Central post-stroke pain: Current evidence

Kumar, Gyanendra; Soni, Chetan Rasiklal

doi:10.1016/j.jns.2009.04.030

Cited by 90 publications

(88 citation statements)

References 102 publications

(121 reference statements)

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“…[16][17][18] However, no standard treatment exists for CPSP. One reason for this lack of an effective standard treatment is that no animal model had been available to determine the mechanisms mediating the development of CPSP.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Adjuvant Analgesics on Cerebral Ischemia-Induced Mechanical Allodynia

Matsuura

Harada

Tokuyama

2016

Biological & Pharmaceutical Bulletin

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Central post-stroke pain (CPSP), a potential sequela of stroke, is classified as neuropathic pain. Although we recently established a CPSP-like model in mice, the effects of adjuvant analgesics as therapeutic drugs for neuropathic pain in this model are unknown. Hence, the aim of the present study was to assess the usefulness of our model by evaluating the effects of adjuvant analgesics used for treating neuropathic pain in this mouse model of CPSP. Male ddY mice were subjected to 30 min of bilateral carotid artery occlusion (BCAO). The development of hind paw mechanical allodynia was measured after BCAO using the von Frey test. The mechanical allodynia was significantly increased on day 3 after BCAO compared with that during the pre-BCAO assessment. BCAO-induced mechanical allodynia was significantly decreased by intraperitoneal injections of imipramine (a tricyclic antidepressant), mexiletine (an antiarrhythmic), gabapentin (an antiepileptic), or a subcutaneous injection of morphine (an opioid receptor agonist) compared with that following vehicle treatment in BCAO-mice. By contrast, milnacipran (a serotonin and norepinephrine reuptake inhibitor), paroxetine (selective serotonin reuptake inhibitor), carbamazepine (antiepileptic), and indomethacin (nonsteroidal anti-inflammatory drug) did not affect the BCAO-induced mechanical allodynia. Our results show that BCAO in mice may be useful as an animal model of CPSP. In addition, BCAO-induced mechanical allodynia may be suppressed by some adjuvant analgesics used to treat neuropathic pain.Key words central post-stroke pain; global ischemia; allodynia; neuropathic pain Pain may occur with actual substantial or even potential histologic lesions, producing uncomfortable sensory and emotional experiences, according to the definition by the International Association for the Study of Pain. One type of pain, neuropathic pain, is caused by dysfunctional peripheral or central nerves and results in the appearance of allodynia and hypersensitivity to pain.1,2) Cerebral stroke patients may experience several types of pain, including musculoskeletal pain, headache, and neuropathic central post-stroke pain (CPSP).Among the different types of neuropathic pain, CPSP is an especially intractable condition to treat. CPSP is associated with various symptoms, such as burning and lancinating pain, and the incidence of CPSP after cerebral stroke is reportedly 1-14%. 3,4) In clinical studies, the risk factors associated with CPSP are the degree of brain infarction, sexual dimorphism, alcohol intake, depression anamnesis, statin use, dyslipidemia, diabetes, and peripheral vascular disorder.5) The pathogenic mechanisms for CPSP and neuropathic pain appear similar at the point of excitation of primary afferent fibers and for epistatic or central excitation or suppression pathway disorders. Recently, we established a CPSP-like animal model by experimentally inducing focal (middle cerebral artery occlusion model) or global cerebral ischemia (bilateral carotid artery occlusion model; BCAO). 6,...

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Section: Discussionmentioning

confidence: 99%

“…Animals All experimental procedures were approved by the ethics committee for animals at Kobe Gakuin University (approval number: [14][15][16][17][18][19][20][21]. The experiments were performed on male ddY mice (5 weeks old, 25-30 g) obtained from SLC (Shizuoka, Japan).…”

Section: Methodsmentioning

confidence: 99%

Effects of Adjuvant Analgesics on Cerebral Ischemia-Induced Mechanical Allodynia

Matsuura

Harada

Tokuyama

2016

Biological & Pharmaceutical Bulletin

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“…Central post-stroke pain (CPSP) is a type of central neuropathic pain that is induced by a primary lesion of the central somatosensory system following ischemic or hemorrhagic stroke [1][2][3]. CPSP occurs most often after strokes that involve the thalamus [4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

