Meclizine
By V. Mine-Boss. University of Florida. 2018.
In one patient given [14C]mitoxantrone intra- venously 25mg meclizine amex medications osteoporosis, who died 35 days after the dose, as much as 15% of the administered dose could be accounted for in the liver, bone marrow, lungs, spleen, kidney and thyroid glands (Alberts et al. In one study, the fraction of unbound drug in plasma at the end of a 30-min infusion was only 3. Because of its limited urinary excretion, little information is available on the meta- bolism of mitoxantrone. Two inactive metabolites were identified in urine as the mono- and dicarboxylic acid derivatives resulting from oxidation of the terminal hydroxy groups of the side-chains (Figure 1) (Chiccarelli et al. The concentrations of mitoxantrone in urine were not altered by pre-incubation with a β-glucuronidase or sulfatase, suggesting that the drug is not excreted renally as either the glucuronide or sulfate conjugate (Smyth et al. This metabolite has been identified in the urine of patients given mitoxantrone (Blanz et al. After two further courses of 6 mg/m2 mitoxantrone, her breast milk contained 120 ng/mL mito- xantrone 3–4 h after dosing and 18 ng/mL by five days, and the concentration remained at this level for 28 days. This finding indicates that the drug is slowly released from a deep tissue compartment (Azuno et al. The drug was not developed for oral use, and in a review mito- xantrone was described as being poorly absorbed when administered orally [species not mentioned] (Batra et al. In rats, dogs and monkeys, the disappearance of intravenously administered [14C]- mitoxantrone from plasma was rapid, followed by a slow terminal elimination phase (James et al. Extensive tissue binding was indicated, with 50, 25 and 30% of the dose still retained 10 days after intravenous administration in rats, dogs and monkeys, respectively. In beagle dogs, tri- exponential elimination from plasma was reported, with a very rapid initial distribution phase with a half-time of 6. Extensive tissue retention was again reported, the higher concentrations 24 h after dosing being found in the liver, kidney and spleen. Two metabolites were detected, accounting for 30% of the radiolabel in plasma and 50% in urine, but were not identified (Lu et al. A rapid distribution and a slow elimination phase were also observed in mice, with retention in body tissues, particularly liver and kidney (Rentsch et al. A naphthoquinoxaline metabolite of mitoxantrone has been reported in rats and pigs, resulting from the oxidation of the phenylenediamine substructure (Blanz et al. In general, mitoxantrone is believed to be active in mammalian cells in vitro in the absence of exogenous metabolic activation; however, inhibition of cyto- chrome P450 mixed-function oxidase by metyrapone in HepG2 hepatoxic cells and rat hepatocytes blocked the cytotoxic activity of mitoxantrone, suggesting that conversion to reactive species might be important (Duthie & Grant, 1989; Mewes et al. Leukopenia is the main dose-limiting effect, the lowest leukocyte counts typically being found 10–14 days after a single dose, with recovery by day 21. In a large European trial, seven of 264 patients experienced cardiac abnormalities (3%). Risk factors that may be predictive of the cardiotoxicity of this drug are previous anthracycline therapy, mediastinal radiotherapy and a history of cardiovascular disease (Crossley, 1983). The number of cardiotoxic events increases with cumulative doses of mitoxantrone > 120 mg/m2 in patients who have previously been treated with anthra- cyclines, and > 160 mg/m2 in patients who were not previously treated. The cumulative dose at which a patient has a 50% probability of having to discontinue treatment because of cardiotoxicity was estimated to be 182 mg/m2, representing approximately 13 courses of treatment. Other toxic effects seen with standard doses of mitoxantrone (12–14 mg/m2) include nausea and vomiting (in approximately 50% of patients), diarrhoea (15%), stomatitis and mucositis (20%) and alopecia (50%), although these effects are usually mild and transient (Crossley, 1983). As the drug is an intense blue colour, discolouration of urine and skin is not uncommon. With higher doses (40–90 mg/m2 or 12 mg/m2 on days 1–3), the toxic effects are typically more severe, and hepatotoxicity has been reported (Feldman et al. After intraperitoneal dosing, peritonitis is the dose-limiting toxic effect (Alberts et al. Many of the studies of the toxicity of mitoxantrone have focused on its cardiac effects, particularly in comparison with doxorubicin, another anthracycline known to be toxic to the heart. At doses > 2 mg/kg bw, mito- xantrone induced cardiovascular and renal toxicity in rabbits (Hulhoven et al. Two cats died of complications that may have been attributable to mitoxantrone: one of cardiomyopathy and the other of pulmonary oedema (Ogilvie et al.
