Plat de Resistance

            What is it about people and change? What is about people and the unknown? When really the unknown isn't all that “unknown.” The unknown is something more like we know, but we don’t like all the necessary steps between me and that. I mean, don’t get me wrong. I’m not totally callous to the issue. It isn't totally foreign to me merely because I’m the one on the other end advocating for that most dread of all things, change. No, please do not misunderstand. I’ve been on the “Forced to change” “Need to change” “I’m afraid of change” end of the stick myself. Yes, it’s true I do make a paycheck from resistance and it’s opposite; to some degree if it didn't exist then neither would I professionally. So, yes it is a bit of tangle for me; a “love/hate” sort of thing. But c’mon, it is the thorniest of thorns in my back side. If I could only somehow exist in alternate plain of reality where resistance was at least less resistant so when I encounter it I don't come off as bruised by the experience. Or if I somehow developed a neuromechanical device that I could implant in my limbic system allowing me to not feel the full of weight of resistance wrath then I would be much happier indeed.

            The long and short of it is, to really help I do have to allow some bruising of myself in order to help the other in their nastiest ways of being. For at the heart of resistance is fear and an absence of trust. Fear of being without protection, and absent in trust because change is facing the unknown. In order for the change to happen there must be a safety net of relationship in place. I have seen in my experience especially for the one trying to help, they must be willing to plumb the depths. Because the absent trust has thrust its victim deep, deep down into inner layers of self and isolation. Obstinately at this moment, as uncomfortable as a truth that this is, I am reminded of the protoevangelium- a ten cent term that refers to something further elaborated in Isaiah 53. THE Savior in order to save had to be hurt in the process. If I were smart, and took my cue from His example, I would realize this same principle applies to the everyday. All those “Little savings” require the bruising of the savior’s heel. I can’t help unless in my attempt to help I’ve allowed my heel to be bruised in the process. Then as the strongman C.S. Lewis described, can reach down into the depths carrying its prize with it to the sunlight.

How Family-of-Origins Impact Future Marital Relationships

        This study discussed the effects that a dysfunctional family-of-origin has on premarital couples and the maladaptive behaviors brought henceforth into future marriages. Many factors lead to marital dissolution and unhappiness, however, one of the leading causal factors in marital discord is hostile conflict. Researchers (Amato, 1996; Holman & Birch, 2001) have shown that disrupted and dysfunctional family-of-origin histories exert influence on future marital discord if issues are not recognized and worked through. I've heard it said that families are the laboratory of life, which means that we do most of our learning in the family context. The family is where we do the majority of leaning that impacts the rest of our lives. I think of it like training, the way your family of origin deals and respond to conflict teaches us how to deal with and respond to conflict in future relationships. How families manage money, perceive time, work, love, affection and so on affects all our future relationships. 

        Many people who come from "broken" family contexts leave thinking that they're leave all the drama, conflict and pain behind, only to unwittingly respond to future issues in similar ways they did when in their family context. Wherever we go we take with us all our past hurts, joys, pains, relationships, events and actions. Our response to various stimuli is a complex interaction of past events, actions and relationships with the new set of variables. This isn't to say that we don't grow and change, but to some varying degrees, we can never extricate ourselves from our family contexts. Our past and memories largely constitute our identity.

The intention of this study was to understand was to demonstrate empirically what was discussed above, how “select family-of-origin variables, measured premaritally, were predictive of hostile conflict in early marriage” (Topham, Larson & Holman, 2005). For premarital couples, having an understanding of what factors may cause hostile marital conflict in their future marriage would be incredibly valuable information. Unfortunately little to no research has been conducted on the connection between premarital factors and marital hostile conflict, there have only been correlations discovered between premarital factors and marital dissolution and unhappiness.  

        The theoretical frameworks Topham et al based their hypotheses on were Social Learning theory, Multi-generational family theory and Attachment theory. Each of these theories look at the role family-of-origin play in offspring’s future marital satisfaction, stability and the transmission of dangerous behaviors. Six hypotheses were tested but for the sake of brevity I will only mention those which provided statistical significance. The predictive factors for marital conflict included the wives’ family-of-origin environment and approach to discipline. This reinforces the notion that wives are the “gate-keepers” of marriage relationships, since those factors didn't significantly affect husbands. Topham et al proposed this may be that after marriage the wife's family maintains active contact with their daughter and new husband. This, in general, is not true of the husband’s family, they tend to "let go" easier. Therefore, it is likely that unhealthy behaviors, relationships and mindsets are maintained because of the wives’ continued contact with her family. This has been consistent with my own observations as well.

        The theories were well chosen for the issue of research and provided much insight into the phenomenon. The importance of this study is that it provides a tool for couples coming from dysfunctional families, allowing them to consciously recognize their family’s influence on their behavior and cognitions, and take steps to ensure a stronger and better informed marriage. To be forewarned is to be forearmed. The better understanding one can have of the problem, the more effectively one can step towards healing and growth.

