Episodic ataxia type 2 (EA2) is characterized by recurrent vertigo and ataxia due to mutations in that encodes the α-subunit of the P/Q-type voltage-gated calcium channel. This study aimed to determine intellectual function in EA2.

CGG repeat expansion in the 5' untranslated region (5'UTR) of the Notch 2 N-terminal-like C gene () has been associated with neuronal intranuclear inclusion disease (NIID) and oculopharyngodistal myopathy type 3 (OPDM3). Few OPDM3 patients have been reported. This report describes two OPDM3 patients with novel imaging findings who presented the typical features of NIID, and reviews all OPDM3 cases available in the literature.

Syncope is characterized by the temporary loss of consciousness and is commonly associated with migraine. However, the genetic factors that contribute to this association are not well understood. This study investigated the specific genetic loci that make patients with migraine more susceptible to syncope as well as the genetic factors contributing to syncope and migraine comorbidity in a Han Chinese population in Taiwan.

Secondary progressive multiple sclerosis (SPMS) presents with a challenging clinical phenotype, and siponimod has a potential to treat the active clinical phenotype of this disease. This single-center longitudinal study aimed to determine the therapeutic effects of siponimod in patients with active SPMS over 12 months.

An intracranial vertebral artery dissecting aneurysm (iVADA) increases the risk of future subarachnoid hemorrhage, which is a severe complication with high rebleeding rates and poor outcomes. Identifying potential risk factors associated with iVADA growth is crucial for their effective management.

The estimated prevalence of hereditary transthyretin-related familial amyloid polyneuropathy (TTR-FAP) and the small number of known patients in Germany indicate that many patients with TTR-FAP remain undiagnosed, and may instead be classified as "idiopathic." The aim of this study was to identify biomarkers for detecting TTR-FAP among a cohort of patients with idiopathic polyneuropathy (PNP).

Complications that occur during cancer therapy have emerged as a major contributor to the poor quality of life experienced by cancer patients as they live longer due to improved treatments. Many studies have investigated chemotherapy-induced peripheral neuropathy, but few have investigated the autonomic nervous system. Cardiovascular autonomic dysfunction (CAD) contributes to the distressing symptoms experienced by cancer patients, and it is also related to poor treatment outcomes. CAD has a multifactorial etiology in patients with cancer: it can be caused by the cancer itself, chemotherapy or radiation therapy, or other comorbidities. Its symptoms are nonspecific, and they include orthostatic hypotension, resting tachycardia, dizziness, chest tightness, and exertional dyspnea. It is important to suspect CAD and perform therapeutic interventions in a clinical context, because a patient who is more frail is less like to endure the treatment process. The quality of life of patients receiving active cancer treatments can be improved by evaluating the risk of CAD before and after chemotherapy, and combining both nonpharmacological and pharmacological management. Here we review the prevalence, pathogenesis, diagnosis, and treatment of CAD, which is the most common and a sometimes serious symptom in cancer patients.

We delineated the association between otolithic dysfunction and blood pressure (BP) variability.

This corrects the article on p. 454 in vol. 19, PMID: 37488957.

Visual perceptual learning (VPL) may improve visual field defects (VFDs) after chronic stroke, but the optimal training duration and location remain unknown. This prospective study aimed to determine the efficacy of 8 weeks of VFD-customized visual discrimination training in improving poststroke VFDs.

Migraine is one of the most common chronic neurological diseases worldwide. Although diverse treatment regimens have been recommended, there is insufficient evidence for which treatment patterns to apply in routine clinical settings.

Neonatal encephalopathy (NE) is a neurological syndrome that presents with severe neurological impairments and complications. Hypoxic-ischemic encephalopathy is a major contributor to poor outcomes, being responsible for 50%-80% of admissions to neonatal intensive care units. However, some cases of NE accompanied by hypoxic brain damage cannot be solely attributed to hypoxia-ischemia. We aimed to identify diverse pathogenic genetic variations that may be associated with cases of NE accompanied by hypoxic brain damage rather than hypoxia-ischemia.