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

Chapter 15. The Neurology of Emotion

CHAPTER PREVIEW

Emotion may seem like a strange topic to include when discussing neuroanatomy for communication sciences and disorders. It is a relevant topic for two reasons. First, our patients are emotional beings and will express emotion to us at some point in time. Second, some of our patients, like those with autism, will have difficulty with their emotions or reading the emotions of others. Thus, the topic of emotion is a highly relevant topic for speech-language pathologists and audiologists, especially as it intersects with counseling patients and their caregivers.

CHAPTER OUTLINE

IN THIS CHAPTER

In this chapter, we will . . .

 Define what emotions are

 Consider the concept of emotional intelligence

 Survey three theories of emotion

 Explore the neurology of emotion

 Survey examples of emotional disorders

LEARNING OBJECTIVES

1. The learner will define what emotion and emotional intelligence are.

2. The learner will describe three theories of emotion.

3. The learner will list and describe neural structures involved with emotional processing.

4. The learner will describe three conditions in which there is a disruption in emotion: Kluver-Bucy syndrome, autism, and lability.

5. The learner will describe the connection between patient emotions, like fear, and the need for counseling in speechlanguage pathology and audiology.

 Introduction

 Emotional Intelligence

 Theories of Emotion

 The Neural Basis of Emotion

 The Limbic System

 The Amygdala

 The Cingulate Cortex

 The Insular Cortex

 The Prefrontal Cortex

 Disorders of Emotion

 Kluver-Bucy Syndrome

 Autism

 Lability

 Working With Patients' Emotions: Counseling

 A Tale of Two Minds

 The Therapist's Response to Patient Loss

 Counseling as a Critical Skill in Medicine

 Training Particular Counseling Skills

 Conclusion

 Summary of Learning Objectives

 Key Terms

 Draw It to Know It

 Questions for Deeper Reflection

 Case Study

 Suggested Projects

 References

 Introduction

In its various iterations, the Star Trek series has explored the balance between rational thought and emotions. Vulcans, a humanoid species, have learned to suppress their emotions over many centuries in order to live by logic. They at times despise humans, who to them are ruled by their emotions. One of the fun parts of the series is to see Vulcans begin to get in touch with their suppressed emotions and become more like humans. Dr. Spock, who is part human and part Vulcan, is one of the best examples of this struggle. To appreciate emotions, think about what life would be like without them. What would it be like not to experience happiness, sadness, or anger? What would it be like to be Vulcan?

What is emotion? To answer this question, we can view emotion objectively or we can view it subjectively. Objectively, emotions can be defined as a certain set of physiological responses to certain stimuli. For example, if I encounter a rattlesnake coiled and ready to strike, my heart starts beating fast, my muscles get tense, and I flee from danger. All these responses can be either observed directly or measured in some way. Subjectively, emotion can also refer to a conscious internal experience of feelings. When I see the snake, I have an internal, conscious feeling of fear. When I see my wife, I have an internal, conscious feeling of love. As we shall see, theorists have taken one definition or the other in exploring the topic of emotion. For our purposes, we will define emotion as both the subjective, conscious affective experience (e.g., fear, joy) and the parallel objective, physiological reactions (e.g., change in blood pressure) to stimuli in the environment.

The purpose of this chapter is to explore the neural basis of emotion. It might seem curious to discuss the neurology of emotion, but many speech-language pathologists (SLPs) and audiologists work with people with autism, who have differences in emotional processing. Having a basic understanding of emotion and its neuroanatomy will be helpful in understanding, being empathetic toward, and helping this population.

 Emotional Intelligence

More and more, emotions are being seen as a very important part of being human. For years, scientists have talked a lot about intelligence quotients (i.e., a person’s IQ score), but a new breed of affective neuroscientists, like Daniel Goleman, are reminding the rest of us that humans possess multiple intelligences, one of which is emotional intelligence (EI). The subject of EI has become popularized only in recent decades. It is our ability to understand our own emotions as well as those of others that guides us in our personal relationships. It is a concept that has been around for a long, long time. Aristotle in The Nicomachean Ethics stated:

Those who are not angry at the things they should be angry at are thought to be fools, and so are those who are not angry in the right way at the right time, or with the right persons; for such a man is thought not to feel things nor to be pained by them, and, since he does not get angry, he is thought unlikely to defend himself.

(Book 4, Chapter 5)

Salovey and Mayer (as cited in Colman, 2014c) formally defined EI along four competencies:

(a) the ability to perceive, appraise, and express emotions accurately, (b) the ability to access and evoke emotions when they facilitate cognition, (c) the ability to comprehend emotional messages and to make use of emotional information, and (d) the ability to regulate one’s own emotions to promote growth and well-being.

(Colman, 2014c)

Think of how important each of these competencies is to being an SLP or audiologist. Our patients will express emotion to us at some point about their speech, language, cognitive, or hearing loss, and we need to be able to read the intents of our patients’ messages. Some of these intents will be informational (e.g., “Could you explain what the larynx is?”), but other messages will be emotional (e.g., “I am so frustrated with these new hearing aids. All the kids are teasing me about them.”). Our ability to perceive, appraise, and comprehend our patients’ emotions (e.g., “this is sadness”) and emotional messages is critical not only for establishing rapport, support, and trust in the clinical relationship but also for making appropriate referrals to other professionals (e.g., psychologist).

As clinicians, we must also consider our own emotions. We are emotional creatures and, as clinicians, we need to be able to perceive, appraise, and comprehend our own emotions as well as regulate them appropriately so they do not overburden our patients. In essence, we want to be able to hold our patients emotionally so their emotions do not overwhelm us but also regulate our own emotions so as not to create unhealthy emotional bonds that might overwhelm them. At times, some clinicians have developed an unhealthy attachment to their patients, finding satisfaction for the clinician’s own emotional needs. This is not good for our patients or us.

Our emotional life, as well as that of the people with whom we work, is important. Through EI, we navigate the patient-clinician relationship. Many patients and caregivers report that they want clinicians who are not only competent but also empathetic and supportive. To be this type of clinician, we must take advantage of our EI. We must also realize that EI can be impaired in our patients through various neuropathologies. It is the neurological side of emotion to which we now turn.

