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Journal of Health Sciences & Practice

2011 January Volume: 2 Issue: 1

The Link Between Stress, Psychopathology, Immunity and Somatoform Disorders: A Review
Timothy R. Test, Sr., Ph.D.

ABSTRACT
Human studies on the effects of psychosocial factors on immunity have steadily increased within the past decade and even more so in recent years. As an overview to the effects of psychosocial factors on immunity, illness, and somatoform disorders, a review of the research was conducted. Historical antecedents and mechanisms are discussed as well as implication for further research.

Journal of Health Sciences & Practice

2011 January Volume: 2 Issue: 1

Introduction Over the past decade, there have been great strides in the research validating the connection between psychosocial stressors and immune response. Although the psychological effects on immunity seem very apparent prima fascia, little in the way of human studies were actually conducted for conclusive validation. Human studies on the effects of psychosocial factors on immunity have steadily increased within the past decade and even more so in recent years. As an over view to the effects of psychosocial factors on immunity, a review of the literature was conducted. A summary of these articles will be given along with the effects that these stressors have on bodily function. Moreover, an examination will be made into the underlying mechanisms at work and various ways of testing the effects that these psychosocial stressors have on the body. Stress and Immune Response: Historical Antecedents Coe and Laudenslager (2007) conducted a thorough review of Brain, Behavior and Immunity (BBI) spanning from 1987-2006, and discovered an emergence of three prominent behavior types that were studied; immune response changes due to stress, the correlation between immune function, psychopathology and personality, and immune response in relation to behavioral conditioning. Coe and Laudenslager (2007) found that most of the preliminary research was focused on proving scientifically that psychological processes have a significant impact on immune response to the point that they can create a negative impact on health and disease. Over time, research progressed from rat studies to human studies, examining how psychosocial processes such as personality and psychopathology affect immunity (Coe & Laudenslager, 2007). More recently, research has focused on how stressful or traumatic events affect immune response (Coe & Laudenslager, 2007). For example, studies were conducted that measured the number and types of leukocytes as well as the levels of antibody generated following immunizations. In addition, emphasis on research has also focused on how positive influences may enhance well-being as well as affect the life span (Coe & Laudenslager, 2007).
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2011 January Volume: 2 Issue: 1

Early studies funded by the National Institute of Mental Health (NIMH), were guided by the outbreak of AIDS, and an attempt to discover which factors influenced viral infections and the progression of the disease was undertaken (Coe & Laudenslager, 2007). Of particular interest at that time were the benefits of social support systems, personality traits, and stress affected survival. In addition, studies were conducted to examine the correlation of depression and immunity by measuring cytokines. Post-Traumatic Stress Disorder (PTSD) was also of interest, and studies were conducted on the correlation of PTSD and hormones and immunity (Coe & Laudenslager, 2007). As time progressed, considerable efforts were made to measure the correlation between cognitive and emotions and immunity at the cellular level (Coe & Laudenslager, 2007). By measuring the changes in the brain or hormone secretion within the endocrine system, correlations could be made between stressors and immunity (Coe & Laudenslager, 2007). In particular, an increase of hormone secretion by the hypothalamic-pituitary-adrenal axis, as well as increased activity in the parasympathetic nervous system, could be linked to the immune system. Moreover, NK (natural killer) cell activity with in vitro cytolytic assays was studied (Coe & Laudenslager, 2007). Following a stressful event, rapid change of NK cells in circulation could occur within minutes. Additionally, lytic activity would experience great reductions and would be sustained for periods of up to weeks, following such an event (Coe & Laudenslager, 2007). In the latter decade, researchers such as Robert Ader (1983) advocated that experiences during early rearing of a childs life could have an effect on the normal development of the brain and immune system and in turn affect the susceptibility of the individual to illness, etc. In addition, studies done by Kiecolt-Glaser (1999) examined the effects that loneliness had on cellular immune response. In these studies, Kiecolt-Glaser found that cellular immune response was different in students who were lonely as opposed to those who were satisfied in their social relationships.
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2011 January Volume: 2 Issue: 1

