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A pediatric patient with recurrent pseudotumor cerebri and vitamin B12 deficiency
Sevgi Yetgin1, Orhan Derman, Muhsin Dogan
1Division of Hematology, Hacettepe University Faculty of Medicine, Ankara, Turkey. yetgins@superonline.com
Insights
Pseudotumor cerebri patients may benefit from vitamin B12 treatment. A case study revealed a patient developed cerebral venous thrombosis potentially linked to vitamin B12 deficiency and elevated lipoprotein-a.
Area of Science:
- Neurology
- Vascular Medicine
- Nutritional Science
Background:
- Pseudotumor cerebri (PTC) is characterized by increased intracranial pressure with normal neuroimaging.
- Idiopathic intracranial hypertension is another term for PTC.
- Cerebral venous thrombosis (CVT) is a rare but serious condition.
Observation:
- A patient diagnosed with PTC received vitamin B12 (vit-B12) treatment during two hospital admissions over 2.5 years.
- During the second admission, the patient presented with CVT.
- The CVT was potentially associated with vit-B12 deficiency, hyperhomocysteinemia, and elevated lipoprotein-a.
Findings:
- Vitamin B12 deficiency can lead to hyperhomocysteinemia, a risk factor for thrombosis.
- Elevated lipoprotein-a is also implicated in thrombotic events.
- The interplay between PTC, vit-B12, and CVT warrants further investigation.
Implications:
- This case highlights a potential link between vitamin B12 status and thrombotic complications in PTC patients.
- Monitoring homocysteine and lipoprotein-a levels may be crucial in PTC patients, especially those treated with vit-B12.
- Further research is needed to elucidate the exact mechanisms and guide clinical practice.
Abstract:
Pseudotumor cerebri is a syndrome of increased intracranial pressure, normal cerebrospinal fluid values, and a normal cerebral ventricles on brain imaging studies. A patient with a diagnosis of pseudotumor cerebri was admitted to the authors' hospital twice within a 2.5-year interval and treated with vitamin B12 (vit-B12). At the second admission she also presented with a cerebral venous thrombosis that might have been explained by vit-B12 deficiency, homocysteinemia, and an increased level of lipoprotein-a.