The 2 samples 25 mg meclizine medications japan, standards or blank were added in triplicate to growth inhibition percentages were determined based on the parasite 96-well microtiter plates, followed by 65 l/well of the burdencomparedtothatofuntreatedcontrolcellsthatweremicroscop- freshly prepared reagent. Results this apparent discrepancy is unknown, one explanation could be the appearance of drug resistance in the strain 3. The results are representative of two independent experiments and given as the mean±standard deviation of an experiment performed in duplicate. The extent of the label was analyzed by flow cytometry (A) and fluorescence microscopy (B). The results are representative of one experiment out of three performed in duplicate. The positive labeling (thick continuous line, green) was achieved by incubating the promastigotes with 1mM of H2O2 during 3h and the negative (full peak, blue) was given by the untreated cells. The results are representative of three independent experiments performed in triplicate. Cisplatin induces endoplasmic reticulum stress and nucleus-independent References apoptotic signalling. Clinical and experimental advances in treat- eukaryote (Trypanosoma cruzi): implications for the evolution- ment of visceral leishmaniasis. Determination of glutathione and glutathione trans-platinum complexes which induce programmed cell death in disulfide in biological samples. In vitro screens in the experimental chemotherapy tosis by propidium iodide staining and flow cytometry. Accordingly, plasmid cure shows that these parasites maintain episome even in absence of drug pressure. Accordingly, plasmid cure shows that these parasites maintain episome even in absence of drug pressure. Positive clones were related family members is increasing, functional studies are subjected to restriction map and Southern blot analysis with the required to analyze the biological properties of the different same probe. In more recent bean nuclease and shrimp phosphatase to generate dephos- experiments such approach has been used to define parasite phorylated blunt ends. In this study we used a “reverse” genetic resistance to Blasticidin S (Goyard and Beverley, 2000). Materials and methods digestion was treated by Mug Bean nuclease to obtain blunt ends and ligated into the SmaI site of linearized dephos- 2. Fluorescence gated on forward and side light scatter was collected and displayed 2. The quadrant promastigotes statistic allowed us to determine the percentage of viable cells. Test of deacetylase activity for 2 weeks : G418 (20 μg/ml), Hygromycin B (50 μg/ml), Blasticidin S (30 μg/ml). Furthermore, sensitivity to For inhibition experiments, 250 mM sodium butyrate was blasticidin S has been analyzed by measuring the growth added to the reaction medium. Assays were performed in inhibition index at day 3 of culture=(1−parasite number with triplicate. In vitro macrophage infection Phorbol myristate acetate-treated monocytes (differentiated Late log phase parasites were harvested by centrifugation, macrophages) were incubated with stationary phase amastigotes washed twice in NaCl 0. The lysed in situ by overnight treatment with 5 volumes of cells were fixed with methanol and stained with giemsa. Plugs were washed four times for 30 min in after having counted at least 800 cells per slide. The number of parasites per gram of spleen (parasite burden) was calculated as follows: Amastigote and promastigote multiplication and viability parasite burden=(geometric mean of reciprocal titre from each were determined using flow cytometry analysis. Names and genotypes of the clones obtained during the study are indicated in Table 1. This deacetylase activity is neo) was submitted to a second round of transfection using the not inhibited by sodium butyrate at concentration known to hyg targeted construction. Additional attempt to disrupt the second allele using newly purified hyg targeting construct gave same results. S ch em aticdraw ing ofW and th eneo orhy g targeted i l ocus h e ind targeted constructsand th eirl ocal isationw ith in i l ocusareindicated bydotted l ine.
