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Chronic Fatigue Syndrome

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 Chronic Fatigue Syndrome

Lisa M. Kirk
2005

The pathogens of chronic fatigue syndrome (CFS) are debated within the medical and psychological communities.  The ongoing debate examines whether the origin of CFS is solely a psychological, hypothalamic, immunological disorder, or a mechanism of interplay involving any combination of the three areas of primary focus.  I postulate that an interdisciplinary conceptualization of the treatment of CFS patients may afford both the treatment providers and his or her patients the opportunity to effectively manage the copious disease symptomology. 

Chronic fatigue syndrome is a disease that is besieged by controversy and is a clinical conundrum.  The Center for Disease Control (CDC) has established specific criteria crucial to making a definitive clinical diagnose for CFS (Fakuda, Strauss, Hickie, Sharpe, Dobbins & Komaroff, 1994; Shor,2003; Price, 2000; Akagi & Bass, 2001).  In order to be classified as chronic, the fatigue is required to persist for more than six months (Fakuda, Strauss, Hickie, Sharpe, Dobbins,& Komaroff, 1994; Shor,2003; Price, 2000; Akagi & Bass, 2001).  The reported fatigue cannot be attributed to or associated with the symptomology of another medical condition (Fakuda, Strauss, Hickie, Sharpe, Dobbins & Komaroff, 1994; Shor,2003; Price, 2000; Akagi & Bass, 2001).  A patient must exhibit, or provide documented evidence and/or personal reports of four or more of the seven CDC’s criteria of specific somatic symptoms in order to be diagnosed with CFS (Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Gregg & Jones, 2001).  CFS is characterized by debilitating fatigue with associated myalgias (tenderness/pain in muscles), tender lymph nodes, arthralgias (joint pain), chills, feverish feelings, and postexertional malaise (Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Gregg & Jones, 2001; Shor, 2003).  Patients can also experience psychiatric symptoms such as depression and mood lability (Gregg & Jones 2001; Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994).  CFS can also produce cognitive deficits in memory, concentration and speech (Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Gregg & Jones, 2001; Shor,2003).   The symptoms of CFS can oscillate throughout the disease progression.  The capricious symptomology of CFS may further complicate treatment interventions (Gregg, V.H. & Jones, D., 2001; Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Shor, 2003; Price, 2000; Akagi & Bass, 2001).  The CDC’s definition characterizes the immunological and psychological connection associated with the complex symptomology and treatment of CFS.

The primary source of clinical controversy includes skepticism of the validity of CFS as a medical disorder.  A second point of contention lies in the identification of primary instigate of CFS and whether it be physiological versus psychological, or a disorder of duality (Burns, Kubilus,  Bruehl,  Harden, Norman & Lofland, 2003; Leibing, Pfingsten, Bartmann, Rueger & Schuessler, 1999; Bradley, McKendree-Smith, & Cianfrini, 2003). 

The hypothesis that equates the onset of CFS with an immunological disturbance is supported by selective investigative findings.  These findings have identified that an infectious agent precedes the onset of the disorder (Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Shor,2003; Price, 2000; Akagi & Bass, 2001).   Investigators have also noted that there is a reported heightened sensitivity to allergens, as well as inflamed, painful lymph nodes accompanied by “flu like” symptoms (Landay, Jessop, Lennette & Levy, 1991; Lloyd, Hickie, Wilso & Wakefield, 1994; Tirelli, Marotta & Pinto, 1994; Burns, Kubilus, Bruehl, Harden, Norman, & Lofland, K., 2003; Leibing,  Pfingsten, Bartmann , Rueger & Schuessler,1999; Bradley, McKendree-Smith, & Cianfrini, 2003; Gregg, & Jones, 2001; Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Shor, 2003; Price, 2000; Akagi & Bass, 2001).  The investigators also noted that many of the patients had increased cytokine levels, which is reportedly indicative of an immunological abnormality (Shor, 2003; Price, 2000; Akagi & Bass, 2001). 

