Effects of amphetamine on local cerebral metabolism in normal and schizophrenic subjects as determined by positron emission tomography

Wolkin, Adam; Angrist, Burton; Wolf, Alfred P.; Brodie, Jonathan D.; Wolkin, B.; Jaeger, Judith; Cancro, Robert; Rotrosen, John

doi:10.1007/bf00177923

Cited by 98 publications

(47 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…33 Reduction of cortical CMRglc is a common response to acute administration of drugs of abuse, 34 as observed with opiates, 35 barbiturates, 36 benzodiazepines, 37 cocaine 38 and amphetamine. 39 This commonality is consistent with a classic theory proposing that activity in subcortical emotion circuits alters human consciousness more when cortical inhibition is suppressed. 40 In this view, metabolic effects of intoxication represent release of subcortical regions from cortical inhibition, resulting in heightened emotions.…”

Section: Importance Of Absolute Measuressupporting

confidence: 87%

“…A total of 10 regions of interest (ROIs) were selected because of prior demonstrations of functional abnormalities associated with MA abuse: parietal cortex (Brodmann areas (BAs) 1,2,3,5,7,19,39,40), thalamus, dorsal striatum, ventral striatum, medial orbitofrontal cortex (gyrus rectus and medial orbital gyrus; BA 11), lateral orbitofrontal cortex (lateral, posterior orbital and inferior frontal gyri; BAs 47, 11), infragenual ACC (BAs 25, 32), supragenual ACC (BAs 24, 32, 33), insula (BA 13) and amygdala. 1,6,8,9 ROIs were drawn on the structural MR template provided in SPM2, using MEDx Software (Sensor Systems, Sterling, VA, USA).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Changes in cerebral glucose metabolism during early abstinence from chronic methamphetamine abuse

et al. 2007

View full text Add to dashboard Cite

Changes in brain function during the initial weeks of abstinence from chronic methamphetamine abuse may substantially affect clinical outcome, but are not well understood. We used positron emission tomography with [F-18]fluorodeoxyglucose (FDG) to quantify regional cerebral glucose metabolism, an index of brain function, during performance of a vigilance task. A total of 10 methamphetamine-dependent subjects were tested after 5-9 days of abstinence, and after 4 additional weeks of supervised abstinence. A total of 12 healthy control subjects were tested at corresponding times. Global glucose metabolism increased between tests (P = 0.01), more in methamphetamine-dependent (10.9%, P = 0.02) than control subjects (1.9%, NS). Glucose metabolism did not change in subcortical regions of methamphetaminedependent subjects, but increased in neocortex, with maximal increase ( > 20%) in parietal regions. Changes in reaction time and self-reports of negative affect varied more in methamphetamine-dependent than in control subjects, and correlated both with the increase in parietal glucose metabolism, and decrease in relative activity (after scaling to the global mean) in some regions. A robust relationship between change in self-reports of depressive symptoms and relative activity in the ventral striatum may have great relevance to treatment success because of the role of this region in drug abuse-related behaviors. Shifts in corticalsubcortical metabolic balance either reflect new processes that occur during early abstinence, or the unmasking of effects of chronic methamphetamine abuse that are obscured by suppression of cortical glucose metabolism that continues for at least 5-9 days after cessation of methamphetamine self-administration.

show abstract

Section: Importance Of Absolute Measuressupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Changes in cerebral glucose metabolism during early abstinence from chronic methamphetamine abuse

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Diminished cortical activity has been described in several studies with both depressant and stimulant drugs of abuse such as benzodiazepines, morphine, amphetamines, and cocaine (Mathew and Wilson 1991;London et al 1990aLondon et al , 1990bWolkin et al 1987) and has been viewed as a correlate of euphoria (London et al 1990a(London et al , 1990bPearlson et al 1993). However, in our studies, both cortical hypometabolism and cerebellar hypermetabolism were not associated with positive, but rather with unpleasant feelings such as anxiety and depression, cognitive disturbances, and general psychopathological signs.…”

Section: Neurometabolic Effects Of the Drugs And Correlations With Psmentioning

confidence: 99%

“…Several studies with other psychotropic substances with both stimulant and sedative properties (cocaine, morphine, benzodiazepines, barbiturates) reported decreased cortical activity (London et al 1990a,b;Mathew and Wilson 1991). Studies on the effects of stimulant amphetamines are inconsistent with reports of decreases, no effects, or increases of glucose metabolism or cerebral blood flow (Wolkin et al 1987;Kahn et al 1989;Metz et al 1991;Devous et al 1995;Ernst et al 1997). A recent study with intravenous d-amphetamine administration reported no global change, but frontal, limbic, subcortical, and cerebellar increases of regional glucose metabolic rates (Ernst et al 1997).…”

mentioning

confidence: 99%

Neurometabolic Effects of Psilocybin, 3,4-Methylenedioxyethylamphetamine (MDE) and d-Methamphetamine in Healthy Volunteers A Double-Blind, Placebo-Controlled PET Study with [18F]FDG

