Incongruent changes in heart rate variability and body weight after discontinuing aerobic exercise in patients with schizophrenia.

A bidirectional connection exists between obesity and altered heart rate variability (HRV). Schizophrenia has been associated with a high risk of obesity and decreased vagal modulation. Few studies have examined the link between obesity and HRV in patients with schizophrenia. The aim of this study was to investigate the effects of aerobic exercise on body weight and HRV, and if so, whether these effects could be sustained after discontinuation of exercise training. A total of 18 overweight patients with schizophrenia completed an 8-week moderate-intensity aerobic exercise program conducted twice weekly for 50min. Body weight and heart rate variability were measured at baseline, week 8, and 4weeks after discontinuation of exercise training. Compared with the control group (15 overweight patients with schizophrenia without exercise training), the exercise group had reduced 2.3kg at week 8. Furthermore, the exercise program increased the low frequency, high frequency, and low frequency plus high frequency of HRV. However, after discontinuation of the exercise program for 4weeks, the changes in body weight and the HRV parameters diverged. All of the HRV parameters returned to their baseline values, but no change was seen in the reduced body weight. This suggests that HRV analysis is a more sensitive tool to detect health conditions in patients with schizophrenia. Although exercise is an easy and effective way to prevent and improve health problems, mental health providers might have underestimated the benefits of exercise in daily clinical practice. A regular exercise program should be considered as an essential part of treatment strategies for patients with schizophrenia.

Rapid Management of Trigeminal Neuralgia and Comorbid Major Depressive Disorder With Duloxetine.

OBJECTIVE: To describe a case of a patient diagnosed with major depressive disorder whose trigeminal neuralgia was unexpectedly but rapidly and efficiently responsive to duloxetine. CASE SUMMARY: A 37-year-old woman was diagnosed with trigeminal neuralgia, and the initial treatment with carbamazepine 800 mg/d did not improve her pain. In the following 3 years, she was poorly responsive to the combination therapy with several medications, including carbamazepine, valproate, baclofen, diclofenac, and acetaminophen. The repeated gamma knife radiosurgery still did not relieve her symptoms. She developed clinically significant depressive symptoms, and a diagnosis of major depressive disorder was made. Duloxetine 30 mg/d was initiated for the management of depression, with the dose gradually increased to 60 mg/d. Unexpectedly, at the dose of 60 mg/d, the patient reported remarkable relief in her trigeminal neuralgia within the first week. Her depressed mood gradually improved in the following 3 weeks. At the 4-year follow-up, she was gradually tapered off her medications, and her depression and trigeminal neuralgia were well managed on duloxetine 60 mg/d and carbamazepine 600 mg/d. DISCUSSION: The mechanisms may be related to duloxetine's ability to modulate norepinephrine and serotonin and antagonize N-methyl-d-aspartate (NMDA) receptors. The ignition hypothesis is a proposed etiology of trigeminal neuralgia, in that any individual hyperexcitable neuron can spread its discharge quickly to activate the entire population of neurons. We suggest that duloxetine exerts desynchronizing effects through its NMDA antagonism, modulating the hyperexcitable state of the trigeminal afferents. CONCLUSIONS: Duloxetine may be an adjuvant in treatment-resistant trigeminal neuralgia.