Journal of the International Neuropsychological Society

Controversy surrounds the differences of the cognitive profile between mild cognitive impairment resulting from cerebral small vessel disease (MCI-SVD) and mild cognitive impairment associated with prodromal Alzheimer’s disease (MCI-AD). The aim of this study was to explore and compare the cognitive features of MCI-SVD and MCI-AD. MCI-SVD patients (n = 56), MCI-AD patients (n = 30), and normal control subjects (n = 80) were comprehensively evaluated with neuropsychological tests covering five cognitive domains. The performance was compared between groups. Tests that discriminated between MCI-SVD and MCI-AD were identified. Multiple cognitive domains were impaired in MCI-SVD group, while memory and executive function were mainly impaired in MCI-AD group. Compared with MCI-SVD, MCI-AD patients performed relatively worse on memory tasks, but better on processing speed measures. The AVLT Long Delay Free Recall, Digit Symbol Test, and Stroop Test Part A (performance time) in combination categorized 91.1% of MCI-SVD patients and 86.7% of MCI-AD patients correctly. Current study suggested a nonspecific neuropsychological profile for MCI-SVD and a more specific cognitive pattern in MCI-AD. MCI-AD patients demonstrated greater memory impairment with relatively preserved mental processing speed compared with MCI-SVD patients. Tests tapping these two domains might be potentially useful for differentiating MCI-SVD and MCI-AD patients. (JINS, 2009, 15, 898–905.)

Objectives:The worldwide spread of Parkinson’s disease (PD) calls for sensitive and specific measures enabling its early (or, ideally, preclinical) detection. Here, we use language measures revealing deficits in PD to explore whether similar disturbances are present in asymptomatic individualsat riskfor the disease.Methods:We administered executive, semantic, verb-production, and syntactic tasks to sporadic PD patients, genetic PD patients with PARK2 (parkin) or LRRK2 (dardarin) mutation, asymptomatic first-degree relatives of the latter with similar mutations, and socio-demographically matched controls. Moreover, to detectsui generislanguage disturbances, we ran analysis of covariance tests using executive functions as covariate.Results:The two clinical groups showed impairments in all measures, most of which survived covariation with executive functions. However, the key finding concerned asymptomatic mutation carriers. While these subjects showed intact executive, semantic, and action-verb production skills, they evinced deficits in a syntactic test with minimal working memory load.Conclusions:We propose that thissui generisdisturbance may constitute a prodromal sign anticipating eventual development of PD. Moreover, our results suggest that mutations on specific genes (PARK2 and LRRK2) compromising basal ganglia functioning may be subtly related to language-processing mechanisms. (JINS, 2017,23, 150–158)

Objectives: Patients with Parkinson’s disease often experience significant decline in verbal fluency over time; however, deep brain stimulation of the subthalamic nucleus (STN-DBS) is also associated with post-surgical declines in verbal fluency. The purpose of this study was to determine if Parkinson’s patients who have undergone bilateral STN-DBS have greater impairment in verbal fluency compared to Parkinson’s patients treated by medication only. Methods: A literature search yielded over 140 articles and 10 articles met inclusion criteria. A total of 439 patients with Parkinson’s disease who underwent bilateral STN-DBS and 392 non-surgical patients were included. Cohen’s d, a measure of effect size, was calculated using a random effects model to compare post-treatment verbal fluency in patients with Parkinson’s disease who underwent STN-DBS versus those in the non-surgical comparison group. Results: The random effects model demonstrated a medium effect size for letter fluency (d=−0.47) and a small effect size for category fluency (d=−0.31), indicating individuals with bilateral STN-DBS had significantly worse verbal fluency performance than the non-surgical comparison group. Conclusions: Individuals with Parkinson’s disease who have undergone bilateral STN-DBS experience greater deficits in letter and category verbal fluency compared to a non-surgical group. (JINS, 2016, 22, 478–485)

Behavioral neurologists and neuropsychologists have debated the role of the thalamus and basal ganglia in cognition and behavior for more than a century (e.g., Bucy, 1942; Marie, 1906; Penfield & Roberts, 1959; Wernicke, 1874). However, over these 100-plus years, there is little consensus regarding whether or how these structures contribute to cognition. Fortunately, recent research findings are rapidly changing this state of affairs. It is now obvious we will not understand how the brain controls complex activities until we understand the contribution of these deep brain structures. In healthy and brain-damaged individuals, application of methodologies such as semantic priming, event related potentials, and functional neuroimaging to the question of subcortical functions is beginning to resolve this conundrum. This symposium demonstrates the utility of combining these different approaches. It features empirical work from six laboratories that have engaged in systematic inquiries regarding the role of the thalamus and basal ganglia in cognition. This body of work represents both new directions and convergence of recent findings in the quest to integrate our understanding of this complex issue.

