Parkinson’s disease (PD) is a multifarious neurodegenerative disease. Its pathology is characterized by a prominent early death of dopaminergic neurons in the pars compacta of the substantia nigra and the presence of Lewy bodies with aggregated α-synuclein. Although the α-synuclein pathological aggregation and propagation, induced by several factors, is considered one of the most relevant hypotheses, PD pathogenesis is still a matter of debate. Indeed, environmental factors and genetic predisposition play an important role in PD. Mutations associated with a high risk for PD, usually called monogenic PD, underlie 5% to 10% of all PD cases. However, this percentage tends to increase over time because of the continuous identification of new genes associated with PD. The identification of genetic variants that can cause or increase the risk of PD has also given researchers the possibility to explore new personalized therapies. In this narrative review, we discuss the recent advances in the treatment of genetic forms of PD, focusing on different pathophysiologic aspects and ongoing clinical trials.

Subthalamic nucleus deep brain stimulation (STN DBS) is an established therapy for a subset of patients with Parkinson’s disease, and the adjustment of DBS parameters is typically guided by the patients’ rigidity and tremor. Although these cardinal symptoms remain relatively stable over time, progressive worsening of axial symptoms compromise motor function and quality of life. Because many patients report improvements in their global mobility after gait improvement, we have been adjusting DBS parameters during the long-term after surgery based on gait analysis. Here, we describe a practical strategy for troubleshooting gait problems in PD DBS patients by revising stimulation parameters through “hands-on” programming, which can be a useful alternative approach for improving patients’ outcomes after STN DBS.

The relationship between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and neurodegenerative diseases is yet to be fully clarified. Rapid worsening and even new-onset cases of those disorders have been reported in association with coronavirus disease 2019 (COVID-19). We describe three cases of neurodegenerative diseases in patients with SARS-CoV-2: a case of Creutzfeldt–Jakob disease during the COVID-19 acute phase, to our knowledge, is the second one described in the literature; a rapidly progressive Alzheimer's Disease; and a patient with frontotemporal dementia, and a quick decline of both cognitive and behavioral domains. This report suggests an association between SARS-CoV-2 infection and a higher probability of developing or accelerating neurodegenerative chronic neurologic conditions. We reinforce the need for a close cognitive follow-up in the aftermath of Sars-Cov2 infection.

Background: Neuroophthalmological phenotypical particularities of SCA3. Phenomenology: Eyelid opening apraxia and asymmetrical blepharospasm. Educational Value: To illustrate the phenomenology for purposes of education.