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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Whereas the instability of positive symptoms over time is well recognized, the instability of negative symptoms is still debated. This controversy could be due to the fact that different negative symptoms have been studied in different phases of schizophrenia. We, therefore, hypothesized that some negative symptoms would improve whereas others would remain perfectly stable during the remission of the acute phase of illness. We further hypothesized that the changes in these negative symptoms would be linked to changes in other domains such as extrapyramidal, depressive and positive symptomatology. A broadly defined sample of schizophrenic patients was evaluated at admission and discharge of the hospital with the Scale for the Assessment of Negative Symptoms (SANS) and the Scale for the Assessment of Positive Symptoms (SAPS), the Montgomery and Asberg Depression Rating Scale (MADRS) and the Extrapyramidal Symptoms Rating Scale (ESRS). Doses of antipsychotic medications were converted into chlorpromazine-equivalents. Fifty-seven patients (mean age 40.3 years old) were included in the sample and followed-up during their hospitalization. All the sub-scores of the SANS-SAPS decreased significantly but 4 items of the SANS belonging to the affective flattening subscale (unchanging facial expression, decreased spontaneous movements, paucity of expressive gestures and lack of vocal inflections) and one item belonging to the alogia subscale (poverty of speech) did not vary significantly, showing the necessity of taking into account the individual items of the SANS rather than the subscale scores to evaluate the course of negative symptoms. Changes in all the SANS subscores except the alogia subscore were associated with variations in scores of other scales. The change in attentional subscores was positively correlated to the change in the positive formal thought disorder subscores, probably because both belong to the same syndrome. The change in affective flattening subscores was associated with changes in depressive and akinetic scores and 28% of the variance of the change in the affective flattening subscores was explained by the change in the MADRS scores. Changes in avolition-apathy and anhedonia subscores were also associated with changes in MADRS scores but not with the change in akinesia scores.
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PMID:Negative symptoms in schizophrenia: their evolution during an acute phase. 856 93

The debate concerning the stable or instable aspect of schizophrenic symptomatology has lead the authors to study this phenomenon by taking into account, at the time of inclusion of a schizophrenic patient, such parameters as: the phase of the illness (acute, post-acute or stable) or the course (chronicity) as well as the relationship between the negative symptomatology variation and other symptomatic dimension variation (depression, akinesia, etc.), in follow-up studies. The results of these studies are clearly in favour of taking into consideration all or part of these parameters, to evaluate at best the stability of positive and negative schizophrenic symptoms.
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PMID:[Stability of positive/negative symptoms in schizophrenia]. 876 39

Emotional disturbances, such as lack of motivation or depression, are common after stroke. The drugs mainly used to treat these syndromes in Japan are the cerebral metabolic enhancers whose biochemical and pharmacological profiles are similar to those of antidepressant drugs. In order to examine the possible therapeutic effect of T-794 [(5R)-3-(6-(cyclopropylmethoxy) 2-naphthalenyl)-5-(methoxymethyl) 2-oxazolidone], a new reversible inhibitor of monoamine oxidase (MAO) type A, on those emotional disturbances, its antidepressant activity was compared with those of major cerebral metabolic enhancers in rodents with or without treatment of cerebral ischemia. Oral administration of T-794 potently prevented reserpine-induced ptosis (ED50 = 4.41 mg/kg), akinesia (ED50 = 3.29 mg/kg), and hypothermia (minimum effective dose = 3 mg/kg) in mice. It was at least 3.7, 13.0, and 3.3 times more potent than cerebral metabolic enhancers tested (indeloxazine, bifemelane, amantadine and idebenone) in antagonism of the ptosis, the akinesia, and the hypothermia, respectively. Effect of T-794 was also examined in the behavioral despair test in rats subjected to forebrain ischemia. The ischemia was induced by a combination of bilateral common carotid artery occlusion (15 min) and systemic hypotension (sodium nitroprusside 5 mg/kg, s.c). From 13 d after the surgery, drugs were orally administered twice daily 7 times, and following the last administration rats were assessed for their behavior. T-794 reduced the duration of immobility in the behavioral despair test at 30 mg/kg without affecting spontaneous motor activity, whereas indeloxazine showed no significant effect. Antidepressant-like activity of T-794 was suggested in rodents with as well as those without cerebral ischemia. The results suggest that T-794 may make an important contribution to the treatment of emotional disturbances following stroke.
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PMID:Possible therapeutic effect of T-794, a novel reversible inhibitor of monoamine oxidase-A, on post-stroke emotional disturbances, assessed in animal models of depression. 914 8