Advances in the ability to immunophenotype lymphocytes paved the way for further research in measuring the effects of stressors on immunity (Coe & Laudenslager, 2007). By being able to quantify changes in the circulation of the different types of leukocytes, researchers then could identify activation and adhesion markers. Researchers also realized that they could index a humans immune status by examining the activation of the latent Herpes virus (Coe & Laudenslager, 2007). Moreover, by measuring the amount of antibody titers, researchers could measure the effect that being an elderly caregiver for an impaired spouse has on the immune system (Coe & Laudenslager, 2007). These studies provided strong evidence that psychological stress and demands of being a caregiver had a direct effect on the cellular immune response. Also in this latter decade, significant discoveries regarding cytokines emerged (Coe & Laudenslager, 2007). Once though of as primarily intercellular and paracrine mediators of immune activity at the local level, research of psychoneuroimmunology (PNI) led to the realization that cytokines facilitated communication across various physiological systems (Coe & Laudenslager, 2007). Cytokines were shown to have effects on the peripheral body functions as well as serious effects on the brain. Emotional processes, attention, and memory functions were linked to cytokines (Coe & Laudenslager, 2007). Higher levels contributed to loss of appetite, malaise, and fatigue, while lower levels within the central nervous system affected neuroendocrine activity and the creation and retrieval of memories through its acting on the hippocampus. It was also found that the individual can sometimes counteract the effects of cytokines when motivated (Coe & Laudenslager, 2007). One of the most profound effects discovered was concerning wound healing (Coe & Laudenslager, 2007). A negative emotional state had a huge impact on the ability of wounds to heal quickly. This had profound implications for the individuals ability to heal after surgery or trauma. Even such things as routine stress can have a negative impact on the ability of wounds to heal (Coe & Laudenslager, 2007).

Journal of Health Sciences & Practice

2011 January Volume: 2 Issue: 1

Of final note concerning Coe and Laudenslagers article concerns the plasticity of the body. The immune system is normally quite resilient and hardy. In a normally healthy individual, a body is capable of handling a lot of what is thrown at it. However, in a weakened state, the bodys normal defenses could be compromised, giving rise to various issues and vulnerabilities (Coe & Laudenslager, 2007). Like Coe and Laudenslager (2007), Kemeny and Schedlowski (2007) also investigated the historical antecedents of stress on the immune system, focusing on the human studies that have taken place since the inception of the Journal Brain, Behavior, and Immunity. Kemeny and Schedlowski focused on how stress effects viral infections, autoimmune disease, wound healing, and cancer. The neuroendocrine system plays an important role in responding to stressful situations. Kemeny and Schedlowski (2007) points out that the neuroendocrine system stimulates a series of adaptive responses. These changes can occur at the behavioral, cardiovascular, metabolic, and immunological level (Kemeny & Schedlowski, 2007). Within the endocrine system, prolactin and growth hormone can be released from the pituitary gland during stressful situations which can have an effect on the cellular and humoral immune response (Kemeny & Schedlowski, 2007). In addition, neuropeptides such as corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), neuropeptide Y (NPY) and the opioids can also be released, again having an effect on these immune responses (Kemeny & Schedlowski 2007). As Kemeny and Schedlowski (2007) discovered, data collected though both animal and human studies show the following: (1) primary and secondary lymphoid organs are innervated by sympathetic noradrenergic nerve fibers, (2) all lymphoid cells express b-adrenoceptors and some subsets express aadrenoreceptors, and (3) adrenaline and noradrenaline can alter circulation of leukocyte subpopulations and the functional capacity of immuncompetent cells, including cytokine production and release. (Glaser & Kiecolt-Glaser, 2005; Sanders & Kavelaars, 2007)
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2011 January Volume: 2 Issue: 1

Moreover, exposure to acute psychological stress seems to trigger and increase in sympathetic adrenal activity, which in turn has an effect on the immune system (Kemeny & Schedlowski, 2007). In particular, HypothalamicPituitaryAdrenal (HPA) axis-activity (which results in an increase in the release of glucocorticoids) and sympathetic mechanisms are the main mechanisms at work in the reduction or inhibition of cellular and humoral immune responses (Kemeny & Schedlowski, 2007). It has been found that glucocorticoids are responsible for the regulation of immune cell functions in many ways, including responses to bacterial and viral infections as well as inflammation (Kemeny & Schedlowski, 2007). Moreover, sensory peptides, such as Substance P (SP), may also have a correlation in stress and inflammation as can be seen in studies that correlate the loss of immune control of herpesvirus latency during stressful situations (Kemeny & Schedlowski, 2007). Although the cause of chronic inflammatory diseases cannot be directly linked to any dominant cause, there is observational evidence that there is a correlation between stressful life events and the onset of autoimmune diseases (Kemeny & Schedlowski, 2007). Additionally, there have been numerous studies that involved viral challenge response to vaccinations and its effect on the immune system. In these studies, a healthy individual is given a vaccination under controlled circumstances and then examined for evidence of infection and symptoms (Kemeny & Schedlowski, 2007). In addition to strong evidence correlating stress with physical and immune challenges, there has been research into the effects that stressors have on cancer (Spiegel, Bloom, Kraemer, & Gottheil, 1989). While there has been little to confirm the effect of stressors to the onset of cancer, there has been strong correlation in terms of the amount of social support on survival and recovery. Studies found that utilizing a therapeutic approach that had the participant express and deal with negative emotions in a supportive group environment, resulted in a longer survival time (18 month average) (Spiegel et al., 1989).

