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Depression and executive functions in PD

There is controversy about the relationship between depression and cognitive dysfunction in PD patients (Table 6.1). Three possible patterns emerge: (1) depression influences cognition in PD—in this case depression would mainly influence the severity (quantity) of cognitive impairment [12-23]; (2) depression and cognitive impairment are independently induced, though many symptoms of the two conditions might overlap in PD [24-28]; (3) cognitive dysfunctions that are related to PD neuropathology are the substrate of a depressive disorder in PD—in this case a distinct pattern of cognitive impairment (quality) would be associated with depression.

Evidence that depression affects cognition derives from both epidemiological studies that indicate depression to be a risk factor for dementia [29] and from the observation that severely depressed PD (dPD) patients are more cognitively impaired than patients with mild depression. In particular, Starkstein et al. [14] found that PD patients with major depression (MD) reported a significantly worse performance in tasks assessing frontal lobe functions such as verbal fluency, set-shifting, and attention compared with PD patients without MD. No significant difference in cognitive profile between PD patients with minor depression and non-depressed PD patients was found. Consistently, Troster et al. [23] found that depression exacerbates memory and language impairment in PD. However, differences in cognitive performance between dPD and non-dPD patients disappeared when patients were matched for total Mattis Dementia Rating Scale (MDRS) score, suggesting that depression influences the severity rather than the profile of cognitive impairment in PD. One limitation of the two studies mentioned above was the absence of a comparison group including patients with MD but without PD.

Kuzis et al. [15] compared the cognitive profile of dPD and non-dPD patients and depressed patients without PD and found that all depressed patients (with and without PD) reported poorer performance on tasks assessing verbal fluency and auditory attention than non-depressed PD

Table 6.1 Cognitive functions as assessed in Parkinson's disease (PD) patients with and without depression

Study and cognitive task

PD patients with depression

PD patients without depression

Depressed patients without PD

Starkstein et al. (1989) [13]

Wisconsin Card Sorting Test

+

-

Controlled word association

+

-

Digit Span:

Forwards

-

-

Backwards

-

-

Trail Making Test

+

-

Design Fluency Test

+

-

Symbol Digit Modalities

+

-

MMSE

+

-

Troster et al. (1995) [23]

MDRS

+

-

Wisconsin Card Sorting Test

-

-

Boston Naming Test

+

-

Controlled word association

+

-

Animal naming test

+

-

WAIS-R

Digit Span

-

Logical Memory I

+

-

Logical Memory II

-

-

When groups matched for mean MDRS:

Wisconsin Card Sorting Test

-

-

Boston Naming Test

-

-

Controlled word association

-

-

Animal naming test

-

-

WAIS-R:

Digit Span

-

-

Logical Memory I

-

-

Logical Memory II

-

-

Kuzis et al. (1997) [15]

Raven Progressive Matrices

+

-

-

Wisconsin Card Sorting Test

-

-

Study and cognitive task

PD patients with depression

PD patients without depression

Depressed patients without PD

Categories

+

-

-

Perseverations

+

-

+

verbal fluency:

Buschke Total Recall Test

+

-

-

Buschke Delayed Recall Test

-

-

-

Benton visual Retention Test

-

-

-

Digit Span:

Forwards

-

-

-

Backwards

+

-

+

Costa et al. (2006) [21]

Digit Span:

Forwards

-

-

Backwards

-

-

Corsi Test:

Forwards

-

-

Backwards

-

-

Immediate visual memory

+

-

Word list recall:

Immediate recall

-

-

Delayed recall

+

-

Word list recognition: correct items

+

-

Prose recall

Immediate recall

-

-

Delayed recall

-

-

Rey's figure:

Immediate reproduction

-

-

Delayed reproduction

-

-

Freehand copying of drawings

-

-

Copying drawings with landmarks

-

-

Copying Rey's figure

-

-

Sentence construction

+

-

Table 6.1 (continued) Cognitive functions as assessed in Parkinson's disease (PD) patients with and

without depression

Study and cognitive task

PD patients with depression

PD patients without depression

Depressed patients without PD

Raven's Progressive Matrices 47

+

-

Modified Card Sorting Test

Categories achieved

+

-

Perseverative errors

+

-

Non-perseverative errors

-

-

Lexical verbal fluency

+

-

Uekermann et al. (2003) [19]

Digit Span:

Forwards

-

-

-

Backwards

+

-

-

Benton visual Retention Test

-

-

-

Word list recall:

