95. low pressure headache not low csf pressure appears to predict immediate resolution of idiopathic...

94. Antiepileptic drug polytherapy issues in pregnancyFrank J. E Vajda a, Alison A. Hitchcock b, Janet E. Graham b,Terence J. O’Brien c, Cecilie M. Lander d, Mervyn J. Eadie e

a Royal Melbourne Hospital, University of Melbourne, VICb Royal Melbourne Hospital, VICc Royal Melbourne Hospital, University of Melbourne, VICd Royal Brisbane Hospital, University of Queensland, QLDe University of Queensland, QLD

Aim: To assess the relative risks of antiepileptic drug (AED) poly-therapy and monotherapy in relation to foetal malformation duringhuman pregnancy.

Methods: Statistical analysis of data from the Australian Preg-nancy Register and from the literature.

Results: In the Australian Register,791 of 1073 AED exposed preg-nancies received AED monotherapy (73.7%), and 282 AED poly-therapy (26.3%). In the monotherapy group there were 44pregnancies with foetal malformations detected by the neonatal per-iod (5.18%) and 62 (7.84%) reported at 1 year post-natally: in thepolytherapy group the corresponding figures were 11 (3.90%) and15 (5.32%). For pregnancies involving polytherapy as compared withmonotherapy, the Relative Risk (RR) value for associated foetal mal-formations was 0.75 (95% CI = 0.38, 1.44) as determined neonatally,and 0.68 (95% CI = 0.39, 1.17) as determined after the post-natalyear.In 4 of the 14 publications from the literature the individualRR value calculated from published data was statistically signifi-cantly higher for the polytherapy group,in none statistically signifi-cantly lower, and in only 3 below 1.0. The Australian RR value wasappreciably lower than the published ones. The risk was statisticallysignificantly less overall, and also less for a given valproate dose,when valproate was co-administered with other AEDs, in particularlamotrigine.

Conclusions: It may be unwise to generalise regarding foetal haz-ards of AED polytherapy versus monotherapy without assessment ofthe role of valproate. At the same dose, valproate in polytherapy,particularly if lamotrigine is involved, may be significantly less haz-ardous for foetal development than valproate monotherapy.

doi:10.1016/j.jocn.2010.07.095

95. Low pressure headache not low CSF pressure appears topredict immediate resolution of idiopathic intracranial hyper-tension (IIH)Peter Gates, Jakob Christiansen, Gillian Skardoon, Kate Bryan

Neuroscience Department, Geelong Hospital Barwon Health, VIC

Background: The aetiology and underlying pathology of IIH isunknown. Some patients respond to an lumbar puncture (LP) butwhy has not been clear.

Aim: To examine the effect of reducing CSF pressureto < or = 10 cm H2O in patients with IIH.

Method: A study of 31 patients seen at the Geelong hospitalbetween 1998 and 2010 with IIH. (defined as headache, papilloe-dema and CSF pressure > 25 cm H2O).

Results: Closing pressure was documented in a total of 57 of 83LP’s in the 31 patients; in 7 patients no closing pressure wasrecorded. A closing CSF pressure of 10 or less was recorded after14 LP’s in 10 cases. In 4 of these patients the IIH resolved whilst in6 it persisted. The 4 cases that resolved did so after developing alow-pressure headache. The IIH resolved in another 6 patients whodeveloped a low-pressure headache (4 after LP, 1 after lumbar drainand one with a VP shunt) where a closing CSF pressure of 10 or lesswas not recorded. Rapid resolution of IIH did not occur in any patientafter an LP in the absence of low-pressure headache. One patient hada recurrence after 2 years that coincided with regaining weight, allothers remain free of symptoms 1 month to 10 years later (average3 years), 4 patients for more than 5 years.

Conclusion: Low-pressure headache not just low CSF closingpressure appears to predict response to LP in IIH. In an absence ofknowing whether the block to CSF resorption is physiological orpathological a larger multi-centre study is required to assesswhether this applies to all patients with IIH.

doi:10.1016/j.jocn.2010.07.096

1638 Abstracts / Journal of Clinical Neuroscience 17 (2010) 1610–1638