Tremor and myoclonus are among the most common hyperkinetic movement disorders encountered in neurological practice, with tremor being considerably more common than myoclonus in everyday clinical practice, yet distinguishing between them remains a frequent diagnostic challenge. Although their definitions are conceptually distinct, several disorders - including cortical tremor, dystonic tremor, and generalized polymyoclonus - can mimic one another, leading to diagnostic uncertainty and inappropriate management. This practical review provides clinicians with a structured approach to recognizing and differentiating these movement disorders. The initial assessment relies on careful bedside examination, focusing on rhythmicity, movement duration, oscillatory versus jerky phenomenology, stimulus sensitivity, and the identification of negative myoclonus (asterixis). When clinical uncertainty persists, surface electromyography is the key complementary investigation, reliably distinguishing rhythmic tremor from irregular myoclonic bursts while providing valuable clues regarding the underlying generator. Beyond phenomenological diagnosis, this review outlines a practical framework for etiological orientation based on activation conditions, anatomical distribution, temporal evolution, associated neurological signs, and medication history. Common tremor syndromes and the major categories of myoclonus are discussed, with particular emphasis on identifying reversible causes such as metabolic disturbances and drug-induced disorders. Finally, uncommon but important entities - including orthostatic tremor, palatal tremor, geniospasm, Holmes tremor, functional tremor, and myorhythmia - are reviewed with practical bedside clues to facilitate their recognition. By integrating clinical examination with targeted electrophysiological testing, this guide aims to improve diagnostic accuracy, avoid common pitfalls, and promote timely identification of treatable causes in everyday neurological practice.

Tremor is a common and disabling symptom of Parkinson's disease, which classically occurs at rest and often re-emerges during simple actions. The dimmer-switch hypothesis proposes that the basal ganglia trigger tremor, whereas the cerebello-thalamo-cortical circuit amplifies it. Recent findings suggest that this model may be expanded to include a potential anti-tremor network. This bilateral cortical network, comprising somatosensory, posterior parietal, insular, supplementary motor, and dorsal premotor regions, shows activity that is inversely related to tremor amplitude and clinical tremor severity. Its increased coupling with primary motor cortex during periods of low-amplitude tremor supports a potential role in tremor suppression, although so far causal evidence is lacking. We propose an updated pathophysiological model where Parkinson's tremor results from interactions between circuits that suppress (the good), initiate (the bad), and amplify (the ugly) tremor. Understanding these interactions may enable mechanism-based interventions targeting specific components of the tremor network, including non-invasive brain stimulation and behavioural approaches.

Parkinsonian degenerative syndromes, including Parkinson disease (PD), progressive supranuclear palsy (PSP), multiple system atrophy (MSA), corticobasal degeneration (CBD), and dementia with Lewy bodies (DLB), are frequently associated with ophthalmic manifestations that contribute substantially to impaired quality of life, reduced functional independence, and increased falls risk. These visual disturbances remain under-recognised in routine neurological practice despite their diagnostic and therapeutic relevance. This review summarises the spectrum of ophthalmic manifestations across Parkinsonian degenerative syndromes, focusing on ocular motor dysfunction, eyelid and ocular surface disorders, higher-order visual perceptual dysfunction, and treatment-related visual phenomena. Characteristic patterns of eye movement abnormalities, visual hallucinations, visuospatial dysfunction, dry eye disease, and eyelid dysfunction may assist clinical differentiation between syndromes and identify treatable causes of visual impairment. Practical management strategies including ophthalmological assessment, orthoptic interventions, optimisation of refractive correction, and ocular surface treatment are discussed. Emerging technologies including retinal imaging, oculomics, quantitative eye movement analysis, and tear biomarkers may further enhance future diagnosis and disease monitoring, although their clinical utility remains under investigation.

As the global population ages, the incidence of meningiomas rises, and the demand for clinical management of elderly patients also rises. Meningiomas are common intracranial tumors, and their incidence increases with age. Elderly patients with meningiomas are prone to comorbidities, reduced reserve function, atypical manifestations, increased perioperative risks, and impaired functional recovery, making management more difficult. The application of neuroimaging leads to more elderly patients with asymptomatic or incidentally discovered meningiomas. Choosing the best strategy among monitoring, surgery, radiotherapy, and other strategies is therefore key to clinical decision-making. For asymptomatic, small, and radiologically low-risk meningiomas in elderly patients, active surveillance is generally the preferred initial strategy. Surgery is more appropriate for symptomatic tumors, lesions with mass effect, documented growth, progressive peritumoral edema, neurological deterioration, or other high-risk clinical and radiological features. However, the treatment goal for elderly patients should emphasize symptom relief, preservation of neurological function, and quality of life more than pursuing gross total resection as routine. Stereotactic radiosurgery and fractionated radiotherapy provide important supplementary treatments for very elderly patients, high surgical risk patients, and postoperative residual lesions. This article reviews recent advances in understanding meningiomas in elderly and very elderly patients, focuses on epidemiology, clinical characteristics, prognostic factors, and treatment strategies, and also discusses the core principles of individualized management for this population to guide clinical practice.

Knowledge in the field of autosomal-recessive cerebellar ataxia (ARCA) has considerably improved since the discovery of the Friedreich ataxia gene in 1996. Numerous entities have been described in which cerebellar ataxia may be the first sign or appear during the course of the disease. Even though new sequencing tools have made genetic diagnosis much easier, management of patients with ARCA requires careful phenotypic analysis in order to propose the most effective genetic studies, rapidly track down treatable ARCA, and discuss the pathogenicity of new WGS-identified missense variants.