Burden of encephalitis-associated

hospitalizations in the United States,

19982010
1. Neil M. Vora, MD,
2. Robert C. Holman, MS,
3. Jason M. Mehal, MPH,
4. Claudia A. Steiner, MD, MPH,
5. Jesse Blanton, MPHand
6. James Sejvar, MD
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1. Correspondence to Dr. Vora: wii8@cdc.gov
1. Published online before print January 2, 2014,
doi: 10.1212/WNL.0000000000000086Neurology February 4, 2014 vol. 82 no. 5 443-451
Abstract
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ABSTRACT

Objective: To estimate the burden of encephalitis-associated hospitalizations in the United States for 19982010.
Methods: Using the Nationwide Inpatient Sample, a nationally representative database of hospitalizations,
estimated numbers and rates of encephalitis-associated hospitalizations for 19982010 were calculated. Etiology and
outcome of encephalitis-associated hospitalizations were examined, as well as accompanying diagnoses listed along
with encephalitis on the discharge records. Total hospital charges (in 2010 US dollars) were assessed.
Results: An estimated 263,352 (standard error: 3,017) encephalitis-associated hospitalizations occurred in the
United States during 19982010, which corresponds to an average of 20,258 (standard error: 232) encephalitis-
associated hospitalizations per year. A fatal outcome occurred in 5.8% (95% confidence interval [CI]: 5.6%6.0%)
of all encephalitis-associated hospitalizations and in 10.1% (95% CI: 9.2%11.2%) and 17.1% (95% CI: 14.6%
20.0%) of encephalitis-associated hospitalizations in which a code for HIV or a tissue or organ transplant was listed,
respectively. The proportion of encephalitis-associated hospitalizations in which an etiology for encephalitis was
specified was 50.3% (95% CI: 49.6%51.0%) and that for which the etiology was unspecified was 49.7% (95% CI:
49.0%50.4%). Total charges for encephalitis-associated hospitalizations in 2010 were an estimated $2.0 billion.
Conclusions: Encephalitis remains a major public health concern in the United States. Among the large number of
encephalitis-associated hospitalizations for which an etiology is not reported may be novel infectious and
noninfectious forms of encephalitis. Associated conditions such as HIV or transplantation increase the risk of a fatal
outcome from an encephalitis-associated hospitalization and should be monitored.

FOOTNOTES

Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if
any, are provided at the end of the article.
 APOE 4 worsens hippocampal CA1
apical neuropil atrophy and episodic
memory
1. Geoffrey A. Kerchner, MD, PhD,
2. Daniela Berdnik, PhD,
3. Jadon C. Shen, BS,
4. Jeffrey D. Bernstein, BS,
5. Michelle C. Fenesy, BA,
6. Gayle K. Deutsch, PhD,
7. Tony Wyss-Coray, PhD and
8. Brian K. Rutt, PhD
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1. Correspondence to Dr. Kerchner: kerchner@stanford.edu
1. Published online before print January 22, 2014,
doi: 10.1212/WNL.0000000000000154Neurology February 25, 2014 vol. 82 no. 8 691-697
Abstract
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Objectives: Using high-resolution structural MRI, we endeavored to study the relationships among APOE 4,
hippocampal subfield and stratal anatomy, and episodic memory.
Methods: Using a cross-sectional design, we studied 11 patients with Alzheimer disease dementia, 14 patients with
amnestic mild cognitive impairment, and 14 age-matched healthy controls with no group differences in APOE 4
carrier status. Each subject underwent ultra-high-field 7.0-tesla MRI targeted to the hippocampus and
neuropsychological assessment.
Results: We found a selective, dose-dependent association of APOE 4 with greater thinning of the CA1 apical
neuropil, or stratum radiatum/stratum lacunosum-moleculare (CA1-SRLM), a hippocampal subregion known to
exhibit early vulnerability to neurofibrillary pathology in Alzheimer disease. The relationship between the 4 allele
and CA1-SRLM thinning persisted after controlling for dementia severity, and the size of other hippocampal
subfields and the entorhinal cortex did not differ by APOE 4 carrier status. Carriers also exhibited worse episodic
memory function but similar performance in other cognitive domains compared with noncarriers. In a statistical
mediation analysis, we found support for the hypothesis that CA1-SRLM thinning may link the APOE 4 allele to its
phenotypic effects on memory.
Conclusions: The APOE 4 allele segregated dose-dependently and selectively with CA1-SRLM thinning and
worse episodic memory performance in a pool of older subjects across a cognitive spectrum. These findings
highlight a possible role for this gene in influencing a critical hippocampal subregion and an associated symptomatic
manifestation.

FOOTNOTES

Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if
any, are provided at the end of the article.