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)

Cervical dystonia (CD) or spasmodic torticollis is the most frequent form of focal dystonia. Cervical dystonia is characterized by sustained neck spasms, abnormal head posture, head tremor, and pain. A 53-year-old male patient with the diagnosis of CD developed an episode of delusional depression and was treated with electroconvulsive therapy (ECT). An unexpected and dramatic improvement of CD was seen during the first 2 days after each ECT session. That therapeutic effect was not sustained and vanished soon afterward. The effectiveness of ECT for CD, although too brief to be recommended as a useful treatment, may shed light on the pathophysiology of this problematic movement disorder.
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PMID:Short-lived response of cervical dystonia to electroconvulsive therapy. 1914 11

While deep brain stimulation (DBS) surgery is a well-accepted treatment for Parkinson disease (PD) that improves overall quality of life (QoL), its effects across different domains of QoL are unclear. The study reported here directly compared the effects of unilateral DBS in subthalamic nucleus (STN) or globus pallidus (GPi) on QoL in 42 non-demented patients with medication-refractory PD. Patients were enrolled in the COMPARE trial, a randomized clinical trial of cognitive and mood effects of STN versus GPi DBS conducted at the University of Florida Movement Disorders Center. Patients underwent motor, mood, verbal fluency and QoL (Parkinson disease questionnaire: PDQ-39) measures before and 6 months following surgery. Groups experienced motor and mood improvements that did not differ by target. Patients with STN DBS evidenced a slight decrement on letter fluency. On average, all patients endorsed better overall QoL after surgery. However, despite similar motor and mood improvements, GPi patients improved more than STN patients (38 vs. 14%, respectively; P = 0.03). Patients reported better QoL on subscales of mobility, activities of daily living (ADLs), emotional well-being, stigma, cognition and discomfort, but not on those of social support and communication. Improvements on the mobility, ADLs, stigma and social support subscales were greater amongst GPi patients. In regression analyses, only depression changes independently predicted changes in overall QoL as well as emotional well-being and social support changes. Within the STN group only, declining category fluency scores correlated with poorer QoL on the communication subscale. Unilateral DBS in both STN and GPi improved QoL overall and in disparate domains 6 months after surgery. Patients receiving GPi DBS reported greater improvements that cannot be explained by differential mood or motor effects; however, verbal fluency changes may have partially contributed to lesser QoL improvements amongst STN patients.
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PMID:Greater improvement in quality of life following unilateral deep brain stimulation surgery in the globus pallidus as compared to the subthalamic nucleus. 1936 33

Although apathy is among the most frequent behavioral changes in Parkinson's disease (PD), its diagnosis is still problematic, and the overlap with depression and dementia poorly studied. Aim of the study was validate specific criteria to diagnose apathy in PD, and to examine its association with subsyndromes of depression and dementia. A series of 164 patients with PD, 44 patients with "primary" depression and no PD, 23 patients with Alzheimer's disease, and 26 age-comparable healthy controls underwent a comprehensive psychiatric assessment that included a structured psychiatric interview and the Apathy Scale. A set of seven diagnostic criteria showed high sensitivity and specificity for clinically diagnosed apathy. Fifty-two of the 164 patients with PD (32%) met diagnostic criteria for apathy. Eighty-three percent of patients with apathy had comorbid depression and 56% had dementia. Only 5 of the 40 PD patients (13%) with neither depression nor dementia had apathy. We validated a set of standardized criteria for the diagnosis of apathy in PD. About one third of a series of patients attending a Movement Disorders Clinic showed apathy. Both depression and dementia were the most frequent comorbid conditions of apathy in PD.
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PMID:The syndromal validity and nosological position of apathy in Parkinson's disease. 1941 42

Consecutive patients in a Movement Disorders Center with Parkinson disease (PD) were offered to undergo complete neuropsychological testing and to complete the Beck Depression Inventory (BDI), regardless of their cognitive and behavioral status. A total of 82 patients were included in this cross-sectional study and had a mean age of 67.7 years, formal education of 14.8 years, PD duration of 101 months, Unified Parkinson Disease Rating Scale-Motor ''off'' score of 36.96, Mini-Mental State Examination (MMSE) score of 27.8 (range 19-30), and BDI score of 10.23 (SD 8.65). Beck Depression Inventory scores did not correlate with disease duration or motor scores but inversely correlated with the MMSE scores (r = -0.40; P < .001) and total Dementia Rating Scale (DRS) scores (r = -0.33; P < .01). Using a univariate regression analysis controlling for age, gender, education, and total Unified Parkinson Disease Rating Scales (UPDRS) score, the BDI scores had a significant and unique relationship with MMSE scores. However, when the BDI scores were correlated with specific cognitive domains, only the Boston Naming Test and the Hopkins Verbal Learning Test (HVLT) delayed recall remained significant after Bonferroni correction. Similarly, when comparing the cognitive performance of patients with PD who scored >14 on the BDI versus those who scored <14, only the mean score of the Boston Naming Test was different between the 2 groups. Our study shows that while depressive symptoms correlated with global cognitive performance, naming, verbal memory, and language are the most susceptible cognitive domains affected with depressive symptoms.
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PMID:Depressive symptoms in Parkinson disease correlate with impaired global and specific cognitive performance. 1942 48

