By V. Gorn. State University of New York College of Agriculture and Technology, Cobleskill. 2019.
Shasmaei purchase glucophage sr 500 mg overnight delivery, Rahimi glucophage sr 500 mg on-line, Zarabian & Sedehi (2008) demonstrated in their controlled clinical trial (N = 120) that the combination treatment of cognitive therapy and pharmacotherapy was significantly more effective than the two treatments alone cheap glucophage sr 500mg without prescription. Combined treatment was also significantly better in severely depressed clients (Thase et al quality glucophage sr 500 mg. The Clinical Guidelines for the Treatment of Depressive Disorders by the Canadian Psychiatric Association and the Canadian Network for Mood and Anxiety Treatments (Segal et al. If the client suffers from both depression and anxiety symptoms, therapy for depression should be seen as the main priority. For clients with mild depression, exercise, guided-self help, or brief psychotherapy or counselling can be considered. It might also be helpful to provide advice on sleep hygiene and anxiety management. Positive outcomes are related to a good therapeutic relationship, proficiency of the therapist and exposure of the client to contents of behavioural or emotional avoidance. The psychological, social and physical characteristics and the relationships of the client should be considered during therapy. Inpatient treatment could be considered for clients with increased suicide risk or risk of self-harm. The psychotherapist or counsellor should be competent to assess and manage the risks, or refer the client to another health professional when necessary. For clients with severe or chronic depression a combination of psychotherapy and antidepressant medication may be helpful and therapists should work in collaboration with the clients medical practitioner, where possible. It has been recommended that antidepressant medication should be continued for at least 4-6 months after full remission (Montgomery, 2006). Summary and conclusion It can be concluded, based on current empirical evidence, that no therapeutic approach seems to be superior to others for the treatment of mild to moderate depression. Interpersonal psychotherapy and behavioural therapy have also received substantial empirical support and can therefore also be recommended for depression. Nondirective supportive treatment seems slightly less efficacious than other treatments (Cuijpers et al. Antidepressants may be used for moderately to severely depressed clients but have not been recommended for the treatment of mild depression. Although empirical results of efficacy studies comparing psychotherapy and drug treatment are inconsistent, results suggest lower relapse rates after psychotherapeutic treatment than antidepressant treatment alone. The literature suggests that a good therapeutic relationship, a therapeutic approach according to the clients choice and adequate length of treatment with continuation of treatment to full remission and relapse prevention, are important for a successful treatment of depression. Practice guidelines for the treatment of patients with major depressive disorder (2nd ed. Evidence-based guidelines for treating depressive disorders with antidepressants: A revision of the 2000 British Association of Psychopharmacology guidelines. Evidence-based guidelines for treating depressive disorders with antidepressants: A revision of the 1993 British Association for Psychopharmacology guidelines. A cost-effectiveness analysis of cognitive behaviour therapy and fluoxetine (prozac) in the treatment of depression. Outcome of time-limited psychotherapy in applied settings: Replicating the second Sheffield psychotherapy project. Sequence of improvement in depressive symptoms across cognitive therapy and pharmacotherapy. Psychological interventions for major depression in primary care: A meta- analytic review of randomized controlled trials. Prevalence of anxiety and depression in Australian adolescents: Comparisons with worldwide data. Psychodynamic psychotherapy and clomipramine in the treatment of major depression. Mindfulness-based cognitive therapy: Evaluating current evidence and informing future research. Psychotherapy for depression in adults: A meta-analysis of comparative outcome studies. Are individual and group treatments equally effective in the treatment of depression in adults? Psychotherapy alone and combined with pharmacotherapy in the treatment of depression. Speed of action: The relative efficacy of short psychodynamic supportive psychotherapy and pharmacotherapy in the first 8 weeks of a treatment algorithm for depression. Short psychodynamic supportive psychotherapy, antidepressants, and their combination in the treatment of major depression: A meta-analysis based on three randomized clinical trials. Relative efficacy of psychotherapy and pharmacotherapy in the treatment of depression: A meta- analysis. A systematic review of research findings on the efficacy of interpersonal therapy for depressive disorders. Empirically supported individual and group psychological treatments for adult mental disorders. Medications versus cognitive behaviour therapy for severely depressed outpatients: meta-analysis of four randomized comparisons. Randomized trial of behavioral activation, cognitive therapy, and antidepressant medication in the acute treatment of adults with major depression. Mindfulness-based cognitive therapy for treatment-resistant depression: A pilot study. Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program. National Institute of Mental Health Treatment of Depression Collaborative Research Program: General effectiveness of treatments. Treating depression: The beyondblue guidelines for treating depression in primary care. Comparative effects of cognitive- behavioral and brief psychodynamic psychotherapies for depressed family caregivers. The effects of adding emotion- focused interventions to the client-centered relationship conditions in the treatment of depression. Experiential therapy of depression: Differential effects of client-centered relationship conditions and process experiential interventions. Development of gender differences in depression: An elaborated cognitive vulnerability-transactional stress theory. Short-term psychodynamic psychotherapy for depression: An examination of statistical, clinically significant, and technique-specific change. Treatment-resistant depressed patients show a good response to mindfulness-based cognitive therapy. New developments in psychosocial interventions for adults with unipolar depression. Comparative effects of short-term psychodynamic psychotherapy and cognitive-behavioral therapy in depression: A meta- analytic approach. Short-term psychodynamic psychotherapy: Review of recent process and outcome studies. Randomised controlled trial of interpersonal psychotherapy and cognitive-behaioural therapy for depression. Mindfulness-based cognitive therapy for depression: Replication and exploration of differential relapse prevention effects. The efficacy of group psychotherapy for depression: A meta-analysis and review of the empirical research. The clinical effectiveness of guided self-help versus waiting-list control in the management of anxiety and depression: a randomized controlled trial. Mindfulness predicts relapse/recurrence in major depressive disorder after mindfulness-based cognitive therapy. Recurrence after recovery from major depressive disorder during 15 years of observational follow-up. Treatments for late-life depressive conditions: A meta-analytic comparison of pharmacotherapy and psychotherapy.
Although an explanation for the unexpected control therapy aimed at reducing A1C 6 generic 500 mg glucophage sr free shipping. The mean duration of dia- glycemia in these trials was 2 to 3 times higher in the intensive betes was 8 years cheap glucophage sr 500mg with visa. Therefore purchase 500 mg glucophage sr visa, it has been suggested that a tight glycemic vascular events in the intensive control group trusted glucophage sr 500mg, mainly through a 21% control with a target A1C of 6. Such multifactorial interventions have recently uria was signicantly reduced in the intensive-treatment partici- been suggested to lead to not only signicant microvascular and pants, with 9. The salient results of this study include: However, during an observational median follow up of 9. Avoid symptom- has been the lack of well-designed, long-term outcome studies atic hyperglycemia and any hypoglycemia. Level 2 (1) for type 2 diabetes] Although, nontraditional glycemic targets, such as fructosamine b. Bajaj reports personal fees from Abbott; grants and per- mizing hypoglycemia duration, severity and frequency. Intensive blood-glucose control Intensive glucose control with lowering A1C values to 7. Effect of intensive com- progression of retinopathy in the diabetic control and complications trial. The association between symptom- 20 studies of 95,783 individuals followed for 12. Diabetes Care atic, severe hypoglycaemia and mortality in type 2 diabetes: Retrospective epi- 1999;22:23340. Is the current denition for diabetes relevant to health gains with plasma glucose level lowering in type 2 diabetes mellitus. The relation of fasting and 2-h postchallenge older adults with tight glycemic control. Postprandial blood glucose predicts car- 21 years follow-up on the Steno-2 randomised trial. Diabetologia 2016;59:2298 diovascular events and all-cause mortality in type 2 diabetes in a 14-year 307. Translating the A1C assay into estimated fasting blood glucose concentration, and risk of vascular disease: A collabora- average glucose values. The effect of intensive treatment of diabetes on the development and patients: Variations with increasing levels of HbA(1c). Diabetes Care progression of long-term complications in insulin-dependent diabetes melli- 2003;26:8815. Intensive insulin therapy prevents the cemia on overall glycemic control in type 2 diabetes Importance of postpran- progression of diabetic microvascular complications in Japanese patients with dial glycemia to achieve target HbA1c levels. Diabetes Res Clin Pract non-insulin-dependent diabetes mellitus: A randomized prospective 6-year study. Writing Team for the Diabetes Control and Complications Trial/Epidemiology precedes stepwise deterioration of fasting with worsening diabetes. Persistent effects of intensive glycemic label, treat-to-target non-inferiority trial. Circulation blood glucose control and vascular outcomes in patients with type 2 diabetes. New Engl J Med 2015;372:2197 in participants with type 2 diabetes at high cardiovascular risk. Variation of fasting plasma glucose: A predictor of ment of type 2 diabetes mellitus on cardiovascular outcomes: A meta-analysis mortality in patients with type 2 diabetes. Can J Diabetes 42 (2018) S47S53 Contents lists available at ScienceDirect Canadian Journal of Diabetes journal homepage: www. In some circumstances, such as when signicant changes blood sampling (days 0 to 30) contributes 50% of the result and the are made to therapy or during pregnancy, it is appropriate to check A1C prior 90 to 120 days contributes 10% (2,3). Testing at 6-month intervals may be consid- capacity to use the information from testing to modify healthy behaviours ered in situations where glycemic targets are consistently achieved or self-adjust antihyperglycemic agents. A1C may also be used for the diagnosis of diabetes in adults (see Screening for Diabetes in Adults chapter, p. In 2007, a consensus statement from the American Diabetes Association, European Association for the Study A1C is a measurement of your average blood glucose control for the last of Diabetes and the International Diabetes Federation called for A1C 2 to 3 months. For those who wish and medication changes that will improve your blood glucose levels. Point-of-care A1C analyzers are bench-top instruments that use a nger-prick capillary blood sample. They are designed for use in a health-care providers oce, a treatment room or at a bedside. The blood is applied to a test cartridge and the sample is analyzed 1499-2671 2018 Canadian Diabetes Association. It can increase ones empowerment and adherence to potential advantages over laboratory A1C testing, including rapid treatment. It can also provide information to both the person with test results to expedite medical decision-making, convenience for diabetes and their diabetes health-care team to facilitate longer-term people with diabetes, potential improved health system eciency treatment modications and titrations as well as shorter-term treat- and improved access to testing for underserved populations (12). Care should be taken to select an appropriate meter with an Most trials in noninsulin-treated people with type 2 diabetes are alternative glucose measurement method in such situations. In the Structured Testing sites other than the ngertip (forearm, palm of the hand, thigh). At 1 year, there was a signicantly greater accurately reect glycemic status than forearm or thigh testing reduction in mean A1C in the structured testing group compared (63,64). In comparison, blood samples taken from the palm near with the active control group (0. Treatment decisions for the A1C cohort were based strictly acetoacetate through urine testing may not identify the onset and on A1C test results. For most individuals with diabetes, A1C should be measured approxi- a preset limit. A blinded (sometimes referred to as professional) mately every 3 months to ensure that glycemic goals are being met or main- tained [Grade D, Consensus]. Testing at least every 6 months should analysis by the health-care provider (typically in conjunction with be performed in adults during periods of treatment and healthy behaviour the user). Individuals with type 1 diabetes should be instructed to perform ketone up to 14 days. Blood ketone testing methods may be Novel Glucose Sensing Technology on Hypoglycaemia in Type 1 preferredoverurineketonetesting,astheyhavebeenassociatedwithearlier detection of ketosis and response to treatment [Grade B, Level 2 (67)]. S36 hypoglycemia by 54%, reduced glycemic variability and improved Targets for Glycemic Control, p. There was a statistical reduction in A1C for Glycemic Management in Adults with Type 1 Diabetes, p. Glycated hemoglobin and the risk of kidney Recommendation Tool for Health-Care Providers disease and retinopathy in adults with and without diabetes. Self-monitoring of blood glucose levels and glycemic control: The Northern California Kaiser Permanente Diabetes reg- istry. Longitudinal study of new