Other pieces of the public awareness campaign intended to change consumer behavior (Akunyili meclizine 25mg without a prescription medicine lookup, 2005). The regulators reasoned that if consumers were informed about falsifed medicines and empowered to make safe choices, they would. To this end, they published lists of known fake products and photos illustrating warning signs in daily newspapers (Akunyili, 2006; Raufu, 2006). Since 2002, the agency has sponsored an es- say contest on medicine safety for students, awarding cash prizes to the winners and computers to their schools (Akunyili, 2006). People in developed coun- tries, who have long taken medicines regulation for granted, are among the least knowledgeable. An Inter-Press Service story reported that 20 percent of Western Europeans did not consider it dangerous to circumvent traditional pharmacies to buy medicine (Stracansky, 2010). The same be- havior has long been normal in the United States, where pharmacy tourism to Canada and Mexico has been common since the 1970s (Rabinovitch, 2005). Chapter 5 will discuss the internet pharmacies that have largely replaced in-person cross-border shopping. Public Action Educating the public on the problems of falsifed and substandard medicines is important, but only insomuch as education empowers people to act. The reasons they gave included doubt that the regulator would act on their information and fear of litigation. Similar attitudes may underlie a lack of reporting of adverse drug reac- tions among health workers in developing countries. Their role in surveil- lance is important in low- and middle-income countries, where falsifed and substandard drugs are common, and less than 27 percent have func- tional pharmacovigilance systems (Pirmohamed et al. Few staff are trained in pharmacovigilance, a practice sometimes seen as adding to the responsibilities of already overworked health professionals (Olsson et al. The increasing awareness of falsifed and substandard medicines could drive improved pharmacovigilance in developing countries. Awareness cam- paigns and investigative reporting reach health workers as well as they reach the rest of the public. There is also a need for targeted health worker education on falsifed and substandard medicines, emphasizing the correct reporting channels health workers can use to confrm suspected cases of falsifed and substandard drugs. Much useful work has been done on the frst steps of this process; clinicians struggling to broach the topic with their patients can consult the World Health Professionals Alliance guidelines on how to inquire about suspicious medicines (see Box 4-8). Chapter 3 describes governments’ and drug companies’ reluctance to share information on substandard and falsifed drugs (Cockburn et al. Pharmaceutical companies fear damage to their branding from Copyright © National Academy of Sciences. Emphasis can be placed on the importance of buying medicine from a pharmacy or other known and reliable sources. It can be suggested that patients check the packaging, the product, and the patient leafet when they purchase medicine. For example: “Was the packaging of the product intact, properly sealed, clearly labeled with dosing, manufacturer, batch number, and expiry date? By explaining what should happen when patients take medicine, health professionals can help patients identify anything unusual. If a medicine is supposed to start relieving symptoms within 24 hours, for example, then patients should know, so that if the medicine does not take efect, then can notify their health professional. These concerns are well grounded, and an appropriate communication strategy will convey accurate information is a way that is sensitive to all stakehold- ers. Falsifed and substandard medicine is a sensitive and dynamic problem, and the public has a right to accurate information about it. This informa- tion can be presented in such a way as to empower the consumer to make safe choices and to build confdence in the regulatory system. Recommendation 4-5: Governments and donor agencies should fund development of effective communication and training programs for consumers and health workers on understanding the quality and safety of medicines. Falsifed and substandard drugs are a potential threat around the world, though risk varies widely from country to country. Awareness of the prob- lem also varies and may be most limited in countries with strong regulatory systems but where, because of the global drug supply chain, substandard and falsifed drugs still reach consumers. An effective communication cam- paign should present accurate information in a way that empowers patients to protect their own health.
