Compensatory neural mechanisms in cognitively unimpaired Parkinson disease.

OBJECTIVE: Cognitive impairments in Parkinson disease (PD) are thought to be caused in part by dopamine dysregulation. However, even when nigrostriatal dopamine neuron loss is severe enough to cause motor symptoms, many patients remain cognitively unimpaired. It is unclear what brain mechanisms allow these patients to remain cognitively unimpaired despite substantial dopamine dysregulation. METHODS: Thirty-one cognitively unimpaired PD participants off dopaminergic medications were scanned using functional magnetic resonance imaging while they performed a working memory task, along with 23 controls. We first compared the PD off medication (PD_OFF) group with controls to determine whether PD participants engage compensatory frontostriatal mechanisms during working memory. We then studied the same PD participants on dopaminergic medications to determine whether these compensatory brain changes are altered with dopamine. RESULTS: Controls and PD showed working memory load-dependent activation in the bilateral putamen, anterior-dorsal insula, supplementary motor area, and anterior cingulate cortex. Compared to controls, PD_OFF showed compensatory hyperactivation of bilateral putamen and posterior insula, and machine learning algorithms identified robust differences in putamen activation patterns. Compared to PD_OFF, the PD on medication group showed reduced compensatory activation in the putamen. Loss of compensatory hyperactivation on dopaminergic medication correlated with slower performance on the working memory task and slower cognitive speed on the Symbol Digit Modality Test. INTERPRETATION: Our results provide novel evidence that PD patients maintain normal cognitive performance through compensatory hyperactivation of the putamen. Dopaminergic medication downregulates this hyperactivation, and the degree of downregulation predicts behavior. Identifying cognitive compensatory mechanisms in PD is important for understanding how some patients maintain intact cognitive performance despite nigrostriatal dopamine loss.

Boston Naming Test: Lose the Noose.

OBJECTIVE: Administering the noose item of the Boston Naming Test (BNT) has been questioned given the cultural, historical, and emotional salience of the noose in American culture. In response, some have modified the BNT by skipping/removing this item and giving the point as if the examinee responded correctly. It is unknown, however, whether modifying standardized administration and scoring in this manner affects clinical interpretation. In the present study, we examined the prevalence of noose item failure, whether demographic and clinical characteristics differed between those who responded correctly versus failed the item, and whether giving a point to those who failed affected clinical interpretation. METHOD: Participants included a mixed clinical sample of 762 adults, ages 18-88 years, seen for neuropsychological evaluation at one of five sites within the USA. RESULTS: Those who failed the item (13.78%) were more likely to be female, non-White, and have primary diagnoses of major neurocognitive disorder, epilepsy, or neurodevelopmental disorder. Noose item failure was associated with lower BNT total score, fewer years of education and lower intellectual functioning, expressive vocabulary, and single word reading. Giving a point to those who failed the item resulted in descriptor category change for 17.1%, primarily for patients with poor overall BNT performance. CONCLUSIONS: Only a small percentage of patients fail the noose item, but adding a point for these has an impact on score interpretation. Factors associated with poorer overall performance on the BNT, rather than specific difficulty with the noose item, likely account for the findings.

Recovery of episodic memory subprocesses in mild and complicated mild traumatic brain injury at 1 and 12 months post injury.

INTRODUCTION: Episodic memory complaints are commonly reported after traumatic brain injury (TBI). The contributions of specific memory subprocesses (encoding, consolidation, and retrieval), however, are not well understood in mild TBI (mTBI). In the present study, we evaluated subprocesses of episodic memory in patients with mTBI using the item-specific deficit approach (ISDA), which analyzes responses on list learning tasks at an item level. We also conducted exploratory analyses to evaluate the effects of complicated mTBI (comp-mTBI) on memory. METHOD: We compared episodic verbal memory performance in mTBI (n = 92) at approximately 1 and 12 months post TBI, as well as in a healthy comparison (HC) group (n = 40) at equivalent time points. Episodic memory was assessed using the California Verbal Learning Test-2nd Edition (CVLT-II), and both standard CVLT-II scores and ISDA indices were evaluated. RESULTS: Compared to the HC group, the mTBI group showed significantly poorer encoding and learning across time, as measured by ISDA and CVLT-II. Further analyses of these mTBI subgroups [(noncomplicated mTBI (NC-mTBI, n = 77) and comp-mTBI (n = 15)], indicated that it was the comp-mTBI group who continued to demonstrate poorer encoding ability than the HC group. When the patient groups were directly compared, the NC-mTBI group improved slightly on the ISDA Encoding Deficit Index. While the comp-mTBI group worsened slightly over time, their poorer encoding ability was not likely clinically meaningful. CONCLUSIONS: These findings indicate that, while the NC-mTBI and HC groups' performances were comparable by 12 months, a primary, long-term deficit in encoding of auditory verbal information remained problematic in the comp-mTBI group.