Kava Withdrawal Treated with Phenobarbital-A Case Report and Literature Review.

ABSTRACT: Kava consumption is a traditional practice in Polynesian and Micronesian cultures. It has recently gained popularity in the United States for therapeutic and recreational use. We report the following case. A man presented to the emergency department after a fall while intoxicated on kava. He was medically admitted for altered mental status, facial and clavicle fractures, and hyponatremia. Psychiatry was consulted for management of delirium. On interview, he reported consuming escalating amounts of kava for weeks despite attempts to stop. He was diagnosed with acute kava withdrawal with hyperactive delirium, treated with phenobarbital load (860 mg) and taper (390 mg). Continuous dexmedetomidine drip to hospital day 3 treated sympathetic activation and breakthrough agitation. By day 4, his delirium resolved and remained in remission until discharge. We performed a systematic review for reports of kava withdrawal, returning 9 studies. Eight assessed withdrawal symptoms after cessation of a low controlled dose of kava extract with no symptoms noted. One reported a case series of heavy kava users with seizure-like events. No publications discussed treatment of kava withdrawal. To our knowledge, this is the first publication to describe kava withdrawal syndrome and its effective treatment with phenobarbital.

Systematic analysis of proximal midgut- and anorectal-originating contractions in larval zebrafish using event feature detection and supervised machine learning algorithms.

BACKGROUND: Zebrafish larvae are translucent, allowing in vivo analysis of gut development and physiology, including gut motility. While recent progress has been made in measuring gut motility in larvae, challenges remain which can influence results, such as how data are interpreted, opportunities for technical user error, and inconsistencies in methods. METHODS: To overcome these challenges, we noninvasively introduced Nile Red fluorescent dye to fill the intraluminal gut space in zebrafish larvae and collected serial confocal microscopic images of gut fluorescence. We automated the detection of fluorescent-contrasted contraction events against the median-subtracted signal and compared it to manually annotated gut contraction events across anatomically defined gut regions. Supervised machine learning (multiple logistic regression) was then used to discriminate between true contraction events and noise. To demonstrate, we analyzed motility in larvae under control and reserpine-treated conditions. We also used automated event detection analysis to compare unfed and fed larvae. KEY RESULTS: Automated analysis retained event features for proximal midgut-originating retrograde and anterograde contractions and anorectal-originating retrograde contractions. While manual annotation showed reserpine disrupted gut motility, machine learning only achieved equivalent contraction discrimination in controls and failed to accurately identify contractions after reserpine due to insufficient intraluminal fluorescence. Automated analysis also showed feeding had no effect on the frequency of anorectal-originating contractions. CONCLUSIONS & INFERENCES: Automated event detection analysis rapidly and accurately annotated contraction events, including the previously neglected phenomenon of anorectal contractions. However, challenges remain to discriminate contraction events based on intraluminal fluorescence under treatment conditions that disrupt functional motility.

Use of Thromboelastography with Platelet Mapping to Identify Prothrombotic Coagulation Profiles in Patients with History of Cardiac Intervention Undergoing Lower Extremity Revascularization.

