Recognition Memory in Parkinson’s Disease With and Without Dementia: Evidence Inconsistent with the Retrieval Deficit Hypothesis

Higginson, Christopher I.; Wheelock, Vicki; Carroll, Kimberly E; Sigvardt, Karen A.

doi:10.1080/13803390490515469

Cited by 87 publications

(83 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The present study corroborates those findings. We used the NOR task, which involves recognition memory and executive functions, both functions that can be impaired in PD [19,20]. Our results corroborated the previous study showing that animals treated with reserpine failed to discriminate the objects in the test session (in the second and third tests, Figure 3).…”

Section: Discussionsupporting

confidence: 80%

Alpha-Tocopherol Counteracts Cognitive and Motor Deficits Induced by Repeated Treatment with Reserpine

Sarmento-Silva¹,

Lima²,

Cabral³

et al. 2015

Biochem Pharmacol (Los Angel)

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 80%

Alpha-Tocopherol Counteracts Cognitive and Motor Deficits Induced by Repeated Treatment with Reserpine

Sarmento-Silva¹,

Lima²,

Cabral³

et al. 2015

Biochem Pharmacol (Los Angel)

View full text Add to dashboard Cite

“…This hypothesis (Higginson, Wheelock, Carroll, & Sigvardt, 2005) establishes that subcortical dementias (PD and Huntington's disease; Cummings & Benson, 1984) are characterized by retrieval rather than encoding deficits. On the other hand, in accordance with the abovementioned literature, we expected to observe deficits in familiarity in the groups of patients affected by dementia.…”

mentioning

confidence: 88%

Recognition by familiarity is preserved in Parkinson's without dementia and Lewy-Body disease.

et al. 2010

View full text Add to dashboard Cite

Objective:The retrieval deficit hypothesis states that the lack of deficit in recognition often observed in patients with Parkinson's disease is because of the low retrieval requirements of the task, given that these patients have retrieval and not encoding deficits. To test this hypothesis we investigated recognition memory by familiarity in Parkinson's patients and in patients with Lewy Bodies disease and Parkinson with dementia. Method: We analyzed to what extent the experimental groups were able to recognize by familiarity in a typical yes/no recognition memory task. The experimental groups were patients with early nondemented Parkinson's disease, advanced nondemented Parkinson's disease, demented Parkinson's patients, and patients with dementia with Lewy Bodies. We compared their performance with a group of young and another group of old healthy participants. The estimation of familiarity was made by analyzing recognition of word targets and distractors consisting of combinations of different letters in comparison with a condition in which targets and distractors were composed of similar letters, even though subjects were unaware of the independent variable. Results: The results indicate that familiarity was used at the same level by controls, patients with early Parkinson's disease and patients with dementia with Lewy Bodies. Although late Parkinson patients also used familiarity, its effect was only marginally significant. Patients with Parkinson's disease and dementia were not capable of using familiarity in recognition memory. Conclusions: Our results support the retrieval deficit hypothesis as Parkinson's patients without dementia show no deficit in a situation in which the retrieval requirements are minimal.

show abstract

“…However, PD is not 'just' a motor disorder. Patients are often impaired at recalling recently experienced information, such as facts and personal events, but have usually been found to be less impaired at recognition of recently encountered stimuli (e.g., Beatty, Staton, Weir, Monson, & Whitaker, 1989;Breen, 1993;Edelstyn, Mayes, Condon, Tunnicliffe, & Ellis, 2007;Edelstyn, Shepherd, Mayes, Sherman, & Ellis, 2010;Flowers, Pearce, & Pearce, 1984;Higginson, Wheelock, Carroll, & Sigvardt, 2005;Shepherd, Edelstyn, Mayes, & Ellis, 2013;Taylor, Saint-Cyr, & Lang, 1986) …”

Section: Q2mentioning

confidence: 99%

Evidence of an amnesia-like cued-recall memory impairment in nondementing idiopathic Parkinson's disease

Edelstyn

John

Shepherd

et al. 2015

Cortex

View full text Add to dashboard Cite

Familiarity Medial temporal lobe Prefrontal cortexParkinson's disease a b s t r a c t Medicated, non-dementing mild-to-moderate Parkinson's disease (PD) patients usually show recall/recollection impairments but have only occasionally shown familiarity impairments. We aimed to assess two explanations of this pattern of impairment.Recollection typically improves when effortful planning of encoding and retrieval processing is engaged. This depends on prefrontally-dependent executive processes, which are often disrupted in PD. Relative to an unguided encoding and retrieval of words condition (C1), giving suitable guidance at encoding alone (C2) or at encoding and retrieval (C3) should, if executive processes are disrupted, improve PD recollection more than control recollection and perhaps raise it to normal levels. Familiarity, being a relatively automatic kind of memory, whether impaired or intact, should be unaffected by guidance. According to the second explanation, PD deficits are amnesia-like and caused by medial temporal lobe dysfunction and although poorer recollection, which is caused by hippocampal disruption, may be improved by guidance, it should not improve more than control recollection. Familiarity impairment will also occur if the perirhinal cortex is disrupted, but will be unimproved by guidance. Without guidance, recollection/ recall was impaired in thirty PD patients relative to twenty-two healthy controls and remained relatively equally impaired when full guidance was provided (C1 vs C3), both groups improving to broadly the same extent. Although impaired, and markedly less so than recollection, familiarity was not improved by guidance in both groups.The patients showed elevated rates of subclinical depressive symptoms, which weakly correlated with recall/recollection in all three conditions. PD executive function was also deficient and correlated with unguided/C1 recollection only. Our results are * Corresponding author. School of Psychology, Keele University, Keele, Staffordshire ST5 5BG, UK.E-mail address: n.edelstyn@keele.ac.uk (N.M.J. Edelstyn).Available online at www.sciencedirect.com ScienceDirectJournal homepage: www.elsevier.com/locate/cortex 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 114 115 116 117 118 119 120 121 122 123 124 125 126 127 128

show abstract

Recognition Memory in Parkinson’s Disease With and Without Dementia: Evidence Inconsistent with the Retrieval Deficit Hypothesis

Cited by 87 publications

References 42 publications

Alpha-Tocopherol Counteracts Cognitive and Motor Deficits Induced by Repeated Treatment with Reserpine

Alpha-Tocopherol Counteracts Cognitive and Motor Deficits Induced by Repeated Treatment with Reserpine

Recognition by familiarity is preserved in Parkinson's without dementia and Lewy-Body disease.

Evidence of an amnesia-like cued-recall memory impairment in nondementing idiopathic Parkinson's disease

Contact Info

Product

Resources

About