Additional femoral catheter in combination with popliteal catheter for analgesia after major ankle surgery.

BACKGROUND: The contribution of the saphenous nerve in pain after major ankle surgery is unknown. The aim of this study was to evaluate its contribution in this context. METHODS: Fifty patients were included in this prospective, randomized, controlled study. In all patients [Group P (popliteal) and Group F (popliteal+femoral)], a popliteal catheter was placed before operation and ropivacaine 0.5% (30 ml) administered via this catheter; major ankle surgery was then performed under spinal anaesthesia. In Group PF patients, an additional femoral catheter was sited before operation and ropivacaine 0.5% (10 ml) administered. Six hours after spinal anaesthesia (defined as T(0)), a continuous infusion of ropivacaine 0.3% (14 ml h(-1)) was started through the popliteal catheter until T(24). Then, the concentration was reduced to 0.2% until T(48). Patients in Group PF received continuous ropivacaine 0.2% (5 ml h(-1)) through the femoral catheter from T(0) to T(48). I.V. morphine patient-controlled analgesia was used as a rescue analgesia. Pain at rest, pain with movement, adverse effects, and i.v. morphine consumption were assessed. Pain at rest and on movement was evaluated 6 months after operation. RESULTS: Pain at rest was comparable in the two groups. In Group PF, patients had significantly reduced pain during movement in the postoperative period (P=0.01) and 6 months after operation (P=0.03). Morphine consumption was significantly reduced in Group PF at T(0)-T(24) and T(24)-T(48) (P=0.01). Adverse effects were comparable in both groups. CONCLUSIONS: The addition of continuous femoral catheter infusion of ropivacaine to a continuous popliteal catheter infusion improved postoperative analgesia during movement after major ankle surgery. This effect was still present 6 months after surgery.

General life satisfaction and domain-specific quality of life in chronic schizophrenic patients.

Subjective quality of life (QOL) has often been assessed through questionnaires or structured interviews focusing on the person's satisfaction with various life domains. In particular, most QOL instruments for psychiatric patients are based on this concept. We report on a study casting some doubts on the rationale of this approach. We investigated the QOL of 48 chronic schizophrenic outpatients with a long-term disease history (at least 20 years) using a German version of the Lancashire QOL Profile. The interrelations between general life satisfaction, satisfaction with specific life domains, psychological well-being and psychopathology were studied using correlation analysis and multiple linear regression. Of the life domains assessed, only two, namely social relations and health, contributed significantly to the patients' general life satisfaction, while the others (including work, leisure, family relations and housing) did not. The subscales on psychological well-being (self-esteem, affective state) as well as psychopathology were found to be more closely associated with general life satisfaction than almost all life domains considered. The findings are discussed with regard to the specific situation of the group of patients investigated. They give indications that the life domain approach to measuring QOL has its limitations, in particular when applied to patients having adapted to a very restricted everyday life.

EEG alterations in patients treated with clozapine in relation to plasma levels.

It is well known that psychotropic drugs can induce EEG alterations. Dose dependence seems established; however, there are no data concerning the impact of plasma levels. The authors investigated the influence of clozapine plasma levels on the frequency of EEG alterations. Data from 29 inpatients (18 male, 11 female, 31.7 +/- 10.2 years) receiving clozapine in a dose range between 25 and 600 mg were collected prospectively. There was no psychotropic or anticholinergic comedication. All patients had normal EEGs before taking clozapine. Fifteen patients showed pathological changes (group 2) and 14 no changes (group 1). Discriminant analysis showed that EEG changes are dependent on plasma levels (P = 0.0009, plasma levels in group 1 mean 81.6 ng/ml, +/- SD 64.6, in group 2 235.7 ng/ml, +/- 169.8). A total of 72.4% of the patients were correctly classified as having either pathological EEG changes or none by this analysis. Variables such as dose, age, sex, weight and duration of treatment were not statistically relevant. It can therefore be suggested that clozapine plasma levels are a valid indicator for the appearance of electrophysiological reactions.

Effects of bright artificial light on monoamines and neuropeptides in eight different brain regions compared in a pigmented and nonpigmented rat strain.

Seasonal affective disorder is a form of depression which recurs at the same time of the year. Exposure to bright artificial light at a dose of 2,500 lux is used to treat seasonal affective disorders. We exposed a pigmented (Brown Norway) and a nonpigmented (Sprague-Dawley) rat strain with bright artificial light for 21 days at two doses (2,500 and 6,100 lux) and analyzed dopamine, dihydroxyphenyl-acetic acid, 5-hydroxytryptamine (5-HT), and 5-hydroxyindole-acetic acid (5-HIAA) by high performance liquid chromatography (HPLC) and electrochemical detection in eight different brain regions. Furthermore, we measured tissue levels of substance P (SP), neurokinins (NK), vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), and neuropeptide Y (NPY) with radioimmunoassay. Our data obtained with light microscopy show that bright artificial light at both doses induced a massive destruction of photoreceptors in the retina of albino rats but not of the pigmented rat strain. Retinal lesion of photoreceptors resulted in increased tissue levels of all measured neuropeptides except SP in the hypothalamus and increased VIP in the ventral tegmental area/substantia nigra. Furthermore, increased 5-HT and 5-HIAA tissue levels were found in the ventral tegmental area/substantia nigra. In contrast, in the frontal cortex there was a significant reduction in 5-HIAA tissue levels and a decreased 5-HIAA/5-HT ratio, indicating decreased 5-HT metabolism. Light exposure of the pigmented rat strain revealed no changes in the measured biogenic amines and neuropeptides in any investigated brain region. Our data suggest that retinal lesion but not direct visual neurotransmission induced changes in neurotransmitters in some brain regions. We conclude that Brown Norway rats but not Sprague-Dawley rats are useful to study neurochemical effects of bright artificial light. However, Sprague-Dawley rats may be a useful tool to study biochemical mechanisms of photoreceptor damage by bright light.