Diagnosis of Parkinsonism is made in two steps: 1. identification of the Parkinson syndrome, a combination of rest tremor, hypertonia, akinesia and postural disturbances; 2. then essentially on the basis of clinical observations, relation to Parkinson's disease. The main risks during the course with L-dopa treatment are, on the one hand, the appearance of akinetic changes and movement disorders, more common in the younger affected patients, and on the other hand, disorders that do not respond to L-dopa, especially postural and cognitive, that are favoured by old age. Anxiety, depression pain, autonomic disorders and insomnia increase the repercussions of the disease and complicate its management.
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PMID:[Diagnosis and course (under treatment) of Parkinson disease]. 920 68

Idiopathic Parkinson's disease (IPD) is a common and universal condition. Although its cause is still unknown, we now have some insights into pathogenetic mechanisms and genetic factors that may be important in causing the selective neuronal loss and presence of Lewy bodies that characterize its pathology. Clinically, as well as the classic features of akinesia, rigidity and often rest tremor, patients may present a wide range of other symptoms including pain, other sensory symptoms, impaired olfaction, personality change, mild executive cognitive deficits, dementia and depression, an extraordinary richness of symptoms and signs rendered even more extraordinary by the long-term effects of drug treatment. While there may be little difficulty recognizing typical cases of IPD, there has been, at least until recently, a considerable misdiagnosis rate in both atremulous (confusion with ageing, vascular disease, multiple system atrophy (MSA) or progressive supranuclear palsy (PSP)) and tremulous (confusion with essential tremor (ET), dystonic tremor, and MSA) forms. However, increasing awareness of the clinical features of all these conditions, together with adherence to exacting diagnostic criteria, is leading to improved diagnosis, which is crucial for patients (who want to know what the future holds for them), for their treatment (giving them the right drug and not the wrong one) and for research (since all the different diseases above have different aetiologies and pathology).
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PMID:Parkinson's disease: clinical features. 942 65

Parkinson's disease (PD) is a common neurological illness and various degrees of depression frequently complicate its course. Risk factors for developing depression with PD include right-sided hemiparkinsonism, akinesia, increased severity of disability, anxiety and psychosis. Onset of parkinsonism at a younger age, female gender and the use of levodopa are arguable risk factors. Depression may be difficult to diagnose in patients with PD because the signs of the 2 disorders overlap. In addition, patients with atypical PD more commonly have depression than patients with classical PD presentations. Antidepressant response to antiparkinsonian treatment has been limited. Enhancement of catecholamine levels in the CNS by selegiline (deprenyl), a monoamine oxidase (MAO) type B inhibitor, has shown potential antidepressant as well as neuroprotective effects. Other MAO inhibitors have shown antidepressant efficacy in animal models but have not been well tolerated by patients with PD. A catechol-O-methyltransferase (COMT) inhibitor combined with an MAO inhibitor might synergistically maximise the levels of catecholamines in the CNS. Antidepressant medications used in patients without PD include tricyclic antidepressants (TCAs) and selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors (SSRIs), but only TCAs have been carefully studied for their antidepressant effects in PD. Electroconvulsive therapy has proven efficacy as antidepressant therapy in patients with PD, and transcranial magnetic stimulation has provided temporary relief of depression under experimental conditions. Adverse effects of polypharmacy in the attempted treatment of depression in patients with PD are common in the elderly. A 'serotonin syndrome' has occurred frequently enough to preclude the coadministration of selegiline with SSRIs or TCAs, and multiple interactions between antiparkinsonian and antidepressant medications further complicate treatment strategies in patients with PD. An algorithmic approach to the pharmacological treatment of depression is described in this article.
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PMID:Depression in Parkinson's disease. Pharmacological characteristics and treatment. 946 87

