Polymorphisms of the vitamin D receptor (VDR) gene have been linked to both multiple sclerosis (MS) and osteoporosis. We examined the frequency of the Taq-I and Bsm-I polymorphisms of the vitamin D receptor (VDR) gene in 69 patients with MS and 81 age and sex-matched healthy individuals. Genotyping of Taq-I (rs731236) and Bsm-I (rs1544410) was performed using TaqMan® SNP Genotyping Assay. All patients and controls had determination of body mass index (BMI), bone mineral density (BMD) and smoking history.

Summary: We retrospectively assessed all patients in a large cohort of patients with epilepsy surgery at the National Hospital for Neurology and Neurosurgery (NHNN) over 12 years, to identify patients with postoperative psychogenic nonepileptic attacks (PNEA). Twenty‐nine patients (23 women) were identified of a total of 790 patients, a frequency of 3.7%. Female gender and presurgical psychiatric diagnosis, other than psychosis, were significant risk factors for PNEA development. In female patients with a preoperative psychiatric diagnosis the chance of developing PNEA after epilepsy surgery was 8.5%. PNEA developed between 2 weeks and 10 years after epilepsy surgery, independently of outcome of epileptic seizures. In most cases, PNEA differed from the present or past epileptic seizures, and motor symptoms were the most common manifestations. Seizures after epilepsy surgery should be carefully evaluated. Physicians should consider the possibility of PNEA, especially in female patients with preoperative psychiatric comorbidity developing “atypical” seizures with motor manifestations postoperatively, even many years after epilepsy surgery.

Mirtazapine is an antidepressant blocking presynaptic alpha2-adrenergic receptors and an antagonist of 5-hydroxytryptamine 2A/2C, 5-hydroxytryptamine 3, and histaminergic (H) postsynaptic receptor. Acute dystonia restless legs syndrome (RLS) and manic syndromes are adverse effects of mirtazapine, whereas only few cases of acute akathisia, after the first doses of mirtazapine, are referred. Instead, mirtazapine is used to treat akathisia probably because of its antagonistic property at H1 postsynaptic receptors and dopaminergic action in the frontal cortex. A 72-year-old woman with depression, on mirtazapine treatment for almost 20 years, was admitted to an outpatient neurology clinic, with 1-week history of 3-kg weight loss and progressive intense "inner restlessness," constant movements of the legs and feet, remarkable distress, insomnia, and pacing up and down. Neurological examination had normal results, no deterioration of the depression was present, a magnetic resonance scan of the brain was unremarkable, and biochemical tests were within reference ranges. The disorder eventually resolved after the permanent withdrawal of the offending medication. After excluding other possible disorders, the diagnosis of severe akathisia, possibly induced by mirtazapine, was made. The reappearance of the symptoms after the patient had been rechallenged with mirtazapine ascertained the diagnosis of akathisia induced by mirtazapine. This report relates akathisia with mirtazapine intake after such a long period of treatment. It illustrates the importance of being alert to any movement disorder emerging in patients treated with mirtazapine, even after many years of treatment.