Coronavirus disease 2019 (COVID-19) is an emerging global health emergency caused by the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The global outbreak of SARS-CoV-2 infection has been declared a global pandemic by the World Health Organization (WHO). The clinical presentation of SARS-CoV-2 infection depends on the severity of the disease and may range from an asymptomatic infection to a severe and lethal illness. Fever, cough, and shortness of breath are among the most common symptoms associated with SARS-CoV-2 infection. Accumulating evidence indicates that COVID-19 patients commonly develop neurological symptoms, such as headache, altered mental status, anosmia, and myalgia. In this comprehensive literature review, we have summarized the most common neurological complications and reported neurological case studies associated with COVID-19, and neurological side effects associated with COVID-19 treatments. Additionally, the post-acute COVID-19 syndrome and long-term neurological complications were discussed. We also explained the proposed mechanisms that are involved in the pathogenesis of these neurological complications.

Glioblastoma multiforme (GBM) is an aggressive tumor that has a poor prognosis with a median survival of 15 months with treatment and 3-4 months without treatment. Subsets of patients are found to survive longer than two years, some survivors lived more than 10 years, and rare cases survived 20 years or more with treatment. Better prognosis has been found to be associated with many factors. Some of these factors are related to patients' characteristics, biological factors that impact tumor aggressiveness, and/or factors associated with treatment. However, the exact contribution for extended survival is still not known. Finding the factors that have a strong impact on the long survival is of high importance and can help give hope to better treat glioblastoma cases. In this report, we present a case of a glioblastoma patient who was diagnosed at the age of 47 years with more than 20-year survival. We further discuss the suggested factors that may have contributed to a better prognosis with a focus on the possible role of varicella-zoster infection in mediating long-term survival.

Neurofibromatosis type 1 is an autosomal dominant genetic disease and a common tumor predisposition syndrome that affects 1 in 3000 to 4000 patients in the USA. Although studies have been conducted to better understand and manage this disease, the underlying pathogenesis of neurofibromatosis type 1 has not been completely elucidated, and this disease is still associated with significant morbidity and mortality. Treatment options are limited to surgery with chemotherapy for tumors in cases of malignant transformation. In this review, we summarize the advances in the development of targeted pharmacological interventions for neurofibromatosis type 1 and related conditions.

Background: Phantom limb syndrome is defined as the perception of intense pain or other sensations that are secondary to a neural lesion in a limb that does not exist. It can be treated using pharmacological and surgical interventions. Most medications are prescribed to improve patients’ lives; however, the response rate is low. In this case report, we present a case of phantom limb syndrome in a 42-year-old female with a history of transradial amputation of the left thoracic limb due to an accidental compression one year before. The patient underwent placement of a deep brain stimulator at the ventral posteromedial nucleus (VPM) on the right side and removal secondary to loss of battery. The patient continued to have a burning pain throughout the limb with a sensation of still having the limb, which was subsequently diagnosed as phantom limb syndrome. After a thorough discussion with the patient, a right stereotactic centro-median thalamotomy was offered. An immediate response was reported with a reduction in pain severity on the visual analogue scale (VAS) from a value of 9–10 preoperative to a value of 2 postoperative, with no postoperative complications. Although phantom limb pain is one of the most difficult to treat conditions, centro-median thalamotomy may provide an effective stereotactic treatment procedure with adequate outcomes.

Metrics & MoreArticle Recommendations D r. Yin and colleagues discussed the possible role of vascular endothelial growth factor (VEGF) in COVD-19-related brain inflammation. The authors claimed that the role of VEGF in COVID-19-related brain inflammation may be mediated through angiopoietins. 1 Although we agree that VEGF may play an important role in the development of cytokine storm in COVID-19-related brain inflammation, the authors mistakenly used angiopoietin and angiotensin interchangeably, and this may confuse the reader. Specifically, the authors used the abbreviation Ang II for angiopoietin 2; however, Ang II is the abbreviation for angiotensin II, and Ang 2 is the correct abbreviation for angiopoietin 2. 2−4 The authors also incorrectly stated that angiopoietin 2, which was abbreviated Ang II in the abstract and subsequent sections of the article, was the product of the SARS-CoV-2-attacking target, angiotensin-converting enzyme 2 (ACE2). In reality, angiotensin II (Ang II) is the product of ACE2; therefore, SARS-CoV-2 actually targets angiotensin II (Ang II), not angiopoietin 2 (Ang 2). 2−4 Further, the authors mentioned that exogenous VEGF and Ang II (alone or combination) facilitated the release of inflammatory cytokines, such as IL-8 and IL-6. The cited reference reports that angiopoietin 2 (Ang 2) and not Ang II is induced by VEGF and facilitates the release of IL-8 and IL-6. 5 On the basis of the context of the article, it may be interpreted that the authors were referring to angiopoietin 2 when they used the abbreviation Ang II; however, this abbreviation was also used for angiotensin II in subsequent text and figures. The authors also conclude that angiotensin II (Ang II) plays a role in the upregulation of TNF-α, IL-1β, IL-6, IL-8, and ICAM-1 in brain inflammation through a vicious cycle. Nonetheless, the literature that was referenced did not support this claim; instead, it described the role of angiopoietin 2 in the upregulation of cytokines. Therefore, it is not clear if the authors have a reference for this conclusion that was unintentionally excluded or if they inadvertently used the previous reference that was used to describe the role of angiopoietin to support this claim.According to findings from previous studies, we believe that VEGF may play a role in the development of cytokine storm and that a biological correlation may exist between angiotensin II (Ang II), VEGF, and angiopoietin 2 (Ang 2). For example, studies have revealed that angiotensin II induces angiopoietin 2 and VEGF, and angiotensin II has also been implicated in angiogenesis. 6−9 Additionally, angiotensin II promotes the inflammation and release of various inflammatory mediators. 10−12 However, we have yet to uncover evidence that supports the role of VEGF in the activation of angiotensin II signaling and COVID-19-related brain inflammation that was described in this article.