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Propofol injection pain: comparing the addition of lignocaine or metoclopramide.

Lignocaine has been shown to reduce the incidence of pain on injection of propofol. Metoclopramide, a weak local anaesthetic and commonly used antiemetic, was combined with propofol and the mixture compared, in a prospective, randomized trial, with a lignocaine-propofol combination. The incidence of injection pain was similar in both groups, as were recovery times and incidence of vomiting. The metoclopramide-propofol group experienced a lower incidence of nausea. One patient in the metoclopramide-propofol group had a minor extrapyramidal reaction. No adverse local or haemodynamic effects were seen.

Adult↗

Prochlorperazine.

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Drug Utilization↗

Basal ganglia: functional anatomy and physiology. Part 1.

Advances in knowledge about basal ganglia structure and connectivity from 1925 to date are reviewed. Current concepts about neuronal populations, transmitters, and input and output of each of the basal ganglia nuclei are presented. The portrayal by Wilson, in 1925, of the striatum as a simple homogeneous structure has been replaced by the recognition, based on staining characteristics, connectivity, and function, that the neostriatum is compartmentalized into striosomes, matrisomes, and matrix compartments. Electrophysiologic studies have further shown the existence, in the neostriatum, of neuronal clusters that represent basic functional units much like the functional columns described much earlier for the cerebral cortex. Whereas the neostriatum is considered the major receiving area of the basal ganglia, the globus pallidus and substantia nigra pars reticulata constitute the major output nuclei. Combined neuroanatomic and neurophysiologic studies have revealed precise somatotopic organization throughout the basal ganglia system such that the leg, arm, and face areas of the cerebral cortex related to respective topographic areas within the striatum, pallidum, substantia nigra, and subthalamus. The previous concept of an inhibitory role for dopamine on striatal neurons has been modified. It is now acknowledged that dopamine exerts an inhibitory effect on striatal neurons that project to the external pallidum and a facilitatory effect on striatal neurons that project to the internal pallidum and substantia nigra pars reticulata. The previous concept of serial connectivity of the neostriatum (funnel concept) has been replaced by the concept of parallel connectivity. Within the internal connectivity of the basal ganglia, there is a fast system in which the neurotransmitter is gamma-aminobutyric acid (GABA) and a slow system modulated by neuropeptides. The slow system is believed to give identity to an otherwise homogenous GABAergic system.

Basal Ganglia↗

Neuropathophysiology of movement disorders in cerebral palsy.

Recent developments in understanding the pathophysiology of disordered motor control in cerebral palsy are reviewed. In spastic cerebral palsy, evidence for abnormal segmental as well as supraspinal control of motor neuron output exists. Impaired Ia inhibition of antagonist muscles has been suggested but recently contested. Evidence also supports the role of decreased presynaptic inhibition of Ia afferents and decreased nonreciprocal Ib inhibition. Furthermore, early cerebral injury results in reorganization of supraspinal (corticospinal) inputs to motor neuron pools. In extrapyramidal cerebral palsy, injury of basal ganglia or thalamus has been demonstrated. A scheme for understanding the neurochemical circuitry of the extrapyramidal system is discussed. Animal models and certain specific human diseases provide examples of how this circuitry may be disturbed, thereby resulting in an imbalance between the direct and indirect striatal output systems and in impaired motor control. Future studies employing postmortem neurochemical analysis, functional magnetic resonance imaging, and positron emission tomographic scanning may foster progress in this area.

Animals↗

Extrapyramidal manifestations complicating organophosphorus insecticide poisoning.

Six patients who developed extrapyramidal manifestations following poisoning with the organophosphorus (OP) insecticide fenthion are reported. The extrapyramidal features, in order of frequency, were dystonia, rest tremor, cog-wheel rigidity, and choreo-athetosis. The delay in onset of these signs, following poisoning, varied from 4 to 40 days, and they disappeared spontaneously in about 1 to 4 weeks in those who survived. The human extrapyramidal system is rich in cholinergic neurons and acetylcholinesterase (AChE). Inhibition of AChE by fenthion, which has ready access to central neurons on account of its lipid solubility, is postulated as the mechanism underlying the extrapyramidal manifestations.

Adult↗

Extrapyramidal reactions and the selective serotonin-reuptake inhibitors.

OBJECTIVE: To review the known published reports of extrapyramidal reactions (EPRs) associated with the use of selective serotonin-reuptake inhibitors (SSRIs). DATA SOURCES: Information was selected from a MEDLINE search (January 1990 to January 1996) of English-language medical literature. Manual searches of pertinent journal article bibliographies were also performed. DATA EXTRACTION: Appropriate information from all reports obtained was included, with specific attention directed toward patient age, gender, primary psychiatric diagnosis, total daily SSRI dosage, dosage escalation strategy, and concurrent psychotropic medications. DATA SYNTHESIS: Reports of EPRs associated with SSRI use have been accumulating in the medical literature for several years. More commonly associated with high-potency antipsychotics, EPRs can have an adverse impact on medication compliance and hospital readmissions. The proposed hypothesis for EPRs occurring with SSRI use involves serotonin's inhibitory actions on extrapyramidal dopamine activity. Other possible contributing factors include pharmacokinetic interactions or drug-disease interactions. EPRs may include dystonias, dyskinesias, akathisia, parkinsonism, exacerbations of Parkinson's disease, and possibly the neuroleptic malignant syndrome. The majority of SSRI-related reactions appear to occur within the first month of treatment. Information from available case reports does not strongly support any consistent risk factor, although some worth considering may include total SSRI daily dose, rapid dose escalation strategies, increased age, female gender, concurrent psychotropics known to also precipitate EPRs, and concurrent disease states such as Parkinson's disease. Since SSRI-related EPRs have occurred in different situations with different possible contributing factors, clinical pharmacy practitioners and other healthcare providers should remain aware of these reactions and carefully consider educating and monitoring their patients accordingly. CONCLUSIONS: The use of SSRIs may be associated with the development of EPRs; therefore, appropriate monitoring should be considered for patients so that optimal pharmaceutical care may be provided.

Basal Ganglia Diseases↗