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)

The 159 patients with Parkinson's disease with onset after the age of 50 (mean: 62.3 years) were studied with reference to diagnosis and treatment. The results were as follows: 1. Other than the characteristic features, the symptoms at onset were depression (6% of the patients), lumbago (4%), hemiplegia-like (4%) and dizziness (3%), causing misdiagnoses in some of the patients. Among 159 patients studied, the severity most frequent was Yahr stage 3 (63%) at first examination, indicating the necessity of earlier diagnosis. 2. Magnetic resonance imaging (MRI) of the substantia nigra and striatum was investigated using a 1.5 Tesla field and T2-weighted images, which gave no specific results concerning diagnosis and severity. However, it was useful in differential diagnosis between this disease and parkinsonism caused by multiple system atrophy and cerebrovascular diseases. 3. With 123I-IMP SPECT, decrease in blood flow in the frontal and temporal lobes correlated with the severity (Yahr stage) of the disease. Regarding cognitive functions the scores of Hasegawa's Dementia Scale and Mini-Mental State showed a highly significant correlation with the amount of blood flow in frontal and parietal lobes, suggesting that dementia might be caused by dysfunction of these lobes. 4. In 98 patients treated with levodopa mixed with dopa-economizers for more than a year, the maximum improvement was small in severely disabled patients of Yahr stage 5 and 4 because none improved to stage 3A or below (3A is an arbitrary criterion meaning mild involvement in stage 3 with 3P meaning more severe cases).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnosis and treatment of Parkinson's disease in the elderly]. 187 Feb 74

Depression is a frequent finding in patients with neurological disorders. These depressions, however, have similar phenomenology, duration, biological markers, and response to treatment as depressions in patients with no known brain injuries (i.e., functional depression). In the present article, we review evidence that suggests the dementia of depression exists among severely depressed patients with cerebrovascular lesions or Parkinson's disease (PD). We conclude that: a) in patients with either stroke lesions or PD, depression is significantly associated with cognitive deficits; b) this association is only true for patients with major depression (i.e., it is not present in patients with minor depression); and c) patients with poststroke depression and patients with PD and depression have a severity and profile of cognitive deficits similar to those found in patients with primary major depression.
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PMID:Dementia of depression in Parkinson's disease and stroke. 191 43

In patients with Parkinson's disease high prevalence of depression has been estimated. This prevalence may be overestimated since the commonly used assessment of depressive complaints neglects the correspondence with physical symptoms of Parkinson's disease and psychosomatic symptoms in depression. To evaluate the effect of this contamination, we presented a frequently used questionnaire for assessing depressive complaints, Beck's Depression Inventory (BDI), to eight neurologists specialized in Parkinson's disease. We asked them to select those items on which Parkinson patients might receive high scores merely because of the physical symptoms of their disease. Based on their consistent judgments, a BDI-version corrected for somatic items was constructed. Next, the scores of the original and the corrected version were computed for 27 outpatients with Parkinson's disease (from mild to very severe) and 52 psychiatric inpatients who were being treated for depression. Prevalence of depression were 74% (original BDI) and 48% (corrected BDI) for the Parkinson group and 75% and 81% respectively for the psychiatric group. Results indicate that great care should be taken in interpreting scores on depression inventories in patients with Parkinson's disease. In general, the results raise doubts on the validity of somatic complaints as indicators of depression in patients with Parkinson's disease.
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PMID:[Physical symptoms of Parkinson's disease and the score on Beck's Depression Inventory]. 192 97

Recent immunohistochemical studies have shown the distribution of histaminergic neurons in the mammalian brain, which are concentrated in the tuberomammillary nucleus of the posterior hypothalamus and project efferent fibers to almost all parts of the brain from the olfactory bulb to the spinal cord. Histaminergic neurons co-express other neuroactive substances, such as gamma-aminobutyric acid, adenosine, substance P, galanin and Met-enkephalin-Arg-Phe. In addition, pharmacological studies have demonstrated the presence of presynaptic histamine H3-receptors (autoreceptor) in addition to H1- and H2-receptors. The specific agonist (alpha-methylhistamine) and antagonist (thioperamide) of H3-receptors were developed. Results from a number of studies indicate a variety of physiological roles of neuronal histamine such as thermoregulation, feeding behavior, sexual activity, sleep-wakefulness cycle, hormonal regulation and so on. Moreover, histaminergic drugs affect not only the emotional behavior, but also are effective to treat some patients of depression, Parkinson's disease, akathisia, motion sickness and so on. The central histaminergic neuron system is also affected by mental disorders and neuropsychopharmacological drugs. This review especially focused on these points and suggests that the central histaminergic neuron system may play an important role in the regulation of mental functions.
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PMID:[Recent advances in neuropsychopharmacology of the central histaminergic neuron system]. 192 57

