Journal of Neurological Research And Therapy

Journal of Neurological Research And Therapy

Current Issue Volume No: 4 Issue No: 2

Case-report Article Open Access
  • Available online freely Peer Reviewed

  • Acute Hypomagnesemia-Induced Cerebellar Down-Beat Nystagmus Syndrome Due To Benign Paroxysmal Positional Vertigo: A Case Report

    1 Audiology and Vestibology Unit, Department of ENT, Ospedale del Mare, ASL Napoli 1 Centro, Napoli, Italy. 

    2 Department of Neuroscience, Reproductive Science and Dentistry, Section of Audiology, 

    3 Department of Neuroscience, Psychology, Drug s Area and Child s Health, University of Florence, Florence, Italy. 

    4 University of Salerno, Faculty of Medicine and Surgery, Salerno, Italy. 

    5 Department of Neurology, Ospedale San Luca di Vallo della Lucania, ASL Salerno, Salerno, Italy. 6Department of ENT, University of Perugia, Perugia, Italy. 

    6 Department of Medicine and Surgery, University of Perugia, Perugia, Italy. 

    Abstract

    Magnesium is essential for the proper functioning of all human cells and is involved in the regulation of neurotransmitter function and neurological function. Acute and chronic hypomagnesemia cause severe neurological symptoms such as neuromuscular irritability, myoclonus, stridor, dysphagia, mainly postural tremor and movement disorders along with vertical downbeat nystagmus. Here we report a case of cerebellar downbeat nystagmus syndrome induced by acute hypomagnesemia (HICS) due to very frequent vomiting in a 75-year-old woman with benign paroxysmal positional vertigo (BPPV). The clinical condition improved with daily intravenous and then oral magnesium supplementation. To our knowledge, this is the first described case of HICS induced by acute hypomagnesemia due to vomiting triggered by a benign peripheral pathology such as BPPV which was then successfully treated once the central syndrome was resolved.
    Author Contributions
    Received Jun 09, 2024     Accepted Jul 15, 2024     Published Jul 17, 2024

    Copyright© 2024 Marcelli Vincenzo, et al.
    License
    Creative Commons License   This work is licensed under a Creative Commons Attribution 4.0 International License. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

    Competing interests

    The authors have no conflict of interest to declare.

    Funding Interests:

    Citation:

    Marcelli Vincenzo, Giannoni Beatrice, Marcelli Edoardo, Volpe Giampiero, Faralli Mario et al. (2024) Acute Hypomagnesemia-Induced Cerebellar Down-Beat Nystagmus Syndrome Due To Benign Paroxysmal Positional Vertigo: A Case Report Journal of Neurological Research And Therapy. - 4(2):1-7
    DOI 10.14302/issn.2470-5020.jnrt-24-5148

    Introduction

    Introduction

    Magnesium, the second most important intracellular cation after potassium1, is essential for the proper functioning of all human cells and is involved, among other processes, in over 600 enzymatic reactions, including energy metabolism, protein synthesis, stabilization of vascular endothelium and regulation of neurotransmitter function 2345, modulating any activity mediated by intracellular calcium concentration fluxes6. In addition, magnesium is involved in the process of myelination7 and in the formation and maintenance of synapses8, making it an element necessary to keep neurons healthy and viable9. Finally, magnesium is an activator of Sirtuin 1, an anti-aging gene important to neurodegeneration and diabetes 101112.

    Magnesium homeostasis is tightly regulated by small intestinal absorption and renal excretion, and the normal plasma magnesium concentration is 1.8 to 2.5 mg/dL. Although often underdiagnosed13, magnesium deficiency, defined as a serum magnesium concentration < 1.8 mg/dL (< 0.70 mmol/L), is commonly found in 10% of patients admitted to a geriatric facility and up to 60% in intensive care units 14151617.

    The clinical picture of hypomagnesemia varies from asymptomatic presentations to complex clinical pictures characterized mainly by symptoms involving the neurological system, including neuromuscular irritability, myoclonus, stridor, dysphagia, mainly postural tremor and movement disorders along with spontaneous and gaze evoked vertical downbeat nystagmus (DBN).

    Here we report a case of acute hypomagnesemia-induced cerebellar downbeat nystagmus syndrome (HICS) due to very frequent vomiting in a 75-year-old woman with an underlying benign paroxysmal positional vertigo.

    Discussion

    Discussion

    We describe a case of benign paroxysmal positional vertigo in which we hypothesized that hypomagnesemia due to uncontrollable vomiting led to severe hypomagnesemia-induced cerebellar syndrome (HICS) among whose signs was an impressive DBN. Our hypothesis was confirmed by the effective response to magnesium therapy within two months.

    The causes of hypomagnesemia can be broadly classified into three categories18: decreased uptake, redistribution from the extracellular to the intracellular compartment, and increased renal or gastrointestinal losses. In our case, it was a magnesium gastrointestinal loss due to neurovegetative reactions from vestibular dysfunction.

    The most commonly used laboratory test to assess magnesium status is serum magnesium concentration. Other clinical laboratory tests include measurement of serum ionized magnesium concentration and twenty-four-hour urinary magnesium excretion. Research tests include the magnesium retention test, red blood cell magnesium concentration, and tissue magnesium concentration.

    If no cause is readily apparent, gastrointestinal and renal losses can be distinguished by measuring 24-hour urinary Mg2 excretion or fractional excretion of Mg2.

    Under normal conditions, magnesium blocks NMDA receptors in the cerebellum, resulting in inhibition of calcium influx and reduction of excitability, and stimulates the GABA-A chloride channel19. Magnesium depletion increases the excitatory effect of glutamate, leading to neuronal hyperexcitability4 and GABAergic channel dysfunction. Dysfunctional GABAergic activity in Purkinje cells causes DBN20. In fact, Purkinje cells send inhibitory projections to the part of the superior vestibular nucleus (SVN) that controls only upward eye movement: disruption of GABAergic activity in Purkinje cells leads to disinhibition of the SVN, resulting in slow upward gaze and DBN21.

    Another possible mechanism by which hypomagnesemia may cause cerebellar suffering is related to the vulnerability of the vascular autoregulation of the posterior circulation22. Severe hypomagnesemia results in elevated intracellular calcium levels, leading to increased contraction and tone23, increased perfusion pressure, and ultimately cytotoxic damage and endothelial dysfunction with subsequent vasogenic edema24. These lesions resemble the clinical and imaging features of posterior reversible encephalopathy syndrome (PRES) and pre-eclampsia, which are characterized by posterior circulation edema 2526.

    In the peripheral nervous system, magnesium acts primarily at the neuromuscular junction27, and decreases endplate sensitivity to the action of acetylcholine28. This explains why hypomagnesemia and hypocalcemia cause tremor.

    Finally, the effect of hypomagnesemia on cognition may be related to the effect of low magnesium levels on cholinergic transmission and the overactivity of NMDA receptors29, which could affect synaptic transmission, and disrupt the establishment of long-term potentiation, which is essential for learning and memory30.

    It is important to note that although the literature almost always reports MR-documented cerebellar edema18associated with hypomagnesemia, we did not observe the same finding in our patient in two consecutive brain MRIs performed approximately 15 days apart. It is possible that, although the authors do not specify the time at which this evaluation was performed in their patients, it was done at a stage in which hypomagnesemia had been present for some time.  In our case, however, a very pronounced hypomagnesemia had developed hyperacutely, and perhaps the cerebellar edema described by other authors had not yet had a chance to develop. To the best of our knowledge, the case of a cerebellar syndrome induced by acute hypomagnesemia as a result of a benign and peripheral disease, has not been described.

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