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Introduction. The management of neuropathic pain remains complex, generally because of the psychiatric comorbidity that is often underdiagnosed. The objectives of our work were to determine the link between depression and the characteristics of NP on the one hand and quality of life on the other hand, in a sample of subjects consulting for neuropathic pain (NP) regardless of etiology. Methods. We conducted a cross-sectional study involving 61 neuropathic pain consulting patients in whom we assessed five parameters, namely, neuropathic pain based on DN4, pain intensity using EVA, anxiety, and depression according to the HADS and quality of life. Results. The study population mean age was 52.71 ± 14.29 years while the sex ratio (m/f) was 0.52. The neuropathic pain’s most common etiologies were postherpetic pain, carpal tunnel syndrome, and diabetic neuropathy. Depression and anxiety prevailed by 65.6% and 73.7%, respectively. The quality of life was impaired with average SF-12 physical and mental scores of 33.76 ± 8.03 and 37.78 ± 11.52, respectively. The overall mean BPI score was 5.53 ± 1.76. Patients with high DN4 scores were significantly more depressed (p=0.025). A significantly positive association was found between the depression score and the pain intensity (p=0.001, r = 0.41). Depressed subjects had a poor quality of life according to SF-12 and BPI. Conclusion. Given the depressive comorbidity impact on the neuropathic pain components as well as the quality of life, screening for this comorbidity should be part of the baseline ND assessment.

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Background Sleep disturbances in schizophrenia are common throughout its course including in the prodrome, and have been mainly attributed to severity of symptoms and antipsychotic use. We aimed to investigate whether early course patients with schizophrenia and young non‐psychotic siblings of patients with schizophrenia also show sleep disturbances and whether sleep correlates with symptoms and functioning. Methods Three study groups, that is, adults newly diagnosed with schizophrenia (n = 54), young non‐psychotic siblings of schizophrenia patients (n = 56) and a sample of healthy controls matched to the patients and siblings (n = 61) were evaluated on Horne and Ostberg Morningness‐Eveningness Questionnaire, Epworth Sleepiness Scale and Pittsburgh Sleep Quality Index. Severity of symptoms and functioning are assessed using the Positive and Negative Syndrome Scale and the Global Assessment of Functioning Scale, respectively. Age, gender, occupation and marital status were regarded as covariates, and differences between the three groups were evaluated using analysis of covariance. Results Early course schizophrenia patients and non‐psychotic siblings of schizophrenia patients showed significantly reduced sleep quality relative to healthy controls (P < .001). Schizophrenia patients had significantly higher daytime sleepiness compared to controls (P < .001). Chronotypes in schizophrenia patients and unaffected siblings did not significantly differ from those of the healthy controls. Conclusions Like chronic medicated schizophrenia patients, early course schizophrenia patients and young non‐psychotic siblings of individuals with schizophrenia have sleep disturbances. These findings indicate that sleep markers can distinguish unaffected siblings of schizophrenia from healthy controls and serve as an endophenotype for schizophrenia.

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Contrary to phenothiazines, butyrophenones are very seldom associated with hepatitis. In particular, the incidence of hepatitis on haloperidol is about 0.002%. Almost all these cases consisted of cholestatic hepatitis. Cytolytic hepatitis induced by haloperidol seems to be exceptional. Objective: To outline the occurrence of haloperidol-induced cytolytic hepatitis. Methods: Case report and review Results: We report the case of a male patient aged 22, with a family history of schizophrenia in two cousins and with a personal history of generalized epilepsy on carbamazepine. The patient was admitted to our department for behavioral disturbances. Psychiatric interview found mystical and grandiosity delusions as well as auditory and visual hallucinations. The patient was started on haloperidol 5mg bid. Routine liver enzymes obtained on day-10 revealed eight-fold elevated transaminases with no associated biological signs of cholestasis. The patient did not report any symptoms suggestive of hepatitis. Serology for viral hepatitis (A, B, and C), EBV and CMV was negative. Hepatic ultrasound examination was normal. Antinuclear, anti-LMK and anti-mitochondrial antibodies were negative. Serum and urine copper levels were normal. The diagnosis of a drug-induced hepatitis was made. Haloperidol was withdrawn and switched to olanzapine. Transaminase levels slowly dropped then normalized within two months, thus consolidating our diagnosis. Conclusions: Cytolytic hepatitis induced by haloperidol is very rare and can be asymptomatic. Routine liver tests when starting antipsychotics are crucially important to diagnose this possibly hazardous side effect.