► Theories of Emotion

Theorists of emotion have asked the question: What is the relationship between emotional experience and emotional expression? In other words, which comes first—the internal subjective emotional experience or the external objective physiological expression? In the 19th century, William James (1842-1910) and Carl Lange (1834-1900) proposed a theory called the James-Lange theory. It proposed that physiological responses (e.g., trembling) to external stimuli lead to emotional experience (Colman, 2014d). This theory can be represented as follows:

Environment → Trembling → Afraid

James and Lange defined emotion as the external, physiological status of the body (e.g., trembling) and a person’s interpretation of the body’s status. For example, if a wild bear approached you, you would begin to tremble. As you trembled, you would say to yourself, “I am trembling. I must be afraid!” This theory proposes that your feelings are never directly connected to the external stimulus (e.g., the bear), but rather are directly tied to your physiological state. What if you were angry, with your heart pounding and your face red? If these emotional expressions were removed, what would be left? Would you still “feel” angry if the physiological feelings were removed? James and Lange would say, “No!”

In the early 20th century, Walter Cannon (18711945) challenged the James-Lange theory. After some modification by his student Philip Bard (1898-1977), the Cannon-Bard theory of emotion became popular. It theorized that an external stimulus simultaneously triggers a physiological response and an emotional experience, both occurring independently of each other (Colman, 2014a). The Cannon-Bard theory can be represented in this way:

Environment → Trembling and Afraid

Using our example of the bear again, as the bear approaches you, you would simultaneously start to tremble and feel afraid. In other words, your feelings (e.g., fear) are tied directly to the external stimulus. Could a person have an emotional experience with no physiological response? Cannon and Bard would respond, “Yes!” For example, there might be a person with locked-in syndrome who experiences emotion but does not express emotion physiologically (i.e., no trembling). Another example is sleep: The body is in a state of rest, but we can experience vivid emotions connected to our dreams.

One last theory of emotion is the two-factor theory (or cognitive-appraisal theory) proposed by Stanley Schachter and Jerome Singer in the 1960s. This theory states that emotion is based on two factors—a physiological state and the interpretation of that state (Colman, 2014b). It can be represented this way:

Trembling → Environment → Afraid

For example, you begin to tremble, so you look to the environment to discover a stimulus that explains why you are trembling. You then see a bear and decide that the trembling is due to the bear.

These three theories differ neurologically. The James-Lange theory posits that the viscera and sensory system are the center of the emotional system. In contrast, the Cannon-Bard theory hypothesizes that the thalamus is the center of the emotional system, sending two parallel yet independent signals. One of these signals goes to the cortex where a subjective emotional experience occurs; the other goes to the sympathetic nervous system via the hypothalamus to induce a physiological response. The two-factor theory relies heavily on the autonomic nervous system and the cognitive aspects of the cortex. It does not address known areas of emotional processing, such as the amygdala.

Which of these three theories is correct? It appears that there are elements of truth in all three theories. For example, it is possible to force yourself to smile a lot and find that happy feelings begin to arise over time; the physiological experience has given rise to the emotional experience (James-Lange). It is equally possible to have an internal emotional experience but have or not have a physiological response (Cannon-Bard). Finally, we may at times look to the environment for an explanation of a physiological response we are having and frame that response emotionally (e.g., fear) based on the environmental stimulus (two-factor).

Setting these theories aside and stepping back, what is the relationship between emotion and our neurological system? Is emotion reducible to the viscera? Or the thalamus? Or the autonomic nervous system? What are the components of the nervous system that process and help us express our emotions?

FIGURE 15-1 Major limbic structures.

► The Neural Basis of Emotion

The Limbic System

An American neuroscientist named James Papez (1883-1958) built on the work of Cannon and Bard and proposed that a series of structures known as the limbic system was the brain’s emotional system. In addition to emotion, the limbic system is involved in olfaction, memory, and homeostasis. Blumenfeld (2010) suggests these four limbic functions can be remembered by the acronym HOME: Homeostasis, Olfaction, Memory, and Emotion. We have all had the experience of smelling something that evoked both memory and emotion; it is the limbic system that integrates the neurological structures behind these experiences.

The limbic system is located between the thalamus and the medial walls of the cerebral hemispheres (FIGURE 15-1). The name limbic, which is Latin for “border,” was given by Paul Broca for the cortical area that is a part of this system.

FIGURE 15-2 The Papez circuit. Note: The purple boxes indicate the basic components of the Papez circuit.

Data from Dalgleish, T. (2004). The emotional brain. Nature Reviews Neuroscience, 5, 583-589.

Papez proposed that a number of structures are involved in this system, not just the thalamic structures. His proposal became known as the Papez circuit. This circuit includes the sensory cortex, cingulate cortex, hippocampus, hypothalamus, and anterior thalamic nuclei (FIGURE 15-2). According to Papez, the body’s sensory experiences are sent to the thalamus and then are routed to the hypothalamus. The hypothalamus then sends ascending fibers through the anterior thalamus and cingulate cortex to the sensory cortex, resulting in conscious emotional experience, especially the coloring of that experience (positive versus negative emotions). To complete the circuit, fibers then descend through the hippocampus, back to the hypothalamus, and to the body, leading to physiological responses (e.g., increased heart rate) (LeDoux & Damasio, 2013). The connections between cortical structures and the hypothalamus are bidirectional, meaning that the two influence each other. This means that both the James-Lange and Cannon-Bard theories are probably correct. Emotional experience can cause emotional expression, and emotional expression can cause emotional experience.

FIGURE 15-3 Overview of the limbic circuitry.

The Papez circuit continues to have explanatory power in neuroscience. Today, this system is known to involve more structures than Papez theorized, including the olfactory bulb, hypothalamus, amygdala, septal nuclei, anterior nucleus of the thalamus, piriform olfactory cortex, hippocampal formation, and limbic cortex (FIGURE 15-3) (Castro, Merchut, Neafsey, & Wurster, 2002). Though the hippocampus is classified as a memory structure by many, there is a clear connection between emotion and memory, because many of our strongest memories have a strong emotional component to them.

The Amygdala

The Papez circuit theory predicts that if any damage occurs within the circuit, there will be effects on emotional behavior. This has not always been found to be true, but one area that clearly results in changes in emotional behavior when damaged is the amygdala. The term amygdala is Greek for “almond,” and there are two of these almond-shaped nuclei deep in our brains. The amygdala is clearly involved in fear and aggression.

The amygdala is situated in the medial temporal lobe and is made up of two groups of nuclei: the cor- ticomedial group and the basolateral group. The cor- ticomedial group is related to olfaction, whereas the basolateral group has extensive cortical connections that are both afferent and efferent. Afferent connections include the olfactory tract, the limbic cortex, and nuclei (solitary and parabrachial) involved with taste and general visceral functions. Efferent connections are made with the hypothalamus, limbic cortex, and various autonomic nervous system centers (Castro et al., 2002).

