Surgical intervention for chronic migraine headache: A systematic review.

AIMS: Migraine is a global phenomenon, affecting more than 10% of the world's population. It is characterized by unilateral headache that may be accompanied by vomiting, nausea, photophobia and phonophobia. Some patients with chronic migraine respond to extra-cranial botulinum toxin type A injection, although the benefits observed are temporary. The rationale for surgical trigger site deactivation is to achieve lasting symptomatic improvement or permanent relief from migraine. METHODS: We performed a PRISMA-compliant systematic review of clinical studies evaluating surgical intervention for migraine by searching Ovid MEDLINE and EMBASE databases from inception to June 2017. Studies were independently screened by two authors. Data were extracted on study characteristics, migraine outcomes, adverse events and recurrence. The quality of evidence was assessed using the GRADE approach. The review protocol was prospectively registered on the PROSPERO database (CRD42017068577). RESULTS: The search strategy identified 789 articles; of them, 18 studies (4 RCTs and 14 case series) were eligible for analysis. Surgical interventions were heterogeneous and variably involved peripheral nerve decompression by myectomy or foraminotomy, nerve excision, artery resection and/or nasal surgery. All studies reported significant reductions in migraine intensity, frequency, duration and composite headache scores following surgery. Study heterogeneity precluded formal meta-analysis. Where reported, adverse event rates varied markedly between studies. The quality of included studies was consistently low or very low. CONCLUSION: There is insufficient evidence to support the effectiveness of any specific surgical intervention for chronic migraine, especially with regard to permanent relief; however, all included studies report improvements in key outcomes following migraine surgery. A definitive, well-powered RCT with objective surgical and patient-reported outcome measures and robust adverse event reporting is required.

Prediction error for free monetary reward in the human prefrontal cortex.

Making predictions about future rewards is an important ability for primates, and its neurophysiological mechanisms have been studied extensively. One important approach is to identify neural systems that process errors related to reward prediction (i.e., areas that register the occurrence of unpredicted rewards and the failure of expected rewards). In monkeys that have learned to predict appetitive rewards during reward-directed behaviors, dopamine neurons reliably signal both types of prediction error. The mechanisms in the human brain involved in processing prediction error for monetary rewards are not well understood. Furthermore, nothing is known of how such systems operate when rewards are not contingent on behavior. We used event-related fMRI to localize responses to both classes of prediction error. Subjects were able to predict a monetary reward or a nonreward on the basis of a prior visual cue. On occasional trials, cue-outcome contingencies were reversed (unpredicted rewards and failure of expected rewards). Subjects were not required to make decisions or actions. We compared each type of prediction error trial with its corresponding control trial in which the same prediction did not fail. Each type of prediction error evoked activity in a distinct frontotemporal circuit. Unexpected reward failure evoked activity in the temporal cortex and frontal pole (area 10). Unpredicted rewards evoked activity in the orbitofrontal cortex, the frontal pole, parahippocampal cortex, and cerebellum. Activity time-locked to prediction errors in frontotemporal circuits suggests that they are involved in encoding the associations between visual cues and monetary rewards in the human brain.

Brain responses to changes in bladder volume and urge to void in healthy men.

Knowledge of how changes in bladder volume and the urge to void affect brain activity is important for understanding brain mechanisms that control urinary continence and micturition. This study used PET to evaluate brain activity associated with different levels of passive bladder filling and the urge to void. Eleven healthy male subjects (three left- and eight right-handed) aged 19-54 years were catheterized and the bladder filled retrogradely per urethra. Twelve PET scans were obtained during two repetitions of each of six bladder volumes, with the subjects rating their perception of urge to void prior to and after each scan. Increased brain activity related to increasing bladder volume was seen in the periaqueductal grey matter (PAG), in the midline pons, in the mid-cingulate cortex and bilaterally in the frontal lobe area. Increased brain activity relating to decreased urge to void was seen in a different portion of the cingulate cortex, in premotor cortex and in the hypothalamus. Both activation patterns were predominantly bilaterally symmetric and none of the effects could be attributed to the presence of the catheter. However, in some subjects, mostly those reporting intrusive sensations from the urethral catheter, there was a discrepancy between filling volume and urge so that they reported high urge with low volumes. As this 'mismatch' decreased, activation increased bilaterally in the somatosensory cortex. Our findings support the hypothesis that the PAG receives information about bladder fullness and relays this information to areas involved in the control of bladder storage. Our results also show that the network of brain regions involved in modulating the perception of the urge to void is distinct from that associated with the appreciation of bladder fullness.

Variability in fMRI: an examination of intersession differences.

The results from a single functional magnetic resonance imaging session are typically reported as indicative of the subject's functional neuroanatomy. Underlying this interpretation is the implicit assumption that there are no responses specific to that particular session, i.e., that the potential variability of response between sessions is negligible. The present study sought to examine this assumption empirically. A total of 99 sessions, comprising 33 repeats of simple motor, visual, and cognitive paradigms, were collected over a period of 2 months on a single male subject. For each paradigm, the inclusion of session-by-condition interactions explained a significant amount of error variance (P < 0.05 corrected for multiple comparisons) over a model assuming a common activation magnitude across all sessions. However, many of those voxels displaying significant session-by-condition interactions were not seen in a multisession fixed-effects analysis of the same data set; i.e., they were not activated on average across all sessions. Most voxels that were both significantly variable and activated on average across all sessions did not survive a random-effects analysis (modeling between-session variance). We interpret our results as demonstrating that correct inference about subject responses to activation tasks can be derived through the use of a statistical model which accounts for both within- and between-session variance, combined with an appropriately large session sample size. If researchers have access to only a single session from a single subject, erroneous conclusions are a possibility, in that responses specific to this single session may be claimed to be typical responses for this subject.

Imaging hypnotic paralysis: implications for conversion hysteria.

In a single case study with positron emission tomography (PET) functional imaging, hypnotic paralysis activated similar brain areas to those in conversion hysteria, supporting the view that hypnosis and hysteria might share common neurophysiological mechanisms.

Transcriptional abnormality in myotonic dystrophy affects DMPK but not neighboring genes.

Myotonic dystrophy (DM) is caused by the expansion of a trinucleotide repeat, CTG, in the 3' untranslated region of a protein kinase gene, DMPK. We set out to determine what effect this expanded repeat has on RNA processing. The subcellular fractionation of RNA and the separate analysis of DMPK transcripts from each allele reveals that transcripts from expanded DMPK alleles are retained within the nucleus and are absent from the cytoplasm of DM cell lines. The nuclear retention of DMPK transcripts occurs above a critical threshold between 80 and 400 CTGs. Further analysis of the nuclear RNA reveals an apparent reduction in the proportion of expansion-derived DMPK transcripts after poly(A)+ selection. Quantitative analysis of RNA also indicates that although the level of cytoplasmic DMPK transcript is altered in DM patients, the levels of transcripts from 59 and DMAHP, two genes that immediately flank DMPK, are unaffected in DM cell lines.