Background and objectives: Movement disorders are an underrecognized phenomenon in Myelin Oligodendrocyte Glycoprotein-Associated Disease (MOGAD). The aim of this paper was to summarize all movement disorders previously described in MOGAD. Materials and Methods: We conducted a systematic literature search in PubMed, Web of Science, and Scopus in English, focusing on patients with MOGAD exhibiting a movement disorder, i.e., ataxia, tremor, dystonia, parkinsonism, chorea, athetosis, myoclonus, ballism, tics, stereotypies, dyskinesia. Results: We included 58 studies, with a total of 91 patients with MOGAD and a movement disorder (45.6% male, 54.4% female). Movement disorders had a mean latency of 2.1 years (±6.9, 0–42) after MOGAD onset; however, they could be the presenting feature (in approximately 70% of cases), especially in pediatric patients. Cerebellar ataxia was the most common movement disorder, occurring in 77 patients (84.6%). Tremor, postural and/or kinetic, was the second most common movement disorder (15%). Dystonia was reported in 8.8%, presenting as cervical, or limb dystonia or stereotyped dystonic episodes. Myoclonus and hypokinetic movement disorders were rare. Subcortical (in 60%), brainstem and cerebellar lesions (in 50% respectively) were the most common imaging findings. The most common accompanying symptoms were encephalopathy, fever and headache. Approximately half of the patients made a full recovery, and the other half showed a significant improvement in the movement disorder after immunomodulatory treatment, most commonly steroids. Conclusions: The new onset of a movement disorder, especially ataxia, in a young patient should prompt the search for MOGAD or can indicate a relapse in patients with an established diagnosis.

Background/Objectives: Guillain–Barré syndrome (GBS) is an acute immune-mediated disorder of the peripheral nervous system. Autonomic involvement in GBS occurs during the acute phase and may persist into the recovery phase. This study aimed to investigate the autonomic nervous system’s function in GBS sufferers. Methods: A cross-sectional exploratory study was conducted at the Clinical Neurophysiology Laboratory, Medical School, University of Cyprus. Eligible patients were previously hospitalized with GBS. Autonomic nervous system assessment included the Ewing battery using the Finapres Nova system as well as sudomotor assessment. Results: Seventeen patients were recruited (53% female; mean age 58.7 ± 14.1 years). The mean follow-up time since diagnosis was 15.5 ± 13.2 months (range 1–45 months). At follow-up, 4/17 patients (24%) demonstrated an abnormal heart rate (HR) response to standing, 3/17 patients (18%) exhibited an abnormal systolic blood pressure (BP) response to standing, and 4/17 patients (24%) exhibited an abnormal diastolic BP response to standing. One patient (6%) demonstrated an abnormal HR response during deep breathing, while another showed an abnormal diastolic BP response during the handgrip test. Overall, 6/17 patients (35%) showed abnormal findings in at least one component of the Ewing battery, and 3/17 (18%) fulfilled the criteria for definite generalised dysautonomia. Two patients (12%) demonstrated abnormal sympathetic skin response (SSR) results; both fulfilling the criteria for dysautonomia based on the Ewing battery. Conclusions: Autonomic dysfunction may be present in GBS patients beyond the acute phase, even in the absence of overt autonomic symptoms. Larger prospective studies with serial autonomic assessments are required to better characterise the long-term course and clinical significance of dysautonomia in GBS.