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Background: This mini-review aims to summarize and discuss previous and recent advances in the clinical presentation, pathophysiology, diagnosis, treatment, and outcome of SARS-CoV-2-associated peripheral neuropathies. Methods: Literature review. Results: Altogether, 105 articles about SARS-CoV-2-associated neuropathy describing 261 patients were retrieved. Peripheral neuropathy in patients with COVID-19 is frequent and predominantly due to immune mechanisms or neurotoxic side effects of drugs used to treat the symptoms of COVID-19 and, to a lesser extent, due to the compression of peripheral nerves resulting from prolonged bedding in the Intensive Care Unit (ICU) and pre-existing risk factors such as diabetes. SARS-CoV-2 does not cause viral neuropathy. Neurotoxic drugs such as daptomycin, linezolid, lopinavir, ritonavir, hydro-chloroquine, cisatracurium, clindamycin, and glucocorticoids should be administered with caution and patients should be appropriately bedded in the ICU to prevent SARS-CoV-2-associated neuropathy. Patients with Guillain-Barré syndrome (GBS) benefit from immunoglobulins, plasma exchange, and steroids. Conclusions: Neuropathies of peripheral nerves in patients with COVID-19 are frequent and mostly result from immune mechanisms or neurotoxic side effects of drugs used to treat the symptoms of COVID-19 and, to a lesser extent, from the compression of peripheral nerves due to prolonged bedding on the ICU. SARS-CoV-2 does not cause infectious neuropathy.

Although several considerations have been raised suggesting a beneficial effect of N-acetyl cysteine (NAC) for the treatment of severe acute respiratory syndrome coronavirus 2 infection, there is currently no clinical evidence that NAC truly prevents coronavirus disease 2019 (COVID-19), reduces the severity of the disease, or improves the outcome. Appropriately designed clinical trials are warranted to prove or disprove a therapeutic effect of NAC for COVID-19 patients.

OBJECTIVES: Affection of the central nervous system and the eyes is increasingly recognized as manifestations of a SARS-CoV-2 infection (COVID-19). This review aims at summarizing and discussing recent advances concerning causes and locations of impaired vision because of an infection with SARS-CoV-2. METHODS: On a literature search through PubMed and ScholarOne, all available publications about COVID-19 patients with impaired vision were retrieved. RESULTS: Visual impairment in SARS-CoV-2-infected patients may be due to infection of lacrimal glands (dacryoadenitis), conjunctivitis, tonic pupils, vitritis, central retinal artery/venous occlusion, retinitis, retinal bleeding, panuveitis, anterior ischemic optic neuropathy, optic nerve stroke, optic neuritis, optic perineuritis, or occipital ischemic stroke. Visual impairment may be the initial manifestation of SARS-CoV-2. CONCLUSIONS: This mini review shows that impaired vision may be the initial manifestation of COVID-19, that all sections of the visual tract may be affected and causative for visual impairment in COVID-19 patients, and that SARS-CoV-2 manifests along the visual tract with ischemia, focal infection, and immunological reactions.

Heavy metal contamination in aquatic environments plays an important role in the exposure of humans to these toxicants. Among these pollutants, mercury (Hg) is one main concern due to its high neurotoxicity and environmental persistence. Even in low concentrations, Hg bioaccumulation is a major threat to human health, with higher impact on populations whose diet has fish as chief consumption. Mercury compounds have high affinity for neuronal receptors and proteins, which gives Hg its cumulative feature and have the ability to cross cell membranes and blood–brain barrier to show their neurotoxicity. Intoxication with Hg increases levels of reactive oxygen species (ROS), thus depleting faster the resource of antioxidant proteins. To evaluate Hg-induced hippocampal ROS production, synaptic plasticity, anxiety, and memory, a total of 11 male Wistar rats were exposed to HgCl2 (Hg30 group) to produce a residual concentration of 8 ng/mL at the end of 30 days. Behavioral tests (plus-maze discriminative avoidance task), in vitro electrophysiology, and ROS assays were performed. Western blot assay showed decreased levels of antioxidant proteins GPx and SOD in Hg30 group. Increased ROS production was observed in the CA1 and CA3 regions in the Hg-exposed group. Plus-maze task detected long-term memory impairment in Hg30 group, linked to poorer in vitro long-term potentiation as compared to control group. Hg intoxication also promoted higher anxiety-like behavior in the exposed animals. In conclusion, our data suggests that low doses of HgCl2 resulted in impaired long-term memory and unbalance between decreased antioxidant protein expression and increased ROS production in the hippocampus.