The onset of CFS has also been attributed to a genetic etiology or predisposition (Buchwald, Herrell & Ashton, 2001).  These investigators conducted a research study which revealed that the incidence of CFS was found to be greater in monozygotic twins [one egg and one sperm] than in dizogotic twins [two eggs and two sperms] (Buchwald, Herrell & Ashton, 2001).  They inferred from this study that CFS is not attributed to a medical or psychiatric condition and may reflect a genetic pathogen in the development of CFS (Buchwald, Herrell & Ashton, 2001). 

Investigators have also hypothesized that CFS is a disturbance of the hypothalamic-pituitary-adrenal (HPA) axis (Demitrack & Crofford, 1998; Demitrack, Cale, Straus, Lane, Listwak & Kruesi, 1991; Pagani & Lucini, 1999; Scott, Medbak & Dinan, 1998).  The researchers observed the significant correlation between stress intensity and the onset of disease (Demitrack & Crofford, 1998; Demitrack, Cale, Straus, Lane, Listwak & Kruesi, 1991; Pagani & Lucini, 1999; Scott, Medbak & Dinan, 1998).  The researchers observed symptoms of autonomic disturbance (e.g., poor thermo-regulation, palpitations, disequilibrium) and coinciding endocrine disturbance such as low cortisol levels (Demitrack & Crofford, 1998; Demitrack, Cale, Straus, Lane, Listwak & Kruesi, 1991; Pagani & Lucini, 1999; Scott, Medbak & Dinan, 1998).

“The Peroxynitrite Hypothesis” explores the cellular mechanism of oxidative stress that may potentially result in the development and chronicity of CFS (Pall, 2002).
Peroxynitrite is a potent oxidant created from the reaction of two moderately nonreactive free radicals, nitric acid and superoxide (Pall, 2002).  The result of this interaction can result in the inflammations of the following cytokines: interferon, interleukin-1B, interleukin- 6, and tumor necrosis factor-oc (Pall, 2002).   There is also a reported correlation that the inflamed cytokines and viral infection or the presence of a bacterial antigen (Pall, 2002).  Pall (2002) proposed that numerous mechanisms that result in intensified peroxynitrite levels which, reportedly impacts the HPA axis.

Those medical professionals that attribute CFS to a physiological pathogen acknowledge the possibility of coexisting psychological and cognitive disturbances (Shor, 2003; Scott, Medbak & Dinana, 1998).  The psychiatric and cognitive disturbances are suggested to be a secondary facet to the primary physiological disturbance (Demitrack & Crofford, 1998; Demitrack, Cale, Straus, Lane, Listwak & Kruesi, 1991; Pagani & Lucini, 1999; Scott, Medbak & Dinan, 1998). The belief is that once the physiological dimensions of the symptoms of CFS are treated and better managed then the psychiatric and cognitive symptoms will either dissipate or the symptom will be better managed (Akagi & Bass, 2001; Demitrack & Crofford, 1998; Demitrack, Cale, Straus, Lane, Listwak & Kruesi, 1991; Pagani & Lucini, 1999; Scott, Medbak & Dinan, 1998; Shor, 2003).

There are also medical investigators who hypothesized that the primary causation of the CFS disorder is a psychiatric reaction to a traumatic physiological event (Fry & Martin, 1996; Lawrie, MacHale, Power & Goodwin, 1997; Wessely, Hotopf & Sharpe, 1998).  These investigators hypothesized that CFS patients had  interpreted physiological symptoms in a negative, catastrophic manner (Fry & Martin, 1996; Lawrie, MacHale, Power & Goodwin, 1997; Wessely, Hotopf & Sharpe, 1998).  This response, in conjunction with a perfectionist personality, may result in an inaccurate learned response to a bodily function (Fry & Martin, 1996; Lawrie, MacHale, Power & Goodwin, 1997; Wessely, Hotopf & Sharpe, 1998).  Investigators assert that patients who suffer from cognitive misinterpretation of a bodily function limit his or her physical activities.  This reaction can further perpetuate poor health and under-utilization of muscles.  This corollary can result in an increase in joint/muscle pain and overall malaises (Fry & Martin, 1996; Lawrie, MacHale, Power & Goodwin, 1997; Wessely, Hotopf & Sharpe, 1998). Investigators, who support the hypothesis that CFS is derivative of a psychiatric disorder, suggest a primary treatment approach that incorporates cognitive and behavioral interventions (Fry & Martin, 1996; Lawrie, MacHale, Power & Goodwin, 1997; Wessely, Hotopf & Sharpe, 1998).  These investigators assert that Cognitive/Behavioral treatment provides a patient with skills to accurately interpret bodily functions and develop appropriate, healthy responses to those functions.

