Objectives-i) to assess the diagnostic specificity of MRI-defined hippocampal atrophy for Alzheimer's disease (AD) among individuals with a variety of pathologically confirmed conditions associated with dementia as well as changes attributable to typical aging, and, ii) to measure correlations among pre-mortem MRI measurements of hippocampal atrophy, mental status exam performance, and the pathologic stage of AD. Methods-An un-selected series of 67 individuals participating in the Mayo Alzheimer's DiseaseResearch Center/Alzheimer's Disease Patient Registry were identified who had undergone a standardized antemortem MRI study and also post-mortem examination. Hippocampal volumes were measured from antemortem MRI. Each post-mortem specimen was assigned a pathologic diagnosis, and in addition, the severity of AD pathology was staged using the method of Braak and Braak.Results-Individuals with an isolated pathologic diagnosis of AD, hippocampal sclerosis, frontotemporal degeneration, and neurofibrillary tangle-only degeneration usually had substantial hippocampal atrophy while those with changes of typical aging did not. Among all 67 subjects, correlations (all p<0.001) were observed between hippocampal volume and Braak stage (r = −0.39), between hippocampal volume and MMSE score (r = 0.60), and between MMSE score and Braak stage (r = −0.41).Conclusions-Hippocampal atrophy, while not specific for AD, was a fairly sensitive marker of the pathologic AD stage [particularly among subjects with isolated AD pathology (r = −0.63, p = 0.001)] and consequent cognitive status.

MRI-based hippocampal volumetry accurately depicts the structural-functional relationships between memory loss and hippocampal damage across the spectrum from normal aging to dementia.

decayed, missing, filled teeth in primary dentition (dmft); receiver operation characteristics (ROC); relative risk (RR); confidence interval (CI); National Institutes of Health (NIH); World Health Organization (WHO); US Department of Health and Human Services (US/DHHS); American Academy of Pediatric Dentistry (AAPD).

Objective: To determine if posttraumatic nonconvulsive electrographic seizures result in longterm brain atrophy. Methods:Prospective continuous EEG (cEEG) monitoring was done in 140 patients with moderate to severe traumatic brain injury (TBI) and in-depth study of 16 selected patients was done using serial volumetric MRI acutely and at 6 months after TBI. Fluorodeoxyglucose PET was done in the acute stage in 14/16 patients. These data were retrospectively analyzed after collection of data for 7 years.Results: cEEG detected seizures in 32/140 (23%) of the entire cohort. In the selected imaging subgroup, 6 patients with seizures were compared with a cohort of 10 age-and GCS-matched patients with TBI without seizures. In this subgroup, the seizures were repetitive and constituted status epilepticus in 4/6 patients. Patients with seizures had greater hippocampal atrophy as compared to those without seizures (21 Ϯ 9 vs 12 Ϯ 6%, p ϭ 0.017). Hippocampi ipsilateral to the electrographic seizure focus demonstrated a greater degree of volumetric atrophy as compared with nonseizure hippocampi (28 Ϯ 5 vs 13 Ϯ 9%, p ϭ 0.007). A single patient had an ictal PET scan which demonstrated increased hippocampal glucose uptake. Conclusion:Acute posttraumatic nonconvulsive seizures occur frequently after TBI and, in a selected subgroup, appear to be associated with disproportionate long-term hippocampal atrophy. These data suggest anatomic damage is potentially elicited by nonconvulsive seizures in the acute postinjury setting. Neurology ® 2010;75:792-798 GLOSSARY cEEG ϭ continuous EEG; FLAIR ϭ fluid-attenuated inversion recovery; GCS ϭ Glasgow Coma Scale score; GRE ϭ gradient recalled echo; ICU ϭ intensive care unit; TBI ϭ traumatic brain injury.Neurologic critical care of traumatic brain injury (TBI) focuses on avoiding secondary insults.

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