Mirtazapine in the treatment of essential tremor: an open-label, observer-blind study

Essential tremor (ET) is the most common movement disorder in the adult population. At present ET treatment shows limited efficacy, particularly in patients with severe and disabling symptoms. This study evaluates the clinical efficacy of mirtazapine in an untreated ET patient population

Automatic perimetry abnormalities in Vigabatrin chronically treated epileptic patients

Sixty epileptic patients chronically receiving GVG underwent to automatic perimetry and to flash electroretinogram (ERG) and visual evoked potentials (VEPs). All patients suffered from partial epilepsy. The mean GVG dose was 2887±871 mg/die (ranging from 1000 to 4000). The mean treatment duration was 56.6±43.5 months (ranging from 2 to 182). In 50 patients GVG was associated with other antiepileptic drugs (carbamazepine in 46 of them). One of them complained of visual symptoms. ERG was normal in all the subjects. The VF evaluation was normal in 13 and not reliable in 10 subjects. Thirty-seven subjects showed different kind of VF defects, which were explainable by a retinal/prechiasmatic lesion in 22 of them (17 subjects showed a binasal defect, 5 a concentric costriction). In these patients VEPs were normal in 17 subjects and showed a delayed latency in 4, a reduced amplitude in 1. The VF alterations occurred more frequently in the patients with a treatment duration longer than 18 months. Our data show that asymptomatic VF defects occur frequently in patients with partial epilepsy chronically receiving GVG. The relationship between the occurrence of VF defect and treatment duration suggest that GVG plays a pathophysiological role

Do changes in SSEP amplitude over time predict the outcome of comatose survivors of cardiac arrest?

Aim: To assess if the amplitude of the N20 wave (N20Amp) of somatosensory evoked potentials (SSEPs) changes between 12–24 h and 72 h from the return of spontaneous circulation (ROSC) after cardiac arrest and if an N20Amp decrease predicts poor neurological outcome (CPC 3–5) at six months. Setting: Retrospective analysis of the ProNeCA multicentre prognostication study dataset. (NCT03849911). Methods: In adult comatose cardiac arrest survivors whose SSEPs were recorded at both 12–24 h and 72 h after ROSC, we measured the median N20Amp at each timepoint and the individual change in N20Amp across the two timepoints. We identified their cutoffs for predicting poor outcome with 0% false positive rate (FPR) and compared their sensitivities. Results: We included 236 patients. The median [IQR] N20Amp increased from 1.90 [0.78–4.22] µV to 2.86 [1.52–5.10] µV between 12–24 h and 72 h (p = 0.0019). The N20Amp cutoff for 0% FPR increased from 0.6 µV at 12–24 h to 1.23 µV at 72 h, and its sensitivity increased from 56[48–64]% to 71[63–77]%. Between 12–24 h and 72 h, an N20Amp decrease > 53% predicted poor outcome with 0[0–5]% FPR and 26[19–35]% sensitivity. Its combination with an N20Amp < 1.23 µV at 72 h increased sensitivity by 1% to 72[64–79]%. Conclusion: In comatose cardiac arrest survivors, the median N20Amp and its cutoff for predicting poor neurological outcome increase between 12–24 and 72 h after ROSC. An N20Amp decrease greater than 53% between these two timepoints predicts poor outcome with 0% FPR, confirming the unfavourable prognostic signal of a low N20Amp at 72 h

Neurophysiology for predicting good and poor neurological outcome at 12 and 72\u2009h after cardiac arrest: The ProNeCA multicentre prospective study

Aims: To assess the accuracy of electroencephalogram (EEG) and somatosensory evoked potentials (SEPs) recorded at 12 and 72 h from resuscitation for predicting six-months neurological outcome in patients who are comatose after cardiac arrest. Methods: Prospective multicentre prognostication study. EEG was classified according to the American Clinical Neurophysiology Society terminology. SEPs were graded according to the presence and amplitude of their cortical responses. Neurological outcome was defined as good (cerebral performance categories [CPC] 1\u20133) vs. poor (CPC 4\u20135). None of the patients underwent withdrawal of life-sustaining treatment. Results: A total of 351 patients were included, of whom 134 (38%) had good neurological outcome. At 12 h, a continuous, nearly continuous and low-voltage EEG pattern predicted good neurological outcome with 71[61\u201380]% sensitivity, while an isoelectric EEG and a bilaterally absent/absent-pathological amplitude (AA/AP) cortical SEP pattern predicted poor neurological outcome with 14[8\u201321]% and 59[50\u201368]% sensitivity, respectively. Specificity was 100[97\u2013100]% for all predictors. At 72 h, both an isoelectric, suppression or burst-suppression pattern on EEG and an AA/AP SEP pattern predicted poor outcome with 100[97\u2013100]% specificity. Their sensitivities were 63[55\u201370]% and 66[58\u201374]%, respectively. When EEG and SEPs were combined, sensitivity for poor outcome prediction increased to 79%. Conclusions: In comatose resuscitated patients, EEG and SEPs predicted good and poor neurological outcome respectively, with 100% specificity as early as 12 h after cardiac arrest. At 72 h after arrest, unfavourable EEG and SEP patterns predicted poor neurological outcome with 100% specificity and high sensitivity, which further increased after their combination

Family study of epilepsy in first degree relatives: Data from the Italian Episcreen study

Objective: To evaluate the family history of epilepsy in first degree relatives of probands with epilepsy. Methods: A sample of 10787 patients with epilepsy with complete information about first degree relatives (parents, siblings and offspring) was selected from the database of the Episcreen Project, the largest Italian observational study on epilepsy. Family history was assessed by: (1) prevalence estimates of epilepsy among proband's relatives, (2) modified cumulative risks (MCR), adjusted using proband's age as censoring time in life tables, (3) standardised morbidity ratios (SMR), using a sub-group of symptomatic epilepsies as control group. Results: Patients (9.1%) had a family history of epilepsy. The overall prevalence of epilepsy among first degree relatives was 2.6%. Idiopathic generalised epilepsies had the highest prevalence (5.3%). Cryptogenetic epilepsies had a lower prevalence (2.1%) than idiopathic epilepsies, but higher then symptomatic epilepsies (1.5%), both in generalised and focal forms (3.8% vs. 2.0% and 1.8% vs. 1.3%). A similar tendency was detected using MCR and SMR, with the higher values of risks/ratios for idiopathic and generalised epilepsies. Probands with idiopathic generalised epilepsies were highly concordant with respect to their relatives' type of epilepsy. Considering other strata factors, risks were higher in proband's epilepsies with an onset less then 14 years of age, while sex played no definite role in differentiating the family history. Conclusions: The Episcreen model permits a variety of stratification factors to measure family risk, including age at onset, epilepsy localisation and aetiology with a large sample of more than 10 000 probands and 1065/40 544 relatives affected and classified. © 2002 BEA Trading Ltd. Published by Elsevier Science Ltd. All rights reserved