Current knowledge of cognitive dysfunction in Parkinson's disease (PD) has largely been obtained from studies of chronically treated patients in whom effects of disease chronicity, treatment, depression and dementia are confounding factors. Studies of untreated patients have examined few cognitive domains and relationships between cognition, depression and motor disability have been incompletely explored. Accordingly, we studied 60 consecutive patients with newly diagnosed, untreated, idiopathic PD and 37 matched, healthy control subjects; no subject had clinical dementia or depression. All subjects received tests of specific processes of memory and cognition, including working memory, verbal and non-verbal short- and long-term memory, language, visuospatial capacity, set-formation and shifting and sequencing. Patients also received quantitative global clinical measures of severity of dementia, depression and motor disability. The PD group as a whole showed deficits in immediate recall of verbal material, language production and semantic fluency, set-formation, cognitive sequencing and working memory and visuomotor construction. However, this group was unimpaired in immediate memory span, long-term forgetting, naming, comprehension and visual perception. Language deficits and more severe frontal lobe impairments were confined to those PD patients scoring abnormally on a Mini Mental State examination. Motor disability correlated strongly with severity of depression but weakly with cognitive impairment. Cognitive sequencing, set-formation and set-shifting deficits tended to associate with depression, but otherwise there was no association between cognition and depression. The results indicate dissociation of cognition and motor control in early PD which suggests that cognitive dysfunction is largely independent of frontostriatal dopamine deficiency underlying motor disability. Some, but not all, of the frontal lobe deficits of chronic disease are detectable in early, untreated PD. The pathogenesis of the cognitive deficits shown here appears to involve extrastriatal dopamine systems or non-dopaminergic pathology. Longitudinal study is necessary to determine whether increasing disease duration exacerbates the early cognitive deficits and affects new cognitive domains, in addition to producing increasing motor disability.
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PMID:Cognitive impairment in early, untreated Parkinson's disease and its relationship to motor disability. 193 36

The Kraepelinian subtypes, developed early in the century, recognize the heterogeneity of schizophrenia but do not reliably predict differences in response to classical neuroleptics. The newer distinction of positive and negative syndromes in schizophrenia carry promise as an approach to identifying meaningful clinical and neurobiological dimensions. The present review summarizes the supportive evidence from a series of investigations using the Positive and Negative Syndrome Scale (PANSS), and a hypothesis on the pathophysiology of negative and positive symptoms is advanced. Our data suggest that: (a) positive and negative syndromes in schizophrenia represent stable, independent dimensions and not co-exclusive subtypes; (b) both are unrelated to the progression of illness; (c) they are differentially related to fundamental aspects of schizophrenia, including premorbid adjustment, cognitive development, family psychiatric history, the cognitive and neuropsychiatric profiles, dopaminergic functions, drug response, and subsequent course; (d) together with depression and excitement, they comprise the fundamental symptomatic components of schizophrenia, which, in their interaction, can account for the specific Kraepelinian subtypes. We have proposed that negative symptoms represent the core pathology in schizophrenia and may be understood as a variant of parkinsonism, hence characterized by dopaminergic deficiency and increased cholinergic activity. This view is supported by the striking overlap with Parkinsonism in regard to clinical features, neurochemistry, pharmacology, neuropathology, and neuroradiology. Positive symptoms are thought to reflect increased dopaminergic activity, which may arise as a compensatory adaptive mechanism to overcome the progressive dopamine loss in the maturing brain. The early onset of schizophrenia by comparison to Parkinson's disease may explain why schizophrenia entails more pronounced positive symptoms, development deficits, and cognitive, social, and emotional impairments. We describe evidence that pineal calcification, which may reflect disturbance of melatonin functions, appears to be a nongenetic factor in schizophrenia associated with perinatal injury. This may in part underlie the negative syndrome and its response to antipsychotic compounds with serotonergic (5-HT) antagonism.
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PMID:Experimental models of schizophrenia. 193 75