BACKGROUND: Patients with concomitant coronary and peripheral artery disease (CAD and PAD) are at significant risk for major adverse limb events (MALEs). Prevention of thrombosis in this population is of paramount importance. Identifying prothrombotic coagulation profiles in this cohort may facilitate targeted thromboprophylaxis. We compared coagulation profiles of those with CAD and PAD to those with PAD alone during the perioperative period of lower extremity revascularization. STUDY DESIGN: Patients undergoing lower extremity revascularization underwent thromboelastography-platelet mapping (TEG-PM) analysis preoperatively and at serial intervals for up to 6 months. Coagulation profiles of patients with significant CAD (defined as history of coronary artery bypass graft or percutaneous coronary intervention) and PAD were compared with those with PAD alone. MALE in the postoperative period was recorded. RESULTS: Four hundred seventy-seven TEG-PM samples from 114 patients were analyzed; 28.1% had a history of significant CAD. The incidence of atrial fibrillation was higher in this group. The significant CAD group had lower ADP-platelet inhibition, higher ADP-platelet aggregation, and greater maximum clot strength compared with patients with PAD alone. Patients with significant CAD were more frequently on full-dose anticoagulation, but less frequently on dual antiplatelet therapy; 28.1% of patients with significant CAD developed postoperative MALE compared with 22.9% of patients with PAD alone (p = 0.40). For both groups, patients who developed postoperative MALE demonstrated greater ADP-platelet aggregation and lower ADP-platelet inhibition. CONCLUSIONS: Patients with a history of significant CAD undergoing lower extremity revascularization demonstrated prothrombotic TEG-PM profiles, less frequent use of dual antiplatelet therapy, and greater rates of full-dose anticoagulation. Decreased platelet inhibition was also associated with postoperative MALE. This study underscores the potential utility of viscoelastic assays for coagulation profiling in complex cardiovascular patients.

Electrophysiological Alterations Driving Pain-Associated Spontaneous Activity in Human Sensory Neuron Somata Parallel Alterations Described in Spontaneously Active Rodent Nociceptors.

Neuropathic pain in rodents can be driven by ectopic spontaneous activity (SA) generated by sensory neurons in dorsal root ganglia (DRG). The recent demonstration that SA in dissociated human DRG neurons is associated with reported neuropathic pain in patients enables a detailed comparison of pain-linked electrophysiological alterations driving SA in human DRG neurons to alterations that distinguish SA in nociceptors from SA in low-threshold mechanoreceptors (LTMRs) in rodent neuropathy models. Analysis of recordings from dissociated somata of patient-derived DRG neurons showed that SA and corresponding pain in both sexes were significantly associated with the three functional electrophysiological alterations sufficient to generate SA in the absence of extrinsic depolarizing inputs. These include enhancement of depolarizing spontaneous fluctuations of membrane potential (DSFs), which were analyzed quantitatively for the first time in human DRG neurons. The functional alterations were indistinguishable from SA-driving alterations reported for nociceptors in rodent chronic pain models. Irregular, low-frequency DSFs in human DRG neurons closely resemble DSFs described in rodent nociceptors while differing substantially from the high-frequency sinusoidal oscillations described in rodent LTMRs. These findings suggest that conserved physiological mechanisms of SA in human nociceptor somata can drive neuropathic pain despite documented cellular differences between human and rodent DRG neurons. PERSPECTIVE: Electrophysiological alterations in human sensory neurons associated with patient-reported neuropathic pain include all three of the functional alterations that logically can promote spontaneous activity. The similarity of distinctively altered spontaneous depolarizations in human DRG neurons and rodent nociceptors suggests that spontaneously active human nociceptors can persistently promote neuropathic pain in patients.

Neuroprogression in post-traumatic stress disorder: a systematic review

Abstract Introduction Neuroprogression has been proposed as the pathological rewiring of the brain that takes place in parallel with clinical and neurocognitive deterioration in the course of psychiatric disorders. This study aims to review the biological underpinnings and clinical outcomes related to neuroprogression in post-traumatic stress disorder (PTSD). Methods We performed a systematic review by searching PubMed, Embase, and Web of Science for articles published between January 1, 1960, and January 6, 2020. Inclusion criteria were met when articles assessed brain changes, neurocognition, functioning, inflammation, oxidative stress, and neurotrophins in patients with PTSD. Narrative review articles, case reports, and preclinical studies were excluded. Results A total of 965 abstracts were identified and 15 articles were included in our systematic review. It seems that for a subset of patients whose symptoms worsen or are maintained at a high intensity there is a progressive change in the frontal lobe, especially the prefrontal cortex, and worsening of both neurocognition (verbal memory and facial recognition) and functioning (physical, psychological, social and environmental). Conclusion Although current findings associate progressive reduction in frontal lobe size with neurocognitive impairment, further research is needed to characterize PTSD as a neuroprogressive disorder.

