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Results for “Paranoid Behavior”

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At least 595 records · Page 33Linked to original sources
PubMed1993

The pharmacology and neural circuitry of sensitization to psychostimulants.

Behavioral sensitization to amphetamine-like psychostimulants is manifest as a progressive increase in drug-induced anxiety and paranoia which can culminate in psychopathologies, such as paranoid psychosis and panic attacks. Sensitization may also mediate the facilitation of drug relapse in addicts by increasing the reinforcing value of acute drug administration. The primary animal model for psychostimulant-induced psychopathologies involves repeated, non-contingent administration of drug to rodents, which can produce a progressive and enduring augmentation in motor activity and increased susceptibility to drug self-administration. Because of the mature literature implicating mesoaccumbens dopamine transmission in the acute motor and reinforcing effects of amphetamine-like stimulants, investigation into the neural basis of behavioral sensitization has focused on this projection. Over the last decade, with a few exceptions, the neurochemical and molecular literature that has emerged from this effort is replete with inconsistencies. In contrast, the presence of behavioral sensitization is a highly replicable event. It is proposed that behavioral sensitization arises from an alteration in the neural circuitry that subserves the translation of motivationally relevant stimuli into adaptive motor responses. The mesoaccumbens dopamine projection is embedded in this circuit and an enduring change in dopamine transmission may alter the functional state of the circuit to produce behavioral sensitization. However, combinations of alterations in other connections within the circuit can also support behavioral sensitization. The specific changes in the circuit that promote behavioral sensitization are under the control of experimental parameters, such as the drug employed, dosage regimen, withdrawal period and the presence of conditioning cues. Thus, the profile of neurochemical alterations observed after exposure to repeated psychostimulants may vary depending upon the experimental protocol and strain of animals, even though all laboratories report the presence of behavioral sensitization.

Journal Article↗
PubMed1991

Cocaine-induced psychosis.

BACKGROUND: Chronic stimulant use can produce a paranoid psychosis that is similar to acute paranoid schizophrenia. While this phenomenon has been systematically explored in amphetamine abusers, it has been relatively unexplored in a systematic fashion in cocaine abusers. METHOD: The experience of cocaine-induced psychosis was evaluated in 55 individuals consecutively admitted for treatment of DSM-III-R cocaine dependence. Each subject was interviewed about their experiences of psychosis while intoxicated by means of a standardized, semistructured interview. RESULTS: Fifty-three percent (29/55) of those interviewed reported experiencing transient cocaine-induced psychosis. There was no significant difference in lifetime amount of cocaine use or amount of cocaine use in the month before admission between those who experienced psychosis and those who did not. The psychosis-positive group used significantly more cocaine in the year prior to admission (p less than or equal to .02) and had a longer duration of use (p less than or equal to .01). Males were significantly (p less than or equal to .05) more likely than females to develop psychosis. Ninety percent (26/29) developed paranoid delusions directly related to drug use. Ninety-six percent (28/29) of the subjects experienced hallucinations: 83% (24/29), auditory hallucinations; 38% (11/29), visual hallucinations; and 21% (6/29), tactile hallucinations. Twenty-seven percent (15/55) of subjects developed transient behavioral stereotypies. CONCLUSION: Cocaine-induced paranoia is a common experience among chronic users. Amount and duration of use are related to its development. Implications for a kindling model of cocaine-induced psychosis will be discussed.

Administration, Inhalation↗
PubMed1990

Hoarding as a psychiatric symptom.

Collecting is a normal behavior in childhood and adulthood, while hoarding--the gathering, ordering, and disposal of articles without clear conscious motivation or control--is characterized as the pathologic counterpart of collecting. The literature describing the characteristics of collecting and the theories concerning its underlying mechanisms is presented along with eight case studies of adults who exhibited hoarding as a prominent symptom. It is apparent that hoarding is the final common pathway for a variety of processes: compulsive hoarding in obsessive compulsive disorder, fears of theft and poisoning in paranoid delusions, and the deterioration of habits in organic mental disorder.

Adult↗
PubMed1997

Delirium in Alzheimer disease.

