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Post-dural puncture headache (PDPH), an alternative cause of posterior reversible encephalopathy syndrome (PRES)
Abstract Number: T 39
Abstract Type: Case Report/Case Series
There have been few published reports of post-dural puncture headaches (PDPH) in the setting of posterior reversible encephalopathy syndrome (PRES), and the following case presents this potentially new etiology for PRES. PDPH is characterized by CSF leaking from a dural puncture, causing a loss of CSF pressure in the spine and a loss of buoyancy supporting the brain. When the patient assumes an upright posture, the brain sags, and tension on the meninges and other intracranial structures creates the pain seen with PDPH (1). PRES is a reversible condition, characterized by white matter changes in the posterior circulation, resulting in headaches, altered mental status, seizures, vision loss, and loss of consciousness (4).
The patient presented herein, a G3P1, received epidural anesthesia for natural vaginal delivery and suffered a frank “wet tap” which resulted in a profound PDPH. Ultimately her headache was recurrent despite an autologous epidural blood patch. Patient then received a second blood patch, resolving her headache. However, several days later, the patient presented to her obestetrician’s office with new-onset patchy visual loss, fixed lateral gaze, and upper extremity proprioceptive deficits.
Given the nature of these symptoms, patient was admitted to hospital for neurologic evaluation, which ultimately revealed a PRES syndrome, diagnosed radiologically in the background of the aforementioned symptoms.
Initially, given these radiologic findings, patient was diagnosed with atypical preeclampsia, as it was the only previously accepted etiology of PRES that had been published in the obstetric literature. However, patient did not have typical features of preeclampsia. She was normotensive, without proteinuria, nor significant edema. Since the patient responded to magnesium sulfate, resolving her PRES symptoms, the obstetric team was even more convinced of this atypical preeclampsia-induced PRES syndrome.
However, magnesium sulfate is a known calcium channel blocker, with anti-vasospastic action, potentially resolving our patient’s PRES, absent preeclampsia. Thus, the patient was misdiagnosed with preeclampsia. Ho et al describes PRES with vasospasm in a post-partum woman following spinal anesthesia who developed a PDPH (5). We suggest a similar mechanism at play in this case, where the patient’s PDPH, via traction on the posterior cerebral artery from displacement of the brain, produced a cerebral vasospasm that resulted in PRES.
Despite the paucity of epidemiology available on PRES, the literature does describe several accepted causes of PRES, which include: hypertension, eclampsia and preeclampsia, immunosuppressive medications such as cyclosporine, various antineoplastic agents, severe hypercalcemia, thrombocytopenic syndromes, Henoch-Schönlein purpura, hemolytic uremic syndrome, amyloid angiopathy, SLE, and various causes of renal failure (4). We suggest PDPH as an alternative cause of PRES.