Journal of Health Sciences & Practice

2011 January Volume: 2 Issue: 1

While none of these two articles involve any one particular study, what they show is a progression in human studies that have provided definite linkages between the emotional state of an individual and immune response, as well as the effect disease and illness can have on the psychological state. Mechanisms within the hypothalamic-pituitary-adrenal (HPA) and the sympathetic nervous system (SNS) can compromise and inhibit cytokines producing vulnerabilities and susceptibilities to illness. Various methods for measuring this response have been employed, to include measuring the leukocytes and NK cells in the bloodstream, as well as the release of hormones, as well as through survey instruments and observation. While there have been numerous advances in the testing methods, much progress is still being made. As magnetic resonance imaging (MRI) and positron emission tomography (PET) technology advance, so can our understanding of the mechanisms at work. This can lead to more effective preventative measures as well as therapeutic treatment to reduce the instances of immune vulnerability. Having a thorough understanding and knowledge of the linkage between stress and immunity, better prevention strategies can be implemented. The Link Between Stress and Risk of Physical Ailments Other studies have focused on the link between stress and negative emotion, thoughts, and feelings and increased risks in developing Irritable Bowel Syndrome, heart disease, and other conditions (Smith & Ruiz, 2002). Smith and Ruiz (2002) examined the psychosocial influences that can play a role in the development and progression of coronary heart disease. At the time of the article, coronary heart disease (CHD) was the leading cause of death in the United States (American Heart Association, 2001). Enormous amounts of money have been devoted to this disease with regard to prevention, treatment, disability and loss of work (Smith & Ruiz, 2002; American Heart Association, 2001). In the attempts to find ways to address this disease, Smith and Ruiz (2002) brought to light three major topics that encompassed behavioral medicine and health psychology; modifiable behavioral risk factors and behavior change, stress and disease or psychosomatics,
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Journal of Health Sciences & Practice

2011 January Volume: 2 Issue: 1

and psychosocial aspects of medical illness and care (Smith & Ruiz, 2002). Smith and Ruiz (2002) focused mainly on how psychosocial influences impact the development and course of Coronary Heart Disease. In addition, Smith and Ruiz (2002) looked at interventions for psychosocial risk factors and the psychophysiological mechanisms at work. Smith and Ruizs main tenant was that these interventions can reduce the number of deaths related to CHD as well as its severity. Worthy of notation is the categorization of CHD. CHD is actually one symptom or manifestation of Coronary Arterial Disease (CAD) (Smith & Ruiz, 2002). There is strong evidence that indicates that stress and negative emotions can initiate and/or quicken the development of CAD (Smith & Ruiz, 2002). Several studies were highlighted in the article that indicates that Cardio Vascular Reactivity (CVR) promotes development of CAD (Smith & Ruiz, 2002). The extent to which CVR occurs is linked with the severity of the progression of carotid artery atherosclerosis (Smith & Ruiz, 2002). In addition, the differences in CVR can exacerbate the effects of low socioeconomic status or other risk factors on CAA (Smith & Ruiz, 2002). Therefore, the magnitude of stress-induced situations has a positive correlation to the severity of CAA (Smith & Ruiz, 2002). More recent research has shown that higher levels of parasympathetically mediated heart rate have a negative correlation with CHD morbidity and mortality (Smith & Ruiz, 2002). In addition, the fact that negative emotions and stress have an effect on immune response and healing can in turn have an effect on the onset of CAD and CHD (Smith & Ruiz, 2002). Factors such as hostility can have an effect on the progression of atherosclerosis although there are some distinctions between cynical hostility and outward anger (Smith & Ruiz, 2002). Evidence supports that social isolation and low levels of perceived social support have a negative correlation with the risk of CHD (Smith & Ruiz, 2002). Moreover, among patients with cardiovascular disease, conflicts in their personal relationships have a negative effect (Smith & Ruiz, 2002). For example, women with CHD who experienced a lot of marital conflict were
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2011 January Volume: 2 Issue: 1

