The value of single photon emission tomography in psychopharmacology

Abstract

Functional neuroimaging with SPET and PET offers the opportunity to visualize brain function either in terms of blood flow and metabolism or receptor function using specific ligands. SPET is a more widely available and cheaper technology than PET. Continuously developing and being refined, this technology will help the understanding of brain function generally and of brain dysfunction in psychiatric disorders specifically. SPET may also be used to study how these measures of brain function change with pharmacological intervention. Receptor imaging allows the study of drug-receptor interactions in vivo. As yet, the precise role and value of these techniques have not been established, but they do provide complementary tools to structural imaging and may ultimately provide prognostic information and facilitate refinement of the pharmacotherapeutic rationale underlying clinical practice.KEY WORDS-Imaging, psychiatry, receptors, blood flow. INTRODUCTIONFunctional neuroimaging includes studies with radionuclides (either single photon or positron emitters) as well as more recently developed magnetic resonance imaging sequences and spectroscopy. With the use of tomography to construct threedimensional images, we thus have two main types of emission tomography: single photon emission tomography (SPET) and positron emission tomography (PET). Although PET has greater spatial resolution, clinical applications of SPET may be more practicable because of its wider availability and lower cost. With PET and SPET, we can visualize certain brain functions, namely blood flow, metabolism and neurotransmission.Psychopharmacology, by improving our understanding of ligandheceptor interactions, has as its ultimate goal the modification of pathological behaviours using drug treatments. Potential drug treatments are initially evaluated using animal models and then must be explored in humans and finally in the clinical setting. The most important measure of a pharmacological action will be clinical, that is its effect on behaviour. It is not always clear, however, how these clinical effects correlate with drug action at receptor level; the exact relationship between the neuropharmacology of a drug and its psychopharmacology is often ill defined. Thus, although we may well know the psychopharmacological profile of a drug, its effects on normal and abnormal behaviours, that knowledge is likely to have come about serendipitously. If we understood better the physiology and pharmacology of behaviour, and at the molecular level of those drugs which treat pathological behaviours, we could better develop drugs with specific behavioural effects. Any technological or conceptual advance which would allow us to examine the relationship between a drug's psychopharmacology and its neuropharmacology in more detail would help us in the development of such 'designer drugs'. Functional neuroimaging with Single Photon Emission Tomography (SPET) and Positron Emission Tomography (PET) offers such an advance. BACKGROUNDThe 1970s saw the advent of tomography for ...

Correlation of the vesicular acetylcholine transporter densities in the striata to the clinical abilities of women with rett syndrome

“…[ 3 H]vesamicol binds to the vesicular acetylcholine transporter (ACVT) (Wenk and Mobley, 1996). (−)‐( 2R,3R )‐2‐hydroxy‐3‐(4‐phenylpiperidino)‐5‐[ 123 I]iodotetralin, (−)‐5‐[ 123 I]iodobenzovesamicol ([ 123 I] IBVM] provides the means to estimate the density of the acetylcholine vesicular transporters in the living human brain by single‐photon emission‐computed tomography (SPECT) (Barret et al, 2008; Jung et al, 1996; Mach et al, 1997; Moriarty, 1994; Zea‐Ponce et al, 2005). [ 123 I]IBVM binds to the acetylcholine (ACh) transporter of presynaptic vesicles in the living human brain of healthy adult volunteers (Kuhl et al, 1994, 1996) and in Alzheimer's (Mazère et al, 2008) and Parkinson's diseases (Kuhl et al, 1996).…”

“…The development of an in vivo procedure to map the integrity of cholinergic neurons in the brains of people with RTT will likely then provide the means to safely and effectively determine the results of pharmacological and other interventions for this disorder. The presynaptic density and distribution of vesicular acetylcholine transporters can be estimated in the living human brain by SPECT (Moriarty, 1994) following the intravenous administration of [ 123 I]IBVM (Barret et al, 2008). Binding potentials estimated using reference tissue methods are comparable with those using arterial blood sampling (Barret et al, 2008).…”