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)

In the late-stage idiopathic Parkinson's disease (IDP), comorbid conditions such as depression and drug-induced psychosis may be observed. A patient with Parkinson disease, major depression, and paranoid psychosis who developed neuroleptic malignant syndrome (NMS) as the result of the sudden termination of high-dose (1200 mg/d) levodopa treatment is presented in this report. Because the patient did not respond to other treatment modalities, electroconvulsive therapy (ECT) was applied, and a rapid improvement was observed both in the patient's NMS and also in Parkinson's and psychiatric symptoms, with no additional side effects other than transient post-ictal confusions. The application of ECT allowed the patient to remain stable for a 5-year period with a quite low dose of levodopa (300 mg/d). Later, the patient had two episodes of depressive and psychotic symptoms, which were again successfully treated with the ECT. We suggest that ECT might be an effective and life-saving therapy in patients with severe, drug-resistant NMS.
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PMID:Electroconvulsive therapy in drug-induced psychiatric states and neuroleptic malignant syndrome. 1590 57

Recent evidence has demonstrated the efficacy of pegylated interferon-alpha (IFN-alpha) in treating hepatitis C virus infection. Neuropsychiatric complications commonly occur during the course of IFN treatment, with depressive symptoms usually appearing within the first 12 weeks. Few cases of the pegylated interferon-alpha-induced psychosis and depression have been reported compared to standard interferon-alpha therapy. We report the first case of a major depressive episode with psychotic features induced by pegylated IFN-alpha-2b and ribavirin in the last 2 weeks of therapy.
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PMID:Major depressive episode with psychotic features induced by pegylated interferon-alpha-2b and ribavirin treatment. 1609 20

This double-blind randomized study examined the effect of quetiapine (QTP) on drug-induced psychosis (DIP) in Parkinson's disease (PD). Conventional antipsychotic drugs are associated with adverse extrapyramidal effects. QTP is a new atypical antipsychotic drug used in the treatment of psychosis in PD. A total of 58 consecutive psychotic PD patients (mean age, 75 +/- 8.3 years; mean disease duration, 10.5 +/- 6.4 years; 29 with dementia) were randomly assigned to 2 groups: 30 were treated with QTP (mean dose, 119.2 +/- 56.4 mg) and 28 received placebo for 3 months. The motor part of the Unified Parkinson's Disease Rating Scale, the Brief Psychiatric Rating Scale, the Mini-Mental State Examination, the Hamilton Rating Scale for Depression, the Epworth Sleepiness Score, and the Clinical Global Impression Scale were administered before and during the study. No significant difference was found between the groups in all parameters. There were 32 PD patients (55%) completed the 3-month study (15 [26%] QTP and 17 [29%] placebo). Treatment was interrupted in 15 patients in the QTP and 11 in the placebo groups. This double-blind study did not show a beneficial effect of QTP for the treatment of DIP in PD. The high rate of withdrawal probably influenced the results. Larger double-blind studies are required.
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PMID:Effect of quetiapine in psychotic Parkinson's disease patients: a double-blind labeled study of 3 months' duration. 1703 6

To investigate whether transcranial brain sonography (TCS) discriminates different courses of idiopathic Parkinson's disease (PD), 101 patients with clinically definite PD were studied. In four patients, TCS was not possible due to insufficient acoustic temporal bone windows. Substantia nigra (SN) hyperechogenicity was found in 96% of assessable patients. Larger SN echogenic size correlated with younger age at PD onset (Spearman correlation, r = -0.383; P < 0.001), but not with age, PD duration, or severity. Marked bilateral SN hyperechogenicity indicated early-onset rather than late-onset PD, and akinetic-rigid (AR) or mixed-type (MX) PD rather than tremor-dominant PD. SN echogenic sizes were larger contralateral to the clinically more affected side in AR PD and MX PD patients. Reduced echogenicity of brainstem raphe was associated with depression (RR = 1.61; 95% CI = 1.05-2.46; P = 0.044) but not with other clinical features. Caudate nucleus hyperechogenicity was, independently from PD duration, related to drug-induced psychosis (RR = 2.40; CI = 1.36-4.22; P = 0.001), but not to motor fluctuations. Lenticular nucleus hyperechogenicity indicated AR PD rather than tremor-dominant PD (RR = 1.44; CI = 1.11-1.86; P = 0.040). Frontal horn dilatation > 15.4 mm (mean of bilateral measurements) indicated increased risk of dementia (RR = 4.11; CI = 1.51-11.2; P = 0.001). We conclude that TCS displays characteristic changes of deep brain structures in different clinical manifestations of PD.
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PMID:Transcranial brain sonography findings in clinical subgroups of idiopathic Parkinson's disease. 1708 96

