Analysis of the Perception of and Reactivity to Pain and Heat in Patients With Wallenberg Syndrome and Severe Spinothalamic Tract Dysfunction

Abstract

Background-The aim of the study was to assess the consequences of severe spinothalamic tract lesions resulting from lateral medullary infarct and to show that a specific pain perception can be elicited by strong thermal stimulation. Case Descriptions-Both patients examined presented with severe thermoalgic dissociation of the limbs contralateral to the lesion, with normal discriminative somatosensory perception and motor strength. They reported pain perception when touching very warm (Ͼ50°C to 60°C) objects and a brisk, occasionally uncontrolled withdrawal reaction of the arm and hand under the same conditions, without any perception of the heat nature of the stimulus. Warm stimulation, Ͻ45°C, elicited no thermal perception or discrimination. Pain perception could be elicited in both patients by increasing the temperature, with a reproducible threshold of 47°C to 49°C. Pain always occurred after a prolonged delay of 8 to 10 seconds in response to threshold heat, and was described as deep and osseous, and clearly different from that perceived on the nonaffected side. The delay was much shorter when the temperature was increased by 4°C to 5°C. Cold stimulation elicited similar pain perception in one patient. Analysis of subjective perception of laser stimulation showed a much higher pain threshold on the affected hand. There were no laser-evoked potentials on this side, which suggested major spinothalamic injury. Assessment of the RIII noxious reflex revealed persistent response withdrawal reactions, with an increased threshold on the affected side, and partial consciousness of the noxious nature of the stimulus. Conclusions-To

Representation of Somatosensory Modalities in Pathways Ascending from the Spinal Anterolateral Funiculus to the Thalamus Demonstrated by Lesions in Man

“…In two instances, the pathways for mechanically induced and thermally induced pain are dissociated within the spinal cord (table 2). In addition to the cases described here, Rousseaux et al [36] have described two Wallenberg syndrome patients in whom there is dissociation between heat pain and innocuous thermal sensation, as in 3 of our crossed (No. 6, 8 and 9) and 1 uncrossed (No.…”

Neurophysiologic study of central pain in patients with Parkinson disease

“…40 The hyperalgesia to pain stimuli found in our PD-PCP patients is in line with the results obtained from previous QST studies done in patients with PD using various stimulus modalities. 6,13,35,41 This finding is in contrast with the observation of elevated warm and heat pain thresholds observed in stroke 8,9 or patients with MS 11 with central pain, where a structural damage of spino-thalamo-cortical tract may lead to both elevated thresholds and chronic deafferentation pain. 30 Our patients had no lesions in pain pathways, which could explain the absence of high thermal thresholds.…”

“…Usually, LEPs are of reduced amplitude in central neuropathic pain conditions. 9,19,20 Laser stimuli can also activate structures involved in pain processing at a subcortical level 21 and cause reflex autonomic responses such as the sudomotor skin response (SSR). 18,22,23 The laserinduced SSR (l-SSR) results from a synchronized change in sympathetic outflow to sweat glands and, therefore, it may provide information on involuntary physiologic reactions to pain stimuli, such as arousal or alarm.…”

Imaging central pain syndromes

“…An ongoing debate on which specific thalamic nuclei are involved in pain and thermal sensibility has mainly focused on the lateral ventroposterior thalamic nucleus, corresponding to Vc [20•], and the ventral medial posterior thalamic nucleus (VMpo) [21]. Supraspinal lesions giving rise to central pain mainly involve the lateral medulla of the brainstem, but lesions in other structures such as the pons, cerebellum, midbrain, and basal ganglia also have been reported [1,2,5,[22][23][24]. Cortical lesions were mainly identified in the somatosensory pathway, including the parietal lobe, SII, and insula [1,2,6,[25][26][27][28].…”