Neuroprogression in post-traumatic stress disorder: a systematic review.

INTRODUCTION: Neuroprogression has been proposed as the pathological rewiring of the brain that takes place in parallel with clinical and neurocognitive deterioration in the course of psychiatric disorders. This study aims to review the biological underpinnings and clinical outcomes related to neuroprogression in post-traumatic stress disorder (PTSD). METHODS: We performed a systematic review by searching PubMed, Embase, and Web of Science for articles published between January 1, 1960, and January 6, 2020. Inclusion criteria were met when articles assessed brain changes, neurocognition, functioning, inflammation, oxidative stress, and neurotrophins in patients with PTSD. Narrative review articles, case reports, and preclinical studies were excluded. RESULTS: A total of 965 abstracts were identified and 15 articles were included in our systematic review. It seems that for a subset of patients whose symptoms worsen or are maintained at a high intensity there is a progressive change in the frontal lobe, especially the prefrontal cortex, and worsening of both neurocognition (verbal memory and facial recognition) and functioning (physical, psychological, social and environmental). CONCLUSION: Although current findings associate progressive reduction in frontal lobe size with neurocognitive impairment, further research is needed to characterize PTSD as a neuroprogressive disorder.

Chronic BDNF simultaneously inhibits and unmasks superficial dorsal horn neuronal activity.

Brain-derived neurotrophic factor (BDNF) is critically involved in the pathophysiology of chronic pain. However, the mechanisms of BDNF action on specific neuronal populations in the spinal superficial dorsal horn (SDH) requires further study. We used chronic BDNF treatment (200 ng/ml, 5-6 days) of defined-medium, serum-free spinal organotypic cultures to study intracellular calcium ([Ca2+]i) fluctuations. A detailed quantitative analysis of these fluctuations using the Frequency-independent biological signal identification (FIBSI) program revealed that BDNF simultaneously depressed activity in some SDH neurons while it unmasked a particular subpopulation of 'silent' neurons causing them to become spontaneously active. Blockade of gap junctions disinhibited a subpopulation of SDH neurons and reduced BDNF-induced synchrony in BDNF-treated cultures. BDNF reduced neuronal excitability assessed by measuring spontaneous excitatory postsynaptic currents. This was similar to the depressive effect of BDNF on the [Ca2+]i fluctuations. This study reveals novel regulatory mechanisms of SDH neuronal excitability in response to BDNF.

Paraventricular hypothalamus mediates diurnal rhythm of metabolism.

Defective rhythmic metabolism is associated with high-fat high-caloric diet (HFD) feeding, ageing and obesity; however, the neural basis underlying HFD effects on diurnal metabolism remains elusive. Here we show that deletion of BMAL1, a core clock gene, in paraventricular hypothalamic (PVH) neurons reduces diurnal rhythmicity in metabolism, causes obesity and diminishes PVH neuron activation in response to fast-refeeding. Animal models mimicking deficiency in PVH neuron responsiveness, achieved through clamping PVH neuron activity at high or low levels, both show obesity and reduced diurnal rhythmicity in metabolism. Interestingly, the PVH exhibits BMAL1-controlled rhythmic expression of GABA-A receptor γ2 subunit, and dampening rhythmicity of GABAergic input to the PVH reduces diurnal rhythmicity in metabolism and causes obesity. Finally, BMAL1 deletion blunts PVH neuron responses to external stressors, an effect mimicked by HFD feeding. Thus, BMAL1-driven PVH neuron responsiveness in dynamic activity changes involving rhythmic GABAergic neurotransmission mediates diurnal rhythmicity in metabolism and is implicated in diet-induced obesity.

Disrupted hypothalamic CRH neuron responsiveness contributes to diet-induced obesity.

