Background/Objectives: Anti-IgLON5 disease is a neurological disorder characterized by the presence of autoantibodies directed against the neuronal cell adhesion protein IgLON5. Pathophysiology involves both autoimmune inflammation and neurodegenerative processes. The most common causes of death are sudden death, central hypoventilation, dysphagia, and aspiration. However, the high rate of largely unclear sudden deaths calls for further research in this area. Methods: We performed a systematic search of the literature on causes of death in anti-IgLON5 disease following the PRISMA guidelines. In addition, we present a new case that was followed up in our clinic until death. Results: Of 258 publications with anti-IgLON5 disease, 21 publications comprising 61 cases that reported the causes of death were included in the analysis. The most common cause of death was death due to complications at 36.1%, followed by sudden death, accounting for 32.8% of the cases. Other causes include respiratory, cardiac, and unknown causes. The patient presented here as a case report was also diagnosed with cardiac amyloidosis and died from a cardiac cause of sudden death. Conclusions: Sudden death in anti-IgLON5 disease is one of the most common causes of death in the literature. A progressive neurodegenerative process in the brain stem causing central hypoventilation is generally assumed as a major causative factor. The case reported here had concomitant cardiac amyloidosis, which may raise the question as to whether unrecognized cardiac causes, which are not routinely screened for in this population, might represent another cause of sudden death, which would have important therapeutic implications.

Psychosis after weight loss during continuous subcutaneous foslevodopa/foscarbidopa therapy - a case series

Tremor and Other Hyperkinetic Movements (TOHM) [ISSN: 2160-8288], a fully open access peer-reviewed journal, publishes clinical and scientific papers on tremor and hyperkinetic movements. TOHM is indexed in PubMed and PubMed Central. In contrast to other publications focusing on disorders of hypokinesia (i.e., mainly Parkinson’s disease), TOHM emphasizes the hyperkinetic movements, giving center stage to clinical observations and research in this area. Papers on Parkinson’s disease and related disorders will be considered if they relate to the hyperkinetic features of these diseases (e.g., tremor, dystonia, dyskinesias). The average turnaround time from submission to first decision is roughly 24 days (~3.5 weeks). The average turnaround time from acceptance to publication is 18 days (~2.5 weeks) with a median of 14 days (2 weeks). Tremor and Other Hyperkinetic Movements is indexed with the Web of Science Emerging Sources Citation Index. As of 2024, Tremor has a Journal Impact Factor of 2.5.

The role of neurodegeneration in essential tremor (ET) remains debated, particularly in patients with late disease onset. Neuropathological studies have identified structural changes in the Purkinje cells and its connections. Recent studies additionally suggested a role of cerebellar astrocytes. Increased levels of serum glial fibrillary acidic protein (sGFAP), an astrocytic intermediate filament, were found in various neuroinflammatory and neurodegenerative diseases. The objective of this case–control study was to investigate the role of sGFAP in ET focusing on early-stage late-onset patients. sGFAP was quantified by single molecule array at baseline and follow-up in 36 ET-patients (median follow-up period 5.3 years) and 36 age-matched healthy controls (4.9 years). ET-patients were assessed both at baseline and follow-up using the Fahn–Tolosa–Marin–Tremor-Rating-Scale. The ET group was stratified (1) by median age at onset and median disease duration in early-stage late-onset and early-onset/late-stage ET, and (2) by median sGFAP-level at baseline. Early-stage late-onset ET-patients had higher baseline-sGFAP than controls (p = 0.023) and higher follow-up-sGFAP and annual sGFAP-increase than both controls (p = 0.023; p = 0.007) and early-onset/late-stage ET-patients (p = 0.021; p = 0.024). Baseline sGFAP-level correlated with tremor severity at follow-up in the early-stage late-onset (r_s = 0.704, p = 0.011) but not in the early-onset/late-stage group. Patients with high compared to low sGFAP-baseline levels had later disease onset (p < 0.001) and sGFAP-increase was associated to tremor progression only in high sGFAP-patients (p = 0.041). ET-plus and pure-ET-patients did not differ in any of the sGFAP-parameters. sGFAP is elevated in early stages of late-onset ET and associated to tremor progression, substantiating the role of a neurodegenerative process in ET in this subgroup.

Background: Parkinson's disease (PD) is a progressive neurodegenerative disorder clinically defined by three cardinal motor symptoms: bradykinesia, rigidity, and tremor. Although the natural history of bradykinesia and rigidity is well described, the evolution of tremor as the disease progresses remains controversial. Objectives: The goal was to clinically characterize long‐term trajectories of rest, postural, and action tremor in PD and examine their neural network correlates using longitudinal resting‐state functional magnetic resonance imaging (rs‐fMRI). Methods: In this retrospective longitudinal cohort study, we analyzed 93 tremor‐positive PD patients (mean disease duration: 3.6 years), each with up to six clinical assessments over 4.2 years. Linear mixed‐effects models assessed temporal change in Movement Disorder Society‐Unified Parkinson's Disease Rating Scale (MDS‐UPDRS) and Fahn–Tolosa–Marín Tremor Rating Scale (FTM‐TRS) scores. Rs‐fMRI data from 30 tremor‐affected patients (mean interval, 3.35 years) were analyzed for seed‐to–whole‐brain connectivity and connectivity between predefined brain regions. Results: Bradykinesia (β = +0.09, P < 0.001) and rigidity (β = +0.06, P < 0.001) worsened, whereas total FTM‐TRS scores declined by 0.49 points/year ( P = 0.037), driven by reductions in postural ( P < 0.001) and action tremor ( P = 0.033); resting tremor remained stable. Rs‐fMRI revealed longitudinal changes in cerebellar‐ and thalamic‐seed‐to‐whole‐brain connectivity. Conclusions: Tremor in PD evolves along distinct clinical courses, often stabilizing or improving as other motor features worsen. These findings are consistent with partially adaptive reorganization within tremor‐related networks and underscore the importance of identifying patient subtypes with divergent trajectories to inform prognosis and optimize therapy. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.