References:

Amato, P. R. (1996). Explaining the intergenerational transmission of divorce, Journal of Marriage and the Family, 58, 628–640.

Holman, T. B. & Birch, P. J. (2001). Family-of-origin structures and processes and adult children’s marital quality. In T. B. Holman & Associates (Eds.), Premarital prediction of marital quality or break up: Research, theory, and practice. New York: Plenum Press.

Topham, G. L., Larson, J. H., & Holman, T. B. (2005). Family-of-origin predictors of hostile conflict in early marriage, Contemporary Family Therapy: An International Journal, 27, 101-121.

Ever Wonder if Your Mom was a Double? Part 3

Treatment for Capgras Syndrome

When looking for treatments of Capgras Syndrome, the search yielded little results. Most of the research offered psychodynamic interventions for patients suffering from Capgras Syndrome. The lack of neurological treatment for CS is largely due to the fact that not much is known organically about CS. In the past CS was thought to be purely a psychological issue, therefore explanations and subsequent treatments have been based on psychodynamic theory. Yet there is much debate over etiology, therefore, much research on psychopathology and neuropathology has continued. CS is usually co-morbid with schizophrenia and other mental illnesses. Treatment typically follows a therapeutic regimen of antipsychotic medication and supportive therapy in which areas of cognitive-behavioral strength are used to overcome weaker areas of functioning.  

Evidence is lacking that medications, principally antipsychotics, are effective in treating delusional disorder, yet delusions in the context of another psychotic disorder, such as schizophrenia, may respond better to treatment. It is necessary to note that subtypes of delusional disorder as specified in the Diagnostic and Statistical Manual of Mental Disorders (4th ed.; American Psychiatric Association, 1994) tend in general to be resistant to treatment. Particularly when assessing geriatric patients with delusions, it is important to consider delirium, dementia, and other organic etiologies underlying the thought disturbance.

Antipsychotics: 1^st Generation

The first-generation diphenylbutylpiperidine agent Pimozide (Orap) has been most closely studied in the context of the broader category of schizophrenia-like disorders but has been suggested by some to be differentially effective in the management of delusional disorder. Again, however, systematic trials are lacking (Manschreck, 2000) and initiation of the use of Pimozide to treat at least one form of delusional disorder (somatic delusions) has been traced to a case report involving no more than 5 patients (Elmer, George, & Peterson, 2000). These authors detailed the numerous adverse side effects associated with Pimozide use, particularly extrapyramidal reactions, the risks of Tardive Dyskinesia, and, notably, cardiac conduction defects. Other authors have not found Pimozide to be an effective agent in management of delusional disorder (Silva et al, 1998). A recent Cochrane review (Sultana & McMonagle, 2000) found that the use of Pimozide did prolong time to relapse in a range of psychotic disorders, including delusional disorder, although with a relatively wide confidence interval.

The cardiac side-effect profile of Pimozide is significant, and the U.S. Food and Drug Administration (FDA) has recently instructed the manufacturers of Pimozide to expand the warning label to reflect the risk of cardiac events (prolongation of the QT interval) when this medication is combined with numerous other compounds. This letter also addresses the risks of using Pimozide in patients with imbalances in serum potassium or magnesium (Food and Drug Administration, 2002). Baseline electrocardiography and special informed consent are recommended prior to its use.

Antipsychotics: 2^nd Generation

DeVane & Mintzer, (2003) reviewed studies which tested the efficacy of the drug Risperidone in a geriatric population with dementia, schizophrenia, delusional disorder, and other psychological and neurological disorder. There were some positive results, yet as Devane and Mintzer pointed out there were several problems with these studies that may invalidate their positive results. Just a few examples of the problems these studies had, the population were on several other drugs, the reductions of symptoms noted in the studies were of aggression and agitation and not of psychotic symptoms. DeVane and Mintzer (2003) did cite one study where adults and elderly patients were given low doses of Risperidone and rated on their improvement. On average, patients with schizophrenia, schizophreniform and delusional disorder were rated by therapists as having improved.

Lee et al. (2004) also did a meta-analysis of the research being done on Second Generation Atypical Antipsychotics, and found mixed results. Some studies showed a superiority of SGA’s to placebo, other studies showed little difference between second and first antipsychotics and others that found positive results. Their conclusion was that the evidence was mixed and in desperate need of further investigation before SGA’s can be recommended as a preferred treatment.

Even though atypical (i.e., second-generation) antipsychotics are increasingly prescribed for delusions or other behavioral or psychological manifestations of dementia and other neurological disease, none are indicated for this condition in the United States. These cautions notwithstanding, a recently published Expert Consensus Guideline for management of delusional disorder in older persons recommended risperidone, 0.75–2.5 mg/day, as the preferred treatment. Olanzapine, 5–10 mg/day, and quetiapine, 50–200 mg/day, were also listed as “high second line” treatments. Clozapine and first-generation antipsychotics were listed as third line treatments (Alexopoulos, Strehm, Carpenter, & Docherty, 2004).