Psychogenic tremor is a variant of psychogenic movement disorder. Psychogenic tremor often starts in an abrupt manner and affects voluntary motor function, rapidly reaching maximum impairment for the patient. Patients often present with comorbid psychiatric disorders, including depression, anxiety and personality disorders. Overall prognosis is poor, with 80 to 90 percent of patients symptomatic after one year. The authors present the case of a 33-year-old woman who experienced an acute episode of psychogenic tremor. They review the literature on psychiatric and neurologic manifestations of psychogenic tremor, consider diagnostic and treatment implications and discuss overall prognosis of recovery for patients afflicted with psychogenic tremor.
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PMID:Psychogenic tremor in a patient with a major depressive episode. 1965 Feb 75

Parkinson's disease (PD) is the second most common neurodegenerative disease and primarily considered as a movement disorder defined by the presence of motor symptoms, such as bradykinesia, tremor and rigidity. However, it is nowadays widely accepted that PD is associated with a wide variety of non-motor features, which affect the vast majority of patients during the course of the disease and may even precede the onset of motor symptoms. The spectrum of these non-motor disturbances is very broad and comprises neuropsychiatric conditions, such as depression, dementia and hallucinations, as well as autonomic, sensory and sleep disorders. Physicians need to be aware of these non-motor features, since they have substantial impact on the health-related quality of life of PD patients, even ahead of motor symptoms. This article aims to provide an overview of frequently observed non-motor features in PD and discusses prospects and limitations of currently available options for symptomatic treatment of these disturbances.
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PMID:Beyond tremor and rigidity: non-motor features of Parkinson's disease. 1968 May 98

Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) are second only to Alzheimer's disease (AD) in frequency. In particular it is evident that up to 80% of people with PD will develop dementia towards the end of their life. While the neurobiology of movement disorder has been well studied in PD, much less attention has been given to mechanisms underlying the cognitive and behavioural symptoms associated with DLB and PDD. To date, the best correlate of cognitive impairment appears to be cortical Lewy bodies; however, new emphasis has been placed on small aggregates of synuclein. Furthermore, very few studies have attempted to investigate the neurochemical correlates of behavioural disorders in DLB/PDD and whether these are similar or distinct from AD. Aggregated alpha-synuclein forms the core component of Lewy bodies, a major pathological feature of Parkinson's-related conditions. The 26S proteasome is an ATP-dependent protease that catalyses the breakdown of alpha-synuclein. Previous studies have implicated alterations in the proteasome in PD. Furthermore, proteasome inhibitors have been reported to induce alpha-synuclein aggregation and Lewy body-like inclusions, resulting in neuronal loss both in vitro and in vivo. Our preliminary results indicate that selective alterations in the expression of proteosome sub-units are a feature of both DLB and PDD, while changes in activity are restricted to PDD. Depression is a common symptom in DLB/PDD, yet the evidence base for standard treatment with SSRIs is limited. In contrast to previous studies of AD, our results indicate that there is no association between depression and the 5-HT transporter, while there was a significant increase in the number of 5-HT1A receptors in those DLB/PDD patients with depression. These data may provide an insight into the lack of success of current treatments and suggest alternative approaches.
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PMID:Biochemical and pathological correlates of cognitive and behavioural change in DLB/PDD. 1971 Nov 17

