A Young Female with SARS-CoV-2 Infection Presenting with Concurrent Neurological and Pulmonary Manifestations: A Case Report

Coronavirus disease 2019 (COVID-19), besides its well-known deleterious effects on the respiratory system, is also reported to affect the central nervous system (CNS), presenting with neurological manifestations, that are commoner among older patients with associated co-morbidities and in the critically ill with COVID pneumonia. Infective, cerebrovascular, and hypoxic-toxic-metabolic etiology have been implicated. Reported outcomes have been poor with persistent neurological deficits among the majority who have survived. We report a young lady who presented with neurological manifestations alongside moderately severe COVID-19 pneumonia. Diagnosed early and managed as severe encephalopathy after excluding infective and cerebrovascular aetiology. Responded well to conservative measures and made a complete recovery. Early recognition of neurological manifestations of COVID-19 disease followed by the institution of appropriate therapies improved the outcomes.

Neurological manifestation in COVID-19 disease with neuroimaging studies.

OBJECTIVE: Magnetic resonance imaging (MRI) of the brain or spine examines the findings as well as the time interval between the onset of symptoms and other adverse effects in coronavirus disease that first appeared in 2019 (COVID-19) patients. The goal of this study is to look at studies that use neuroimaging to look at neurological and neuroradiological symptoms in COVID-19 patients. METHODS: We try to put together all of the research on how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes neurological symptoms and cognitive-behavioral changes and give a full picture. RESULTS: We have categorized neuroimaging findings into subtitles such as: headache and dizziness; cerebrovascular complications after stroke; Intracerebral Hemorrhage (ICH); Cerebral Microbleeds (CMBs); encephalopathy; meningitis; encephalitis and myelitis; altered mental status (AMS) and delirium; seizure; neuropsychiatric symptoms; Guillain-Barre Syndrome (GBS) and its variants; smell and taste disorders; peripheral neuropathy; Mild Cognitive Impairment (MCI); and myopathy and myositis. CONCLUSION: In this review study, we talked about some MRI findings that show how COVID-19 affects the nervous system based on what we found.

The Spectrum of Neuro-COVID is Broader than Frequently Anticipated.

The spectrum of neuro-COVID is broader than anticipated. Neurological disease in COVID-19 may be due to a direct attack of the virus, due to the immune response against the virus, secondary due to affection of the heart or arteries, or due to side effects from the treatment applied against COVID-19. How to cite this article: Finsterer J. The Spectrum of Neuro-COVID is Broader than Frequently Anticipated. Indian J Crit Care Med 2023;27(5):366-367.

Associations of the neutrophil/lymphocyte ratio, monocyte/ lymphocyte ratio, and platelet/lymphocyte ratio with COVID-19 disease severity in patients with neurological symptoms: A cross-sectional monocentric study.

Objectives: Data are limited regarding the relationship of neutrophil/lymphocyte ratio (NLR), monocyte/lymphocyte ratio (MLR), and platelet/ lymphocyte ratio (PLR) with neurological symptoms (NS) in COVID-19 patients. This study is the first to assess the utility of the NLR, MLR, and PLR for predicting COVID-19 severity in infected patients with NS. Materials and Methods: Consecutive 192 PCR-positive COVID-19 patients with NS were included in this cross-sectional and prospective study. The patients were classified into the non-severe and severe groups. We analyzed routinely complete blood count in these groups in terms of COVID-19 disease severity. Results: Advanced age, a higher body mass index, and comorbidities were significantly more common in the severe group (P < 0.001). Among the NS, anosmia (P = 0.001) and memory loss (P = 0.041) were significantly more common in the non-severe group. In the severe group, the lymphocytes and monocyte counts and the hemoglobin level were significantly lower, while the neutrophil count, NLR, and PLR were significantly higher (all P < 0.001). In the multivariate model, advanced age and a higher neutrophil count were independently associated with severe disease (both P < 0.001) but the NLR and PLR were not (both P > 0.05). Conclusion: We found positive associations of COVID-19 severity with the NLR and PLR in infected patients with NS. Further research is required to shed more light on the role of neurological involvement in disease prognosis and outcomes.

