Causes, treatment, and outcome of hyphema, fibrin, and vitreal hemorrhage in horses: 219 cases (2012-2023).

Objective: To determine the causes, time to resolution, effect of therapeutics, and ocular sequelae of hyphema, fibrin, and/or vitreal hemorrhage in horses.

Animals: 225 horses (219 eyes) who were diagnosed with hyphema, fibrin, and/or vitreal hemorrhage.

Methods: Records were retrospectively reviewed for the horses.

The Millon Clinical Multiaxial Inventory-IV (MCMI-IV) and Millon Adolescent Clinical Inventory-II (MACI-II) in Legal Settings.

The MCMI-IV and MACI-II are the most recent iterations of the primary Millon clinical inventories and have become well-established instruments over the course of multiple editions. The MCMI, in particular in its prior editions, and to a lesser extent, the original MACI, have joined the canon of commonly-used psychological instruments in several forensic settings, though they have been met with significant controversy. This controversy is due in large part to complicated and sometimes questionable psychometric and normative referencing qualities that evaluators may find difficult to defend in a court setting.

A prototype closed-loop brain-machine interface for the study and treatment of pain.

Chronic pain is characterized by discrete pain episodes of unpredictable frequency and duration. This hinders the study of pain mechanisms and contributes to the use of pharmacological treatments associated with side effects, addiction and drug tolerance. Here, we show that a closed-loop brain-machine interface (BMI) can modulate sensory-affective experiences in real time in freely behaving rats by coupling neural codes for nociception directly with therapeutic cortical stimulation.

Ketamine normalizes high-gamma power in the anterior cingulate cortex in a rat chronic pain model.

Chronic pain alters cortical and subcortical plasticity, causing enhanced sensory and affective responses to peripheral nociceptive inputs. Previous studies have shown that ketamine had the potential to inhibit abnormally amplified affective responses of single neurons by suppressing hyperactivity in the anterior cingulate cortex (ACC). However, the mechanism of this enduring effect has yet to be understood at the network level.