Neural basis of eye surface sensations
At a recent international eye meeting, Carlos Belmonte, MD, PhD, Alicante, Spain, gave the EuCornea Medal Lecture on the topic of
“Neural basis of eye surface sensations. From dryness to pain.”
Many surgeons have resorted to innovative surgical procedures, such as meibomian gland probing with or without platelet rich plasma insertion, Intense Pulsed Light, and even autologous stem cells inserted into the meibomian glands, in efforts to help patients find relief of debilitating pain conditions.
Pain in and around the eye can be very frustrating to treat. This pain goes by many names: eye pain, neuropathic pain, pain without stain, trigeminal neuralgia, chronic foreign body sensation, headache, and even migraine.
Many surgeons have resorted to innovative surgical procedures, such as meibomian gland probing with or without platelet rich plasma insertion, Intense Pulsed Light, and even autologous stem cells inserted into the meibomian glands, in efforts to help patients find relief of debilitating pain conditions.
These new procedures have sparked an interest in really trying now to understand the underlying pathophysiology of eye Lai.
Eye pain is similar to pain in other parts of the body: nociceptive pain and neuropathic pain.
Pain referred to the ocular surface represents a variety of conditions, diseases, and environmental factors wherein the underlying mechanisms leads to the common phenotypic feature of pain.
The below is from ESCRS:
Dr. Belmonte notes the eye surface is innervated by distinct trigeminal ganglion neuron classes that differ in their expression of ion channels, responsiveness to natural stimuli, and behavior under pathological conditions.
Mechano- and polymodal corneal nociceptor neurons respond to injurious mechanical, chemical, and thermal noxious stimuli and mediate pain sensations.
Low and high threshold thermoreceptor neurons respond respectively to moderate or intense cooling and to osmolarity and mediate unpleasant dryness sensations evoked by excessive evaporation and high tear osmolarity, he said.
Dr. Belmonte added that hyperexcitability and spontaneous activity of eye neurons is a common feature in ocular pain and may arise from several processes, such as altered expression, trafficking, and function of ion channels. They lead to amplification of the sensory message sent by primary sensory neurons to the brain, he said. Additionally, aggressions to the corneal surface cause local inflammation and nerve-terminal damage, whose relative importance depends on the nature of the pathological process.
Injury causes decreased sensitivity to natural stimuli and also aberrant spontaneous activity in all types of corneal neurons, Dr. Belmonte said, and inflammation enhances responsiveness of polymodal- and mechano-nociceptors and decreases activity of cold thermoreceptors.
He concluded saying that, in pathological processes affecting the eye surface, nerve injury and/or inflammation make a variable contribution to the final disturbances experienced by eye sensory neurons, and this may partially explain the differences in neurosensory and autonomic symptoms shown by each pathology.
Dr. Belmonte notes the eye surface is innervated by distinct trigeminal ganglion neuron classes that differ in their expression of ion channels, responsiveness to natural stimuli, and behavior under pathological conditions.
Mechano- and polymodal corneal nociceptor neurons respond to injurious mechanical, chemical, and thermal noxious stimuli and mediate pain sensations.
Low and high threshold thermoreceptor neurons respond respectively to moderate or intense cooling and to osmolarity and mediate unpleasant dryness sensations evoked by excessive evaporation and high tear osmolarity, he said.
Dr. Belmonte added that hyperexcitability and spontaneous activity of eye neurons is a common feature in ocular pain and may arise from several processes, such as altered expression, trafficking, and function of ion channels. They lead to amplification of the sensory message sent by primary sensory neurons to the brain, he said. Additionally, aggressions to the corneal surface cause local inflammation and nerve-terminal damage, whose relative importance depends on the nature of the pathological process.
Injury causes decreased sensitivity to natural stimuli and also aberrant spontaneous activity in all types of corneal neurons, Dr. Belmonte said, and inflammation enhances responsiveness of polymodal- and mechano-nociceptors and decreases activity of cold thermoreceptors.
He concluded saying that, in pathological processes affecting the eye surface, nerve injury and/or inflammation make a variable contribution to the final disturbances experienced by eye sensory neurons, and this may partially explain the differences in neurosensory and autonomic symptoms shown by each pathology.
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What this all means is that the cause of eye pain is very complex and the treatment is complex. What was name of pt Thank you again. have amazing new treatments that work if the patient comes in early enough before permanent scar tissue forms in multiple tissue layers. Otherwise, potential chronic pain conditions start which can lead to a lifetime of needing pain pills, steroids, and now even medical marijuana.