Pseudotumor Cerebri in a 43-Year-Old Woman on Triptorelin
Pseudotumor Cerebri in a 43-Year-Old Woman on Triptorelin
BIH, also known as pseudotumor cerebri, has an incidence of 1.6 to 3.5 per 100,000 in women and is much higher at 7.9 to 20 per 100,000 in women who are overweight and of reproductive age. Although by definition the etiology of BIH is unknown, a plethora of drugs and systemic conditions are associated with this condition. To explain the mechanism of BIH, some hypotheses have been put forward. These include the link between BIH and relatively obstructive segments in the distal transverse sinus, unrecognized sinus thrombosis (undetected by MRI or MRV scans), or the presence of increased arterial inflow with an accompanying low-grade stenosis of the transverse sinus.
Administration of triptorelin initially stimulates the anterior pituitary gland to release the gonadotrophins luteinizing hormone and follicle-stimulating hormone. However, its sustained use leads to their suppression.
To explain the BIH in this case, we speculate that the Triptorelin-induced initial surge of gonadal steroids may have caused non-occlusive thrombosis of the dural venous sinuses by creating a venous hypertensive state and impeding CSF drainage.
BIH usually develops several weeks to months after the intake of the offending medication. In our case, the dramatic presentation and the very high CSF opening pressure (43 cm) suggest a possible idiosyncratic effect in our patient. Nevertheless, after stopping the drug, our patient's visual improvement and the resolution of the papilledema were also very dramatic. Such a causal relationship strongly suggests triptorelin to be the cause of the BIH.
BIH has also been documented with the use of leuprorelin, which is similar in structure to triptorelin, and this only strengthens the basis of our report. In 1994, Radhakrishnan et al. reviewed the literature on BIH associated with other diseases and with drugs. Within their study, the authors insisted that the following criteria should be met to include the disease or drug within their list of causally related associations: at least two cases should have been described; the reported cases should have met all the criteria for the diagnosis of idiopathic intracranial hypertension; and intracranial dural sinus thrombosis should have been ruled out with reasonable certainty.
Therefore gonadotrophin-releasing hormone analogues fulfill the authors' criteria as a causative agent for BIH.
Discussion
BIH, also known as pseudotumor cerebri, has an incidence of 1.6 to 3.5 per 100,000 in women and is much higher at 7.9 to 20 per 100,000 in women who are overweight and of reproductive age. Although by definition the etiology of BIH is unknown, a plethora of drugs and systemic conditions are associated with this condition. To explain the mechanism of BIH, some hypotheses have been put forward. These include the link between BIH and relatively obstructive segments in the distal transverse sinus, unrecognized sinus thrombosis (undetected by MRI or MRV scans), or the presence of increased arterial inflow with an accompanying low-grade stenosis of the transverse sinus.
Administration of triptorelin initially stimulates the anterior pituitary gland to release the gonadotrophins luteinizing hormone and follicle-stimulating hormone. However, its sustained use leads to their suppression.
To explain the BIH in this case, we speculate that the Triptorelin-induced initial surge of gonadal steroids may have caused non-occlusive thrombosis of the dural venous sinuses by creating a venous hypertensive state and impeding CSF drainage.
BIH usually develops several weeks to months after the intake of the offending medication. In our case, the dramatic presentation and the very high CSF opening pressure (43 cm) suggest a possible idiosyncratic effect in our patient. Nevertheless, after stopping the drug, our patient's visual improvement and the resolution of the papilledema were also very dramatic. Such a causal relationship strongly suggests triptorelin to be the cause of the BIH.
BIH has also been documented with the use of leuprorelin, which is similar in structure to triptorelin, and this only strengthens the basis of our report. In 1994, Radhakrishnan et al. reviewed the literature on BIH associated with other diseases and with drugs. Within their study, the authors insisted that the following criteria should be met to include the disease or drug within their list of causally related associations: at least two cases should have been described; the reported cases should have met all the criteria for the diagnosis of idiopathic intracranial hypertension; and intracranial dural sinus thrombosis should have been ruled out with reasonable certainty.
Therefore gonadotrophin-releasing hormone analogues fulfill the authors' criteria as a causative agent for BIH.
Source...