The involvement of cranial nerves is being increasingly recognised in COVID-19. This review aims to summarize and discuss the recent advances concerning the clinical presentation, pathophysiology, diagnosis, treatment, and outcomes of SARS-CoV-2 associated cranial nerve mononeuropathies or polyneuropathies. Therefore, a systematic review of articles from PubMed and Google Scholar was conducted. Altogether 36 articles regarding SARS-CoV-2 associated neuropathy of cranial nerves describing 56 patients were retrieved. Out of these 56 patients, cranial nerves were compromised without the involvement of peripheral nerves in 32 of the patients, while Guillain-Barre syndrome (GBS) with cranial nerve involvement was described in 24 patients. A single cranial nerve was involved either unilaterally or bilaterally in 36 patients, while in 19 patients multiple cranial nerves were involved. Bilateral involvement was more prevalent in the GBS group (n=11) as compared to the cohort with isolated cranial nerve involvement (n=5). Treatment of cranial nerve neuropathy included steroids (n=18), intravenous immunoglobulins (IVIG) (n=18), acyclovir/valacyclovir (n=3), and plasma exchange (n=1). The outcome was classified as “complete recovery” in 21 patients and as ”partial recovery” in 30 patients. One patient had a lethal outcome. In conclusion, any cranial nerve can be involved in COVID-19, but cranial nerves VII, VI, and III are the most frequently affected. The involvement of cranial nerves in COVID-19 may or may not be associated with GBS. In patients with cranial nerve involvement, COVID-19 infections are usually mild. Isolated cranial nerve palsy without GBS usually responds favorably to steroids. Cranial nerve involvement with GBS benefits from IVIG.

Parkinson’s disease (PD) is one of the most common age-related neurodegenerative disorders. Several studies over the last few years have shown that PD is accompanied by high rates of premature death compared with healthy controls. Death in PD patients is usually caused by determinant factors such as pneumonia, and cerebrovascular and cardiovascular diseases. During recent years it has emerged that dehydration may also contribute to mortality in PD. Interestingly, it has been documented that a substantial proportion of patients with PD die suddenly (known as sudden and unexpected death in PD). In this article, we focus on the magnitude of the problem of sudden and unexpected death in PD, with special reference to the daily water consumption of PD patients.

Affection of the central nervous system and the eyes is increasingly recognized as manifestations of a SARS-CoV-2 infection (COVID-19). This review aims at summarizing and discussing recent advances concerning causes and locations of impaired vision because of an infection with SARS-CoV-2.On a literature search through PubMed and ScholarOne, all available publications about COVID-19 patients with impaired vision were retrieved.Visual impairment in SARS-CoV-2-infected patients may be due to infection of lacrimal glands (dacryoadenitis), conjunctivitis, tonic pupils, vitritis, central retinal artery/venous occlusion, retinitis, retinal bleeding, panuveitis, anterior ischemic optic neuropathy, optic nerve stroke, optic neuritis, optic perineuritis, or occipital ischemic stroke. Visual impairment may be the initial manifestation of SARS-CoV-2.This mini review shows that impaired vision may be the initial manifestation of COVID-19, that all sections of the visual tract may be affected and causative for visual impairment in COVID-19 patients, and that SARS-CoV-2 manifests along the visual tract with ischemia, focal infection, and immunological reactions.