“…The quality of life of patients with CPSP is very poor due to daily paroxysms of persistent spontaneous pain and hypersensitivity to noxious (hyperalgesia and allodynia) and non-noxious stimuli (paresthesia and dysesthesia) [10][11][12][13]. So far, the clinical treatment of CPSP has been inadequate due to resistance to both drug and non-drug therapies in about half of the affected patients [1,2,[14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Yang

et al. 2016

Neurosci. Bull.

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The a 2 d-1 subunit of the voltage-gated Ca 2? channel (VGCC) is a molecular target of gabapentin (GBP), which has been used as a first-line drug for the relief of neuropathic pain. GBP exerts its anti-nociceptive effects by disrupting trafficking of the a 2 d-1 subunit to the presynaptic membrane, resulting in decreased neurotransmitter release. We previously showed that GBP has an antiallodynic effect in the first two weeks; but this is followed by insensitivity in the later stage after repeated administration in a rat model of central post-stroke pain (CPSP) hypersensitivity induced by intra-thalamic hemorrhage. To explore the mechanisms underlying GBP insensitivity, the cellular localization and time-course of expression of the a 2 d-1 subunit in both the thalamus and spinal dorsal horn were studied in the same model. We found that the a 2 d-1 subunit was mostly localized in neurons, but not astrocytes and microglia. The level of a 2 d-1 protein increased in the first two weeks after injury but then decreased in the third week, when GBP insensitivity occurred. Furthermore, the a 2 d-1 down-regulation was likely caused by later neuronal loss in the injured thalamus through a mechanism other than apoptosis. In summary, the present results suggest that the GBP receptor a 2 d-1 is mainly expressed in thalamic neurons in which it is up-regulated in the early stage of CPSP but this is followed by dramatic down-regulation, which is likely associated with GBP insensitivity after long-term use.Keywords Central post-stroke pain Á Calcium channel a 2 d subunit Á Gabapentinoid Á Thalamic hemorrhagic stroke Á Thalamus Á Spinal dorsal horn

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“…15 The percentage may be higher in patients with strokes involving the spinothalamic pathway or central pain processing areas. [16][17][18] Antidepressants are considered the first line of treatment, followed by anticonvulsants and opiates.…”

Section: Discussionmentioning

confidence: 99%

The Nucleus Accumbens as a Potential Target for Central Poststroke Pain

Mallory

Abulseoud

Hwang

et al. 2012

Mayo Clinic Proceedings

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Although deep brain stimulation (DBS) has been found to be efficacious for some chronic pain syndromes, its usefulness in patients with central poststroke pain (CPSP) has been disappointing. The most common DBS targets for pain are the periventricular gray region (PVG) and the ventralis caudalis of the thalamus. Despite the limited success of DBS for CPSP, few alternative targets have been explored. The nucleus accumbens (NAC), a limbic structure within the ventral striatum that is involved in reward and pain processing, has emerged as an effective target for psychiatric disease. There is also evidence that it may be an effective target for pain. We describe a 72-year-old woman with a large right hemisphere infarct who subsequently experienced refractory left hemibody pain. She underwent placement of 3 electrodes in the right PVG, ventralis caudalis of the thalamus, and NAC. Individual stimulation of the NAC and PVG provided substantial improvement in pain rating. The patient underwent implantation of permanent electrodes in both targets, and combined stimulation has provided sustained pain relief at nearly 1 year after the procedure. These results suggest that the NAC may be an effective DBS target for CPSP.

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Central post-stroke pain: Current evidence

Cited by 90 publications

References 102 publications

Effects of Adjuvant Analgesics on Cerebral Ischemia-Induced Mechanical Allodynia

Effects of Adjuvant Analgesics on Cerebral Ischemia-Induced Mechanical Allodynia

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

The Nucleus Accumbens as a Potential Target for Central Poststroke Pain

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