much more likely (almost 3 times) to have a recurrent coronary event as opposed to married women in non-distressed relationships (Smith & Ruiz, 2002). In effect, even among those who are initially healthy but at high risk, an increase in marital stress had a positive correlation with risk of death from Coronary Heart Disease (Smith & Ruiz, 2002). Moreover, positive social ties have a negative correlation with CAD and CHD (Smith & Ruiz, 2002). Finally, it was often found that job stress is correlated with CVR and other stress responses (Smith & Ruiz, 2002). Stress, Somatoform, and Psychogenic Disorders Stressors not only have an effect on immune response and the onset of physical symptoms; there has been an emergence of somatoform disorders that have been correlated with stressors (Brown, 2004). There are many documented cases of individuals being plagued by unexplained illnesses. These illnesses affect the individual as much as any explained illness with the exception that the symptomology cannot be explained scientifically. By all medical standards, these individuals should have no symptoms, and there is no basis for the onset or pathology of the disorder. Brown (2004) summarized theories of medically unexplained illnesses. These were based on three concepts; namely dissociation, conversion, and somatization (Brown, 2004). Among patients being seen in family practice, between 25% and 60% of patients symptomology cannot be explained medically (Brown, 2004). The Diagnostic and Statistical Manual of Mental Disorders (DSM IV, 2001) categorizes somatoform disorders and encompasses such symptoms as pain, fatigue, and general malaise that does not have a general identifiable pathology. Brown (2004) classifies symptoms as medically unexplained if adequate investigation has failed to identify a plausible physical cause for their occurrence or their associated level of impairment. In addition, these symptoms must be distressful enough to meet diagnostic criteria or actually cause functional disability (Brown, 2004). Finally, one cannot attribute the symptoms solely to anxiety, depression, hypochondriasis, or psychosis (Brown, 2004).

Journal of Health Sciences & Practice

2011 January Volume: 2 Issue: 1

There have been three major theories that have emerged which attempt to explain this phenomenon; dissociation, conversion, and somatization (Brown, 2004). Dissociation was first introduced by Janet (Brown, 2004). According to this theory, when individuals are exposed to traumatic events, they experience a spontaneous narrowing of attention (Brown, 2004). This in turn leads to the onset of unexplained symptoms by limiting the number of sensory channels that can be attended to at the same time and by developing tendency to focus on sensory channels at the expense of others (Brown, 2004). More modern accounts in dissociation tend to differ with Janets in one fundamental way (Brown, 2004). Whereas Janet viewed dissociation as an abnormal process provoked by stressors, contemporary models take the stance that dissociation is a normal psychological process that is used as a defense mechanism. There has been some criticism of this theory. Frankel (1994) made the argument that the concept of dissociation has been so overused within a clinical setting that it has become more of a description rather than having solid significance as a mechanism. Moreover, as Brown (2004) pointed out, one can draw a link between somatoform symptoms and hypnotic phenomena without using dissociation as the theoretical link. Conversion was introduced by Breuer and Freud who contended that the brain attempts to regulate the conscious experience of negative affect by unconsciously suppressing (or repressing) the conscious recall of memories associated with personal trauma. In essence, the repressed memories are kept out of our awareness through an amnesic barrier. This is done in order to protect ourselves from a potentially negative affect from the experience. In this theory, unexplained symptoms act as a defense mechanism. This theory is also not without its criticisms. There are challenges that symptoms are the result of unresolved and psychological conflict within our unconscious (Brown, 2004). Somatization as defined by Lipowski (1968) is the tendency to experience or express psychological distress as the symptoms of physical illness. Rather than trying to explain the specific mechanisms involved in unexplained illness, somatization focuses on the processes of
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2011 January Volume: 2 Issue: 1

