The utility of the lumbar puncture in idiopathic intracranial hypertension

Lumbar puncture (LP) is an essential element in the diagnostic workup of idiopathic intracranial hypertension (IIH) (1,2) to prove the pathological increase in CSF pressure and to exclude secondary causes. Beyond that, it is occasionally used as a therapeutic tool as it is commonly assumed that it leads to an improvement of the IIH-associated headache and papilledema. However, as plausible as this may seem, given the current pathophysiological understanding of the disorder, the therapeutic efficacy and the sustainability of a potential improvement remain largely unknown as prospective data is scarce (3). Given that the LP is an intervention that may cause anxiety and local discomfort as well as complications, which in rare cases may even be severe, it is very important to question if repeated LPs are really a useful tool to use for the (short-term) treatment of IIH.

Yiangou et al. have addressed this question, assessing the effect of lumbar puncture on headache intensity and papilledema following LP at 1, 4 and 6 hours and daily for 7 days. The authors showed that despite the fact that the majority of IIH patients showed an improvement at some point during the first week after LP, the benefit was small and LP-induced headache exacerbations were common. The improvement was greatest in patients presenting with severe headache, and the risk of headache deterioration was most pronounced in patients with mild headache prior to the LP. In line with the current literature, the authors did not observe a positive correlation between CSF opening pressure and headache (3–5), nor any relationship between the post-LP headache response and papilledema grade. Considering that the LP-induced reduction of intracranial pressure is only short-lived (6), and that even under effective long-term normalization of CSF pressure with carboanhydrase inhibitors headache does not remit sustainably in the majority of IIH patients (7), the utility of repeated LPs is questionable.

The same holds true in most cases for the utility of repeated LPs for the treatment of the papilledema. Alterations in intracranial pressure are reflected in the CSF pressure of the optic nerve sheath with a substantial delay (8), and papilledema itself is the result of a pressure-induced axoplasmic stasis in the prelaminar section of the optic nerve (optic disc) which also takes time to develop (8–10). It is therefore hard to believe that an LP-induced, short-lived normalization of intracranial pressure may have a significant effect on papilledema and visual deterioration.

Beyond addressing the utility of therapeutic LP for the clinical management of IIH, the study by Yiangou et al. questions the underlying mechanisms that drive the IIH-associated headache. It seems obvious that the chronic elevation in intracranial pressure plays a significant role, but it remains unclear why a direct correlation between headache intensity and intracranial pressure was never proven in IIH and why the headache frequently does not remit despite pressure normalization (3). This is particularly interesting given that other IIH-associated symptoms such as papilledema and olfactory disturbances do improve under effective long-term therapy (11,12). These observations suggest that specific neuronal mechanisms, such as for example a sensitization of nociceptive trigeminal pathways or an alteration of central processing of trigeminal pain, may occur after an extended time of increased intracranial pressure and do not simply recover after its original cause has been treated. Although this study was not conceived to answer these questions, it brings them back on the table and highlights the need for further studies in this direction.