Mucosal proteolytic enzymes are com- posed of exopeptidases meclizine 25mg discount medications like zoloft, such as mono and diaminopeptidases, and endopeptidases, such as serine, cysteine, and aspartic peptidases. Examples of common peptidase inhibitors include amastatin, aprotinin, bestatin, boroleucine, borovaline, leupeptin, pepstatin, and trypsin inhibitors. Antibacterial agents, such as azelaic acid, fusidic acid, and puromycin, exhibit activity against peptidases. Other enzyme inhibitors, such as p-chloromercuribenzoate, phenylmethylsulfonyl fuoride, thiomersal, and chelate metal ions, are essential for proteolytic activity. The bioavailabil- ity of mucosal delivered peptide drugs can be dramatically improved by solubilizing the drug with permeation enhancers that improve solubility, enhance membrane fu- idity, or open tight junctions [24]. Tight junctions are the gaps between the margins of adjacent endothelial cells with several transmembrane proteins that project into and seal the gaps. The need for an adjuvant to enhance the penetration of peptide drugs in order to obtain adequate absorption for practical use is especially true for larger molecules and those having relatively high water solubility. However, most absorption enhancers can potentially damage the mucosa, especially when used con- tinuously or chronically, because the increase in membrane permeability may cause unpleasant sensations or local irritation [25]. Mucolytic agents, such as amino acid N-acetyl-l-cysteine, reduce the viscosity and tenacity of mucus, the frst layer, to allow surfactant molecules to diffuse more effciently onto the endothelial membrane, the second layer, to increase membrane fuidity and mucosal permeability. This mucolytic peptide drug is admin- istered to the lungs of cystic fbrosis patients through a nebulizer. Fatty acids, such as palmitic acid and oleic acid, as well as lipids are used to moisturize and soften the cell layers, thereby increasing membrane fuidity. Signal transduction substances, such as enzyme pro- tein kinase C, regulates the tight junctions, as junction modulating peptides to permit the entry of the drug into the bloodstream. The use of a mixed solvent system, that is, cosolvent, could facilitate drug sol- ubilization but has not shown any clear advantage when one considers the higher risk of mucosal irritability [26]. In developing a salt form, one should ascertain that the salt form of the peptide drug would not cause intolerable mucosal irritation. In the unfortunate event that mucosal irritation does occur, protecting the ionizable functional group with a readily cleavable protective group could circumvent the problem. Inert polysaccharides can be intentionally conjugated to the drug to form a more hydrophilic and solubilizable prodrug. It should be noted that if the drug is still conju- gated when it is in the bloodstream, it is more readily cleared from the body. Ideally, the prodrug should convert to the parent drug once it reaches the bloodstream. Polysaccharides have a fair number of hydroxy groups that can conjugate to carboxylate drugs by esterifcation. More often, oxidation of a hydroxy group is performed to obtain a reactive aldehyde, which then can be more readily conjugated to the parent drug. Polysaccharides such as algi- nate, cellulose, chitosan, pectin, cyclodextrin, dextrans, and inulin are biodegradable carriers that can release the parent drug [27]. In particular to peptides, chitosan dis- played an improved paracellular route of absorption, that is, transport between cells, of peptide drugs [28]. Interestingly, cyclodextrins form dynamic molecular inclusion complexes, in which the lipophilic part of the peptide drug can be incorporated into the lipophilic cavity of cyclodextrin. In simpler words, cyclodextrin hides the drug inside of its funnel-like structure. While polysaccharides are conjugated to improve hydrophilicity, liposaccharides can be used to increase the lipophilicity of peptide drugs and thereby improve their membrane permeability. Lipidic α-amino acids possessing a long alkyl side-chain have been used to provide protection for peptide drugs from enzymatic attack and improve oral absorption [29]. To balance out the high lipophilicity, lipoamino acids can be conjugated to mono and polysaccharides, resulting in amphipathic liposaccharides. Other than being conjugated to the parent drug, liposaccharides can form particulate structures and used as colloidal carriers for oral administered drugs.
