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At least 19 recordsLinked to original sources
PubMed1995

Electroencephalographic correlates of marihuana-induced euphoria.

The present study was conducted to determine if there is a neurophysiological correlate of marihuana-induced good effects or euphoria. Three groups of 6 male occasional marihuana smokers were prepared for electroencephalographic (EEG) recording and smoked either placebo or marihuana cigarettes containing 1.26% or 2.53% delta 9-tetrahydrocannabinol (delta 9-THC) in a controlled laboratory setting. Using a continuously available non-verbal joystick device and a questionnaire, subjects reported changes in their subjective mood state while EEG activity was continuously recorded. Subjects reported multiple episodes of intense good effects or euphoria during the first 15 min after marihuana. These episodes of euphoria occurred while plasma delta 9-THC levels were rapidly rising. EEG alpha power during these discrete episodes of euphoria was significantly higher suggesting that these transient EEG changes may reflect a neurophysiological correlate of the reinforcing effects of marihuana.

Adult↗
PubMed1986

Neuroleptic reduction of cocaine-induced paranoia but not euphoria?

Central dopaminergic activation is hypothesized to underly schizophrenia and, paradoxically, stimulant euphoria. Four cocaine abusers with histories of stimulant-induced paranoid psychoses reported selective reduction in psychotic symptoms but not euphoria when treated with dopamine blockers. This provides preliminary evidence against efficacy of neuroleptics in cocaine abuse prevention, and suggests euphoria and paranoia may have discriminable neurophysiological substrates.

Antipsychotic Agents↗
PubMed2006

Low-carb diets, fasting and euphoria: Is there a link between ketosis and gamma-hydroxybutyrate (GHB)?

Anecdotal evidence links the initial phase of fasting or a low-carbohydrate diet with feelings of well-being and mild euphoria. These feelings have often been attributed to ketosis, the production of ketone bodies which can replace glucose as an energy source for the brain. One of these ketone bodies, beta-hydroxybutyrate (BHB), is an isomer of the notorious drug of abuse, GHB (gamma-hydroxybutyrate). GHB is also of interest in relation to its potential as a treatment for alcohol and opiate dependence and narcolepsy-associated cataplexy. Here I hypothesize that, the mild euphoria often noted with fasting or low-carbohydrate diets may be due to shared actions of BHB and GHB on the brain. Specifically, I propose that BHB, like GHB, induces mild euphoria by being a weak partial agonist for GABA(B) receptors. I outline several approaches that would test the hypothesis, including receptor binding studies in cultured cells, perception studies in trained rodents, and psychometric testing and functional magnetic resonance imaging in humans. These and other studies investigating whether BHB and GHB share common effects on brain chemistry and mood are timely and warranted, especially when considering their structural similarities and the popularity of ketogenic diets and GHB as a drug of abuse.

Brain↗
PubMed2005

Cocaine craving, euphoria, and self-administration: a preliminary study of the effect of catecholamine precursor depletion.

The authors used the acute phenylalanine-tyrosine depletion (APTD) method to test the effect of transient catecholamine precursor depletion on cocaine craving, euphoria, and self-administration. Eight nondependent, nontreatment-seeking cocaine users self-administered 3 doses of cocaine (0.6, 1.5, 3.0 mg/kg, taken intranasally) following ingestion of (a) a nutritionally balanced amino acid mixture, (b) APTD, and (c) APTD followed by L-dopa/carbidopa (2x100 mg/25 mg). APTD decreased both cue and cocaine-induced drug craving but not euphoria or self-administration. APTD+L-dopa also decreased drug craving, possibly reflecting the ability of L-dopa to transiently decrease dopamine cell firing. Together, these preliminary results suggest that the craving elicited by cocaine and cocaine cues is related to changes in catecholamine neurotransmission. Euphoria and the self-administration of freely available drugs by regular users, in comparison, might be better accounted for by other mechanisms.

Adult↗
PubMed2001

[Hypochondriacal euphoria as a special form of monopolar affective psychosis].

BACKGROUND: In contemporary concepts of affective psychoses the existence of monopolar manias is widely questioned. Nevertheless, cases of manias with monomorphous symptomatology are reported repeatedly from all over the world. Based upon subtle observation of signs and course over many years, Karl Leonhard developed a concept of affective psychoses that permits a distinction of monopolar from bipolar forms, e.g. monopolar manias and euphoric euphorias. METHODS: As an example for the pure forms of euphorias we present two cases of hypochondriacal euphoria. CONCLUSION: We discuss some of the literature relevant to the issue and propose the application of a differentiated psychopathological analysis for the discrimination of monopolar from bipolar manias.