and preva- Author Disclosures lent use of self-monitoring of blood glucose. Woo has self-monitoring on metabolic control and quality of life in type 2 diabetic patients: An urgent need for better educational strategies. Self-management education for adults with type 2 diabetes: A meta-analysis of the effect on glycemic control. Integrating medical management with diabetes self-management training: A randomized control trial of the Diabe- 1. Mean blood glucose and biological varia- tes Outpatient Intensive Treatment program. Diabetes Care 2003;26:3048 tion have greater inuence on HbA1c levels than glucose instability: An analy- 53. Diabe- treated type 2 diabetes: Results from the Structured Testing Program study. Guidelines and recommendations for improves glycemic control in stable, insulin-treated veterans with type 2 laboratory analysis in the diagnosis and management of diabetes mellitus. The effect of intensive treatment of diabetes on the development and national Diabetes Federation.
Diagnosis is difficult in cysticercosis buy 500mg glucophage sr with mastercard, which is done by different clinical and laboratory criteria discount glucophage sr 500mg. Hatching of eggs occurs in the small intestine where they penetrate the villus and become cysticercoid cheap 500 mg glucophage sr with amex. Since this tapeworm consumes a lot of vitamin B12 and interferes with its absorption purchase 500mg glucophage sr free shipping, it can cause vitamin B12 deficiency; and some patients develop megaloblastic anemia. Diagnosis: Diagnosis is reached by demonstration of characteristic eggs in the stool. B further reading Module on intestinal parasitosis, by Health Science College, Hawassa University 55 Internal Medicine 3. List the etiologies & animal reservoirs of the different types of leishmaniasis 4. Refer suspected cases of leishmaniasis to hospitals for investigation & treatment 12. Design appropriate methods of prevention andcontrol of leishmaniasis Definition: is an infectious disease caused by the protozoa called Leishmania Classification of leishmaniasis There are three major clinical forms of leishmaniasis: Visceral leishmaniasis Cutaneous leishmaniasis Mucocutaneous leishmaniasis Etiologic Agents The different clinical forms of leishmaniasis (listed above) are caused by different species of leishmanial parasites which are listed under each of these diseases. The parasites are seen in two forms Leishmanial form:- ( amastogote ) this is non flagellate form seen in man and extra human vertebrate reservoir Leptomonad forms (also called promastigotes) are flagellated forms The parasite is transmitted by the bite of vectors of the species phlebotomus, Sand flies 56 Internal Medicine Life Cycle of Leshimaniasis Transmitted by the bite of an infected female phlebotomine Sand fly, the leishmaniases are globally widespread diseases. Sand flies are primarily infected by animal reservoir hosts, but humans are also a reservoir for some forms. Animal Reservoirs: include Rodents - Commonly in East Africa, Ethiopia, the Sudan and Kenya and Canines - Mediterranean and Asia. As the sandfly feeds, promastigote forms of the leishmanial parasite enter the human host via the proboscis. Within the human host, the promastigote forms of the parasite are ingested by macrophage where they metamorphose into amastigote forms and reproduce by binary fission. They increase in number until the cell eventually bursts, then infect other phagocyctic cells and continue the cycle. The parasites are transformed inside the fly and delivered to a new host, and the life-cycle continues Fig 3. It is characterized by chronic irregular fever, profound wasting, debility and hepatosplenomegally. Epidemiology Visceral leishmaniasis affects many countries in Africa, mainly Ethiopia and the Sudan the Middle East, Southern soviet union, India and S. Transmission The commonest way of transmission is by inoculation of promastigotes into humans by the bite of sand flies which breed in termite hills and forests. The source of the aflagellate forms may be either humans or extra human vertebrate reservoirs, and the disease may have life cycles that involve humans and sand flies only, or humans, sand flies and extra human vertebrate reservoirs together. Pathogenesis The common site of entrance is the skin where primary cutaneous lesion appears at the sites of sand fly bite. Here a cellular reaction by lymphocytes and plasma cells develop around the amasitigote-filled histiocytes in the dermis. As immune response develops epitheloid and giant cells appear, to be followed in some by healing. In others usually 4-6 months later amastigotes escape to the blood in macrophages, hematogeneous spread occurs and colonize the cells of reticuloendothelial system, where they multiply further and released after rupture of the cells and transported to new cells. The cells affected