Browsing by Author "Gupta, Kunal"

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    Case Report: Novel Anchoring Technique and Surgical Nuances for Trigeminal Ganglion Stimulation in the Treatment of Post-Herpetic Trigeminal Neuropathic Facial Pain
    (Frontiers Media, 2022-03-17) Gupta, Kunal; Neurological Surgery, School of Medicine
    Introduction: Trigeminal ganglion stimulation is a neuromodulatory surgical procedure utilized to treat trigeminal neuropathic pain. This technique involves the placement of a stimulating electrode adjacent to the trigeminal ganglion and can be trialed before permanent implantation. Wider adoption by surgical practitioners is currently limited by complications such as lead migration from the trigeminal ganglion, which can result in loss of therapy and cannot be rectified without repeat surgery. We describe a novel surgical modification that successfully anchors the trigeminal ganglion electrode long-term. Objective: To describe a novel surgical technique for the anchoring of trigeminal ganglion stimulation electrodes and a case report of a patient with post-herpetic trigeminal neuropathic pain treated with this approach. Methods: An electrode was inserted percutaneously through the foramen ovale into Meckel's cave, adjacent to the trigeminal ganglion. The lead was anchored using a modification of an existing anchoring device, which was inserted into the buccal incision. The lead was connected to a generator for therapeutic stimulation. The location of the lead was followed radiographically using serial lateral skull radiographs. Results: A 74-year-old male with post-herpetic trigeminal neuropathic pain, who had failed prior surgical therapies, underwent trigeminal ganglion stimulation. The trial lead was anchored using standard techniques and migrated outward within 7 days, rendering the trial electrode ineffective. The permanent lead was anchored using the described novel technique and remained in position without clinically significant outward migration nor loss in targeted stimulation until the last follow-up at 6 months. Conclusion: Trigeminal ganglion stimulation is an effective therapeutic option for medically refractory trigeminal neuropathic pain. The novel surgical adaptation described prevents the outward migration of the lead and enables stable long-term lead placement.
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    Novel Strategies for the Prevention of Post-Stroke Epilepsy and Sudden Unexpected Death in Epilepsy Patients
    (2022-10) Adhikari, Yadav Prasad; Truitt, William; Witkin, Jeffrey M.; Gupta, Kunal; Brutkiewicz, Randy; Jin, Xiaoming
    Stroke is the second leading cause of mortality worldwide, accounting for 5.5 million deaths annually. In addition to its high mortality rate, stroke is the most common cause of acquired epilepsy. Three to thirty percent of stroke survivors develop post-stroke epilepsy. Although currently available therapies such as thrombolytics and mechanical thrombectomy prevent immediate mortality by restoring blood flow after stroke, these treatments do not target the cellular and molecular mechanisms that lead to post-stroke epileptogenesis. With the increasing number of stroke survivors, there is an urgent need for therapies that prevent epilepsy development in this population. Here, we showed that homeostatic plasticity is involved in the development of hyperexcitability after stroke and can be targeted to prevent the development of post-stroke epilepsy. Using two-photon calcium imaging, we found that homeostatic regulation leads to cortical hyperexcitability after stroke. We also found that activity enhancement by optogenetic and pharmacological approaches can target homeostatic plasticity to prevent post-stroke epilepsy. This study demonstrates the high translational potential of activity enhancement as a novel strategy to prevent post-stroke epilepsy through regulating cortical homeostatic plasticity. Sudden premature death is a leading cause of death in patients with medically refractory epilepsy. This unanticipated death of a relatively healthy person with epilepsy in which no structural or toxicological cause of death can be identified after postmortem analysis is referred to as sudden unexpected death in epilepsy patients (SUDEP). Respiratory failure during seizures is an important underlying mechanism of SUDEP. Here, we showed that LPS-induced peripheral inflammation is protective against SUDEP. This protection is mediated at least in part via enhancing serotonergic function in the brain stem. To the best of our knowledge, this is the first study demonstrating the relationship between peripheral inflammation and SUDEP prevention.
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    Susceptibility-Weighted MRI Approximates Intraoperative Microelectrode Recording During Deep Brain Stimulation of the Subthalamic Nucleus for Parkinson's Disease
    (Elsevier, 2024-01) Budnick, Hailey C.; Schneider, Dylan; Zauber, S. Elizabeth; Witt, Thomas C.; Gupta, Kunal; Neurological Surgery, School of Medicine
    Background Deep brain stimulation of the subthalamic nucleus (STN-DBS) for Parkinson's disease can be performed with intraoperative neurophysiological and radiographic guidance. Conventional T2-weighted magnetic resonance imaging sequences, however, often fail to provide definitive borders of the STN. Novel magnetic resonance imaging sequences, such as susceptibility-weighted imaging (SWI), might better localize the STN borders and facilitate radiographic targeting. We compared the radiographic location of the dorsal and ventral borders of the STN using SWI with intraoperative microelectrode recording (MER) during awake STN-DBS for Parkinson's disease. Methods Thirteen consecutive patients who underwent placement of 24 STN-DBS leads for Parkinson's disease were analyzed retrospectively. Preoperative targeting was performed with SWI, and MER data were obtained from intraoperative electrophysiology records. The boundaries of the STN on SWI were identified by a blinded investigator. Results The final electrode position differed significantly from the planned coordinates in depth but not in length or width, indicating that MER guided the final electrode depth. When we compared the boundaries of the STN by MER and SWI, SWI accurately predicted the entry into the STN but underestimated the length and ventral boundary of the STN by 1.2 mm. This extent of error approximates the span of a DBS contact and could affect the placement of directional contacts within the STN. Conclusions MER might continue to have a role in STN-DBS. This could potentially be mitigated by further refinement of imaging protocols to better image the ventral boundary of the STN.
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    Transcriptome Profiling of the Hippocampal Seizure Network Implicates a Role for Wnt Signaling during Epileptogenesis in a Mouse Model of Temporal Lobe Epilepsy
    (MDPI, 2022-10) Mardones, Muriel D.; Gupta, Kunal; Neurological Surgery, School of Medicine
    Mesial temporal lobe epilepsy (mTLE) is a life-threatening condition characterized by recurrent hippocampal seizures. mTLE can develop after exposure to risk factors such as febrile seizure, trauma, and infection. Within the latent period between exposure and onset of epilepsy, pathological remodeling events occur that contribute to epileptogenesis. The molecular mechanisms responsible are currently unclear. We used the mouse intrahippocampal kainite model of mTLE to investigate transcriptional dysregulation in the ipsilateral and contralateral dentate gyrus (DG), representing the epileptogenic zone (EZ) and peri-ictal zone (PIZ). DG were analyzed after 3, 7, and 14 days by RNA sequencing. In both the EZ and PIZ, transcriptional dysregulation was dynamic over the epileptogenic period with early expression of genes representing cell signaling, migration, and proliferation. Canonical Wnt signaling was upregulated in the EZ and PIZ at 3 days. Expression of inflammatory genes differed between the EZ and PIZ, with early expression after 3 days in the PIZ and delayed expression after 7–14 days in the EZ. This suggests that critical gene changes occur early in the hippocampal seizure network and that Wnt signaling may play a role within the latent epileptogenic period. These findings may help to identify novel therapeutic targets that could prevent epileptogenesis.