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In addition to an understanding of the primary and secondary symptoms of PTSD, awareness of the various subtypes and course of the disorder are necessary for assessment and diagnostic procedures.

There has been a growing literature on the subject of PTSD in children. The literature consistently points to children’s vulnerability to the de­velopment of PTSD after severe trauma. In earlier work, such as the evaluation of the children who survived the Buffalo Creek disaster (Newman, 1976), PTSD per se is rarely discussed. Nevertheless, New­man (1976) reported that most of the 224 children were “significantly or severely emotionally impaired.” Examples of symptoms often con­formed to one or several diagnostic criteria consistent with PTSD.

As noted earlier, stress-response syndromes have been resisted by the mental health community until relatively recently. Indeed, it is still the cause of debate between various theoretical positions. As Figley and Sprenkle (1978) and Schultz (1984) stress, the families of PTSD patients have also been largely ignored. Consequently, as Scurfield (1985) states, little attention has been given to the impact of PTSD on families and family treatment of families with a member suffering from PTSD.

Before moving to the specific assessment process of PTSD, let us place this particular disorder in the context of evaluation in general. Before clinicians can go about making the detailed diagnostic assessment that will be discussed momentarily, they must be sensitized to the possibility that a patient might suffer from a trauma-related disorder.

Perhaps the symptom that is the sine qua non of PTSD is the reexperiencing of the event through intrusive imagery. The dissociative quality of these experiences (that is, the perceived nonvolitional aspect of the experience) was part of the unsuccessful impetus to place PTSD under the dissociative disorders in the DSM-III-R (Keane, personal communication, March 1988). Yet, some people who are traumatized develop PTSD, while others do not. Is it possible that people who develop PTSD are more hypnotizable than those who do not?

Unfortunately, there has been little published material on the therapy of children who have experienced trauma or disaster. Generally, there are three types of specialized interventions that have been described: Individual Psychodynamic (Pynoos & Eth, 1986), Group Play Therapy (Galante & Foa, 1986) and Group Stress Inoculation Training (Ayalon, 1983). It is not clear how the majority of children who experience trauma receive treatment. Presumably, they are either treated in family therapy (see Chapter 13) or general individual play therapy (usually psychodynamic in nature).

WR-2721 (S-2(3-aminopropylaminoethyl) phosphorothioic acid) is an organic thiophosphate derivative of cysteamine which was developed under the auspices of the Walter Reed Army Institute of Research in an attempt to develop non-toxic means of introducing thiol-containing compounds into tissues. Thiols are known to protect cells against the toxic effects of ionizing radiation and alkylating agent chemotherapy, however agents with free sulfhydryl groups such as cysteamine are very toxic. To avert the toxicity of this reactive group, several thioester derivatives were synthesized (1). Yuhas (2) found that one of the thiophosphates, WR-2721, is accumulated by, and provides radioprotection to normal tissues, but not certain tumors in experimental animals. The mechanism of this tissue selectivity is unknown. In studies in animals and humans, there are few side effects at doses providing radioprotection (3). During initial trials of its efficacy as a radio- and a chemoprotective agent in patients with malignancies, acute transient hypocalcemia was noted; intravenous WR-2721 produced a 20% fall in the serum calcium concentration at four hours and serum calcium levels remained depressed at 24 hours. Serum concentrations of immunoreactive PTH were reduced after infusion of WR-2721 instead of increasing in response to hypocalcemia suggesting that WR-2721 causes hypocalcemia by reducing secretion of PTH (4).

The elucidation of the metabolism of vitamin D has increased our understanding of mineral homeostasis. Vitamin D is produced in the skin as cholecalciferol (vitamin D3) and is absorbed in the small bowel as both vitamin D3 and D2 (ergocalciferol). Since the parent compound cannot be readily measured, estimates of vitamin D stores are made from assays of the circulating 25-hydroxy metabolites. In normal individuals, dermal synthesis seems to be much more important than the diet as a source of vitamin D. Circulating 25(OH)D3 is more abundant than 25(OH)D2 even in the winter and despite vitamin D2 dietary supplementation (Poskitt et al., 1979). Since vitamin D2 and D3 are hydroxylated at a comparable rate (Whyte et al., 1979), this implies that dermal synthesis is more important than diet in normal circumstances. Similarly, 25(OH)D levels correlate, not with dietary intake, but rather with recorded sunlight and season of the year (Stryd et al., 1979). Conversion to 25(OH)D occurs mainly in the microsomal fraction of the liver. This conversion is inhibited mainly by the liver and plasma pool of vitamin D and 25(OH)D, rather than by calcium and phosphate (Bhattacharya and DeLuca, 1973; Mawer, 1977). Control is not rigorous, however, and 25(OH)D levels do reflect provision of parent vitamin D to the liver. By contrast, the circulating levels of the 1,25(OH)2D metabolites do not correlate well with nutritional vitamin D status and are normal or low with vitamin D loading (Hughes et al., 1976). Circulating levels of 25(OH)D are 10–40 ng/ml in the United States, depending on season and latitude, and lower in Great Britain. 25(OH)D undergoes enterohepatic circulation (Arnaud et al., 1975), but the significance of this observation remains unclear; possibly, enhanced delivery to the intestine facilitates 24-hydroxylation (see below).