Psychiatric disorders frequently occur in patients with epilepsy, but the relationship between epilepsy and psychopathology is poorly understood. Frequent comorbidities in epilepsy patients comprise major depression, anxiety disorders, psychosis and cognitive dysfunction. Animal models of epilepsy, such as the pilocarpine model of acquired epilepsy, are useful to study the relationship between epilepsy and behavioral dysfunctions. However, despite the advantages of mice in studying the genetic underpinning of behavioral alterations in epilepsy, mice have only rarely been used to characterize behavioral correlates of epilepsy. This prompted us to study the behavioral and cognitive alterations developing in NMRI mice in the pilocarpine model of epilepsy, using an anxiety test battery as well as tests for depression, drug-induced psychosis, spatial memory, and motor functions. In order to ensure the occurrence of status epilepticus (SE) and decrease mortality, individual dosing of pilocarpine was performed by ramping up the dose until onset of SE. This protocol was used for studying the consequences of SE, i.e. hippocampal damage, incidence of epilepsy with spontaneous recurrent seizures, and behavioral alterations. SE was terminated by diazepam after either 60, 90 or 120 min. All mice that survived SE developed epilepsy, but the severity of hippocampal damage varied depending on SE length. In all anxiety tests, except the elevated plus maze test, epileptic mice exhibited significant increases of anxiety-related behavior. Surprisingly, a decrease in depression-like behavior was observed in the forced swimming and tail suspension tests. Furthermore, epileptic mice were less sensitive than controls to most of the behavioral effects induced by MK-801 (dizocilpine). Learning and memory were impaired in epileptic mice irrespective of SE duration. Thus, the pilocarpine-treated mice seem to reflect several of the behavioral and cognitive disturbances that are associated with epilepsy in humans. This makes these animals an ideal model to study the neurobiological mechanisms underlying the association between epilepsy and psychopathology.
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PMID:Behavioral alterations in the pilocarpine model of temporal lobe epilepsy in mice. 1771 5

We analysed acute and long-term effects of the N-methyl-d-aspartate receptor antagonist MK-801 on long-term heterosynaptic population spike depression (LTHPSD) evoked by high-frequency stimulation of the direct cortical input in female rat hippocampal slices to understand disturbances in cognitive functions associated with an acute phencyclidine-induced psychosis. High-frequency stimulation (HFS) of the direct cortical input (dCI) to cornu ammonis area 1 (CA1) induced homosynaptic long-term potentiation (LTP) while simultaneously evoking LTHPSD at the Schaffer collateral input. Animals treated with a single intraperitoneal application of MK-801 (5 mg/kg body weight) showed severe behavioural alterations for 24 h, although histological examination of CA1 did not reveal any morphological changes. However, after application of MK-801, homosynaptic LTP of the dCI was suppressed for up to 7 days and recovered within 4 weeks. Likewise, LTHPSD in response to HFS of the dCI to CA1 was abolished for at least 1 week post-treatment, with partial recovery occurring after 4 weeks. Homosynaptic LTP, induced by HFS of Schaffer collaterals, was also disturbed for at least 24 h, with recovery after 7 days. Remarkably, bath application of MK-801 (50 microM) converted LTHPSD, induced by dCI HFS, into persistent heterosynaptic long-term enhancement of stratum radiatum-evoked responses. The acute effects of MK-801 on synaptic plasticity seen in this study may contribute to the observed severe behavioural alterations and long-term effects and may explain some of the long-lasting symptoms remaining after an acute psychotic episode in humans.
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PMID:Acute and long-term effects of MK-801 on direct cortical input evoked homosynaptic and heterosynaptic plasticity in the CA1 region of the female rat. 1800 Dec 84