FIGURE 15-4 The amygdala's role in fear and self-preservation.

The amygdala is a central structure in our ability to preserve ourselves and respond to environmental danger. FIGURE 15-4 illustrates this function by showing how the amygdala might protect us if we were to spot a ferocious lion. It would increase our heart rate and blood pressure via the hypothalamus and invoke a flight response away from danger.

Other behaviors the amygdala directs include feeding and drinking, fighting, mating, maternal care, and our response to physical or emotional stress.

The amygdala is also important in emotional learning and emotional memory. These processes are implicit in nature, meaning that this learning and memory occur unconsciously. Emotional learning and memory can become explicit in times of danger, though. In these situations, those structures involved in explicit memory (e.g., hippocampus) are brought online to record the experience so it can be consciously recalled later (LeDoux & Damasio, 2013). For example, when this author was a child, he touched the engine of a running tractor, resulting in burns to his hands. It is safe to say that a strong emotional memory was formed that day and he never touched a running engine again!

Studies have shown that damage to the amygdala flattens emotions and produces difficulty recognizing facial emotions in others. When the amygdala is bilaterally damaged, subjects will have an explicit memory of a conditioning experience (e.g., electrical shock), but no physiological responses (e.g., avoidance) when the source of the shock is displayed. For example, if I were the subject, I could tell you about my experience touching the tractor’s engine, but you could not record any physiological responses (e.g., increased blood pressure) if a running engine were brought into the room. In contrast, patients with bilateral hippocampi damage have physiological responses (and implicit learning) when the source of the shock is displayed, but no explicit recall of the experience.

If the opposite occurs and the amygdala’s function is altered or overstimulated in some way, the result may be abnormal fear, aggression, and anxiety. Thus, the amygdala is implicated in a number of psychiatric disorders, including depression, anxiety, and posttraumatic stress disorder (PTSD) (LeDoux & Damasio, 2013). It is also involved in positive experiences, like pleasure and rewards. Pleasurable experiences induced through alcohol and drugs can result in addictions. The architecture of structures like the amygdala can change when substances are abused, resulting in anxiety and stress as levels of these substances decrease in the body. This stress and anxiety can then only be eased by the continued, and often increased, abuse of these substances.

The Cingulate Cortex

The cingulate cortex is an arch-shaped band of cortical tissue located in the medial region of the cerebral cortex (Figure 15-3). Superior to the cingulate cortex is the cingulate sulcus, and above the cingulate sulcus are the lobes of the brain. Inferior to the cingulate is the corpus callosum.

Papez (1937) was one of the first to theorize that the cingulate cortex is important in emotional processing and social behavior, but the exact nature of this processing has proven elusive. Lesion studies in animals have demonstrated that damage to the cingulate cortex results in decreases in social behavior, reduced time spent with others, and a decrease in vocalizations. Subjects also demonstrate an increase in time with inanimate objects (Hadland, Rushworth, Gaffan, & Passingham, 2003). Activation in the cingulate has been noted when subjects are exposed to negative emotion, such as pictures of angry faces (Blair, Morris, Frith, Perrett, & Dolan, 1999; Etkin, Egner, & Kalisch, 2011; Lane, Chua, & Dolan, 1999). The resolution of emotional conflict and thus the regulation of emotions have been associated with activation of the anterior cingulate cortex (Etkin, Egner, & Kalisch, 2011; Etkin, Egner, Peraza, Kandel, & Hirsch, 2006). The anterior cingulate cortex also seems to play a role in attention, especially in filtering out irrelevant information, even perhaps irrelevant emotional signals (Kozlovskiv, Vartanov, Nikonova, Pyasik, & Velichkovsky, 2012; Mohanty et al., 2007).

It is difficult to separate emotion from cognition. The cingulate cortex plays a role in cognition through its connections with the prefrontal cortex. For example, activations have also been noted in tasks that require theory of mind (ToM) abilities (Frith & Frith, 1999; Gallagher et al., 2000). ToM is the ability to understand that I have a mind, that you have a mind, and that our minds are different from one another. This ability is obviously important in having empathy for others.

Damage to the cingulate cortex has been associated with disorders such as depression and schizophrenia. Drevets, Savitz, and Trimble (2008) have reported abnormal reduction in cingulate tissue near the genu of the corpus callosum associated with mood disorders like major depression and bipolar disorder. Adams and David (2007) found that the cingulate was either underactive or overactive in people with schizophrenia in comparison to normal subjects, but psychiatric medications returned the cingulate to normal activation patterns.

The Insular Cortex

The insular cortex is located at the medial temporal lobes and has many connections to structures involved in emotional processing, including the amygdala, hypothalamus, and other areas. It plays a role in the expression of some negative emotions, like disgust (Jezzini, Caruana, Stoianov, Gallese, & Rizzolatti, 2012). It also plays an important role in emotional awareness, a key ability in EI (Craig, 2009). Lamm and Singer (2010) concluded that the insula is involved in empathy, compassion, fairness, and cooperation. These are all important intrapersonal abilities that would flow from emotional awareness of self and others. This obviously relates to ToM.

The Prefrontal Cortex

The prefrontal cortex plays an important role not only in cognition but also in emotion. This is not surprising given the heavy interconnectedness between it and other limbic areas, especially the anterior cingulate cortex. People who have experienced prefrontal cortex damage often have impaired abilities in social emotions. Because of this, they may experience the loss of stable social relationships with spouses and friends (LeDoux & Damasio, 2013). One patient I had several years ago had prefrontal cortex damage after a minor car accident. He reported that after the accident, he did not love his wife anymore. His wife reported that he did not have any interest in her or their son since the accident. The husband alienated all of their friends, and the marriage eventually ended in divorce.

The ventromedial region of the prefrontal cortex (Brodmann areas [BAs] 10, 11, 12), the anterior cingulate cortex (BAs 25, 32), and the amygdala appear to be critically important in emotion. Lesions in the prefrontal cortex can result in a disconnection with the anterior cingulate and amygdala and a flattening of emotional responses. Patients will no longer have physiological emotional reactions to stimuli that people normally have (LeDoux & Damasio, 2013). Some people become the opposite though—explosively emotional. Several studies have found that people with prefrontal cortex damage have difficulty reading facial emotions and identifying vocal expressions of emotion (Blair & Cipolotti, 2000; Hornak, Rolls, & Wade, 1996; Hornak et al., 2003).