A microcomputer-based approach to the quantification of facial expression was used to measure and compare the smiling behavior of a group of Parkinson's disease sufferers, a group of patients with major depression, and a control group of comparable age. Subjects were asked to view a series of amusing slides and their expressions were recorded. The most animated smile for each subject was chosen for analysis and scores on 12 computer-generated measures were obtained using the Facial Expression Measurement program. These measures are end-lip measure, mouth width measure, mouth-opening measure, mid-top measure, mid-lower lip measure, top lip-thickness measure, lower lip-thickness measure, eye-opening measure, top eyelid/iris intersect measure, lower eyelid/iris intersect measure, inner eyebrow measure, and mid-eyebrow measure. The depressed group differed significantly from the other groups, with higher scores on end-lip measure, mid-top lip measure, and mid-eyebrow measure. All subjects completed the Levine-Pilowsky Depression Questionnaire. The depressed patients obtained higher depression scores than the parkinsonian group, who in turn had significantly higher depression scores than the control group. The depression score was correlated with end-lip measure, mouth width measure, mid-top lip measure, eye-opening measure, and mid-eyebrow measure in the population as a whole. A significant negative correlation emerged between the depression score and mid-eyebrow measure in the depressed group. Both the depressed group and the parkinsonian group were found to smile significantly less often during the slide session when compared with the control group. These results are discussed in the light of earlier findings.
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PMID:A controlled quantitative study of facial expression in Parkinson's disease and depression. 194 Aug 92

Seventeen patients with Parkinson's disease which was markedly asymmetric and worse on the right side of the body (RHP) were compared with 13 patients whose signs were worse on the left (LHP). The two groups of patients were well matched for age, duration of symptoms, disability, overall severity of signs, and medication. The mean scores on ratings of depression, using both a self-rating scale and semi-structured interview rating, were almost twice as great in the LHP group. The LHP group also had significantly more symptoms of anxiety. The prevalence of clinically significant psychopathology was increased about five fold in the LHP group compared with the RHP group. There was a close correlation between anxiety and depressive symptoms. The depression experienced by the patients was 'atypical', with relatively little anhedonia and evidence of a negative view of self, and prominent symptoms of anxiety. The best predictor of symptoms of depression and anxiety was a measure of social support and stress. They also correlated with the overall severity of Parkinson's disease.
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PMID:Left-sided Parkinson's disease is associated with greater anxiety and depression. 194 51

Depression is the major psychiatric complication of Parkinson's disease, and it occurs in approximately one-third of all cases. Diagnosis of depression is complicated by the overlap of depressive and parkinsonian symptoms. Its etiology is not fully understood but involves changes in dopamine and serotonin. Depression has significant clinical impact; depressed patients are more disabled (less independent). The depressive symptoms respond to treatment with antidepressants and electroconvulsive therapy.
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PMID:The etiology of depression in Parkinson's disease patients. 196 50

High-speed memory scanning (Sternberg paradigm) was tested in a collective of 20 parkinsonian patients (10 newly diagnosed, untreated patients, duration of the disease 0.5-3.8, mean 1.5 years; 10 levodopa-treated patients, duration of the disease 4.2 to 11, mean 7.6 years). The levodopa-treated patients stopped taking levodopa before the test. There was a tendency towards retarded memory scanning in the patients' collective compared with 20 healthy controls with similar ages and verbal IQs (p = 0.076, Mann-Whitney U test). The mental slowing correlated significantly with bradykinesia and the sum-score of the Columbia University Parkinson Rating Scale (p = 0.021 and 0.019; Spearman rank correlation). Kruskal-Wallis ANOVA revealed a significant mental slowing in the subgroup of patients with Parkinson's disease for greater than 4 years compared with the newly diagnosed patients and the controls (H = 8.54; p = 0.019 and 0.006, Mann-Whitney U test). The findings suggest a mental slowing in Parkinson's disease, which is associated with the progression of parkinsonian motor symptoms and not with depression.
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PMID:Slowing of high-speed memory scanning in Parkinson's disease is related to the severity of parkinsonian motor symptoms. 196 55


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