Ecological aspects of pain in sensory modulation disorder.

BACKGROUND: Sensory Modulation Disorder (SMD) interferes with the daily life participation of otherwise healthy individuals and is characterized by over-, under- or seeking responsiveness to naturally occurring sensory stimuli. Previous laboratory findings indicate pain hyper-sensitivity in SMD individuals suggesting CNS alteration in pain processing and modulation. However, laboratory studies lack ecological validity, and warrant clinical completion in order to elicit a sound understanding of the phenomenon studied. Thus, this study explored the association between sensory modulation and pain in a daily life context in a general population sample. METHODS: Daily life context of pain and sensations were measured in 250 adults (aged 23-40 years; 49.6% males) using 4 self-report questionnaires: Pain Sensitivity Questionnaire (PSQ) and Pain Catastrophizing Scale (PCS) to evaluate the sensory and cognitive aspects of pain; the Sensory Responsiveness Questionnaire (SRQ) to appraise SMD; and the Short Form - 36 Health Survey, version 2 (SF36) to assess health related Quality of Life (QoL). RESULTS: Thirty two individuals (12.8%) were found with over-responsiveness type of SMD, forming the SOR-SMD group. While no group differences (SOR-SMD vs. Non-SMD) were found, low-to-moderate total sample correlations were demonstrated between the SRQ-Aversive sub-scale and i) PSQ total (r=0.31, p<0.01) and sub-scales scores (r=0.27-0.28, p<0.01), as well as ii) PCS total and the sub-scales of Rumination and Helplessness scores (r=0.15, p<0.05). PSQ total and sub-scale scores were more highly correlated with SRQ-Aversive in the SOR-SMD group (r=0.57-0.68, p=0.03-<0.01) compared to Non-SMD group. The Physical Health - Total score (but not the Mental Health - Total) of the SF36 was lower for the SOR-SMD group (p=0.03), mainly due to the difference in the Body pain sub-scale (p=0.04). CONCLUSIONS: Results suggest that SOR-SMD is strongly associated with the sensory aspect of pain but weakly associated with the cognitive aspect. This indicates that SMD co-occurs with daily pain sensitivity, thus reducing QoL, but less with the cognitive-catastrophizing manifestation of pain perception.

Atypical central pain processing in sensory modulation disorder: absence of temporal summation and higher after-sensation.

Sensory over-responsivity (SOR), a subtype of the proposed sensory modulation disorder (SMD), is characterized by over-responsiveness to stimuli in several sensory modalities. SMD individuals demonstrate abnormal responses to naturally occurring stimuli in a manner that interferes with daily life participation. Previous psychophysical testing of the somatosensory system revealed that SOR individuals rated pain sensations higher than controls, demonstrating hyperalgesia that can be centrally mediated. Temporal summation (TS) of second pain and after-sensation are manifestations of central sensitization; therefore, this study explored these measures for better characterization of central pain processing in SOR. Twelve SOR adults and 12 healthy controls participated. TS was produced by a train of fifteen repetitive heat pulses, 0.7 s duration each, and 2 s of inter-stimulus interval, applied to the thenar-eminence, while four pain ratings were obtained. An after-sensation was then measured for 5 min, obtaining six pain ratings. No TS of pain was indicated in the SOR group (SOR: p = 0.36; control: p < 0.001). Further, while controls reported a gradual disappearance of pain after-sensation, individuals with SOR continued to report pain for the duration of the 5 min measured (p = 0.002). These results demonstrate an atypical response pattern, suggesting alteration in pain processing and/or modulation at a central level in individuals with SOR. These possible neural changes may manifest themselves as interference with daily functioning as well as shed light on some of the between-subject variability seen in psychophysical testing in non-painful subjects.

Brainstem projections to the ventromedial medulla in cat: retrograde transport horseradish peroxidase and immunohistochemical studies.