normal somatic perception as well as on the biopsychosocial context of the experience of physical and mental illness. One of the major complaints of this theory is the fact that it is very general in its explanation of the psychological mechanisms involved. As such, it underplays etiological differences between varying types of somatization that could be important (Brown, 2004). Brown (2004) attempted to bridge the gap in these theories and presented and integrated conceptual model. Brown (2004) posited that his model integrated dissociation, conversion, and somatization within a common explanatory framework. Brown (2004) viewed his model as an extension of these theories as opposed to an alternative or replacement for these theories. This model makes the assumption that genuine somatoform symptoms are subjectively real to that individual (Brown, 2004). In other words, the symptoms are very similar these individuals to physical symptoms that are explained (Brown, 2004). Brown (2004) tried to provide a theoretical framework on how it is possible to experience these unexplained symptoms without underlying pathology. Moreover, Brown (2004) attempted to clarify how the development and maintenance of these unexplained symptoms are controlled or differentiated by different risk factors associated with the phenomenon. Brown (2004) attempted to provide an explanation of unexplained illness that did not rely on the concept of psychosocial precipitation but demonstrated its importance. Based on cognitive psychological principles, stored information in the cognitive system disrupts the interaction between conscious and preconscious aspects of information processing, which in turn causes unexplained symptoms (Brown, 2004). This process is often driven by a defensive reaction that functions to reduce the individuals exposure to a traumatic affect (Brown, 2004). Symptom-focused attention is at the core and forms the foundation to the creation and maintenance of unexplained symptoms and illuminates the important role of catastrophic misinterpretation, illness beliefs, rumination, worry, illness behavior, negative affect, and personality features in this process (Brown, 2004). Brown (2004) attempted to place the understanding of these phenomena back into everyday
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psychology and normalize how this occurs. In this manner, more effective strategies can be developed for treatment (Brown, 2004). Unexplained symptoms have been a source of frustration among the medical profession and a quandary for many Psychologists to attempt to get at the root of this problem. Brown attempted to meld the three theories into a model that was more eclectic. It has become more apparent that, as opposed to viewing this phenomenon as an abnormal response to a traumatic event or events, this mechanism is a normal mechanism that protects us from more harm. By understanding these mechanisms involved, Psychologists can be more effective in their treatment of these symptoms. More effort and collaboration needs to take place between the medical profession and Psychologists. When symptomology that has no pathological etiology manifests itself, a collaborative effort can be made to identify the catalyst that initiated the onset of these symptoms. In this manner, treatment can be more specific and targeted to the individual with the goal of recovery being at the forefront. Moreover, by normalizing these symptoms, the patient does not have the attached stigma of being crazy or delusional. They can realize that it is a normal reaction and can concentrate on the root cause of the symptoms. We must realize that the mind and body are not two separate entities, but they are rather intertwined. According to Lickerman (2010), evidence is beginning to mount that our physical brains and our subjective experience of them---that is, our minds---are also "two but not two". To treat them as such not only does a disservice to the patients, but to the profession as a whole. It is imperative to realize the interconnectedness of our minds and the effects it has on the manifestation of symptoms, perceived or real. Psychogenic symptoms are not only unpopular, but very common (Benbadis, 2005). According to Benbadis (2005), it is estimated that at least 10% of all medical services provided are for psychogenic symptoms. Additionally, approximately 9% of inpatient neurology admissions are for psychogenic symptoms, and this number increases for outpatient visits
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(Benbadis, 2005). These symptoms can be frustrating to both the patient as well as the health care provider, and these symptoms can be extremely difficult to treat. Benbadis (2005) posited that among the varying types of psychogenic symptoms, psychogenic seizures, otherwise known as psychogenic nonepileptic seizures (PNES), are very unique. Not only are they very common among the symptoms, they can be diagnosed with near certainty (Benbadis, 2005). Moreover, as Benbadis (2005) pointed out, almost everything that occurs within PNES can be applied to other psychogenic symptoms, which makes it an excellent foundation for studying other psychogenic symptoms. In contrast to the literature which paints a picture of PNES representing a unique disorder, Benbadis (2005) contended that in reality, PNES are but one type of somatoform disorder. Regardless of the expression of the psychopathology, the underlying psychopathology, the prognosis of the disorder, as well as how it is managed is the same (Benbadis, 2005). Regardless of the symptoms, this is a very difficult disorder to treat, and Benbadis (2005) attempted to bring to the surface the important features of psychogenic symptoms utilizing PNES as a model. It is very common for an individual to be falsely diagnosed with epilepsy (Benbadis, 2005). Approximately 25% of patients who had been previously diagnosed with epilepsy and were not responding to the drugs and treatment were found to be misdiagnosed (Benbadis, 2005). Additionally, most of these misdiagnosed patients are eventually shown to have either PNES or syncope (Benbadis, 2005). Other symptoms such as migraines, sleep disorders, and paroxysmal movement disorders can be misdiagnosed as epilepsy (Benbadis, 2005). PNES are the most common conditions; in fact, 30% of patients diagnosed with posttraumatic epilepsy are actually experiencing PNES, and Benbadis (2005) estimated that the prevalence of PNES within the general population was 2 to 33 per 100,000. Once a patient is diagnosed with epilepsy, it is very hard to undo. One thing that should tip off the clinician that the seizures are psychogenic is the fact that the patient is not responsive to antiepileptic drugs (Benbadis, 2005). There are certain motor
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2011 January Volume: 2 Issue: 1

(convulsive) phenomena characteristics of PNES that include slow or very gradual onset or termination (Benbadis, 2005). Additionally, there are unusual precipitating factors that include discontinuous, interrupted, and irregular or asynchronous (out-of-phase) movements (Benbadis, 2005). Moreover, symptoms such as side-to-side head shaking, pelvic thrusting, opisthotonic posturing, etc. are for the most part specific to PNES (Benbadis, 2005). The main tool for diagnosing is the EEG and the recording of the habitual event in an effort to show that there is no change in the EEG during the episodes and that the episodes are not consistent with the EEG (Benbadis, 2005). In addition to PNES, psychogenic symptoms are relatively common in neurology (Benbadis, 2005). Some of the symptoms that emerge are paralysis, mutism, visual symptoms, sensory symptoms, movement disorders, gait or balance problems, and pain (Benbadis, 2005). There have been tests such as the Hoovers test (for limb weakness) designed to differentiate organic from nonorganic symptoms (Benbadis, 2005). For the most part, the neurologist tries to invoke symptoms that do not make neuroanatomical sense (Benbadis, 2005). Medicine in general has a lot of psychogenic symptoms and transcends every specialty (Benbadis, 2005). Symptoms within gastroenterology include vomiting, dysphagia, abdominal pain, and diarrhea (Benbadis, 2005). Symptoms within cardiology include chest pain that is noncardiac (Benbadis, 2005). Other symptoms may include shortness of breath, cough, globus and dysphonia, excoriations, erectile dysfunction, blindness, and convergence spasms (Benbadis, 2005). Symptoms can emerge as pain to include tension headaches, chronic back pain, limb pain, rectal pain, and sexual organ pain. As it is very difficult to make a case for psychogenic pain, it can be very difficult to attach that label to it (Benbadis, 2005). In addition, diagnoses such as fibromyalgia, fibrositis, myofascial pain, chronic fatigue, irritable bowel syndrome, and multiple chemical sensitivity have a largely psychogenic (either partly or wholly) component to them (Benbadis, 2005).