Parkinson's disease is a movement disorder resulting from neurodegeneration of the basal ganglia. Parkinson's disease is usually diagnosed at approximately 55-60 years of age and affects approximately 1% of the population over 60 years. Dopaminergic cells located in the substantia nigra and whose terminals extend to the striatum degenerate slowly such that 60% of cells are already lost when clinical motor symptoms first become evident. In addition to the classic triad of Parkinson's disease symptoms, rest tremor, muscular rigidity and bradykinesia, abnormalities in postural reflexes, dementia and depression are important comorbid conditions. Current therapies are aimed primarily at replacing dopamine with the dopamine precursor L-dopa or by the use of direct acting dopamine receptor agonists. Adjunctive treatments with monoamine oxidase inhibitors, catechol-O-methyl transferase inhibitors and amantadine are also used. While providing very effective symptomatic therapy in early stages of the disease, these agents fail to halt disease progression. Thus, while these treatments generally provide excellent results for 2-5 years, quality of life for Parkinson's disease patients becomes increasingly poor 5-10 years after diagnosis. Symptoms that become increasingly problematic with disease progression include inconsistencies in motor control (response fluctuations), gait and balance abnormalities, cognitive loss, hypophonia and dysphagia. Therefore, in order to maintain an acceptable quality of life for patients with Parkinson's disease, therapies that provide not only symptomatic improvement, but also slow or stop disease progression are greatly needed. In this review, we will discuss possible mechanisms of cell death in Parkinson's disease and related potentially disease-modifying therapies. These therapies include dopaminergic cell tranplantation and the use of growth factors. Small molecules that may act as antioxidants, nicotinic receptor agonists, nitric oxide synthase inhibitors, immunophilins, excitatory amino acid-related (iGluR and mGluR agonists and antagonists) drugs and anti-inflammatory drugs will also be discussed.
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PMID:Pharmacological approaches to disease-modifying therapies in Parkinson's disease. 1981 Sep 16

Machado-Joseph disease or spinocerebellar ataxia 3 (MJD/SCA3) is a clinically heterogeneous, neurodegenerative disorder characterized by varying degrees of ataxia, ophthalmoplegia, peripheral neuropathy, pyramidal dysfunction and movement disorder. MJD/SCA3 is caused by a CAG repeat expansion mutation in the protein coding region of the ATXN3 gene located at chromosome 14q32.1. Current hypotheses regarding pathogenesis favor the view that mutated ataxin-3, with its polyglutamine expansion, is prone to adopt an abnormal conformation, engage in altered protein-protein interactions and aggregate. Expanded CAG repeat length correlates with the range and severity of the clinical manifestations and inversely correlates with age of disease onset. Though MJD/SCA3 is classically described as affecting the cerebellum, brainstem and basal ganglia, recent neuropathology and neuroimaging series demonstrate involvement of other areas such as the thalamus and cerebral cortex. Clinically, much emphasis has been placed in the description and recognition of the non-motor symptoms observed in these patients, such as pain, cramps, fatigue and depression. Currently, no disease modifying treatment exists for MJD/SCA3. Standard of care includes genetic counseling, exercise/physical therapy programs, and speech and swallow evaluation. Symptomatic treatment for clinical findings such as depression, sleep disorders, parkinsonism, dystonia, cramps, and pain is important to improve the quality of life for those with MJD/SCA3.
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PMID:Caring for Machado-Joseph disease: current understanding and how to help patients. 1981 45

Sporadic Parkinson's disease (sPD) is a nervous system-wide disease that presents with a bradykinetic movement disorder and frequently progresses to include depression and cognitive impairment. Cybrid models of sPD are based on expression of sPD platelet mitochondrial DNA (mtDNA) in neural cells and demonstrate some similarities to sPD brains. In sPD and CTL cybrids we characterized aspects of mitochondrial biogenesis, mtDNA genomics, composition of the respirasome and the relationships among isolated mitochondrial and intact cell respiration. Cybrid mtDNA levels varied and correlated with expression of PGC-1 alpha, a transcriptional co-activator regulator of mitochondrial biogenesis. Levels of mtDNA heteroplasmic mutations were asymmetrically distributed across the mitochondrial genome; numbers of heteroplasmies were more evenly distributed. Neither levels nor numbers of heteroplasmies distinguished sPD from CTL. sPD cybrid mitochondrial ETC subunit protein levels were not altered. Isolated mitochondrial complex I respiration rates showed limited correlation with whole cell complex I respiration rates in both sPD and CTL cybrids. Intact cell respiration during the normoxic-anoxic transition yielded K(m) values for oxygen that directly related to respiration rates in CTL but not in sPD cell lines. Both sPD and CTL cybrid cells are substantially heterogeneous in mitochondrial genomic and physiologic properties. Our results suggest that mtDNA depletion may occur in sPD neurons and could reflect impairment of mitochondrial biogenesis. Cybrids remain a valuable model for some aspects of sPD but their heterogeneity mitigates against a simple designation of sPD phenotype in this cell model.
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PMID:Cybrid models of Parkinson's disease show variable mitochondrial biogenesis and genotype-respiration relationships. 1981 14


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