Purpose: To determine the effectiveness of two dissemination and implementation strategies to implement a national guideline for epilepsy management in primary care settings.Methods: Three-arm cluster-randomized controlled trial. The participants were general practitioners from 68 practices in Tayside, Scotland, and 1, 133 of their patients with self-reported epilepsy treated with antiepileptic medications (AEDs). Practices were randomized blind to a control, intermediate, or intensive intervention. Control: Postal dissemination of a nationally developed clinical guideline. Intermediate intervention: Postal dissemination of the guideline supported by interactive, accredited workshops, and dedicated, structured protocol documents. Intensive intervention: Intermediate intervention plus a nurse specialist who supported and educated practices in the establishment of epilepsy review clinics. The primary outcome was the SF-36 health-related quality-of-life instrument. Secondary measures were a battery of prevalidated epilepsy-specific quality-of-life instruments. These were administered at baseline and after the intervention phase. Process of care was assessed by case-note review on number of review meetings and counseling sessions for epilepsy before and after the interventions.Results: None of the intervention groups showed any change in the primary or secondary outcome measures or process-of-care measures.Conclusions: None of the intervention strategies led to improvements in patient quality of life or quality of epilepsy care. Further research is needed to discover why the interventions failed, to identify barriers to adoption of guidelines, and to develop strategies that might improve implementation and uptake in the future.

Lipid peroxidation (LPx) products were measured as thiobarbituric acid-reactive substances (TS) and lipid-soluble fluorescent pigments (FP) in both plasma and CSF from MS patients and controls. Although no significant changes were found in MS plasma, we report here for the first time increases in both TS and FP in MS CSF (p<0.05 and p<0.01, respectively, compared with patients with other neurological diseases), indicating that increased LPx in CNS may be a feature of MS. Levels of transferrin were normal but caeruloplasmin (CP), a major antioxidant plasma protein, was significantly raised in MS patients (p<0.01) and this may represent an adaptive response to increased oxidative challenge. Neither of these proteins was detectable in CSF using radial immunodiffusion. There was no significant correlation between the severity or duration of the disease nor the period since the last relapse and either LPx products of CP suggesting that the changes observed in this work are not simply the direct result of demyelination and tissue damage.