Therefore purchase 25 mg meclizine with visa 4 medications list, it is possible that the comparison of cases with asymptomatic controls may have provided a misleading estimate of association. These controls were identified from the records of one treatment centre; the same matching criteria were used as described for the comparison with asymptomatic controls. Twenty-five to 40 mice from each group were used only for haematological examinations and for determinations of the plasma concentration of the drug. At day 91, anaemia was seen in animals at the intermediate and high doses, and the doses were lowered to 20, 30 and 40 mg/kg bw per day. Two separate groups of 85 male and 85 female mice were left untreated or were given the vehicle alone. The study was terminated at 19 and 22 months for male and female mice, respectively. Tissues from all mice in the untreated, vehicle control and high-dose groups were examined microscopically. In addition, the vaginas from all mice at the low and intermediate doses were examined. Treatment with zidovudine did not affect the survival rate in either sex, and the rate at 18 months was 50%. The incidences of vaginal squamous-cell carcinomas were 0/60, 0/60, 0/60, 0/60 and 5/60 [p = 0. One squamous- cell papilloma of the vagina was seen at the intermediate dose and one at the high dose. Squamous-cell hyperplasia of the vaginal epithelium was seen in all groups of mice, including the controls, and the incidence of moderate to severe hyperplasia was dose- relatedly increased in mice given the intermediate or high dose of zidovudine. Treatment did not affect the incidence of any other benign or malignant tumour in any tissue or organ examined [specific tumour incidences not reported] (Ayers et al. Groups of 95 male and 95 female B6C3F1 mice, seven to eight weeks of age, were treated with zidovudine (~98% pure) in 0. Each group of 95 animals of each sex comprised 50 animals of each sex for evaluation of carcinogenic response, 30 animals of each sex for evaluation of haematological end-points and bone-marrow cellularity, and 15 animals of each sex from which blood was drawn for determination of the plasma concentrations of zidovudine at week 54. The survival and mean body weights of mice exposed to zidovudine were similar to those of the vehicle control groups. Squamous- cell carcinomas or papillomas (combined) of the vagina occurred in 0/50, 0/49, 5/45 (p = 0. The incidences of Harderian gland tumours in male mice were 3/50, 5/50, 2/50 and 10/50 (p = 0. At day 91, the high dose was lowered to 450 mg/kg bw per day because of the occurrence of anaemia. Progression of anaemia led to a further reduction of the high dose to 300 mg/kg bw per day on day 278. Two separate groups of 60 male and 60 female rats were left untreated or were given the vehicle alone. The study was terminated at 24 and 22 months for male and female rats, respectively. Tissues from all rats in the untreated, vehicle control and high-dose groups were examined microscopically. In addition, the vaginas from all female rats at the low and intermediate doses were examined. Treatment with zidovudine did not affect the survival rate in either of the sexes, and the rate at 18 months was 50% or greater. Two squamous-cell carcinomas of the distal vagina were observed in females at the high dose, but no vaginal tumours occurred in the other groups, or in the untreated or vehicle control groups. Treatment with zidovudine did not affect the incidence of any other benign or malignant tumour in any tissue or organ examined [specific tumour incidences not reported] (Ayers et al. At weaning, zidovudine was admi- nistered to the offspring at the same doses in the drinking-water for 17–35 days and then by gavage for 24 months. Two additional groups were treated similarly with 40 mg/kg bw per day, but one group was treated only until day 21 of lactation and the second by gavage for 90 days after birth. Two groups each of 60 female mice were either untreated or were given the vehicle, beginning on day 10 of gestation and throughout gestation, parturition and lactation, and then in the drinking-water for 17–35 days, followed by daily gavage for 24 months. The study was designed to give a total of 70 male and 70 female progeny in each dose group.