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Even with EEGs which can diagnose PNES with near certainty, the actual diagnosis of PNES can take a very long time, with 80% of these patients receiving antiepileptic drugs before PNES diagnosis (Benbadis, 2005). This has implications for other psychogenic symptoms. If this can occur for misdiagnosed epilepsy, then it is likely that the same applies to other symptoms (Benbadis, 2005). There have been some techniques being used in order to tease out PNES, although they are controversial due to ethical concerns (Benbadis, 2005). Benbadis (2005) refers to these techniques as provocative techniques or inductions. However, when these are done correctly and interpreted appropriately, their specificity for the diagnosis of PNES approaches 100% (Benbadis, 2005). Inductions are another technique and offer a lot of advantages but raise ethical concerns (Benbadis, 2005). Provocative techniques utilize the principle of suggestibility. Particularly in psychogenic symptoms, suggesting a change in symptoms, they may induce a change and can be used as diagnostic criteria for psychogenic mechanisms (Benbadis, 2005). Moreover, suggestibility can also be useful in the treatment of psychogenic symptoms. In conversion symptoms, for example, suggesting a cure is usually successful (Benbadis, 2005). The first and most important step in treating these symptoms is in the diagnosis. When the clinician fears making the diagnosis of psychogenic symptoms and starts off with an organic disorder (epilepsy), the patients generally will exhibit signs of anger and hostility, as well as denying or disbelieving that their symptoms are psychogenic (Benbadis, 2005). It can be helpful for clinicians to use written information to back up verbal explanations of the symptoms, although it can be difficult to find due to lack of availability (Benbadis, 2005). Even the American Psychological Association (APA) does not have any written information on somatoform disorders (Benbadis, 2005). If the patients and their families do not accept the diagnosis, they are not going to comply with treatments, and as such, communicating the diagnosis effectively is crucial and must be
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done clearly and with compassion (Benbadis, 2005). These types of symptoms require psychotherapy, and more effort needs to be made to provide this therapy to the patients (Benbadis, 2005). In addition, the neurologist or other specialists should continue to follow the patients progress in order to provide the necessary support and help them not to feel abandoned while eliminating unnecessary treatments (Benbadis, 2005). Overall, Benbadis (2005) posited that psychogenic symptoms have been underemphasized and required more research. A search of the journal Neurology from the years 19942003 for articles that contained psycho-genic within the title, only 21 articles were found (Benbadis, 2005). Of those, only 4 were related to topics other than psychogenic seizures (Benbadis, 2005). Moreover, a similar search in the New England Journal of Medicine found no articles with psychogenic in the title (Benbadis, 2005). Two articles were found with psychogenic in the abstract, and both of those were related to erectile dysfunction (Benbadis, 2005). In order to improve the diagnosing and treatment of psychogenic symptoms, it is imperative for them to be addressed rather than ignored. To improve the diagnosis and outcome of psychogenic symptoms, the problems discussed here need to be confronted head-on. There is a need for more research and more effective communication between the medical and psychological communities. Baker (2003) illustrated some of the ways psychogenic symptoms can manifest. Baker (2003) did a case study on psychogenic voice disorders due to traumatic stress. Baker (2003) defined psychogenic dysphonia as the loss of voice where there is insufficient structural or neurological pathology to account for the nature and severity of the dysphonia, and where loss of volitional control over phonation seems to be related to psychological processes such as anxiety, depression, conversion reaction, or personality disorder (p. 308).

