Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical and clinical literature without systematic methodology.
What was done
Narrative review synthesizing findings from animal and human studies on the causes of magnesium deficiency, its impact on cerebrospinal fluid (CSF) and brain tissue concentrations, associated neurological and psychiatric symptoms, and underlying mechanisms such as NMDA receptor regulation.
What was found
Magnesium deficiency lowers CSF magnesium concentrations, although the decline is less pronounced and slower than in plasma. Animal models demonstrate that lower CSF magnesium correlates with reduced brain extracellular magnesium. While supplementation can restore normal central levels, high-dose magnesium therapy (e.g., in eclampsia) raises CSF magnesium by only approximately 11% to 18% above baseline in adults, though neonatal swine achieve CSF concentrations closer to plasma levels. Clinical manifestations include hyperexcitability, convulsions, apathy, and psychosis; low-magnesium epileptiform activity in the central nervous system was reported to be blocked by NMDA receptor antagonists.
Why it matters
The review summarizes blood-brain barrier transport dynamics for magnesium and links central magnesium deficits to NMDA receptor disinhibition and neuroexcitatory disorders.
Limits
The paper is a non-systematic narrative review with no defined search protocol, unified study counts, or quantitative synthesis. Findings from animal models and human clinical data are conflated without clear distinction of effect sizes.