Peripheral Nervous System Complications Research Articles

Neurological involvement in patients with primary immunodeficiency.

Primary immunodeficiency diseases (PID) are defined by recurrent infections, allergies, autoimmunity, and malignancies. Neurologic symptoms are one of the major components of some immunodeficiency syndromes, such as Ataxia-Telangiectasia (AT), Nijmegen breakage syndrome (NBS), and Purine Nucleoside Phosphorylase (PNP) deficiency, which are considered as the primary involvement. Various pathological mechanisms, DNA repair disorders, metabolic abnormalities, and autoimmune phenomena have also been linked with neurological conditions. We retrospectively assessed the neurological involvement in 108 patients out of 6000 with PID in this study. The female/male ratio of the cases was 49/59, and the median age was 13 years (min = 1; max = 60). Neurological problems were detected at a median age of 7 years (min = 0.5; max = 30). Di George Syndrome (DGS) and CVID (common variable immunodeficiency) were the most common diseases in our cohort (n = 31, 30% and n = 30, 27%, respectively). The most frequent outcomes were cognitive delay (n = 63, 58%), epilepsy (n = 25, 23%), and ataxia (n = 20, 18%). Central nervous system involvement was found in 99% of the patients (n = 107), and peripheral nervous system complication was found in only one patient with CVID and chronic inflammatory demyelinating polyneuropathy (CDIP). Cranial MRI was found to be abnormal in 74% (n = 80) of the patients. MRI findings included cerebellar atrophy (n = 33, 34%), white matter lesion (n = 27, 28.4%), cerebral atrophy (n = 21, 22.3%), gray matter lesion (n = 6, 6.3%), hydrocephalus (n = 5, 5,3%), and pituitary gland lesion (n = 3, 3.2%), intracranial hemorrhage (n = 3, 3%), intracranial vasculitis (n = 3, 2.7%), and arterio-venous malformation (n = 1, 0,9%). Primary involvement (a component of the disease) was 60% (n = 65), and secondary (infection or autoimmunity) and tertiary involvements (structural or incidental lesions) contributed 20% (n = 20) each in the patients. In this study, we describe the various neurologic findings of patients with PID. The neurologic presentation may represent the initial manifestation of certain types of PID. Early diagnosis and treatment are essential to prevent or reduce further neurologic damages.

Systemic Lupus Erythematosus Patients in the Qassim Region, Saudi Arabia: Insights on Peripheral Nervous System Involvements

Background: Systemic lupus erythematosus (SLE) is a complex autoimmune disorder with diverse clinical manifestations. This study aimed to investigate the prevalence, clinical features, and risk factors associated with peripheral nervous system (PNS) involvement in SLE patients. Materials and Methods: This study encompassed a retrospective analysis involving 377 SLE patients diagnosed according to the European Alliance of Associations for Rheumatology/American College of Rheumatology criteria at Qassim region in Saudi Arabia, conducted through a meticulous chart review facilitated by proficient data collectors. A structured data collection form/checklist, incorporating explicit definitions and instructions, was utilized for extracting information from patient files, papers, and databases. Additionally, the SLE Quality of Life Questionnaire was employed to evaluate the quality of life among the participants. A multivariate logistic regression model was employed to identify independent predictors of PNS involvement. Results: Distinct clinical patterns were observed in SLE patients with PNS involvement, including a higher prevalence of nonscarring alopecia, acute cutaneous lesions, oral ulcers, and seizures. Diabetes and chronic kidney disease emerged as significant positive predictors for PNS complications. Hematological abnormalities, renal involvement, and vitamin deficiencies were prevalent, contributing to an overall poor quality of life among these patients. Conclusion: This study underscores the need for heightened clinical awareness of PNS complications in SLE, emphasizing the impact of diabetes and chronic kidney disease as significant risk factors. Early detection and targeted interventions are crucial to improving outcomes and enhancing the overall quality of life for SLE patients with PNS involvement.

Molecular Pathogenesis of Central and Peripheral Nervous System Complications in Anderson-Fabry Disease.

