Trends in prescribing of buprenorphine.
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Buprenorphine↗
Biomedical subjects
Laurence Reed
Publications and source records attributed to Laurence Reed.
Benzodiazepine co-dependence exacerbates the opiate withdrawal syndrome.
Patients seeking treatment for opiate withdrawal are commonly also dependent on benzodiazepines, although the interactions between benzodiazepine and opiate dependence and withdrawal syndromes have been subject to little systematic investigation. This is the first study comparing type, severity and course of opiate withdrawal symptoms between opiate dependent patients with, and without, concurrent benzodiazepine dependence. Patients dependent only on opiates (n = 39), and patients dependent on both opiates and benzodiazepines (n = 22), were recruited from consecutive admissions to an in-patient drug treatment unit. Quantity and duration of prior opiate use was similar for both groups. Patients completed daily self-ratings of opiate withdrawal (SOWS) for the duration of a standard in-patient detoxification treatment. Co-dependent patients were detoxified from benzodiazepines and opiates concurrently. Co-dependent patients reported a more severe withdrawal symptoms than patients withdrawing from opiates alone. Co-dependent patients had significantly more severe opiate withdrawal symptoms. Concurrent benzodiazepine withdrawal exacerbates opiate specific withdrawal symptoms. Possible psychological and neurophysiological mechanisms for the observed sensitisation are discussed.
Adult↗
Practice and difficulty evoke anatomically and pharmacologically dissociable brain activation dynamics.
Brain activation is adaptive to task difficulty and practice. We used functional MRI to map brain systems activated by an object-location learning task in 24 healthy elderly volunteers each scanned following placebo and two of four active drugs studied. We distinguished a fronto-striatal system adaptive to difficulty from a posterior system adaptive to practice. Fronto-striatal response to increased cognitive load was significantly attenuated by scopolamine, sulpiride and methylphenidate; practice effects were not modulated by these drugs but were enhanced by diazepam. We also found enhancement by methylphenidate, and attenuation by sulpiride, of load response in premotor, cingulate and parietal regions comprising a spatial attention network. Difficulty and practice evoke anatomically and pharmacologically dissociable brain activation dynamics, which are probably mediated by different neurotransmitter systems in humans.
Adrenergic Uptake Inhibitors↗
The role of insulin in human brain glucose metabolism: an 18fluoro-deoxyglucose positron emission tomography study.
The effect of basal insulin on global and regional brain glucose uptake and metabolism in humans was studied using 18-fluorodeoxyglucose and positron emission tomography (FDG-PET). Eight healthy male volunteers aged 49.3 +/- 5.1 years were studied twice in random order. On each occasion, they received an infusion of 0.1 mg. kg(-1). min(-1) somatostatin to suppress endogenous insulin production. In one study 0.3 mU. kg(-1). min(-1) insulin was infused to replace basal circulating insulin levels, and in the other study a saline infusion was used as control. We sought stimulatory effects of basal insulin on brain glucose metabolism particularly in regions with deficiencies in the blood-brain barrier and high density of insulin receptors. Insulin levels were 27.07 +/- 1.3 mU/l with insulin replacement and 3.51 +/- 0.4 mU/l without (P = 0.001). Mean global rate of brain glucose utilization was 0.215 +/- 0.030 mmol. kg(-1). min(-1) without insulin and 0.245 +/- 0.021 mmol. kg(-1). min(-1) with insulin (P = 0.008, an average difference of 15.3 +/- 12.5%). Regional analysis using statistical parametric mapping showed that the effect of basal insulin was significantly less in the cerebellum (Z = 5.53, corrected P = 0.031). We conclude that basal insulin has a role in regulating global brain glucose uptake in humans, mostly marked in cortical areas.
Adult↗