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According to Bakers research, psychogenic voice disorders occur more commonly in women than men, with a ratio of approximately 8:1. Baker (2003) stated that psychogenic dysphonias can develop into post-viral infections with laryngitis and can often be linked to some recent emotional or psychological stressor where underlies a conflict with speaking out. House and Andrew (1987) provided an almost picture perfect scenario where one can link the onset of the disorder with some stressful event(s) or conflict. This in turn has some meaning and relevance to this individual. In addition, it has implications for the therapist, who can then implement an effective treatment plan. However, Baker (2003) asked whether the validity of the model that House and Andrew (1987) had posited held in cases where there seemed to be no connection to a certain event or life experience and the onset of symptoms. Baker (2003) pointed out that many times in these situations, the symptoms disappear after brief therapy, and the person leaves therapy content. Moreover, Baker (2003) questioned those instances where a sequence of events related to the onset of symptoms is identified and explored, yet the voice does not return. Baker (2003) posited that there is something that is operating at a deeper level beyond the understanding of either the patient or the therapist. Three possible hypotheses are presented; first, sufficient time may not have been given to develop a trusting and safe relationship that would allow for addressing of more delicate issues; second, the questions were not asked appropriately that would allow for recall; or third, the therapist is not asking the right questions. Baker (2003) stated the model of conflict over speaking out in relation to identifiable and consciously recalled stressful life events in close proximity to onset is not, in its present form, a sufficient explanation (p. 311). Two recent cases outlined briefly below may add to this discussion and our understanding of the phenomenology of psychogenic dysphonia (Baker, 2003). The first case study in involved a 23-year-old female student who developed prima fascia viral laryngitis, loss of voice, and whispery dysphonia (Baker, 2003). This had been going on for 3weeks. Upon first examination, her laryngologist informed her that her dysphonia was more than likely related to
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the viral infection and some protective tension of the laryngeal muscles, which would be alleviated by learning to use her voice properly. Following speech therapy with no progression, a full psychosocial interview and speech pathology assessment was conducted, and according to the method advocated by Aronson25, speech pathology assessment revealed psychogenic dysphonia. The only stressors or events that could be attributed to the psychogenic dysphonia were work pressure and ongoing studies at school. Although this individual entertained this as a cause, it did not sit right with her as being significant enough. She was asked to come back for a second interview to make sure that all issues with her normal voice had been resolved and to see if there might be another explanation. Upon returning, her voice was perfectly normal, and her disposition was happy and calm. Close to the end of that session, the client asked the therapist whether it was possible for an event that occurred 4 months earlier to have an influence upon the symptoms the client experienced. The client had been in a situation where a fellow student raped her while on a date. She decided to put it behind her and to move forward, but at upon the young man who raped her being assigned to her immediate work environment, she developed the laryngitis and dysphonia (Baker, 2003). In the second case, a 50-year-old health professional suffered acute hoarseness after a viral infection followed by dysphonia 6 months later (Baker, 2003). This woman went through various procedures to include medialization with gelfoam of the paralyzed vocal fold and fat injections designed to improve vocalizations (Baker, 2003). The laryngologist then referred the patient for a second opinion and speech pathology, where psychogenic dysphonia was suspected (Baker, 2003). By all accounts, the patient reported being content with her relationships with family, her employment, and as a single woman. She was not able to pinpoint any event that would account for the psychogenic dysphonia and subsequent aphonia (Baker, 2003). She was quite concerned and wanted answers to why this might have occurred and was not seeking any kind of compensation. The aphonia was attributed to stressful events from the removal of the plug, the corrective procedure, her residual dysphonia, and her anger and disappointment in her
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doctors. Her therapy continued in an effort to help her to understand which factors might be relevant to her particular situation, and given that nothing seemed relevant, they focused on circumstances surrounding her earlier illness, the medical treatments, surgical difficulties, and on the fact that she may need to express her ambivalence more directly. Following the lack of response, explorations were made as to possible traumatic experiences she may have had or witnessed in her early life. A week later she came into the session talking with a clear and strong voice. She inquired as to whether dreams could have any relevance of things that occurred in the far past. She then described a recent dream of a drowning episode that she had experienced at the age of 15, where she had been hit on the head with a ball and fell off her flotation device. She remembered not being able to breathe and could not call out. She was rescued before she totally drowned. She then related these feelings to those she had from her recent operation. Following this, her vocalization stabilized. She was feeling content with her therapy. Toward the end of the therapy sessions, the therapist was discussing some of Freuds theories on conversion, particularly the aspect that it is inevitably linked with early sexual abuse. The therapist remarked how it did not make sense in the clients case. The client then recounted that at the age of 12 she was assaulted by an elderly workman who thrust his tongue down into her throat (Baker, 2003). Baker (2003) pointed out that what made these cases unique was that neither of them were recent, they werent readily recalled, nor were they recognized as being linked with the onset of the psychogenic symptomology. As Baker (2003) stated, The issues related to conflict over speaking out only came to light after more extensive probing and, possibly, in less experienced or persistent hands, might never had been revealed. (p. 315). As such, the models presented where recent stressful events cause a conflict over speaking out is not appropriate for these case studies (Baker, 2003). As is evidenced above, there are examples where patients are first fitted with an organic diagnosis that is later found to be psychogenic in nature. This has serious implications for
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clinicians and the medical community to work together, communicate, and work towards viable treatment options. There must be an awareness of psychogenic symptomology and more research needs to be done. As Cassady et al., (2005) stated, clinicians should be aware of the potential for outbreaks of psychogenic illness and work to address the challenges of developing effective intervention strategies. (p. 291). Conclusion In conclusion, human studies on the effects of psychosocial factors on immunity, wound healing, physical illness, and somatoform disorders have steadily increased within the past decade and even more so in recent years. Psychosocial factors play a major role on the overall health of the body and can profoundly impact the medical community. Emotional processes, attention, and memory functions were linked to cytokine release, which can contribute to loss of appetite, malaise, fatigue, altered neuroendocrine activity, and the creation and retrieval of memories. In addition, social isolation and low levels of perceived social support has a negative correlation with the risk of CHD as well as negative effects for patients with cardiovascular disease who have conflicts in their personal relationships. Moreover, stressors or trauma can lead to somatoform and psychogenic disorders, which can tax the profession and leave the patient frustrated. Understanding these mechanisms can lay the foundation needed to implement efficacious treatments that can maximize the patients ability to recover. Additionally, initiating a preventative approach can help to minimize the impact on the costs of healthcare and promote healthier individuals. There is a need for awareness, and diagnostics need to be improved. It is only through the implementation of studies that more viable diagnoses and treatments can be explored and validated.