Fabry disease (FD) is a recessive monogenic disease linked to chromosome X due to more than two hundred mutations in the alfa-galactosidase A (GLA) gene. Modifications of the GLA gene may cause the progressive accumulation of globotriaosylceramide (Gb3) and its deacylated form, globotriasylsphingosine (lyso-Gb3), in lysosomes of several types of cells of the heart, kidneys, skin, eyes, peripheral and central nervous system (not clearly and fully demonstrated), and gut with different and pleiotropic clinical symptoms. Among the main symptoms are acroparesthesias and pain crisis (involving the peripheral nervous system), hypohidrosis, abdominal pain, gut motility abnormalities (involving the autonomic system), and finally, cerebrovascular ischemic events due to macrovascular involvement (TIA and stroke) and lacunar strokes and white matter abnormalities due to a small vessel disease (SVS). Gb3 lysosomal accumulation causes cytoplasmatic disruption and subsequent cell death. Additional consequences of Gb3 deposits are inflammatory processes, abnormalities of leukocyte function, and impaired trafficking of some types of immune cells, including lymphocytes, monocytes, CD8+ cells, B cells, and dendritic cells. The involvement of inflammation in AFD pathogenesis conflicts with the reported poor correlation between CRP levels as an inflammation marker and clinical scores such as the Mainz Severity Score Index (MSSI). Also, some authors have suggested an autoimmune reaction is involved in the disease's pathogenetic mechanism after the α-galactosidase A deficiency. Some studies have reported a high degree of neuronal apoptosis inhibiting protein as a critical anti-apoptotic mediator in children with Fabry disease compared to healthy controls. Notably, this apoptotic upregulation did not change after treatment with enzymatic replacement therapy (ERT), with a further upregulation of the apoptosis-inducing factor after ERT started. Gb3-accumulation has been reported to increase the degree of oxidative stress indexes and the production of reactive oxygen species (ROS). Lipids and proteins have been reported as oxidized and not functioning. Thus, neurological complications are linked to different pathogenetic molecular mechanisms. Progressive accumulation of Gb3 represents a possible pathogenetic event of peripheral nerve involvement. In contrast, central nervous system participation in the clinical setting of cerebrovascular ischemic events seems to be due to the epitheliopathy of Anderson-Fabry disease with lacunar lesions and white matter hyperintensities (WMHs). In this review manuscript, we revised molecular mechanisms of peripheral and central neurological complications of Anderson-Fabry Disease. The management of Fabry disease may be improved by the identification of biomarkers that reflect the clinical course, severity, and progression of the disease. Intensive research on biomarkers has been conducted over the years to detect novel markers that may potentially be used in clinical practice as a screening tool, in the context of the diagnostic process and as an indicator of response to treatment. Recent proteomic or metabolomic studies are in progress, investigating plasma proteome profiles in Fabry patients: these assessments may be useful to characterize the molecular pathology of the disease, improve the diagnostic process, and monitor the response to treatment.

Predictors for the development of neurological immune-related adverse events of immune checkpoint inhibitors and impact on mortality.

Little is known about risk factors for developing neurological immunological adverse events (neuro-irAEs) from immune checkpoint inhibitors (ICIs). We report the incidence, predictors for development, impact on mortality of neuro-irAEs, and impact of ICIs on pre-existing neurological conditions in a large clinical cohort. Patients who received ICIs between January 2011 and December 2018 were identified from a tertiary cancer center registry. Descriptive statistics were used to summarize patient, cancer, and treatment data. Odds ratios from univariable and multivariable logistic regression models were calculated to identify potential predictors for developing a neuro-irAE. Impact of neuro-irAEs on overall survival was estimated by Kaplan-Meier and Cox proportional hazard models. Overall frequency of neurological irAEs was 2.3%. Peripheral nervous system complications were most frequent (53.6%). Melanoma, younger age, prior chemotherapy, prior resection, CTLA-4 ICIs exposure, and combination PD-1 and CTLA-4 ICIs exposure had significantly higher odds for developing a neuro-irAE (p < 0.05) in univariate but not multivariate models. Those with a neuro-irAE were less likely to die at 3 years compared to those without a neuro-irAE (69% vs. 55%, p = 0.004) in univariate but not multivariate model. Flare of pre-existing neurological condition after exposure to ICIs was present (15.4%, 2 of 13 patients) but manageable. One patient was rechallenged with ICIs without recurrent flare. Neuro-irAEs are not associated with increase in overall mortality. Potential predictors for the development of neuro-irAEs are younger age, melanoma, prior chemotherapy and resection, CTLA-4, or combination ICIs exposure.