Advanced age and dementia are well-known risk factors for delirium, and most studies of delirium have concentrated on hospitalized populations. We reviewed the records of 199 community-dwelling Alzheimer disease (AD) patients and identified 43 (22%) who had had episodes of delirium during their dementing illness. These patients were matched for age, gender, and disease duration to AD patients without previous episodes of delirium. Variables examined included causes of delirium, Mini-Mental State Examination scores, Clinical Dementia Rating scores. Blessed Activities of Daily Living (ADL) scores, years of education, neuropsychological performance, and incidence of behavioral symptoms on the Brief Psychiatric Rating Scale. In six of 198 (3%) patients delirium was an initial symptom of AD. Conditions associated with onset of delirium were urinary tract infections, stressful events, surgery, medical illnesses, and medications. No significant differences were found between groups on neuropsychological testing. Patients with previous episodes of delirium had worse ADL scores and higher disease-course incidences of hallucinations and paranoid delusions, mostly occurring during the delirious episode. We conclude that delirium is common in AD, but it is an unusual initial symptom and it occurs in diverse clinical settings. Measures of behavioral symptoms and ADLs are more likely to reflect the impact of delirium on clinical status than measures of cognition or stage of dementia.

Aged↗
PubMed2005

Distinct temporal phases in the behavioral pharmacology of LSD: dopamine D2 receptor-mediated effects in the rat and implications for psychosis.

RATIONALE: The effect of LSD in humans has been described as occurring in two temporal phases. The behavioral effects in rats also occur in two temporal phases: an initial suppression of exploration followed by increased locomotor activity. OBJECTIVES: We decided to investigate this phenomenon from the perspective that the pharmacology might have relevance to the neurochemical mechanisms underlying psychosis. METHODS: Twenty-five male Sprague-Dawley rats were trained to discriminate LSD (186 nmol/kg, 0.08 mg/kg, i.p.) with a 30-min preinjection time (LSD-30, N=12) and LSD (372 nmol/kg, 0.16 mg/kg, i.p.) with a 90-min preinjection time (LSD-90, N=13) from saline, using a two-lever, food-reinforced operant conditioning task. RESULTS: LSD (186 or 372 nmol/kg, 0.08 or 0.16 mg/kg) given 30 min prior to training produced a cue that was completely antagonized by 5-HT2A antagonists and lasted no longer than 1 h. LSD (372 nmol/kg, 0.16 mg/kg) injected 90 min before training produced a cue that was not fully blocked by 5-HT2A antagonists, but instead was significantly inhibited by haloperidol. In these rats, substitution no longer occurred with the 5-HT2 agonists DOI or LSD (30 min preinjection), but full substitution was obtained with the D2 agonists apomorphine, N-propyldihydrexidine, and quinelorane. CONCLUSION: The discriminative stimulus effect of LSD in rats occurs in two phases, and these studies provide evidence that the later temporal phase is mediated by D2 dopamine receptor stimulation. A second temporal phase that involves dopaminergic pathways would be consistent with the widespread belief that excessive dopaminergic activity may be an underlying cause of paranoid psychosis.

Amphetamine↗
PubMed1995

Subjective reports on the effects of the MDMA ('ecstasy') experience in humans.

1. The objective of this paper was to provide an understanding of methylenedioxymethamphetamine (MDMA) use. This investigation provides the subjective effects that were reported by MDMA users. 2. There were a total of (500) humans who participated in this study. 3. Using a survey device, data from users were collected. Symptomatology associated with both the consumption of MDMA and its residual effects are documented. 4. Tables have been constructed to present prevalent psychological and physical side-effects associated with MDMA intake. 5. The results suggest that MDMA has significant implications with various psychological disorders and physical manifestations.

Adolescent↗
PubMed2002

Assessment of dysfunctional beliefs in borderline personality disorder.

