Neurocognitive Effects of Ketamine and Association with Antidepressant Response in Individuals with Treatment-Resistant Depression: A Randomized Controlled Trial

The glutamate N-methyl-D-aspartate (NMDA) receptor antagonist ketamine displays rapid antidepressant effects in patients with treatment-resistant depression (TRD); however, the potential for adverse neurocognitive effects in this population has not received adequate study. The current study was designed to investigate the delayed neurocognitive impact of ketamine in TRD and examine baseline antidepressant response predictors in the context of a randomized controlled trial. In the current study, 62 patients (mean age=46.2±12.2) with TRD free of concomitant antidepressant medication underwent neurocognitive assessments using components of the MATRICS Consensus Cognitive Battery (MCCB) before and after a single intravenous infusion of ketamine (0.5 mg/kg) or midazolam (0.045 mg/kg). Participants were randomized to ketamine or midazolam in a 2:1 fashion under double-blind conditions and underwent depression symptom assessments at 24, 48, 72 h, and 7 days post treatment using the Montgomery–Asberg Depression Rating Scale (MADRS). Post-treatment neurocognitive assessment was conducted once at 7 days. Neurocognitive performance improved following the treatment regardless of treatment condition. There was no differential effect of treatment on neurocognitive performance and no association with antidepressant response. Slower processing speed at baseline uniquely predicted greater improvement in depression at 24 h following ketamine (t=2.3, p=0.027), while controlling for age, depression severity, and performance on other neurocognitive domains. In the current study, we found that ketamine was devoid of adverse neurocognitive effects at 7 days post treatment and that slower baseline processing speed was associated with greater antidepressant response. Future studies are required to further define the neurocognitive profile of ketamine in clinical samples and to identify clinically useful response moderators.     

Mycophenolate in idiopathic inflammatory myositis: outcome data of a large South Asian cohort

Clinical Rheumatology - Consensus on treatment of idiopathic inflammatory myositis (IIM), particularly with regard to flares and interstitial lung disease (ILD), does not exist. We studied the...     

Orthostatic hypotension: A commonly unrecognized cause of symptoms in mitral valve prolapse

To test the hypothesis that orthostatic hypotension could represent an alternative mechanism contributing to the symptoms of mitral valve prolapse, the systolic and diastolic arterial blood pressures were measured in the supine and standing positions in 86 patients with the diagnosis confirmed by echocardiography. Orthostatic hypotension was demonstrated in 12 patients. Ten of them presented with a history of recurrent lightheadedness, dizziness or syncope and constitute 59 percent of the total number of patients with such symptoms in this series. Although nine of these 10 patients reported transient lightheadedness or dizziness during periods of ambulatory electrocardiographic recording, in only one were the symptoms chronologically related to cardiac arrhythmias. On the other hand, eight of them described lightheadedness and two experienced near-syncope during the postural test in association with the orthostatic drop in blood pressure. Improvement in symptoms and correction of the orthostatic hypotension were demonstrated in seven patients after beta-adrenergic blockade with propranolol. Before therapy, the mean systolic blood pressure dropped from 114 ± 3 mm Hg in the supine position to 78 ± 1 mm Hg upon standing (p < 0.001). In repeated postural tests performed after four weeks of treatment, the systolic blood pressure changed from 120 ± 3 mm Hg supine to 115 ± 1 mm Hg upon standing (p > 0.01).We conclude that orthostatic hypotension is a commonly unrecognized mechanism responsible for some of the symptoms of mitral valve prolapse, particularly in patients affected by recurrent lightheadedness, dizziness or syncope.     

Long-term survival of a patient with left ventricular free wall rupture without surgical repair

This report describes the case of a patient who developed postinfarction left ventricular free wall rupture and cardiac tamponade. He was managed conservatively, made a successful recovery, and is alive and asymptomatic 10 months after the index episode. Only 17 cases in which the patients survived subacute rupture of the ventricular free wall over the long term without surgical repair have been reported in the literature.     

Hemodynamics and annuloplasty in isolated mitral regurgitation in children.

Isolated mitral insufficiency in children is quantitated angiographically by comparing the stroke volumes of the right ventricle and left ventricle. The disease results in greater enlargement of the left atrium than of the left ventricle and is accompanied by a significant increase in left atrial "distensibility." Right and left heart pressures may be normal or may be increased; they tend to be elevated in the group with regurgitant fractions of over 50%. Annuloplasty results in marked clinical and hemodynamic improvement and may even be corrective.