Central and Peripheral Nervous System Complications of Vasculitis Syndromes from Pathology to Bedside: Part 2-Peripheral Nervous System.

Peripheral nervous system vasculitides (PNSV) are a heterogeneous group of disorders with a clinical subset that may differ in prognosis and therapy. We provide a comprehensive update on the clinical assessment, diagnosis, complications, treatment, and follow-up of PNSV. Progress in neuroimaging, molecular testing, and peripheral nerve biopsy has improved clinical assessment and decision-making of PNSV, also providing novel insights on how to prevent misdiagnosis and increase diagnostic certainty. Advances in imaging techniques, allowing to clearly display the vessel walls, have also enhanced the possibility to differentiate inflammatory from non-inflammatory vascular lesions, while recent histopathology data have identified the main morphological criteria for more accurate diagnosis and differential diagnoses. Overall, the identification of peculiar morphological findings tends to improve diagnostic accuracy by defining a clearer boundary between systemic and non-systemic neuropathies. Therefore, the definition of epineurium vessel wall damage, type of vascular lesion, characterization of lymphocyte populations, antibodies, and inflammatory factors, as well as the identification of direct nerve damage or degeneration, are the common goals for pathologists and clinicians, who will both benefit for data integration and findings translation. Nevertheless, to date, treatment is still largely empiric and, in some cases, unsatisfactory, thus often precluding precise prognostic prediction. In this context, new diagnostic techniques and multidisciplinary management will be essential in the proper diagnosis and prompt management of PNSV, as highlighted in the present review. Thirty to fifty percent of all patients with vasculitis have signs of polyneuropathy. Neuropathies associated with systemic vasculitis are best managed according to the guidelines of the underlying disease because appropriate workup and initiation of treatment can reduce morbidity. Steroids, or in severe or progressive cases, cyclophosphamide pulse therapy is the standard therapy in non-systemic vasculitic neuropathies. Some patients need long-term immunosuppression. The use of novel technologies for high-throughput genotyping will permit to determine the genetic influence of related phenotypes in patients with PNSV.

Predictors for the Development of Neurological Immune-Related Adverse Events of Immune Checkpoint Inhibitors and Impact on Mortality

Objective To report the incidence, predictors for development, impact on mortality, and impact on pre-existing neurological conditions of neurological immune-related adverse events (irAEs) in a large clinical cohort. Background Immune checkpoint inhibitors (ICI) are associated with irAEs. Although neurological complications have been described, little is known about risk factors for their development and their impact on mortality. The impact of ICIs on pre-existing neurological conditions is also not well understood. Design/Methods Patients who received ICI between January 2013 and December 2018 were identified using a tertiary cancer center registry. Patient demographics, cancer characteristics, treatment type, and concurrent oncologic therapy were summarized using descriptive statistics. Patients with neuro-irAE were compared to those without neuro-irAE during the study timeframe. Odds ratios from univariable and penalized multivariable logistic regression models were calculated to identify potential predictors for developing a neuro-irAE. The impact of a neuro-irAE on overall survival was estimated by Kaplan-Meier and multivariable Cox proportional-hazard models. Results Overall frequency of neurological irAEs was 2.3% (28/1228). Peripheral nervous system complications such as myasthenia gravis, myositis, and neuropathies were the most frequent (53.6%). Melanoma, younger age, prior chemotherapy, prior resection, CTLA-4 ICI exposure, and combination ICI exposure had significantly higher odds for developing a neuro-irAE (p &lt;0.05), but these findings were not statistically significant in the multivariable models. Those with a neuro-irAE had greater survival at 3 years compared to those without a neuro-irAE (69% vs 55%, p = 0.004), but after adjusting for patient and cancer characteristics, this effect was no longer statistically significant. Relapse rate of pre-existing neurological condition after exposure to ICI was 15.4% (2/13). Conclusions Neuro-irAEs are rare and are not associated with an increase in mortality. Potential predictors for the development of neuro irAEs are younger age, melanoma, prior chemotherapy and resection, CTLA-4, or combination ICI exposure. Relapse of a pre-existing neurological condition was uncommon.

