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Wouter I. Schievink, Marc S. Schwartz, M. Marcel Maya, Franklin G. Moser, and Todd D. Rozen

Object

Spontaneous intracranial hypotension is an important cause of headaches and an underlying spinal CSF leak can be demonstrated in most patients. Whether CSF leaks at the level of the skull base can cause spontaneous intracranial hypotension remains a matter of controversy. The authors' aim was to examine the frequency of skull base CSF leaks as the cause of spontaneous intracranial hypotension.

Methods

Demographic, clinical, and radiological data were collected from a consecutive group of patients evaluated for spontaneous intracranial hypotension during a 9-year period.

Results

Among 273 patients who met the diagnostic criteria for spontaneous intracranial hypotension and 42 who did not, not a single instance of CSF leak at the skull base was encountered. Clear nasal drainage was reported by 41 patients, but a diagnosis of CSF rhinorrhea could not be established. Four patients underwent exploratory surgery for presumed CSF rhinorrhea. In addition, the authors treated 3 patients who had a postoperative CSF leak at the skull base following the resection of a cerebellopontine angle tumor and developed orthostatic headaches; spinal imaging, however, demonstrated the presence of a spinal source of CSF leakage in all 3 patients.

Conclusions

There is no evidence for an association between spontaneous intracranial hypotension and CSF leaks at the level of the skull base. Moreover, the authors' study suggests that a spinal source for CSF leakage should even be suspected in patients with orthostatic headaches who have a documented skull base CSF leak.

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Wouter I. Schievink, Miriam Nuño, Todd D. Rozen, M. Marcel Maya, Adam N. Mamelak, John Carmichael, and Vivien S. Bonert

OBJECT

Spontaneous intracranial hypotension is an increasingly recognized cause of headaches. Pituitary enlargement and brain sagging are common findings on MRI in patients with this disorder. The authors therefore investigated pituitary function in patients with spontaneous intracranial hypotension.

METHODS

Pituitary hormones were measured in a group of 42 consecutive patients with spontaneous intracranial hypotension. For patients with hyperprolactinemia, prolactin levels also were measured following treatment. Magnetic resonance imaging was performed prior to and following treatment.

RESULTS

The study group consisted of 27 women and 15 men with a mean age at onset of symptoms of 52.2 ± 10.7 years (mean ± SD; range 17–72 years). Hyperprolactinemia was detected in 10 patients (24%), ranging from 16 ng/ml to 96.6 ng/ml in men (normal range 3–14.7 ng/ml) and from 31.3 ng/ml to 102.5 ng/ml in women (normal range 3.8–23.2 ng/ml). In a multivariate analysis, only brain sagging on MRI was associated with hyperprolactinemia. Brain sagging was present in 60% of patients with hyperprolactinemia and in 19% of patients with normal prolactin levels (p = 0.02). Following successful treatment of the spontaneous intracranial hypotension, hyperprolactinemia resolved, along with normalization of brain MRI findings in all 10 patients.

CONCLUSIONS

Spontaneous intracranial hypotension is a previously undescribed cause of hyperprolactinemia. Brain sagging causing distortion of the pituitary stalk (stalk effect) may be responsible for the hyperprolactinemia.