Neurological Symptoms Common in Covid-19 Patients: A Retrospective Observational Study

In December 2019, a novel coronavirus outbreak spread rapidly all over the world. The virus is known to be neuroinvasive, but much is still unknown. In this study, we aimed to pres-ent the main neurologic symptoms in patients who were diagnosed with coronavirus disease 2019 (COVID-19). The study was conducted retrospectively by phoning 156 patients in Turkey diagnosed with COVID-19 through real-time polymerase chain reaction;only 100 patients could be reached. Data about their demographics, initial symptoms, neurological symptoms, and sleeping habits were collected. During the disease process, 66% had at least one neurological symptom, 55% had central nervous system symptoms, 42% had peripheral nervous system symptoms, and 64% had sleep disturbances and myalgia. Impaired consciousness, smell and taste impairments, and sleep disturbances were significantly higher in patients with positive chest computed tomography imaging (p < 0.05). Neurological symptoms were observed in COVID-19, as in other coronaviruses. Headache in particular was the most common symptom in our population. In patients with respiratory system findings, the detec-tion of certain neurological symptoms such as smell-taste impairments, impaired consciousness, and sleep disorders were more common. We concluded that COVID-19 patients should be approached in a more holistic way, taking the nervous system into account.Copyright © 2022, Dr. Mladen Stojanovic University Hospital. All rights reserved.

Neurological manifestations of COVID-19 infection in acute and late phases: A case-control study

Background & Objective: The late-term neurological effects of COVID-19 are not fully understood yet. Herein, we aimed to determine if COVID-19-related acute and late-term neurological symptoms exist in the patient group that differs from the general population during the pandemic period. Methods: Two hundred fifty patients with a history of COVID-19, whose treatments were completed at least one month before enrollment, were examined together with a control group consisting of 150 individuals that lived in the same socio-cultural environment during the same period. A survey that included questions about possible neurological symptoms that might be related to the COVID-19 infection was completed in both groups. Results: The patient and control groups were mostly similar regarding the neurological symptoms in the pre-pandemic period. The control group did not report any new symptoms except ageusia during the pandemic period. Whereas a number of neurological symptoms such as headache, ageusia and anosmia, difficulty in thinking and planning, forgetfulness, clumsiness of one or both hands, dizziness, unsteadiness, numbness in both hands and feet, and neuropathic pain occurred during the infection. Neurological symptoms, except headache and unsteadiness, prolonged to the late-term with a decreased prevalence. Conclusion: The emergence of new neurological symptoms during the pandemic in those with COVID-19 disease, unlike the control group, suggested that these symptoms are related to the infection itself. © 2023, ASEAN Neurological Association. All rights reserved.

Lactoferrin for Mental Health: Neuro-Redox Regulation and Neuroprotective Effects across the Blood-Brain Barrier with Special Reference to Neuro-COVID-19.

Overall mental health depends in part on the blood-brain barrier, which regulates nutrient transfer in-and-out of the brain and its central nervous system. Lactoferrin, an innate metal-transport protein, synthesized in the substantia nigra, particularly in dopaminergic neurons and activated microglia is vital for brain physiology. Lactoferrin rapidly crosses the blood-brain barrier via receptor-mediated transcytosis and accumulates in the brain capillary endothelial cells. Lactoferrin receptors are additionally present on glioma cells, brain micro-vessels, and neurons. As a regulator of neuro-redox, microglial lactoferrin is critical for protection/repair of neurons and healthy brain function. Iron imbalance and oxidative stress are common among patients with neurodegenerative disorders such as Parkinson's disease, Alzheimer's disease, dementia, depression, and multiple sclerosis. As an endogenous iron-chelator, lactoferrin prevents iron accumulation and dopamine depletion in Parkinson's disease patients. Oral lactoferrin supplementation could modulate the p-Akt/PTEN pathway, reduce Aß deposition, and ameliorate cognitive decline in Alzheimer's disease. Novel lactoferrin-based nano-therapeutics have emerged as effective drug-delivery systems for clinical management of neurodegenerative disorders. Recent emergence of the Coronavirus disease-2019 (COVID-19) pandemic, initially considered a respiratory illness, demonstrated a broader virulence spectrum with the ability to cross the blood-brain barrier and inflict a plethora of neuropathological manifestations in the brain - the Neuro-COVID-19. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections are widely reported in Parkinson's disease, Alzheimer's disease, dementia, and multiple sclerosis patients with aggravated clinical outcomes. Lactoferrin, credited with several neuroprotective benefits in the brain could serve as a potential adjuvant in the clinical management of Neuro-COVID-19.