Bipolar Disorder↗
PubMed1977

Lithium: effects on subjective functioning and morphine-induced euphoria.

The therapeutic usefulness of lithium in decreasing the euphoria and other symptoms associated with manic behavior and the hypothesis of a common final mechanism for elevations in mood have led to speculation that lithium may block the euphoria induced by drugs of abuse. In this study, lithium alone was antieuphoric in drug-free opiate addicts and, further, did not block morphine-induced euphoria.

Clinical Trials as Topic↗
PubMed1994

Biopsychological changes after bungee jumping: beta-endorphin immunoreactivity as a mediator of euphoria?

A study on 12 novice bungee jumpers was performed to investigate the influence of acute psychological stress on levels of cortisol in saliva, beta-endorphin immunoreactivity as well as the number of leukocytes in peripheral blood. In addition, heart rate and blood pressure as well as ratings on emotional states were recorded. Furthermore, correlations between ratings on mood and biochemical stress markers were computed. As expected, subjective ratings on anxiety were increased prior to the jump and were markedly reduced after the jump. Salivary cortisol was also increased after the jump and decreased to baseline within the next hour. In contrast, ratings on euphoria increased markedly after performing the jump and remained highly elevated for the next 30 min. An increase of more than 200% in beta-endorphin immunoreactivity after the jump was observed. In contrast to levels of cortisol, the concentration of beta-endorphin recorded immediately after the jump was significantly correlated with ratings on euphoria obtained at subsequent measurements indicating a relationship between beta-endorphins and euphoria. Additional increase of the number of blood leukocytes and of heart rate and blood pressure indicate that various systems of the organism are markedly affected by the exceptional eustress of bungee jumping.

Adult↗
PubMed2004

Construct validity and frequency of euphoria sclerotica in multiple sclerosis.

Using the Neuropsychiatric Inventory (NPI), we studied euphoria and other behavioral changes in 75 consecutive, unselected multiple sclerosis (MS) patients and 25 healthy controls. We also assessed disease duration, clinical course, physical disability, personality, depression, insight, cognition, and caregiver distress. Factor analysis identified a cluster of symptoms--labeled euphoria/disinhibition--similar to the euphoria sclerotica syndrome originally described by Charcot and others. The euphoria/disinhibition factor score was elevated in 9% of patients and associated with secondary-progressive course, low agreeableness, poor insight, impaired cognition, and high caregiver distress. Thus, we used the NPI to validate the euphoria syndrome in multiple sclerosis (MS) and determined its frequency, and its neurological and psychological correlates.

Adolescent↗
PubMed1985

Brain mechanisms of drug reward and euphoria.

Drugs of abuse have in common the fact that they serve as biological rewards. They presumably do so because of their ability to activate endogenous brain circuitry. By determining the brain circuitry activated by rewarding drug injections, much can be learned about the degree to which there is a common basis for the abuse liability of seemingly different drugs. The brain circuitry activated by two classes of abused drugs, psychomotor stimulants and opiates, is now partially understood; the current evidence suggests a shared mechanism of stimulant reward and opiate reward. The identified portion of the circuitry involves dopamine-containing cells of the ventral tegmental area and their fiber projections to the cells of the nucleus accumbens. Morphine activates these cells in the region of the cell bodies; it may have direct actions on receptors imbedded in the dopaminergic cell membrane, or it may act on afferent terminals that synapse on the dopaminergic cell bodies or dendrites. Cocaine and amphetamine act at the terminals of the dopaminergic fibers to nucleus accumbens and perhaps other structures. The shared activation of the dopaminergic input to nucleus accumbens accounts for the behaviorally activating and the rewarding effects of both stimulants and opiates (the opiate stimulant action is not widely known because it is usually masked by depressant actions of opiates in other, antagonistic, brain circuits). The activation of dopaminergic systems also accounts for amphetamine euphoria; it almost certainly accounts for cocaine euphoria and it probably accounts for opiate euphoria as well. Opiates and psychomotor stimulants clearly have many other actions which are not shared; nonshared actions must account for the well-known differences in the subjective effects of opiates and stimulants. One of the major nonshared actions is physical dependence. Opiates gain access to a major component of the circuitry mediating opiate physical dependence through opiate receptors in the periaqueductal gray matter. This receptor population is anatomically distinct from the population mediating the rewarding effects of opiates in nondependent animals. While both opiates and stimulants can activate (though by quite different mechanisms and at quite different loci) the dopaminergic circuitry underlying reward phenomena, only opiates activate the separate circuitry underlying dependence phenomena.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Lithium attenuates the activation-euphoria but not the psychosis induced by d-amphetamine in schizophrenia.

