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

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 consistent with a major cause of the patients' recall/recollection impairments being hippocampal disruption, probably exacerbated by subclinical depressive symptoms. However, the results do not exclude a lesser prefrontal cortex contribution because patient executive functions were impaired and correlated solely with unguided overall recollection.

Recollection deficiencies in patients with major depressive disorder.

Neuropsychological research suggests that recognition memory (RM) and recall memory are impaired in patients with a major depressive disorder or a dysphoric mood state. This study examines the proposal that abnormalities in recollection (a form of recall) result from a breakdown in frontal strategic memory processes involved in encoding and retrieval, and executive functions linked to reality monitoring, planning, problem-solving, reasoning and decision-making. We investigated two predictions arising from this theory. Firstly, patients diagnosed with a major depressive disorder (MDD) will display a dissociation between (deficient) recollection and (preserved) familiarity. Secondly, if recollection impairments are indicative of a breakdown in prefrontal strategic memory processes which are dependent, at least in part, on executive processes, then an explicit correlational approach predicts that recollection will be positively associated with the severity of executive dysfunction in MDD patients. The remember/know paradigm was used to investigate RM for words and neutral faces in 16 MDD patients and 16 healthy volunteers, matched for age, gender and estimates of premorbid IQ. Measures of executive function included working memory, reasoning and decision-making. Applying the Dual Process Signal Detection interpretation of the remember/know data, the MDD group displayed significant impairments in RM and recollection rates for both verbal and neutral facial memoranda. In contrast, familiarity-aware rates were preserved. There was no evidence of executive dysfunction in the patient group, and little evidence that recollection rates correlated with executive function. Furthermore, a single process signal detection approach suggested that the MDD patients displayed a reduction in sensitivity for RM and remember rates but not know responses. The criteria for detecting studied from unstudied items, and remembering from knowing, were the same in both patient and healthy control groups. Taken together, these findings are consistent with the view that MDD is marked by a decline in RM, which is underpinned by an impairment in recollection rather than familiarity processes. The extent to which the recollection deficiencies arise from disruption of strategic memory and executive processes requires further investigation.

Reality monitoring in anosognosia for hemiplegia.

Anosognosia for hemiplegia (AHP) is a lack of awareness about paralysis following stroke. Recent explanations use a 'forward model' of movement to suggest that AHP patients fail to register discrepancies between internally- and externally-generated sensory information. We predicted that this failure would impair the ability to recall from memory whether information is internally- or externally-generated (i.e., reality monitor). Two experiments examined this prediction. Experiment 1 demonstrated that AHP patients exhibit a reality monitoring deficit for non-motor information (i.e., perceived vs. imagined drawings), whilst hemiplegic controls without anosognosia (nonAHP) perform like age-matched healthy volunteers (HVs). Experiment 2 explored if this deficit occurs when AHP patients discriminate performed, imagined, or observed movement. Results showed impaired reality monitoring for movements in AHP and nonAHP patients relative to HVs. Findings suggest that reality monitoring processes not directly related to movement, together with a failure to reality monitor movements, contribute to the pathogenesis of AHP.

Auditory recognition memory, conscious recollection, and executive function in patients with schizophrenia.

BACKGROUND: Dual-process models propose that recognition memory (RM) involves two processes: conscious recollection and familiarity-aware memory. Studies investigating RM in schizophrenia report a selective deficit in conscious recollection and intact levels of familiarity-driven RM for stimuli presented in the visual and olfactory domains. It has been suggested that abnormalities in conscious recollection result from a breakdown in frontal strategic memory processes involved in encoding and retrieval and executive functions linked to reality monitoring and decision making. We investigated three predictions arising from these proposals. Firstly, if conscious recollection abnormalities arise from a central impairment, then these abnormalities should not be domain specific. Secondly, if the deficits in conscious recollection arise from a breakdown in executive processes, deficiencies should be correlated with executive dysfunction. Finally, the conscious recollection deficiencies are likely to be more severe in schizophrenia, a condition associated with marked executive dysfunction relative to Major Depressive Disorder, Recurrent (MDDR), in which executive dysfunction is less marked. METHODS: The remember/know paradigm was used to investigate RM for voices in three groups: patients with schizophrenia (n = 14), patients with MDDR (n = 16), and normal controls (n = 16). Executive function was assessed using the Wisconsin Card Sorting Task. RESULTS: Patients with schizophrenia made significantly fewer remember responses than normal controls (p < 0.01), despite normal levels of discrimination and familiarity-driven auditory RM. Patients with MDDR did not differ significantly from either normal controls or patients with schizophrenia. Executive dysfunction was limited to the schizophrenia group and was not correlated with conscious recollection deficiencies. CONCLUSIONS: Patients with schizophrenia exhibit a deficit in conscious recollection for auditory RM of voices. These findings, when considered alongside remember/know data collected from the same set of patients for olfactory and visual RM, support proposals that abnormalities in conscious recollection stem from a breakdown in central rather than domain-specific processes.