COVID-19-induced neurological symptoms: focus on the role of metal ions.

Neurological symptoms are prevalent in both the acute and post-acute phases of coronavirus disease 2019 (COVID-19), and they are becoming a major concern for the prognosis of COVID-19 patients. Accumulation evidence has suggested that metal ion disorders occur in the central nervous system (CNS) of COVID-19 patients. Metal ions participate in the development, metabolism, redox and neurotransmitter transmission in the CNS and are tightly regulated by metal ion channels. COVID-19 infection causes neurological metal disorders and metal ion channels abnormal switching, subsequently resulting in neuroinflammation, oxidative stress, excitotoxicity, neuronal cell death, and eventually eliciting a series of COVID-19-induced neurological symptoms. Therefore, metal homeostasis-related signaling pathways are emerging as promising therapeutic targets for mitigating COVID-19-induced neurological symptoms. This review provides a summary for the latest advances in research related to the physiological and pathophysiological functions of metal ions and metal ion channels, as well as their role in COVID-19-induced neurological symptoms. In addition, currently available modulators of metal ions and their channels are also discussed. Collectively, the current work offers a few recommendations according to published reports and in-depth reflections to ameliorate COVID-19-induced neurological symptoms. Further studies need to focus on the crosstalk and interactions between different metal ions and their channels. Simultaneous pharmacological intervention of two or more metal signaling pathway disorders may provide clinical advantages in treating COVID-19-induced neurological symptoms.

Cavernous Sinus Thrombosis Linked to COVID-19 Infection: a Case Report.

The severity of SARS-CoV-2 virus infection is mainly related to its respiratory complications. However, it can also lead to a large variety of thromboembolic events. Symptoms may include headache, fever, and neurological disorders. Since 2020, the clinical presentation of COVID-19 infection has become increasingly varied, leading in some cases to complex symptom associations, including numerous neurological symptoms. SARS-CoV-2 may lead to neurotropism which could reach the central nervous system and all cranial nerves. Cavernous sinus thrombosis is a rare condition and may occur as a complication of ear, nose, and throat (ENT) or facial infections. A 73-year-old man without personal or family history of thrombosis was referred to the emergency room for a sudden appearance of diplopia and ptosis, 3 days after testing positive for COVID-19 infection. An initial head CT-scan found no signs of stroke. He underwent a cerebral MRI 7 days later, which revealed a thrombosis of his right cavernous sinus. A brain CT scan 7 days later showed regression of the thrombosis with complete recanalization of the cavernous sinus. This was accompanied by a complete regression of diplopia and fever. He was discharged from the hospital 10 days after hospital admission. In this case report, we describe a rare event of cavernous thrombophlebitis following a COVID-19 infection.

Two Cases of COVID-19 With Concomitant Unexplained Dental Pain: Coincidence or Related?

As the rapidly evolving Covid-19 pandemic spread and became a global concern and the study of the disease's features became possible, its signs and symptoms were elucidated in many studies around the world. In addition to other fairly typical symptoms including fever, cough, sore throat, and shortness of breath, the Covid-19 pandemic has several neurological symptoms that have been noted and documented, including headaches, muscle, and joint discomfort, loss of taste and smell, as well as generalized body aches. However, there were a few unusual symptoms that were noted, one of which we will focus on in this report, namely, tooth pain. The Covid-19 virus has caused tooth pain and discomfort in two Lebanese patients. The reported pain is not related to any local aggression; therefore, it is likely a neurological consequence of the viral infection by the SARS-Cov-2 virus.

The Very Long COVID: Persistence of Symptoms after 12-18 Months from the Onset of Infection and Hospitalization.

According to the World Health Organization's definition, long COVID is the persistence or development of new symptoms 3 months after the initial infection. Various conditions have been explored in studies with up to one-year follow-up but very few looked further. This prospective cohort study addresses the presence of a wide spectrum of symptoms in 121 patients hospitalized during the acute phase of COVID-19 infection, and the association between factors related to the acute phase of the disease and the presence of residual symptoms after one year or longer from hospitalization. The main results are as follows: (i) post-COVID symptoms persist in up to 60% of the patient population at a mean follow-up of 17 months; (ii) the most frequent symptoms are fatigue and dyspnea, but neuropsychological disturbances persist in about 30% of the patients (iii) when corrected for the duration of follow-up with a freedom-from-event analysis; only complete (2 doses) vaccination at the time of hospital admission remained independently associated with persistence of the major physical symptoms, while vaccination and previous neuropsychological symptoms remained independently associated with persistence of major neuropsychological symptoms.

