- Case report
- Open Access
- Open Peer Review
Graves' disease presenting as pseudotumor cerebri: a case report
- Ester Coutinho1Email author,
- Ana M Silva2,
- Cláudia Freitas1 and
- Ernestina Santos1
https://doi.org/10.1186/1752-1947-5-68
© Coutinho et al; licensee BioMed Central Ltd. 2011
- Received: 22 October 2009
- Accepted: 15 February 2011
- Published: 15 February 2011
Abstract
Introduction
Pseudotumor cerebri is an entity characterized by elevated intracranial pressure with normal cerebrospinal fluid and no structural abnormalities detected on brain MRI scans. Common secondary causes include endocrine pathologies. Hyperthyroidism is very rarely associated and only three case reports have been published so far.
Case presentation
We report the case of a 31-year-old Luso-African woman with clinical symptoms and laboratory confirmation of Graves' disease that presented as pseudotumor cerebri.
Conclusion
This is a rare form of presentation of Graves' disease and a rare cause of pseudotumor cerebri. It should be remembered that hyperthyroidism is a potential cause of pseudotumor cerebri.
Keywords
- Hyperthyroidism
- Intracranial Hypertension
- Acetazolamide
- Papilledema
- Elevated Intracranial Pressure
Introduction
Pseudotumor cerebri (PTC) is an entity characterized by elevated intracranial pressure with normal cerebrospinal fluid (CSF) and no structural abnormalities detected on brain MRI scans. The neurological symptoms and signs can be totally attributed to intracranial hypertension, and these include headaches, transient visual obscurations, visual loss and intracranial tinnitus, papilledema being the hallmark of PTC. This syndrome includes both idiopathic and secondary causes. Common secondary causes include endocrine pathologies. Thyroid disturbances have a unique correlation, since hypothyroidism, hyperthyroidism and thyreostimulin suppression hormone therapy have all been reported in association with this disorder. Hyperthyroidism is very rarely associated with the disorder and only three case reports [1–3] have been published to date, one of them [3] in association with hypovitaminosis A.
Case presentation
Brain MRI scan with venography. A brain MRI scan showing normal morphology, ventricular dimensions and venous drainage.
Thyroid scintigraphy. Technetium 99 m pertechnetate thyroid images showing the goiter with diffusely increased radiotracer uptake.
Conclusion
Considering that other causes were excluded and there was neurological improvement once hyperthyroidism treatment was started, a relationship between hyperthyroidism and PTC can be assumed. Although acetazolamide was also used during the symptomatic phase, and this could represent a confounder, we are convinced that the thyroid disease treatment was the major reason for improvement. This is a rare form of presentation of Graves' disease and a rare cause of PTC.
The pathophysiologic basis of PTC is still a matter of debate, but a relationship has been established [4, 5] with elevated intracranial venous pressure. The increase in resistance of CSF absorption is thought to be caused by an insufficiently high driving pressure gradient from the subarachnoidal space to the venous system. Thyroxine, being a major regulator of sodium transport, can contribute to altered CSF dynamics. The effect of thyroid hormone raising venous pressure may justify the association between those two entities. In fact, there is a previously reported association between thyrotoxicosis and cerebral vein thrombosis [6], with additional procoagulant influences probably required in such cases.
We would like to emphasize that hyperthyroidism should be considered among the causes of PTC and that this association should be given further attention. Optic fundus examination with screening for papilledema in patients with thyroid diseases could detect more patients with intracranial hypertension, helping to prevent visual sequelae.
Consent
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
Declarations
Authors’ Affiliations
References
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Copyright
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