Behavioural disorders in Parkinson's disease can grossly be subdivided in primary disturbances and those which are related to drug treatment. Depression and anxiety are a common feature in parkinsonian patients. Both occur independently of drug treatment. In general, most current antidepressive and anxiolytic drugs could be administered in Parkinson's disease with the same precautions as in the normal population. However, in single case reports modern serotonin reuptake blockers in Parkinson's disease have been accused to worsen parkinsonian motor condition. Combinations of serotonin reuptake inhibitors with MAO-inhibitors like selegiline should be used with caution. In the case of cognitive decline firstly an underlying depression should be disclosed or if existent be treated. Depression seems to be the single most important factor associated with the severity of dementia and early antidepressant treatment seems to decrease cognitive decline in depressed parkinsonian patients. Anticholinergic medications should be discontinued since they may cause mental side effects. Sleep disorders in Parkinson's disease are mainly caused by nocturnal akinesia, which causes sleep fragmentation or altered dreaming and nightmares, which might be a side-effect of dopaminergic treatment. In the first case the administration of a controlled release preparation of levodopa at bedtime may be indicated. If the sleep disorder is considered to be due to dopaminergic medication, a reduction of long-term acting agents like modern dopamine agonists and controlled-release levodopa should be considered. In severe psychotic states related to drug treatment antiparkinsonian therapy must be carefully analysed and, if possible, reduced. If motor condition worsens and/or psychiatric symptoms do not improve, initiation with "atypical" neuroleptics like clozapine is indicated. The pharmacological and clinical properties of new antipsychotic drugs that can be used in Parkinson's disease are revised.
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PMID:Treatment of behavioural disturbances in Parkinson's disease. 947 Jan 38