include that of spleen, liver, bone marrow and lymphatic glands, where the parasite multiplies and cause overcrowding of cells and as a result these organs are enlarged. The liver with its Kuppfer cells packed with amastigotes is enlarged & progress to cirrhosis. Clinical Features Incubation period usually varies from weeks to months but can be as long as years. Diagnosis Definitive diagnosis is based on demonstration of the Parasite - Giemsa stained smear of peripheral blood (in Indian form) and tissue touch preparation of organ aspirates and examined by light microscopy. Following the bite of sand flies, leishmania multiply in the macrophages of the skin. Single or multiple painless nodules occur on exposed areas (mainly the face) within one week to 3 months of the bite. The nodules may enlarge and ulcerate with erythematous raised border and overlying crust which may spontaneously heal over months to years. Different clinical patterns are described depending on the etiologic agents as follows:- 60 Internal Medicine Table I- 3. Investigation for Diagnosis Giemsa staining of smear from a split skin: This demonstrates leishmania in 80% of cases Culture followed by smear 61 Internal Medicine Leishmanin skin test is positive in over 90% of cases although it is negative in diffuse cutaneous leishmaniasis. However large lesions or those on cosmetically important sites require treatment either 0 Locally - by surgery, curettage, cryotherapy or hyperthermia (40-42 c) or Systemic therapy: with drugs like Pentostam. Treatment is less successful than visceral leishmaniasis as antimonials are poorly concentrated in the skin L. Bolivia, Uruguay and Northern Argentina) In the early stage it affects the skin, but in secondary stage of the disease it involves the upper respiratory mucosa. This leads to nasal obstruction, ulceration, septal perforations and destruction of the nasal cartilage called Espundia. Death usually occurs from secondary bacterial infection 62 Internal Medicine References: th 1. Tuberculosis Learning Objective: At the end of this unit the student will be able to 1. Understand the different treatment categories of Tuberculosis be able to categorize any type of Tuberculosis 11. Refer complicated cases of Tuberculosis diseases to hospitals for better management 14. Design appropriate methods of prevention and control of Tuberculosis Definition: Tuberculosis is a Chronic necrotizing disease caused by Mycobacterium tuberculosis complex. The rate of clinical disease is highest during late adolescence and early adulthood, but the reasons are not clear. Activated alveolar macrophages ingest the bacilli; after which they release chemicals to activate other immune system components and try to control the infection or multiplication of bacilli. These activated cells aggregate around the lesion and the center becomes necrotic, soft cheese like material called caseous necrosis. But if the bacteria inside the macrophage multiply rapidly, they will kill the macrophage and are released but to be taken up 66 Internal Medicine by other macrophages again. Clinical Manifestations Pulmonary Tuberculosis: - This can be classified as primary or post primary (Secondary). Primary disease: Clinical illness directly after infection is called primary tuberculosis; this is common in children <4 years of age. Post primary disease: -If no clinical disease is developed after the primary infection, dormant bacilli may persist for years or decades before being reactivated, when this happens, it is called secondary (or post primary) tuberculosis. Most patients have cough, which may be dry at first, but later becomes productive of whitish sputum; it is frequently blood streaked. Chest x-ray findings are non-specific; infiltrations, consolidation or cavitory lesions may be present. Pleural tuberculosis:- Pleural involvement may be asymptomatic or patients could have fever, pleuritic chest pain and dyspnea. Patients may present with swelling and pain on the back with or without paraparesis or paraplegia due to cord compression. Patients present with progressive joint swelling, usually with pain and limitation of movement. Gastro Intestinal Tuberculosis:- Tuberculosis can affect anywhere from the mouth to the anus. Patients usually present with abdominal swelling and pain, weight loss, fever and night sweating. Milliary tuberculosis:- This is secondary to hematogenous dissemination of the bacilli. Patients who have suggestive symptoms and signs for tuberculosis should undergo further tests. If all 3 sputum smears are negative and the patient has suggestive clinical and chest x-ray findings, first the patient should be treated with broad spectrum antibiotics to rule out other bacterial causes. However the bacillus is slowly multiplying and it takes several weeks to grow the bacilli in a culture media. Although any radiographic finding is possible, typically there will be nodular infiltrates and cavities in the upper lobe; pleural effusion is also common.
