Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven patients who had been maintained on tricyclic antidepressants developed signs of hypomania or mania shortly (two-seven days) after drug withdrawal. Three patients responded promptly to treatment with neuroleptics. One patient receiving lithium and three others who received no further drug treatment experienced more gradual resolution of symptoms. Tricyclic withdrawal is accompanied by changes in the turnover rate of individual neurotransmitters as well as by shifts in the equilibrium between various transmitter systems. These events may be accompanied by alterations in mood. Although relapse to depression is more common, hypomania or mania may also occur.
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PMID:Hypomania and mania after withdrawal of tricyclic antidepressants. 744 89

The clinical experience of a psychiatrist working in a pain clinic is described. One hundred and seventy two patients were assessed over a 4-year period. The modal age was 45-54 years with a male : female ratio of 7 : 10. The model duration of pain was 1-5 years, the back being the commonest site. Depression was diagnosed in 30% of cases. PErsonality disorder, traumatic neurosis, anxiety, hysteria and drug dependence were the next most common diagnoses. Treatment was instituted in half of the patients seen and half of the treated patients improved or recovered. Drug withdrawal, EMG feedback and brief psychotherapy were associated with more improvement than pharmacotherapy or treatment at a psychiatric unit. The response to antidepressant medication was particularly disappointing and possible reasons for this are discussed.
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PMID:The psychiatrist and the chronic pain patient: 172 anecdotes. 745 87

Exploration of the neurochemistry of psychiatric and substance use disorders in dual diagnosis patients may help explain the greater than chance comorbidity of these disorders and lead to advances in treatment. This paper will focus on the hypothesized neurochemical changes associated with primary substance use disorders which might lead to secondary psychiatric disorders by mimicking the hypothesized neurochemical changes of primary psychiatric disorders. For example, hypothesized serotonergic deficits in alcoholism, endorphin deficits in opioid dependence, and dopamine depletion in cocaine dependence all might predispose to depression. A vicious cycle of cocaine dependence and depression and a vicious cycle of alcohol and drug dependence and panic anxiety are reviewed as models for hypothesized alcohol or drug withdrawal related neurochemical changes predisposing to continued chemical dependency. Exploration of the neurochemistry of dual diagnosis patients reinforces the need for treatment approaches that take into account both aspects of illness.
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PMID:Hypothesized neurochemical models for psychiatric syndromes in alcohol and drug dependence. 750 27

We studied the long-term effects after withdrawal of enalapril, an angiotensin-converting enzyme inhibitor, on tail systolic pressure and cardiovascular structural properties in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Observations in control rats were from 4 to 35 weeks of age, whereas treated rats received enalapril from 4 to 20 weeks and were studied for a further 15 weeks. We measured blood pressure and the ratio of left ventricle weight to body weight and derived methoxamine log dose-perfusion pressure curves in the isolated hindquarter bed. From the changes in resistance properties we also estimated the changes in structure using a model developed previously. During therapy, blood pressure was depressed to a common value in both strains. After drug withdrawal, by age 35 weeks, previously treated SHR developed only mild hypertension, whereas blood pressure of WKY had recovered to the corresponding control level. At 21 weeks, soon after enalapril was stopped, left ventricular development was depressed in both strains; the depression was slightly greater in SHR, but that of vascular resistance was proportionately similar in each strain. Late cardiovascular development between 21 and 35 weeks was attenuated in the previously treated groups. For the left ventricle, it was similar in each strain, but for the vasculature, late development was relatively smaller in SHR than WKY. In the former, the pattern of development between 21 and 35 weeks was the same as in untreated controls and appeared to be mediated in response to the rise in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular development after enalapril in spontaneously hypertensive and Wistar-Kyoto rats. 772 5

