We found evidence for distinct neuronal network damage in mesial temporal lobe epilepsy (mTLE) and cryptogenic TLE (cTLE) which is more widespread in patients with left-sided seizure focus. Atrophy of the cingulum was a common feature in left- but not in right-sided mTLE and cTLE.

These findings are consistent with dysfunction of antinociceptive systems in MOH, which is influenced by anxiety. Dysfunction of the reward system may be a neurobiological basis for dependence in a subgroup of MOH patients.

Patients with chronic daily headache and overuse of analgesics, triptans, or other acute headache compounds, are considered to suffer from medication-overuse headache (MOH). This implies that medication overuse is the cause of headache chronification. It remains a key question why only two-thirds of patients with chronic migraine-like headache and overuse of pain medication improve after detoxification, whereas the remainder continue to have chronic headache. In the present longitudinal MRI study, we used voxel-based morphometry to investigate gray matter changes related to medication withdrawal in a group of humans with MOH. As a main result, we found that only patients with significant clinical improvement showed a significant decrease of previously increased gray matter in the midbrain including periaqueductal gray matter and nucleus cuneiformis, whereas patients without improvement did not. Patients without treatment response had less gray matter in the orbitofrontal cortex. Another striking result is the correlation of treatment response with the amount of orbitofrontal gray matter. Thus, we demonstrate adaptive gray matter changes within the pain modulatory system in patients with MOH who responded to detoxification, probably reflecting neuronal plasticity. Decreased gray matter in the orbitofrontal cortex at baseline may be predictive of poor response to treatment.

No abstract

The objective of this study was to evaluate whether the quality of sleep and the degree of fatigue and daytime sleepiness are related to migraine. We investigated 489 subjects comprising 97 patients with eight or more, 77 patients with five to seven and 196 patients with one to four migraine days per month, and 119 migraine-free controls with fewer than six headache days per year. The patients were recruited via articles in newspapers not stressing the subject of the study. All participants underwent a semistructured interview and completed the Pittsburgh Sleep Quality Index (PSQI), the Fatigue Severity Scale (FSS), the Epworth Sleepiness Scale (ESS) and the Self-rating Depression Scale and the Self-rating Anxiety Scale. For statistical analysis we used two way manovas, post hoc univariate two-way anovas and Hochberg's GT2 tests as well as three-way mixed design anovas. The PSQI total score was highest in patients with frequent migraine (5.9 +/- 4.3) and lowest in controls (4.3 +/- 2.5, P = 0.04). Four subscores of the PSQI showed similar statistically significant differences. The FSS and ESS scores did not differ in the four study groups. Analysing depression and anxiety revealed a significant impact on PSQI, FSS and ESS, but did not demonstrate interactions with migraine, thus suggesting that the impact of migraine is similar in patients without and with psychiatric comorbidity. In conclusion, the quality of sleep is decreased in patients with migraine, whereas fatigue and daytime sleepiness do not differ from healthy controls. The decreased quality of sleep in migraineurs is also a consequence of migraine itself and cannot be explained exclusively by comorbidity with depression or anxiety.