Stimulation of the nucleus magnocellularis (NMC) of the medulla produces changes in locomotion, muscle tone, heart rate, and blood pressure. Glutamatergic input has been found to modulate muscle tone, whereas cholinergic input has been found to mediate cardiovascular changes produced by stimulation of the NMC. The current study was designed to identify the brainstem afferents to NMC by using retrograde transport of wheat germ agglutinin and horseradish peroxidase (WGA-HRP) combined with glutamate and choline acetyltransferase (ChAT) immunohistochemical and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemical techniques. Fifty nanoliters of 2.5% WGA-HRP were microinjected into the NMC in the cat. A heavy density of WGA-HRP-labeled neurons was found in the ipsilateral mesencephalic reticular formation (MRF), periaqueductal gray, Kolliker-Fuse nucleus, and pontis centralis caudalis (PoC), in the contralateral pontis centralis oralis (PoO), and bilaterally in the nucleus paragigantocellularis lateralis. A moderate density of retrogradely labeled neurons was found in the ipsilateral side of the nuclei parvocellularis, retrorubral (RRN), PoO, and vestibular complex, in the contralateral PoC and nucleus gigantocellularis, and bilaterally in the inferior vestibular nucleus. Retrograde HRP/glutamate-positive cells could be found throughout the brainstem, with a high percentage in RRN, PoO, PoC, and MRF. Double-labeled WGA-HRP/ChAT neurons were found in the pedunculopontine nucleus. Double-labeled WGA-HRP/NADPH-d-positive neurons could be seen in many nuclei of the brainstem, although the number of labeled neurons was small. The dense glutamatergic projections to the NMC support the hypothesis that rostral brainstem glutamatergic mechanisms regulate muscle activity and locomotor coordination via the NMC, whereas the pontine cholinergic projections to the NMC participate in cardiovascular regulation.

Sleep in the platypus.

We have conducted the first study of sleep in the platypus Ornithorhynchus anatinus. Periods of quiet sleep, characterized by raised arousal thresholds, elevated electroencephalogram amplitude and motor and autonomic quiescence, occupied 6-8 h/day. The platypus also had rapid eye movement sleep as defined by atonia with rapid eye movements, twitching and the electrocardiogram pattern of rapid eye movement. However, this state occurred while the electroencephalogram was moderate or high in voltage, as in non-rapid eye movement sleep in adult and marsupial mammals. This suggests that the low-voltage electroencephalogram is a more recently evolved feature of mammalian rapid eye movement sleep. Rapid eye movement sleep occupied 5.8-8 h/day in the platypus, more than in any other animal. Our findings indicate that rapid eye movement sleep may have been present in large amounts in the first mammals and suggest that it may have evolved in pre-mammalian reptiles.

Neurotoxic N-methyl-D-aspartate lesion of the ventral midbrain and mesopontine junction alters sleep-wake organization.

The dorsal regions of the midbrain and pons have been found to participate in sleep regulation. However, the physiological role of the ventral brainstem in sleep regulation remains unclear. We used N-methyl-D-aspartate-induced lesions of the ventral midbrain and pons to address this question. Unlike dorsal mesencephalic reticular formation lesions, which produce somnolence and electroencephalogram synchronization, we found that ventral midbrain lesions produce insomnia and hyperactivity. Marked increases in waking and decreases in slow wave sleep stage 1 (S1), stage 2 (S2) and rapid eye movement sleep were found immediately after the lesion. Sleep gradually increased, but never returned to baseline levels (baseline/month 1 post-lesion: waking, 30.6 +/- 4.58%/62.3 +/- 10.1%; S1, 5.1 +/- 0.74/3.9 +/- 1.91%; S2, 46.2 +/- 4.74%/23.1 +/- 5.47%; rapid eye movement sleep, 14.1 +/- 3.15%/7.2 +/- 5.42%). These changes are comparable in magnitude to those seen after basal forebrain lesions. Neuronal degeneration was found in the ventral rostral pons and midbrain, including the substantia nigra, ventral tegmental area, retrorubral nucleus, and ventral mesencephalic and rostroventral pontine reticular formation. We conclude that nuclei within the ventral mesencephalon and rostroventral pons play an important role in sleep regulation.