Since SGA’s have low side effects much research has been done on this drug class, yet mostly with elderly populations. This is because elderly patients who have been unsuccessful with other medications have shown positive responses to SGA’s. Yet, SGA’s are not the perfect medication; they do cause weight and increase the risk for diabetes, which are huge risk factors for elderly patients. Their also associated with cardiac conduction problems, sedation, and orthostatic hypotension.

            Psychotropics have been shown not to be an effective medication for treating delusions. Because some patients with severe depression may express delusions (Maina, Albert, Bada, & Bogetto, 2001), and because delusions may have a strikingly obsessive quality to them, some authors have recommended treatment with antidepressants, particularly the selective serotonin reuptake inhibitors. This application, however, has not received systematic review, and the literature is limited to a handful of case studies. In a small case series (n = 4), patients with somatic delusions responded to the antidepressant clomipramine (Wada, Kawakatsu, Nadaoka, Okuyama, & Otani, 1999). As is the case for pharmacological treatment of delusional disorder, systematized studies of nondrug interventions are few. Some authors have presented data suggesting that cognitive-behavioral treatment was efficacious in treating delusions, but much of this is also based on single case studies (Garcelan & Yust, 2000).

Other authors have found that treatment of various psychoses, including delusional  psychosis, with an integrated model utilizing psychological and psychosocial treatments with a minimal medication regimen resulted in outcomes that were equal to or somewhat better than outcomes for patients treated with a standard medication regime. Lehtinen, Aaltonen, Koffert, Raekkoelaeinen, and Syvaelahti (2000) found that provision of an integrated treatment model allowed a much larger percentage of patients (42.9%) to avoid medication after the initial course of treatment. In contrast, only 5.9% of those in standard treatment groups required no medication.

We have only general guidelines to guide the use of psychopharmacology in delusional disorder. Limited data suggest that the disorder is not particularly responsive, and that response is not dose-related. It seems that low dose may be the best route for patients. The few case studies that address combined treatments suggest that patients have more sustained response and require less medication than those treated with drugs alone. There are not, however, standard rules that suggest the most efficacious integrated treatment regimens. Further study of the relative contributions of psychotherapy and medication in managing this challenging disorder are needed. However, it seems that an integrated treatment model have proven to be the most helpful thus far.

References

Alexopoulos, G. S., Strehm, J., Carpenter, D., & Docherty, J. P. ( 2004). The expert consensus guideline series: Using antipsychotic agents in older patients. Journal of Clinical Psychiatry, 65, (Suppl.2) 1– 41.

American Diabetes Association, et al. ( 2004). Consensus development conference on antipsychotic drugs and obesity and diabetes. Journal of Clinical Psychiatry, 65, 267– 272.

American Psychiatric Association. ( 1994). Diagnostic and statistical manual of mental disorders ( 4th ed.). Washington, DC: Author.

Alexander, M.P., Stuss, D.T., & Benson, D.F. (1979). Capgras's syndrome: A reduplicative phenomenon, Neurology, 29, 334-339.

Anderson, J.R. (1980). Cognitive psychology and its implications, San Francisco: W.H. Freeman.

Bekelman, D. B., & Hallenbeck, J. (2006). Capgras syndrome associated with morphine treatment, Journal of Palliative Medicine, 9, 810-813.

Berson, R. (1983). Capgras syndrome, American Journal of Psychiatry, 140, 969-978.

Berrios, G. E., Luque, R. (1995). Cotard’s syndrome: analysis of 100 cases, Acta

Psychiatr Scand, 91, 185-8.

Bourget, D., Whitehurst, L. (2004). Capgras syndrome: a review of the neurophysiological correlates and presenting clinical features in cases involving physical violence, Can J Psychiatry, 49, 719-25.

Brighetti, G., Bonifacci, P., Borlimi, R., & Ottaviani, C. (2007). ‘‘Far from the heart far from the eye’’: Evidence from the Capgras delusion, Cognitive Neuropsychiatry, 12, 189-197.

Christodoulou, G.N. (1977b). Treatment of the syndrome of doubles, Acta Psychiatrica Belgique, 77, 254-259.

DeVane, C. L., & Mintzer, J. ( 2003). Risperidone in the management of psychiatric and neurodegenerative disease in the elderly: An update. Psychopharmacology Bulletin, 31, 116– 132.

Doran, J. M. (1990). The Capgras syndrome: Neurological/neuropsychological perspectives, Neuropsychology, 4, 29-42.

Elmer, K. B., George, R. M., & Peterson, K. ( 2000). Therapeutic update: Use of Risperidone for the treatment of monosymptomatic hypochondriacal psychosis. Journal of the American Academy of Dermatology, 43, 683– 686.

