Acute Vascular Ischemic Events in Patients With Central Retinal Artery Occlusion in the United States: A Nationwide Study 2003-2014.

PURPOSE: Central retinal artery occlusion (CRAO) confers a high risk of acute vascular ischemic events, including stroke and myocardial infarction (MI). Understanding the burden and risk factor profile of these ischemic events can serve as a valuable guide for ophthalmologists in the management and appropriate referral of these patients. DESIGN: Retrospective cross-sectional study. METHODS: The Nationwide Inpatient Sample (NIS) was queried to identify all inpatient admissions with a diagnosis of CRAO in the United States between the years 2003 and 2014. The primary outcome measure was the incidence of in-hospital acute vascular ischemic events. RESULTS: There were an estimated 17 117 CRAO inpatient admissions. The mean age was 68.4 ± 0.1 years and 53% of patients were female. The incidence of in-hospital stroke and acute MI were 12.9% and 3.7%. The incidence of stroke showed an increasing trend over the years, almost doubling in 2014 in comparison to 2003 (15.3% vs 7.7%). The combined risk of in-hospital stroke, transient ischemic attack, acute MI, or mortality was 19%. Female sex, hypertension, carotid artery stenosis, aortic valve disease, smoking, and alcohol dependence or abuse were positive predictors of in-hospital stroke. CONCLUSION: There is a significant burden of vascular risk factors, associated with an increased risk of in-hospital stroke, acute MI, and death in CRAO patients. The risk of CRAO-associated stroke is highest in women and in those with a history of hypertension, carotid artery stenosis, aortic valve disease, smoking, or alcohol abuse.

Loss of neurons from laminas I-III of the spinal dorsal horn is not required for development of tactile allodynia in the spared nerve injury model of neuropathic pain.

It has been proposed that death of inhibitory interneurons in the dorsal horn contributes to the neuropathic pain that follows partial nerve injury. In this study, we have used two approaches to test whether there is neuronal death in the dorsal horn in the spared nerve injury (SNI) model. We performed a stereological analysis of the packing density of neurons in laminas I-III 4 weeks after operation and found no reduction on the ipsilateral side compared with that seen on the contralateral side or in sham-operated or naive rats. In addition, we used two markers of apoptosis, terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) staining and immunocytochemical detection of cleaved (activated) caspase-3. Neither of these methods demonstrated apoptotic neurons in the dorsal spinal cord 1 week after operation. Although TUNEL-positive cells were present throughout the gray and white matter at this stage, they were virtually all labeled with antibody against ionized calcium-binding adapter molecule 1, a marker for microglia. All animals that underwent SNI showed clear signs of tactile allodynia affecting the ipsilateral hindpaw. These results suggest that a significant loss of neurons from the dorsal horn is not necessary for the development of tactile allodynia in the SNI model.