ACUTE DISSEMINATED ENCEPHALOMYELITIS POST SARS-COV-2 VACCINATION

Many of the central and peripheral nervous system complications related to severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection have been recently described. An efficient mass vaccination program is required in order to effectively reduce the spreading of the infection and, therefore, minimize long-term sequelae, including neurological ones. Nonetheless, as more patients are accessing the 2019 coronavirus (COVID-19) vaccines, it is important to report potential adverse events. For this reason, we report here, the case of a patient with no remarkable medical history, having developed acute disseminated encephalomyelitis (ADEM) 3 weeks after being vaccinated against COVID-19 Diagnostic criteria for possible autoimmune encephalitis were fulfilled. Our patient showed a good response to plasmapheresis therapy after a failure of corticosteroid one. The Complications of post-vaccination encephalitis following SINOPHARM vaccination still seem to be very rare, but should be diagnosed and treated appropriately.

COVID-19 and the peripheral nervous system. A 2-year review from the pandemic to the vaccine era.

Increasing literature has linked COVID‐19 to peripheral nervous system (PNS) diseases. In addition, as we move from the pandemic to the vaccination era, literature interest is shifting towards the potential association between COVID‐19 vaccines and PNS manifestations. We reviewed published literature on COVID‐19, COVID‐19 vaccines and PNS manifestations between 1 January 2020 and 1 December 2021. For Guillain‐Barré syndrome (GBS), isolated cranial neuropathy (ICN) and myositis associated with COVID‐19, the demographic, clinical, laboratory, electrophysiological and imaging features were included in a narrative synthesis. We identified 169 studies on COVID‐19‐associated complications, including 63 papers (92 patients) on GBS, 29 papers (37 patients) on ICN and 11 papers (18 patients) on myositis. Additional clinical phenotypes included chronic inflammatory demyelinating polyneuropathy, vasculitic neuropathies, neuralgic amyotrophy, critical care‐related complications, and myasthenia gravis. PNS complications secondary to COVID‐19 vaccines have been reported during randomized clinical trials, in real‐world case reports, and during large‐scale surveillance programs. These mainly include cases of GBS, Bell's palsy, and cases of neuralgic amyotrophy. Based on our extensive review of the literature, any conclusion about a pathophysiological correlation between COVID‐19 and PNS disorders remains premature, and solely supported by their temporal association, while epidemiological and pathological data are insufficient. The occurrence of PNS complications after COVID‐19 vaccines seems limited to a possible higher risk of facial nerve palsy and GBS, to a degree that widespread access to the ongoing vaccination campaign should not be discouraged, while awaiting for more definitive data from large‐scale surveillance studies.

Neurological Manifestations of SARS-CoV-2 Infection and the Role of Complement Activation

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, while considered a respiratory illness, is associated with a wide range of neurological manifestations, with severity ranging from transient deficit to permanent disability and death. These neurological manifestations can be divided into central nervous system complications, which include cerebrovascular disease and encephalopathies, and peripheral nervous system complications, which involve the muscle (i.e. muscle injuries, myositis, and peripheral and cranial neuropathies). Complement overactivation has been observed clinically in many studies and is hypothesized to be involved in a variety of pathogenic mechanisms of SARS-CoV-2 infection. These include endothelial damage, thrombosis and hyperinflammation, all of which are completely interconnected and integrated. This article broadly describes the diverse neurological effects of coronavirus disease 2019 and delves into the current literature available on complement in this context.

Central and Peripheral Nervous System Complications of Vasculitis Syndromes From Pathology to Bedside: Part 1-Central Nervous System.

Purpose of ReviewThe aim of this review is to provide a comprehensive update on the clinical assessment, diagnosis, complications, and treatment of primary central nervous system vasculitis (PCNSV).Recent FindingsThe developments in neuroimaging, molecular testing, and cerebral biopsy have enhanced clinical assessment and decision making, providing novel insights to prevent misdiagnosis increasing diagnostic certainty. Advances in imaging techniques visualizing the wall of intracranial vessels have improved the possibility to distinguish inflammatory from non-inflammatory vascular lesions. Large recent studies have revealed a more varied histopathological pictures and disclosed an association with amyloid angiopathy. Unfortunately, therapy remains largely empiric.SummaryPCNSV is a heterogeneous group of disorders encompassing different clinical subsets that may differ in terms of prognosis and therapy. Recent evidence has described a more benign course, with good response to therapy. New diagnostic techniques will play soon a pivotal role in the appropriate diagnosis and prompt management of PCNSV.

