PubMed · 9747395
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D Healy, M Savage. 1998. Reserpine exhumed.. https://doi.org/10.1192/bjp.172.5.376
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The author describes the development and evaluation of the Psychiatric Discomfort Scale, a self-report instrument that provides a quantitative measurement of patients' discomfort with psychiatric symptoms that change over time. Initially, a 60-item instrument was evaluated with 55 psychiatric inpatients in a Veterans Affairs (VA) medical center and a comparison group of 71 medical outpatients in the VA system. It was revised and tested again with 292 outpatients in treatment for psychosis. The resulting 23-item instrument was found to be internally consistent and responsive to changes in a patient's condition over time.
An increase in emotional defecation in rats in a well-habituated environment induced by neuroleptic drugs (NDef) has been proposed as a model for neuroleptic-induced akathisia. We examined the effects of dopamine receptor antagonists and agonists on this model. A selective dopamine D1 antagonist (SCH 23390) and a selective D2 antagonist (raclopride) induced increased defecation at higher doses, and demonstrated a synergistic effect at lower doses. Selective D1 (SKF 82958) and D2 (quinpirole) agonists did not have a significant effect on defecation, nor did they reverse the effect of haloperidol. In a further pilot study, we explored the effects of typical and atypical neuroleptics on this model. The haloperidol and risperidone treated rats produced more faecal boli than those treated with clozapine, thioridazine and chlorpromazine, with the former being non-significantly greater than the vehicle-treated group. The results of our studies suggest that NDef is most probably an effect of central dopamine antagonism that is not specific to D1 or D2 receptors, but that the two receptor subtypes have a synergistic effect. It is unlikely to be due to actions of neuroleptics on 5HT2 or alpha1 receptors as has sometimes been suggested. The results have implications for our understanding of the pathogenesis of akathisia.
PURPOSE: There are no rodent models of chronic epidural catheterisation which can induce clinically relevant analgesic effects of morphine (potency ratio of intrathecal:epidural = 10 to 30:1). The purpose of this study was to investigate a new rat model of chronic epidural catheterisation by comparing the analgesic effect of epidural and intrathecal morphine. METHODS: In Sprague-Dawley rats, for epidural catheterisation, a skin incision and muscle dissection were made at T13 level in the midline. The intervertebral ligament was cut to insert an epidural catheter (polyethylene tube; outer diameter 0.14 mm) 2 cm caudally. The distal end of the catheter (0.61 mm) was passed s.c. to exit in the dorsal neck area. For intrathecal catheterisation, the atlanto-occipital membrane was incised to insert a catheter (0.61 mm) 8.5 cm caudally. The effects of morphine (1, 3, 10, 30, or 100 micrograms.10 microliters-1 intrathecally, and 30, 100, or 300 micrograms.5, 10, or 20 microliters-1 epidurally) on thermal escape latency were investigated by a hot box test. Behaviour and motor function were also tested. RESULTS: A volume of 20 microliters induced greater analgesic effect than 5 and 10 microliters epidural administration. The ED50 of epidural morphine (94.1 micrograms) was 30 times more than that of intrathecal morphine (3.1 micrograms). CONCLUSION: A new rat model of chronic epidural catheterisation is described, which provides a similar analgesic epidural: intrathecal potency ratio for morphine to that in humans when morphine is administered in a volume of 20 microliters.