This article investigates the effects of postherpetic neuralgia (PHN) on resting-state brain activity utilizing arterial spin labeling (ASL) techniques. Features of static and dynamic cerebral blood flow (CBF) were analyzed to reflect the specific brain response to PHN pain. Eleven consecutive patients suffering from PHN and 11 age- and gender-matched control subjects underwent perfusion functional magnetic resonance imaging brain scanning during the resting state. Group comparison was conducted to detect the regions with significant changes of CBF in PHN patients. Then we chose those regions that were highly correlated with the self-reported pain intensity as "seeds" to calculate the functional connectivity of both groups. Absolute CBF values of these regions were also compared across PHN patients and control subjects. Significant increases in CBF of the patient group were observed in left striatum, right thalamus, left primary somatosensory cortex (S1), left insula, left amygdala, left primary somatomotor cortex, and left inferior parietal lobule. Significant decreases in CBF were mainly located in the frontal cortex. Regional CBF in the left caudate, left insula, left S1, and right thalamus was highly correlated with the pain intensity, and further comparison showed that the regional CBF in these regions is significantly higher in PHN groups. Functional connectivity results demonstrated that the reward circuitry involved in striatum, prefrontal cortex, amygdala, and parahippocampal gyrus and the circuitry among striatum, thalamus, and insula were highly correlated with each element in PHN patients. In addition, noninvasive brain perfusion imaging at rest may provide novel insights into the central mechanisms underlying PHN pain.

No abstract

Purpose:To test the hypothesis that lidocaine prolongs the safe period of circulatory arrest during deep hypothermia. Methods: Sixteen dogs were subjected to cooling, first surface cooling to 30~ and then core cooling to 20~ rectal temperature). The circulation was then stopped for 90 rain. In the lidocaine group, 4 mg.kg-' lidocaine was injected into the oxygenator two minutes before circulatory arrest and 2 mg.kg-' at the beginning of reperfusion and rewarming. The control group received equivalent volumes of normal saline. Post-operatively, using a neurological deficit scoring system (maximum deficit score -100; minimum -zero indicating that no scored deficit could be detected). Neurological function was evaluated hourly for six houm and then daily for one week. the pharmacokinetic parameters were calculated using one compartment model. Results: On the seventh day, the neurological deficit score and overall performance were better in the lidocaine (0.83 -+ 2.04) than in the control group (8.33 -+ 4.08 P < 0.05). During the experiment, the base excess values were also better in the lidocaine than in the control group (at 30 min reperfusion:-4.24 _+ 1.30 vs -8.20 _ 2.82 P < 0.01, at 60 min reperfusion was -3.34 _+ 1.87 vs -7.52 _+ 2.40 (P < 0.01). On the eighth day the extent of pathological changes were milder in the lidocaine group than that in the control group. The elimination half life of lidocaine was 40.44 _ 7.99 during hypothermia and 2.01 -+ 4.56 during rewarming. Conclusions:In dogs lidocaine prolongs the safe duration of circulatory arrest during hypothermia.Objectif : V&ifier I'hypoth&e qui veut que la lidoca~ne prolonge la p&iode sans risque d'arr& circulatoire sous hypothermie profonde. M~thode : Seize chiens ont ~t~ soumis ~ un refroidissement, externe d'abord jusqu'~ 30 ~ puis interne jusqu'~ une temp&ature rectale de 20 ~ La circulation a ~t~ arr&& ensuite pendant 90 min. Dans le groupe ayant re~u de la lidoca'ine, 4 mgxkg-' de lidocafne ont ~t~ inject& dans I'oxyg~nateur deux minutes avant I'arr& de la circulation et 2 mgxkg "~ au d~but de la reperfusion et du r&hauffement. Le groupe t~moin a re~u des quantit& ~quivalentes de solution salve. Apt& rintervention, au moyen d'un syst~me de cotation du d~ficit neurologique (d~ficit maximal -100; minimal -z&o, indiquant qu'aucune baisse n'a &~ d&ect~e dans cette &helle de cotation), la fonction neurologique a ~t~ ~valu& ~ toutes les heures pendant six heures et, par la suite, ~ chaque jour pendant une semaine. Les param&res pharmacocin~tiques ont ~te~ calculus avec I'emploi d'un module monocompartimental. K~sultats : Le septi~me jour, la cotation du d~ficit neurologique et le rendement global ont ~t~ meilleurs dans le groupe avec la lidocaine (0,83 -+ 2,04) que dans le groupe t~moin (8,33 -+ 4,08 P < 0,05). Pendant I'exp&ience, les valeum de I'exc~s basique ont aussi ~t~ meilleures dans le groupe avec lidoca'fne que dans le groupe t(~moin (30 min. apr& le d~but de la reperfusion: -4,24 + 1,30 vs -8,20 + 2,82 P < 0,01; ~ 60 min. -3,34 _ 1,87 vs -7,52...

In this study, we aimed to investigate the functional network changes that occur in patients with lower back pain (LBP). We also investigated the link between LBP and the small-world properties of functional networks within the brain. Functional MRI (fMRI) was performed on 20 individuals with LBP and 17 age and gender-matched normal controls during the resting state. The severity of the pain in the individuals with LBP ranged from 5 to 8 on a 0-10 scale, with 0 indicating no pain. Network-based statistics were performed to investigate the differences between the brain networks of individuals with LBP and those of normal controls. Several small-world parameters of brain networks were calculated, including the clustering coefficient, characteristic path length, local efficiency, and global efficiency. These criteria reflect the overall network efficiency. The brain networks in the individuals with LBP due to herniation of a lumbar disc demonstrated a significantly longer characteristic path length as well as a lower clustering coefficient, global efficiency, and local efficiency compared to those in control subjects. We found that LBP patients tended to have unstable and inefficient brain networks when compared with healthy controls. In addition, LBP individuals showed significantly decreased functional connectivity in the anterior cingulate cortex, middle cingulate cortex, post cingulate cortex, inferior frontal gyrus, middle temporal gyrus, occipital gyrus, postcentral gyrus, precentral gyrus, supplementary motor area, thalamus, fusiform, caudate, and cerebellum. We believe that these regions may be involved in the pathophysiology of lower back pain. small-world network, brain functional networks, resting-state fMRI, low back pain