Parkinson's disease (PD) is characterized by progressive neuronal loss associated with Lewy bodies in many subcortical nuclei leading to multiple biochemical and pathophysiological changes of clinical relevance. Loss of nigral neurons causing striatal dopamine deficiency is related to both the duration and clinical stages (severity) of the disease. The clinical subtypes of PD have different morphological lesion patterns: a) The akinetic-rigid type shows more severe cell loss in the ventrolateral part of substantia nigra zona compacta (SNZC) that projects to the dorsal putamen than the medial part projecting to caudate nucleus and anterior putamen, with negative correlation between SNZC cell counts, severity of akinesia-rigidity, and dopamine loss in the posterior putamen. Reduced dopaminergic input causes overactivity of the GABA ergic inhibitory striatal neurons projecting via the "indirect loop" to SN zona reticulata (SNZR) and medial pallidum (GPI) leading to inhibition of the glutamatergic thalamo-cortical motor loop and reduced cortical activation. b) The tremor-dominant type shows more severe neuron loss in medial than in lateral SNZC and damage to the retrorubral field A8 containing only few tyrosine hydroxylase and dopamine transporter immunoreactive (IR) neurons but mainly calretinin-IR cells. A8 that is rather preserved in rigid-akinetic PD (protective role of calcium-binding protein?) projects to the matrix of dorsolateral striatum and ventromedial thalamus. Together with area A10 it influences the strial efflux via SNZR to thalamus and from there to prefrontal cortex. Rest tremor in PD is associated with increased metabolism in the thalamus, subthalamus, pons, and premotor-cortical network suggesting an increased functional activity of thalamo-motor projections. In essential tremor, no significant pathomorphological changes but overactivity of cerebello-thalamic loop have been observed. c) In the akinetic-rigid forms of multisystem atrophy, degeneration is more severe in the lateral SNZC with severe loss of calbindin-IR cells reflecting initial degeneration of the striatal matrix in the caudal putamen with transsynaptic degeneration of striatonigral efferences that remain intact in PD. This fact and loss of striatal D2 receptors--as in advanced stages of PD--are reasons for negative response to L-dopa substitution. These data suggest different pathophysiological mechanisms of the clinical subtypes of PD that have important therapeutic implications. d) Involvement of extranigral structures in PD includes the mesocortical dopaminergic system, the noradrenergic locus coeruleus, dorsal vagal nucleus and medullary nuclei, serotonergic dorsal raphe, nucleus basalis of Meynert and other cholinergic brainstem nuclei, e.g. Westphal-Edinger nucleus (controlling pupillomotor function), posterolateral hypothalamus and the limbic system, e.g. amygdaloid nucleus, part of hippocampal formation, limbic thalamic nuclei with prefrontal projections, etc. Damage to multiple neuronal systems by the progressing degenerative process causing complex biochemical changes may explain the variable clinical picture of PD including vegetative, behavioural and cognitive dysfunctions, depression, pharmacotoxic psychoses, etc. Future comparative clinico-morphological and pathobiochemical studies will further elucidate the pathophysiological basis of specific clinical symptoms of PD and related disorders providing a broader basis for effective treatment strategies. Parkinson's disease (PD) is characterized by progressive degeneration of the nigrostriatal dopaminergic system and other subcortical neuronal systems leading to striatal dopamine deficiency and other biochemical deficits related to the variable clinical signs and symptoms of the disorder. (ABSTRACT TRUNCATED)
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PMID:Post mortem studies in Parkinson's disease--is it possible to detect brain areas for specific symptoms? 1037 Sep 1

Negative symptoms in schizophrenia represent a diagnostic and therapeutic challenge. Diagnostically, they need to be differentiated from depression and treatment-related variables. The latter include akinesia, a part of drug-induced Parkinsonism, sedation, and effects of understimulation, as they have been reported in patients institutionalised for long periods of time. Other patients show negative symptoms as sequelae of positive symptoms: Commanding voices that tell patients to stay in the house or forbid them to speak to other people, or persecutory delusions may result in social withdrawal and alogia. All of the above, often summarised as secondary negative symptoms, have to be distinguished from primary negative symptoms, sometimes also referred to as the deficit state of schizophrenia. These are considered illness inherent problems and usually have an enduring, chronic course. They are often seen in the absence of positive symptoms, as in simple schizophrenia. The chronicity of the disorder, the lack of obviously disturbed and aberrant behavior and the fact that these patients tend to lead secluded lives lead to an underrepresentation of these patients in clinical psychiatry. Next to a description of clinical symptoms a review of means to aid differential diagnosis is provided. Negative symptoms call for sound differential diagnosis provided by a specialist in order to be able to provide optimal management to prevent the negative consequences of a chronic negative syndrome.
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PMID:Negative symptoms in patients with schizophrenia with special reference to the primary versus secondary distinction. 1129 57

Parkinson's disease (PD) is associated with sleep disorders which are attributed mainly to dopamine deficiency, nocturnal akinesia, drug therapy, and cofactors such as age and depression. These disturbances affect the macro- and microstructure of both REM and non-REM sleep and motor, respiratory, and autonomic functions. Excessive daytime sleepiness and the interactions between sleep and daytime motor performance in PD are not yet completely understood. Correct diagnosis and treatment of sleep disorders is essential due to the risk of harm to the patient and others and due to their effect on quality of life for all concerned. As sleep disorders in PD are extremely common (about 70%) and may have severe consequences, a systematic sleep history and specific therapy should be considered integral to treatment in every PD patient.
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PMID:[Pathophysiology, clinical aspects and therapy of sleep disorders in Parkinson disease]. 1143


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