This study had two aims: to test the hypothesis that borderline personality disorder (BPD) patients hold numerous dysfunctional beliefs associated with a variety of Axis II disorders, and to construct a BPD belief scale which captures these beliefs. Beliefs were measured using the Personality Belief Questionnaire (PBQ) which is designed to assess beliefs associated with various personality disorders, although not specifically BPD. Eighty-four BPD patients and 204 patients with other personality disorders (OPD) were randomly split into two study samples. Fourteen PBQ items were found to discriminate BPD from OPD patients in both samples. These items came from the PBQ Dependent, Paranoid, Avoidant, and Histrionic scales and reflect themes of dependency, helplessness, distrust, fears of rejection/abandonment/losing emotional control, and extreme attention-seeking behavior. A BPD beliefs scale constructed from these items showed good internal consistency and diagnostic validity among the 288 study patients. The scale may be used to assist in diagnosis and cognitive therapy of BPD.

Adult↗
PubMed1998

Are psychoactive-drug-induced changes in plasma lipid and lipoprotein levels of significance for clinical remission in psychiatric disorders?

In the present pilot study, our aim was to investigate whether associations could be demonstrated in psychiatric patients between the changes in plasma lipid and lipoprotein levels expected during treatment with psychoactive drugs and the changes in the patients' depressive and hostile behavior. One hundred and fourteen patients with various psychiatric disorders (depressive episode in bipolar affective disorder, depressive episode or recurrent depressive disorder, paranoid schizophrenia, and schizoaffective disorders) were included in the study. The following examinations were carried out in each patient on admission and at discharge: (1) the plasma lipid parameters total cholesterol (TC), low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), high-density lipoprotein (HDL), and triglycerides (TRI) were determined, and (2) the psychopathological features were recorded employing the AMDP system and the AMDP Syndrome Scales. Within the context of a naturalistic clinical setting with a choice of psychoactive drugs available, patients were subdivided at the end of treatment into eight treatment groups, as follows: group 1, treatment with butyrophenones; group 2, treatment with tricyclics; group 3, treatment with butyrophenones and tricyclics; group 4, treatment with butyrophenones, tricyclics and selective serotonin reuptake inhibitors; group 5, treatment with butyrophenones and lithium; group 6, treatment with tricyclics and lithium; group 7, treatment with butyrophenones, tricyclics and lithium; and group 8, treatment with butyrophenones, tricyclics, selective serotonin reuptake inhibitors and lithium. To compare the changes in the eight treatment groups, mixed general linear models including diagnosis, gender, age, body mass index changes, and baseline values were applied using proc GLM of SAS. Butyrophenones induce an increase in TC, LDL, and TC/TRI ratio, whereas tricyclics lead to an increase in TC, LDL, VLDL, and TRI. In combined medication of butyrophenones and tricyclics the effects of tricyclics predominate. Comedication of lithium inhibits the increase in TC and LDL induced by butyrophenones and/or tricyclics. Treatment groups with lipid changes of the same type (decrease, no change, or increase) were combined in "lipid change groups". Analyses of variance or covariance (with psychopathological admission value as covariate where there were significant differences in psychopathological admission mean values between the groups) of these lipid change groups with regard to the changes in the Depressive Syndrome Scale and the Hostility Syndrome Scale gave results which are interpreted as follows: an increase in TC or LDL inhibits the remission of hostility, whereas an increase in TRI with concomitant decrease in TC, or else a relatively greater increase in TRI than in TC promotes the remission of hostility. A decrease in TRI or VLDL promotes the remission of depression. Our data and findings published in the literature may suggest that systemic changes in plasma lipid parameters, at the cellular level, induce changes in the fluidity of brain cell membranes. We hypothesize that an increase in plasma TC or LDL and/or a decrease in plasma TRI or VLDL may induce a relative decrease in brain cell membrane fluidity with decreased presynaptic serotonin reuptake and increased postsynaptic serotonin function. This proposed increase in brain serotonin function would finally result in an anti-depressive, aggression-promoting effect. Conversely, a decrease in plasma TC or LDL and/or an increase in plasma TRI or VLDL may induce a relative increase in brain cell membrane fluidity with increased presynaptic serotonin reuptake and decreased postsynaptic serotonin function. This proposed decrease in brain serotonin function would result in an anti-aggressive, depression-promoting effect.

Adult↗