The current obesity epidemic mainly results from high-fat high-caloric diet (HFD) feeding and may also be contributed by chronic stress; however, the neural basis underlying stress-related diet-induced obesity remains unknown. Corticotropin-releasing hormone (CRH) neurons in the paraventricular hypothalamus (PVH), a known body weight-regulating region, represent one key group of stress-responsive neurons. Here, we found that HFD feeding blunted PVH CRH neuron response to nutritional challenges as well as stress stimuli and dexamethesone, which normally produce rapid activation and inhibition on these neurons, respectively. We generated mouse models with the activity of these neurons clamped at high or low levels, both of which showed HFD-mimicking, blunted PVH CRH neuron responsiveness. Strikingly, both models developed rapid HFD-induced obesity, associated with HFD-mimicking, reduced diurnal rhythmicity in feeding and energy expenditure. Thus, blunted responsiveness of PVH CRH neurons, but not their absolute activity levels, underlies HFD-induced obesity and may also contribute to stress-induced obesity.

Neuregulin 3 rs10748842 polymorphism contributes to the effect of body mass index on cognitive impairment in patients with schizophrenia.

There is evidence that obesity or higher body mass index is correlated with cognitive impairment in schizophrenia. Recent studies have demonstrated that genetic risk factors, such as the NRG3, are correlated with both elevated BMI and reduced cognitive function. In present study, we aimed to determine whether possession of the NRG3 rs10748842 influences the correlation between elevated BMI and reduced cognitive ability in schizophrenia. To our knowledge, this has never been examined before. A total of 625 inpatients with schizophrenia and 400 controls were recruited. The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) was performed to assess cognitive function. We used multiple analysis of covariance (MANCOVA), analyses of covariance (ANCOVA), Pearson correlations, partial correlations, and multivariate regression analysis to test the influence of NRG3 rs10748842 on the aforementioned variables. All RBANS five sub-scores and total score were lower in patients than those in controls (all p < 0.001). Patients carrying NRG3 rs10748842 TC + CC heterozygous genotype had lower attention score compared to TT homozygous genotype (adjusted F = 4.77, p = 0.029). BMI was positively associated with language score in patients (ß = 0.387, t = 2.59, p = 0.01). Interestingly, we further found positive association between BMI and language score in TT carriers (partial correlations: r = 0.13, adjusted p = 0.004; multivariate regression: ß = 0.42, t = 2.66, p = 0.008), but not in CT + CC carrier (p > 0.05). Our study demonstrated that NRG3 rs10748842 was associated with cognitive impairments, especially attention performance in schizophrenia. Moreover, NRG3 rs10748842 altered the effect of BMI on cognitive impairments as measured by the RBANS language score in chronic patients with schizophrenia.

The prevalence, risk factors and clinical correlates of diabetes mellitus in Chinese patients with schizophrenia.

Diabetes is one of the most common comorbid diseases in patients with schizophrenia. The present study examined the prevalence of diabetes and its clinical correlates in a large sample of Chinese patients with schizophrenia, which has not been examined systemically. In this cross-sectional study, a total of 1189 patients (males/females = 938/251; average age: 48.51 ± 10.09 years) were recruited. Fasting blood samples were collected to diagnose diabetes. Psychiatric symptoms were measured with the Positive and Negative Syndrome Scale (PANSS). The prevalence of diabetes was 12.53% with a significant gender difference (males: 10.87% versus females: 18.73%). Compared to patients without diabetes, those with diabetes were older, had a later age of onset, had a higher BMI, had higher positive symptom scores and had higher level of metabolic indices, including triglyceride, cholesterol and HDL cholesterol. After stepwise binary logistic regression analysis, age, BMI, and triglyceride level remained significantly associated with diabetes. This study suggests that diabetes occur with high prevalence in Chinese schizophrenia patients. In addition, age, BMI, and triglyceride level possibly are useful markers predicting an increased risk for diabetes.

Risk factors for suicidality in patients with panic disorder: A systematic review and meta-analysis.

