hyperalgesia/mŕtvica

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Allodynia in the flank after thalamic stroke.

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Lesions responsible for thalamic pain are often thought to involve the ventral posteromedial nucleus and ventral posterolateral nucleus of the thalamus. We describe two patients with allodynia and hyperpathia in the contralateral flank caused by a small lesion in the posteroventral part of the

Post-stroke tactile allodynia and its modulation by vestibular stimulation: a MEG case study.

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BACKGROUND There is behavioural evidence that caloric vestibular stimulation (CVS) can alleviate central pain. Several such patients have also noted that it reduces tactile allodynia, an especially ill-understood phenomenon in these patients. OBJECTIVE The first aim is to use magnetoencephalography

[Relationship between cutaneous temperature and hand edema and allodynia after stroke--the etiology of shoulder-hand syndrome].

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The etiology of shoulder-hand syndrome is as yet unknown. We hypothesized that it may be due to damaged unmyelinated fibers in front of the subscapular muscle. We examined the existence of edema and hypersensitivity to pain in the hands of stroke patients during the subacute stage and their

Aβ and Aδ but not C-fibres are involved in stroke related pain and allodynia: an experimental study in mice.

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OBJECTIVE Cerebral ischaemia is a leading cause of death and disability, including severe complications such as memory disturbance, palsy, and spasticity. Central post-stroke pain (CPSP) is a complication of cerebral ischaemia, and is characterized clinically by spontaneous pain and attacks of

Allodynia in relation to lesion site in central post-stroke pain.

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Seventy-one percent of 122 patients with central post-stroke pain (CPSP) had allodynia that was tactile-, cold-, or movement-evoked. Site of thalamic (and some infratentorial) lesions as revealed by magnetic resonance imaging (MRI) was correlated in some cases with allodynia type and sensory

Allodynia in patients with post-stroke central pain (CPSP) studied by statistical quantitative sensory testing within individuals.

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The disinhibition hypothesis of post-stroke central pain (CPSP) suggests that 'the excessive response (dysesthesia/hyperalgesia/allodynia) is accompanied by a em leader loss of sensation' resulting from a lesion of a 'lateral nucleus' of thalamus or of 'cortico-thalamic paths' [Brain 34 (1911) 102].

Influence of heterotopic noxious conditioning stimulation on spontaneous pain and dynamic mechanical allodynia in central post-stroke pain patients.

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In 10 patients with central post-stroke pain (CPSP), the influence of ischemia-induced heterotopic noxious conditioning stimulation (HNCS) on the intensity of spontaneous ongoing- and brush-evoked pain was examined. In addition, the modulating effect of ongoing pain and HNCS on pain sensitivity in a

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

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Approximately 20% of patients suffering from stroke with pure or predominant sensory symptoms (referred to as sensory stroke patients) develop central poststroke pain (CPSP). It is largely unknown what distinguishes these patients from those who remain pain free. Using quantitative sensory testing

[Central post-stroke pain].

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Central post-stroke pain (CPSP) is known since the famous Dejerine-Roussy syndrome and its description has not improved. The subject has however been revived over the last decade thanks to advances in central nervous system imaging with magnetic resonance imaging (MRI), the description of allodynia

Establishment of a central post-stroke pain model using global cerebral ischaemic mice.

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OBJECTIVE Stroke is the leading cause of disability in the world. Central post-stroke pain (CPSP), an intractable secondary disease, is a serious problem that occurs following cerebral stroke. However, the detailed mechanisms underlying CPSP and standard treatments for it are not well established.

Late-onset thermal hypersensitivity after focal ischemic thalamic infarcts as a model for central post-stroke pain in rats.

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Central post-stroke pain (CPSP) is a neuropathic pain syndrome that often develops in a delayed manner after thalamic stroke. Here, we describe a new model of CPSP by stereotaxic thalamic injection of endothelin-1. Stroke rats (n = 12), but not saline-injected controls (n = 12), developed a

Successful deep brain stimulation for central post-stroke pain and dystonia in a single operation.

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BACKGROUND Central post-stroke pain is known to be refractory to medications and difficult to manage. We present a case of central post-stroke pain associated with dystonia. Both conditions were successfully treated with a single deep brain stimulation (DBS) operation. METHODS A 60-year-old female

Post-stroke pain caused by peripheral sensory hypersensitization after transient focal cerebral ischemia in rats.

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The mechanisms underlying central post-stroke pain are not well understood and there is no satisfactory treatment. Here, in a rat model of stroke, we measured nociceptive threshold using current stimulation of primary afferent neurons in both hind paws. Male Wistar rats underwent middle cerebral

The effect of upper-extremity aerobic exercise on complex regional pain syndrome type I: a randomized controlled study on subacute stroke.

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OBJECTIVE Complex regional pain syndrome type I (CPRS I), is a complex of symptoms characterized by diffuse pain usually with associated swelling, vasomotor instability, and severe functional impairment of the affected extremity in stroke patients. Pain is a prominent feature and is often refractory

Autoradiographic Measurements of [14C]-Iodoantipyrine in Rat Brain Following Central Post-Stroke Pain.

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Approximately 8% of stroke patients present symptoms of central post-stroke pain (CPSP). CPSP is associated with allodynia and hypersensitivity to nociceptive stimuli. Although some studies have shown that neuropathic pain may involve the dorsolateral prefrontal cortex, rostral anterior cingulate

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