Ophthalmologic nvolvement in SARS-CoV-infected patients is variegated. One of the ophthalmologic pathologies is optic neuritis. Optic neuritis in SARS-CoV-infected patients may precede the classical pulmonary manifestations of COVID-19 and can be unilateral or bilateral. Optic neuritis has been repeatedly reported in COVID-19 patients and may occur with or without affection of other cranial nerves. Since cerebro-spinal fluid parameters can be abnormal in COVID-19 associated optic neuritis, these patients require a spinal tap. Before diagnosing SARS-CoV-2 associated optic neuritis various differentials need to be excluded. Since SARS-CoV-2 causes endothelial damage complicated by thrombus formation and thromboembolism, ophthalmologic vascular complication due to an infection with SARS-CoV-2 such as anterior ischemic optic neuropathy (AION), central retinal artery occlusion (CRAO), and retinal vein occlusion need to be excluded. CRAO may result from arterial hypertension, myocarditis, heart failure, Takotsubo syndrome, atrial fibrillation, or atrial flutter, frequent cardiac complications of COVID-19. Since CRAO can be accompanied by ischemic stroke, patients with SARS-CoV-2 associated optic neuritis need to undergo a cerebral MRI.

Coronavirus disease 2019 (COVID-19) has become an urgent global health priority. Although most patients with COVID-19 manifest with fever and respiratory tract symptoms, COVID-19 infections may also involve other organs and extrarespiratory manifestations, including cardiac, gastrointestinal, hepatic, renal, and neurological symptoms. This case describes a 16-year-old boy who presented with fever, sore throat, myalgia, and subsequently with shortness of breath. A diagnosis of COVID-19 was confirmed by polymerase chain reaction. His condition deteriorated and he died within 3 days of admission. An evaluation of his past medical history confirmed an episode of viral illness which had progressed to myositis and rhabdomyolysis 1 year prior. Clinicians should be aware of this complication and maintain a high index of suspicion in cases of COVID-19 presenting with extrapulmonary symptoms.

INTRODUCTION Although Parkinson’s disease (PD) primarily affects the central nervous system, it is a multi-organ disease which also affects the eyes and the peripheral nervous system, including the autonomic fibers (,). PD-related disturbance of the peripheral nerves may result in sensory, motor, or autonomic neuropathy. Autonomic dysfunction can manifest as sicca syndrome, hypo-/hyperhidrosis, orthostatic hypotension, reduced blood pressure variability, reduced heart rate variability, nausea, constipation, vomiting, urinary dysfunction, or erectile dysfunction (). Non-motor manifestations, such as hyposmia, rapid eye movement [...]

To compare the incidence and clinical features of individuals presenting in emergency rooms (ER) with facial palsy during the Italian COVID-19 outbreak and in the same period of 2019.We retrospectively reviewed the medical records for all accesses to the six ER in the province of Reggio Emilia, Italy, during the first phase of the COVID-19 pandemic (27 February-3 May 2020) to identify all cases of diagnosed facial palsy. Clinical information was retrieved for each patient and compared with that of facial palsy cases presenting in 2019.Between 27 February and 3 May 2020, 38 patients presented to provincial ERs for facial palsy; in 2019, there were 22 cases, for an incidence rate ratio of 1.73 (95% CI 1.02-2.92) for the 2020 cohort. Of the 2020 cohort, eight patients (21%) presented with active or recent symptoms consistent with COVID-19 infection, compared with 2 (9%) in 2019 (p = .299); one was tested and resulted positive for SARS-CoV-2. Moreover, patients were younger (-11 years, p = .037) than those of the previous year and manifested a longer lag (+1.1 days, p = .001) between symptoms onset and ER presentation.We observed a higher occurrence of facial palsy during the COVID-19 outbreak compared to the same period of the previous year; 21% of patients presenting with facial palsy had active or recent symptoms consistent with SARS-CoV-2 infection, suggesting an excess risk of facial palsy during or after COVID-19. These patients searched for medical attention later, probably because of the fear of contracting COVID-19 during assistance.