Behavioral Models of Etiology Conditioning Theories of Paraphilia Theorists of classical conditioning have proposed that some forms of fetishism can be explained by early learned associations between sexual stimulation and common objects of infancy such as diapers generic 500 mg glucophage sr fast delivery, bottles purchase glucophage sr 500mg, and paciers (22) cheap 500 mg glucophage sr visa. However order 500 mg glucophage sr fast delivery, etiological explanations based on responses to treatment have limited validity. Clinical work in the Internet era provides observational support for the role of conditioning in the paraphilias. Exposure to Internet-based sexually explicit material and accompanying high levels of sexual arousal appear to, in some indi- viduals, profoundly inuence the development of conditioned sexual fantasy and arousal responses. Therefore, caution must be exercised in drawing conclusions about any direct causative effects of exposureInternet or otherwiseon the development or latensication of psychosexual pathology. Fisher and Barak have presented eloquent reviews on the effects of exposure to pornography, concluding that it is difcult to distinguish between the effects of exposure and the effects of pre-existing underlying personality factors in individuals who seek such exposure (97). In contrast to classic conditioning is the theory of imprinting, which pro- poses that early childhood is a critical period in which animals instinctually grow attached to a primary object. Species such as precocial birds are thought to become imprinted, or physiologically programed to follow whatever crea- ture or object they see shortly after hatching (98). Binet hypothesized pathologi- cal imprinting in humans as a possible explanation for the development of fetishes (41). Owing to events in sensitive developmental periods, an association between arousal and a particular object or experience becomes imprinted. Overall, empirical attempts to validate conditioning theories in the etiology of paraphilias have produced mixed results. Junginger pointed out the possible relevance of the two-process learning theory, which has earned acceptance as an explanation of avoidance behavior in obsessive-compulsive disorder, to the development of fetishism (46). The rewards inherent in sexual arousal and orgasm then serve as positive reinforcement. Deviant Arousal Theory of Paraphilia Some behaviorists have examined the role of deviant arousalarousal in response to deviant or nonnormative stimuliin the etiology of sexual offending behaviors. Some have found evidence of deviant arousal in pedophilia and others have found deviant arousal in exhibitionism, although with concurrent higher arousal to normative stimuli (99101). The inconsistent ndings suggest that deviant arousal is present in some men with paraphilia and less so or not at all in others (102). Why that is the case is unknown and there is no current explanation for the presence or development of the deviant arousal. Voyeurism is viewed as a disturbance in the rst phase, exhi- bitionism as a disturbance of the second, frotteurism of the third, and preferential rape as a disturbance of the fourth phase. Personality Theories of the Paraphilias Efforts to identify associations between personality and variant sexual behavior have been inconsistently fruitful. One of the authors own studies compared person- ality proles of men diagnosed with a paraphilia with those of men with sexual dysfunction and with a normative sample (105). Proles of men diagnosed with a paraphilia showed a distinctive group prole marked by higher neuroticism, lower agreeableness, and lower conscientiousness than those of sexually dysfunc- tional men, whose proles were comparable with the normative group. These ndings are consistent with earlier suggestions that men with paraphilias have difculty with attachment and intimacy, and are commonly self-centered, antagonistic, and autonomically prone to distress (106109). Consistent with the nding by Fagan and colleagues that the para- philia group was higher in openness to fantasy, others have observed that men with paraphilias often experience fantasy as a central aspect of their sexuality (110,111). A recent study of pedophilic sex offenders found that 60% of the sample met criteria for a personality disorder (25). Biological Theories of the Paraphilias Understanding of the neurobiology of sexual functioning, both normal and deviant, is incomplete. Nevertheless, it is clear that sexual interest and function derive from both the central nervous system and endocrine factors. In normal sexual arousal, central nervous system involvement includes a cascade of con- nections from the neocortex to the limbic system and the