The diagnosis of CFS is primarily determined by the exclusion of other possible physiological disorders.  This exclusionary process is due to the lack of a diagnostic medical test that is specific to CFS (Greg & Jones, 2001; Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Kroenke, 1991; Holmes, 1991).   Investigators recommend that several diagnostic evaluations be conducted on a routine basis to monitor possible physiological permutations: complete blood count, monitoring of erythrocyte sedimentation rate, biochemistry profile (to include electrolytes, serum creatinine and serum transaminases) and thyroid functioning tests (Gregg & Jones, 2001; Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Kroenke, 1991; Holmes, 1991; Manu, Lane, Matthews, 1993).  Many of the investigators report little justification in ordering elaborate and extensive studies such as CAT (computerized axial tomography) scans, MRI’s (magnetic resonance imaging), PET (positron emission tomography), SPECT (single-photon emission computed tomography) or BEAM (a brain scan that incorporates measurements of electrical brain activity) ( Kroenke, 1991; Holmes, 1991; Manu, Lane, Matthews, 1993; Shor, 2003). The studies have not shown to produce significant useful clinical information (Kroenke, 1991; Holmes, 1991; Manu, Lane, Matthews, 1993; Shor, 2003; Price, 2000; Akagi & Bass, 2001; Demitrack & Crofford, 1998; Demitrack, Cale, Straus, Lane, Listwak & Kruesi, 1991; Pagani & Lucini, 1999; Scott, Medbak & Dinan, 1998; Shor, 2003). 

Medical researchers continue to examine the many possible etiologic agents that may trigger the onset of CFS.  It is known that CFS is a heterogeneous disorder possibly involving an interaction of a number of physiological and psychiatric systems (Landay, Jessop, Lennette, & Levy, 1991; Lloyd, Hickie, Wilson, & Wakefield, 1994; Tirelli, Marotta, Improta, & Pinto, 1994; Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Gregg & Jones, 2001).  The exploration of the differential diagnostic process is essential to eliminating or identifying other possible medical conditions that mimic CFS.  A few of the medical conditions that may mimic CFS include hypoglycaemia, myophosphorylase deficiency, phosphofructokinase deficiency, metabolic muscle disorder, lipid storage myopathies, carnitine palmityltransferase and numerous other rare metabolic and endocrine disorders (Kroenke, 1991; Holmes, 1991; Manu, Lane, Matthews, 1993; Shor, 2003; Price, 2000; Akagi & Bass, 2001; Demitrack & Crofford, 1998; Demitrack, Cale, Straus, Lane, Listwak & Kruesi, 1991; Pagani & Lucini, 1999; Scott, Medbak & Dinan, 1998).  Other medical disorder such as fibromyalgia, irritable bowel syndrome, depression, and chronic headaches may coexist with CFS or be the primary medical disorder for related symptoms (Landay, Jessop, Lennette, & Levy, 1991; Lloyd, Hickie, Wilson, & Wakefield, 1994).   Therefore, the multifaceted symptomology associated with CFS ought to be considered when implementing a patient’s comprehensive diagnostic treatment plan (Landay, Jessop, Lennette, & Levy, 1991; Lloyd, Hickie, Wilson, & Wakefield, 1994; Tirelli, Marotta, Improta, & Pinto, 1994; Shor; 2003).

