Differentiation of clinical phenotypes of inflammatory and neuropathic ocular pain conditions with morphologic measures and functional brain neuroimaging
NIH/NEI U01EY034686 Grant
Chronic ocular surface pain can occur from two different mechanisms: neuropathy and inflammation. Neuropathic pain involves damage to the somatosensory nervous system, a network of neural circuits to detect sensory information such as temperature, touch, texture, and pain. Neuropathic pain is commonly caused by disease or lesions. Inflammatory/nociceptive pain is caused by harmful stimuli being detected by nociceptors in the body. Nociceptors are a type of sensory receptor that transduces noxious stimuli into a neural signal. Our lab is collaborating with the University of Miami and Massachusetts Eye and Ear Infirmary to differentiate the neural circuitry in patients who have neuropathic ocular pain from those with inflammatory pain. With the use of quantitative sensory testing (QST), in vivo confocal microscopy (IVCM), diffusion tensor imaging (DTI), and functional magnetic resonance imaging (fMRI), we will determine the measurable structural and functional differences in the central nervous system and peripheral nervous systems between controls and the pain sub-types. By understanding the neural pathways of different pain mechanisms, we hope to better define clinical phenotypes with the goal to better treat ocular pain with precision treatments.
Neural plasticity of pain pathways and corneal afferent regeneration following corneal cross-linking (CXL) in keratoconus patients
The Cathedral Fund/David Borsook Project Fund Award
Our long-term objective is the characterization of the short-term and long-term impact of CXL, a corneal surgery, on nervous system pathways of pain. Using functional neuroimaging and in vivo corneal microscopy (IVCM), this project examines whether long-term changes can be quantified and predicted based on risk factors. Our hypothesis is that CXL damages trigeminal afferents to cause acute pain, and that neuroplastic changes in trigeminal circuitry, corneal afferent regeneration, and psychological factors are related to postoperative chronic pain outcomes. The project hopes to define the neuroplastic changes that take place during recovery or the transition into corneal neuropathic pain and determine whether the extent of corneal afferent damage following CXL is connected with the development of chronic pain.
Neural mechanisms underlying photophobia and dry eye
VA CSR&D Merit Review Award I01 CX002015 in collaboration with Anat Galor at the VA Miami
Photophobia is a debilitating condition that describes painful sensitivity to light. Photophobia is a symptom of dry eye (DE), which in extreme cases includes a component of chronic ocular pain. Photophobia affects many daily activities, including the ability to go outdoors, watch television, and use a computer. Our overall hypothesis is that photophobia is an indicator of central pathologic plasticity of 1) trigeminal pathways, and 2) melanopsin pathways. In this program, we use fMRI to examine the neural underpinnings of photophobia and ocular pain. This groundbreaking research aims to advance understanding of ocular pain in order to enhance treatment options.
The trigeminal nociceptive-pain pathway in pediatric mTBI: peripheral and central contributions to photophobia
NIH/NEI R01EY034135 Grant
Concussion, also referred to as mild traumatic brain injury (mTBI), is a neurological disorder that causes disability in children and predisposes them to challenges later in life, including significant physical, cognitive, and psychological disability. The trigeminal nerve innervates the majority of the face and eyes, may be impacted by mTBI. Our theory is that the trigeminal nerve and downstream neural circuits are adversely impacted in mTBI. This project characterizes trigeminal nerve pathology in patients with mTBI using quantitative sensory testing (QST), in vivo corneal nerve microscopy (IVCM), and diffusion tensor imaging (DTI). fMRI and DTI are used to assess central nervous system alterations to light-induced pathways associated with mTBI-related photophobia.