BACKGROUND: Subjects with panic disorder are nearly 4 times as likely to attempt suicide as compared to subjects without this condition. METHODS: We searched the literature from Jan 1, 1960 to May, 4, 2019. Articles that reported a dichotomous sample of patients with panic disorder with and without suicidal behavior were included. OUTCOMES: Twelve studies with 1958 participants were included. Comorbid depression (k = 3, ES = 4.47 [2.63; 7.60]), depressive symptoms (k = 2, ES = 1.98 [1.26; 3.11]), older age (k = 3, ES = 1.66 [1.32; 2.10]), younger age of panic disorder onset (k = 2, ES = 0.65 [0.45; 0.94]), and history of alcohol dependence (k = 2, ES = 8.70 [1.20; 63.04]) were associated with suicide attempt in panic disorder. Depressive symptoms (k = 2, ES = 2.29 (1.60; 3.37]), anxiety symptoms (k = 2, ES = 1.90 [1.33; 2.69]), longer illness duration (k = 2, ES = 3.31 [1.90; 5.74]), comorbid depressive disorder (k = 4, ES = 3.88 [2.03; 7.41]), agoraphobia (k = 2, ES = 4.60 [1.47; 14.42]) and younger age of onset (k = 2, ES = 0.60 [0.38; 0.96]) were associated with suicidal ideation in panic disorder. INTERPRETATION: Our findings provide a framework for the development of suicide prevention strategies in this population.

Identification of a neurocircuit underlying regulation of feeding by stress-related emotional responses.

Feeding is known to be profoundly affected by stress-related emotional states and eating disorders are comorbid with psychiatric symptoms and altered emotional responses. The neural basis underlying feeding regulation by stress-related emotional changes is poorly understood. Here, we identify a novel projection from the paraventricular hypothalamus (PVH) to the ventral lateral septum (LSv) that shows a scalable regulation on feeding and behavioral changes related to emotion. Weak photostimulation of glutamatergic PVH→LSv terminals elicits stress-related self-grooming and strong photostimulation causes fear-related escape jumping associated with respective weak and strong inhibition on feeding. In contrast, inhibition of glutamatergic inputs to LSv increases feeding with signs of reduced anxiety. LSv-projecting neurons are concentrated in rostral PVH. LSv and LSv-projecting PVH neurons are activated by stressors in vivo, whereas feeding bouts were associated with reduced activity of these neurons. Thus, PVH→LSv neurotransmission underlies dynamic feeding by orchestrating emotional states, providing a novel neural circuit substrate underlying comorbidity between eating abnormalities and psychiatric disorders.

Defensive Behaviors Driven by a Hypothalamic-Ventral Midbrain Circuit.

The paraventricular hypothalamus (PVH) regulates stress, feeding behaviors and other homeostatic processes, but whether PVH also drives defensive states remains unknown. Here we showed that photostimulation of PVH neurons in mice elicited escape jumping, a typical defensive behavior. We mapped PVH outputs that densely terminate in the ventral midbrain (vMB) area, and found that activation of the PVH→vMB circuit produced profound defensive behavioral changes, including escape jumping, hiding, hyperlocomotion, and learned aversion. Electrophysiological recordings showed excitatory postsynaptic input onto vMB neurons via PVH fiber activation, and in vivo studies demonstrated that glutamate transmission from PVH→vMB was required for the evoked behavioral responses. Photostimulation of PVH→vMB fibers induced cFos expression mainly in non-dopaminergic neurons. Using a dual optogenetic-chemogenetic strategy, we further revealed that escape jumping and hiding were partially contributed by the activation of midbrain glutamatergic neurons. Taken together, our work unveils a hypothalamic-vMB circuit that encodes defensive properties, which may be implicated in stress-induced defensive responses.

Association of Brain-Derived Neurotrophic Factor With Cognitive Function: An Investigation of Sex Differences in Patients With Type 2 Diabetes.