Kinetic homogeneity describes the predictable relationship between plasma drug concentration and concentration at the receptor site buy meclizine 25 mg treatment 4s syndrome. Model a simplified mathematical simulation of physiologic processes used to predict the time course of drug concentrations or effect in the body. Model-independent parameter a pharmacokinetic parameter, such as clearance, that can be calculated without the use of a specific model. Model-independent pharmacokinetics pharmacokinetic calculations using parameters that do not require the use of specific compartmental models (e. Pharmacodynamics the relationship between drug concentrations at the site of action and the resulting effect, including the time course and intensity of therapeutic and adverse effects. Pharmacokinetics the relationship of drug dose to the time course of drug absorption, distribution, metabolism, and excretion. Plasma the fluid portion of blood (including soluble proteins but not formed elements). Receptor a structure on the surface of a cell to which a drug binds and causes an effect within the cell. Serum the fluid portion of blood that remains when the soluble protein fibrinogen is removed from plasma. Steady state the point at which, after multiple doses, the amount of drug administered over a dosing interval equals the amount of drug being eliminated over that same period. Therapeutic range the plasma concentration range that is effective and safe in treating specific diseases. Volume of distribution (V) an important indicator of the extent of drug distribution into body fluids and tissues, V relates the amount of drug in the body to the measured concentration in the plasma. Studies of drug regulation are of course nothing like a blank territory in the history of science, medicine and technology. Among the industrial goods, pharmaceuticals are certainly This is the path taken by the marketing of Thalidomid in Brasil. The pictogram of a crossed-out pregnant woman on the package however evoked contradictory associations by each consumer. One reason for the pervasiveness of the idea of regulation in the case of pharmaceuticals is certainly that therapeutic agents are not goods as any other. Their sale and purchase constitute a very peculiar market whose control and surveillance in order to protect “public health”, meaning avoid poisoning as well as the creation of monopolies that might threaten reasonable conditions of access, has been considered a duty of the state since the early days of the transformation of pharmaceutical craft into a profession in the early 19th century. As a consequence of this situation, the historiography of drugs has given regulatory issues a rather institutional meaning. Within this perspective, the words “drug regulation” are usually employed with a narrow understanding, which focuses on the actions taken by the government or other political bodies in order to control the activities of drug makers. Studies then focus on the administrative features that have been used to tame the market or safeguard production, i. Industrial drug making as it developed within the large capitalistic corporations of is the focus of analysis approaching the 20th century highly visible conficts between frms, physicians and public authorities caught within a web of market forces and public health defense. Daemmerich have accordingly highlighted the affairs, controversies and public debates, which have reshaped the agency, enlarging its responsibilities if not its power, shifting pre-marketing evaluation from a mere control of composition to an assessment of toxicity and in the second half of the 20th century an assessment of effcacy. As the above mentioned example of Contergan suggests, this form of state administration has been associated with or superimposed on other forms of collective management, of “regulation”, which did not only target sales and commercialization, but the entire trajectory of drugs, i. The perspective adopted for the workshop that provided the background for the essays assembled in this preprint was therefore that the historiography of science, technology and medicine needs a broader approach of regulation. Contemporary studies of science and technology have often made the point that the production and uses of knowledge are interactive, undetermined, and complex processes. This must also be Without making any attempt to offer a bibliography of drug trajectories or even a selection of existing studies on drugs and regulation, we simply invite the reader to take the beneft of the references included in the individual papers of the collection. In the last two centuries, drugs have become central elements in complex health systems. It is the belated product of a long-term transformation, which began in the second half of the 19th century when the industrialization of drug making coincided both with the rising infuence of experimental sciences and laboratory practices in medicine, and the emergence of hospitals as the place where insurance-based health care accessible to the working class would be routinely provided. Although, state and professional forms of regulation can be traced back to the early 19th century, this conjunction deeply affected – diversifed – regulatory practices, setting the pace for new forms of control emphasis standards, homogeneous protocols or statistical effcacy. Our contention is also that various levels of comparison must be chosen in order to explore the relations between research, therapeutic intervention, and commercialization.