► Disorders of Emotion

Kluver-Bucy Syndrome

Though very rare in humans, Kluver-Bucy syndrome has been induced through experiments performing bilateral amygdalectomies on wild rhesus monkeys (Dicks, Myers, & Kling, 1969). After the surgery, the monkeys were released into the wild and 2 weeks later were found dead. They had either starved, drowned, or been killed by other animals. After their surgery, the monkeys could not see or avoid potentially dangerous situations. Those running the experiment concluded that the monkeys had lost their ability to fear and that fear is tied to having intact amygdalae. Kluver-Bucy syndrome is caused by bilateral damage to the amygdala and results in diminished fears, overeating, oral fixation, heightened sex drive, and visual agnosia. In humans, the condition has been documented as occurring after temporal lobectomies, encephalitis, or bilateral stroke (Victor & Ropper, 2001).

One famous case of living without amygdalae is the case of S. M., who unlike the rhesus monkeys is still alive today. Her case was first described in 1994 by Adolphs, Tranel, Damasio, and Damasio. S. M. has a rare genetic condition called Urbach-Wiethe disease, of which there have been only about 400 reported cases worldwide since the early 20th century. It results in skin wrinkles, lesions, and scars; hoarse voice due to thickened vocal cords; and papules (i.e., skin bumps) around the eyelids. In addition, the condition hardens tissues in the medial temporal lobes. In S. M.’s case, this hardening began happening when she was a young girl, most prominently in the amygdalae. She was referred to a neurologist when she was 20 years of age and met Dr. Daniel Tranel. They began a professional relationship that remains in place to this day. Computed tomography and magnetic resonance imaging revealed that both amygdalae had almost completely calcified. Behaviorally, experiments showed that S. M. did not have any kind of fear response. Experimenters exposed her to items such as snakes and spiders as well as horror films and observed she did not exhibit fear. Instead, interest and curiosity were observed. S. M. has no fear of strangers, cannot read fear or other negative emotions on other people’s faces, and tends to be very positive about people and situations. As such, S. M. is at great risk of being taken advantage of by others, and the researchers who have been studying her are very careful in not revealing her identity or where she lives. She has already been the victim of violent crime but has never demonstrated any of the normal behavioral fear or distress responses to those situations.

Most of us would do anything to rid ourselves of fear, but the case of S. M. shows that the right amount of fear helps us negotiate a sometimes dangerous world. Too much fear can paralyze us in life (e.g., PTSD), but too little can leave us open to being abused by others. As stated by Feinstein, Adolphs, and Tranel (2016), “When it comes to survival, no other emotion is as imperative as fear” (p. 7).

Autism

Autism is a neurological developmental disorder that occurs in 1 in 59 children in the United States (Centers for Disease Control and Prevention, 2018). The disorder is characterized by problems in social interaction, communication problems, and stereotyped behaviors, all of which are diagnosed before a child is 3 years of age. Autism is five times more likely in boys than in girls. Twin studies have demonstrated that if one twin has autism, there is a 60% to 96% chance that the other twin will have it as well, suggesting a strong genetic causal component.

It has been argued that children with autism have brains that differ from the brains of their typical counterparts in significant ways. The cerebral cortex, hippocampus, basal ganglia, corpus callosum, brainstem, cerebellum, and amygdala are all thought to have neuroanatomical differences in autism. One theory is neuron overgrowth in these areas leading to overconnectivity between brain areas. In addition, both the amygdala and the fusiform gyrus may show underactivation in these children (Corbett et al., 2009). This may explain at least in part why children with autism process emotion differently than do typical children. A recent, large-scale study by Haar, Berman, Behr- mann, and Dinstein (2016) has challenged these neurological difference theories put forward by previous small-scale studies. These researchers report that people with autism have the same basic brain anatomy as people without autism. They acknowledge that while many subgroups of people with autism do have brain differences, the vast majority of people with autism have brains that are fundamentally the same as anyone else’s.

Both aggression and difficulty interpreting the emotional behavior of others have been frequently reported in cases of autism (Amaral, Schumann, & Nordahl, 2008; Schumann et al., 2004). People with autism have a kind of emotional agnosia when it comes to reading the emotions of other people, whether they are expressed as facial expression, vocal intonation, or body language. Because of possible dysfunction in both the amygdala and fusiform gyrus, it is not surprising that these children experience these issues. If neurological difference theories do prove true, the dysfunction in the amygdala leads to emotional processing problems, and the dysfunction in the fusiform gyrus leads to a kind of prosopagnosia, or face blindness, to facial emotions (not a real prosopagnosia because they can still recognize familiar faces). This inability to read people’s emotions is thought to be related to their deficits in ToM (Hobson, 1995). Children with autism have obvious difficulty in reading the mental states of others and typically fail ToM tests. The result of these deficits is a lack of empathy toward others (Clark, Winkielman, & McIntosh, 2008).

Rizzolatti and Craighero (2004) made an interesting discovery regarding the mirror-neuron system that may have application to autism. Motor command neurons are found in the premotor cortex and they fire when a person performs a certain action, like raising his or her hand. What Rizzolatti and Craighero discovered was that about 20% of these neurons also fire when we watch someone else carry out a motor command. These are called mirror neurons because they mirror what other people do, and they are important in our ability to watch others and learn new skills.

Mirror neurons are also found in the somatosensory cortex and work in the same way with touch. The mirror neurons fire when I am being touched, but they also fire when I see someone else being touched. This is a form of empathy. Ramachandran (2009) summarizes the functions of these neurons as follows:

The mirror neuron system underlies the interface allowing you to rethink about issues like consciousness, representation of self, what separates you from other human beings, what allows you to empathize with other human beings, and also even things like the emergence of culture and civilization, which is unique to human beings.

Lability

Emotional lability (or emotionalism) is an involuntary display of emotion that can sometimes be the result of a neuropathology. As human beings mature, their ability to control their emotions matures as well. The degree to which this is true depends on culture, gender, and ethnicity (Victor & Ropper, 2001).

As we have seen, there are connections between the cortex, especially the prefrontal cortex, and the cingulate cortex, amygdala, and hypothalamus. The prefrontal cortex acts as a regulator of our emotions; when there is damage to it, a person’s emotional life may change. Some patients experience flatness to their emotional life, whereas others experience “emotional incontinence” after a stroke or traumatic brain injury. A sudden outburst of laughing or crying might occur, though patients will report later that they did not feel particularly happy or sad when the outburst occurred. Patients report that these episodes are “both distressing and socially disabling” (House, Dennis, Molyneux, Warlow, & Hawton, 1989, p. 994). This sudden and seemingly strange display of emotion can shock many clinicians. When an episode occurs, it is best to stop all activities and allow the patient a few moments to compose himself or herself, after which many patients can usually resume therapy tasks. Trying to delve into why the person was crying is often not helpful or productive, because there is no underlying reason for it.