Neurological Complications of Pulmonary Embolism: a Literature Review.

Purpose of ReviewThe present review discusses in-depth about neurological complications following acute venous thromboembolism (VTE).Recent FindingsIntracranial hemorrhage, acute ischemic cerebrovascular events, and VTE in brain tumors are described as central nervous system (CNS) complications of PE, while peripheral neuropathy and neuropathic pain are reported as peripheral nervous system (PNS) sequelae of PE. Syncope and seizure are illustrated as atypical neurological presentations of PE.SummaryMounting evidence suggests higher risk of venous thromboembolism (VTE) in patients with neurological diseases, but data on reverse, i.e., neurological sequelae following VTE, is underexplored. The present review is an attempt to explore some of the latter issues categorized into CNS, PNS, and atypical complications following VTE.

Neurological complications of COVID-19: A monocentric experience of a neurological outpatient clinic

Since the onset of the COVID-19 pandemic, numerous central and peripheral nervous system complications related to the virus have been observed. Here we present a case series of neurological complications from our outpatient clinic dedicated to patients with previous SARS-CoV-2 infection.

Peripheral Nervous System Involvement in Non-Primary Pediatric Cancer: From Neurotoxicity to Possible Etiologies.

Peripheral neuropathy is a well described complication in children with cancer. Oncologists are generally well aware of the toxicity of the main agents, but fear the side effects of new drugs. As chemotherapeutic agents have been correlated with the activation of the immune system such as in Chemotherapy Induced Peripheral Neuropathy (CIPN), an abnormal response can lead to Autoimmune Peripheral Neuropathy (APN). Although less frequent but more severe, Radiation Induced Peripheral Neuropathy may be related to irreversible peripheral nervous system (PNS). Pediatric cancer patients also have a higher risk of entering a Pediatric Intensive Care Unit for complications related to therapy and disease. Injury to peripheral nerves is cumulative, and frequently, the additional stress of a malignancy and its therapy can unmask a subclinical neuropathy. Emerging risk factors for CIPN include treatment factors such as dose, duration and concurrent medication along with patient factors, namely age and inherited susceptibilities. The recent identification of individual genetic variations has advanced the understanding of physiopathological mechanisms and may direct future treatment approaches. More research is needed on pharmacological agents for the prevention or treatment of the condition as well as rehabilitation interventions, in order to allow for the simultaneous delivery of optimal cancer therapy and the mitigation of toxicity associated with pain and functional impairment. The aim of this paper is to review literature data regarding PNS complications in non-primary pediatric cancer.

Neurological Complications in Patients with Heart Transplantation.

Neurological complications after heart transplantation are common and include cerebrovascular events (ischemic strokes, hemorrhagic strokes, and transient ischemic attacks), seizures, encephalopathy, central nervous system (CNS) infections, malignancies, and peripheral nervous system complications. Although most neurological complications are transient, strokes and CNS infections can result in high mortality and morbidity. Early recognition and timely management of these serious complications are crucial to improve survival and recovery. Diagnosing CNS infections can be challenging because their clinical presentation can be subtle in the setting of immunosuppression. Immunosuppressive medications themselves can cause a broad spectrum of neurological complications including seizures and posterior reversible encephalopathy syndrome. This article provides a review of the diagnosis and management of neurological complications after cardiac transplantation.