OBJECTIVE: Although a reduction in brain-derived neurotrophic factor (BDNF) has been implicated as a cause of cognitive impairment in type 2 diabetes mellitus (T2DM), the role of sex in moderating this effect has not been explored. METHODS: We compared the difference in serum BDNF and performance on the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) between 96 men and 134 women with T2DM. We compared this with the difference in serum BDNF and performance in the control group (104 men, 144 women). RESULTS: Patients with T2DM performed worse on most RBANS indices (η = 0.372, all p < .05); within T2DM patients, men performed worse than women on the delayed memory score (74.1 (12.1) versus 79.9 (11.5), p = .002) and on the total score (71.4 (11.5) versus 76.5 (10.8), p = .025). Serum BDNF was lower in patients with T2DM versus controls (7.5 (2.7) ng/ml versus 11.5 (2.7) ng/ml, p < .001), and in men compared with women (6.9 (2.4) versus 7.9 (2.8), p = .024). Serum BDNF levels positively correlated with delayed memory score in patients with T2DM (ß = 0.19, p = .007). However, this association was only observed in women, not in men (pinteraction = 0.04). Among healthy controls, no sex differences were noted in either RBANS or BDNF levels (η = 0.04, Cohen's d < 0.163, all p > .05). CONCLUSIONS: Our results show sex differences in poorer cognitive performance, lower BDNF concentration, and their relationship in T2DM patients, suggesting that female sex may be a protective factor for cognitive decline in T2DM patients. However, the findings should be regarded as preliminary because of the cross-sectional design and chronicity of the diabetes.

A lateral hypothalamus to basal forebrain neurocircuit promotes feeding by suppressing responses to anxiogenic environmental cues.

Animals must consider competing information before deciding to eat: internal signals indicating the desirability of food and external signals indicating the risk involved in eating within a particular environment. The behaviors driven by the former are manifestations of hunger, and the latter, anxiety. The connection between pathologic anxiety and reduced eating in conditions like typical depression and anorexia is well known. Conversely, anti-anxiety drugs such as benzodiazepines increase appetite. Here, we show that GABAergic neurons in the diagonal band of Broca (DBBGABA) are responsive to indications of risk and receive monosynaptic inhibitory input from lateral hypothalamus GABAergic neurons (LHGABA). Activation of this circuit reduces anxiety and causes indiscriminate feeding. We also found that diazepam rapidly reduces DBBGABA activity while inducing indiscriminate feeding. Our study reveals that the LHGABA→DBBGABA neurocircuit overrides anxiogenic environmental cues to allow feeding and that this pathway may underlie the link between eating and anxiety-related disorders.

Psychological distress in cancer patients in a large Chinese cross-sectional study.

BACKGROUND: Although psychological distress is common among patients with chronic diseases, the degree of risk for developing psychological distress is not well-established. Our aim with this study is to determine the odds ratio for psychological distress in patients with cancer as compared to either 1) patients with chronic disease patients without cancer, or 2) healthy controls in a large representative sample of Chinese population. METHODS: Using a multistage, stratified cluster sampling method, 21,101 subjects 18-79 years old were interviewed face-to-face in Jilin province, China. Their psychological status was assessed with the 12-item General Health Questionnaire (GHQ-12). A total score of ≥4 was used as the threshold for determining psychological distress. RESULTS: The prevalence of psychological distress was 14.08% across the entire sample: 10.63% in healthy controls; 14.81% in patients with chronic diseases; and 20% in patients with cancer. Multiple logistic regression analysis indicated that, as compared to the health controls, both cancer (OR = 1.609, 95%CI = 1.245-2.081) and chronic disease patients (OR = 1.330, 95%CI = 1.189-1.478) were more likely to suffer from psychological distress. Moreover, cancer patients had a higher risk of psychological distress than patients with chronic diseases (OR = 1.295, 95%CI = 1.049-1.600; p = 0.016). In addition, the cancer group (2.68 ±â€¯0.114) demonstrated a higher GHQ score than the patients with chronic diseases (2.30 ±â€¯0.017) and healthy controls (1.98 ±â€¯0.029) (both p < 0.001). CONCLUSION: Our results showed both a higher rate and greater degree of psychological distress in patients with cancer. This suggests a need for better psychological management in cancer patients to help alleviate their distress.

