Population-based study of central post-stroke pain in Rimini district, Italy

Raffaeli, William; Minella, Cristina E.; Magnani, Francesco; Sarti, Donatella

doi:10.2147/jpr.s46553

Cited by 18 publications

(14 citation statements)

References 30 publications

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“…This was the expected result; CPSP affected the physical function, pain, and physical score components of the SF-36 QoLS poorly, but the other components of the SF-36 QoLS were not affected in our patients. Previous studies showed that CPSP affected not only physical functions but also mental functions poorly 26 , 27 , 28 ) . We thought that this difference was due to the protocol of our study which was a controlled study.…”

Section: Discussionmentioning

confidence: 99%

The effects of central post-stroke pain on quality of life and depression in patients with stroke

Şahin-Onat¹,

Ünsal-Delialioğlu²,

Kulaklı³

et al. 2016

J Phys Ther Sci

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[Purpose] The aim of this study was to assess the effects of central poststroke pain on quality of life, functionality, and depression in stroke. [Subjects and Methods] Twenty-four patients with stroke having central poststroke pain (a mean age of 60.6±8.5 years; 14 males, 10 females; Group I) and 24 similar age-and gender-matched patients with stroke without central poststroke pain (Group II) were enrolled. Characteristics of pain were recorded in patients with stroke having central poststroke pain. The Visual Analogue Scale and Leeds Assessment of Neuropathic Symptoms and Signs pain scale were used to evaluate pain. The Functional Independence Measure was used to assess functionality, the 36-Item Short-Form Health Survey was used to assess quality of life (QoL), and the Beck Depression Inventory was used to assess depression. [Results] There were no significant differences in Functional Independence Measure and Beck Depression Inventory. Some of the 36-Item Short-Form Health Survey domains (physical role limitations, pain, and physical scores) in Group II were significantly higher than those in Group I. Additionally, we found that a unit increase in Leeds Assessment of Neuropathic Symptoms and Signs score led to 0.679 decrease in physical score and 0.387 decrease in mental score. [Conclusion] The physical component of the 36-Item Short-Form Health Survey is negatively affected in patient with central poststroke pain, but the mood and mental components of the scale unaffected.

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Section: Discussionmentioning

confidence: 99%

The effects of central post-stroke pain on quality of life and depression in patients with stroke

Şahin-Onat¹,

Ünsal-Delialioğlu²,

Kulaklı³

et al. 2016

J Phys Ther Sci

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“…CPSP has been identified in 1%–50% of total patients after stroke of both IS and ICH origins [7,13–17] ; however, CPSP is more common in patients with a thalamic stroke, and varies from 11% to 32% [18–23] . CPSP patients most often present with spontaneous and/or evoked pain (hyperalgesia and allodynia) or paresthesia/dysesthesia in a persistent and/ or paroxysmal form [5–7,24] .…”

Section: Introductionmentioning

confidence: 99%

Post-stroke pain hypersensitivity induced by experimental thalamic hemorrhage in rats is region-specific and demonstrates limited efficacy of gabapentin

Yang

Han

et al. 2014

Neurosci. Bull.

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Intractable central post-stroke pain (CPSP) is one of the most common sequelae of stroke, but has been inadequately studied to date. In this study, we first determined the relationship between the lesion site and changes in mechanical or thermal pain sensitivity in a rat CPSP model with experimental thalamic hemorrhage produced by unilateral intra-thalamic collagenase IV (ITC) injection. Then, we evaluated the efficacy of gabapentin (GBP), an anticonvulsant that binds the voltage-gated Ca2+ channel α2δ and a commonly used anti-neuropathic pain medication. Histological case-by-case analysis showed that only lesions confined to the medial lemniscus and the ventroposterior lateral/medial nuclei of the thalamus and/or the posterior thalamic nucleus resulted in bilateral mechanical pain hypersensitivity. All of the animals displaying CPSP also had impaired motor coordination, while control rats with intra-thalamic saline developed no central pain or motor deficits. GBP had a dose-related anti-allodynic effect after a single administration (1, 10, or 100 mg/kg) on day 7 post-ITC, with significant effects lasting at least 5 h for the higher doses. However, repeated treatment, once a day for two weeks, resulted in complete loss of effectiveness (drug tolerance) at 10 mg/kg, while effectiveness remained at 100 mg/kg, although the time period of efficacious analgesia was reduced. In addition, GBP did not change the basal pain sensitivity and the motor impairment caused by the ITC lesion, suggesting selective action of GBP on the somatosensory system.

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“…Neuropathic pain refers to the douleur anormale (abnormal pain), caused by damage and dysfunction of the central or peripheral nervous system [1,2]. Neuropathic pain is one type of chronic pain, whose main clinical manifestations include hyperalgesia, paresthesia, ambulatory pain and allodynia [3,4]. According to statistics, the prevalence rate is 0.6-1.5% and with the aging of the population, the prevalence rate increases gradually [5].…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine alleviated neuropathic pain in dorsal root ganglion neurons by inhibition of anaerobic glycolysis activity and enhancement of ROS tolerance

et al. 2020

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Neuropathic pain is a kind of chronic pain that is triggered or caused primarily by damage to the nervous system and neurological dysfunction. It’s known that dexmedetomidine is a new type of highly selective alpha2-adrenoceptor agonist with sedation, anti-anxiety, analgesic and other effects. However, the function and mechanism of dexmedetomidine on neuropathic pain are not clear. Rat DRG neurons were isolated and identified using immunofluorescence assay. Following treatment with H2O2, dexmedetomidine or ROS inhibitor (NAC), the apoptosis and ROS levels were examined by flow cytometery; apoptosis- and anaerobic glycolysis-related proteins were determined by Western blot assay; glucose consumption, pyruvic acid, lactic acid and ATP/ADP ratios were also measured. The results revealed that dexmedetomidine inhibited H2O2-induced apoptosis and reactive oxygen species (ROS) in rat DRG neurons and in addition, dexmedetomidine down-regulated the expression levels of anaerobic glycolysis-related proteins, significantly reduced glucose, pyruvic acid and lactic acid levels. It also increased the ATP/ADP ratio in H2O2-treated rat dorsal root ganglion (DRG) neurons. Moreover, we also demonstrated that ROS inhibitor (NAC) also inhibited H2O2-induced apoptosis and anaerobic glycolysis in rat DRG neurons. In conclusion, dexmedetomidine suppressed H2O2-induced apoptosis and anaerobic glycolysis activity by inhibiting ROS, in rat DRG neurons. Therefore, dexmedetomidine might play a pivotal role in neuropathic pain by the inhibition of ROS.

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Population-based study of central post-stroke pain in Rimini district, Italy

Cited by 18 publications

References 30 publications

The effects of central post-stroke pain on quality of life and depression in patients with stroke

The effects of central post-stroke pain on quality of life and depression in patients with stroke

Post-stroke pain hypersensitivity induced by experimental thalamic hemorrhage in rats is region-specific and demonstrates limited efficacy of gabapentin

Dexmedetomidine alleviated neuropathic pain in dorsal root ganglion neurons by inhibition of anaerobic glycolysis activity and enhancement of ROS tolerance

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