BackgroundLhermitte–Duclos disease (LDD) is a rare cerebellar lesion characterized by a hamartomatous lesion in the posterior fossa. Mainly diagnosed by MRI, the clinical presentation is usually made of neurological symptoms.Case presentationWe present here a rare case of a woman who developed depressive symptoms that inaugurated the clinical presentation of LDD.ConclusionPsychiatric symptoms may occur in all brain lesions, delaying the diagnosis and causing therapeutic escalation. More attention should be given by practitioners to psychiatric aspects of LDD.

Introduction and aimEating disorders (EDs) are complex, multifactorial diseases linked to biological, developmental, psychological, and sociocultural factors. Medical students are among subjects at high risk of EDs. The aim of the present investigation was to evaluate EDs among 710 Moroccan medical students with a focus on cognition and behavior related to EDs.MethodsSociodemographic, economic, and clinical data were collected. Validated questionnaires, such as the SCOFF (Sick, Control, One Stone, Fat, Food) questionnaire and the Eating Disorder Inventory 2 (EDI2), were administered.ResultsThe male:female ratio was 0.53, mean age was 21±2 years, 11.1% of participants were underweight, 13.4% were overweight, and 1.8% were obese. A middle socioeconomic level was found in 84.9% of cases. The prevalence of EDs in students was 32.8% (37.6% among females and 23.7% among males) and that of weight-control behaviors 18.5%. Increased body-mass index values were significantly associated with dieting (P<0.001), fasting (P=0.044), and the use of appetite suppressants (P=0.037).ConclusionIt appears that the impact of EDs is high, affecting a third of medical students, with significant use of harmful weight-control behaviors. We also found that dimensions of bulimia, perfectionism, body dissatisfaction, and ineffectiveness, parts of the core of EDs, were found in future medical practitioners.

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O UR PATIENT, A 40-year-old woman with bipolar disorder, was admitted to our unit complaining of dizziness and diplopia for the last 2 days. The patient had been undergoing stable carbamazepine (CBZ) treatment (600 mg/day) for 10 years. CBZ levels were regularly measured and they were within therapeutic range (7.3 mg/mL, 16 days before admission). Four days before the patient's admission she was prescribed fluconazole (150 mg/day) for a fungal cervical infection. After 2 days of antimycotic treatment, the patient noted double vision, nausea, vomiting and dizziness, which gradually worsened. Neurological examination during her admission revealed a symmetrical, horizontal, high-frequency, gaze-evoked nystagmus. In the examination of the eye smooth pursuit movements, many saccades were noted. All the other neurological examinations, including tests for ataxia or certain eye muscle palsy, were normal. In addition, full blood tests and a brain computed tomography scan were obtained, without any pathological findings. However a toxic, nearly twofold increase of the plasma CBZ levels was noted (plasma CBZ levels were 18 mg/dL, with a therapeutic range 5-10 mg/dL in our laboratory). A day after fluconazole withdrawal, the patient reported that all her symptoms disappeared and the neurological examination was perfectly normal. CBZ plasma levels returned to normal limits (9 mg/mL) 5 days after the antimycotic treatment cessation. All plasma concentrations of CBZ were measured in a morning blood sample, obtained prior to the drug administration.The aforementioned adverse effects were most likely associated with CBZ-fluconazole co-administration. Some first reports of potential stupor 1 or asymptomatic transient increase of CBZ plasma levels 2 after fluconazole and CBZ co-administration have implied a toxicity of this drug combination. The originality of our report is that the symptoms emerged in a patient treated with CBZ as a mood stabilizer for bipolar disorder, in a much lower dosage (600 mg/day) compared with Ulivelli's case report (1200 mg/day). 3The explanation of the above toxic effects could be the metabolism interaction of the two drugs. CBZ is primarily metabolized by the cytochrome P450 3A4 isoenzyme.4,5 CBZ is involved in pharmacokinetic interactions of clinical significance due to its co-administration with other drugs known to inhibit or induce CYP3A4 or other relative isoforms.4 Fluconazole is excreted by the kidney, but has been noted to inhibit CYP3A4 and P2C9 isoenzymes. However, clinically significant drug interactions may occur only in certain patients, 6 depending on several individual characteristics, such as genetics, health, nutrition, age, and concomitant drug administration.Our observation suggests that the interaction between fluconazole and CBZ requires further investigation and clinical attention. The incidence of fungal infections is high in everyday clinical practice. Thus both neurologists and psychiatrists, who use CBZ for its multiple indications, should be aware of toxic effects that may...

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by multisystemic involvement and diverse manifestations. Neuropsychiatric systemic lupus erythematosus (NPSLE) is a complex neurological disorder characterized by neuropsychological dysfunction. NPSLE is associated with increased morbidity and mortality. In 1999, the American College of Rheumatology developed 19 discrete neuropsychiatric syndromes that comprised NPSLE. Nervous system disease in systemic lupus erythematosus is manifested by a wide variety of clinical manifestations. The pathogenesis of NPSLE is due to autoantibodies, neuronal and non neuronal antigens and the generation of proinflammatory cytokines and mediators. Anatomopathological lesions are attributed to in situ thrombosis, edema, hemorrhage, vasculitis, atherosclerosis or atheroembolism. The diagnosis of NPSLE remains largely one of exclusion and is approached by clinical evaluation, and supported when necessary by autoantibody profiles, diagnostic imaging, electrophysiologic studies and objective assessment of cognitive performance. Brain MRI abnormalities in NPSLE might show small punctate focal lesions in white matter being the most common MRI finding, followed by cortical atrophy, ventricular dilation, cerebral edema, diffuse white matter abnormalities, focal atrophy, cerebral infarction, acute leukoencephalopathy and intracranial hemorrhage. The treatment is based on the use of symptomatic therapies, immunosuppressives and non-pharmacologic interventions. This review paper was designed to understand the pathophysiology for better management of NPSLE.