1. 1. The loss or diminution of the spontaneous electrical discharges of the sensory cortex following lesions or destruction of the ipsilateral ventral posterior thalamic nuclei is often only transitory (experiments in cats). It may be followed by a tendency to periodic burst discharges or by a continuous activity of increased amplitude that may be subject to spontaneous fluctuations. 2. 2. The development of a hypersensitivity of the respective cortical area to toxins such as Mecholyl or Metrazol could be demonstrated. Mecholyl may accentuate an existing or bring to light a latent assymetry of the spontaneous discharges and/or the tendency to burst discharges. 3. 3. Stimulation of sensory nerves (ulnar, sciatic) is still able to elicit evoked potentials (secondary responses of Forbes) in the sensory cortex deprived of its connections with the ventral posterior thalamic nuclei. On bilateral peripheral stimulation with single shocks, one notices that the secondary response is more pronounced in the sensory area corresponding to the thalamic lesion than in the opposite cortex; this difference becomes more marked under the effect of Mecholyl. 4. 4. These findings may have a bearing upon the development of pain and hyperpathia in cerebral lesions extending into the white matter below the sensory cortex.