While nystagmus is an involuntary ocular movement relatively frequent, well described, and easily recognized by most practitioners, non-nystagmus hyperkinetic eye movement disorders (NHEMD) are less obvious and can be overlooked. NHEMD may arise from intrinsic abnormalities in ocular muscles and oculomotor nerves, brain and brainstem lesions, systemic diseases, dysimmune disorders, drugs or can even be functional in nature. Given that some treatable disorders initially manifest with NHEMD, their knowledge becomes crucial. This review aims to offer a practical and comprehensive guide to recognize specific types of NHEMD, to choose the appropriate diagnostic tests and treatments. The review approaches individual NHEMD based on the location of anatomical lesions and the underlying pathophysiological mechanisms; therefore, it begins with those arising from abnormalities in extraocular muscles or oculomotor nerves (as for example, superior oblique myokymia and ocular neuromyotonia), then moves to NHEMD due to brainstem and brain involvement (as for example, ocular bobbing, opsoclonus, and tonic downward gaze deviation). Lastly, functional NHEMD and nonnystagmus ocular hyperkinesias associated with specific neurological disorders, such as Parkinson’s disease or blepharospasm will be considered. Overall, the review offers a comprehensive reappraisal of hyperkinetic disorders of eye motility.

BACKGROUND AND PURPOSE:Core clinical manifestations of COVID-19 include influenza-like and respiratory symptoms. However, it is now evident that neurological involvement may occur during SARS-CoV-2 infection, covering an extensive spectrum of phenotypical manifestations. A major challenge arising from this pandemic is represented by detecting emerging neurological complications following recovery from SARS-CoV-2 infection. To date, a few post-COVID-19-infected subjects diagnosed with Parkinson disease (PD) have been described, raising the possibility of a connection between the infection and neurodegenerative processes. Here, we describe a case series of six subjects who developed PD after COVID-19.METHODS:Patients were observed at Scientific Institute for Research and Health Care Mondino Foundation Hospital, Pavia (Italy), and San Paolo University Hospital of Milan (Italy) between March 2021 and June 2022. In all subjects, SARS-CoV-2 infection was confirmed by means of reverse transcriptase polymerase chain reaction from a nasopharyngeal swab. Subjects underwent an accurate neurological evaluation, and neuroimaging studies were performed.RESULTS:We describe six subjects who developed PD with an average time window after SARS-CoV-2 infection of 4-7 weeks. Apparently, no relationship with COVID-19 severity emerged, and no overt structural brain abnormalities were found. All subjects experienced unilateral resting tremor at onset and showed a satisfactory response to dopaminergic treatment.CONCLUSIONS:Immune responses to SARS-CoV-2 infection have been shown to shape the individual susceptibility to develop long-term consequences. We hypothesize that, in these subjects, COVID-19 has unmasked a latent neurodegenerative process. Characterization of the neuroinflammatory signatures in larger cohorts is warranted, which might provide novel insights into the pathogenesis of PD.

The presence of respiratory symptoms in Parkinson's disease (PD) has been known since the first description of the disease, even though the prevalence and incidence of these disturbances are not well defined. Several causes have been reported, comprising obstructive and restrictive pulmonary disease and changes in the central ventilatory control, and different pathogenetic mechanisms have been postulated accordingly. In our review, we encompass the current knowledge about respiratory abnormalities in PD, as well as the impact of anti-Parkinsonian drugs as either risk or protective factors. A description of putative pathogenetic mechanisms is also provided, and possible treatments are discussed, focusing on the importance of recognising and treating respiratory symptoms as a key manifestation of the disease itself. A brief description of respiratory dysfunctions in atypical Parkinsonism, especially a-synucleinopathies, is also provided.

Hyperkinetic movement disorders may be difficult to treat, but cases where patients respond to alcohol and/or drugs with similar effects have been described. We report the case of a 64-year-old man with tardive dyskinesia characterized by severe uncontrolled dystonic and myoclonic jerks of the face, shoulders, and arm and forearm muscles, which improved with oral sodium oxybate. Our case suggests the possibility to test sodium oxybate in patients with severe, drug-resistant hyperkinetic syndromes, especially when they are known to improve with alcohol.

