hyperalgesia/infartarse

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Author's experience of lateral medullary infarction--thermal perception and muscle allodynia.

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The patient, the author (S.K.), is a 67-year-old male. He has the typical dissociated pain, altered temperature sensation and ataxia often encountered by patients with lateral medullary infarction. This started at the time of his admission to hospital. Several weeks after discharge, he experienced

Allodynia after lateral-medullary (Wallenberg) infarct. A PET study.

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We used PET to study regional cerebral blood flow (rCBF) changes in nine patients with unilateral central pain after a lateral medullary infarct (Wallenberg's syndrome). All patients presented, on the abnormal side, a combination of hypaesthesia to noxious and thermal stimuli and allodynia to

[Hyperalgesia with loss of temperature sensation in one side of the body due to pinpoint infarction of contralateral spinothalamic tract].

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We report a 67-year-old man who presented sudden loss of temperature sensation associated with hyperalgesia in the left trunk and extremities. No abnormal lesions were found on routine magnetic resonance image (MRI) in the brain and spinal cord. He did not show common manifestations of the lateral

[Studies on white blood cells in regions of cutaneous hyperalgesia in myocardial infarction and in stenocardia].

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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

Cheiro-pedal syndrome following pontine infarction.

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We report the case of a 64-year-old man with sudden onset of numbness in the right hand and foot. Neurological examinations were normal except for hypersthesia, and hyperalgesia of the right hand and foot. Brain MRI demonstrated a high signal intensity on T2-weighted image and a low signal intensity

Thalamic thermo-algesic transmission: ventral posterior (VP) complex versus VMpo in the light of a thalamic infarct with central pain.

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The respective roles of the ventral posterior complex (VP) and of the more recently described VMpo (posterior part of the ventral medial nucleus) as thalamic relays for pain and temperature pathways have recently been the subject of controversy. Data we obtained in one patient after a limited left

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

Baroreceptor reflex is suppressed in rats that develop hyperalgesia behavior after nerve injury.

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The baroreceptor reflex buffers autonomic changes by decreasing sympathetic activity and increasing vagal activity in response to blood pressure elevations, and by the reverse actions when the blood pressure falls. Because of the many bidirectional interactions of pain and autonomic function, we

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

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Central poststroke pain (CPSP) is an infrequently recognized complication of lateral medullary infarction (LMI). We determined the frequency, nature, and predictors of this complication in 63 patients with LMI. The hypothesis tested was that the degree of clinical sensory loss and extent of

Altered experimental pain perception after cerebellar infarction.

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Animal studies have suggested that the cerebellum, in addition to its motor functions, also has a role in pain processing and modulation, possibly because of its extensive connections with the prefrontal cortex and with brainstem regions involved in descending pain control. Consistently, human

Phantom limb pain: are cutaneous nociceptors and spinothalamic neurons involved in the signaling and maintenance of spontaneous and touch-evoked pain? A case report.

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A patient suffered multiple fractures of the right leg and a left brain-stem infarction involving the anterolateral fasciculus of the central nociceptive system following multiple trauma. Later, the right leg was amputated, resulting in spontaneous and touch-evoked phantom pain and mechanical stump

Neuropathic pain attenuates ischemia reperfusion injury through β2-adrenergic pathway.

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OBJECTIVE The relationship between neuropathic pain and myocardial infarction (MI) was uncertain because of some medication or underlying diseases. This study investigated the impact of neuropathic pain on ischemia reperfusion injury using isolated rat hearts and cardiomyocytes. METHODS Male

P2X2/3 receptor activity of rat nodose ganglion neurons contributing to myocardial ischemic nociceptive signaling.

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Myocardial ischemia causes the production of a variety of chemical substances, which act on the cardiac afferent nerve to cause pain. Myocardial damage can affect cardiac vagal afferent activity. Survivors of myocardial infarction are often left with impaired activity of cardiac vagal sensory

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

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