Carl Y. Saab

ORCID: 0000-0003-4665-9946
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About
Contact & Profiles
Research Areas
  • Pain Mechanisms and Treatments
  • Musculoskeletal pain and rehabilitation
  • Neuroscience and Neuropharmacology Research
  • Ion channel regulation and function
  • EEG and Brain-Computer Interfaces
  • Neural dynamics and brain function
  • Neuroscience and Neural Engineering
  • Spinal Cord Injury Research
  • Pain Management and Treatment
  • Neuroscience of respiration and sleep
  • Pain Management and Placebo Effect
  • Sleep and Wakefulness Research
  • Obstructive Sleep Apnea Research
  • Vestibular and auditory disorders
  • Olfactory and Sensory Function Studies
  • Neuropeptides and Animal Physiology
  • Nerve injury and regeneration
  • Migraine and Headache Studies
  • Transcranial Magnetic Stimulation Studies
  • Neurogenesis and neuroplasticity mechanisms
  • Neural and Behavioral Psychology Studies
  • Multiple Sclerosis Research Studies
  • Anesthesia and Neurotoxicity Research
  • Vagus Nerve Stimulation Research
  • Pharmacological Effects of Natural Compounds

Brown University
2015-2025

Cleveland Clinic Lerner College of Medicine
2022-2025

Cleveland Clinic
2022-2025

Rhode Island Hospital
2013-2024

Case Western Reserve University
2020-2024

Providence College
2006-2024

University School
2023

Allen Institute for Brain Science
2019-2021

Island Hospital
2021

John Brown University
2021

Spinal cord injury (SCI) can result in hyperexcitability of dorsal horn neurons and central neuropathic pain. We hypothesized that these phenomena are consequences, part, dysregulated expression voltage-gated sodium channels. Because the rapidly repriming TTX-sensitive channel Nav1.3 has been implicated peripheral pain, we investigated its role pain after SCI. In this study, adult male Sprague Dawley rats underwent T9 spinal contusion injury. Four weeks when extracellular recordings...

10.1523/jneurosci.23-26-08881.2003 article EN Journal of Neuroscience 2003-10-01

Peripheral nerve injury is known to upregulate the rapidly repriming Na v 1.3 sodium channel within first-order spinal sensory neurons. In this study, we hypothesized that (1) after peripheral injury, second-order dorsal horn neurons abnormally express 1.3, which (2) contributes responsiveness of these and pain-related behaviors. To test hypotheses, adult rats underwent chronic constriction (CCI) sciatic nerve. Ten days CCI, allodynia hyperalgesia were evident. situ hybridization,...

10.1523/jneurosci.0300-04.2004 article EN cc-by-nc-sa Journal of Neuroscience 2004-05-19

Spinal cord contusion injury (SCI) is known to induce pain-related behaviour, as well hyperresponsiveness in lumbar dorsal horn nociceptive neurons associated with the aberrant expression of Nav1.3, a rapidly repriming voltage-gated sodium channel. Many these second-order project third-order ventrobasal complex thalamus. In this study we hypothesized that, following SCI, thalamus undergo electrophysiological changes linked Nav1.3. Adult male Sprague-Dawley rats underwent SCI at T9 thoracic...

10.1093/brain/awh623 article EN Brain 2005-08-18

<title>Abstract</title> Clinical diagnosis of sleep disorders, which are recognized contributors to morbidity and mortality, often relies on polysomnography (PSG) data. However, the vast physiologic data collected during PSG is underutilized, presenting a key opportunity enhance characterization dysfunction predict clinical outcomes. We introduce foundation model that uniquely integrates time-series signals electronic medical record Using diverse dataset (n=10,000; mean observation period...

10.21203/rs.3.rs-6307069/v1 preprint EN Research Square (Research Square) 2025-04-10

Axonal degeneration within the spinal cord contributes substantially to neurological disability in multiple sclerosis (MS). Thus neuroprotective therapies that preserve axons, so they maintain their integrity and continue function, might be expected result improved outcome. Sodium channels are known provide a route for sodium influx can drive calcium influx, via reverse operation of Na+/Ca2+ exchanger, after injury axons CNS, channel blockers have been shown protect CNS from experimental...

10.1152/jn.00434.2003 article EN Journal of Neurophysiology 2003-11-01

Axonal degeneration is a major contributor to non-remitting deficits in multiple sclerosis, and there thus considerable current interest the development of strategies that might prevent axonal loss neuroinflammatory disease. Dysregulation sodium ion homeostasis has been implicated mechanisms leading degeneration, several studies have shown blockade channels can ameliorate axon damage following anoxic, traumatic nitric oxide-induced CNS injury. Two channel blockers, phenytoin flecainide,...

10.1093/brain/awl216 article EN Brain 2006-06-09

Thalamocortical oscillations are critical for sensory perception. Although pain is known to disrupt synchrony in thalamocortical oscillations, evidence the literature controversial. coherence has been reported be increased patients with neurogenic but decreased a rat model of central pain. Moreover, theta (4 8 Hz) primary somatosensory (S1) cortex speculated predict humans. To date, link between and network animal models understudied. Thus, we tested hypothesis that disrupts S1 power two We...

10.1016/j.pain.2014.01.013 article EN Pain 2014-01-20

We recently showed that spinal cord contusion injury (SCI) at the thoracic level induces pain-related behaviors and increased spontaneous discharges, hyperresponsiveness to innocuous noxious peripheral stimuli, enlarged receptive fields in neurons ventral posterolateral (VPL) nucleus of thalamus. These changes are linked abnormal expression Na(v)1.3, a rapidly repriming voltage-gated sodium channel. In this study, we examined burst firing properties VPL after SCI. Adult male Sprague-Dawley...

