RESUMEN
Neuropathic pain (NP), resulting from damage to the somatosensory system, is characterized by either spontaneous or evoked pain. In the context of NP, wherein aberrant signaling pathways contribute to the perception of pain, the thalamus emerges as a key player. This structure is integral to the pain network that includes connections to the dorsal horn of the spinal cord, highlighting its role in the affective-motivational aspects of pain perception. Given its significant involvement, the thalamus is targeted in advanced treatments such as thalamotomy and deep brain stimulation (DBS) when traditional therapies fail, emphasizing the need to understand its function in NP to improve management strategies. This review aimed to provide an overview of the role of the thalamus in the transmission of nociceptive information in NP by discussing the existing evidence, including the effectiveness and safety of current techniques in the management and treatment of NP. This is an integrative review involving the qualitative analysis of scientific articles published in PubMed/MEDLINE, Embase, Scopus, and Web of Science. A total of 687 articles were identified, and after selection, 15 articles were included in this study. All studies reviewed demonstrated varying degrees of effectiveness of DBS and thalamotomy in alleviating painful symptoms, although the relief was often temporary. Many studies noted a reduction in pain perception at the conclusion of treatment compared to pre-treatment levels, with this decrease maintained throughout patient follow-ups. However, adverse events associated with these treatments were also reported. In conclusion, there are some benefits, albeit temporary, to using thalamotomy and DBS to alleviate the painful symptoms of NP. Both procedures are considered advanced forms of surgical intervention that aim to modulate pain pathways in the brain, providing significant relief for patients suffering from chronic pain resistant to conventional treatment. Despite limitations, these surgical interventions offer renewed hope for patients facing disabling chronic pain and can provide a significant improvement in quality of life.
RESUMEN
Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS). Neuropathic pain in MS is a debilitating symptom that significantly impairs the quality of life for a substantial proportion of MS patients. Neuropathic pain in MS stems primarily from demyelination, axonal loss, CNS inflammation, and direct damage to the myelin sheath, leading to pain manifestations such as ongoing extremity pain, Lhermitte's phenomenon, and trigeminal neuralgia (TN). The pathophysiological mechanisms behind MS-related neuropathic pain are explored in this review, highlighting central sensitization, neural dysfunction, spinal thalamic tract dysfunction, and inflammatory processes that exacerbate neuronal damage. Neuropathic pain in MS necessitates comprehensive assessment tools and neurophysiological tests to differentiate neuropathic pain from other MS symptoms accurately. Treatment strategies for MS-related neuropathic pain encompass pharmacological interventions, including anticonvulsants and antidepressants, and emerging therapies targeting specific inflammatory processes. The review advocates for a holistic approach to management, incorporating innovative treatments and multidisciplinary strategies to address both the physical symptoms and psychosocial aspects of this disorder. This comprehensive overview underscores the importance of ongoing research into targeted therapies to improve patient outcomes and enhance the quality of life for those affected by MS.
RESUMEN
Brugada syndrome (BrS) is an inherited arrhythmogenic disorder marked by distinctive ST-segment elevations on electrocardiograms (ECG) and an increased risk of sudden cardiac death. Characterized by mutations primarily in the SCN5A gene, BrS disrupts cardiac ion channel function, leading to abnormal electrical activity and arrhythmias. Although BrS primarily affects young, healthy males, it poses significant diagnostic challenges due to its often concealed or intermittent ECG manifestations and clinical presentation that can mimic other cardiac disorders. Current management strategies focus on symptom control and prevention of sudden death, with implantable cardioverter-defibrillators (ICD) serving as the primary intervention for high-risk patients. However, the complications associated with ICDs and the lack of effective pharmacological options necessitate a cautious and personalized approach. Recent advancements in catheter ablation have shown promise, particularly for managing ventricular fibrillation (VF) storms and reducing ICD shocks. Additionally, pharmacological treatments such as quinidine have been effective in specific cases, though their use is limited by availability and side effects. This review highlights significant gaps in the BrS literature, particularly in terms of long-term management and novel therapeutic approaches. The importance of genetic screening and tailored treatment strategies to better identify and manage at-risk individuals is emphasized. The review aims to enhance the understanding of BrS and improve patient outcomes, advocating for a multidisciplinary approach to this complex syndrome.
RESUMEN
Long QT syndrome (LQTS) is a cardiac disorder characterized by prolonged repolarization of the heart's electrical cycle, which can be observed as an extended QT interval on an electrocardiogram (ECG). The safe and effective management of LQTS often necessitates a multifaceted approach encompassing pharmacological treatment, lifestyle modifications, and, in high-risk cases, the implantation of implantable cardioverter-defibrillators (ICDs). Beta-blockers, particularly nadolol and propranolol, are foundational in treating LQTS, especially for high-risk patients, though ICDs are recommended for those with a history of cardiac arrest or recurrent arrhythmic episodes. Intermediate and low-risk patients are usually managed with medical therapy and regular monitoring. Lifestyle modifications, such as avoiding strenuous physical activities and certain medications, play a critical role. Additionally, psychological support is essential due to the anxiety and depression associated with LQTS. Left cardiac sympathetic denervation (LCSD) offers an alternative for those intolerant to beta-blockers or ICDs. For diagnosis and management, advancements in artificial intelligence (AI) are proving beneficial, enhancing early detection and risk stratification. Despite these developments, significant gaps in understanding the pathophysiology and optimal management strategies for LQTS remain. Future research should focus on refining risk stratification, developing new therapeutic approaches, and generating robust data to guide treatment decisions, ultimately aiming for a personalized medicine approach.