F58. Separation of human central pain and temperature pathways

Abstract

Facial sensations of sharp (pin), warm, cool and touch are transmitted by different peripheral fibers. Animal studies show separate trigeminal nucleus caudalis (NC) neurons responding to pain and temperature modalities but also possibly some polymodal neurons. Traditionally, the animal and human central sensory pathways are described as follows. Pain and temperature fibers travel together to synapse in the inferior trigeminal spinal nucleus, NC. Post-synaptic axons cross the midline in a single pathway to form the pain and temperature trigemino-thalamic pathway. Larger myelinated touch fibers synapse in the brainstem 5th nucleus but smaller touch fibers synapse in spinal nuclei. Disruption of crossing fibers at the midline causes simultaneous pain and temperature deficits in syringomyelia. This report describes 11 syringomyelia patients whose deficits provide evidence for separate, central afferent, post-synaptic pathways for facial pain, warm and cool sensations. Evaluations: MRIs and exams including stimuli at 21–22 °C and 40–41 °C. Exams show discrepancies between warm and cool sensations and between pin and temperature sensations. Preserved touch is present in 3 patients with pin deficit. Three cases lack MRI abnormalities appropriate to their deficit, but 2 of those probably had syringes that were previously larger. Translation of experimental animal studies to human function benefits from verification. Unlike human case reports and animal studies, the spinal cord lesions in our patients did not cause symmetrical pain and temperature deficits. Most human reports of temperature sensation don’t indicate what thermal stimulus was used. Use of careful warm and cool stimuli would likely find additional discrepant cases that also suggest distinct but probably adjacent pain, warm and cool central sensory pathways. Differences between touch and pin sensation may be due to the bilateral touch pathways.