d-Amphetamine (20 mg) was administered intravenously in a double-blind design to 17 schizophrenic patients with and without concurrent 3-week lithium carbonate pretreatment to evaluate the lithium attenuation of d-amphetamine effects which we had observed in affective disorder patients. Lithium significantly attenuated the acute d-amphetamine-induced changes in an activation-euphoria cluster and in the mannerisms and posturing item of the Brief Psychiatric Rating Scale. Because the psychosis-increasing effects of d-amphetamine were not significantly decreased, it is conceivable that the d-amphetamine-induced changes in activation and euphoria and in psychosis are regulated by different dopamine mechanisms. The small clinical effects seen at 3 weeks of lithium treatment in schizophrenic patients could be mediated by dopamine.

Adolescent↗
PubMed1992

Cocaine euphoria, dysphoria, and tolerance assessed using drug-induced changes in brain-stimulation reward.

The time course of cocaine-induced changes in self-stimulation thresholds were used to evaluate cocaine euphoria and dysphoria as a function of the chronicity of drug treatment, dosage level, and the spacing of injections. It was assumed that cocaine-induced decreases in thresholds were indicative of cocaine euphoria, while increases in thresholds reflected rebound dysphoric responses to cocaine administration. Three experiments were performed using self-stimulating rats implanted with ventral tegmental area electrodes. Cocaine's threshold-lowering effects were evident 15 min postinjection (IP) with thresholds returning to baseline by approximately 3.0 h after treatment. Little evidence for cocaine-induced increases in thresholds was observed during periods of chronic cocaine treatment. However, thresholds were slightly elevated upon withdrawal from chronic cocaine treatment in Experiments 2 and 3. No evidence of tolerance or sensitization to cocaine-induced shifts in thresholds was noted with single daily injections, while multiple daily injections produced tolerance to cocaine's threshold-lowering effects. It is concluded that cocaine's ability to enhance brain-stimulation reward is highly reliable and robust, while decreases in brain-stimulation reward associated with chronic cocaine treatment are less reliable and difficult to demonstrate. The possible influence of drug dosage on the induction of cocaine dysphoria and the ability of various self-stimulation procedures to measure dysphoric effects are discussed.

Animals↗
PubMed1997

High dose pimozide does not block amphetamine-induced euphoria in normal volunteers.

Studies with laboratory animals have shown that dopamine antagonists block the rewarding and interoceptive effects of amphetamine. However, studies using dopamine antagonists with humans have not consistently shown blockade of amphetamine-induced euphoria. The unexpected results in humans may relate to the low doses of dopamine antagonists tested. The purpose of this study was to evaluate the effects of a relatively high acute dose (8 mg) of the dopamine receptor antagonist, pimozide, on responses to d-amphetamine (10 and 20 mg) in normal volunteers. Male and female volunteers (N = 12) attended six sessions on which they received pimozide or placebo (7:30 am) followed by d-amphetamine or placebo (9:30 am). Subjective, physiological and behavioral measures were obtained at baseline (7:15 am) and hourly over a 5 h period. d-Amphetamine and pimozide, when administered alone, produced significant and opposite effects on ratings of Elation and Vigor, as well as on psychomotor performance and physiological measures. However, there were few significant interactions between pimozide and d-amphetamine. Thus, pimozide failed to consistently antagonize the effects of d-amphetamine, even at doses of pimozide that had behavioral and physiological effects when administered alone. Possible reasons for lack of robust dopamine antagonism of amphetamine-induced euphoria in humans are discussed.

Adult↗
PubMed1976

Peptide transmitters: a unifying hypothesis for euphoria, respiration, sleep, and the action of lithium.

Actions of morphine include analgesia, sleep, euphoria, and depression of respiration. Transmitter or modulator substances in the brain that have actions similar to morphine may control these functions in man. This hypothesis proposes that enkephalin is a controlling neurotransmitter and its binding to opiate receptors determines mood state as well as influencing respiratory and sleep patterns. Lithium may act through modification of the opiate receptor affinity for an endogenous morphine-like substance. The theory predicts blocking action of naloxone in mania and in most drug-induced euphorias. It implies a new chemical pathophysiological basis for the phenomenology of mental illness.

Brain↗
PubMed1999

Selegiline effects on cocaine-induced changes in medial temporal lobe metabolism and subjective ratings of euphoria.