The pathological hallmark of Parkinson's disease (PD) is a degeneration of the dopamine (DA) producing cells in the substantia nigra and the ventral tegmentum, resulting in a dopamine deficiency in the dopaminergic projection areas with defective functioning of specific cortico-subcortical extrapyramidal circuits. Depending on which circuits (;motor', ;association' or ;limbic') are involved, and on the extent of the accompanying noradrenergic, serotonergic and cholinergic detrition in PD, dysfunction may result in motor deficits, mood disturbances or cognitive deficits, sometimes proceeding to dementia. Drug-induced psychosis occurs in approximately 15-20% of patients treated with dopaminergic agents. In PD, mainly nigrostriatal dopamine (A9) is depleted, leading to progressive motor dysfunction with subtle cognitive disturbances. As a rule, the neuropsychological deficit in PD might be described as the inability to switch cortical behavioral programmes in situations requiring the internal regulation of behavior. In daily life, in most patients these deficits do not become manifest, due to the abundance of external information to guide behavior. When the ability to use environmental information or external cues is lost as well, significant cell loss in the ventral tegmental area, with reduced DA-innervation of the mesocorticolimbic regions and the nucleus accumbens, must be suspected. This leads to clinically overt defects not only in the ;motor' but also in the ;limbic' and ;association' circuits. In addition to more severe cognitive disturbances or even dementia, this may also lead to mood disorders and drug-induced psychosis. Depression then occurs as the cortical modulation of limbic activity has become deficient, leading to emotional reactions disproportionate to the thoughts that evoke them. The proposed mechanism of psychosis in PD is that cortical sensory input is misinterpreted, leading to misperceptions (hallucinations) or false beliefs about reality due to a reduced ;signal-to-noise' ratio by insufficient processing of relevant information.
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PMID:Mental dysfunction in Parkinson's disease. 1859 Oct 98

There is a growing awareness that emotion, motivation, and reward values are important determinants of our behavior. The habenula is uniquely positioned both anatomically and functionally to participate in the circuit mediating some forms of emotive decision making. In the last few years there has been a surge of interest in this structure, especially the lateral habenula (LHb). The new studies suggest that the LHb plays a pivotal role in controlling motor and cognitive behaviors by influencing the activity of dopamine and serotonin neurons. Further, dysfunctions of the LHb have also been implicated in psychiatric disorders, such as depression, schizophrenia, and drug-induced psychosis.
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PMID:Habenula: crossroad between the basal ganglia and the limbic system. 1900 47

A patient with multiple psychosomatic disorder developed a steroid induced rare bipolar mood disorder (both mania and depression). The "unmasking effect" of steroids and a positive family history of psychiatric disorder as a possible risk factor, hitherto undocumented, is suggested in steroid induced psychosis.
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PMID:Steroid induced rare bipolar mood disorder. 1969 51

Transcranial sonography (TCS) allows high resolution imaging of deep brain structures, provided sufficient imaging conditions and adequate qualification of the investigator. Since TCS can display changes of midbrain structures and basal ganglia that are not or only heavily detected with other neuroimaging methods, TCS has yielded new insights into the pathogenesis also of non-motor features of PD. Abnormal increased echogenicity ('hyperechogenicity') of substantia nigra is not only a characteristic finding in PD, but is also related to increased risk of depression in PD patients (relative risk [RR], 1.9). Reduced echogenicity ('hypoechogenicity') of midbrain raphe indicated increased risk of depression (RR, 2.0) and urinary incontinence (RR, 4.7) in PD patients. Caudate nucleus hyperechogenicity was associated with drug-induced psychosis (RR, 2.4), and frontal-horn dilatation >20mm with dementia (RR, 3.6). TCS findings support the hypothesis of a pathogenetic link between depression and PD. Further studies are warranted to find out whether TCS is useful for detecting increased risk for non-motor complications, such as depression, psychosis, or urinary incontinence, already before they become clinically obvious.
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PMID:Transcranial sonography findings related to non-motor features of Parkinson's disease. 1973 25


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