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A growing importance has been placed on the recognition and supervision of non-motor features of Parkinson's disease (PD). Depression has been estimated to affect one in three individuals with PD and can lead to worse health outcomes and decreased quality of life. Anxiety, apathy and anhedonia further complicate PD outcomes. In this double-blind, placebo-controlled trial, participants (individuals with mild to moderate PD; n = 24) were randomly assigned to treatment (800 mg/d docosahexaenoic acid (DHA) and 290 mg/d eicosapentaenoic acid, a precursor to DHA) or placebo (an equicaloric amount of corn oil). Treatment duration was 6 months. Treatment had no statistically significant effect on rate of change on either Unified Parkinson's Disease Rating Scale or Hoehn-Yahr Scale score. However, 75% of DHA-treated patients, reduced Hamilton Rating Scale for Depression total score by at least 50%, compared with only 25% into the placebo group. At the end of the six-month study, DHA integration reduced the depressive symptoms.

Anhedonia is present in Parkinson's Disease (PD) as well as in addictive behaviors. Pathological Gambling (PG) and other Impulse Control Disorders (ICDs) have emerged as iatrogenic complications associated with dopamine replacement therapy. We studied 154 PD patients, divided into three groups: 11 with PG, 23 with other ICDs (compulsive buying, hypersexuality, binge eating), 120 without ICDs. All patients underwent a thorough clinical, neuropsychological and psychiatric evaluation. The PG-group, compared to the ICDs-group and PD-controls, reported a significantly higher incidence of anhedonia (45% vs. 9% vs. 14% respectively), higher Snaith–Hamilton Pleasure Scale (SHAPS) scores (2.0±1.3 vs. 1.0±1.1 vs. 1.0±1.2), higher levels of impulsivity traits as measured by the Barratt Impulsiveness Scale (70.0±10.6 vs. 64.8±11 vs. 60.9±9.3) and more severe frontal dysfunctions (Frontal Assessment Battery, FAB: 12.4±4.9 vs. 15.5±1.6 vs. 14.4±3). A model for PG (incorporating anhedonia, impulsivity levels and frontal impairment) is discussed in the context of the pathophysiology of addictive behaviors. The impairment of hedonic capacity, possibly resulting from an underlying neuropsychological dysfunction, might facilitate loss of control over reward-related behavior, thus favoring the shift towards predominantly habit-based compulsive behaviors.

Objective We aimed at evaluating the association between appetite and symptoms of depression and anxiety, cognitive dysfunction, fatigue, and comorbidities in patients on hemodialysis (HD). Design A cross-sectional study was conducted. Setting The study was conducted in an outpatient HD service of a tertiary level academic hospital. Patients A total of 90 patients on HD were evaluated for appetite (during the past week, how would you rate your appetite?), symptoms of depression (Beck Depression Inventory [BDI]) and anxiety (Hamilton Anxiety Rating Scale [HARS]), cognitive dysfunction (Mini Mental State Examination [MMSE]), and comorbidities (Charlson Comorbidity Index). Main Outcome Measure Relationship between appetite and symptoms of depression and/or anxiety, cognitive dysfunction, and comorbidities was assessed. Results In 43 patients, the appetite was very good/good (group 1), in 22, it was fair (group 2), and in 25, it was poor/very poor (group 3). Mean and median BDI were significantly higher in group 3 as well as the percentage of patients with BDI ≥16. Mean and median HARS and the percentage of patients with HARS >13 were significantly higher in group 3. MMSE was significantly lower in group 3 as well as the percentage of patients with MMSE ≤23. Multiple linear regression analysis showed a dependence of appetite by age and BDI ( P = .007 and P = .002, respectively). Conclusions Anorexia is associated with older age and symptoms of depression in patients on HD.

Studies performed in animals and humans have suggested a functional interaction between opioid and cholinergic systems in the control of growth hormone (GH) secretion. Moreover, the sex-dependent modulation of GH secretion in humans is well established. To investigate the role of sex and food intake in the regulation of the reciprocal influences of opioids and acetylcholine in the modulation of GH secretion, we studied the GH response to pyridostigmine (PYR) alone and during a naloxone (NAL) infusion in a group of normal men and women before a meal (at 1:00 PM) and postprandially. In women, the response of GH to PYR alone before the meal was significantly lower than in the men (area under the curve [AUC], mean +/- SEM, 320.18 +/- 87.16 v 1,031.06 +/- 333.21 micrograms/L/90 min, P < .01). Before the meal, NAL completely abolished the response of GH to PYR in men (AUC, 1,031.06 +/- 333.21 v 16.50 +/- 7.50 micrograms/L/90 min, P < .01), whereas infusion of NAL did not significantly modify the GH response to PYR in women. Consumption of the meal significantly decreased PYR-induced GH release in both women (AUC, 21.75 +/- 12.75 v 320.18 +/- 87.16 micrograms/L/90 min, P < .05) and men (AUC, 45.75 +/- 18.75 v 1,031.06 +/- 333.21 micrograms/L/90 min, P < .01). Conversely, food intake did not change the effects of NAL infusion on the GH response to PYR either in women or in men. We conclude that the sex-dependent opioid modulation of PYR-induced GH secretion is observed before a meal but not in the postprandial state. Food intake may be hypothesized to influence the cholinergic regulation of GH secretion and the sex-dependent opioid modulation of central cholinergic tone.

