To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Suicide is a devastating public health problem and very few biological treatments have been found to be effective for quickly reducing the intensity of suicidal ideation (SI). We have previously shown that a single dose of ketamine, a glutamate N-methyl-d-aspartate (NMDA) receptor antagonist, is associated with a rapid reduction in depressive symptom severity and SI in patients with treatment-resistant depression.
We conducted a randomized, controlled trial of ketamine in patients with mood and anxiety spectrum disorders who presented with clinically significant SI (n = 24). Patients received a single infusion of ketamine or midazolam (as an active placebo) in addition to standard of care. SI measured using the Beck Scale for Suicidal Ideation (BSI) 24 h post-treatment represented the primary outcome. Secondary outcomes included the Montgomery–Asberg Depression Rating Scale – Suicidal Ideation (MADRS-SI) score at 24 h and additional measures beyond the 24-h time-point.
The intervention was well tolerated and no dropouts occurred during the primary 7-day assessment period. BSI score was not different between the treatment groups at 24 h (p = 0.32); however, a significant difference emerged at 48 h (p = 0.047). MADRS-SI score was lower in the ketamine group compared to midazolam group at 24 h (p = 0.05). The treatment effect was no longer significant at the end of the 7-day assessment period.
The current findings provide initial support for the safety and tolerability of ketamine as an intervention for SI in patients who are at elevated risk for suicidal behavior. Larger, well-powered studies are warranted.
James W. Murrough, Department of Psychiatry Mount Sinai School of Medicine New York, NY, USA,
Sanjay J. Mathew, Department of Psychiatry and Behavioral Sciences Baylor College of Medicine Houston, TX, USA
This chapter reviews the neurochemical imaging literature in the anxiety disorders, focusing on key findings in post-traumatic stress disorder (PTSD), panic disorder (PD), social anxiety disorder (SAD) and generalized anxiety disorder (GAD). It provides a partial review of preclinical and human investigations of several neurochemical systems relevant to neurochemical imaging of anxiety disorders: namely the 5-HT, gamma-aminobutyric acid-benzodiazepine (GABA-BZD) and dopamine (DA) systems. Genetic analyses of polymorphisms of the major DA metabolizing enzyme catechol-O-methyltransferase (COMT) have suggested an association between specific polymorphisms and anxiety disorders, although these findings await replication. Several studies have utilized 1H-magnetic resonance spectroscopy (MRS) to investigate potential abnormalities in N-acetyl-aspartate (NAA), choline (CHO), creatine (CR) or lactate in GAD. As anxiety disorders are frequently comorbid with mood disorders, investigations of patients with anxious depression may be informative in determining specificity of neurochemical abnormalities.
Email your librarian or administrator to recommend adding this to your organisation's collection.