Obesity, altered oxidative stress, and clinical correlates in chronic schizophrenia patients.

Antipsychotic pharmacotherapy is strongly obesogenic and is associated with increased oxidative stress in patients with schizophrenia. However, whether these changes reflect psychopathology, antipsychotic efficacy, or some other factor is not known. Our study aims to investigate the degree of oxidative stress in different BMI categories and to identify clinical symptomatology that may be paired with increased oxidative stress in a schizophrenia population. To this end, we performed a cross-sectional study and recruited 89 long-term inpatients with schizophrenia and collected the following variables: plasma malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), routine biochemical analysis, and psychopathology through the Positive and Negative Syndrome Scale (PANSS). The results indicate that the levels of the lipid peroxidation product, MDA, were significantly higher in the high BMI group than the low (normal) BMI group. As expected, high BMI was associated with an atherogenic lipid profile; however, it was also associated with fewer psychopathological symptoms. Multiple regression analysis found that MDA levels, the PANSS general psychopathology subscore, and triglyceride levels (all p < 0.05) were independent contributors to the BMI in patients. These results suggested that oxidative stress may play an important role in antipsychotic-induced weight gain. Further investigations using the longitudinal design in first-episode schizophrenia patients are needed to explore the beneficial effect of antioxidants on the abnormal lipid metabolism mediated by antipsychotic treatment.

Prevalence and Clinical Correlates of and Cognitive Function at the Time of Suicide Attempts in First-Episode and Drug-Naive Patients With Schizophrenia.

BACKGROUND: It is well established that patients with chronic schizophrenia have a substantially higher rate of attempted and completed suicide than the general population. However, the actual prevalence of suicide attempts at first-episode psychosis is relatively unknown. Previous studies showed that suicidal schizophrenia patients demonstrate higher cognitive function than nonsuicidal patients, though with inconsistent results. The aims of the study were to examine the prevalence of suicide attempts and the association of this prevalence with demographic and clinical variables and cognitive function in Chinese first-episode, drug-naive (FEDN) schizophrenia patients using a cross-sectional and case-control design. METHOD: A total of 357 FEDN inpatients meeting DSM-IV criteria for schizophrenia and 380 healthy controls were enrolled and completed a detailed in-house questionnaire. The suicide attempt data were collected from medical records and interviews with the patients and their family members. The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) was administered to measure cognition in the 28 patients with and 95 patients without a history of suicide attempt and 151 healthy controls. Also, patients were rated on the Positive and Negative Syndrome Scale (PANSS). This study was conducted from June 2013 to December 2015. RESULTS: A suicide attempt rate of 12.0% was found in inpatients with first-episode schizophrenia. The attempters were more likely to smoke (34.4% vs 17.9%; χ² = 5.49, P = .019) and had lower severity of negative symptoms (F1,354 = 4.12, P = .043) as compared to FEDN patients without a suicide attempt. All 5 RBANS subscales (all P < .001) except for the Visuospatial/Constructional index (P > .05) showed significantly lower cognitive performance for FEDN patients than for healthy controls. Among the FEDN patients, the suicide attempters performed better than nonattempters on attention (F1,121 = 5.12, P = .025), with an effect size of 0.49. The following variables were independently associated with suicide attempt as shown by multivariate regression analysis: PANSS negative symptom subscale score (Wald χ²1 = 7.90 P = .005; adjusted OR = 0.807, 95% CI, 0.696-0.936) and Attention (Wald χ²1 = 4.69, P = .03; adjusted OR = 0.957, 95% CI, 0.918-0.997). CONCLUSIONS: FEDN patients with schizophrenia attempt suicide more often than the general population. The suicidal patients were more likely to smoke, had lower severity of negative symptoms, and showed better attention than nonsuicidal patients.