Rehabilitation challenges in COVID-19 induced acute polyradiculoneuropathies

Introduction. SARS-COV 2 infection causes damage of the peripheral nervous system: loss of smell loss of taste and demyelination or axonal injury in the spinal roots and motor and sensory nerves with acute polyradiculoneuritis. As many people are affected by COVID-19, the number of patients with secondary peripheral nervous system damage is increasing. Material and method. There are a significant number of Guillain Barre syndrome (GBS) cases reported in COVID-19 positive patients, leading to the recognition of GBS as one of the peripheral nervous system complications of SARS-COV 2 infection. We are trying to summarise the particularities of specific rehabilitation in post-COVID patients. Results and discussions. The rehabilitation of a COVID patients has particularities, first – because of infectious risk carried by the patient during the procedures, second by the patient’s pulmonary and physical impairments induced by the Coronavirus. Conclusions. There is scarce evidence for rehabilitation interventions, and many recommendations are based on methods developed in other viral infections or chronic pulmonary and neurologic conditions. There is a urgent need for studies regarding the efficacy of interventions in COVID rehabilitation, as the number of patients is constantly increasing. Keywords: therapeutic plasma exchange, plasmapheresis, neuroimmune disorders,rehabilitation,

Neurological and neurourological complications of electrical injuries.

Electrical injury can affect any system and organ. Central nervous system (CNS) complications are especially well recognised, causing an increased risk of morbidity, while peripheral nervous system (PNS) complications, neurourological and cognitive and psychological abnormalities are less predictable after electrical injuries. PubMed was searched for English language clinical observational, retrospective, review and case studies published in the last 30 years using the key words: electrical injury, electrocution, complications, sequelae, neurological, cognitive, psychological, urological, neuropsychological, neurourological, neurogenic, and bladder. In this review, the broad spectrum of neurological, cognitive, psychological and neurourological consequences of electrical trauma are discussed, and clinical features characteristic of an underlying neurological, psychological or neurourological disorder are identified. The latest information about the most recently discovered forms of nervous system disorders secondary to electrical trauma, such as the presentation of neurological sequelae years after electrocution, in other words long-term sequelae, are presented. Unexpected central nervous system or muscular complications such as hydrocephalus, brain venous thrombosis, and amyotrophic lateral sclerosis are described. Common and uncommon neuropsychological syndromes after electrical trauma are defined. Neurourological sequelae secondary to spinal cord or brain trauma or as independent consequences of electrical shock are also highlighted.

Overview of COVID-19 and neurological complications.

The sudden and storming onset of coronavirus 2 infection (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) was associated by severe acute respiratory syndrome. Recently, corona virus disease 19 (COVID-19) has appeared as a pandemic throughout the world. The mutational nature of the virus, along with the different means of entering and spreading throughout the body has involved different organs. Thus, patients are faced with a wide range ofsymptoms and signs. Neurological symptoms, such as anosmia, agnosia, stroke, paralysis, cranial nerve deficits, encephalopathy, meningitis, delirium and seizures, are reported as common complications affecting the course of the disease and its treatment. In this review, special attention was paid to reports that addressed the acute or chronic neurological manifestations in COVID-19 patients who may present acute respiratory syndrome or not. Moreover, we discussed the central (CNS) and peripheral nervous system (PNS) complications in SARS-Cov2-infected patients, and also the pathophysiology of neurological abnormalities in COVID-19.

Central and peripheral nervous system complications of COVID-19: a prospective tertiary center cohort with 3-month follow-up

ObjectiveTo systematically describe central (CNS) and peripheral (PNS) nervous system complications in hospitalized COVID-19 patients.MethodsWe conducted a prospective, consecutive, observational study of adult patients from a tertiary referral center with confirmed COVID-19. All patients were screened daily for neurological and neuropsychiatric symptoms during admission and discharge. Three-month follow-up data were collected using electronic health records. We classified complications as caused by SARS-CoV-2 neurotropism, immune-mediated or critical illness-related.ResultsFrom April to September 2020, we enrolled 61 consecutively admitted COVID-19 patients, 35 (57%) of whom required intensive care (ICU) management for respiratory failure. Forty-one CNS/PNS complications were identified in 28 of 61 (45.9%) patients and were more frequent in ICU compared to non-ICU patients. The most common CNS complication was encephalopathy (n = 19, 31.1%), which was severe in 13 patients (GCS ≤ 12), including 8 with akinetic mutism. Length of ICU admission was independently associated with encephalopathy (OR = 1.22). Other CNS complications included ischemic stroke, a biopsy-proven acute necrotizing encephalitis, and transverse myelitis. The most common PNS complication was critical illness polyneuromyopathy (13.1%), with prolonged ICU stay as independent predictor (OR = 1.14). Treatment-related PNS complications included meralgia paresthetica. Of 41 complications in total, 3 were para/post-infectious, 34 were secondary to critical illness or other causes, and 4 remained unresolved. Cerebrospinal fluid was negative for SARS-CoV-2 RNA in all 5 patients investigated.ConclusionCNS and PNS complications were common in hospitalized COVID-19 patients, particularly in the ICU, and often attributable to critical illness. When COVID-19 was the primary cause for neurological disease, no signs of viral neurotropism were detected, but laboratory changes suggested autoimmune-mediated mechanisms.

