Vivek Sanker

All Publications

• Efficacy of Additional Surgical Decompression on Functional Outcome in Pyogenic Spinal Epidural Abscess With No Neurological Deficit. Korean journal of neurotrauma Kim, M. S., Desai, A., Yu, D., Sanker, V., Kim, S. W., Jeon, I. 2024; 20 (4): 276-288

  Abstract

  The aim of this study was to investigate the efficacy of additional surgical decompression with antibiotics to treat pyogenic spinal epidural abscess (SEA) with no neurological deficits.We retrospectively reviewed the data of patients diagnosed with spontaneous pyogenic SEA in the thoracolumbosacral area who presented with sciatica and no motor deficits in the lower extremities. The treatment took place in a single tertiary hospital. The effects of additional surgical decompression (decompressive laminectomy) and other clinical variables on functional outcome were assessed using the short form 36 (SF-36).Fifty-nine patients (49 men and 10 women, mean age 65.73±12.29 [41-89] years) were included in the analysis. Surgical decompression had been performed in 31 patients (Group S, treated with additional surgical decompression and antibiotics). There were five (15.2%, 5/33) unplanned operations to control leg sciatica among the patients with initially non-surgical plans, and 28 patients were finally treated with only antibiotics (group N-S). Group S showed a statistically significant increased cost of hospitalization compared to group N-S (15,856.37±7,952.83 vs. 10,672.62±4,654.17 US dollars, p=0.004) with no superiority of 6-month functional outcome after the completion of antibiotic treatment (53.65±4.74 vs. 51.75±7.96 SF-36 scores, p=0.266).Although there is a possibility of requiring an unplanned operation to control leg sciatica during conservative antibiotic treatment, overall, additional surgical decompression in pyogenic SEA presenting with no motor deficit of the lower extremity showed increased medical burden and no greater benefit in terms of functional outcomes.

  View details for DOI 10.13004/kjnt.2024.20.e48

  View details for PubMedID 39803337

  View details for PubMedCentralID PMC11711023

• Sonic hedgehog signalling pathway in CNS tumours: its role and therapeutic implications. Molecular brain Wireko, A. A., Ben-Jaafar, A., Kong, J. S., Mannan, K. M., Sanker, V., Rosenke, S. L., Boye, A. N., Nkrumah-Boateng, P. A., Poornaselvan, J., Shah, M. H., Abdul-Rahman, T., Atallah, O. 2024; 17 (1): 83

  Abstract

  CNS tumours encompass a diverse group of neoplasms with significant morbidity and mortality. The SHH signalling pathway plays a critical role in the pathogenesis of several CNS tumours, including gliomas, medulloblastomas and others. By influencing cellular proliferation, differentiation and migration in CNS tumours, the SHH pathway has emerged as a promising target for therapeutic intervention. Current strategies such as vismodegib and sonidegib have shown efficacy in targeting SHH pathway activation. However, challenges such as resistance mechanisms and paradoxical effects observed in clinical settings underscore the complexity of effectively targeting this pathway. Advances in gene editing technologies, particularly CRISPR/Cas9, have provided valuable tools for studying SHH pathway biology, validating therapeutic targets and exploring novel treatment modalities. These innovations have paved the way for a better understanding of pathway dynamics and the development of more precise therapeutic interventions. In addition, the identification and validation of biomarkers of SHH pathway activation are critical to guide clinical decision making and improve patient outcomes. Molecular profiling and biomarker discovery efforts are critical steps towards personalised medicine approaches in the treatment of SHH pathway-associated CNS tumours. While significant progress has been made in understanding the role of the SHH pathway in CNS tumorigenesis, ongoing research is essential to overcome current therapeutic challenges and refine treatment strategies. The integration of molecular insights with advanced technologies and clinical expertise holds great promise for developing more effective and personalised therapies for patients with SHH pathway-driven CNS tumours.

  View details for DOI 10.1186/s13041-024-01155-w

  View details for PubMedID 39568072

  View details for PubMedCentralID PMC11580395

• Theranostics advances in the treatment and diagnosis of neurological and neurosurgical diseases. Archives of medical research Awuah, W. A., Ahluwalia, A., Tan, J. K., Sanker, V., Roy, S., Ben-Jaafar, A., Shah, D. M., Tenkorang, P. O., Aderinto, N., Abdul-Rahman, T., Atallah, O., Alexiou, A. 2024; 56 (1): 103085

