Annals of Clinical and Translational Neurology最新文献

Article AID: ACN352114

Table 1

On Page 4, age at first evaluation for HSCT asymptomatic group should have a maximum of 40.7 not 40.1.

For initial psychosine levels, please update natural history median to 22.3 and range to 0.99–82.3, symptomatic HSCT median to 28.1 and range to 4.09–54.0, and asymptomatic HSCT range to 1.03–29.1.

For initial GALC levels, please update symptomatic HSCT median to 0.01 and asymptomatic HSCT range to 0.02–0.23.

Table 2

On Page 5, please update heading to say, “Summary of the growth percentiles in Natural History, Symptomatic HSCT, and Asymptomatic HSCT patients, indicating percentages below the third percentile for head circumference and below the fifth percentile for height, weight, and body mass index.”

Sitting

On Page 8, please update the last sentence from “52%” to “53%,” and replace “Table S6” with “Table S7” in the last sentence.

Neurodevelopmental Function

On Pages 10–11, the last sentence in the first paragraph of Page 11 (“The Asympt HSCT group showed higher scores and greater gains over time than both the NH and Sympt HSCT groups for all domains (all p < 0.001) (Table S9).”) needs to be moved to Page 10 just after “(Figs. S2 and S3, Table S8).” and before “The group performed slightly better….”

Supporting Information

Table S4

Table S4 is incorrectly listed as Table S5.

Tables S7, S8, and S9

Table S7 is incorrectly listed as Table S9. Table S8 is incorrectly listed as Table S7. Table S9 is incorrectly listed as Table S8.

Additionally, the tables and figures under Supporting Information do not have numbers or legends when downloaded. To address all issues, we have prepared new, reformatted PDFs with correct figure numbers and legends to be included in Supporting Information. Please just replace those files with the new ones provided. Thank you!

We apologize for these errors.

Episodic memory is a critical cognitive function that enables the encoding, storage, and retrieval of new information. Memory consolidation, a key stage of episodic memory, stabilizes this newly encoded information into long-lasting brain “storage.” Studies using fMRI to investigate post-encoding awake rest holds promise to shed light on early, immediate consolidation mechanisms. Here, we review fMRI studies during episodic memory to document common methods to investigate post-encoding consolidation, such as multivoxel pattern analysis (MVPA) and functional connectivity, and the current state of the science in both healthy younger and older adults. In young adults, post-encoding reactivation of stimuli-specific neural patterns in the hippocampus and its connectivity with cortical and subcortical areas (e.g., visual-temporal cortex, medial prefrontal, and medial parietal cortex) correlate with subsequent memory performance. Conversely, studies in older adults highlight the importance of large-scale brain networks during post-encoding rest, particularly the default mode network (DMN). Alterations in connectivity between the DMN and task-positive networks may help older adults maintain episodic memory. Furthermore, non-invasive brain stimulation techniques can enhance these post-encoding consolidation processes and improve memory performance in both younger and older adults. Notably, a lack of studies has investigated post-encoding memory consolidation in neurodegenerative disorders. This review underscores the importance of understanding how post-encoding neural reactivation and connectivity evolve with age to partially explain age-related declines in episodic memory performance and how such declines can be restored.

Patient is a 57-year-old Hispanic female with a past medical history of hypertension, asthma, and type II diabetes mellitus who presented to the emergency room (ER) for evaluation of 7 days of altered mental status. Upon initial presentation, the patient had difficulty following one step commands and was not fully oriented. Additionally, she appeared to be responding to external auditory and visual stimuli. Magnetic resonance imaging (MRI) completed in the ER was without acute intracranial abnormality (Figure 1), and electroencephalogram (EEG) was significant for diffuse slowing but no epileptiform activity was noted. She was admitted to the neurology service for further workup and treatment for possible autoimmune encephalitis, plasma exchange (PLEX), high-dose steroids, as well as intravenous immunoglobulin (IVIG) treatments. However, despite treatments, the patient continued to remain altered. Therefore, psychiatry was consulted as well as a cognitive specialist. Per patient's husband, he was able to recall that she had in fact had several years of cognitive decline, periods of altered mental status, hallucinations, and slowed gait. During her admission she had periods of not recognizing her husband, and identified him as an imposter, consistent with Capgras syndrome.¹ Given clinical findings, our cognitive team determined the patient's most likely diagnosis and started her on rivastigmine 1.5 mg bid with improvement.²

Lewy body dementia.

This study evaluated disease activity in people with Multiple Sclerosis (PwMS) who received immune checkpoint inhibitors (ICIs) compared to PwMS not treated with ICIs. There were 108 PwMS included (27 PwMS+ICIs and 81 PwMS controls), matched on age, sex, disease duration, DMTs, and MS disease course. Of 27 PwMS+ICIs, one (4%) had a relapse and four (15%) developed new MRI lesions without clinical symptoms. Time to relapse and MRI activity were compared using Kaplan–Meier curves and Cox regression models. There was no significant difference for either time to relapse (p = 0.34) or MRI activity (p = 0.15) in PwMS+ICIs compared to controls.