Previous studies have shown that food ingestion is not capable of inhibiting the GHRH-induced GH release in anorexia nervosa, at variance with what is observed in normal subjects. Moreover, a cholinergic alteration has been hypothesized in this disorder. In a group of 24 anorectic patients in a stabilized phase of the illness, we tested, before and after a standard meal, the GH response to GHRH alone and after pre-treatment with pyridostigmine, an inhibitor of acetylcholinesterase, and, on a different day, with oxiracetam, which stimulates the central cholinergic neurones. The GH response to GHRH was significantly increased by both drugs in a fasting state. The postprandial response was not significantly modified by pyridostigmine nor by oxiracetam. Neither of these compounds was able to enhance the postprandial GH ‘paradoxical’ response to GHRH in anorectic patients. The lack of effect of both drugs postprandially also suggests a suppression of somatostatinergic activity.

Previously, we have shown that in the opposite extremes of nutritional status, obesity and anorexia nervosa (AN), growth hormone (GH) response to growth hormone-releasing hormone (GH-RH) is not inhibited by the ingestion of a normal 800-cal meal consumed at lunch time (1 pm), which is at variance with results in normal subjects. However, in obese patients the postprandial increase in GH response to GH-RH is inhibited by an infusion of naloxone (NAL). In this study we have tested anorectic patients, performing the following tests at 1 pm: GH-RH test (50 μg IV) or, in a different day session, NAL (1.6 mg/h, starting 30 minutes before GH-RH) + GH-RH test (50 μg IV). The tests were performed in the following three different experimental conditions: (1) short-term fasting studies (lasting from breakfast), (2) long-term fasting studies (from midnight of the day before) and (3) postprandial studies (after a standard meal consumed 1 hour before the test). In AN, the GH response to GH-RH was not influenced by NAL infusion at 1 pm, in both short-and long-term fasting studies (short-term fasting: peak values after GH-RH alone, 26.5 ± 6.5 ng/mL, duirng NAL, 28.0 ± 3.3 ng/mL; long-term fasting: peak values after GH-RH alone, 32.2 ± 6.8 ng/mL, during NAL, 30.6 ± 4.0 ng/mL). A partial NAL-inhibitory effect was instead observed in postprandial studies, as evidenced by the calculation of areas under the curve ([AUCs] 1,662.1 ± 90.0 after GH-RH alone v 1,090.5 ± 245.4 ng/mL/h during NAL). These findings indicate that NAL exerts differential effects in AN before and after a meal. Comparison to the results previously obtained in normal and obese subjects seems to suggest a differential opioid modulation of GH response to GH-RH in AN patients versus normal subjects or patients with obesity.

The alpha-2-adrenoceptor agonist clonidine is able to stimulate GHRH secretion directly or via beta-endorphin and, therefore, induces a GH release in normal subjects. This effect has been shown to be blunted in alcoholism during early abstinence, due to central alterations of adrenergic mechanisms. To evaluate pituitary responsiveness to direct stimulation with GHRH, we have studied the GH and PRL response to GHRH in 10 alcoholics during early abstinence. Our data indicate that the pituitary response to GHRH is intact in abstinent alcoholics, except in obese patients, who displayed a blunted GH response. GHRH did not increase PRL. The dissociation between clonidine and GHRH in GH stimulation could reveal a different neuroendocrine mechanism, in comparison with other psychiatric disorders (anorexia nervosa), in which such a dissociation is accompanied by a PRL response to GHRH.

Erratum to “Correlates of symptoms of depression and anxiety in chronic hemodialysis patients” [General Hospital Psychiatry 32 (2010) 125–131] Maurizio Bossola, M.D.⁎, Claudia Ciciarelli, M.D., Enrico Di Stasio, M.D., Gian Luigi Conte, M.D., Carlo Vulpio, M.D., Giovanna Luciani, M.D., Luigi Tazza, M.D. Servizio Emodialisi, Istituto di Clinica Chirurgica, Universita Cattolica del Sacro Cuore, 8-00168 Rome, Italy Istituto di Psichiatria, Universita Cattolica del Sacro Cuore, 8-00168 Rome, Italy Istituto di Chimica Clinica, Universita Cattolica del Sacro Cuore, 8-00168 Rome, Italy