The interrogator generic meclizine 25 mg medicine 20th century, however, can keep his prime sources separated so that there is no cross-fertilization, and also he can attempt to extinguish malingering in the group by exposing and punishing an unsuccessful malingerer. Thus he can give himself or the unit the reputation for being a shrewd detector of deception and a harsh punisher of such duplicity. Once the prisoner gets the feeling that his pretense is endangered, the interrogator may supply him with many face-saving devices which would allow him to relinquish the symptoms that prevent him from cooperating, but without forcing him to admit his guilt. Already mentioned was the technique of giving the prisoner "treatment" for his illness, one that is guaranteed to bring about a cure. Thus the prisoner may behave as if the pills or the electroshock did produce a cure or that the hypnosis or narcosis did allow him to recover his memory, and there will be no need to admit the malingering or suffer punishment for it. The prisoner may use this way out if he gets the impression that the interrogator is becoming wise or is demanding recovery. Another honorable way out for the prisoner could be to remain "ill" but not to allow the illness to interfere with the communication of relevant information. The interrogator might allow the prisoner to keep his simulated depression, delusions, or posturing and gesturing, but he would insist that these symptoms in no way interfere with his ability to recall and communicate important facts. To augment -298- this approach, the interrogator might "treat" only those symptoms which cause memory or communication difficulty, reassuring the prisoner that the other symptoms will remain for a while and that he will be hospitalized and be given more care and privileges than he might otherwise receive. This approach makes it possible for the prisoner to cooperate without revealing his deception, and it offers a substitute goal for the malingering — that of better treatment and privileges. Direct confrontation could conceivably produce a real psychic disorder, especially in those persons who are borderline psychotics to begin with and whose symptoms are exaggerations of their own latent tendences. As Hurst (44) and Eissler (22) point out, that which was feigned at one time may show up as a real illness at a later time. If forced compliance to the interrogator would produce more anxiety and guilt than would malingering, a serious disorder may be the alternative which the prisoner will take. Conclusions Detection of Malingering Exact procedures for the determination of malingering are not available. Few true psychotics display the exact symptoms of the textbook cases, and this wide range of variability among psychotics requires evaluations of a wide variety of symptom patterns for the detection of malingering. The malingerer may demonstrate a set of symptoms which must be entertained as a possible deviation from the more usual syndromes. It is only through rather skillful and lengthy observations that an examiner may be able to come to the conclusion -299- that the patient is feigning his condition. Hurst (44) feels that malingering can be diagnosed with certainty only when the simulator is caught flagrante delicto or gives an unforced confession. Eissler (22) doubts the validity of confessions, since psychotics or borderline psychotics may feign malingering. The fact that borderline schizophrenics may try to malinger complicates the matter and makes diagnosis more difficult. Another complicating but undetermined factor is the effect the role may have upon the malingerer. Hurst (44) suggests that what was simulated may become a truly hysterical symptom after a time. There are therapeutic techniques which are dedicated to the proposition that a person may unconsciously take over portions of roles which he has consciously enacted (48, 64). Effectiveness of Malingering as Countermanipulation The advantages of malingering to an individual resisting coercive attempts to influence his behavior lie primarily in the cultural definitions of the psychotic as incompetent and not responsible for his acts. The discouragement of malingering involves principally the creation of the impression that psychosis is no excuse or that the person who is detected in malingering will be treated even more harshly than he might otherwise have been. When the value conflict is sufficiently great, however, neither threat nor actual punishment may be capable of forcing the person to abandon malingering as defense. The prudence in the use of threat and punishment forced on a rational interrogator by the possibility of creating a genuine disorder confers an additional advantage on the malingerer. Risks of Malingering In considering recommendations of malingering as a resistance tactic in training military personnel for the event of capture, certain dangers follow from these same three factors: the cultural definitions of the insane person, the rationality of the interrogator, and the possibility of a genuine disorder being created. Captors may not operate with humane cultural definitions toward the psychotic, and -300- they may not be constrained by rationality in their use of threats and punishments. The risk the malingerer takes must be evaluated in terms of the importance of the goal of resistance and the possible effectiveness of alternative modes of resistance and evasion open to him. The risks involve both the damage the captor may inflict upon him and the possibilities of a real and lasting personality disorder resulting from his simulation. To the best of our knowl- Executive Publisher edge, these procedures reflect currently accepted practice.
