The Occurrence of Depression in Parkinson's Disease

Tandberg, Elise

doi:10.1001/archneur.1996.00550020087019

Cited by 394 publications

(297 citation statements)

References 24 publications

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“…In our study, in agreement with other works, depression in PD is more frequent than in the general population, 4,5,47,48 supporting the idea that depression is a genuine part of the PD syndrome. 49 In our study, the severity of depression in PD was similar to other reports.…”

Section: Discussionsupporting

confidence: 93%

“…49 In our study, the severity of depression in PD was similar to other reports. 5,50 In patients with PD, there are no, however, differences of prevalence of depression related to gender. 51 In our patients with PD, depression was more frequent in those subjects with a predominant akinetic-rigid syndrome than in those with a predominant tremor or with mixed phenotype.…”

Section: Discussionmentioning

confidence: 99%

“…3 The rate of depression in PD varies widely in different studies, with a mean prevalence of 40% and with limits from 4 to 70%. [4][5][6] The clinical manifestations of depression are usually of low to moderate severity. 6,7 Its pathogenesis is unclear.…”

Section: Introductionmentioning

confidence: 99%

“…4,8 Others suggest that mood alterations are just a direct consequence of the neurodegeneration of certain brain nuclei in patients with PD, 6,9 regardless of the severity of the motor disability. It appears that there is a relationship between severity and duration of motor symptoms in PD and depression, [10][11][12] but depression is more frequent in PD than in other chronic neurological diseases, 5 suggesting that this symptom belongs, at least in part, to the core of PD, and is not only reactive to a reduced quality of life.…”

Section: Introductionmentioning

confidence: 99%

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Depression in Parkinson's disease is related to a genetic polymorphism of the cannabinoid receptor gene (CNR1)

et al. 2005

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Depression is a common symptom in Parkinson's disease (PD) and it is present in up to 40% of the patients. The cause of depression in PD is thought to be related to disturbance of monoamine neurotransmission. The endogenous cannabinoid system mediates different brain processes that play a role in the control of behaviour and emotions. Cannabinoid function may be altered in neuropsychiatry diseases, directly or through interactions with monoamine, GABA and glutamate systems. For this reason, we have investigated whether there is a genetic risk factor for depression in PD linked to the polymorphisms of CB1 receptor gene. Depression was more frequent in patients with PD than in controls with osteoarthritis. The presence of depression did not correlate with the stage of the disease but it was more frequent in patients with pure akinetic syndrome than in those with tremoric or mixed type PD. The CB1 receptor gene polymorphism (AAT)n is considered to modify the transcription of the gene and, therefore, it may have functional relevance. We analysed the length of the polymorphic triplet (AAT)n of the gene that encodes CB1 (CNR1) receptor in 89 subjects (48 PD patients and 41 controls). In patients with PD, the presence of two long alleles, with more than 16 repeated AAT trinucleotides in the CNR1 gene, was associated with a reduced prevalence of depression (Fisher's exact test: P ¼ 0.003). This association did not reach significant differences in the control group, but the number of control individuals with depression was too small to allow for statistical analysis. Since the alleles with long expansions may have functional impact in cannabinoid neurotransmission, our data suggest that the pharmacological manipulation of cannabinoid neurotransmission could open a new therapeutic approach for the treatment of depression in PD and possibly in other conditions.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Depression in Parkinson's disease is related to a genetic polymorphism of the cannabinoid receptor gene (CNR1)

et al. 2005

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“…20 -22 Furthermore, the majority of patients with PD have depressive symptoms not fulfilling the criteria for major depressive episode. 23 …”

Section: Differences Between Depression Without Pd and Dpdmentioning

confidence: 99%

Depression rating scales in Parkinson's disease: Critique and recommendations

Schrag¹,

Barone²,

Brown³

et al. 2007

Movement Disorders

594

348

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Depression is a common comorbid condition in Parkinson's disease (PD) and a major contributor to poor quality of life and disability. However, depression can be difficult to assess in patients with PD due to overlapping symptoms and difficulties in the assessment of depression in cognitively impaired patients. As several rating scales have been used to assess depression in PD (dPD), the Movement Disorder Society commissioned a task force to assess their clinimetric properties and make clinical recommendations regarding their use. A systematic literature review was conducted to explore the use of depression scales in PD and determine which scales should be selected for this review. The scales reviewed were the Beck Depression Inventory (BDI), Hamilton Depression Scale (Ham-D), Hospital Anxiety and Depression Scale (HADS), Zung Self-Rating Depression Scale (SDS), Geriatric Depression Scale (GDS), Montgomery-Asberg Depression Rating Scale (MADRS), Unified Parkinson's Disease Rating Scale (UPDRS) Part I, Cornell Scale for the Assessment of Depression in Dementia (CSDD), and the Center for Epidemiologic Studies Depression Scale (CES-D). Seven clinical researchers with clinical and research experience in the assessment of dPD were assigned to review the scales using a structured format. The most appropriate scale is dependent on the clinical or research goal. However, observer-rated scales are preferred if the study or clinical situation permits. For screening purposes, the HAM-D, BDI, HADS, MADRS, and GDS are valid in dPD. The CES-D and CSDD are alternative instruments that need validation in dPD. For measurement of severity of depressive symptoms, the Ham-D, MADRS, BDI, and SDS scales are recommended. Further studies are needed to validate the CSDD, which could be particularly useful for the assessment of severity of dPD in patients with comorbid dementia. To account for overlapping motor and nonmotor symptoms of depression, adjusted instrument cutoff scores may be needed for dPD, and scales to assess severity of motor symptoms (e.g., UPDRS) should also be included to help adjust for confounding factors. The HADS and the GDS include limited motor symptom assessment and may, therefore, be most useful in rating depression severity across a range of PD severity; however, these scales appear insensitive in severe depression. The complex and time-consuming task of developing a new scale to measure depression specifically for patients with PD is currently not warranted.

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