Ellis, H. D., Lewis, M. B., Moselhy, H., & Young, A. W. (2000). Automatic without autonomic responses to familiar faces: Differential components of implicit face recognition in a case of Capgras delusion, Cognitive Neuropsychiatry, 5, 255 -269.

Enoch, D., Ball, H. (2001). Uncommon psychiatric syndromes, 4th edn. London : Arnold , 1–19.

Fialkov, M. J. and Robins, A. H. (1978). An unusual case of the Capgras syndrome, British Journal of Psychiatry, 132, 403-404.

Food and Drug Administration. ( 2002, Nov. 22). Letter to Teva Pharmaceuticals. Retrieved February 7, 2005, from www.fda.gov/cder/foi/appletter/2002/17473slr038ltr.pdf

Garcelan, S. P., & Yust, C. C. ( 2000). Effectiveness of individual cognitive-behavioural therapy applied to psychotic symptoms: Review of single case experimental designs applied to the treatment of delusional beliefs. Psychology in Spain, 4, 3– 12.

Gainotti, G. (1972). Emotional behavior and hemispheric side of the lesion, Cortex, 8, 41-55.

Gluckman, I.K. (1968). A case of Capgras syndrome, Australian and New Zealand Journal of Psychiatry, 2, 39-43.

Hacaen, H., & Angelergues, R. (1962). Agnosia for faces (prosopagnosia), Archives of Neurology, 7, 92-100.

Hayman, M.K., & Abrams, R. (1977). Capgras syndrome and cerebral dysfunction, British Journal of Psychiatry, 130, 68-71.

Koritar, E., & Steiner, W. (1988). Capgras syndrome: A synthesis of various viewpoints, Canadian Journal of Psychiatry, 33, 62-66.

Lee, P. E., Gill, S. S., Freedman, M., Bronskill, S. E., Hillmer, M. P., & Rochon, P. A. (2004). Atypical antipsychotic drugs in the treatment of behavioral and psychological symptoms of dementia:Systematic review. British Medical Journal, 329, 75– 78.

Lehtinen, V., Aaltonen, J., Koffert, T., Rakekkoelaeinen, V., & Syvaelahti, E. ( 2000). Two year outcome in first-episode psychosis treated according to an integrated model: Is immediate neuroleptization always needed?European Psychiatry, 15, 312– 320.

MacCallum, W. A.G. (1973). Capgras syndrome with an organic basis, British Journal of Psychiatry, 123, 639-642.

Manschreck, T. C. ( 2000). Delusional disorder and shared psychotic disorder. In B. J.Sadock & V. A.Sadock, Comprehensive textbook of psychiatry ( 7th ed., (pp. 1243– 1264). Baltimore: Williams & Wilkins.

Maina, G., Albert, U., Bada, A., & Bogetto, F. ( 2001). Occurrence and clinical correlates of psychiatric co-morbidity in delusional disorder. European Psychiatry, 16, 222– 228.

Milner, B. (1968). Visual recognition and recall after right temporal lobe excision in man,

Neuropsychologia, 6, 191-209.

Mullan, S., & Penfield, W. (1959). Illusions of comaprative interpretation and emotion, Archives of Neurology and Psychiatry, 81, 269-284.

Nejad A.G., Toofani K. (2006). A variant of Capgras syndrome with delusional conviction of inanimate doubles in a patient with grandmal epilepsy, Acta Neuropsychiatrica, 18, 52–54.

Paterson, A., & Zangwill, O.L. (1944). Disorders of visual spatial perception associated with lesions of the right cerebral hemisphere, Brain, 67, 331-358.

Pick, A. (1903). Zur pathologie des bekanntheitsgefu¨ hls (Bekanntheitsqualita¨ t), Neurol Centralblatt, 22, 2–7.

Ramachandran, V. S., & Blakeslee, S. (1998). Phantoms in the brain, Quill, 158-173.

Quinn, D. (1981). The Capgras syndrome: Two case reports and a review, Canadian Journal of Psychiatry, 26, 126-129.

Sautter, S. W., & Farkas, L. B. K. (1991). A neuropsychological profile of Capgras syndrome, Neuropsychology, 5, 139-150.

Schraberg, D., & Weitzel, W.D. (1979). Prosopagnosia and the Capgras syndrome, Journal of Clinical Psychiatry, 40, 313-316.

Schweinberger, R., & Burton , M. (2003). Covert recognition and the neural system for face processing, Cortex, 39, 9-30.

Sinkman, A. (2008). The syndrome of Capgras, Psychiatry, 71,371-378.

Silva, H., Jerez, S., Ramirez, A., Renteria, P., Aravena, N., Salazar, D., & LaBarca, R. ( 1998). Effects of pimozide on the psychopathology of delusional disorder. Progress in Neuropsychopharmacology and Biological Psychiatry, 22, 331– 340.

Staton, R.D., Brumback, R.A., & Wilson, H. (1982). Reduplicative paramnesia: A disconnection syndrome of memory, Cortex, 18, 23-36.