-

Immediate

-

-

-

Delayed

-

-

-

Semantic verbal fluency

-

-

-

Lexical verbal fluency

+

-

-

Hayling Test

-

-

Stefanova et al. (2006) [20]

WAIS-R:

verbal IQ

-

-

Performance of IQ

+

-

Rey Auditory verbal Learning Test:

Recall

-

-

Delayed recall

-

-

Letter (lexical) fluency

+

-

Category (semantic) fluency

+

-

Boston Naming Task

+

-

Hooper Test

-

-

Trail Making Test:

Form A

-

-

Form B

-

-

Study and cognitive task

PD patients with depression

PD patients without depression

Depressed patients without PD

Silberman et al. (2006) [28]

Stroop Test

-

-

Emotional Stroop Test

-

-

MMSE, Mini-Mental State Examination; MDRS, Mattis Dementia Rating Scale; WAIS-R, Wechsler Adult Intelligence Scale-Revised.

+, altered performance on cognitive tasks; -, normal performance on cognitive tasks.

patients. Moreover, dPD patients showed a significantly worse performance on frontal tasks evaluating concept formation and set-shifting compared with non-depressed PD patients, patients with depression alone, and normal subjects of a control group. This finding suggests that alteration of frontal lobe functions, such as concept formation and set-shifting, may result from an interaction between PD neuropathology and the mechanism of MD. Consistently, Costa et al. [21] found that PD patients with MD performed worse than non-depressed PD patients on long-term verbal episodic memory tasks, abstract reasoning tasks, and tasks assessing executive functioning. They concluded that MD in PD is specifically associated with a qualitatively distinct neuropsychological profile that may be related to the alteration of prefrontal and limbic cortical areas.

Since the duration of PD might be an important factor for both neuropathological and cognitive changes, Uekermann et al. [19] explored cognitive functions in early PD, finding poorer performance on short-term memory and lexical fluency tasks in dPD patients compared with non-dPD patients, depressed patients without PD, and control subjects. Similarly in early PD patients, Stefanova et al. [20] found that MD in PD patients was associated with cognitive impairment of specific domains (visuospatial memory, spatial working memory, language) and more profound executive and visuospatial deficits, whereas dysthymic disorder was associated only with a quantitative increase in executive dysfunctions observed in non-dPD. They concluded that cognitive impairment in early PD may be predicted by the severity of depression. Since depression is reported to be associated with right-side disease onset and disease duration, Foster et al. [30] explored whether mood disturbances are associated with side of onset and disease duration in patients with PD and affect cognitive functioning. They found that parkinsonian patients with right hemibody onset of motor symptoms experienced more depression as the PD progressed and that they showed more severe alterations of cognitive functioning than PD patients with left hemibody onset.

Evidence that depression and cognitive dysfunctions are independent derives from a variety of studies mainly focusing on general screening tools for dementia, such as the Mini-Mental State Examination [24-27]. In one study, executive dysfunction, as explored by the Stroop and Emotional Stroop Tests, was related neither to depression nor to the severity of PD [28].

The relationship between depression and executive dysfunction is generally thought to be one of depression affecting the severity of cognitive impairment. Conversely, executive dysfunction, which is related to neuropathology of PD, might be responsible for depressive symptoms, especially considering that the DSM-IV criteria for diagnosis of MD do not separate anhedonia from apathy (DSM-IVA, Criterion 2). Santangelo et al. [31] subtyped PD patients with MD according to the occurrence of apathy/anhedonia (DSM-IVA, Criterion 2). They found that dPD patients with high levels of apathy and/or anhedonia scored significantly worse on frontal tasks than patients with depressed mood (DSM-IVA, Criterion 1) and non-depressed patients. These findings suggest that the combination of apathy, anhedonia, and frontal lobe dysfunction might contribute to the overdiagnosis of depression in PD. More recently, Varanese et al. [32] found that depression, unlike apathy, was not associated with executive impairment in PD patients. These findings indirectly support the idea that apathy and depression are two independent non-motor symptoms of PD.

Subthreshold depression (SD) is characterized by depressive symptoms not meeting the criteria for MD. SD is not associated with objective cognitive deficits (assessed by means of screening tools for dementia) [33-36] but is related to subjective cognitive complaints [36]. Therefore, it should be investigated accurately because it might reduce quality of life and might be a predictor of development of MD in PD, as demonstrated in the general population [37].

 
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