Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Social anxiety disorder has only recently garnered recognition as a unique anxiety disorder. Although social anxiety disorder is distinguishable from other psychiatric disorders, there are several areas in which this distinction is not straightforward. Furthermore, social anxiety disorder is associated with considerable comorbidity with other disorders, which may render differential diagnosis a challenging endeavor. This article will review those disorders that must be differentiated from social anxiety disorder, including major depression, panic disorder with agoraphobia, generalized anxiety disorder, obsessive-compulsive disorder, and body dysmorphic disorder. In addition, the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) provides specific examples of disorders, e.g., verbal dysfluency (stuttering) and Parkinson's disease, in the context of which social anxiety disorder is not to be diagnosed. Social anxiety disorder is also frequently comorbid with the Axis II avoidant personality disorder. Interestingly, this may present a prime example of "comorbidity by committee," because it is growing increasingly clear that much avoidant personality disorder as defined by DSM-IV merely denotes a subgroup of patients with generalized social anxiety disorder. Because social anxiety disorder has a chronic course and is associated with significant morbidity, it is critical that patients receive an accurate diagnosis and appropriate treatment.
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PMID:The history, epidemiology, and differential diagnosis of social anxiety disorder. 1033 73

In this pilot study, we performed an oral yohimbine challenge in 6 patients with Parkinson's disease (PD) and anxiety or depression, 2 parkinsonian patients without psychiatric illness, and 2 healthy control subjects to determine whether patients with Parkinson's disease and anxiety respond to this adrenergic agent in the same way patients with idiopathic anxiety disorders respond. Given the atypical nature of depression in Parkinson's disease (characterized by prominent anxiety), we also wanted to see if patients with Parkinson's disease and depression (but no history of anxiety) are susceptible to yohimbine-induced panic. Parkinsonian patients with anxiety developed panic attacks at frequencies comparable to primary psychiatric patients with panic disorder. The one patient with PD and a history of major depression alone developed a panic attack. Regardless of their history of anxiety or depression, parkinsonian patients demonstrated a vulnerability to yohimbine-induced somatic symptoms.
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PMID:Parkinson's disease: a preliminary study of yohimbine challenge in patients with anxiety. 1036 82

Major depression, opioid addiction, neurodegenerative diseases, and glial tumors are associated with disturbances of imidazoline receptors (IR) in the human brain. In depression, the level of a 45-kD IR protein (putative I1-IR) is increased in the brain of suicide victims (51%) and in platelets of depressed patients (40%). The density of platelet I1-IR ([125I]-p-iodoclonidine binding) is also increased in depression (135%). The 29/30-kD IR protein (putative I2B-IR) is downregulated (19%) in suicide victims in parallel with a reduction (40%) in the density of I2B-IR ([3H]idazoxan binding). Antidepressant drugs induce downregulation of 45-kD IR protein and I1-sites in platelets of depressed patients and upregulation of I2-sites in rat brain. The densities of I2B-IR and the related 29/30-kD IR protein are decreased (39% and 28%) in the brain of heroin addicts. The density of I2B-IR is increased in Alzheimer's disease (63%) and decreased in Huntington's disease (56%). Brain I2B-IR is not altered in Parkinson's disease. The level of I2-IR in glial tumors is increased (two-fivefold) in parallel with the abundance of the related 29/30-kD IR protein (39%), whereas the level of 45-kD IR protein is decreased (39%). The possible functional relevance of these findings in the context of the pathogenesis of these disorders remains to be elucidated.
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PMID:Imidazoline receptors and human brain disorders. 1041 44

An involvement of immunological events in the process of neurodegeneration has frequently been reported. We investigated the cytokine producing capacity for interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) in whole blood cultures of de-novo patients with idiopathic Parkinson's disease (PD) at the time of first diagnosis and after oral amantadine treatment. Before treatment, productions of IL-2 and IFN-gamma were markedly decreased in PD patients compared to patients with major depressive disorder and healthy controls. After amantadine treatment, the in vitro IL-2 secretion defect was corrected to normal levels in half of the patients, and the increase in IL-2 production was correlated with an increase in IFN-gamma secretion. Our findings suggest that immunological abnormalities occur in the course of PD and that a formerly unappreciated therapeutic potential of amantadine may arise from its immunomodulatory effects on altered T cell function in patients with PD.
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PMID:Effects of amantadine treatment on in vitro production of interleukin-2 in de-novo patients with idiopathic Parkinson's disease. 1043 55

Tolcapone is a catechol-O-methyltransferase (COMT) inhibitor that has shown efficacy in the treatment of Parkinson's disease. The authors undertook the first study on the efficacy of this COMT inhibitor in the treatment of major depressive disorder (MDD). The authors also wanted to assess the effects of tolcapone on the choline and myoinositol resonances in the left caudate and dorsolateral frontal lobe through proton magnetic resonance spectroscopy and on whole blood levels of S-adenosyl-L-methionine (SAMe). The study enrolled 21 adults (10 men and 11 women; mean age, 42.6 +/- 9.6 years) with MDD, which was diagnosed using the Structured Clinical Interview for DSM-IV, and an initial score of > or = 16 on the 17-item Hamilton Rating Scale for Depression (HAM-D-17). Patients were then treated openly for 8 weeks with tolcapone 400 mg twice daily. Treatment efficacy was assessed with the HAM-D-17, the Clinical Global Impressions Severity (CGI-S) scale, and the Beck Depression Inventory (BDI). Among all subjects (N = 21), there were significant (p < .0001) decreases at endpoint in HAM-D-17 scores (from 19.4 +/- 2.9 to 10.7 +/- 5.5), CGI-S scores (from 3.9 +/- 0.6 to 2.4 +/- 1.1), and BDI scores (from 21.6 +/- 8.1 to 12.3 +/- 8.6). Eight patients (38%) dropped out before completing the 8-week open study because of diarrhea, elevated liver function tests, increased anxiety, and noncompliance. No significant effects were noted on choline and myoinositol resonance or on SAMe levels in whole blood before and after 2 weeks of tolcapone treatment. The preliminary results suggest that tolcapone may be a promising agent in the treatment of MDD. Furthermore, double-blind, placebo-controlled studies are necessary to confirm this impression.
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PMID:Open study of the catechol-O-methyltransferase inhibitor tolcapone in major depressive disorder. 1077 Apr 81