10.1152/jn.01009.2005 article EN Journal of Neurophysiology 2006-02-16

Summary Rats with peripheral neuropathy manifest a range of abnormal firing patterns single neurons in the ventral posterolateral thalamus, whereas high-frequency, but not low-frequency, microstimulation within thalamus reverses these changes and attenuates hyperalgesia. Chronic neuropathic pain is associated long-term at multiple levels neuroaxis, including brain, where electrical stimulation has been used to manage severe conditions. However, clinical outcome deep brain often mixed,...

10.1016/j.pain.2011.07.011 article EN Pain 2011-09-09

Oscillations are fundamental to communication between neuronal ensembles. We previously reported that pain in awake rats enhances synchrony primary somatosensory cortex (S1) and attenuates coherence S1 ventral posterolateral (VPL) thalamus. Here, we asked whether similar changes occur anesthetized modulates phase-amplitude coupling VPL S1. also hypothesized the suppression of burst firing using Z944, a novel T-type calcium channel blocker, restores thalamocortical connectivity. Local field...

10.1097/j.pain.0000000000000362 article EN Pain 2015-09-23

Abstract Pain modulates rhythmic neuronal activity recorded by Electroencephalography (EEG) in humans. Our laboratory previously showed that rat models of acute and neuropathic pain manifest increased power primary somatosensory cortex (S1) electrocorticography (ECoG). In this study, we hypothesized increases EEG corticocortical coherence different pain, whereas treatments with clinically effective analgesics reverse these changes. results show cortical over S1 prefrontal (PFC) awake, freely...

10.1097/j.pain.0000000000000652 article EN Pain 2016-06-20

Pain is a multidimensional experience mediated by distributed neural networks in the brain. To study this phenomenon, EEGs were collected from 20 subjects with chronic lumbar radiculopathy, age and gender matched healthy subjects, 17 pain scheduled to receive an implanted spinal cord stimulator. Analysis of power spectral density, coherence, phase-amplitude coupling using conventional statistics showed that there no significant differences between radiculopathy control groups after...

10.1016/j.neuroimage.2020.117256 article EN cc-by NeuroImage 2020-08-29

Ketamine is an N-Methyl-D-Aspartate (NMDA) receptor antagonist, which has been found to effectively treat somatic and neuropathic pain. This study examines the effect (on pain) of preemptive ketamine using different routes administration (intrathecal versus intraperitoneal).The Institutional Animal Care Use Committee approved study. Thirty male Sprague-Dawley rats (250-275 g) were divided into three treatment groups [intrathecal saline/intraperitoneal saline or Control (CTL), intrathecal...

10.1016/s1098-7339(99)90129-3 article EN Regional Anesthesia & Pain Medicine 1999-05-01

Fractalkine (FKN) evokes nociceptive behavior in nai ve rats, whereas minocycline attenuates pain acutely after neuronal injury. We show that, FKN causes hyperresponsiveness of lumbar wide dynamic range neurons to brush, pressure and pinch applied the hindpaw. One day spinal nerve ligation (SNL), after-discharge responses brush pressure. In contrast, does not alter evoked 10 days SNL or sciatic constriction, but increases spontaneous discharge. speculate that microglia rapidly sensory...

10.1016/j.febslet.2006.06.087 article EN FEBS Letters 2006-07-07

Abstract Magneto- and/or electro-encephalography (M/EEG) are non-invasive clinically relevant tools that have long been used to measure electromagnetic fields in the somatosensory cortex evoked by innocuous and noxious stimuli. Two commonly applied stimulation paradigms produce distinct responses primary (SI) linked sensations electrical median nerve (MN) cutaneous laser-evoked (LE) dorsum of hand, respectively. Despite their prevalence, physiological mechanisms stereotypic macroscale MN LE...

10.1162/imag_a_00095 article EN cc-by Imaging Neuroscience 2024-02-01

Spinal cord stimulation (SCS) utilizing time-dynamic pulses (TDPs) is an emergent field of neuromodulation that continuously and automatically modulates pulse parameters. We previously demonstrated TDPs delivered for 60 min at paresthesia-free or minimal paresthesia amplitudes significantly reversed allodynia in a rat model neuropathic pain. Because the anti-allodynic effect was observed to persist post-stimulation, we hypothesized anti-nociceptive effects may longer than those tonic...

10.3389/fpain.2025.1541078 article EN cc-by Frontiers in Pain Research 2025-04-09

Cerebellar dysfunction in multiple sclerosis (MS) contributes significantly to disability, is relatively refractory symptomatic therapy, and often progresses despite treatment with disease-modifying agents. We previously observed that sodium channel Nav1.8, whose expression normally restricted the peripheral nervous system, present cerebellar Purkinje neurons a mouse model of MS (experimental autoimmune encephalomyelitis [EAE]) humans MS. Here, we tested hypothesis upregulation Nav1.8...

10.1002/ana.22665 article EN Annals of Neurology 2011-11-02

We tested the relation between pain behavior, theta (4-8 Hz) oscillations in somatosensory cortex and burst firing thalamic neurons vivo. Optically-induced bursts attenuated cortical mechanical allodynia. It is proposed that are an adaptive response to de-synchronizes decreases sensory salience.

10.1038/s41598-017-02753-6 article EN cc-by Scientific Reports 2017-05-23
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