This week in the Journal of Neuroscience, researchers mapped the thalamic nuclei in which damage specifically produces allodynia, a painful response to normally innocuous mechanical or cold stimuli. Lesions to posterior regions of the thalamus produce poststroke central pain (CPSP), as well as loss or reduction of sensation. This week in the Journal of Neuroscience, Kim et al. [1] mapped the thalamic nuclei in which damage specifically produces allodynia, a painful response to normally innocuous mechanical or cold stimuli.

The subjects had experienced small thalamic strokes. The authors used somatosensory testing and atlas-based mapping with positron emission tomography and magnetic resonance imaging.

The authors hypothesized that damage to ventral caudal (Vc) and ventral medial posterior (VMpo) nuclei would be necessary to alter cold sensations and produce CPSP. Although all subjects had lesions to the Vc, the VMpo remained intact.

Nevertheless, sensitivity to cold and tactile pain was compromised in each case. Unlike other subjects, the patient with the best-preserved Vc had a normal threshold for cold sensation. Heat pain thresholds were unaffected, revealing subnuclear modality specificity within the thalamus.


[1] Jong H. Kim, Joel D. Greenspan, Robert C. Coghill, Shinji Ohara, and Frederick A. Lenz