A meta-analysis was conducted on 25 longitudinal studies involving 901 initially non-demented Parkinson's disease (PD) patients to examine the magnitude of decline across multiple cognitive domains associated with disease progression. Pooled effect sizes reflecting the standardized difference between baseline and follow-up neuropsychological performance were calculated for 8 cognitive domains using a random-effects model. Relatively small effect sizes were found across all cognitive domains (d= .00 − .40). During a mean follow-up interval of 29 months, significant declines were detected in global cognitive ability (d= .40), visuoconstructive skills (d= .32), and memory (d= .29). Age showed a significant relation with decline in global cognitive ability and memory. Lower educational level was associated with greater decline in all cognitive domains. Studies with longer follow-up intervals yielded larger effect sizes for global cognitive ability. In non-demented PD patients, changes in cognitive functions over time appear to be modest. Educational level, age, and length of the follow-up interval are likely to affect the magnitude of decline in several domains. Methodological flaws, such as selection bias and uncontrolled practice effects, may have caused underestimation of the true extent of decline (JINS, 2007,13, 920–932.)

A meta-analysis of 68 studies with a total of 4644 participants was conducted to investigate the sensitivity of tests of verbal fluency to the presence of Parkinson's disease (PD) relative to healthy controls. Both phonemic and semantic fluency were moderately impaired but neither deficit qualified as a differential deficit relative to verbal intelligence or psychomotor speed. However, PD patients were significantly more impaired on semantic relative to phonemic fluency (rs = .37vs..33, respectively), and confrontation naming, a test of semantic memory that imposes only minimal demands upon cognitive speed and effortful retrieval, was associated with a deficit that was of a comparable magnitude to the deficits upon each of these types of fluency. Thus, the disorder appears to be associated with particular problems with semantic memory. Tests that impose heavy demands upon switching may also be disproportionately affected. Demented and non-demented PD patients differ quantitatively but not qualitatively in terms of the relative prominence of deficits on tests of phonemic and semantic fluency. However, patients with dementia of the Alzheimer's type and demented PD patients can be differentiated from one another by the relative magnitude of deficits upon these two measures. (JINS, 2004,10, 608–622.)

Executive function impairments in Parkinson’s disease (PD) are well documented. However, uncertainties remain regarding the impact of these deficits on other areas of cognitive functioning. The goal of this study was to provide a comprehensive assessment of cognitive characteristics in patients with PD without dementia and to assess how any such deficits affected other areas of cognitive functioning. Forty PD patients without dementia were compared to healthy controls using measures of attention and speed of processing and a comprehensive set of executive function tests including working memory, planning, and problem solving. Measures of memory/learning and visuospatial skills were also included to examine the relationship between aspects of executive function and other areas of cognition. Patients with PD showed deficits on measures of executive function, problem solving, and visuospatial skills. However, they were unimpaired on measures of planning, attention, and memory/learning. Deficits in problem solving were only evident for tasks with a high visuospatial content and were no longer significant when visuospatial skills were controlled for. While deficits in executive function and visuospatial skills were apparent for PD patients compared to controls, many aspects of cognition remained intact. These can provide a focus for cognitive intervention strategies that can be effective in delaying decline for PD patients. (JINS, 2010, 16, 268–277.)

The goal of this study was to further characterize episodic memory functioning in schizophrenia. This study compared verbal and visual learning and memory performance in (1) patients with schizophrenia (N = 35), (2) patients with temporal lobe epilepsy (TLE; N = 30), and (3) normal controls (N = 25). Results indicated significant memory impairments in patients with schizophrenia and TLE. “Savings” score measures of memory decay showed that the loss of information in schizophrenia and TLE was approximately equal, and quantitatively mild compared to that found in most neurologic groups with memory disorders. The severe difficulty shown by the schizophrenia group on a task of incidental recall suggested that the absence of instructional set added to a vulnerability to memory deficit. In contrast, relatively mildly impaired performance on paired associate learning suggested that patients with schizophrenia benefited from retrieval cues, multiple trials, and short (nonsupraspan) informational loads. Because patients with schizophrenia consisted of a relatively nonchronic sample with a mean IQ of 99.7, their memory disorder could not be attributed to schizophrenic dementia, nor was it accounted for by other potential confounds. Patients with schizophrenia, even those relatively early in the course of illness, have a mild episodic memory disorder. (JINS, 1998, 4, 342–352.)