Chronic sensory stroke with and without central pain is associated with bilaterally distributed sensory abnormalities as detected by quantitative sensory testing

Pain ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 194-202 ◽  
Author(s):  
Thomas Krause ◽  
Susanna Asseyer ◽  
Frederik Geisler ◽  
Jochen B. Fiebach ◽  
Jochen Oeltjenbruns ◽  
...  
PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e37524 ◽  
Author(s):  
Karl-Heinz Konopka ◽  
Marten Harbers ◽  
Andrea Houghton ◽  
Rudie Kortekaas ◽  
Andre van Vliet ◽  
...  

2013 ◽  
Vol 24 (5) ◽  
pp. 893-899 ◽  
Author(s):  
Mette H. Lauridsen ◽  
Anders D. Kristensen ◽  
Vibeke E. Hjortdal ◽  
Troels S. Jensen ◽  
Lone Nikolajsen

AbstractIntroductionChronic pain is common after sternotomy in adults with reported prevalence rates of 20–50%. So far, no studies have examined whether children develop chronic pain after sternotomy.Material and methodsPostal questionnaires were sent to 171 children 10–60 months after undergoing cardiac surgery via sternotomy at the age of 0–12 years. The children were asked to recall the intensity and duration of their post-operative pain, if necessary with the help from their parents, and to describe the intensity and character of any present pain. Another group of 13 children underwent quantitative sensory testing of the scar area 3 months after sternotomy.ResultsA total of 121 children, median (range) age 7.7 (4.2–16.9) years, answered the questionnaire. Their age at the time of surgery was median (range) 3.8 (0–12.9) years, and the follow-up period was median (range) 4 (0.8–5.1) years. In all, 26 children (21%) reported present pain and/or pain within the last week located in the scar area; in 12 (46%) out of the 26 children, the intensity was ≥4 on a numeric rating scale (0–10). Quantitative sensory testing of the scar area revealed sensory abnormalities – pinprick hyperalgesia and brush and cold allodynia – in 10 out of 13 children.ConclusionChronic pain after cardiac surgery via sternotomy in children is a problem that should not be neglected. The pain is likely to have a neuropathic component as suggested by the sensory abnormalities demonstrated by quantitative sensory testing.


2009 ◽  
Vol 25 (7) ◽  
pp. 641-647 ◽  
Author(s):  
Miroslav-Misha Backonja ◽  
David Walk ◽  
Robert R. Edwards ◽  
Nalini Sehgal ◽  
Toby Moeller-Bertram ◽  
...  

2016 ◽  
Vol 7;19 (7;9) ◽  
pp. 507-517
Author(s):  
Joachim K. Krauss

Background: Trigeminal neuralgia (TN) is characterized by paroxysmal pain attacks affecting the somatosensory distributions of the trigeminal nerve. It is thought to be associated with a neurovascular conflict most frequently, but pathomechanisms have not been fully elucidated. In general, no sensory deficit is found in routine clinical examination. There is limited data available, however, showing subtle subclinical sensory deficits upon extensive testing. Objective: We used quantitative sensory testing (QST) to detect abnormalities in sensory processing in patients with TN by comparing the affected and non-affected nerve branches with their contralateral counterparts and by comparing the results of the patients with those of controls. Study Design: Observational study. Setting: University Hospital, Departments of Neurosurgery, Institute for Cognitive and Clinical Neuroscience. Methods: QST was conducted on 48 patients with idiopathic TN and 27 controls matched for age and gender using the standardized protocol of the German Neuropathic Pain Network. Stimulations were performed bilaterally in the distribution of the trigeminal branches. The patients had no prior invasive treatment, and medications at the time of examination were noted. Results: In patients with TN deficits in warm and cold sensory detection thresholds in the affected and also the non-affected nerve branches were found. Tactile sensation thresholds were elevated in the involved nerve branches compared to the contralateral side. Limitations: More data are needed on the correlation of such findings with the length of history of TN and with changes of the morphology of the trigeminal nerve. Conclusions: QST shows subtle sensory abnormalities in patients with TN despite not being detected in routine clinical examination. Our data may provide a basis for further research on the development of TN and also on improvement after treatment. Key words: Quantitative sensory testing, trigeminal neuralgia, facial pain, neuropathic pain, microvascular decompression, cranial nerve


2019 ◽  
Vol 21 (5) ◽  
pp. 519-531
Author(s):  
Sabrina Bouferguène ◽  
Alexandra Lapierre ◽  
Bérengère Houzé ◽  
Pierre Rainville ◽  
Caroline Arbour

Background: Central pain associated with changes in sensory thresholds is one of the most enduring consequences of major trauma. Yet it remains sparsely studied among community-dwelling survivors of moderate-to-severe traumatic brain injury (TBI). Purpose: To describe and compare thermal and mechanical sensory thresholds in home-based patients with and without central pain after moderate-to-severe TBI with a cohort of healthy controls. Design: Cross-sectional. Method: Thresholds for cold/heat detection, thermal pain, touch, and distorted sensation were gathered using quantitative sensory testing (QST). QST was performed on the painful and contralateral pain-free body regions in TBI participants with pain (TBI-P) and on both forearms in TBI participants without pain (TBI-NP) and healthy controls (HC). Central pain was characterized using the Brief Pain Inventory–Short Form. Results: We tested 16 TBI-P patients, 17 TBI-NP patients, and 16 HC. Mean time since injury for TBI patients was 24 ± 15 months. TBI-P and TBI-NP patients showed significant loss in innocuous mechanical sensitivity compared to HC ( F = 18.929; Bonferroni-adjusted p ≤ .001). Right–left differences in cold pain sensations were significantly larger in TBI-P than in TBI-NP and HC participants ( F = 14.352; Bonferroni-adjusted p ≤ .001). Elevated heat sensitivity thresholds were also observed in TBI-P participants but remained within normal range. Conclusion: Damage to cutaneous mechanoreceptors is a necessary, but not sufficient, condition for the development of chronic central pain following TBI. Damage or incomplete recovery of cutaneous thermoreceptors may be a contributing factor to chronic pain after TBI.


Sign in / Sign up

Export Citation Format

Share Document