The significance of multimodality approach in the management of non-lesional drug-resistant focal parietal lobe epilepsies.

Due to extensive connectivity of the parietal lobe, non-lesional drug-resistant (DRE) parietal lobe epilepsies (PLEs) are difficult to localize and often imitate other epilepsies. Therefore, patients with PLEs have low rates of seizure freedom following epilepsy surgery. Previous studies have highlighted the need to combine EEG and semiology for more accurate localization of PLEs. As sophisticated tools for localization become more available, the use of multiple different neuroimaging and neurophysiologic diagnostic tests may more readily identify PLE. We hereby report a unique case of a complex localization in a non-lesional PLE, which was initially falsely localized to frontal lobe. This case underscores the utility of voxel-based morphometry (VBM) in identifying an epileptogenic lesion on a non-lesional MRI and the significance of multimodality approach including PET, magnetoencephalopathy (MEG), interictal and ictal EEG, semiology and cortical stimulation for accurate localization of PLEs. Understanding epilepsy through multimodality approach in this fashion can help with accurate localization especially in difficulty to localize and deceptive non-lesional PLEs. PLAIN LANGUAGE SUMMARY: Parietal lobe epilepsies are hard to pinpoint in the brain and can mimic other types of epilepsy, especially when brain MRIs appear normal. As sophisticated tools for locating epilepsies in the brain become more available, using multiple diagnostic tests may help identify parietal lobe epilepsies more easily. We describe a unique case of a parietal lobe epilepsy patient with normal brain MRI whose epilepsy was initially misidentified as being in the frontal lobe. Using various advanced diagnostic tests, we accurately found the epilepsy's true location in the parietal lobe and successfully treated the patient with surgery.

Interrelationship of Sleep Disturbances and Cognitive Status on Mortality.

Sleep disturbances may promote the development and advancement of Alzheimer's disease. Our purpose was to determine if sleep disturbances were associated with earlier mortality while accounting for cognition. The National Alzheimer's Coordinating Center database was used to evaluate mortality risk conferred by sleep, and the Montreal Cognitive Assessment score determined cognitive status. Demographics, sleep disturbances, cognitive status, and comorbid/other neuropsychiatric conditions were examined as predictors of survival time via Cox regression. The sample (N = 31,110) had a median age [interquartile range] of 72 [66, 79] years, MoCA score of 23 [16, 26], and survival time of 106.0 months [104.0,108.0]; 10,278 (33%) died during follow-up; 21% (n = 6461) experienced sleep disturbances. Sleep disturbances impacted survival time depending on cognition, with the greatest effect in transition from normal to cognitive impairment (P < .001). Findings support that sleep disturbances negatively impact survival time, and the impact of sleep disturbances on survival time is interrelated with cognition.

Association of Seizure Control With Cognition in People With Normal Cognition and Mild Cognitive Impairment.

BACKGROUND AND OBJECTIVES: Seizures are common in dementia and associated with accelerated cognitive decline. However, the impact of active vs remote seizures on cognition remains understudied. This study aimed to investigate the impact of active vs remote seizures on cognition in people with normal cognition and mild cognitive impairment (MCI). METHODS: This longitudinal, multicenter cohort is based on National Alzheimer's Coordinating Center data of participants recruited from 39 Alzheimer's Disease Centers in the United States from September 2005 to December 2021. All participants with normal cognition and MCI and at least 2 visits were included. Primary outcome, that is, cognitive decline, was determined using Clinical Dementia Rating (CDR) from (1) normal-to-impaired (CDR ≥0.5) and (2) MCI-to-dementia (CDR ≥1) groups. The effect of active seizures (over the preceding 12 months), remote seizures (previous seizures but none over the preceding 12 months), and no seizures (controls) on cognition was assessed. Subgroups of chronic seizures at enrollment and new-onset seizures were further analyzed. Cox regression models assessed the risk of all-cause MCI and/or dementia. All models were adjusted for age, sex, education, race, hypertension, and diabetes. RESULTS: Of the 13,726 participants with normal cognition at enrollment (9,002 [66%] female; median age 71 years), 118 had active seizures and 226 had remote seizures. Of the 11,372 participants with MCI at enrollment (5,605 [49%] female; median age 73 years), 197 had active seizures and 226 had remote seizures. Active seizures were associated with 2.1 times higher risk of cognitive impairment (adjusted hazard ratio [aHR] 2.13, 95% CI 1.60-2.84, p < 0.001) in cognitively healthy adults (median years to decline: active seizures = ∼1, remote seizures = ∼3, no seizures = ∼3) and 1.6 times higher risk of dementia (aHR 1.58, 95% CI 1.24-2.01, p < 0.001) in those with MCI (median years to decline: active seizures = ∼1, remote seizures = ∼2, controls = ∼2). This risk was not observed with remote seizures. DISCUSSION: In this study, active seizures but not remote seizures were associated with earlier cognitive decline in both cognitively normal adults and those with MCI, independent of other dementia risk factors. Therefore, early identification and management of seizures may present a path to mitigation of cognitive decline in the aging epileptic population. A limitation is that causality cannot be confirmed in our observational longitudinal study.