Endogenous pain in patients with Parkinson disease is accompanied by increased sensitivity to some painful stimuli, suggesting that basal ganglia abnormality also involves pain encoding.

The aim of the present study was to examine the possible role of personality traits in determining the variability of pain perception among individuals. More specifically, it was intended to test whether or not the three personality dimensions suggested by Cloninger in 1987 - mainly harm avoidance (HA), but also reward dependence (RD), and novelty seeking (NS), can predict interpersonal differences in responsiveness to experimental pain. Seventy healthy volunteers participated in the study. Their personality traits were evaluated through Cloninger's tridimensional personality questionnaire (TPQ). Pain threshold (latency to pain onset), pain magnitude (VAS), and pain tolerance (time to withdrawal) were measured by using the cold pressor test. Bonferroni-adjusted correlations were found between HA and the pain parameters as follows: a negative correlation between HA and threshold (rho=-0.297, P(adj)=0.039); no significant correlation between HA and tolerance (rho=-0.219, P(adj)=0.207); and a trend for a positive correlation between HA and VAS (rho=0.266, P(adj)=0.081). Possible correlations between pain perception and the various possible combinations of high and low scoring for each of the three traits were also investigated. Correlations were found only for the combinations of high/low HA and high/low RD. The low HA/low RD combination demonstrated the lowest responsiveness to pain (VAS 65.2+/-21.4; tolerance 107.6+/-71.8 s), whereas the high HA/low RD combination was correlated with the highest responsiveness (VAS 83.3+/-10.8; tolerance 30.8+/-28.4 s). The results indicate that HA personality trait correlates best with pain responsiveness. As such, a high HA are likely to predict a heightened pain response. RD may modify this pattern. The possible relevant behavioral and neuro-chemical mechanisms are discussed.

Several lines of evidence support involvement of the parasympathetic system in migraine: (i) migraine-associated symptoms, such as exaggerated facial flushing, lacrimation and rhinorrhea; (ii) increased levels of cranial venous vasoactive intestinal peptide in migraineurs during attacks; and (iii) reports of migraine pain alleviation by intranasal instillation of lidocaine, which can block some of the parasympathetic outflow to the cranium. This study assessed cranial parasympathetic function in migraineurs in between attacks, assuming that abnormal function might imply involvement of the parasympathetics in migraine pathogenesis. We tested 39 female migraineurs outside attacks, of whom 11 had bilateral pain, 20 unilateral at a specific side and eight alternating unilateral head pain, and 16 controls. The trigemino-parasympathetic reflex was studied, using soapy and saline eye drops for stimulation of the afferent limb of the reflex arch, and cutaneous vascular response at the forehead for the efferent limb. The latter was recorded by photoplethysmography on both sides of the forehead. We found no difference in vasodilatation between migraineurs as a group and controls (83.7 +/- 6.5% and 80.8 +/- 7.6%, respectively, not significant). However, when analysing data by the site of pain, we found that those with bilateral pain had the largest vasodilatation response (141.6 +/- 16.2%, P < 0.05 versus controls, analysis of varance, post hoc Tukey-Kramer HSD), while those with unilateral pain had the least vasodilatation (45.5 +/- 3.3%, P < 0.05). The response of patients with alternating pain (97.2 +/- 12.6%) did not differ from controls. It is concluded that cranial parasympathetic function does differ among patients with various migraine types at rest. Based on the understanding of dysfunctional brainstem pain modulation in migraine, we suggest a model of within-brainstem interaction between the two locus coeruleus nuclei, which are involved in control of pain and cranial parasympathetic outflow. The model assumes various levels of inhibitory inter-relationships between these two nuclei; diminution or absence of the normal reciprocal inhibitory relationships between them may underlie the augmented cranial parasympathetic response in bilateral migraineurs, while an excess of reciprocal inhibitory relationship between them may underlie the diminished cranial parasympathetic response in unilateral migraineurs. These findings might help in clarifying inter-relationships between brainstem nuclei in the context of migraine pathogenesis.

In 12 epileptic patients suffering from "absences" 8-channel EEG was recorded by telemetry. The autoregressive model was applied to the signal and the prediction coefficients being the basis for calculation of the poles of the predictor. The location of the poles in the z- and s-planes was described as a function of time for 0.1 s steps along the pre-seizure EEG. In 10 of the 12 patients, and in 25 of the 28 recorded seizures this presentation of the poles of the predictor showed specific pattern linked with the occurrence of the seizure. The trajectory of the "most mobile pole" during the pre-seizure period could aid in the prediction of the seizure by several seconds.

