What vitamin deficiencies are associated with diplopia?

Vitamin Deficiencies Associated with Diplopia

Vitamin B1 (thiamine), vitamin B12, and vitamin A deficiencies are the most significant vitamin deficiencies associated with diplopia, with thiamine deficiency being the most urgent to address due to its potential for causing irreversible neurological damage.

Thiamine (Vitamin B1) Deficiency

Thiamine deficiency is strongly associated with diplopia through its role in causing Wernicke's encephalopathy, which presents with a classic triad:

• Diplopia and ophthalmoplegia (horizontal and vertical gaze palsy, nystagmus)
• Ataxia
• Confusion/altered mental status

Risk Factors:

• Bariatric surgery patients 1
• Malabsorption conditions 1
• Prolonged vomiting 1
• Alcoholism 2
• Anorexia nervosa 3

Management:

• Immediate treatment is essential to prevent irreversible neurological damage
• For suspected acute deficiency: 500 mg thiamine IV daily for 3-5 days, then 250 mg daily for 3-5 days until symptoms resolve 1
• Maintenance therapy: oral administration of 100 mg daily as needed 1
• Never administer glucose before thiamine repletion as it can precipitate or worsen Wernicke's encephalopathy 1

Vitamin B12 Deficiency

Vitamin B12 deficiency can cause diplopia through demyelination in the central nervous system and peripheral neuropathy affecting cranial nerves.

Neurological Manifestations:

• Diplopia
• Paraesthesia
• Muscle weakness
• Abnormal reflexes
• Gait ataxia
• Myelopathies and myelo-neuropathies 1

Risk Factors:

• Bariatric surgery (especially RYGB and BPD procedures) 1, 4
• Ileal resection >20 cm 4
• Pernicious anemia 5
• Vegan/vegetarian diet 4
• Metformin use 4
• Proton pump inhibitor or H2 blocker use 4

Management:

• For neurological symptoms: 1000-2000 μg B12 daily sublingual or IM 1, 4
• Post-bariatric surgery: 1000 μg oral B12 daily indefinitely 4
• Ileal resection >20 cm: 1000 μg vitamin B12 intramuscularly monthly for life 4
• Neurological symptoms require more aggressive treatment, potentially including initial parenteral therapy 4

Vitamin A Deficiency

Vitamin A deficiency can lead to visual problems including diplopia.

Manifestations:

• Xerophthalmia
• Night blindness
• Diplopia 1

Risk Factors:

• Malabsorptive bariatric procedures (especially BPD) 1
• Fat malabsorption 1
• Bacterial overgrowth 1

Management:

• For vitamin A deficiency without corneal changes: 10,000-25,000 IU/day orally 1
• For vitamin A deficiency with corneal changes: 50,000-100,000 IU IM for 3 days followed by 50,000 IU/day for 2 weeks IM 1
• Maintenance: 6000 IU vitamin A should be included in routine multivitamin 1

Vitamin E Deficiency

Vitamin E deficiency can cause neurological symptoms that may include diplopia.

Manifestations:

• Peripheral neuropathy
• Ataxia
• Muscle weakness 1
• Potential visual disturbances including diplopia

Management:

• Treatment: 800-1200 IU/day to reach normal serum concentrations 1
• For severe deficiency: oral vitamin E 100-400 IU daily has been recommended 1

Clinical Approach to Diplopia with Suspected Vitamin Deficiency

1. Assess risk factors for vitamin deficiencies:

   • History of bariatric surgery
   • Malabsorption conditions
   • Prolonged vomiting
   • Alcoholism
   • Restrictive diets

2. Evaluate for associated symptoms:

   • Nystagmus
   • Ataxia
   • Confusion
   • Peripheral neuropathy
   • Night blindness

3. Laboratory testing:

   • Serum thiamine levels
   • Vitamin B12 levels (consider methylmalonic acid for indeterminate results)
   • Vitamin A levels
   • Vitamin E levels

4. Imaging:

   • If 3rd nerve palsy is present, MRI with gadolinium and MRA or CTA is recommended to rule out compressive lesions 1

5. Treatment:

   • Begin empiric thiamine supplementation immediately if Wernicke's encephalopathy is suspected
   • Add appropriate vitamin supplementation based on deficiencies identified
   • Monitor response to therapy

Important Considerations

• Diplopia from vitamin deficiencies often occurs with other neurological symptoms
• Multiple vitamin deficiencies may coexist, particularly in malabsorptive conditions 5
• Prompt recognition and treatment of thiamine deficiency is critical to prevent permanent neurological damage 6, 3
• Vitamin deficiencies can occur despite compliance with standard post-bariatric surgery supplementation 6
• Never administer glucose before thiamine repletion in suspected deficiency 1

By addressing vitamin deficiencies promptly and appropriately, the risk of permanent neurological damage and visual impairment can be minimized.