Stewart, J. T. (2004) Capgras syndrome related to diazepam treatment, Southern Medical Journal, 97, p65-66.

Sultana, A., & McMonagle, T. ( 2000). Pimozide for schizophrenia or related psychoses. In Cochrane Database of Systematic Reviews, 2000: Vol. 2Retrieved from www.cochran.org

Synodinou, C., Christodoulou, G.N., & Tzavaros, A. (1977). Capgras' syndrome and prosopagnosia, British Journal of Psychiatry, 132, 413-414.

Wada, T., Kawakatsu, S., Nadaoka, T., Okuyama, N., & Otani, K. (1999). Clomipramine treatment of delusional disorder, somatic type. International Clinical Psychopharmacology, 14, 181– 183.

Weston, M.J., & Whitlock, F.A. (1971). The Capgras syndrome following head injury, British Journal of Psychiatry, 119, 25-31.

Yalin, S., Varol Tas, F., Guvenir, T. (2008). The coexistence of Capgras, Fregoli and Cotard’s syndromes in an adolescent case, Archives of Neuropsychiatry, 45, 149-151.

Ever Wonder if You're Mom was Double? Part 2

Search for an Explanation

        What makes CS such an interesting subject for neuroscientists is the fact that CS patients believe that loved ones such as family members, long-time friends, and close co-workers have been replaced. But this delusional belief of doubles or impostors does not extend to those who they have no emotional connection with. In most CS cases the patients do not regard acquaintances, nurses, grocery store clerks or anyone else that they do not have a strong emotional tie with as a double or impostor (Ramachandran, 1998). Furthermore, in most CS case reports, patients believe that they are addressing their actual loved ones or family members when speaking to them on the phone (Yalin et al, 2008; Ramachandran, 1998). This point was further illustrated by a study done by Pick (1903), in which he studied a young man who believed that his mother had been replaced by an impostor when he looked at her. However, “her voice still elicited a strong feeling of familiarity.” This suggests that the cause of CS may be contained to an optical malfunction or lesion in the visual pathway; since patients do not experience any CS symptoms when listening to their loved ones.

        Ellis, Lewis, Moselhy & Young, (2000) and Schweinberger & Burton, (2003) wanted to see if there was any validity to the optical theory. They discovered that individuals with Capgras syndrome do not have any optical impairment. If patients did this finding would explain their inability to recognize family members, friends and co-workers faces. But the research showed that they do recognize faces; however, they lack the ability to match a face that they recognized with the any emotions. “Opposite to the pattern observed in prosopoagnosia, Capgras subjects recognize the structural features of familiar faces but may have impairments in the affective route to face recognition as documented by the SCR hyporesponsiveness”( Brighetti, Bonifacci, Borlimi & Ottaviani, 2007). Ellis et al. and Schweinberger et al. demonstrated that CS patients have no optical malfunctions and that they can recognize loved ones faces normally. CS patients possess the ability of emotional expression and of facial recognition; however, there seems to be a severing in the link between the primary emotional and recognition centers. In his book, “Phantoms in the Brain”, Ramachandran proposes his own theory for CS. He thought there was a neurological disconnection between temporal lobe areas involved with facial recognition, such as the Hippocampus, and the emotional center in the brain, the amygdala. Along with Ramachandran many other neuroscientists are arriving at similar conclusions, that CS has an organic basis in the brain.

        As stated before, investigations into the neurological causation of Capgras Syndrome are a recent phenomenon, taking place within the last forty years. One of the first studies that drew attention to the organic etiology of CS was done by Gluckman in 1968. The woman he studied believed that her husband was an impostor; she was subsequently diagnosed with paranoid Schizophrenia. Gluckman put her through a computerized axial tomography scan and found “severe cerebral atrophy” (Doran, 1990). This study and the growing suspicion of other researchers, that CS has an organic causation, opened the door to further neurological research. Three years later Weston & Whitlock (1971) presented their case of a twenty year old man who underwent severe head trauma and then exhibited symptoms of CS. Weston & Whitlock (1971) described the damage as “frontal lobe syndrome with evidence of bilateral temporoparietal damage, a severe memory defect, and mixed dysphasia along with generalized impairment” (Doran, 1990). They suggested that this damage to the temporal and parietal lobes lead to the patient’s inability to “integrate memory, perception, and affect.” And that these dysfunctions were primary factors in the formation of CS (Doran, 1990).

         Other studies have demonstrated a strong link between CS and physical disorders. In certain cases CS symptoms remitted at the same time that the physical illness remitted (Christodoulou, 1977b).  Further evidence of CS’s organic basis was found by MacCallum (1973). In three out of five cases MacCullum demonstrated the onset of CS as a result of “anoxia, basilar migraine, [and] alcoholic encephalopathy” (Doran, 1990). He also observed that when the physical symptoms were remedied so were the delusional perceptions and beliefs of the patients.  Based on these results, “MacCallum hypothesized that these organic conditions caused a change in the patients' affects and perceptions, which then led to the appearance of the Capgras syndrome. With a remission of the organic condition, affect and perception returned to normal” (Doran, 1990). These findings strongly support the suggestion that CS is caused by organic factors. Other studies have linked CS with “right-sided cerebral dysfunction” (Hayman & Abrams, 1977), which turns the focus of this discussion to current emerging theories of CS.

