Effect of meditation on intracerebral EEG in a patient with temporal lobe epilepsy: A case report.

Meditation has been deemed a miracle cure for a wide range of neurological disorders. However, it is unclear whether meditation practice would be beneficial for patients suffering from epilepsy. Here we report on the comparison of the effects of focused-attention meditation and a control task on electroencephalographic (EEG) activity in a patient undergoing stereoencephalographic (SEEG) investigation for drug-resistant epilepsy. The patient routinely practiced focused-attention meditation and reported that she found it beneficial. During the SEEG investigation, intracerebral EEG data were recorded during meditation as well as during mind-wandering task. The EEG data were analyzed for type of electrical activity (labeled) by two expert epileptologists. We found that the proportion of EEG segments containing activity classified as interictal epileptiform discharges (IEDs; abnormal electrical activity that occurs between seizures) increased significantly during meditation practice. Although the finding was surprising, this increase in IEDs may not correlate with an increase in seizure frequency, and the patient might still benefit from practicing meditation. The finding does, however, warrant further studies on the influence of meditation on epileptic activity.

Etiological assessment of status epilepticus.

Status epilepticus (SE) is a potentially serious condition that can affect vital and functional prognosis and requires urgent treatment. Etiology is a determining factor in the patient's functional outcome and in almost half of all cases justifies specific treatment to stop progression. Therefore, identifying and addressing the cause of SE is a key priority in SE management. However, the etiology can be difficult to identify among acute and remote causes, which can also be multiple and interrelated. The most common etiologies are the discontinuation of antiepileptic medication in patients with a prior history of epilepsy, and acute brain aggression in cases of new onset SE (cerebrovascular pathologies are the most common). The list of remaining possible etiologies includes heterogeneous pathological contexts. Refractory SE and especially New-Onset Refractory Status Epilepticus (NORSE) lead to an extension of the etiological assessment in the search for encephalitis of autoimmune or infectious origin in adults and in children, as well as a genetic pathology in children in particular. This is an overview of current knowledge of SE etiologies and a pragmatic approach for carrying out an etiological assessment based on the following steps: - Which etiological orientation is identified according to the field and clinical presentation?; - Which etiologies to look for in an inaugural SE?; - Which first-line assessment should be carried out? The place of the biological, EEG and imaging assessment is discussed; - Which etiologies to look for in case of refractory SE?

[Facial linear scleroderma associated with neurological abnormalities relating to microangiopathy]. / Sclérodermie linéaire de la face associée à des anomalies neurologiques par microangiopathie.

BACKGROUND: Linear scleroderma is a fibrotic disease affecting the skin and sometimes the deeper tissues. We describe a case of scleroderma associated with neurological anomalies not previously reported in the literature. PATIENTS AND METHODS: A 16-year-old male patient presented in 2009 for hemifacial linear scleroderma. Treatment with methotrexate for 14 months resulted in stabilization of the disease. In 2013, we noted worsening of the patient's skin lesions as well as homolateral ptosis. Head MRI revealed unilateral hemispherical signal abnormalities with T2 hypersignal in the basal gangliaand punctate foci of T2* hyposignal corresponding to microbleeds. In 2014 and 2015, the patient presented three brief episodes of right hemicorpus paresthesia (with temporary aphasia followed by headache during the first episode). The head MRI showed worsening of the anomalies, suggesting progressing cerebral microangiopathy. DISCUSSION: Clinicians may not always be familiar with the neurological abnormalities associated with localized facial scleroderma even if such abnormalities are not uncommon (their exact prevalence is unknown). Clinical signs vary but, in most cases, the radiological features are calcifications and hyperintense foci of white matter lesions in T2. As far as we are aware, there have been no reports to date of microbleeding as observed in our patient. The worsening with time of these neurological anomalies of unknown origin does not appear to be correlated with the dermatological lesions. It is important for dermatologists be aware of these complications of facial linear scleroderma.

Bilateral Wada test: amobarbital or propofol?

PURPOSE: The Wada test is still the gold standard procedure to predict language and memory deficits before temporal lobe epilepsy surgery. As amobarbital was no longer available, our aim was to validate propofol as an alternative. METHOD: We retrospectively studied 47 patients who underwent a bilateral intracarotid procedure, performed with amobarbital (18), or propofol (29), between 2000 and 2010 during the preoperative evaluation of temporal lobe epilepsy. RESULTS: The number of patients experiencing an adverse event (mostly transient disturbance of consciousness or benign ocular symptoms) during both injections did not differ significantly between amobarbital and propofol. Hemispheric dominance was successfully determined in 96.5% patients with propofol vs. 94.4% with amobarbital for language, and in 72.4% under propofol vs. 77.7% under amobarbital for memory with no significant difference between groups. CONCLUSION: Propofol can be used for the Wada test with an efficacy and safety comparable to amobarbital.