A 44-Year-Old Alcohol-Dependent Man Who Recovered from Central Pontine Myelinolysis with Supportive Physical Therapy

Abstract

BACKGROUND Central pontine myelinolysis (CPM) includes symmetric demyelination of the central pons. CPM is a rare neurological disorder that generally develops after rapid correction of hyponatremia in individuals having underlying conditions, such as malnutrition, alcoholism, and severe burns. It can cause severe long-term disabilities. However, there is currently no pharmacotherapy capable of promoting remyelination, a process crucial for recovery from CPM. We present the case of a patient with alcoholism and malnutrition-related CPM, which developed following rapid correction of hyponatremia but then improved remarkably with supportive physical therapy. CASE REPORT A 44-year-old alcoholic and malnourished man was admitted to an emergency hospital for disorientation due to overdrinking, but later developed bulbar palsy after hyponatremia was unexpectedly, but rapidly, corrected. Axial scans of the diffusion-weighted brain MRI revealed a characteristic lesion known as a piglet sign in the central pons. Based on his underlying conditions, present episode of sodium correction, and MRI finding, the patient was diagnosed as having CPM, which progressively worsened, resulting in locked-in syndrome after 12 days. The patient was then transferred to a long-term care unit and received simple motion exercise daily, but no specific medication. His symptoms gradually improved, achieving discontinuation of tube feeding on day 21, independent walking on day 110, and discharge after 6 months. CONCLUSIONS This report highlights the importance of physical therapy, the potential of which is often underestimated despite its broad benefits for human health, as a readily applicable intervention for patients with CPM. Further understanding of mechanisms underlying exercise-induced myelination should contribute to establishing novel therapies for a wide spectrum of brain disorders.

Figure 1.

Axial MRI scans taken on the day of disease onset. (A) T2-weighted (T2W) image at the level of the pons. (B) Enlarged T2W image of the square region indicated in (A) showing the central pontine lesion as a slightly high-signal area. (C) Enlarged T1-weighted (T1W) image of the square region indicated in (A) showing the central pontine lesion as a slightly low-signal area. (D) Enlarged diffusion-weighted (DW) image of the square region indicated in (A) showing the central pontine lesion as an apparently high-signal area resembling a piglet sign. Arrows indicate relatively spared descending corticospinal and corticobulbar tracts (the nostrils of the pig snout) within the lesion.

Figure 2.

Axial MRI scans taken 11 weeks after disease onset. (A) T2W image at the level of pons. (B) Enlarged T2W image of the square region indicated in (A) showing the clear central pontine piglet sign as a well-defined high-density area. Arrows indicate spared descending corticospinal and corticobulbar tracts (the nostrils of the pig snout) within the lesion. (C) Enlarged T1W image of the square region indicated in (A) showing the central pontine piglet sign as a low-density area.

Figure 3.

Schematic summarizing 2 major pathways involved in exercise-induced CNS remyelination. Physical exercise excites related neurons in the brain and promotes their myelination via axonal action potentials (white arrows). Physical exercise also stimulates secretion and increases serum levels of myelination-promoting factors that subsequently enter the CNS via blood circulation (gray arrows).