Search PubMed⌕ Search

PubMed · 9541160

Article commended.

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E C Lauterbach, J M Meyer, G M Simpson. 1998. Article commended.. https://doi.org/10.4088/jcp.v59n0308d

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

[Receptor mapping in living human beings by means of positron emission tomography].

PET can map neurotransmitter synthesis, storage, release, binding to receptors, and re-uptake in the brain with tracer concentrations in the picomolar or nanomolar range. Tracers are analogues of naturally occurring precursors or ligands, or are drugs, which bind with varying degrees of specificity to receptor subtypes in the brain. Tracers have been synthesised for many transmitter systems, but dopaminergic and serotonergic neurotransmissions are the main foci of current efforts to selectively trace synthesis, storage, re-uptake, or post-synaptic binding of neurotransmitters. Common measures of the tracer uptake and binding include precursor clearance (k3), a measure of transmitter synthesis and trapping, and binding potential (pB), a measure of the receptor binding per unit of unbound tracer, and hence a measure of the release of the endogenous transmitter, or the occupancy of a drug. Dopamine tracers are used in diseases of the basal ganglia, whereas serotonin, benzodiazepine, and opiate tracers are used in lesions of the cerebral cortex. PET has revealed loss of dopaminergic terminals and dopamine synthetic capacity in Parkinson's disease, MPTP intoxication, and Lesch-Nyhan's syndrome; release of dopamine after administration of cocaine and amphetamine, and in motor activity and cognition; increased synaptic dopamine and release of dopamine, and the 70-90% neuroleptic occupancy of dopamine receptors in the striatum, in patients with schizophrenia; loss of muscarinic and nicotinergic receptors in Alzheimer's disease, and benzodiazepine and opiate receptors in stroke, epilepsy, and Huntington's chorea; altered opiate receptors in chronic pain and drug abuse; and release of opiates in analgesia; but changes in serotonin synthesis, transport, and binding in affective or psychotic disorders remain elusive.

Basal Ganglia Diseases↗

Neuroimaging in basal ganglia disorders: perspectives for transcranial ultrasound.

Transcranial sonography is a new diagnostic tool, allowing not only the evaluation of cerebral arteries but also the two-dimensional display of the brain parenchyma. In this review we will summarize basics of the application, the ultrasound anatomy of the brain and sonographic findings in some movement disorders. While in normal adults basal ganglia nuclei are hypoechogenic, they are hyperechogenic in certain basal ganglia disorders. In Parkinson's disease, for example, the substantia nigra can be depicted as a distinctly echogenic area. An elevated echogenicity of the lentiform nuclei was noticed in patients with primary adult-onset dystonia. In both disorders the altered echogenicity may arise from higher heavy metal tissue content (i.e. iron in Parkinson's disease and copper in primary dystonia). Our findings converge to the hypothesis that transcranial ultrasound sensitively detects pathological metal accumulation not identified by other neuroimaging techniques (CT and MRI) and therefore provides new insights in the diagnosis of basal ganglia disorders. The implications of these findings for the understanding of the pathogenesis and its usefulness for the early diagnosis of movement disorders are outlined.

Basal Ganglia Diseases↗