The relationship of surgical castration to sexual recidivism in a sexually violent predator/sexually dangerous person (SVP/SDP) population is reviewed. A review of the literature on castrated sex offenders reveals a very low incidence of sexual recidivism. The low sexual recidivism rates reported are critiqued in light of the methodologic limitations of the studies. Better designed testicular/prostate cancer studies have demonstrated that, while sexual desire is reduced by orchiectomy, the capacity to develop an erection in response to sexually stimulating material is not eliminated. The relevance of this literature to SVP/SDP commitment decisions and ethics is discussed. Two vignettes of castrated, high-risk sex offenders illustrate how to address risk reduction. Two tables are presented: the first outlines individual case data from a difficult-to-obtain report, and the second summarizes the most frequently cited castration studies on sexual recidivism. Orchiectomy may have a role in risk assessments; however, other variables should be considered, particularly as the effects can be reversed by replacement testosterone.

The most recent type of civil commitment for dangerous sex offenders is found under the sexually violent predator laws. Forensic psychiatrists or psychologists must render an opinion as to whether the sex offender has a diagnosed mental disorder and, as such, represents a risk to public safety if released from custody into the community. Thus, expert testimony provided by these professionals has taken a central role in the commitment determinations. There is considerable debate as to what disorders predispose individuals to sexual recidivism and what the term "likely" signifies. In this article, the authors explore the debate in terms of whether Antisocial Personality Disorder is a qualifying diagnosed mental disorder for classification as a sexually violent predator and how a likely threshold of risk of sexual recidivism can be conceptualized.

Forensic psychiatrists and psychologists are often called on to provide opinions and render testimony in which minor head trauma accompanied by persistent somatic, cognitive, and/or emotional symptoms is alleged. The frequency of persistent symptoms following such minor head injury is generally low. The forensic clinician therefore must differentiate between subtle brain dysfunction, symptom amplification, psychogenic-based causes for the presence of cognitive and other deficits, or frank malingering. The purpose of this article is twofold: first, to review critical issues related to the assessment of malingering and symptom exaggeration in mild head injury cases; and second, to offer a practical model for the assessment of amplified neuropsychological and psychiatric deficits in civil litigants in cases of minor head trauma.

An innovative animal model of posttraumatic stress disorder (PTSD) is proposed in which nonhabituation of the acoustic startle response is developed in rats subsequent to tailshock exposure. Subjects (n = 31) received 30 minutes of intermittent tail shock on 2 days followed by exposure to the tailshock apparatus on the third day. Compared to baseline startle reactions, 9 of 31 tailshock-exposed rats developed nonhabituation of startle response reactions during the subsequent 3 weeks of testing. No control rats developed nonhabituation of startle reactions over a similar time period. These data suggest that this system models useful aspects of clinical PTSD emphasizing nonhabituation of startle reactions as a dependent variable. The method consistently identifies a subgroup of rats that develop persistent nonhabituation of startle in response to a tailshock-stress paradigm.

Risk assessment in the area of identification of violence has been dichotomized by several prominent researchers as the "clinical approach" versus the "actuarial method". The proponents of the actuarial approach argue for actuarially derived decisions to replace existing clinical practice. The actuarial method requires no clinical input, just a translation of the relevant material from the records to calculate the risk score. A risk appraisal approach based upon a sole actuarial method raises several questions: those of public safety, peer-accepted standards of practice, liability issues, and concordance with evidence-based medicine practice. We conclude that the sole actuarial approach fails to satisfy these critical issues.

Morrow, N. S. and T. Garrick. Effects of intermittent tail shock or water avoidance on proximal colonic motor contractility in rats. Physiol Behav 62(2) 233–239, 1997.—Changes in proximal colonic mechanical activity and defecation during exposure to three different types of experimental stressors were examined in rats chronically implanted with 2 force transducers on the proximal colon. To validate the integrity of the recording system, meal-induced changes in proximal colonic contractility were initially measured in all rats 1–2 days prior to stress induction. Different groups of ad lib fed rats were then exposed to tail shock, re-exposure to the shock chamber or water avoidance for 1 h over the next 1–2 days. Two types of phasic colonic contractions, long (0–3/min) and short (67ndash;8/min) duration, were analyzed separately using a computer. Long duration contractions were significantly elevated 21–71% over fasting basal values from 61–120 min following a meal. No other consistent changes during the prandial or postprandial period were observed. Tail shock significantly suppressed proximal colonic contractility from pre-shock values and increased fecal output and fluid content when compared to ad lib fed rats that were not shocked. Fecal output increased but proximal colonic contractility did not change when previously shocked rats were re-exposed to the tail shock chamber but not shocked. In rats exposed to water avoidance, proximal colonic contractility was minimally suppressed but defecation was significantly greater than home cage control animals. These results indicate that proximal colonic contractile activity is differentially altered by exposure to different environmental stressors and may be a contributing factor in stress-induced bowel dysfunction.

Nonhabituation of the acoustic startle response is used to identify rat subjects with altered alarm responses subsequent to trauma exposure. Subjects (n = 31) were exposed to 30 minutes of intermittent tail shock on 2 days followed by exposure to the apparatus on the third day. Twenty-nine percent of traumatized rats developed nonhabituation of startle over the subsequent 3 weeks of testing. No control rats developed nonhabituation of startle reactions over a similar time period. These data suggest that this system represents a more accurate representation of clinical PTSD than do other animal models.