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References Ader, R. (1983). Developmental psychoneuroimmunology. Developmental Psychobiology, 16, 251-267. Baker, J. (2003). Psychogenic voice disorders and traumatic stress experience: A discussion paper with two case reports, Journal of Voice, 17(3), 308-313. Benbadis, S. R. (2005). The problem of psychogenic symptoms: is the psychiatric community in denial? Epilepsy & Behavior, 6, 914. Brown, R. J. (2004). Psychological mechanisms of medically unexplained symptoms: An integrative conceptual model. Psychological Bulletin, 130(5), 793-812. Cassady, J. D., Kirschke, D. L., Jones, T. F., Craig, A. S., Bermudez, O. B., & Schaffner, W. (2005). Case series: Outbreak of conversion disorder among Amish adolescent girls. The Journal of the American Academy of Child & Adolescent Psychiatry, 44(3), 291-297. Coe, C. L., & Laudenslager, M. L. (2007). Psychosocial influences on immunity, including effects on immune maturation and senescence. Brain Behavior and Immunity, 21(8): 10001008. doi:10.1016/j.bbi.2007.06.015. Frankel, F. H. (1994). Dissociation in hysteria and hypnosis: A concept aggrandized. In S. J. Lynn & J. W. Rhue (Eds.), Dissociation: Clinical and theoretical perspectives (pp. 80 93). New York: Guilford Press. Glaser, R., & Kiecolt-Glaser, J. K. (2005). Stress-induced immune dysfunction: Implications for health. Immunology, 17, 321-328. House A. O., & Andrews H. B. (1987). The psychiatric and social characteristics of patients with functional dysphonia. J PsychosomRes, 7(31), 483490. Kemeny, M. E., & Schedlowski, M. (2007). Understanding the interaction between psychosocial stress and immune-related diseases: A stepwise progression. Brain, Behavior, and Immunity, 21, 1009-1018.

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Kiecolt-Glaser, J. K. (1999). Stress, personal relationships, and immune function: Health implications. Brain, Behavior, and Immunity, 13(1), 61-72. Lickerman, A. (2010). Happiness in this world. Psychology Today. Retrieved from http://www.psychologytoday.com/blog/happiness-in-world/201003/psychosomaticsymptoms Lipowski, Z. J. (1968). Review of consultation psychiatry and psychosomatic medicine. III. Theoretical issues. Psychosomatic Medicine, 30,395422. Sanders, V. M., & Kavelaars, A. (2007). Adregenic regulation of immunity. In: Ader, R., Felton, D.L., Cohens, N. (Eds.), Psychoneuroimmunology. New York: Academic Press Smith, T. W., & Ruiz, J. M. (2002). Psychosocial Influences on the Development and Course of Coronary Heart Disease: Current Status and Implications for Research and Practice. Journal of Consulting and Clinical Psychology, 70(3), 548568. Spiegel, D., Bloom, J. R., Kraemer, H. C., & Gottheil, E. (1989). Effect of psychosocial treatment on survival of patients with mestastatic breast cancer. Lancet, 2, 888-891.

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Author Information: Timothy R. Test, Sr. Ph.D., is currently enrolled in the Ph.D. program in Health and Behavioral Medicine Psychology with Northcentral University, Prescott, AZ. He is an Adjunct Professor with National College of Business and Technology, Bristol, TN and Everest College of Phoenix Online. Dr. Test is also a counselor with Test & Test Natural Wellness Center, Erwin, TN where he concentrates on holistic wellness with his wife, Charlotte.

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