Depersonalization: a self-relations perspective.
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Biomedical subjects
Publications and source records attributed to M Sacks.
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Operations at the clinical-research interface exert a signal influence on the therapy of patients being treated on investigative units. The effect on the treatment milieu has been described but the impact of a research climate on individual psychotheraphy of hospitalized patients has not. We observed research-therapy interaction in 25 acutely schizophrenic patients. Analytically oriented psychotherapy was carried out on a National Institutes of Health clinical research unit where drugs are only occasionally used, and patients are subjects in psychobiological investigation. The subtle, and often neglected, interplay between therapy and research is examined, with emphasis on the shifting meanings of the patient's participation or refusal to participate in therapy, research, or both. A research transference and countertransference are defined, and some special behavioral patterns of research patients receiving dynamic therapy are considered in this framework.
A group pf 19 acute, medication-free schizophrenic patients was studied, using average-evoked responses (AERs) to four intensities of light. Comparison with age- and sex-matched normal controls and patients with bipolar affective disorders showed that schizophrenics had smaller AER amplitudes and either no increase or an actual decrease in amplitude with increasing stimulus intensity. Normal subjects and schizophrenic patients were discriminated with 71% accuracy using AER variables; normals, patients with bipolar disorders, and schizophrenic patients with 64% accuracy. Patients who evidenced this AER "reducing" pattern to a noticeable extent early in hospitalization showed greater improvement and tended to have relatively good premorbid histories.
The authors describe their experience in carrying out clinical and psychobiological research in a therapeutic milieu setting. The clinical-research meeting, composed of clinical-care staff with secondary research responsibilities, researchers, and acutely psychotic patients, proved to be a useful mechanism for identifying and resolving inevitable problems at the clinical-research interface and enhanced the effectiveness of research implementation and patient care. The authors discuss three specific areas where covert issues threatened to undermine the work of the unit-the abrogation of research responsibility, the abrogation of clinical responsibility, and intergroup competition and envy.
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This study is based on a simple chemical interaction of peroxynitrite (O = N-O-O-) and luminol, which produces blue light upon oxidation. Since peroxynitrite has a half-life of about 1 s, a drug known as linsidomine (SIN-1) is used as a peroxynitrite generator. Peroxynitrite can oxidize lipids, proteins and nucleic acids. Upon the stimulation of inflammation and/or infection, macrophages and neutrophils can be induced to produce large amounts of peroxynitrite, which can oxidize phenols and sulphhydryl-containing compounds. Therefore, phenols and sulphhydryls eliminate peroxynitrite. This is an example of the Yin-Yang hypothesis e.g. oxidation-reduction. Acetaminophen (Tylenol) can inhibit fever and some types of pain without being a particularly effective anti-inflammatory. Since it is a phenol, it could act as a nitration target for peroxynitrite. Then peroxynitrite, the possible cause of pain and elevated temperature, might be destroyed in the reaction. Acetaminophen is a phenolic compound which produces a clear inhibitory dose-response curve with peroxynitrite in its range of clinical effectiveness. Whether acetaminophen actually works as we suggest is to be proven. Three different types of reaction could decrease the amount of peroxynitrite: (a) interference with base-catalysed opening of the SIN-1 molecule; (b) destruction of one or both substances needed to form it--superoxide and/or nitric oxide; when the SIN-1 degrades to superoxide and nitric oxide, the former may be destroyed by superoxide dismutase (SOD); (c) peroxynitrite may react directly with phenols (mono-, di-, tri- and tetraphenols), possibly by nitration. Nordihydroguaiaretic acid and 2-hydroxyestradiol (catechol estrogen) are potent inhibitors of luminol light emission. Epineprine, isoproterenol, pyrogallol, catechol and ascorbic acid (a classic antioxidant) are all inhibitors of luminol chemiluminescence. Isoproterenol, norepinephrine/and epinephrine first inhibit light but overall stimulate the light production. Initially, SIN-1 degrades to produce peroxynitrite, which reacts with luminol to produce blue light. If any of three catecholamines are present with the reaction that produces light, there is an initial inhibition of light production, and then a marked stimulation. A possible reason for this is that these catechols are oxidized and the metabolized phenol stimulates the production of light from luminol. Also, during oxidation of catecholamines superoxide is sometimes formed, which could stimulate production of peroxynitrite. This simple screening system is introduced to find useful antioxidants against peroxynitrite.
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Digitalis is a ubiquitous drug in modern clinical medicine and digitoxicity is one of the more common iatrogenic disorders. Psychiatric problems are often overlooked as manifestations of digitalis excess and may range from mild disorientation, lethargy, or restlessness to full blown delirium. In this paper we discuss two patients who presented to a psychiatric inpatient unit and were later found to be digitoxic. Psychiatrists are advised to consider digitalis as a possible cause of mental abnormalities and are reminded that psychiatric signs may be the first indication of a potentially lethal drug toxicity. Psychiatric patients may also be at special risk for the development of digitoxicity because of erratic drug taking, electrolyte imbalance or increased autonomic tone.
Ectopic pituitary adenoma of the sphenoid sinus in a 68-year-old woman is presented. The confusing discrepancy between the imaging features and the mild clinical manifestations of extensive bone destruction of the skull base is emphasized. A definite diagnosis can be established only by histopathological examination supported by immunohistochemical studies.
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