The neurologic complications of COVID-19 infection are frequent in hospitalized patients; a high percentage of them present neurologic manifestations at some point during the course of their disease. Headache, muscle pain, encephalopathy and dizziness are among the most common complications. Encephalitis is an inflammatory condition with many etiologies. There are several forms of encephalitis associated with antibodies against intracellular neuronal proteins, cell surfaces or synaptic proteins, referred to as autoimmune encephalitis. Several case reports published in the literature document autoimmune encephalitis cases triggered by COVID-19 infection. Our paper first presents our experience in this issue and then systematically reviews the literature on autoimmune encephalitis that developed in the background of SARS-CoV-2 infections and also discusses the possible pathophysiological mechanisms of auto-immune-mediated damage to the nervous system. This review contributes to improve the management and prognosis of COVID-19-related autoimmune encephalitis.

The disruption of blood–brain barrier (BBB) for multiple sclerosis (MS) pathogenesis has a double effect: early on during the onset of the immune attack and later for the CNS self-sustained ‘inside-out’ demyelination and neurodegeneration processes. This review presents the characteristics of BBB malfunction in MS but mostly highlights current developments regarding the impairment of the neurovascular unit (NVU) and the metabolic and mitochondrial dysfunctions of the BBB’s endothelial cells. The hypoxic hypothesis is largely studied and agreed upon recently in the pathologic processes in MS. Hypoxia in MS might be produced per se by the NVU malfunction or secondary to mitochondria dysfunction. We present three different but related terms that denominate the ongoing neurodegenerative process in progressive forms of MS that are indirectly related to BBB disruption: progression independent of relapses, no evidence of disease activity and smoldering demyelination or silent progression. Dimethyl fumarate (DMF), modulators of S1P receptor, cladribine and laquinimode are DMTs that are able to cross the BBB and exhibit beneficial direct effects in the CNS with very different mechanisms of action, providing hope that a combined therapy might be effective in treating MS. Detailed mechanisms of action of these DMTs are described and also illustrated in dedicated images. With increasing knowledge about the involvement of BBB in MS pathology, BBB might become a therapeutic target in MS not only to make it impenetrable against activated immune cells but also to allow molecules that have a neuroprotective effect in reaching the cell target inside the CNS.

Depression remains an underdiagnosed comorbidity which significantly decreases the quality of life in amyotrophic lateral sclerosis (ALS) patients. We aimed to investigate the prevalence of depression in a cohort of ALS patients with more than one year of disease evolution. A total of 50 ALS patients were evaluated with the Beck Depression Inventory II (BDI-II) and cognition, using the Mini-Cog Standardized Instrument (MCSI). The clinical disability was evaluated using the ALS Functional Rating Scale (ALSFRS). The prevalence of depression was 42.8%. A lower BDI-II score was significantly correlated with a higher education level, the spouse as a caregiver, spiritual devotion, and employment status (p < 0.05). A multiple linear regression analysis between the BDI-II score as the dependent variable and various independent variables such as spirituality, caregiver status, educational level, and occupational status revealed that only the type of caregiver (spouse or parent/child) significantly affected the BDI-II total score (p = 0.006). The functional disability significantly correlated with loss of appetite and loss of libido (p < 0.001). A high education, spiritual devotion, high ALSFRS, and the presence of the spouse as the caregiver were associated with the absence of depression.