Antagonists of the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors and agonists of the glycine-B coagonist site of these receptors have been important tools for characterizing the contributions of NMDA receptor pathophysiology to a large number of neuropsychiatric conditions and for treating these conditions. Among these disorders are Alzheimer's disease, chronic pain syndromes, epilepsy, schizophrenia, Parkinson's disease, Huntington's disease, addiction disorders, major depression, and anxiety disorders. This review will examine pathophysiological and therapeutic hypotheses generated or supported by clinical studies employing NMDA antagonists and glycine-B agonists and partial agonists. It will also consider ethical issues related to human psychopharmacological studies employing glutamatergic probes.
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PMID:NMDA agonists and antagonists as probes of glutamatergic dysfunction and pharmacotherapies in neuropsychiatric disorders. 1048 32

This is a naturalistic review of maintenance electroconvulsive therapy (MECT) during the first 4 1/2 years of a university ECT service. A total of 56 patients, ages 30-84, received MECT. Patients could be classified under five different clinical groups: major depression; bipolar disorder; combined depression and axis 2 disorder; Parkinson's disease plus depression; and schizophrenia. Effectiveness in the different groups and issues related to partial improvement or treatment failure are discussed.
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PMID:A naturalistic review of maintenance ECT at a university setting. 1061 33

Clinical observation points to similarities between psychomotor retardation in major depression and bradykinesia in Parkinson's disease (PD). While common elements of neuropathology have been proposed to account for this, experimental investigations of this possible link have been few and inconclusive. The present study attempts to determine whether patients with depression display the characteristically Parkinsonian reliance on external cues; and if so, whether this is common to both melancholic and non-melancholic patients. Twenty three patients with unipolar major depression (11 melancholic and 12 non-melancholic) and 24 age-matched healthy controls performed a serial choice reaction time task known to be sensitive to Parkinsonian movement deficits. The melancholic patients showed a Parkinsonian pattern of impairment on the task, exhibiting a particular difficulty when initiating movements in the absence of external cues. This was largely alleviated when a moderate amount of external cueing was provided. At a high level of advance information, melancholic patients were again slow relative to controls. A base-line measure of bradykinesia and a derived measure of dependence upon external cues both correlated significantly with CORE (measure of psychomotor disturbance) ratings. The non-melancholic patients did not show any measurable motor impairment. This cue-dependent deficit may be due to an underlying basal ganglia dysfunction similar to that involved in PD, i.e. a failure of internal cueing. Difficulty with a high level of external cueing might reflect bradyphrenia or a prefrontal motor deficit of ability to plan multiple upcoming movements simultaneously. The results suggest that depression subtypes involve differing patterns of fronto-striatal impairment.
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PMID:Parkinsonian motor characteristics in unipolar major depression. 1077 37

Maintenance of motor set in patients with unipolar major depression was examined. Twelve melancholic and 12 non-melancholic depressed patients and 24 age matched controls performed a serial choice reaction time task while external cues aiding maintenance of a motor set were systematically removed. Melancholic patients were significantly slower than controls with no reduction in external cues and with a moderate reduction in external cues. At a high level of reduction in external cues, seven of 12 melancholic patients (but only three of 12 non-melancholic patients and controls) were unable to complete the task; suggesting a greater reliance on external cues, perhaps implicating a failure of motor planning ability in melancholic patients. This, in turn, may point to a prefrontal (premotor) deficit in melancholic depression, with possible commonalities with Parkinson's disease.
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PMID:Reliance on external cues during serial sequential movement in major depression. 1089

Given the many clinical parallels between melancholia and disorders associated with impaired dopaminergic function such as Parkinson's Disease (PD), it has been hypothesised that major depressive disorder, and in particular the psychomotor features of melancholic depression, may also be associated with a hypodopaminergic state. If this is the case, then the use of a dopamine agonist might lead to reversal of both the cognitive and motor impairments seen in these patients. A double-blind, placebo-controlled cross-over design was used to test the effect of apomorphine on motor and cognitive function in seven melancholic subjects (as defined by the CORE instrument) and five control subjects. The testing battery included the following items: finger tapping, rapid alternating movements, verbal fluency, Rey Auditory Verbal Learning Task, digit symbol substitution task and simple and complex reaction times. The independent t-test, after covarying for age, revealed significant impairment in melancholic subjects for the walking task and digit symbol substitution at baseline. Results of the ANCOVA revealed no impact of time or drug condition, either alone or in combination, upon task performance in either group whether assessed separately or jointly. Results of a MANCOVA revealed that apomorphine impaired performance on some cognitive tasks, and that this was seen to a lesser extent in melancholics than control subjects. There was no evidence that the dopamine agonist apomorphine improved cognitive or motor function in subjects with strictly defined melancholia, suggesting that psychomotor retardation is not associated with a hypodopaminergic state. Our conclusions, however, were limited by small sample size; minimal baseline task impairment in depressed compared to control subjects; mild sedation in many subjects during task performance; and lack of serum apomorphine levels.
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PMID:Effect of apomorphine on motor and cognitive function in melancholic patients: a preliminary report. 1116 91


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