Abstract
The thalamus is the final relay nucleus in the ascending pain pathway and receives its major nociceptive inputs from the spinothalamic and trigeminothalamic tracts (TTTs). These tracts terminate in several regions of medial and lateral thalamus. The terminations of nociceptive-specific neurons in lamina I of the spinal and medullary dorsal horn are to the posterior ventromedial nucleus (VMpo), ventroposterior inferior nucleus (VPI), and the ventrocaudal medial dorsal nucleus (MDvc), whereas the terminations of the nociceptive neurons in the deeper layers are in the ventroposterior nucleus (VP) as well as in VPI and the central lateral nucleus (CL). The main cortical targets of the thalamic regions receiving lamina I neuron projections are the insular cortex via the VMpo and the anterior cingulate cortex via the MDvc, whereas the VP that receives nociceptive inputs primarily from the deep dorsal horn is to primary somatosensory cortex. Nociceptive-specific neurons are located in VMpo and are topographically arranged. VP that contains primarily neurons responding to innocuous tactile stimuli also contains nociceptive neurons in register with the somatotopic pattern of the low-threshold neurons. Stimulation in the human VPI and VMpo region can produce pain, but stimulation in VP is rarely painful. Damage to the lateral thalamus, usually as a result of a stroke, can lead to chronic central pain. The thalamus may play a prominent role in the pathophysiology of central neuropathic pain.
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