        Doran (1990) reviewed the current neurological theory on Capgras Syndrome. He pointed out that initial importance is given to the distinction between the reduplication of a person or place. In neurological literature the reduplication of a place is termed “reduplicative paramnesia”; however, within psychiatric literature the reduplication of a person is termed Capgras Syndrome. The common perception is that these reduplicative disorders are one in the same; the only difference between the two is the object of the duplication, a person or a place. Doran went on to say that, “The cerebral localization and mechanism of action could essentially be the same.” Alexander, Stuss & Benson (1979) and Staton, Brumback & Wilson (1982) both had cases in which duplication of a “person” and of a “place” were demonstrated in their patient. Lesions in the right hemisphere have been found to be the primary cause of duplicative symptoms.

        This finding leads to the central thrust of this theory, the right hemisphere. Research of the,

“Right hemisphere lesions may lead to disturbed visuospatial analysis (Paterson & Zangwill, 1944), impaired facial recognition and memory (Hacaen & Angelergues, 1962; Milner, 1968), abnormal sensations of general familiarity andjamais vu (Mullan & Penfield, 1959), and abnormally flat or euphoric disorders (Gainotti, 1972)”(Doran, 1990). Furthermore, the right hemisphere has connections between “facial recognition, visual memory, and feeling and familiarity” (Quinn, 1980; Schraberg & Weitzel, 1979; Synodinou, Christodoulou, & Tzavaros, 1977).

         According to these findings, Alexander (1979) and numerous other researchers concluded that the “right hemisphere is the seat of dysfunction producing the delusional symptom of Capgras” (emphasis in original).  The dysfunctions that occur if the right hemisphere is damaged fit the descriptions of Capgras Syndrome perfectly. Staton (1982) hypothesized that a disconnection occurs between old memory stores and new memory registration. He also suggests this area of damage happens specifically in the “right posterior hippocampus and right temporo-parieto-occipital junction.” Another recent study proposes that the dysfunction is subcortical (Anderson, 1980). Based on this evidence, it is hypothesized that Capgras Syndrome is the result of a disconnect between the “hippocampus and the hypothalamic/amygdala circuit” (Doran, 1990). In other words, a CS patient still recognizes a loved one in every sensory way, but does not recognize them emotionally; due to a disconnection between emotion and memory. This conclusion, again, supports the previous assertion that Capgras Syndrome is the result of an organic disconnection between emotion and memory made by Ramachandran, Ellis (2000), and Schweinberger (2003).

Ever Wonder if Your Mom was a Double? Part 1

           In 1923 there was an unusual case in Paris of a woman who complained to the police that there were strange children imprisoned in her basement. She was also convinced that there were more children imprisoned throughout the city. Her delusional state consisted of an elaborate system which centered around two main themes: first, the belief that she had been substituted at birth and was an heiress. Second, the belief of an elaborate plot against her that involved thefts, poisonings, changes in her body’s appearance and substitutions of her family, herself and others in her environment (Sinkman, 2008). Accompanying her misidentification symptoms were psychotic features, persecutory hallucinations and other signs of severe mental illness.  This odd set of symptoms caught the attention of French psychiatrist Joseph Capgras. Capgras’ and Reboul-Lachaux’s research on this woman, later referred to as Mme M., eventually became the basis for a new set of disorders, categorized as “misidentity” or “false identity” syndromes.

Delusional Misidentity Syndrome

            Research with Mme. M led subsequent researchers to discover a whole range of disorders which they classified as Delusional Misidentity Syndrome (DMS). Included in the category is, firstly, Fregoli Syndrome (FS), in which a patient “holds the belief that a persecutor takes on the appearance of various people at different times” (Sinkman, 2008). FS can be associated with a persecutory misidentification of people; however, this is not always the case. It can also be an over-misidentification of one face on others. FS can also extend to misidentification of places as well as people. Second is Intermetamorphosis Syndrome, where the patient believes that an individual can transform into another person. Third, Cotard Syndrome, a disorder consisting of the delusional perception that one is dead or that a particular body part is dead (Berrios & Luque, 1995). Finally, Capgras Syndrome (CS), which will be discussed in detail later on. Variations of misidentity syndromes have arisen in the past; nevertheless, those listed above are the main syndromes within the DMS category. Patients who are diagnosed with a misidentity syndrome often have co-occurring or comorbid disorders such as schizophrenia and paranoia, or other misidentity syndromes (Fialkov & Robins, 1978; Koritar & Steiner, 1988).