Association of the matrix metalloproteinases (MMPs) family gene polymorphisms and the risk of coronavirus disease 2019 (COVID-19); implications of contribution for development of neurological symptoms in the COVID-19 patients.

BACKGROUND: Seemingly, the Matrix metalloproteinases (MMPs) play a role in the etiopathogenesis of coronavirus disease 2019 (COVID-19). Here in this study, we determined the association of MMP9 rs3918242, MMP3 rs3025058, and MMP2 rs243865 polymorphisms with the risk of COVID-19, especially in those with neurological syndrome (NS). METHODS: We enrolled 500 patients with COVID-19 and 500 healthy individuals. To genotype the target SNPs, the Real-time allelic discrimination technique was used. To determine serum levels of MMPs, Enzyme-linked immunosorbent assay (ELISA) was exerted. RESULTS: The MMP9 gene rs3918242 and MMP3 gene rs3025058 SNP were significantly associated with increased COVID-19 risk and susceptibility to COVID-19 with NS. The serum level of MMP-9 and MMP-3 was significantly higher in COVID-19 cases compared with the healthy controls. Serum MMP-9 and MMP-3 levels were also higher in COVID-19 subjects with NS in comparison to the healthy controls. The polymorphisms in MMP genes were not associated with serum level of MMPs. CONCLUSION: MMP9 and MMP3 gene polymorphisms increases the susceptibility to COVID-19 as well as COVID-19 with neurologic syndrome, but they probably have no role in the regulation of serum MMP-9 and MMP-3 levels.

Neurological symptoms and neuronal damage markers in acute COVID-19: Is there a correlation? A pilot study.

A wide spectrum of neurological symptoms (NS) has been described in patients with COVID-19. We examined the plasma levels of neuron-specific enolase (NSE) and neurofilament light chain (NFL) together, as neuronal damage markers, and their relationships with clinical severity in patients with NS at acute COVID-19. A total of 20 healthy controls and 59 patients with confirmed COVID-19 were enrolled in this pilot prospective study. Serum NSE and NFL levels were measured by using the enzyme-linked immunoassay method from serum samples. Serum NSE levels were found to be significantly higher in the severe group than in the nonsevere group (p = 0.034). However, serum NFL levels were similar between the control and disease groups (p > 0.05). For the mild group, serum NFL levels were significantly higher in patients with the sampling time ≥5 days than in those with the sampling time <5 days (p = 0.019). However, no significant results for NSE and NFL were obtained in patients with either single or multiple NS across the groups (p > 0.05). Increased serum NSE levels were associated with disease severity regardless of accompanied NS in patients with acute COVID-19 infection. However, serum NFL levels may have a role at the subacute phase of COVID-19.

Functional neurological disorder in people with long COVID: A systematic review.

BACKGROUND AND PURPOSE: Acute health events, including infections, can trigger the onset of functional neurological disorder (FND). It was hypothesized that a proportion of people with long COVID might be experiencing functional symptoms. METHODS: A systematic review of studies containing original data on long COVID was performed. The frequency and characteristics of neurological symptoms were reviewed, looking for positive evidence suggesting an underlying functional disorder and the hypothesized causes of long COVID. RESULTS: In all, 102 studies were included in our narrative synthesis. The most consistently reported neurological symptoms were cognitive difficulties, headaches, pain, dizziness, fatigue, sleep-related symptoms and ageusia/anosmia. Overall, no evidence was found that any authors had systematically looked for positive features of FND. An exception was three studies describing temporal inconsistency. In general, the neurological symptoms were insufficiently characterized to support or refute a diagnosis of FND. Moreover, only 13 studies specifically focused on long COVID after mild infection, where the impact of confounders from the general effects of severe illness would be mitigated. Only one study hypothesized that some people with long COVID might have a functional disorder, and another eight studies a chronic-fatigue-syndrome-like response. DISCUSSION: Neurological symptoms are prevalent in long COVID, but poorly characterized. The similarities between some manifestations of long COVID and functional disorders triggered by acute illnesses are striking. Unfortunately, the current literature is plagued by confounders, including the mixing of patients with initial mild infection with those with severe acute medical complications. The hypothesis that long COVID might in part correspond to a functional disorder remains untested.