► Working With Patients’ Emotions: Counseling

A Tale of Two Minds

Daniel Goleman (1995) said that every person has two minds, one that is thinking in nature and another that is feeling. Tanner (1980), understanding the feeling mind, stated that SLPs should regard their clients as being in a state of grief over their communication loss. Several researchers have written about stages of grief connected to the death of a loved one (Kubler-Ross, 1969; Maciejewski, Zhang, Block, & Prigerson, 2007; Powers & Singer, 1993; Schneider, 1984), but others have confirmed that grief can occur when a patient has experienced a disability, like a communication disorder (Davis, 1987; Riesz, 2004; Robinson, Clare, & Evans, 2005; Rybarczyk, Edwards, & Behel, 2004; Sanders & Adams, 2005). Death grief is often thought of as being temporary, whereas grief associated with disease and disability is often chronic and episodic (Friehe, Bloedow, & Hesse, 2003; Kurtzer-White & Luterman, 2003). According to Spillers (2007), “Grief is a normal human response to loss, and loss permeates disability. Grief allows a person to separate from the loss and make some sense out of it” (p. 191).

Various researchers have explored different dimensions of grief associated with the loss associated with disability. Gilhome-Herbst and Humphrey (1980) found that 27% of their subjects were in a state of denial about their diagnoses. Martin, George, O’Neal, and Daly (1987) discovered that two of the most common reactions to a diagnosis of hearing loss are sorrow and depression. Clark (1990a) reported that patients often intellectualize their diagnoses in order to keep their condition at a distance. Kurtzer-White and Luterman (2003) stated that parents of children with hearing loss often feel overwhelmed and inadequate. Luterman (2001) reported two additional patient responses to communication loss, namely vulnerability and confusion. Friehe, Bloedow, & Hesse (2003) also reported confusion as well as shock and fear.

The Therapist’s Response to Patient Loss

In light of these patient reactions, our therapy plans should include “the facilitation of the grieving process and the ultimate acceptance of the loss by the patient” (Tanner, 1980, p. 928). However, patients often report that professionals do not understand their emotional difficulties in adjusting to a communication disorder (Martin, Krall, & O’Neal, 1989). For example, a patient might report feeling depressed because of his or her diagnosis of dysarthria; the clinician may respond that dysarthria is a term that describes slurred speech and that the patient will need to learn some speech techniques to reduce the slurring. In this example, the patient is using his or her feeling mind while the clinician is responding to the patient’s thinking mind. In other words, the clinician has not correctly read and matched the patient’s communication intent (i.e., poor EI), resulting in a well-intentioned but useless patient pep talk (Clark, 1990b). The clinician is playing the part of the expert instead of connecting to his or her patient on an emotional level (Beazely & Moore, 1995). The danger of not connecting on this emotional level is the development of patient stress, both in the clinician-patient relationship and within the patient’s family (Zraick & Boone, 1991).

Counseling as a Critical Skill in Medicine

Physicians have long recognized the importance of patient counseling in establishing patient trust (Epstein et al., 2007; Fiscella, Meldrum, & Franks, 2004). Part of this counseling includes physicians understanding patients’ feelings. Unfortunately, patient concerns are not always expressed in a straightforward manner. In fact, they often use “affectively loaded questions” and statements, which “are often superficially straightforward, but reflect underlying feelings of fear, anger, or apprehension that should be addressed” (Epstein et al., 2007, p. 1731). Patients leave it up to the physician to explore these topics further, and if physicians do not, patients then assume that these emotions are either not important or the physician does not care (Salmon, Peters, & Stanley, 1999; Seaburn et al., 2005). When physicians do take interest in patients’ emotions, patients report higher satisfaction in that they trust and feel more supported by their physicians. Unfortunately, researchers have shown the reality to be that “patient concerns are minimized” and “expressions of empathy and support are uncommon” (Epstein et al., 2007, p. 1732).

As in medicine, counseling is seen as crucial to a patient’s and family’s adjustment to a communication disorder (Toner & Shadden, 2002). The American Speech Language Hearing Association (2004), in its statements on preferred practice patterns and scope of practice for SLPs, stated that counseling is part of the SLP’s responsibilities in the rehabilitative process.

Training Particular Counseling Skills

A crucial part of entering the patient’s inner world through counseling is the skill of being empathetic (Riley, 2002). In fact, patients and caregivers have reported that they want not only skillful clinicians, “but also an empathetic, supportive counselor” (Luterman & Kurtzer-White, 1999, p. 16). The Merriam-Webster’s Collegiate Dictionary (2007) defines empathy as “the action of understanding, being aware of, being sensitive to, and vicariously experiencing the feelings, thoughts, and experience of another of either the past or present without having the feelings, thoughts, and experience fully communicated in an objectively explicit manner.”

Margulies (1984) divided empathy into two modes. First, there is resonant empathy, which is a form of empathy in which the clinician listens attentively to the patient’s expressions of emotions. Second, there is imaginative empathy, in which the clinician uses his or her imagination to step into the patient’s shoes and construct what the patient’s inner world might be like. To be effective SLPs and audiologists, clinicians must have not only resonant empathetic skills, but also knowledge about the possible emotions, struggles, and other characteristics of a patient to effectively engage the patient in imaginative empathy.

Important clinical skills in both resonant and imaginative empathy include the abilities to pay attention, listen well, and determine and match patients’ communicative intents (Eagen, 2001; Ivey, 2001). According to Holland (2005), good listening “involves sensitivity to both what a message’s manifest (surface) content and its latent (deeper emotional) content are, and whether or not these two messages are in agreement” (p. 13). Caldwell (2004) describes these clinical communication skills as “the currency of therapy” and states that “high-quality, non-judgmental attention can be a balm directly applied to a client’s wound, which soothes immediately and heals over time” (p. 35). Luterman (2006) describes the role of the counselor as follows:

The counseling relationship is not a conventional one; it places a different set of demands on the professional. It is a relationship that requires deep, selfless listening. The professional must be willing to put aside his or her agenda and listen to the client. Therefore, the professional can have no point of view other than trying to hear and understand where the client is coming from, and in many cases, reflect that back to the client. Within a counseling relationship, there is the understanding that wisdom resides within the client; therefore, all professional judgments are suspended. Because nonjudgmental listening offers a high degree of emotional safety for the client, he or she can begin the process of resolving problems. When interacting with clients, professionals must learn to listen for the “faint knocking” that is the client’s affect because clients are often unaware of how they feel. By listening deeply we can elicit the feelings and provide the support. (p. 9)

► Conclusion

Emotions are not a typical topic of study in the field of communication disorders, but much is communicated through emotion. Sometimes emotions can even betray a person by contradicting the very thing the person is saying (e.g., saying “I’m just fine” while gritting teeth and red faced). As clinicians, we will encounter many patients and caregivers going through the stages of grief. Others will be struggling with emotional deficits due to neurological disorders. Clinicians must stand ready to understand not only their own emotions but also the emotions of their patients. By doing this, we will be the supportive and empathetic counselors our patients desire.

