisc.uab.edu/Public/Facts%20and%20Figures%20-%20 2017.pdf

Saladin, K. S. (2007). Anatomy and physiology: The unity of form and function. Dubuque, IA: McGraw-Hill.

Seikel, J. A., King, D. W., & Drumright, D. G. (2010). Anatomy and physiology for speech, language, and hearing. Clifton Park, NY: Delmar.

Victor, M., & Ropper, A. H. (2001). Principles of neurology (7th ed.). New York, NY: McGraw-Hill.

Yu, F., Jiang, Q.-J., Sun, X.-Y., Zhang, R.-W. (2014). A new case of complete primary cerebellar agenesis: Clinical and imaging findings in a living patient. Brain, 138(6), e353. https://doi .org/10.1093/brain/awu239

Zemlin, W R. (1998). Speech and hearing science: Anatomy and physiology. Boston, MA: Allyn and Bacon.



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