  Abstract

  Theranostics represents a significant advance in the fields of neurology and neurosurgery, offering innovative approaches that combine the diagnosis and treatment of various neurological disorders. This innovation serves as a cornerstone of personalized medicine, where therapeutic strategies are closely integrated with diagnostic tools to enable precise and targeted interventions. Primary research results emphasize the profound impact of theranostics in Neuro Oncol. In this context, it has provided valuable insights into the complexity of the tumor microenvironment and mechanisms of resistance. In addition, in the field of neurodegenerative diseases (NDs), theranostics has facilitated the identification of distinct disease subtypes and novel therapeutic targets. It has also unravelled the intricate pathophysiology underlying conditions such as cerebrovascular disease (CVD) and epilepsy, setting the stage for more refined treatment approaches. As theranostics continues to evolve through ongoing research and refinement, its goals include further advancing the field of precision medicine, developing practical biomarkers for clinical use, and opening doors to new therapeutic opportunities. Nevertheless, the integration of these approaches into clinical settings presents challenges, including ethical considerations, the need for advanced data interpretation, standardization of procedures, and ensuring cost-effectiveness. Despite these obstacles, the promise of theranostics to significantly improve patient outcomes in the fields of neurology and neurosurgery remains a source of optimism for the future of healthcare.

  View details for DOI 10.1016/j.arcmed.2024.103085

  View details for PubMedID 39369666

• Novel insights into the role of TREM2 in cerebrovascular diseases. Brain research Awuah, W. A., Ben-Jaafar, A., Kong, J. S., Sanker, V., Shah, M. H., Poornaselvan, J., Frimpong, M., Imran, S., Alocious, T., Abdul-Rahman, T., Atallah, O. 2024; 1846: 149245

  Abstract

  Cerebrovascular diseases (CVDs) include conditions such as stroke, cerebral amyloid angiopathy (CAA) and cerebral small vessel disease (CSVD), which contribute significantly to global morbidity and healthcare burden. The pathophysiology of CVD is complex, involving inflammatory, cellular and vascular mechanisms. Recently, research has focused on triggering receptor expressed on myeloid cells 2 (TREM2), an immune receptor predominantly found on microglia. TREM2 interacts with multiple signalling pathways, particularly toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB), inhibiting patients' inflammatory response. This receptor plays an essential role in both immune regulation and neuroprotection. TREM2 deficiency or dysfunction is associated with impaired microglial responses, exacerbated neurodegeneration and neuroinflammation. Up until recently, TREM2 related studies have focused on neurodegenerative diseases (NDs), however a shift in focus towards CVDs is beginning to take place. Advancements in CVD research have focused on developing therapeutic strategies targeting TREM2 to enhance recovery and reduce long-term deficits. These include the exploration of TREM2 agonists and combination therapies with other anti-inflammatory agents, which may synergistically reduce neuroinflammation and promote neuroprotection. The modulation of TREM2 activity holds potential for innovative treatment approaches aimed at improving patient outcomes following cerebrovascular insults. This review compiles current research on TREM2, emphasising its molecular mechanisms, therapeutic potential, and advancements in CNS disease research.

  View details for DOI 10.1016/j.brainres.2024.149245

  View details for PubMedID 39305972

• Unusual giant plunging sublingual epidermoid cyst: A case report and review of literature. Clinical case reports Safwan, M., Godbole, A. A., Médéus, A. J., García-González, O. Y., Sanker, V., Prashanth, P. S., Dave, T. 2024; 12 (6): e9067

  Abstract

  When treating a painless or asymptomatic mass in the submental or floor of the mouth, sublingual epidermoid cyst should be considered. Despite its irregularity, preventing malignant transformation is essential for a successful outcome.Dermoid and epidermoid cysts are rarely found in the head and neck region. They account for less than 0.01% of all oral cavity cysts. This is a rare case of a sublingual epidermoid cyst of the oral cavity in a 25-year-old male. The patient presented with a painless sublingual swelling for a duration of 1 month. The clinical examination revealed a non-tender swelling in the sublingual region extending to the submental triangle. Magnetic resonance imaging confirmed a 6.2 × 7.7 × 3.2 cm cystic lesion in the sublingual space. Fine needle aspiration cytology confirmed dermoid cyst contents. Intra-oral surgical excision under general anesthesia was performed successfully. Histopathological analysis revealed that the cyst wall was lined by stratified squamous epithelium. The presence of a prominent granular layer and keratin flakes confirmed the diagnosis of an epidermoid cyst. Postoperative recovery was good, and no recurrence was observed during follow-up. This case emphasizes the infrequent and unusual presentation of a case of a giant plunging sublingual epidermoid cyst and promotes awareness and potential studies in the enhancement of patient care in this area.

  View details for DOI 10.1002/ccr3.9067

  View details for PubMedID 38868117

  View details for PubMedCentralID PMC11166552