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.

1. The learner will define what emotion and emotional intelligence are.

• Emotion: Objectively, emotions can be defined as a certain set of physiological responses to certain stimuli. Subjectively,

emotion can also refer to a conscious internal experience of feelings.

• Emotional intelligence (EI): Colman (2014c) defines EI along four competencies:

 The ability to perceive, appraise, and express emotions accurately

 The ability to access and evoke emotions when they facilitate cognition

 The ability to comprehend emotional messages and to make use of emotional information

 The ability to regulate one’s own emotions to promote growth and well-being

2. The learner will describe three theories of emotion.

 James-Lange theory: Proposes that physiological responses (e.g., trembling) to external stimuli lead to emotional experience (Environment -> Trembling -> Afraid).

 Cannon-Bard theory: Theorizes that an external stimulus simultaneously triggers a physiological response and an emotional experience, both occurring independently of each other (Environment -> Trembling and Afraid).

 Two-factor theory: States that emotion is based on two factors: a physiological state and the interpretation of that state (Trembling -> Environment -> Afraid).

3. The learner will list and describe neural structures involved with emotional processing.

 Limbic system: Proposed by Papez (1937) to be the brain’s emotional system.

 Amygdala: Directs feeding and drinking, fighting, mating, maternal care, our response to physical or emotional stress, emotional learning, and emotional memory.

 Cingulate cortex: important in emotional processing and social behavior.

 Insular cortex: Plays a role in the expression of some negative emotions, like disgust, and also emotional awareness.

 Prefrontal cortex: important for reading facial emotions and identifying vocal expressions of emotions. Damage can leave a person flat or explosively emotional.

4. The learner will describe three conditions in which there is a disruption in emotion: Kluver- Bucy syndrome, autism, and lability.

 Kluver-Bucy syndrome: a condition caused by bilateral damage to the amygdala, resulting in diminished fears, overeating, oral fixation, heightened sex drive, and visual agnosia

 Autism: a condition that involves emotional issues, namely aggression and difficulty interpreting the emotional behavior of others

 Lability: an involuntary display of emotion that can sometimes be the result of a neuropathology

5. The learner will describe the connection between patient emotions, like fear, and the need for counseling in speech-language pathology and audiology.

 Communication disorders are a form of loss, and with that loss comes a patient grieving process.

 Grief due to a communication disorder involves many emotions, such as fear, shame, guilt, and worry.

 Clinicians should be ready to enter grieving patients’ worlds by using their feeling mind (EI) and using empathy as a tool to connect with patients and patient emotions.

 This process is called counseling, and it is a critical skill found in the scope of practice for both speech-language pathologists and audiologists scope.

 The purpose of counseling is for the patient to adjust in a healthy manner to his or her new communication disorder.

KEY TERMS

Amygdala

Autism

Cannon-Bard theory

Emotion

Emotional intelligence (EI)

Emotional lability Empathy HOME

James-Lange theory Kluver-Bucy syndrome

Mirror neurons Papez circuit Prefrontal cortex Theory of mind (ToM) Two-factor theory

DRAW IT TO KNOW IT

1. Draw the Papez circuit from memory as presented in Figure 15-2. Indicate the basic components of this circuit.

QUESTIONS FOR DEEPER REFLECTION

1. Compare and contrast the three theories of emotion presented in this chapter.

2. List the neuroanatomical areas known to be involved in emotion and state their contribution to it.

3. Describe the emotional challenges people with autism face.

4. Explain how you might handle a patient who demonstrates emotional lability.

CASE STUDY

Ana is a 54-year-old female who suffered a (L) cerebrovascular accident (CVA) approximately 3 weeks ago. She spent a few days in acute care, but now is receiving physical therapy (PT), occupational therapy (OT), and speech therapy (ST) in the hospital’s acute rehabilitation (AR) unit. One of Ana’s behaviors you have observed in therapy is that Ana will suddenly burst out crying during therapy and that these

outbursts do not seem connected to anything specific in therapy. Ana is scheduled to be discharged from the AR in 2 days to her home. Home health PT, OT, and ST have been ordered for Ana.

1. What label would you give to Ana’s crying outbursts?

2. What counsel would you give to Ana’s home health ST?

SUGGESTED PROJECTS

1. Pick a partner from class and use your smartphone to make a movie in which you and your partner describe and act out the three theories of emotion presented in this chapter.

2. Access the “How Emotionally Intelligent Are You?” test online (Cherry, 2016). Take the test to determine your emotional intelligence.

3. Write a three- to four-page paper on the emotional life and challenges of those with autism.

4. Write a two- to three-page paper on mirror neurons using three or four scholarly resources.

5. Read Temple Grandin’s book Thinking in Pictures and write a two- to three-page reflection paper on it. Half your paper should be a summary of the book and the other half should include your reflections/reactions to the book.

6. Read the original article about S. M. in Adolphs, Tranel, Damasio, and Damasio (1994), and give a 10-minute oral presentation of the case to your class.

REFERENCES

Adams, R., & David, A. S. (2007). Patterns of anterior cingulate activation in schizophrenia: A selective review. Neuropsychiatric Disease and Treatment, 3(1), 87-101.

Adolphs, R., Tranel, D., Damasio, H., & Damasio, A. (1994). Impaired recognition of emotion in facial expressions following bilateral damage to the human amygdala. Nature, 372(6507), 669.

Amaral, D. G., Schumann, C. M., & Nordahl, C. W (2008). Neuroanatomy of autism. Trends in Neurosciences, 31(3), 137-145.

American Speech Language Hearing Association. (2004). Scope of practice in speech language pathology. Rockville, MD: Author.

