Central poststroke pain and Wallenberg's lateral medullary infarction: Frequency, character, and determinants in 63 patients

MacGowan, Daniel; Janal, Mel; Clark, W C; Wharton, Ralph N.; Lazar, Ronald M.; Sacco, Ralph L.; Mohr, J. P.

doi:10.1212/wnl.49.1.120

Cited by 153 publications

(92 citation statements)

References 11 publications

(14 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As a result, thalamic lesions were thought to be required for development of pain, and the syndrome was referred to for decades by the misleading term "thalamic pain." Research since that time has established that CPS can result from damage to any structure along spinothalamo-cortical pathways that convey pain and temperature information (Boivie 2005;Bowsher 1996;Finnerup et al 2003;Kim et al 2007;MacGowan et al 1997;Peyron et al 2000;Schmahmann and Leifer 1992).…”

Section: Introductionmentioning

confidence: 99%

Zona Incerta: A Role in Central Pain

Masri¹,

Quiton²,

Lucas³

et al. 2009

Journal of Neurophysiology

139

174

View full text Add to dashboard Cite

pain syndrome (CPS) is a debilitating condition that affects a large number of patients with a primary lesion or dysfunction in the CNS. Despite its discovery over a century ago, the pathophysiological processes underlying the development and maintenance of CPS are poorly understood. We recently demonstrated that activity in the posterior thalamus (PO) is tightly regulated by inhibitory inputs from zona incerta (ZI). Here we test the hypothesis that CPS is associated with abnormal inhibitory regulation of PO by ZI. We recorded single units from ZI and PO in animals with CPS resulting from spinal cord lesions. Consistent with our hypothesis, the spontaneous firing rate and somatosensory evoked responses of ZI neurons were lower in lesioned animals compared with sham-operated controls. In PO, neurons recorded from lesioned rats exhibited significantly higher spontaneous firing rates and greater responses to noxious and innocuous stimuli applied to the hindpaw and to the face. These changes were not associated with increased afferent drive from the spinal trigeminal nucleus or changes in the ventroposterior thalamus. Thus CPS can result from suppressed inputs from the inhibitory nucleus zona incerta to the posterior thalamus.

show abstract

Section: Introductionmentioning

confidence: 99%

Zona Incerta: A Role in Central Pain

Masri¹,

Quiton²,

Lucas³

et al. 2009

Journal of Neurophysiology

139

174

View full text Add to dashboard Cite

show abstract

“…Thus, LEPs are inappropriate to reflect the slowly emerging, ill-defined and long-lasting phenomena that underlie over-reaction symptoms (hyperalgaesia and allodynia), which are thought to depend on spino-reticulo-thalamic projection systems. [31][32][33] In other words, the slope of energy change associated to allodynic or hyperalgaesic symptoms is commonly not abrupt enough to generate LEPs. Thus, LEPs accurately reflect the spinothalamic deafferentation leading to pain discrimination deficits, but do not index the neural events underlying allodynia and hyperalgaesia.…”

Section: Nature Of the Painmentioning

confidence: 99%

“…44 This figure increases to 25-60% in syringomyelia or brainstem infarcts. 33,37 As pain usually does not develop immediately but commonly one to six months after the triggering event, preventative therapy may be attempted early if we could reliably determine those patients prone to develop neuropathic pain.…”

Section: Laser-evoked Potentials Abnormalities Depend On Both Lesion mentioning

confidence: 99%

Diagnostic Role of Laser-Evoked Potentials in Central Neuropathic Pain

García-Larrea¹,

Godinho²

2007

European Neurological Review

View full text Add to dashboard Cite

“…[2][3][4][5] To date, the largest prospective study, which enrolled 15 754 participants with ischemic stroke from 35 countries, found that 2.7% of patients developed CPSP at 1 year after stroke.…”

mentioning

confidence: 99%

Management of Central Poststroke Pain

Mulla

Wang

Khokhar

et al. 2015

Stroke

View full text Add to dashboard Cite

C entral poststroke pain (CPSP) is a chronic (≥3 months) neuropathic disorder that can occur after a lesion or disease affecting the central somatosensory system. 1 The pain may be spontaneous, occurring either constantly or intermittently, or evoked in response to external stimuli.1 It may develop immediately after a stroke, or years later. [2][3][4][5] To date, the largest prospective study, which enrolled 15 754 participants with ischemic stroke from 35 countries, found that 2.7% of patients developed CPSP at 1 year after stroke.6 Because CPSP case definition is complex, 1 however, its reported prevalence is variable, and dependent on the site of lesion: 1 study, for instance, found that 25% of patients with brain stem infarcts developed CPSP within 6 months. 4 Individuals with CPSP commonly experience sensory abnormalities, including increased tactile and thermal sensitivities, which impair their quality of life. [7][8][9] The underlying mechanisms of CPSP are poorly understood, 1 contributing to challenges in its management.There are several pharmacological and nonpharmacological therapies available for patients with CPSP; few systematic Background and Purpose-Central poststroke pain is a chronic neuropathic disorder that follows a stroke. Current research on its management is limited, and no review has evaluated all therapies for central poststroke pain. Methods-We conducted a systematic review of randomized controlled trials to evaluate therapies for central poststroke pain. We identified eligible trials, in any language, by systematic searches of AMED, CENTRAL, CINAHL, DARE, EMBASE, HealthSTAR, MEDLINE, and PsychINFO. Eligible trials (1) enrolled ≥10 patients with central poststroke pain; (2) randomly assigned them to an active therapy or a control arm; and (3) collected outcome data ≥14 days after treatment. Pairs of reviewers, independently and in duplicate, screened titles and abstracts of identified citations, reviewed full texts of potentially eligible trials, and extracted information from eligible studies. We used a modified Cochrane tool to evaluate risk of bias of eligible studies, and collected patient-important outcomes according to recommendations by the Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials. We conducted, when possible, random effects meta-analyses, and evaluated our certainty in treatment effects using the Grading of Recommendations Assessment, Development, and Evaluation System. Results-Eight eligible English language randomized controlled trials (459 patients) tested anticonvulsants, an antidepressant, an opioid antagonist, repetitive transcranial magnetic stimulation, and acupuncture. Results suggested that all therapies had little to no effect on pain and other patient-important outcomes. Our certainty in the treatment estimates ranged from very low to low. Conclusions-Our

show abstract

Central poststroke pain and Wallenberg's lateral medullary infarction: Frequency, character, and determinants in 63 patients

Cited by 153 publications

References 11 publications

Zona Incerta: A Role in Central Pain

Zona Incerta: A Role in Central Pain

Diagnostic Role of Laser-Evoked Potentials in Central Neuropathic Pain

Management of Central Poststroke Pain

Contact Info

Product

Resources

About