The Journal of Neuroscience, May 2, 2007, 27(18):4995-5004; doi:10.1523/JNEUROSCI.0716-07.2007
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Neurobiology of Disease
Lesions Limited to the Human Thalamic Principal Somatosensory Nucleus (Ventral Caudal) Are Associated with Loss of Cold Sensations and Central Pain
Jong H. Kim,1
Joel D. Greenspan,2
Robert C. Coghill,3
Shinji Ohara,4 and
Frederick A. Lenz1
1Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland 21287-7713, 2Department of Biomedical Sciences, University of Maryland Dental School and University of Maryland Program in Neuroscience, Baltimore, Maryland 21201, 3Department of Neurobiology and Anatomy, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, and 4Department of Neurosurgery, Kyoto Kizugawa Hospital, Kyoto 610-0101, Japan
Correspondence should be addressed to Frederick A. Lenz, Department of Neurosurgery, Johns Hopkins Hospital, Meyer Building 8-181, 600 North Wolfe Street, Baltimore, MD 21287-7713. Email: flenz1{at}jhmi.edu
Central pain is neuropathic pain resulting from a lesion of the CNS, such as a stroke [poststroke central pain (CPSP)]. Lesions involving the posterior thalamus lead to reduction or loss of sensation and to CPSP, although the responsible nuclei have not been identified. We now examine the hypotheses that thalamic lesions must extend posterior to the ventral caudal nucleus (Vc) and include ventral medial posterior nucleus (VMpo), to result in loss of cold sensibility and CPSP. Patients with small thalamic strokes associated with CPSP were evaluated by atlas-based mapping of magnetic resonance imaging scans, and by somatosensory testing. All lesions involved posterior Vc; two lesions also involved nuclei posterior to Vc, but not VMpo. All patients tested had alterations of cold pain sensation and tactile sensation, as measured by von Frey hairs. Three patients had altered cool sensation, and the patient with the least involvement of Vc had normal cool thresholds, suggesting that a critical volume of Vc must be involved before cool sensation is impaired. Perception of warm was impaired only in lesions involving nuclei posterior to Vc. Heat pain perception was never affected. In a subject with cold allodynia, a single-subject protocol PET study measured the responses to immersion of either hand in a 20°C waterbath. The scan during stimulation of the affected hand was characterized by intense activation of contralateral sensorimotor cortex. Therefore, there are modality-specific subnuclear structures in the posterior thalamus, but lesions of Vc not involving VMpo are sufficient to impair cold sensibility and to produce CPSP.
Key words: pain; cold; ventral posterior thalamus; stroke; human; somatosensory
Received Feb. 16, 2007;
revised March 29, 2007;
accepted April 1, 2007.
Correspondence should be addressed to Frederick A. Lenz, Department of Neurosurgery, Johns Hopkins Hospital, Meyer Building 8-181, 600 North Wolfe Street, Baltimore, MD 21287-7713. Email: flenz1{at}jhmi.edu
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