The effect on gastric contractility following bilateral microinjection of thyrotropin-releasing hormone (TRH) analog. RX 77368, into the central nucleus of the amygdala was examined in fasted. urethane-anesthetized rats. Extraluminal force transducers were used to measure gastric corpus contractility. Bilateral microinjection of RX 77368 (0.5 μg. 1.0 μg,n = 6 each) stimulated gastric contractility for up to 120 min post-injection,P < 0.05. Gastric contractility was not significantly stimulated by microinjection of 0.1 μg RX 77368. 0.1% bovine serum albumin (BSA) into the central nucleus or RX 77368 (0.5 μg. 1.0 μg) into sites adjacent to the central nucleus. Peak responses (1.0 μg) occurred 40 min post-injection and represented a 16-26-fold increase over basal values. The frequency of gastric contraction waves was attenuated for 0–90 min in rats receiving central amygdaloid microinjection of RX 77368 (0.1. 0.5 or 1.0 μg) versus rats microinjected with the vehicle or RX 77368 into sites adjacent to the central nuclei. The stimulatory effect of RX 77368 (1.0 μg) on gastric contractility was abolished by subdiaphragmatic vagotomy. These results indicate that the TRH analog. RX 77368, acts within the central amygdala to vagally stimulate gastric contractility.

The effect of murine interleukin-1 beta (mIL-1 beta) microinjected into the dorsal vagal complex (DVC) on thyrotropin-releasing hormone (TRH) analogue (RX-77368)-induced stimulation of gastric contractility was examined in fasted, urethan-anesthetized rats. Gastric corpus contractions were measured with extraluminal force transducers and analyzed by computer. Microinjection of RX-77368 (30 ng) into the right DVC with mIL-1 beta microinjected either into the right (100, 250 pg) or into the left (100, 500 pg) DVC inhibited gastric contractility for 30-120 min postinjection. Peak suppression of gastric contractility (64-78%) occurred at 50-60 min postinjection. Microinjection of mIL-1 beta into the DVC at a lower dose (10 pg) or into sites adjacent to the DVC (100-500 pg) did not suppress the stimulated gastric contractility pattern. Injection of mIL-1 beta (250 pg) or 0.1% bovine serum albumin into the DVC alone did not alter basal gastric contractility. Intracisternal injection of the IL-1 receptor antagonist (250 ng/10 microliters) abolished the inhibitory effect of mIL-1 beta (250 pg) on gastric contractility. These results demonstrate that mIL-1 beta acts in the DVC to inhibit vagally stimulated gastric contractility, and its action is mediated by IL-1 receptors.

Forensic psychiatrists are not as vulnerable to liability as general psychiatrists. The absence of a traditional physician-patient relationship and judicial and quasijudicial immunity are all protective against malpractice actions. Although the absence of a doctor-patient relationship removes an essential element of malpractice, other types of liability such as defamation and ordinary negligence are possible and may not be covered by malpractice insurance. A model is proposed for forensic psychiatry of a partial secondary doctor-patient relationship out-weighted in most circumstances by duties to truth and/or the hiring attorney. Such a model seems most consistent with conflicting duties currently forced on all psychiatrists. This model has advantages of a duty, a violation of which is likely to be covered by malpractice insurance. Rather than deemphasizing partial secondary physician-patient responsibilities, it is advised to stress the important protection provided by judicial and quasijudicial immunity.

Changes in gastric contractility following microinjection of thyrotropin-releasing hormone (TRH) into the paraventricular nucleus of the hypothalamus (PVN) were examined in fasted, urethane-anesthetized rats. Gastric contractility was measured with extraluminal force transducers and analysed by computer. Unilateral and bilateral PVN microinjections of TRH (0.5 and 1.0 microgram) significantly increased the force index of gastric contractions from 0 to 60 min postinjection, when compared with animals microinjected with 0.1 microgram TRH, 0.1% BSA or TRH (0.5 and 1.0 microgram TRH) in sites adjacent to the PVN. The gastric force index was also significantly elevated from 61 to 120 min postinjection in rats receiving bilateral PVN microinjections of TRH (0.5 and 1.0 microgram). Peak gastric responses occurred within 10-20 min postinjection and represented an approximately eight-fold increase over basal values. In the remaining groups, the force index was not significantly altered from preinjection values. The excitatory action of TRH (1.0 microgram) on gastric contractility was completely abolished by subdiaphragmatic vagotomy. These results suggest that TRH acts within the PVN to stimulate gastric contractility via vagal-dependent pathways.

The role of thyrotropin releasing hormone (TRH) in the dorsal vagal complex (DVC) in mediating the enhanced gastric contractility induced by glutamate (100 pmol) microinjected into the raphe pallidus (Rpa) was investigated in urethane-anesthetized rats acutely implanted with miniature strain gauge force transducers on the corpus of the stomach. Glutamate-induced stimulation of gastric contractility was dose-dependently inhibited by bilateral microinjection into the DVC of TRH antibody (0.17, 0.85 or 1.7 μg/100 nl/site) but not by vehicle. TRH antibody microinjected into the dorsal medullary reticular field had no effect. These data indicate that activation of Rpa neurons by glutamate increases gastric motor function through TRH release in the DVC.

Changes in gastric contractility following lateral hypothalamic (LH) lesions with and without bilateral cervical vagotomy were measured in urethan-anesthetized rats. LH lesions were induced with direct current passed through stereotaxically placed electrodes. Gastric contractility was recorded continuously for 4 h with acutely implanted strain gauge force transducers and analyzed by computer. LH lesions consistently stimulated gastric contractility and caused more gastric mucosal injury than control conditions. Vagotomy blocked both gastric mucosal injury and high-amplitude gastric contractions. In rats with LH lesions and exogenously infused intragastric hydrochloric acid, atropine methyl nitrate inhibited high-amplitude gastric contractions and gastric erosions. These findings indicate that LH lesions stimulate vagally mediated high-amplitude gastric contractions, which, in the presence of hydrochloric acid, cause gastric mucosal erosions.