Implementation of stroke teams and simulation training shortened process times in a regional stroke network-A network-wide prospective trial.

BACKGROUND: To meet the requirements imposed by the time-dependency of acute stroke therapies, it is necessary 1) to initiate structural and cultural changes in the breadth of stroke-ready hospitals and 2) to find new ways to train the personnel treating patients with acute stroke. We aimed to implement and validate a composite intervention of a stroke team algorithm and simulation-based stroke team training as an effective quality initiative in our regional interdisciplinary neurovascular network consisting of 7 stroke units. METHODS: We recorded door-to-needle times of all consecutive stroke patients receiving thrombolysis at seven stroke units for 3 months before and after a 2 month intervention which included setting up a team-based stroke workflow at each stroke unit, a train-the-trainer seminar for stroke team simulation training and a stroke team simulation training session at each hospital as well as a recommendation to take up regular stroke team trainings. RESULTS: The intervention reduced the network-wide median door-to-needle time by 12 minutes from 43,0 (IQR 29,8-60,0, n = 122) to 31,0 (IQR 24,0-42,0, n = 112) minutes (p < 0.001) and substantially increased the share of patients receiving thrombolysis within 30 minutes of hospital arrival from 41.5% to 59.6% (p < 0.001). Stroke team training participants stated a significant increase in knowledge on the topic of acute stroke care and in the perception of patient safety. The overall course concept was regarded as highly useful by most participants from different professional backgrounds. CONCLUSIONS: The composite intervention of a binding team-based algorithm and stroke team simulation training showed to be well-transferable in our regional stroke network. We provide suggestions and materials for similar campaigns in other stroke networks.

Interictal alterations of cytokines and leukocytes in patients with active epilepsy.

BACKGROUND: Involvement of the innate immune system in the pathogenesis of epilepsies has been suggested but possible interactions between the immune system and human epilepsy remain unclear. We analyzed the interictal immuno-phenotype of leukocyte subsets and proinflammatory cytokine profiles in epileptic patients and correlated them with the epilepsy syndrome. METHODS: 101 patients with active focal or generalized epilepsy were prospectively included and compared to 36 healthy controls. Immuno-phenotype of leukocyte subsets and cytokines IL-1ß, IL-6 and tnfα were measured in peripheral blood. Multivariate analyses were performed to test group differences. RESULTS: As compared to controls, the patients showed an elevated percentage of monocytes (18.06±7.08% vs. 12.68±4.55%, p<0.001), NK cells (14.88±7.08% vs. 11.43±5.41%, p=0.019) and IL-6 concentration (3.33±3.11 pg/ml vs. 1.5±1.36 pg/ml, p=0.002). This remained true when focal epilepsies or generalized epilepsies were compared separately to controls but only focal epilepsies showed additionally a decrease in B lymphocyts (8.16±3.76% vs. 11.54±4.2%, p<0.001). Treatment with lamotrigine was associated with a higher percentage of B lymphocytes and valproate with an increased percentage of CD4(+) T lymphocytes. Therapy with levetiracetam showed a trend towards decreased CD8(+) T cell counts. No significant differences were seen between focal and generalized epilepsies and between temporal and extratemporal lobe epilepsies. CONCLUSION: Patients with active epilepsy revealed interictal alterations of the immune system which varied among specific syndromes and were influenced by antiepileptic drug treatment.

Etiology and site of temporal lobe epilepsy influence postictal cytokine release.

Inflammatory mechanisms are involved in the pathogenesis of epilepsy. Vice versa, immune functions are regulated by the brain. We measured postictal changes in serum levels of the immuno-modulating cytokines IL-1beta, IL-6 and TNFalpha in patients with well-defined temporal lobe epilepsy (TLE) and determined modifying factors. Serum levels of IL-1beta, IL-6 and TNFalpha were quantified by ELISA at baseline as well as immediately, 1h and 24h after a complex partial (CPS) or secondary generalized tonic-clonic seizure (GTCS) during video-EEG monitoring in 25 patients suffering from temporal epilepsy. IL-6 increased by 51% immediately after the seizure (p<0.01) and remained elevated for 24h. This increase lacked in patients with hippocampal sclerosis (HS; n=16, mean increase 28%, p>0.5, vs. 112%, p<0.01 in patients without HS). IL-6 levels were higher after right-sided seizures as compared to left-sided seizures 24h after the seizure (8.7pg/mL vs. 3.4pg/mL, p<0.05). In patients taking valproate (VPA, n=9), the levels of IL-1beta were higher as compared to patients not treated with VPA. The results suggest a relationship between the cytokine system and characteristics of TLE such as side and pathology.

NK and CD4+ T cell changes in blood after seizures in temporal lobe epilepsy.

UNLABELLED: Immunological phenomena may affect the course of focal epilepsy. We analyzed prospectively the pre- and postictal distribution of leukocyte subsets in epileptic patients. METHODS: Twenty-two patients (age 36.6+/-10.8 years, 50% men) with temporal lobe epilepsy were included. Distribution of leukocyte subsets and serum levels of epinephrine were measured in peripheral blood immediately and 24 h after seizures and compared to baseline values. RESULTS: In the immediate postictal state (10+/-6 min), we observed a significant relative increase of total leukocytes (42%, p=0.0004), neutrophil leukocytes (55%, p=0.0007), total lymphocytes (45%, p=0.0019), natural killer (NK) cells (104%, p=0.0017), and epinephrine (454%, p=0.0014). CD4(+) T cells decreased by 13% (p=0.0113). These postictal changes remained significant considering only complex partial seizures (n=17). The alterations were more pronounced in patients with hippocampal sclerosis. Treatment with valproic acid (VPA) was accompanied by a greater postictal decrease of CD4(+) T cells (25% compared to 5% in patients without VPA, p=0.041) while treatment with levetiracetam (LEV) correlated with a low postictal increase of NK-like T cells (4% versus 41%, p=0.016). Twenty-four hours after the seizures the alterations had resolved. CONCLUSION: Profound postictal changes in the immune cell composition of the peripheral blood may have been mediated by epinephrine release. The greater immune response in patients with mesial temporal lobe epilepsy due to hippocampal sclerosis may reflect a close relationship between mesial temporal structures and the sympathetic nerve system. VPA and LEV may have an impact on seizure induced immunological changes.

Status epilepticus and seizures induced by iopamidol myelography.

PURPOSE: To report that iopamidol myelography can induce status epilepticus (SE) in patients carrying the diagnosis of symptomatic epilepsy and to estimate the incidence of seizures in patients undergoing iopamidol myelography. METHODS: We retrospectively identified all patients with seizures/SE associated with 1350 iopamidol myelographies during the last 5 years at our institution. The impact of cervical versus lumbar myelography was analysed. RESULTS: Induced by iopamidol myelography two non-epileptic patients suffered from first generalised tonic-clonic seizures and a 67-year-old women with symptomatic epilepsy after a remote ischemic stroke developed a generalised tonic-clonic seizure evolving into a dialeptic and right nystagmus SE (i.e. complex focal status) of 5-hour duration. The incidence of seizures in non-epileptic patients was 0.15%. The incidence of seizure induction for lumbar myelography was lower than for myelographies that included the cervical subarachnoid space. CONCLUSIONS: Iopamidol myelography (especially if cervical) is associated with a risk of seizures in non-epileptic individuals and can induce SE in patients with epilepsy. Patients should be informed about the risk of seizure induction.