Beazely, S., & Moore, M. (1995). Deaf children, their families, and professionals: Dismantling barriers. London, UK: David Fulton Publishers.

Blair, R. J. R., & Cipolotti, L. (2000). Impaired social response reversal: A case of acquired sociopathy. Brain, 123(6), 1122-1141.

Blair, R. J. R., Morris, J. S., Frith, C. D., Perrett, D. I., & Dolan, R. J. (1999). Dissociable neural responses to facial expressions of sadness and anger. Brain, 122, 883-893.

Blumenfeld, H. (2010). Neuroanatomy through clinical cases. Sunderland, MA: Sinauer Associates.

Caldwell, C. (2004, July-August). Caring for the caregiver: The art of oscillating attention. Psychotherapy Networker, 34-35.

Castro, A. J., Merchut, M. P., Neafsey, E. J., & Wurster, R. D. (2002). Neuroscience: An outline approach. St. Louis, MO: Mosby.

Centers for Disease Control and Prevention (CDC). (2018). Autism spectrum disorder (ASD): Data and statistics. CDC, Division of Birth Defects, National Center on Birth Defects and Developmental Disabilities. Retrieved from http://www .cdc.gov /ncbddd/autism/data.html

Cherry, K. (2016). How emotionally intelligent are you? Very Well Mind. Retrieved from https://www.verywellmind.com /how-emotionally-intelligent-are-you-2796099

Clark, J. G. (1990a, June/July). Emotional response transformations: Redirections and projections. ASHA, 28, 67-68.

Clark, J. G. (1990b). The “don’t worry, be happy” professional response. Hearing Journal, 43(1), 21-23.

Clark, T. F., Winkielman, P., & McIntosh, D. N. (2008). Autism and the extraction of emotion from briefly presented facial expressions: Stumbling at the first step of empathy. Emotion, 8(6), 803-809.

Colman, A. M. (2014a). Cannon-Bard theory. In A. M. Colman (Ed.), Oxford dictionary of psychology. Oxford, UK: Oxford University Press.

Colman, A. M. (2014b). Cognitive-appraisal theory. In A. M. Colman (Ed.), Oxford dictionary of psychology. Oxford, UK: Oxford University Press.

Colman, A. (2014c). Emotional intelligence. In A. M. Colman (Ed.), Oxford dictionary of psychology. Oxford, UK: Oxford University Press.

Colman, A. (2014d). James-Lange theory. In A. M. Colman (Ed.), Oxford dictionary of psychology. Oxford, UK: Oxford University Press.

Corbett, B. A., Carmean, V., Ravizza, S., Wendelken, C., Henry, M. L., Carter, C., & Rivera, S. M. (2009). A functional and structural study of emotion and face processing in children with autism. Psychiatry Research: Neuroimaging, 173(3), 196-205.

Craig, A. D. (2009). How do you feel—now? The anterior insula and human awareness. Nature Reviews Neuroscience, 10, 59-70.

Dalgleish, T. (2004). The emotional brain. Nature Reviews Neuroscience, 5, 583-589.

Davis, B. H. (1987). Disability and grief. Social Casework: The Journal of Contemporary Social Work, 68, 352-357.

Dicks, D., Myers, R. E., & Kling, A. (1969). Uncus and amygdala lesions: Effects on social behavior in the free-ranging rhesus monkey. Science, 165(3888), 69-71.

Drevets, W C., Savitz, J., & Trimble, M. (2008). The subgenual anterior cingulate cortex in mood disorders. CNS Spectrums, 13(8), 663.

Eagen, G. (2001). The skilled helper. Monterey, CA: Brooks/Cole Publishing.

Empathy. (2007). Merriam-Webster’s collegiate dictionary (11th ed.). Springfield, MA: Merriam-Webster.

Epstein, R., Hadee, T., Carroll, J., Meldrum, S., Lardner, J., & Shields, C. (2007). “Could this be something serious?” Reassurance, uncertainty, and empathy in response to patients’ expressions of worry. Journal of General Internal Medicine, 22, 1731-1739.

Etkin, A., Egner, T., & Kalisch, R. (2011). Emotional processing in anterior cingulate and medial prefrontal cortex. Trends in Cognitive Sciences, 15(2), 85-93.

Etkin, A., Egner, T., Peraza, D. M., Kandel, E. R., & Hirsch, J. (2006). Resolving emotional conflict: A role for the rostral anterior cingulate cortex in modulating activity in the amygdala. Neuron, 51(6), 871-882.

Feinstein, J. S., Adolphs, R., & Tranel, D. (2016). A tale of survival from the world of patient S. M. In D. G. Amaral & R. Adolphs (Eds.), Living without an amygdala (pp. 1-38). New York, NY: The Guilford Press.

Fiscella, K., Meldrum, S., & Franks, P. (2004). Patient trust: Is it related to patient-centered behavior of primary care physicians? Medical Care, 42, 1049-1055.

Friehe, M. J., Bloedow, A., & Hesse, S. (2003). Counseling families of children with communication disorders. Communication Disorders Quarterly, 24, 211-220.

Frith, C. D., & Frith, U. (1999). Interacting minds: A biological basis. Science, 286, 1692-1695.

Gallagher, H. L., Happe, F., Brunswick, N., Fletcher, P. C., Frith, U., & Frith, C. D. (2000). Reading the mind in cartoons and stories: An fMRI study of theory of mind in verbal and nonverbal tasks. Neuropsychologia, 38, 11-21.

Gilhome-Herbst, K. & Humphrey, C. (1980). Hearing impairments and mental state in the elderly living at home. British Medical Journal, 281, 903-905.

Goleman, D. (1995). Emotional intelligence. New York, NY: Bantam Books.

Hadland, K. A., Rushworth, M. F. S., Gaffan, D., & Passingham, R. E. (2003). The effect of cingulate lesions on social behaviour and emotion. Neuropsychologia, 41(8), 919-931.

Haar, S., Berman, S. Behrmann, M., & Dinstein, I. (2016). Anatomical abnormalities in autism? Cerebral Cortex, 26(4), 1440-1452.

Hobson, R. P. (1995). Autism and the development of mind. New York, NY: Psychology Press.

Holland, A. L. (2005, Winter). Counseling families and adults with speech and language disorders: The view from a wellness perspective. CSHA Magazine, 35, 12-16.

Hornak, J., Bramham, J., Rolls, E. T., Morris, R. G., O’Doherty, J., Bullock, P. R., & Polkey, C. E. (2003). Changes in emotion after circumscribed surgical lesions of the orbitofrontal and cingulate cortices. Brain, 126(7), 1691-1712.

