ABSTRACT
BACKGROUND: Acute symptomatic epileptic seizures are frequently seen in neurocritical care. To prevent subsequent unprovoked seizures, long-term treatments with antiseizure medications are often initiated although supporting evidence is lacking. This study aimed at prospectively assessing the risk of unprovoked seizure relapse with respect to the use of antiseizure medications. It was hypothesized that after a first acute symptomatic seizure of structural etiology, the cumulative 12-month risk of unprovoked seizure relapse is ≤ 25%. METHODS: Inclusion criteria were age ≥ 18 and acute symptomatic first-ever epileptic seizure; patients with status epilepticus were excluded. Using telephone and mail interviews, participants were followed for 12 months after the acute symptomatic first seizure. Primary endpoint was the occurrence and timing of a first unprovoked seizure relapse. In addition, neuro-intensivists in Germany were interviewed about their antiseizure treatment strategies through an anonymous online survey. RESULTS: Eleven of 122 participants with structural etiology had an unprovoked seizure relapse, resulting in a cumulative 12-month risk of 10.7% (95%CI, 4.7%-16.7%). None of 19 participants with a non-structural etiology had a subsequent unprovoked seizure. Compared to structural etiology alone, combined infectious and structural etiology was independently associated with unprovoked seizure relapse (OR 11.1; 95%CI, 1.8-69.7). Median duration of antiseizure treatment was 3.4 months (IQR 0-9.3). Seven out of 11 participants had their unprovoked seizure relapse while taking antiseizure medication; longer treatment durations were not associated with decreased risk of unprovoked seizure relapse. Following the non-representative online survey, most neuro-intensivists consider 3 months or less of antiseizure medication to be adequate. CONCLUSIONS: Even in case of structural etiology, acute symptomatic seizures bear a low risk of subsequent unprovoked seizures. There is still no evidence favoring long-term treatments with antiseizure medications. Hence, individual constellations with an increased risk of unprovoked seizure relapse should be identified, such as central nervous system infections causing structural brain damage. However, in the absence of high-risk features, antiseizure medications should be discontinued early to avoid overtreatment.
ABSTRACT
The presented prospective study investigated whether structural brain damage, measured with the Fazekas score, could predict hearing rehabilitation outcomes with cochlear implantation (CI). With a follow-up period of 24 months, this study included 49 bilaterally, postlingually hearing impaired CI candidates for unilateral CI (67.3 ± 8.7 years; 20 men, 29 women) older than 50 at the time of implantation. The differences in the predictive value between two age groups, 50-70 year-olds (mid-age; n = 26) and over 70-year-olds (elderly; n = 23), were analyzed. The patients were evaluated using speech perception (SP) measured in quiet (Freiburg monosyllabic test; FMT) and noise (Oldenburg sentence test; OLSA). The subjective hearing ability was assessed using Oldenburg inventory (OI). The Fazekas PVWM score predicted postoperative speech perception two years after CI in the mid-age population. The periventricular white matter lesions (PVWM) could explain 27.4% of the speech perception (FMT) variance. Our findings support the hypothesis about the influence of pre-existing WMLs on CI outcome. We recommend the evaluation of Fazekas score as a predictive factor for post-implantation hearing ability.
ABSTRACT
The binding properties of neural cell adhesion molecule are modulated by a polysialic acid moiety. This plays an important role in the migration of adult born neuroblasts from their area of origin, the subventricular zone, towards the olfactory bulb. Polysialisation increases the migration speed of the cells and helps to prevent the neuroblasts from leaving their migration route, the rostral migratory stream. Here, we evaluated the potential of intraventricular application of endoneuraminidase-N, an enzyme that specifically cleaves polysialic acid from neural cell adhesion molecule, in a rat model for structural prefrontal cortex damage. As expected, endoneuraminidase-N caused the rostral migratory stream to become wider, with a less uniform cellular orientation. Furthermore, endoneuraminidase-N treatment caused the neuroblasts to leave the rostral migratory stream and migrate towards the lesioned tissue. Despite the neuroblasts not being differentiated into neurons after a survival time of three weeks, this technique provides a solid animal model for future work on the migration and differentiation of relocated neuroblasts and might provide a basis for a future endogenous stem cell-based therapy for structural brain damage. The experiments were approved by the local animal care committee (522-27-11/02-00, 115; Senatorin für Wissenschaft, Gesundheit und Verbraucherschutz, Bremen, Germany) on February 10, 2016.
ABSTRACT
What is the long-term trajectory of semantic memory deficits in patients who have suffered structural brain damage? Memory is, per definition, a changing faculty. The traditional view is that after an initial recovery period, the mature human brain has little capacity to repair or reorganize. More recently, it has been suggested that the central nervous system may be more plastic with the ability to change in neural structure, connectivity, and function. The latter observations are, however, largely based on normal learning in healthy subjects. Here, we report a patient who suffered bilateral ventro-medial damage after presumed herpes encephalitis in 1971. He was seen regularly in the eighties, and we recently had the opportunity to re-assess his semantic memory deficits. On semantic category fluency, he showed a very clear category-specific deficit performing better that control data on non-living categories and significantly worse on living items. Recent testing showed that his impairments have remained unchanged for more than 40 years. We suggest cautiousness when extrapolating the concept of brain plasticity, as observed during normal learning, to plasticity in the context of structural brain damage.