Magnesium is the second most abundant intracellular cation. Deficiency can cause several neurological complications, including cerebellar syndromes, with various MRI findings. These include cerebellar oedema, presumably through a similar mechanism to that in posterior reversible encephalopathy syndrome (PRES). People particularly vulnerable to deficiency include those with high alcohol consumption, excessive loss due to gastrointestinal pathology and those taking certain medications, including proton pump inhibitors. We report three patients with cerebellar syndromes associated with hypomagnesaemia. These cases support the previously reported association between hypomagnesaemia and reversible cerebellar dysfunction and illustrate the range of potential presentations. They highlight an uncommon but treatable cause of cerebellar ataxia that may present to acute neurological liaison services.
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http://dx.doi.org/10.1136/practneurol-2017-001832 | DOI Listing |
J Neurosci
January 2025
Arizona State University, Department of Psychology, Tempe, AZ, 85287 USA.
The cerebellum, identified to be active during cognitive and social behavior, has multisynaptic connections through the cerebellar nuclei (CN) and thalamus to cortical regions, yet formation and modulation of these pathways are not fully understood. Perineuronal nets (PNNs) respond to changes in local cellular activity and emerge during development. PNNs are implicated in learning and neurodevelopmental disorders, but their role in the CN during development is unknown.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Ibadan, Ibadan, Oyo, Nigeria.
Background: The brain is a potential target for aluminium toxicity as it induces oxidative stress, strategies, rich in polyphenolic compound, containing flavonoid and possessing antioxidant property, found in natural plant products, to attenuate aluminium-induced impairments could provide a potential therapeutic intervention and protection for aluminium neurotoxicity.
Method: Forty adult rats weighing between 160 - 165g was used. The rats were divided into four groups (n = 10).
Hum Gene Ther
December 2024
Laboratoire des Maladies Neurodégénératives, MIRCen Institute, Fontenay-aux-Roses, France.
Worldwide, thousands of male patients who carry ATP Binding Cassette Subfamily D Member 1 () mutations develop adrenomyeloneuropathy (AMN) in mid-adulthood, a debilitating axonopathy of the spinal cord. Today AAV gene therapy brings the most hope for this orphan disease. We previously reported that an AAV9-MAG- vector injected intravenously in the neonatal period prevented the disease in 2-year-old mice, the AMN mouse model.
View Article and Find Full Text PDFApoptosis
December 2024
Department of Physiology, University of Calcutta, Kolkata, West Bengal, India.
Arsenic-mediated neurodegenerative disorders affect millions of individuals globally, but the specific impact of environmental arsenic on adult cerebellar degeneration and neurogenesis is incompletely understood. Of particular concern is arsenic-induced apoptosis-driven neurodegeneration. Our major objective was to investigate the molecular signaling intricacies associated with arsenic-induced death of cerebellar neurons and to propose folic acid as a possible intervention.
View Article and Find Full Text PDFEpilepsy Behav Rep
October 2024
Department of Psychiatry and Psychotherapy, Philipps-University Marburg, Marburg, Germany.
This case series describes the clinical features, diagnostic challenges, treatment approaches, and outcomes of three adult patients with COQ8A-related CoQ10 deficiency presenting with focal status epilepticus, who were effectively treated at the Department of Neurology, Philipps University Marburg, Marburg, Germany. The patients, all from consanguineous families with the first two being siblings, presented with a late onset of the disease, characterized by progressive cerebellar ataxia and epilepsy, with clinical deterioration and focal status epilepticus occurring in adulthood. The first patient exhibited myoclonic status, while the second and third patients presented with bilateral tonic-clonic seizures followed by focal status epilepticus manifesting with cortical blindness.
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