Background: Despite the higher theoretical risk of traumatic intracranial hemorrhage (ICH) in anticoagulated patients with mild head injury, the value of sequential head CT scans to identify bleeding remains controversial. This study evaluated the utility of 2 sequential CT scans at a 48-hour interval (CT1 and CT2) in patients with mild head trauma (Glasgow Coma Scale 13-15) taking oral anticoagulants. Methods: We retrospectively evaluated the clinical records of all patients on chronic anticoagulation treatment admitted to the emergency department for mild head injury. Results: A total of 344 patients were included, and 337 (97.9%) had a negative CT1. CT2 was performed on 284 of the 337 patients with a negative CT1 and was positive in 4 patients (1.4%), but none of the patients developed concomitant neurologic worsening or required neurosurgery. Conclusions: Systematic routine use of a second CT scan in mild head trauma in patients taking anticoagulants is expensive and clinically unnecessary.

Early differential diagnosis of motor neuropathies (MN) and lower motor neuron diseases (LMND) is important, as prognosis and therapeutic approaches are different. We evaluated the diagnostic contribution of the biopsy of the motor branch of the obturator nerve and gracilis muscle in 21 consecutive patients in which, after proper clinical and neurophysiological studies, the differential diagnosis was still open. At baseline, motor biopsy was performed; diagnostic confirmation was obtained by 2‐year clinical follow‐up. Our results support the usefulness of this diagnostic procedure for selected cases of MN and LMND. Ann Neurol 2010

Journal of the Peripheral Nervous SystemVolume 14, Issue 3 p. 203-205 Oral methotrexate as adjunctive therapy in patients with multifocal motor neuropathy on chronic IVIg therapy Eduardo Nobile-Orazio, Corresponding Author Eduardo Nobile-Orazio 2nd Neurology, Milan University, IRCCS Humanitas Clinical Institute, Rozzano, Milan, ItalyEduardo Nobile-Orazio, MD, PhD, FAAN, 2nd Neurology, Milan University, IRCCS Humanitas Clinical Institute, Via Manzoni 56, 20089, Rozzano, Milan, Italy. Tel: +390282242209; Fax: +390282242298; E-mail: eduardo.nobile@unimi.itSearch for more papers by this authorFabrizia Terenghi, Fabrizia Terenghi 2nd Neurology, IRCCS Humanitas Clinical Institute, Rozzano, Milan, ItalySearch for more papers by this authorDario Cocito, Dario Cocito Department of Neuroscience, Turin University, Turin, ItalySearch for more papers by this authorFrancesca Gallia, Francesca Gallia 2nd Neurology, IRCCS Humanitas Clinical Institute, Rozzano, Milan, ItalySearch for more papers by this authorChiara Casellato, Chiara Casellato 2nd Neurology, IRCCS Humanitas Clinical Institute, Rozzano, Milan, ItalySearch for more papers by this author Eduardo Nobile-Orazio, Corresponding Author Eduardo Nobile-Orazio 2nd Neurology, Milan University, IRCCS Humanitas Clinical Institute, Rozzano, Milan, ItalyEduardo Nobile-Orazio, MD, PhD, FAAN, 2nd Neurology, Milan University, IRCCS Humanitas Clinical Institute, Via Manzoni 56, 20089, Rozzano, Milan, Italy. Tel: +390282242209; Fax: +390282242298; E-mail: eduardo.nobile@unimi.itSearch for more papers by this authorFabrizia Terenghi, Fabrizia Terenghi 2nd Neurology, IRCCS Humanitas Clinical Institute, Rozzano, Milan, ItalySearch for more papers by this authorDario Cocito, Dario Cocito Department of Neuroscience, Turin University, Turin, ItalySearch for more papers by this authorFrancesca Gallia, Francesca Gallia 2nd Neurology, IRCCS Humanitas Clinical Institute, Rozzano, Milan, ItalySearch for more papers by this authorChiara Casellato, Chiara Casellato 2nd Neurology, IRCCS Humanitas Clinical Institute, Rozzano, Milan, ItalySearch for more papers by this author First published: 10 November 2009 https://doi.org/10.1111/j.1529-8027.2009.00233.xCitations: 12Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume14, Issue3September 2009Pages 203-205 RelatedInformation