Somatic symptom disorder in patients with post-COVID-19 neurological symptoms: A preliminary report from the somatic study (Somatic Symptom Disorder Triggered by COVID-19)

Objectives: To assess the diagnosis of somatic symptom disorder (SSD) in patients with unexplained neurological symptoms occurring after SARS-CoV-2 infection, also referred to as long COVID. Design: Single-centre observational study. Participants: Adult patients experiencing unexplained long-lasting neurological symptoms after mild COVID. Of the 58 consecutive patients referred in our centre, 50 were included. Intervention: Patients were contacted for a standardised psychometric evaluation by phone, followed by a self- survey. Main outcome: Positive diagnosis of SSD according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders-5 (DSM-5). Results: Although the patients did not meet the DSM-5 criteria for a functional neurological symptom disorder specifically, SSD diagnosis based on DSM-5 criteria was positive in 32 (64%) patients. In the remaining 18 patients, SSD was considered possible given the high score on diagnostic scales. Physical examination were normal for all. Brain MRI showed unspecific minor white matter hyperintensities in 8/46 patients. Neuropsychological assessment showed exclusively mild impairment of attention in 14 out of 15 tested patients, in discrepancy with their major subjective complaint. Forty-five (90%) patients met criteria for Chronic Fatigue Syndrome. Seventeen (32%) patients were screened positive for mood-anxiety disorders, 19 (38%) had a history of prior SSD and 27 (54%) reported past trauma. Additional self- survey highlighted post-traumatic stress disorder in 12/43 (28%), high levels of alexithymia traits and perfectionism. Long-lasting symptoms had a major impact with a high rate of insomnia (29/43, 67%), psychiatric follow-up (28/50, 56%) and work or pay loss (25/50, 50%). Conclusion: A majority of patients with unexplained long-lasting neurological symptoms after mild COVID met diagnostic criteria for SSD and may require specific management. (PsycInfo Database Record (c) 2023 APA, all rights reserved)

Does COVID-19 increase risk of stroke?

Aim: In this study, it was aimed to compare the epidemiological characteristics and frequency of patients diagnosed with stroke in Kayseri City Hospital in the pre-COVID-19 pandemic period and during the COVID-19 pandemic and investigate whether COVID-19 increases the frequency of stroke. The true relationship between COVID-19 and the incidence of stroke has yet to be determined. Materials and Methods: A meta-analysis study reported that 1.4% (95%CI: 1.0-1.9) of 108,571 patients with COVID-19 developed acute cerebrovascular disease (CVD). Additionally, although the number of hospital admissions due to clinical presentation of suspected stroke decreased due to the pandemic, it has been suggested that the COVID-19 infection itself may cause a stroke. Results: In the literature, there have been reports of patient groups who developed ischemic stroke 1-2 weeks after diagnosis with typical COVID-19 symptoms, as well as patient groups who developed symptoms such as fever, dry cough, and shortness of breath during follow-up with ischemic stroke and who were subsequently diagnosed with COVID-19. It was observed that patients presented with sudden onset loss of strength showing side without typical COVID-19 symptoms (such as cough, fever), and thoracic CT scans of these patients in the later period revealed pulmonary findings. Conclusion: In other words, COVID-19 patients may present with neurological symptoms such as acute cerebrovascular disease as the first symptom. [ FROM AUTHOR]

Alzheimer's disease risk after COVID-19: a view from the perspective of the infectious hypothesis of neurodegeneration.

In light of the rising evidence of the association between viral and bacterial infections and neurodegeneration, we aimed at revisiting the infectious hypothesis of Alzheimer's disease and analyzing the possible implications of COVID-19 neurological sequelae in long-term neurodegeneration. We wondered how SARS-CoV-2 could be related to the amyloid-ß cascade and how it could lead to the pathological hallmarks of the disease. We also predict a paradigm change in clinical medicine, which now has a great opportunity to conduct prospective surveillance of cognitive sequelae and progression to dementia in people who suffered severe infections together with other risk factors for Alzheimer's disease.