The purpose of this chapter is severalfold. First, it is intended to provide the reader with some of the theoretical bases for the cognitive-behavioral interventions that have been applied recently to delinquent and criminal populations. Second, it briefly outlines some of the recent work by those cognitive-behavioral psychologists who have begun to apply their interventions to the prevention and treatment of delinquent and criminal behavior. Third, it attempts to describe the cognitive-behavioral approach in terms of target skills and/or abilities that have been identified as associated with—in some cases as underlying—other skills in which delinquent and adult offenders are deficient. As to this last point, the chapter will present some data concerning the role played by interpersonal cognitive problem-solving skills in the adjustment process of youthful offenders.

We have developed an immunochemiluminometric assay (ICMA) which has a sensitivity far greater than that of existing immunoassays and which discriminates clearly between euthyroid and hyperthyroid basal TSH levels (1). As part of the clinical validation of this assay, we have measured basal TSH levels in normal and hyperthyroid subjects over a twenty-four hour period. We have also measured the variation in basal TSH levels in a variety of clinically euthyroid patients with acute and chronic non-thyroidal disease.

Anorexia nervosa can be a devastating illness resulting in physical impoverishment and grossly impaired psychosocial functioning. It is characterized primarily by a refusal to eat a sufficient amount of food to sustain an adequate level of nourishment (Slade, 1982). One diagnostic criterion is the maintenance of weight at least 25% below the norm for one’s age (American Psychiatric Association, 1980). Such extensive weight loss plays havoc with a body that is often already under the physiological stress of puberty. Disturbed attitudes toward eating, manifested in preoccupations with food and peculiar patterns of handling food, is another noted feature of the disorder (Cooper & Fairburn, 1984; Garner, 1986; Garner & Bemis, 1982; Halmi, 1982; McFarlane, Bellissimo, & Upton, 1982; Muuss, 1985). Other features include intense fears of weight gain, behaviors directed toward weight loss, excessive physical activity, disturbances in body image, and, in females, amenorrhea (Halmi, 1982; Kissel & Arkins, 1973; Minuchin, Rosman, & Baker, 1978; Muuss, 1985; Slade, 1982).

It is well known that the secretion of the anterior pituitary (AP) hormones, thyrotropin (TSH) and prolactin (PRL), is under tonic stimulatory and inhibitory control, respectively, by the hypothalamus. It is now clear also that the hypothalamic control of AP hormone secretion is mediated by the release into the portal blood vessels of a variety of peptidic and nonpeptidic substances. Data gathered during the last few years have demonstrated that TRH and the central neurotransmitter dopamine (DA) have important actions on TSH and PRL release from the AP. Furthermore, somatostatin and a variety of other central neurotransmitters such as noradrenaline have effects which will be considered briefly.

The isolation and characterization of the growth hormone (GH) releasing peptides 1–37 (GRF 37), 1–40 (GRF 40) and 1–44 (GRF 44) have led to the generation of antibodies which have been used for immunocytochemistry techniques and the development of assays based on standard competitive protein binding principles. These procedures are now being used to measure circulating levels of GRF in man in both normal and disease states and to investigate abnormalities associated with the release of this peptide. Recently, GRF 40 and GRF 44, which are immunologically and biochemically identical to GRF of pancreatic origin, have been demonstrated in human hypothalamic extracts (1,2). Immunohistochemical studies in both rats and primates have demonstrated the presence of GRF-positive neurons in the hypothalamus and median eminence (3). Further immunohistochemical studies have also demonstrated the presence of immunoreactive GRF in several pancreatic endocrine tumors (4-6). In a large retrospective study, GRF immunoreactivity was detected in 4/24 pancreatic carcinoids, 1/5 bronchial carcinoids, 2/15 gut carcinoids, 1/2 thymic carcinoids, 2/20 medullary carcinomas of thyroid, 1/12 pheochromocytomas and 5/20 small cell carcinomas of lung (7). In this series, clinical features of acromegaly were present in only 2 of the 4 pancreatic carcinoids and in the single patient with a bronchial carcinoid tumor. These data are concordant with earlier case reports of acromegaly associated with bronchial and foregut carcinoids (8–11).

The prostaglandins were first isolated from the lungs by Bergstrom and his coworkers more than 14 years ago (1). It is now established that in animal studies all prostaglandins have powerful effects on both respiratory smooth muscle and on pulmonary vascular smooth muscle and that the lungs have an important function in their metabolic degradation, since some 90–95% of infused E and F prostaglandins are removed predominantly by the enzyme 15-prostaglandin dehydrogenase (15-PGDH) on a single passage through the pulmonary circulation. It is of interest that the A prostaglandins, which have a similar but less potent effect than the E prostaglandins, are less readily degraded by 15-PGDH in the lungs of experimental animals. Similar results have been obtained with prostaglandin F2α (PGF2α) man and it is suggested that degradation occurs in the pulmonary endothelial cells (2,3).