Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale
-
Temporal summation due to repeated pain stimulation of deep somatic structures is facilitated in chronic musculoskeletal pain. In this study, the relation between repeated pressure-induced pain and stress/strain distribution within the deep tissue was evaluated to understand whether tissue characteristics may change during repeated stimulation. This information is important for interpret the pain-evoked responses. ⋯ The peak principal strain in adipose tissue was 0.12; in muscle tissue, it was 0.108 during the first stimulus and increased by 16 % in the tenth stimulus. In a model of a one-stimulus paradigm, it was found that a VAS increase of 2.5 cm required a 47 % increase in muscle strain. These findings show that the increase in muscle strain during repeated pressure stimulations is not sufficient to explain the VAS increase; the temporal summation of deep-tissue pain evoked by repetitive pressure stimulations is not likely to be fully explained by peripheral tissue changes.
-
Cerebral arteries subjected to different types of experimental stroke upregulate their expression of certain G-protein-coupled vasoconstrictor receptors, a phenomenon that worsens the ischemic brain damage. Upregulation of contractile endothelin B (ET(B)) and 5-hydroxytryptamine 1B (5-HT(1B)) receptors has been demonstrated after subarachnoid hemorrhage and global ischemic stroke, but the situation is less clear after focal ischemic stroke. Changes in smooth muscle calcium handling have been implicated in different vascular diseases but have not hitherto been investigated in cerebral arteries after stroke. ⋯ Expression and contractile functions of ET(B) and 5-HT(1B) receptors were strongly upregulated and slightly downregulated, respectively, 24 h after experimental stroke or organ culture. ET(B) receptor-mediated contraction was mediated by calcium from intracellular and extracellular sources, whereas 5-HT(1B) receptor-mediated contraction was solely dependent on extracellular calcium. Organ culture and stroke increased basal intracellular calcium levels in MCA smooth muscle cells and decreased the expression of inositol triphosphate receptor and transient receptor potential canonical calcium channels, but not voltage-operated calcium channels.
-
Clinical Trial
Treatment-related changes in brain activation in patients with fibromyalgia syndrome.
Little is known about the effects of successful treatment on brain function in chronic pain. This study examined changes in pain-evoked brain activation following behavioral extinction training in fibromyalgia patients. Using functional magnetic resonance imaging, brain activation to painful mechanical stimuli applied to the 2nd phalanx of the left 2nd digit (m. flexor digitorum) was assessed in 10 patients with fibromyalgia syndrome (FM) before and after behavioral extinction training. ⋯ The pre- to post-treatment reduction in both interference related to pain and pain severity were significantly associated with bilateral activation in pain-evoked activity in the posterior insula, the ipsilateral caudate nucleus/striatum, the contralateral lenticular nucleus, the left thalamus and the primary somatosensory cortex contralateral to the stimulated side. These data show a relation between successful behavioral treatment and higher activation bilaterally in the posterior insula and in the contralateral primary somatosensory cortex. Future studies should compare responders and non-responders for differential treatment effects and examine in more detail the mechanisms underlying these changes.
-
Pain catastrophizing has been associated with phantom limb pain, but so far the cortical processes and the brain regions involved in this relationship have not been investigated. It was therefore tested whether catastrophizing was related to (1) spontaneous pain, (2) somatosensory activity and (3) cortical responses in phantom limb pain patients. The cortical responses were investigated via electroencephalography (EEG) as it has a high temporal resolution which may be ideal for investigating especially the attentional and hypervigilance aspect of catastrophizing to standardized acute stimuli. ⋯ Catastrophizing accounted for significant amounts of the variance in relation to spontaneous pain, especially worst pain (64.1%), and it was significantly associated with thresholds. At the affected side, catastrophizing was significantly related to the power RMS of the N/P135 dipole located in the area around the secondary somatosensory cortex which has been shown to be associated with arousal and expectations. These findings corroborate the attentional model of pain catastrophizing by indicating that even non-painful stimuli are related to enhanced attention to and negative expectations of stimuli, and they suggest that memory processes may be central to understanding the link between catastrophizing and pain.
-
Contralateral transversus abdominis muscle (cTrA) is known to be anticipatory to rapid focal movement. The activation of ipsilateral TrA (iTrA) follows cTrA, but their anticipatory interaction in healthy subjects seems to be delayed in low back pain (LBP) patients. TrA delay in LBP is linked with reorganization of the primary motor cortex (M1), thus supporting that cortical changes underlie the altered postural control. ⋯ Delay of iTrA/IO and the lacking co-activation were not explained by between-group differences of transcranial magnetic stimulation outcomes. TrA/IO co-activation is present during rapid focal movement in healthy subjects only. LBP patients displayed an important alteration of the control of spine stability that can be explained by altered mechanisms of M1 motor programming.