Investigating neurological symptoms of infectious diseases like COVID-19 leading to a deeper understanding of neurodegenerative disorders such as Parkinson's disease.

Apart from common respiratory symptoms, neurological symptoms are prevalent among patients with COVID-19. Research has shown that infection with SARS-CoV-2 accelerated alpha-synuclein aggregation, induced Lewy-body-like pathology, caused dopaminergic neuron senescence, and worsened symptoms in patients with Parkinson's disease (PD). In addition, SARS-CoV-2 infection can induce neuroinflammation and facilitate subsequent neurodegeneration in long COVID, and increase individual vulnerability to PD or parkinsonism. These findings suggest that a post-COVID-19 parkinsonism might follow the COVID-19 pandemic. In order to prevent a possible post-COVID-19 parkinsonism, this paper reviewed neurological symptoms and related findings of COVID-19 and related infectious diseases (influenza and prion disease) and neurodegenerative disorders (Alzheimer's disease, PD and amyotrophic lateral sclerosis), and discussed potential mechanisms underlying the neurological symptoms and the relationship between the infectious diseases and the neurodegenerative disorders, as well as the therapeutic and preventive implications in the neurodegenerative disorders. Infections with a relay of microbes (SARS-CoV-2, influenza A viruses, gut bacteria, etc.) and prion-like alpha-synuclein proteins over time may synergize to induce PD. Therefore, a systematic approach that targets these pathogens and the pathogen-induced neuroinflammation and neurodegeneration may provide cures for neurodegenerative disorders. Further, antiviral/antimicrobial drugs, vaccines, immunotherapies and new therapies (e.g., stem cell therapy) need to work together to treat, manage or prevent these disorders. As medical science and technology advances, it is anticipated that better vaccines for SARS-CoV-2 variants, new antiviral/antimicrobial drugs, effective immunotherapies (alpha-synuclein antibodies, vaccines for PD or parkinsonism, etc.), as well as new therapies will be developed and made available in the near future, which will help prevent a possible post-COVID-19 parkinsonism in the 21st century.

Host Genetic Variants Linked to COVID-19 Neurological Complications and Susceptibility in Young Adults-A Preliminary Analysis.

To date, multiple efforts have been made to use genome-wide association studies (GWAS) to untangle the genetic basis for SARS-CoV-2 infection susceptibility and severe COVID-19. However, data on the genetic-related effects of SARS-CoV-2 infection on the presence of accompanying and long-term post-COVID-19 neurological symptoms in younger individuals remain absent. We aimed to examine the possible association between SNPs found in a GWAS of COVID-19 outcomes and three phenotypes: SARS-CoV-2 infection, neurological complications during disease progression, and long-term neurological complications in young adults with a mild-to-moderate disease course. University students (N = 336, age 18-25 years, European ancestry) with or without COVID-19 and neurological symptoms in anamnesis comprised the study sample. Logistic regression was performed with COVID-19-related phenotypes as outcomes, and the top 25 SNPs from GWAS meta-analyses and an MR study linking COVID-19 and cognitive deficits were found. We replicated previously reported associations of the FURIN and SLC6A20 gene variants (OR = 2.36, 95% CI 1.31-4.24) and OR = 1.94, 95% CI 1.08-3.49, respectively) and remaining neurological complications (OR = 2.12, 95% CI 1.10-4.35 for SLC6A20), while NR1H2 (OR = 2.99, 95% CI 1.39-6.69) and TMPRSS2 (OR = 2.03, 95% CI 1.19-3.50) SNPs were associated with neurological symptoms accompanying COVID-19. Our findings indicate that genetic variants related to a severe COVID-19 course in adults may contribute to the occurrence of neurological repercussions in individuals at a young age.

Wilson-Konovalov disease in a patient after COVID-19 infection

We present a rare clinical case of Wilson-Conovalov disease in a patient after a new coronavirus infection. The development of her neurological symptoms, which allowed to specify the etiology of the already existing liver damage, may have been provoked by the COVID-19 infection, in which the central nervous system is frequently involved in the pathological process. Wilson-Conovalov disease was suspected due to the presence of neurological manifestations and signs of liver cirrhosis. Subsequently, the diagnosis was confirmed genetically, copper metabolism disorders were identified and pathogenetic therapy was prescribed to eliminate excess copper from the body. © 2022 Global Media Technologies. All rights reserved.