The changes in dopamine system regulation occurring during stimulant administration are examined in relation to a new model of dopamine system function. This model is based on the presence of a tonic low level of extracellular dopamine that is released by the presynaptic action of corticostriatal afferents. In contrast, spike-dependent dopamine release results in a phasic, high concentration of dopamine in the synaptic cleft that is rapidly inactivated by reuptake. Tonic dopamine has the ability to down-modulate spike-dependent phasic dopamine release via stimulation of the very sensitive dopamine autoreceptors present on dopamine terminals. Stimulants are known to elicit locomotion and stimulate reward sites by releasing dopamine from terminals in the nucleus accumbens, which is followed by a rebound depression. It is proposed that the initial activating action of stimulants is caused by increasing the release of dopamine into the synaptic cleft to activate the phasic dopamine response. However, by interfering with dopamine uptake, stimulants also allow dopamine to escape the synaptic cleft, thereby depressing subsequent spike-dependent phasic dopamine release by increasing the tonic stimulation of the autoreceptor. In contrast, repeated stimulant administration is proposed to cause long-term sensitization by pharmacological disruption of a cascade of homeostatic compensatory processes. Upon drug withdrawal, the fast compensatory systems that were blocked by stimulants rapidly restore homeostasis to the system at a new steady-state level of interaction. As a consequence, the slowly changing but potentially more destabilizing compensatory responses are prevented from returning to their baseline conditions. This results in a permanent change in the responsivity of the system. Homeostatic systems are geared to compensate for unidimensional alterations in a system, and are capable of restoring function even after massive brain lesions or the continuous presence of stimulant drugs. However, the system did not evolve to deal effectively with repetitive introduction and withdrawal of drugs that disrupt dopamine system regulation. As a consequence, repeated insults to a biological system by application and withdrawal of drugs that interfere with its homeostatic regulation may be capable of inducing non-reversible changes in its response to exogenous and endogenous stimuli.
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PMID:The tonic/phasic model of dopamine system regulation: its relevance for understanding how stimulant abuse can alter basal ganglia function. 775 1

Many of the symptoms of nicotine withdrawal are similar to those of other drug withdrawal syndromes: anxiety, awakening during sleep, depression, difficulty concentrating, impatience, irritability/anger and restlessness. Slowing of the heart rate and weight gain are distinguishing features of tobacco withdrawal. Although nicotine withdrawal may not produce medical consequences, it lasts for several weeks and can be severe in some smokers. Like most other drug withdrawals, nicotine withdrawal is time-limited, occurs in non-humans, is influenced by instructions/expectancy and abates with replacement therapy and gradual reduction. Unlike some other drug withdrawal syndromes, protracted, neonatal or precipitated withdrawal does not occur. Whether nicotine withdrawal is associated with tolerance, acute physical dependence, greater duration and intensity of use, rapid reinstatement, symptom stages, cross-dependence with other nicotine ligands, reduction by non-pharmacological interventions and genetic influences is unclear. Whether nicotine withdrawal plays a major role in relapse to smoking has not been established but this is also true for other drug withdrawal syndromes.
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PMID:Nicotine withdrawal versus other drug withdrawal syndromes: similarities and dissimilarities. 784 57

Forty five patients with refractory partial seizures were studied in a prospective, randomised, placebo controlled, add on, parallel group, double blind trial of the new antiepileptic drug vigabatrin (1.5 g twice daily) followed by open treatment. Seizure frequency was monitored throughout an eight week baseline, 20 weeks double blind, and up to 18 months of open vigabatrin treatment. Cognitive function, including measures of memory and concentration, mood, and behaviour were assessed at baseline and again during the 20th week of treatment. Vigabatrin was associated with a significant reduction in a measure of motor speed and overall score on a design learning test in the first 20 weeks of treatment. In comparison with the baseline period, vigabatrin treatment was associated with a significant reduction in median complex partial seizure frequency four to 12 and 12 to 20 weeks after commencing vigabatrin (-66% and -69% in the vigabatrin group, +50% and +25% in the placebo group). Ten of 20 patients on vigabatrin and four of 23 on placebo showed a > 50% reduction in complex partial seizure frequency in the last eight weeks of double blind treatment. At least 60% of responders had maintained the response to vigabatrin when assessed during the open phase of the trial at 44 weeks. Two patients discontinued vigabatrin because of depression, which resolved on drug withdrawal.
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PMID:Effects of vigabatrin on partial seizures and cognitive function. 808 68