Hornak, J., Rolls, E. T., & Wade, D. (1996). Face and voice expression identification in patients with emotional and behavioural changes following ventral frontal lobe damage. Neuropsychologia, 34(4), 247-261.

House, A., Dennis, M., Molyneux, A., Warlow, C., & Hawton, K. (1989). Emotionalism after stroke. British Medical Journal, 298(6679), 991.

Ivey, A. (2001). Intentional interviewing in counseling (4th ed.). Belmont, CA: Brooks/Cole Publishing.

Jezzini, A., Caruana, F., Stoianov, I., Gallese, V., & Rizzolatti, G. (2012). Functional organization of the insula and inner perisylvian regions. Proceedings of the National Academy of Sciences, 109(25), 10077-10082.

Kozlovskiy, S. A., Vartanov, A. V., Nikonova, E. Y., Pyasik, M. M., & Velichkovsky, B. M. (2012). The cingulate cortex and human memory processes. Psychology in Russia, 5, 231-243.

Kubler-Ross, E. (1969). On death and dying. New York, NY: MacMillan.

Kurtzer-White, E., & Luterman, D. (2003). Families and children with hearing loss: Grief and coping. Mental Retardation and Developmental Disabilities Research Reviews, 9, 232-235.

Lamm, C., & Singer, T. (2010). The role of anterior insular cortex in social emotions. Brain Structure and Function, 214(5-6), 579-591.

Lane, R. D., Chua, M. L., & Dolan, R. J. (1999). Common effects of emotional valence, arousal, and attention on neural activation during visual processing of pictures. Neuropsychologia, 37, 989-998.

LeDoux, J. E., & Damasio, A. R. (2013). Emotions and feelings. In E. R. Kandel, J. H. Schwartz, T. M. Jessell, S. A. Siegelbaum, & A. J. Hudspeth (Eds.), Principles of neural science (pp. 10791094). New York, NY: McGraw-Hill Medical.

Luterman, D. (2001). Counseling persons with communication disorders and their families (4th ed.). Austin, TX: Pro-Ed.

Luterman, D. (2006). The counseling relationship. The ASHA Leader, 11(8-9), 33-38.

Luterman, D., & Kurtzer-White, E. (1999). Identifying hearing loss: Parents’ need. American Journal of Audiology, 8(1), 13-18.

Maciejewski, P. K., Zhang, B., Block, S. D., & Prigerson, H. G. (2007). An empirical examination of the stage theory of grief. Journal of the American Medical Association, 297, 716-723.

Margulies, A. (1984). Toward empathy: The uses of wonder. The American Journal of Psychiatry, 141, 1025-1033.

Martin, F. N., George, K. A., O’Neal, J., & Daly, J. A. (1987, June/ July). Audiologists’ and parents’ attitudes regarding counseling of families of hearing-impaired children. ASHA, 29, 27-33.

Martin, F. N., Krall, L., & O’Neal, J. (1989, February/March). The diagnosis of acquired hearing loss: Patient reactions. ASHA, 31, 47-50.

Mohanty, A., Engels, A. S., Herrington, J. D., Heller, W, Ringo Ho, M. H., & Banich, M. T., . . . Miller, G. A. (2007). Differential engagement of anterior cingulate cortex subdivisions for cognitive and emotional function. Psychophysiology, 44(3), 343-351.

Papez, J. W (1937). A proposed mechanism of emotion. Archives of Neurological Psychiatry, 38, 725-743.

Powers, L., & Singer, G. (1993). Families, disability, and empowerment: Active coping skills and strategies for family interventions. Baltimore, MD: Brookes Publishing.

Ramachandran, V S. (2009). Vilayanur Ramachandran: The neurons that shaped civilization [Video]. Retrieved from https://www.ted .com/talks/vs_ramachandran_the_neurons_that_shaped _civilization

Riesz, E. D. (2004). Loss and transitions: A 30-year perspective on life with a child who has Down syndrome. Journal of Loss and Trauma, 9, 371-382.

Riley, J. (2002). Counseling: An approach for speech-language pathologists. Contemporary Issues in Communication Science and Disorders, 29(1), 6-16.

Rizzolatti, G., & Craighero, L. (2004). The mirror-neuron system. Annual Review of Neuroscience, 27, 169-192.

Robinson, L., Clare, L., & Evans, K. (2005). Making sense of dementia and adjusting to loss: Psychological reactions to a diagnosis of dementia in couples. Aging & Mental Health, 9, 337-347.

Rybarczyk, B., Edwards, R., & Behel, J. (2004). Diversity in adjustment to a leg amputation: Case illustrations of common themes. Disability and Rehabilitation, 26, 944-953.

Salmon, P., Peters, S., & Stanley, I. (1999). Patients’ perceptions of medical explanations for somatisation disorders: Qualitative analysis. British Medical Journal, 318, 372-376.

Salovey, P, & Mayer, J. D. (1990). Emotional intelligence. Imagination, Cognition and Personality, 9(3), 185-211.

Sanders, S., & Adams, K. B. (2005). Grief reactions and depression in caregivers of individuals with Alzheimer’s disease: Results from a pilot study in an urban setting. Health and Social Work, 30, 287-295.

Schneider, J. (1984). Stress, loss, and grief. Baltimore, MD: University Park Press.

Schumann, C. M., Hamstra, J., Goodlin-Jones, B. L., Lotspeich, L. J., Kwon, H., & Buonocore, M. H., . . . Amaral, D. G. (2004). The amygdala is enlarged in children but not adolescents with autism: The hippocampus is enlarged at all ages. Journal of Neuroscience, 24(28), 6392-6401.

Seaburn, D. B., Morse, D., McDaniel, S. H., Beckman, H., Silberman, J., & Epstein, R. M. (2005). Physician responses to ambiguous patient symptoms. Journal of General Internal Medicine, 20, 525-530.

Spillers, C. S. (2007). An existential framework for understanding the counseling needs of clients. American Journal of SpeechLanguage Pathology, 16(3), 191-197.

Tanner, D. C. (1980). Loss and grief: Implications for the speech-language pathologist and audiologist. ASHA, 22, 916-928.

Toner, M. A., & Shadden, B. B. (2002). Counseling challenges: Working with older clients and caregivers. Contemporary Issues in Communication Science and Disorders, 29(2), 68-78.

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

Zraick, R. I., & Boone, D. R. (1991). Spouse attitudes toward the person with aphasia. Journal of Speech and Hearing Research, 34(1), 123-128.


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