Gouzoulis-Mayfrank

1999

Neuropsychopharmacology

181

100

View full text Add to dashboard Cite

The neurometabolic effects of the hallucinogen psilocybin (PSI; 0.2 mg/kg), the entactogen 3,4-methylenedioxyethylamphetamine (MDE; 2 mg/kg) and the stimulant d-methamphetamine (METH; 0.2-0.4 mg/kg) and the drugs' interactions with a prefrontal activation taskwere investigated in a double-blind, placebo-controlled human [F-18]fluorodeoxyglucoseFDG-positron emission tomographicPET study (each group: n ϭ 8 Experimental studies of cerebral blood flow and metabolism with psychoactive drugs in humans aim to explore the interaction of these drugs with human brain function. Recent studies with hallucinogenic, "mind-expanding" drugs in healthy subjects provided evidence in favor of an altered functional interhemispheric balance From the Department of Psychiatry and Psychotherapy (EG-M, BT, HS), University of Technology (RWTH), Aachen, Germany; Department of Nuclear Medicine (MS, OS, CA, UB), University of Technology (RWTH), Aachen, Germany; Department of Psychiatry (MS), University of Ulm, Ulm, Germany; Pharmaceutical Institute (K-AK), University of Tübingen, Tübingen, Germany; Psychiatric and Neurological Hospital Christophsbad (LH), Göppingen, Germany.Address correspondence to: E. Gouzoulis-Mayfrank, M.D., Department of Psychiatry and Psychotherapy, University of Technology (RWTH), Pauwelsstrasse 30, D-52074 Aachen, Germany.Received March 14, 1998, accepted July 20, 1998 566 E. Gouzoulis-Mayfrank et al. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 20 , NO . 6 with right hemispheric dominance and an increased activity in frontocortical regions after acute administration of mescaline, psilocybin, or ketamine (Hermle et al. 1992; Vollenweider et al. 1997a, b). The most profound increase in metabolism was found in the anterior cingulate (Vollenweider et al. 1997a(Vollenweider et al. , 1997b, which is linked to both emotional and attentional functions (Vogt et al. 1992;Devinsky et al. 1995;Murtha et al. 1996). These functions are, in turn, tightly connected to both the effects of hallucinogens and the symptoms of schizophrenic and schizophrenia-spectrum psychoses.Hallucinogenic drug-induced states can be used as models for acute endogenous psychotic states in psychiatric research (Hermle et al. 1992; Vollenweider et al. 1997a, b;Gouzoulis-Mayfrank et al. 1998). Within the framework of this model psychosis paradigm neurometabolic data from the above-mentioned studies can be interpreted in the sense that acute psychotic states with prominent positive symptoms are linked to increased activity in frontal neocortical, and limbic areas. This is in contrast to the majority of functional neuroimaging studies with schizophrenic patients, which demostrate hypofrontality both in resting states (Buchsbaum et al. 1982;Farkas et al. 1984;Wolkin et al. 1988;Siegel et al. 1993) and under cognitive tasks believed to employ frontal brain areas (Cohen et al. 1987;Weinberger et al. 1988;Buchsbaum et al. 1990;Andreasen et al. 1992). However, most of these studies were performed with chronically ill patients on various neuroleptic medications, a...

show abstract

“…PCP administration to rats and ketamine administration to schizophrenic patients increased metabolism in sensory cortices, motor cortex, thalamus, and limbic areas (e.g., Gao et al 1993;Weissman et al 1987;Lahti et al 1995b). D-amphetamine administration to schizophrenic patients decreased metabolism in frontal and temporal cortical areas (e.g., Wolkin et al 1987). It is possible that deficits in the dopamine and glutamate systems may relate to different aspects of symptomatology and metabolic alterations in schizophrenia.…”

mentioning

confidence: 99%

Glutamate Modulation of Dopamine Measured in Vivo with Positron Emission Tomography (PET) and 11C-Raclopride in Normal Human Subjects

Smith

Schloesser

Brodie

et al. 1998

Neuropsychopharmacology

177

View full text Add to dashboard Cite

show abstract

Effects of amphetamine on local cerebral metabolism in normal and schizophrenic subjects as determined by positron emission tomography

Cited by 98 publications

References 40 publications

Changes in cerebral glucose metabolism during early abstinence from chronic methamphetamine abuse

Changes in cerebral glucose metabolism during early abstinence from chronic methamphetamine abuse

Neurometabolic Effects of Psilocybin, 3,4-Methylenedioxyethylamphetamine (MDE) and d-Methamphetamine in Healthy Volunteers A Double-Blind, Placebo-Controlled PET Study with [18F]FDG

Glutamate Modulation of Dopamine Measured in Vivo with Positron Emission Tomography (PET) and 11C-Raclopride in Normal Human Subjects

Contact Info

Product

Resources

About