hypothalamus, particu- larly the preoptic area and the brainstem (113). Sexual arousal begins via either sensory input, such as tactile, visual or olfactory stimulation, or via fantasy in the neocortex. This cortical arousal propagates through the limbic system and hypo- thalamus to enable a progression of physiologic events that promote sexual beha- viors and orgasm. Subcortical brain areas are important for sexual functioning and include the limbic system and the preoptic nuclei in the hypothalamus. Dopamine appears to enhance sexual arousal with particular activity in the mesolimbic system, whereas serotonin diminishes sexual drive and arousal (114,115). Lowering prolactin levels via bromocriptine in women with pituitary adenomas has been shown to increase libidinal drive. The role of estrogen in normal sexuality is not fully elucidated but it is evident that estrogen affects ser- otonin receptors as well as regulates beta endorphin, a peptide that has reduced sexual drive in animal studies (116). Regarding understanding paraphilic dysregulation from a biological per- spective, the most compelling data is found in studies with androgens. It is known that testosterone levels strongly correlate with sexual drive in women, and aggressive sexual offenders often are found to have higher androgen levels than controls (117,118). Among the most robust data supporting biological factors underlying sexually deviant behavior is the elevation of androgen levels found in convicted rapists (119). However, the implications of these nd- ings for the paraphilias are unclear at this time. Early biological hypotheses regarding the paraphilias included Epsteins theory of phylogenetic preparedness of fetishism (120). He observed that a rubber boot, but not leather, evoked penile erection and ejaculation in a chimpan- zee, suggesting that the fetishistic attraction to an unusal object is not limited to humans. Epstein speculated that the wet surface of the boot bore a relationship to the female chimpanzees genitalia during rear mount sexual behavior. There have been reports of elevated plasma epinephrine and norepi- nephrine levels in individuals with pedophilia (121,122). Paraphilias 313 abnormalities are related to underlying anxiety disorders rather than specic to pedophilia has not been discerned. The study also found a signicant association between pedophilia and lower rates of right-handedness, consistent with earlier reports of decreased right-handedness in child sex offenders (124). The studys ndings suggest that early (prebirth) neurodevelopmental pertur- bations of the developing brain may account for some cases of pedophilia. Future studies may clarify what parts of the brain are affected, whether such perturbations reect an independent pathological process or a general risk factor, and whether such ndings have relevance to the development of other paraphilias. In another recent study, an association was identied between pedophilia and retrospectively recalled childhood accidents resulting in unconsciousness (125,126). Twice as many pedophiles as nonpedophiles reported head injuries with unconsciousness before the age of 6, suggesting that neurodevelopmental perturbations occurring in a window of time after birth may also increase the risk of pedophilia. The authors of these studies cautiously point out that more data are needed before the ndings can be interpreted with condence. Whether head injury causes a neurodevelopmental abnormality that increases the risk of pedophilia or whether a pre-existing neurodevelopmental problem increases the risk of both head injury and pedophilia is unknown. Although most studies regarding possible etiological associations between childhood head injury and the paraphilias have focused on pedophilia, some single case studies have been cited suggesting that some fetishistic behavior may also be related to childhood head injury (127). The authors concluded that traumatic brain injury was a signicant etiological factor underlying the offending behaviors. Such studies support the hypothesis that head injury is related to the development of some adult onset cases of paraphilia. Left temporal lobe lesions have been known to result in sexual disinhibition and compulsivity in some individuals. Similarly, is evidence that temporal lobe epilepsy may cause some cases of fetishism and other paraphilias, most commonly exhibitionism (104,129). However, the majority of individuals with temporal lobe epilepsy do not have a paraphilia and, in fact, many are hyposex- ual. Future studies may explain the occurrence of paraphilia in a small subgroup of these individuals. Kafka has suggested that serotonergic factors may provide a biologic explanation for all paraphilias, but there is limited data to conrm this (133). There are also reports of fetishistic cross-dressing across generations in families (134,135).