Brain autonomic control is asymmetrical, the left hemisphere affecting predominantly parasympathetic function and the right hemisphere affecting predominantly sympathetic function. It is not known whether the extent of autonomic activation is altered in migraine, although the fact that some migraineurs express parasympathetic features such as facial flushing, lacrimation and rhinorrhoea might suggest increased parasympathetic activation. We instilled diluted soapy eyedrops and measured (i) the trigemino-parasympathetic reflex by the vasodilator response of forehead skin bilaterally using photoplethysmography; (ii) the somato-sympathetic reflex by vasoconstriction in the index finger; and (iii) heart rate response. We studied 14 left-sided and 15 right-sided unilateral migraineurs outside attacks. We found that left-side migraineurs had significantly higher bilateral parasympathetic vasodilatation, regardless of the stimulation or measurement side (+60.1 +/- 6.4%) compared with right-side migraineurs (+41.9 +/- 6.4%, P < 0.05). Sympathetic vasoconstriction, however, was similar for the two groups (left, -15.9 +/- 4.2%; right, -17.7 +/- 4.1%, NS). Bradycardia was significantly more pronounced for the left-side migraineurs (interbeat, RR interval increase of +6.2 +/- 1.1% versus +3.1 +/- 1.1%, P < 0.04). We conclude that unilateral left-side migraineurs have increased parasympathetic activation in response to pain compared with right-side migraineurs. Sympathetic responses were similar in the two groups and seemed not to be affected by migraine side. Since cranial parasympathetic activity induces cerebral vasodilatation, this augmentation might be an inherent part of the migraine pathophysiology in these patients.

The aim of the present study was to examine the possible role of personality traits, in accordance with Cloninger's theory, and gender, in the variability of responsiveness to opioids. Specifically, it was intended to test whether or not the three personality dimensions - harm avoidance (HA), reward dependence (RD) and novelty seeking (NS) - as suggested by Cloninger, can predict inter-personal differences in responsiveness to morphine after exposure to experimental cold pain. Thirty-four healthy volunteers (15 females, 19 males) were given the cold pressor test (CPT). Pain threshold, tolerance, and magnitude (VAS) were measured before and after (six measures, 30 min apart) the administration of either 0.5 mg/kg oral morphine sulphate (n=21) or 0.33 mg/kg oral active placebo (diphenhydramine) (n=13) in a randomized, double blind design. Assessment of the three personality traits, according to Cloninger's Tridimensional Personality Questionnaire, was performed before the CPT. A high HA score (but not RD, NS, or baseline values of the three pain parameters) predicted a significantly larger pain relief following the administration of morphine sulphate (but not of the placebo). Women exhibited a larger response in response to both treatments, as indicated by a significantly increased threshold and tolerance following morphine sulphate as well as significantly increased tolerance and decreased magnitude following placebo administration. The present study confirms the existence of individual differences in response to analgesic treatment. It suggests that high HA personality trait is associated with better responsiveness to morphine treatment, and that females respond better than men to both morphine and placebo.

While the major pain generation in polyneuropathy is in the somatic peripheral nerves, pathologies at visceral nerves might be involved as well. Decreased vagal afferent activity is known to disinhibit pain perception, and therefore might contribute to pain in polyneuropathy. In this study we explored this potential contribution by employing a rat model of vincristine (VCR)-induced pain after sub-diaphragmatic vagotomy (SDV). Forty rats were divided into 4 groups: VCR, SDV, VCR+SDV and controls. Each rat underwent a variety of pain-related behavioral tests including assessment of spontaneous pain, allodynia and hyperalgesia to thermal and mechanical stimuli. We found that VCR+SDV rats had enhanced painful neuropathy compared to VCR alone, expressed as: (1) earlier development of central sensitization: at the first week in rats that underwent SDV+VCR (p<0.0001) and only at the second week in rats injected with VCR alone (p<0.0001), (2) increased incidence of spontaneous pain behavior (p=0.0036), (3) spreading of the spontaneous pain behavior to the forelimbs, (4) higher mechanical dynamic allodynia (tendency, p=0.08) and (5) augmentation of the response to repetitive painful and non-painful mechanical stimuli (p<0.001). Thus, decreased vagal activity aggravates both the severity and the time course of painful polyneuropathy. Therefore, the two mechanisms add to each other in generating the pain picture.

Computerized analysis of polygraphic sleep recordings was carried out for the evaluation of midazolam, a benzodiazepine hypnotic. The analysis was carried out in real time on a small laboratory computer, and the output included the hypnogram and relative power profiles for the main electroencephalogram activities. Analysis showed a slight "intranight rapid eye movement rebound" during medication and reduction of sleep stage IV after withdrawal. The relative power of the delta frequency band did not change during medication or withdrawal.