Investigators have suggested that a multi-disciplinary treatment approach is the most appropriate treatment modality for a patient diagnosed with CFS (Burns, Kubilus, Bruehl, Harden, Norman, & Lofland, 2003; Leibing, Pfingsten, Bartmann , Rueger, & Schuessler, 1999; Shor, 2003).   Investigators also recommend that the multi-disciplinary team should also include individualized treatment plans to accommodate the medical and psychological needs specific to a patient’s distinctive presentation, medical/personal reports, and psychiatric and physical involvement (Landay, Jessop, Lennette, & Levy, 1991; Lloyd, Hickie, Wilson, & Wakefield, 1994; Tirelli, Marotta, Improta, & Pinto, 1994; Gregg & Jones, 2001; Shor 2003).  Investigators, both medical and psychiatric practitioners, recommend that the treatment of a CFS patient may include exercise, diet, appropriate sleep hygiene, antidepressants, cognitive/behavioral therapy, and adjunct medications, depending on the patient’s idiosyncratic presentations (Craig & Sujani, 2002; Landay, Jessop, Lennette, & Levy, 1991; Lloyd, Hickie, Wilson, & Wakefield, 1994; Fry & Martin, 1996; Lawrie, MacHale, Power & Goodwin, 1997; Wessely, Hotopf & Sharpe, 1998; Shor, 2003; Kroenke, 1991). 

Cognitive/Behavioral Therapy (CBT) has been identified as the most effective psychiatric therapeutic intervention in the treatment of a CFS patient.  A medical practitioner’s role is to provide clinical data which identifies a patient’s physiological status.  The cognitive/behavioral therapist ascertains the patients’ psychiatric response and related symptomology to the medical data (Burns, Kubilus, Bruehl, Harden, Norman, & Lofland, 2003; Leibing, Pfingsten, Bartmann, Rueger & Schuessler, 1999).  This information is utilized by the therapist to determine the functional implications, and possible maladaptive cognitive/behavioral responses to this debilitating disorder (Burns, Kubilus, Bruehl, Harden, Norman, & Lofland, 2003; Leibing, Pfingsten, Bartmann, Rueger & Schuessler, 1999).  Investigators have concluded that a patients cognitive interpretation of pain and a chronic medical condition can potentially influence the development of either adaptive or maladaptive coping skills and related behaviors (Bradley, McKendree-Smith, & Cianfrini, 2003; Williams, 2003; Leibing, Pfingsten, Bartmann, Rueger, & Schuessler, 1999;  Burns, Kubilus, Bruehl, Harden, Norman, & Lofland 2003; Leibing, Pfingsten, Bartmann, Rueger, & Schuessle, 1999).  CBT interventions can be utilized to alter the continuation or possible occurrence of maladaptive and/or counterproductive cognitions and/or behaviors which may affect the quality of overall functional competence (Burns, Kubilus, Bruehl, Harden, Norman, & Lofland, 2003; Leibing, Pfingsten, Bartmann, Rueger, & Schuessle, 1999; Shor, 2003; Price, 2000; Akagi & Bass, 2001; Demitrack & Crofford, 1998; Demitrack, Cale, Straus, Lane, Listwak & Kruesi, 1991; Pagani & Lucini, 1999; Scott, Medbak & Dinan, 1998).

The primary cognitive factors that can be targeted by CBT are catastrophizing events and situations, perceived helplessness, diminished social/familial support system, identification with his/her disability and sense of self, depression, anxiety, and dysfunctional characteralogical features/behaviors that may affect the management of his or her disorder (Burns, Kubilus, Bruehl, Harden, Norman & Lofland,  2003; Leibing, Pfingsten, Bartmann, Rueger & Schuessler, 1999; Bradley, McKendree-Smith & Cianfrini, 2003; Williams, 2003; Leibing, Pfingsten,, Bartmann , Rueger & Schuessler, 1999). 