Neurological Problems in COVID-19 Pandemic

AbstractCoronavirus disease 2019 (COVID-19) is a potentially severe acute respiratory infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This outbreak, which emerged in Wuhan city, rapidly spread throughout China and has now become a global public health concern. SARS-CoV-2 is a highly pathogenic and transmissible virus. Common clinical manifestations of COVID-19 include fever, dry cough, shortness of breath, muscle ache, headache, and confusion. Currently, there is no confirmed effective therapeutic strategy for COVID-19 because the pathological mechanism is poorly understood. In addition to the respiratory system involvement, recent evidence has shown that SARS-CoV-2 can affect other organ systems including nervous, vascular, digestive, and urinary system. Various neurological complications have also been described in various studies. Nervous system involvement in the case of SARS-CoV-2 is explained by direct neuro invasion, immune mechanism, and other systemic factors. Neurological complications due to SARS-CoV-2 include both central and peripheral nervous system involvement. Central nervous system complications range from mild headache to seizures, encephalitis, myelitis, and acute cerebrovascular accidents. Peripheral nervous system complications range from vague muscle pains to Guillain–Barré syndrome. This article briefly discusses the various neurological and mental health issues related to COVID-19.

Fatal central nervous system co-infection with SARS-CoV-2 and tuberculosis in a healthy child

BackgroundCentral and peripheral nervous system symptoms and complications are being increasingly recognized among individuals with pandemic SARS-CoV-2 infections, but actual detection of the virus or its RNA in the central nervous system has rarely been sought or demonstrated. Severe or fatal illnesses are attributed to SARS-CoV-2, generally without attempting to evaluate for alternative causes or co-pathogens.Case presentationA five-year-old girl with fever and headache was diagnosed with acute SARS-CoV-2-associated meningoencephalitis based on the detection of its RNA on a nasopharyngeal swab, cerebrospinal fluid analysis, and magnetic resonance imaging findings. Serial serologic tests for SARS-CoV-2 IgG and IgA showed seroconversion, consistent with an acute infection. Mental status and brain imaging findings gradually worsened despite antiviral therapy and intravenous dexamethasone. Decompressive suboccipital craniectomy for brain herniation with cerebellar biopsy on day 30 of illness, shortly before death, revealed SARS-CoV-2 RNA in cerebellar tissue using the Centers for Disease Control and Prevention 2019-nCoV Real-Time Reverse Transcriptase-PCR Diagnostic Panel. On histopathology, necrotizing granulomas with numerous acid-fast bacilli were visualized, and Mycobacterium tuberculosis complex DNA was detected by PCR. Ventricular cerebrospinal fluid that day was negative for mycobacterial DNA. Tracheal aspirate samples for mycobacterial DNA and culture from days 22 and 27 of illness were negative by PCR but grew Mycobacterium tuberculosis after 8 weeks, long after the child’s passing. She had no known exposures to tuberculosis and no chest radiographic findings to suggest it. All 6 family members had normal chest radiographs and negative interferon-γ release assay results. The source of her tuberculous infection was not identified, and further investigations by the local health department were not possible because of the State of Michigan-mandated lockdown for control of SARS-CoV-2 spread.ConclusionThe detection of SARS-CoV-2 RNA in cerebellar tissue and the demonstration of seroconversion in IgG and IgA assays was consistent with acute SARS-CoV-2 infection of the central nervous infection. However, the cause of death was brain herniation from her rapidly progressive central nervous system tuberculosis. SARS-CoV-2 may mask or worsen occult tuberculous infection with severe or fatal consequences.