When Low Magnesium Masquerades as a Stroke: A Cautionary Case Report

Every minute counts when a patient arrives at the emergency department with a drooping face, a weak arm, and slurred speech. The clinical reflex is immediate: assume stroke, activate the imaging pathway, and prepare thrombolytic therapy if a vessel blockage is confirmed. Yet a growing body of evidence, highlighted by a new case report published in the Journal of Neurology, suggests that one of the most common minerals in the human body can produce a nearly identical picture without a single blood vessel being blocked. The report, authored by David Vidal Bankier, Francis Renard, and Mario Manto of the Department of Neurology at CHU-Charleroi in Belgium, describes a patient whose stroke-like episode of hemiparesis and aphasia resolved completely once his severe hypomagnesemia, a dangerously low blood level of magnesium, was corrected.

The case is striking not only because of the dramatic recovery but also because of the therapeutic history that preceded it. The patient had been treated with a proton pump inhibitor, a class of acid-suppressing drugs used by millions of people worldwide for reflux and ulcer disease, as well as with metformin, the first-line medication for type 2 diabetes. Both drugs are increasingly recognized as causes of magnesium depletion. Proton pump inhibitors interfere with intestinal magnesium absorption, while metformin has been linked to urinary magnesium losses in patients with diabetes. The Belgian authors note that their patient had also experienced unexplained transient neurological deficits in the past, episodes that now appear, in retrospect, to have been heralds of the same underlying electrolyte disturbance.

Magnesium is the fourth most abundant cation in the body and the second most abundant inside cells, and its physiological reach is enormous. It serves as a cofactor for hundreds of enzymatic reactions, stabilizes the electrical gradients of excitable membranes, regulates calcium channels, and modulates the release of neurotransmitters at both central and peripheral synapses. Because roughly two thirds of body magnesium is stored in bone and only a tiny fraction circulates in the plasma, the serum level is an imperfect window into total body stores. This biochemical reality helps explain why hypomagnesemia is frequently overlooked: clinicians may assume that a normal-looking electrolyte panel excludes deficiency, or simply never order the measurement at all during the chaotic early minutes of a suspected stroke.

The neurological consequences of magnesium depletion are well documented in other contexts. Low magnesium lowers the seizure threshold, produces tremor, muscle cramps, and tetany, and can cause characteristic eye-movement abnormalities and ataxia. Severe cases have even produced reversible cerebellar syndrome with brain imaging showing swelling of the cerebellum, a phenomenon described in several case reports over the past decade. What has been far rarer in the literature is the attribution of focal deficits, weakness or speech disturbance confined to one side of the body in a pattern that strongly suggests a localized brain lesion, to magnesium deficiency alone. The Belgian team argues that this rarity is at least partly an artifact of under-testing rather than a true biological rarity.

The mechanisms by which magnesium depletion could produce focal symptoms are biologically plausible. Experimental work on cerebral penetrating arterioles has shown that magnesium promotes vasodilation in these small vessels, so its absence may impair the fine regulation of blood flow in deep brain regions. Magnesium also acts as a natural antagonist of the NMDA receptor, damping excitotoxic cascades that amplify injury during ischemia, and clinical studies in patients with aneurysmal subarachnoid hemorrhage have explored magnesium infusions as a protective agent during episodes of critical perfusion. In a deficient state, the loss of these protective functions could render vulnerable brain circuits transiently dysfunctional, producing deficits that mimic vascular occlusion but reverse when the electrolyte balance is restored.

Stroke mimics are far from a marginal concern in emergency neurology. Large registries of patients referred to stroke services have found that a substantial proportion of code-stroke activations ultimately receive a non-ischemic diagnosis, ranging from seizures and migraines to metabolic derangements and functional disorders. Distinguishing true stroke from mimic is one of the hardest tasks in acute medicine, because the cost of missing a real infarct is measured in dead brain tissue, while the cost of treating a mimic with thrombolytics includes potentially catastrophic bleeding. Imaging tools such as CT perfusion have improved this discrimination, but they depend on recognizing which metabolic conditions can distort the pictures they produce. A severe electrolyte abnormality that resolves with repletion belongs firmly on that list.

The literature review accompanying the Belgian case assembles the scattered evidence that severe hypomagnesemia can indeed present as an acute stroke. Earlier reports have described patients in emergency settings and in rehabilitation units whose hemiparesis and aphasia cleared after magnesium replacement, and a 2025 review in Neurological Sciences explicitly asked whether hypomagnesemia is a rare but overlooked stroke mimic. The pattern across these reports is consistent: the patients often carry risk factors for magnesium wasting, such as proton pump inhibitor use, diuretics, alcohol use, diabetes, or diarrhea, and their deficits improve as the serum level normalizes, a trajectory that would be unusual for a completed infarct. The authors of the new report emphasize that despite this documentation, magnesium levels are rarely measured during the acute phase of a suspected stroke.

Why does this gap persist? Part of the answer lies in the historical organization of emergency testing. A classic study from 1990 found that when serum magnesium was measured routinely rather than only when specifically requested, previously unrecognized hypomagnesemia was detected at a meaningful rate, suggesting that clinicians systematically underestimate its prevalence. Magnesium also interacts closely with potassium homeostasis, so refractory hypokalemia is a well-known clue to coexisting magnesium depletion, yet this teaching point competes with dozens of others in crowded emergency protocols. In the hyperacute stroke pathway, where every additional test is weighed against the clock, magnesium has simply never earned a place on the mandatory panel. The Belgian authors argue that the case they present, together with the accumulating literature, makes a compelling case for changing that practice.

The clinical implications are considerable. For patients on proton pump inhibitors and metformin, the combination seen in this case, the possibility of drug-induced magnesium wasting deserves explicit attention whenever neurological symptoms appear, particularly if the deficits fluctuate or if vascular imaging fails to show an occlusion. For stroke teams, the report suggests that a serum magnesium level, a cheap and rapid assay available in virtually every hospital laboratory, could be added to the initial workup of suspected stroke without meaningfully delaying treatment. Identifying a reversible metabolic mimic before administering thrombolytic drugs would spare patients an unnecessary bleeding risk, and correcting the deficiency could resolve deficits that would otherwise trigger days of admission, monitoring, and secondary stroke workup aimed at a vascular cause that does not exist.

The Belgian case report, approved by the ethics committee of the Hopital Civil Marie Curie in Charleroi and published with the patient’s informed consent, is unlikely to overturn stroke care on its own. But it adds a vivid data point to a quiet shift in neurological thinking: that the electrolyte milieu of the brain is not a background variable but an active determinant of focal function. As the authors and their predecessors in the literature suggest, some of the deficits long assumed to be vascular may instead be the nervous system’s distress signal when a critical mineral runs out. For a condition whose treatment is as simple as magnesium repletion, overlooking it is a luxury that emergency medicine can no longer afford.

Subject of Research: Severe hypomagnesemia as a reversible stroke mimic causing focal neurological deficits

Article Title: Stroke mimic caused by severe hypomagnesemia: a case report and literature review

Article References: Vidal Bankier, D., Renard, F., & Manto, M. (2026). Stroke mimic caused by severe hypomagnesemia: a case report and literature review. Journal of Neurology, 273(10), Article 632. https://doi.org/10.1007/s00415-026-14155-8

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14155-8

Keywords: hypomagnesemia, stroke mimic, magnesium, neurology, proton pump inhibitors, metformin, aphasia, hemiparesis, emergency medicine, electrolytes, case report, Journal of Neurology