Researchers have hypothesized that there are five primary assumptions that inspire CBT interventions (Gregg & Jones 2001; Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Burns, Kubilus, Bruehl, Harden, Norman & Lofland,  2003; Leibing, Pfingsten, Bartmann, Rueger & Schuessler, 1999; Bradley, McKendree-Smith & Cianfrini, 2003; Williams, 2003; Leibing, Pfingsten,, Bartmann , Rueger & Schuessler, 1999).   The first assumption is that the individual’s method of processing information related to events and internal/ external stimuli has been altered with the onset of CFS.  The individual has preconceived societal perceptions concerning the effect of a chronic medical condition upon an individual.   These preconceptions can be negatively internalized concerning his or her chronic physical disorder.  The patient may then project outcomes based on these personal and societal preconceptions.  The second assumption is that cognitions interact with emotional and physiological reactions as well as with behavior.  The individual will possibly make assumptions based upon his or her physiological and emotional status and interpret the situation or event in a destructive framework.  This technique can possibly result in catastrophizing the medical diagnosis, and  episodes of depression and/or anxiety.  The third assumption is that behavioral responses may be influenced by environmental responses.  The influence and actions of providers, support network and societal stigmas may impact behavioral responses to a chronic medical condition.  The fourth assumption of CBT interventions is a holistic approach.  The CBT interventions address the emotional, cognitive and behavioral facets of the patient.  CBT offers the patient an opportunity to identify and define his or her reactions and belief system related to the presenting medical diagnosis.  The fifth assumption is that CBT interventions provide a realistic venue for the individual to become an active participant in developing adaptive coping skills to manage his or her illness.  The adaptive skills have the potential to empower the individual to develop and activate positive new strategies to cope and manage his or her pain and related symptoms associated with the diagnosed medical condition.

The treatment components of cognitive/behavioral interventions as they relate to the treatment of CFS are (1) education; (2) acquisition of skills; (3) rehearsal of reframed cognitive/behavioral responses and reactions; and (4) generalization and maintenance (Burns, Kubilus, Brueh, Harden, Norman, & Lofland, 2003; Leibing, Pfingsten, Bartmann, Rueger & Schuessler, 1999; Bradley, McKendree-Smith & Cianfrini, 2003;Williams, 2003; Leibing, Pfingsten, Bartmann, Rueger & Schuessler, 1999).  CBT can be an effective therapeutic intervention for individuals diagnosed with CFS.  The provision of accurate clinical medical information related to CFS can assist in the reduction the patient’s likelihood to catastrophize the physical and psychological impact of being diagnosed with CFS (Gregg & Jones 2001; Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994).  Accurate information can also preempt probable depressive and anxious responses commonly found in patients once the CFS becomes a definitive diagnosis (Hiroko, Klimes, & Bass, 2001; Shor, 2003,). CFS has numerous physical, cognitive and psychiatric symptoms which have the potential to immobilize and disenfranchise a patient from his or her sense of self (Hiroko, Klimes, & Bass, 2001; Shor, 2003).  The ability to develop strategies to compensate for the symptomology of CFS is essential in assisting the patient to maintain a level of quality and productivity in the his or her life.  These strategies empower the patient’s sense of control as well as enhance his or her possible fragile sense of confidence (Hiroko, Klimes & Bass, 2001; Gregg & Jones, 2001; Fakuda, Strauss, Hickie, Sharpe, Dobbins, & Komaroff, 1994; Shor 2003).  The daily practice and inclusion of these newly acquired skills can reinforce and substantiate the patient’s purpose and value in life as well as reinforce his or her ability to actively participate in living rather than becoming a passive observer.

A chronic medical condition has the potential to destroy or alter an individual’s life and perception of self.  A chronic medical condition, such as CFS, may also result in the development of characteralogical features that develop a patient’s persona of his or her sense of victimization.  This same chronic medical condition also has the potential to empower and challenge the individual to achieve newer heights of personal development, control and courage.  CFS represents a disorder that encompasses numerous physiological components that reportedly malfunction.  This malfunction results in the ineffective interplay of physiological and psychological systems.  The magnitude and unpredictability of CFS ymptomology challenge medical and psychiatric providers. This challenge is to provide a multi-disciplinary treatment approach to assist the patient to manage the many facets of this disease.  Those individuals who strive to develop adaptive strategies can potentially incorporate characteralogical empowerment features which can be a mechanism to manage a chronic medical condition while 
maintaining a productive, positive sense of self-worth, value and control.  CBT in conjunction with a multi-disciplinary medical approach can offer a patient a full array of physiological and psychiatric clinical interventions which has the potential to enhance the patient’s overall functioning. 

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