Capgras Syndrome

            Capgras Syndrome defined by Joseph Capgras was “the illusion of doubles” (Enoch & Ball, 2001). A current definition of classic Capgras syndrome is a state in which “the patient believes that a person usually closely related to him has been replaced by an exact double” (Nejad & Toofani, 2006). Since Capgras Syndrome was first discovered, there has been a dichotomy in thinking. Some believe the source of CS to be psychological; while others believe it to be organic, resulting from a brain lesion or atrophy (Gluckman, 1968).  Unfortunately, the bulk of research since CS was discovered has shed little light onto the neurological causes. It’s only been very recent that neurological research has been conducted on the disorder. So far explanations for its etiology have varied from “neuro-psychiatric or organic and neurological diseases, including dementia, head trauma, epilepsy, cerebrovascular disease, neurodegenerative disease, most commonly lewy body disease and multiple sclerosis” (Bourget, & Whitehurst, 2004). Behavioral and psychodynamic explanations for Capgras range from “psychosis, paranoia, pathological splitting of a significant other, and changes in the crucial interpersonal relationship” (Berson, 1983).

Helpful Website Resources for Premarital and Married Couples, and Families

CYFERnet – www.cyfernet.org

(Description provided by the handout).

Fighting for Your Marriage- the PREP Approach www.prepinc.com

 (Description provided by the handout).

Health and Age – www.healthandage.com

 (Description provided by the handout).

Marriage Alive – www.marriagealive.org

(Description provided by the handout).

Marriage and Couple Relationship Website – http://citnews.unl.edu/marriage/

(Description provided by the handout).

Marriage Builders – www.marriagebuilders.com

(Description provided by the handout).

Michele Weiner Davis – www.divorcebusting.com

(Description provided by the handout).

National Council on Family Relations – www.ncfr.org

(Description provided by the handout).

PREPARE/ENRICH Program – www.lifeinnovations.com

(Description provided by the handout).

Real Relationships- www.realrelationships.com

(Description provided by the handout).

Smart Marriages – www.smartmarriages.com

(Description provided by the handout).

Stepfamily Association of America – www.saafamilies.org

(Description provided by the handout).

Focus on the Family – www.focusonthefamily.com

Provides short and comprehensive articles on various topics relating to marriage. Offers podcasts, times for broadcasts, newsletters, online community and bookstore. One of the main selling points of this website is that you can create a personalized webpage and e-newsletter for your family.

Crown Financial Ministries – www.crown.org

Offers financial resources and tools for financial planning. Locate local budget coaches, read articles concerning financial “hot topics”, listen to free downloadable podcasts on finances. Sells financial literature for couples along with a newsletter.

Blended Families – www.blended-families.com/

Addresses the issues encountered by blended families through a myriad of literature, free newsletter, booking for seminars, remarriage coaching by trained professionals and teleclasses.

Parent Trust For Washington Children – www.parenttruts.org

Comprehensive advice index on a variety of parenting categories (i.e. child development, early learning, health safety, stress management etc…). Also an online video about planning for a family, other options are ideas for fun family activities, education resources (telephone support, new parent services, child and teen services, notifications of community events). Lists books and local classes.

FamilyFun.com – http://familyfun.go.com/

A site filled with fun activities that the whole family can participate in such as game ideas, crafts, how-to videos, travel resources etc…

National Healthy Marriage Resource Center – http://www.healthymarriageinfo.org/

Specializes in providing research, statistics, information about national programs, initiatives and provides an “online library for resources related to research and issues impacting Healthy Marriage.”

FindingStone Counseling Center: A Family Stress Test - http://www.findingstone.com/services/tests/familystresstest.htm

A measurement to help evaluate family stress levels.

Central Oregon Family Resource Center – http://www.frconline.org/about.html

Offers resources for parents and families living in Oregon, other resources are parenting education, community resources and referrals. 

How We See Our Bodies

           What Influences how we view our own bodies and the bodies of others? What basis do we use to judge? What basis do we use to be happy or dissatisfied with our bodies? There is a disorder in the DSM IV-TR called Body Dysmorphic Disorder, also known as BDD. It is defined as “a preoccupation with some imagined defect in appearance by someone who actually looks reasonably normal” (Abnormal Psychology, pg. 185). The presence of this disorder in our society serve to illustrate a point of how we see ourselves and others. We have a distorted basis for judging an attractive or fit body, and because of that we have created undue pain for ourselves. The warning signs for BDD include:

·         Constantly picking at the skin or touching the face

·         Spending excessive time trying to hide the perceived defect with clothing or makeup

·         Constantly comparing body parts to others and seeking reassurance

·         Having problems at work or school because of being overly self-conscious

·         Seeking out multiple dermatologists or plastic surgeons 

(http://www.everydayhealth.com/eating-disorders/distorted-perspective-of-body-dysmorphic-disorder.aspx)

Possible causes may be:

