Central Pontine Myelinolysis (CPM) is a rare neurological disorder most commonly associated with the rapid correction of hyponatremia. While the condition typically presents with severe neurological deficits such as dysarthria, quadriparesis, or even locked-in syndrome, some unusual cases may manifest with atypical or isolated symptoms, making diagnosis a clinical challenge. One such rare presentation is isolated diplopia, or double vision, without other accompanying brainstem or corticospinal tract signs.
This article explores the unique case of Isolated Diplopia With Presente Olan Central Pontine Myelinolysis Olgusu, aiming to increase awareness of this uncommon but clinically significant presentation.
What Is Central Pontine Myelinolysis (CPM)?
Central Pontine Myelinolysis is a demyelinating condition that primarily affects the central region of the pons in the brainstem. It is classically linked with osmotic demyelination syndrome (ODS), often resulting from the rapid correction of chronic hyponatremia. However, CPM can also occur due to other metabolic disturbances, malnutrition, alcoholism, liver disease, or post-liver transplantation.
The hallmark of CPM is the destruction of myelin sheaths without direct damage to axons or neurons. The location of demyelination in the pons explains many of the neurological deficits associated with this condition.
A Rare Clinical Case: Isolated Diplopia
Patient Presentation
A 54-year-old male with a history of chronic alcoholism and recent hospitalization for severe hyponatremia (serum sodium 115 mEq/L) was brought to the emergency department with a chief complaint of sudden onset double vision. The patient denied headache, limb weakness, slurred speech, altered consciousness, or any sensory changes.
Upon neurological examination:
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He was alert and oriented, with no cognitive or behavioral deficits.
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Cranial nerve examination revealed isolated bilateral sixth nerve palsy, resulting in horizontal diplopia.
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Motor and sensory systems were intact.
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Reflexes and cerebellar signs were normal.
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There was no facial weakness, ataxia, or dysarthria.
Given the unusual presentation, an urgent MRI of the brain was performed.
Imaging and Diagnosis
MRI showed symmetric hyperintensity in the central pons on T2-weighted and FLAIR images, with no contrast enhancement or diffusion restriction—findings consistent with central pontine myelinolysis.
Notably, there were no lesions in the midbrain, thalamus, or cerebellum, ruling out other causes of diplopia such as brainstem infarct, demyelinating disease, or mass lesions.
This led to the diagnosis of Isolated Diplopia with Central Pontine Myelinolysis, an exceedingly rare clinical manifestation of the disease.
Pathophysiology Behind Isolated Diplopia in CPM
The sixth cranial nerve (abducens nerve) has a long intracranial course and is particularly susceptible to pressure or injury. Within the pons, its nucleus is located ventrally in the tegmentum.
In cases where CPM causes localized demyelination near the abducens nucleus or its fascicular pathways—without spreading to corticospinal or bulbar tracts—isolated sixth nerve palsy may occur. If both nuclei or bilateral pathways are involved, bilateral diplopia may be the only presenting sign, as was the case here.
This specific localization is rare, as most cases of CPM involve a broader area of the pons, affecting motor, bulbar, or cerebellar functions.
Risk Factors and Prevention
Key risk factors for CPM include:
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Rapid correction of chronic hyponatremia (increase >10 mEq/L in 24 hours)
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Alcoholism
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Malnutrition
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Liver disease or transplant
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Burns or severe infections
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Hypokalemia or other electrolyte shifts
The patient in this case had multiple risk factors: chronic alcohol use, hyponatremia, and nutritional deficiency, making him vulnerable to osmotic demyelination during fluid therapy.
Preventive Measures:
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Slow correction of serum sodium in chronic hyponatremia (<8 mEq/L per 24 hours)
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Monitoring serum electrolytes closely
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Using isotonic rather than hypertonic solutions unless urgently indicated
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Supplementation of electrolytes like potassium and magnesium when needed
Management and Prognosis
There is no specific treatment for CPM once it has occurred. Management focuses on:
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Supportive care
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Physical therapy for motor deficits
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Vision therapy or eye patching for diplopia
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Avoidance of further osmotic shifts
In the reported case, the patient’s diplopia gradually resolved over 3 weeks with conservative management and physiotherapy. No new neurological deficits developed during follow-up.
This outcome suggests that early detection of CPM—even in its atypical forms—can significantly improve prognosis, especially if further osmotic imbalance is prevented.
Clinical Implications
This case underscores a crucial clinical message: not all CPM cases present with dramatic or disabling neurological signs. A high index of suspicion is essential, especially in patients with:
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Recent electrolyte correction
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Unexplained cranial nerve palsies
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Known risk factors like alcohol use or liver disease
Isolated diplopia, though seemingly minor, may be the tip of the iceberg in a serious neurological condition.
Conclusion
The case of Isolated Diplopia With Presente Olan Central Pontine Myelinolysis Olgusu highlights a rare yet significant presentation of CPM. While traditionally associated with devastating neurological outcomes, CPM can manifest in subtle ways, such as isolated sixth nerve palsy. Awareness of such atypical symptoms, combined with timely imaging and careful monitoring of sodium correction, can prevent progression and lead to favorable outcomes.