To test the effect of selegiline, a specific monoamine oxidase B (MAO-B) inhibitor, on the cerebral metabolic and euphorigenic effects of cocaine in experienced users, eight cocaine-dependent (CD) subjects were evaluated using a within-subjects design. Each subject participated in two pairs of [F-18]-fluorodeoxyglucose (FDG)-positron emission tomography (PET) scans (baseline scan followed 24 h later by a second scan obtained in conjunction with a 40-mg cocaine infusion) performed before and after a 1-week period of daily treatment with 10 mg selegiline administered orally. The hippocampus and amygdala were evaluated because of their hypothesized involvement in the addiction process, and the thalamus was evaluated as a comparison region. Following 7 days of selegiline treatment, the magnitude of the subjective euphoria ("high") produced by cocaine infusion was reduced by 40% (cocaine by selegiline interaction F = 7.15, df = 1.21, p = .014). Selegiline treatment also altered glucose utilization (normalized against whole brain counts) in the two limbic regions, but not the thalamus. In the amygdala, the effects of cocaine differed, depending upon whether or not patients were being treated with selegiline (cocaine by selegiline interaction F = 4.67, df = 1,19.8, p = .043). A different effect was observed in the hippocampus, where selegiline treatment decreased metabolic activity irrespective of whether cocaine was given (main effect F = 7.70, df = 1.20, p = .012). The concomitant changes in both the subjective experience of the "high" and normalized amygdala glucose utilization after selegiline treatment, suggest that a relationship exists between cocaine-induced euphoria and limbic metabolism. The data suggest that selegiline may be a useful adjunct in the treatment of cocaine dependence.

Adult↗
PubMed1986

EEG alpha activity increases during transient episodes of ethanol-induced euphoria.

The effects of acute ethanol administration were studied in 18 men to determine the electroencephalographic (EEG) correlates of ethanol-induced behavioral changes. Subjects were instructed to operate an instrumental device to indicate changes in their subjective mood state while EEG activity and plasma ethanol levels were continuously measured. Three groups of 6 subjects consumed either placebo, 0.347 g/kg ethanol or 0.695 g/kg ethanol over a 15 min period. EEG and behavioral changes were directly correlated with plasma ethanol levels during the ascending limb of the plasma ethanol curve. Theta EEG activity increased proportionally as plasma ethanol levels increased during the 2 hr recording session. Alpha EEG activity increased during the first hour and then returned to control levels. The increased alpha activity was most prominent when subjects reported feeling intense pleasure or euphoria. Power spectral analysis of discrete samples of EEG activity revealed that transient increases in alpha activity paralleled the onset of ethanol-induced euphoria. These data suggest that ethanol-induced behavioral effects are associated with discrete changes in brain electrical activity.

Adult↗
PubMed1977

Morphine and shuttle-box self-stimulation in the rat: a model for euphoria.

In a shuttle-box self-stimulation paradigm, analgesic doses of morphine increase the amount of time a rat leaves rewarding brain stimulation on, without altering average OFF times. This paradigm may serve as a model for the euphoria induced by narcotic drugs and as a useful tool for evaluating the reinforcing effects of drugs.

Animals↗
PubMed1988

Electroencephalographic activity and plasma ACTH during ethanol-induced euphoria.

Covariance of brain electrical activity (EEG), plasma adrenocorticotrophic hormone (ACTH) and cortisol levels, and mood states were determined for healthy adult men during the first 2 hr after ingestion of ethanol or ethanol placebo under controlled double-blind conditions. Analysis of integrated plasma ACTH and cortisol levels at 5-min intervals, EEG power spectral analysis during consecutive 2-min epochs, and continuous assessment of mood states with a nonverbal instrumental device were carried out during the ascending phase of the blood ethanol curve. Ethanol induced rapid changes in brain electrical activity and plasma ACTH levels that were significantly correlated with subjective perception of changes in mood. The paroxysmal short epochs of euphoria associated with electroencephalographic and ACTH responses during the ascending phase of the blood ethanol curve may reflect physiological concomitants of pharmacological and behavioral reinforcers that enhance risk for perpetuation of drinking and alcohol abuse.

Adrenocorticotropic Hormone↗
PubMed1996

Burns with inhalation injury and petrol aspiration in adolescents seeking euphoria through hydrocarbon inhalation.

We have recently managed four adolescent boys severely injured while aspirating petrol to achieve euphoria. This is a practice that occurs sporadically in this group in which alcohol and drugs are more difficult to procure by reason of their age and fiscal resources. The injuries sustained included extensive burns all with associated severe inhalation injury secondary to smoke and products of combustion, complicated by hydrocarbon pneumonitis.

Adolescent↗