Abnormalities in saccadic eye movements have been found in schizophrenics with tardive dyskinesia (TD). This finding supports accumulating evidence for a GABAergic dysfunction in the subcortical-cortical circuits controlling motor and oculomotor behavior. We found that in response to muscimol, a direct-acting GABA agonist, changes in the antisaccade error rate and dyskinesia score were strongly correlated. We then looked at the relationship between these measures during single-blind haloperidol withdrawal. Significant changes occurred in antisaccade error during drug withdrawal, but the final measure was not significantly different from the baseline assessment. Antisaccade error change scores were not correlated with dyskinesia change scores. Change score in antisaccade error was positively correlated with change on the Brief Psychiatric Rating Scale, specifically with the Anxiety/Depression factor. These findings suggest that GABAergic mechanisms are more robust than dopaminergic mechanisms in the pathophysiology of persistent tardive dyskinesia.
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PMID:Pharmacologic relationship of antisaccade and dyskinesia in schizophrenic patients. 829 Jun 71

1. The presence of mood disturbances and platelet 3H-imipramine binding, a putative peripheral serotonergic marker, were evaluated in a group of 27 cocaine users three days after drug withdrawal. 2. Parameters of cocaine use and the linkage between cocaine withdrawal and "post-cocaine depression" were also investigated. In a subgroup of 10 patients, both psychopathological and biological measurements were repeated after 5 or 6 weeks. 3. Interpretation of the data by Pearson's analysis showed a statistically significant and positive correlation between Hamilton Rating Scale for Depression (HAM-D) scores and period of use. A trend towards a negative correlation, which however did not reach the statistical significance, was found between 3H-Imipramine binding and period of cocaine use, number of days of abstinence and HAM-D scores 4. When compared with normal volunteers at baseline, patients had significantly lower Bmax and Kd values which returned towards normal values after 5 or 6 weeks of cocaine withdrawal. 5. These results indicate the presence of a decreased platelet imipramine binding during cocaine withdrawal which may be due to the effect of the drug or alternatively, a result of concomitant depression which may be primary or secondary in origin. The decreased imipramine binding is a reversible phenomenon, since it increases with the time, in parallel with the improvement of depressive symptoms.
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PMID:Phenomenology and neurobiology of cocaine withdrawal: are they related? 858 80

The purpose of the study is to determine the relationship between behavioral symptoms of amphetamine withdrawal and the extracellular concentration of dopamine (DA) in the dorsolateral caudate nucleus and the nucleus accumbens across the entire light-dark cycle. This was accomplished using automated on-line microdialysis sampling in behaving rats. Animals were pretreated with escalating doses of d-amphetamine (or saline) over a 6-week period and then were withdrawn from amphetamine for 3, 7, or 28 days before testing. There were regional differences in the effects of amphetamine withdrawal on the concentrations of DA and DA metabolites in dialysate. Early during withdrawal (3 and 7 days), when animals showed postamphetamine withdrawal behavioral depression (nocturnal hypoactivity), there was a significant decrease in DA and DA metabolites in the dorsolateral caudate nucleus and a disruption in the normal circadian pattern of DA activity. In contrast, there was no effect of amphetamine withdrawal on DA dynamics in the nucleus accumbens. By 28 days after the discontinuation of amphetamine pretreatment, after basal DA in the caudate returned to normal, there was a significant increase in basal DA metabolism in both the caudate and the accumbens. This increase in DA metabolism may be related to the expression of sensitization, including a hypersensitivity to an amphetamine challenge. It is concluded that the role of the dorsal striatum in psychostimulant drug withdrawal syndromes deserves further consideration.
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PMID:Regional differences in the effects of amphetamine withdrawal on dopamine dynamics in the striatum. Analysis of circadian patterns using automated on-line microdialysis. 870 1


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