·         Having a close biological relative with body dysmorphic disorder

·         Being teased or bullied as a child

·         Low self-esteem

·         Having an anxious temperament 

(http://www.everydayhealth.com/eating-disorders/distorted-perspective-of-body-dysmorphic-disorder.aspx)

           However, there are two possible causes I would like to look at in detail, that is culture and gender. First, depending upon the culture and or sex of the person dealing with BDD, the definition will remain fairly static, but the presenting symptoms will be modified. Culture is the reason for this modification, for example in Western culture especially with, but not limited, to women there is an overwhelming concern with being thin. However we are seeing some change in this trend. Traditionally men have been expected to attain the "V" shape body type, and women the hourglass body shape. Both men and women are feeling the pressure to conform to an "I" body shape. Historically, people in our culture have struggled with BDD, but are dissatisfied with different body parts and shapes, and this is due to the fluctuating nature of idealized body types in our culture.
          These shapes are obviously not universal law of attractiveness since so many other cultures do not hold these same standards, for example the African-American community highly values a very curvaceous and voluptuous female figure. Other examples range from the Ugandans and Ethiopians inserting large disks into their lower lips to women in Burma wearing brass neck rings to lengthen their necks. And as I've said, these cultural values are subject to change.

           The second factor that influences how we see our bodies is gender. In Western culture when it comes to body image men usually focus on genitals, receding hairline, body building and muscle defects. As opposed to women who tend to focus on breasts, hips and waist size and who predominately develop eating disorders to fit into the mold. Gender like culture plays a significant role in how we perceive our bodies. 

Reference

 Barlow, David H. & Durand, V. Mark (2008).   Abnormal Psychology: An Integrated Approach, CengageNOW™

Understanding the Diagnostic Statistical Manual

            The mulitaxial diagnostic system was first introduced in the DSM-III-R, which evaluates and diagnoses clients on a multi-dimensional level. The multiaxial diagnostic system evaluates a person on five axes or dimensions, allowing the clinician to have a more complete picture of a person. A person may have a psychological disorder that may not affect their functionality, using this model would allow a clinician to come to a better determination than previous models.
            In the current DSM (DSM-IV-TR) the five axes of the multiaxial diagnostic system are: developmental disorders, learning disorders, motor skills disorders and communication disorders are categorized as Axis I. Axis II is personality disorders and mental retardation, Axis 3 is physical disorders and conditions, Axis 4 is psychosocial and environmental problems and Axis 5 which is clinician rated level of adaptive functioning.
           For example, a clinician using the multiaxial model to evaluate a client with OCD, would classify the client as having an Axis 1 category disorder. Yet the process doesn't end here, the client could be dealing with multiple problems related or non-related to his OCD. Let's suppose upon further inquiry it becomes clear that he also suffers from Schizoid personality disorder, which is an Axis 2 category disorder. The man did not have any physical conditions so no diagnosis is needed for Axis 3. In his Axis 4 assessment, the client was dealing with occupational difficulties and marital problems. And the clinicians rated score of the client's functionality was a 55, which shows slight obstruction with his functioning. The patients presenting symptoms and subsequent diagnosis require some information and guidance for treatment, but in light of the multiaxial model just demonstrated the clinician has a clear idea of what the problem is and how to treat the patient. 
         As a side not, this is all likely to change in the very near future since the DSM V is coming out with an entirely new system for diagnosing clients. 

Pathogenesis: Understanding How Disorders Develop

            To understand how disorders develop we need a conceptual framework to understand the disorder. The Diathesis-stress model is one of the more recent model that give us a way of understanding disorders, the model is also called the Epigenetic model. The Model proposes that people have a genetic tendency for a behavioral trait inherited from their parents that is activated under certain environmental conditions. In the textbook Abnormal Psychology: An Integrated Approach written by Barlow and Durand an example is provided of a girl who had “blood-injury-injection phobia”. This girl never had any episodes of fainting or becoming nauseated at the sight of blood or of any other injury, until she was unintentionally forced to watch a video of an animal dissection. This environmental trigger activated the gene expression which altered her behavior. Henceforward, at the mere mention of a cut or blood she would faint. The Barlow and Durand go on to say that if this girl had never taken a biology course the gene expression (diathesis) caused by an environmental trigger would have never happened and she would have gone through her life without knowing of her own tendency for swooning at the sight of blood.
            This model allows us to understand how twins possessing identical genetic makeup could in one circumstance develop a disorder and not in the other. Separated at birth, parents divorce, one twin is kidnapped and raised by his captors, there are many possibilities in which twins could be separated and raised in two different environments thus exposing one twin to certain environmental triggers and not to the other. Therefore, one twin experiencing different environment triggers could develop a disorder like clinical depression and the other twin experiencing a different environment could not. According to this model it would all be determined by the environment and the genetic tendencies inherited by that person’s parents.

Reference

 Barlow, David H. & Durand, V. Mark (2008).   Abnormal Psychology: An Integrated Approach, CengageNOW™