BACKGROUND: Since papilledema in idiopathic intracranial hypertension is a passive event not primarily affecting the visual tract, resolution with restitution ad integrum is expected if intracranial pressure is rebalanced. Retinal nerve fiber swelling due to papilledema in the acute phase and possible axon loss after long-lasting elevated intracranial pressure was investigated in a controlled cross-sectional study by scanning laser polarimetry. METHODS: A cohort of 23 patients with idiopathic intracranial hypertension according to the modified Dandy diagnostic criteria, and 23 controls matched for age and gender were investigated. All patients received neurological and ophthalmologic examination including scanning laser polarimetry (GDx VCC). Patients were divided into groups depending on the presence of a papilledema (group 1) or the regression of the papilledema after initiation of therapy (group 2). Therapy was based on recommendations of the German Society of Neurology. RESULTS: Scanning laser polarimetry showed an increase of nerve fiber thickness in group 1, and a decrease of the nerve fiber thickness in group 2 compared to controls. Ten of 13 patients showed signs of a regional axon loss in the deviation map of the GDx report, and six had a Nerve Fiber Index above 30. All patients with regressive papilledema and coincidence of visual field damage and pale optic disc appearance had a pathologic result in the GDx examination, but only four of ten patients with a pathologic GDx examination showed coincidence of pale optic disc appearance and visual field damage as sign of underlying optic disc atrophy. CONCLUSION: In patients with apparently effective treatment of clinical symptoms and a regression of papilledema in idiopathic intracranial hypertension, a retinal axon loss was detected by scanning laser polarimetry. Axon loss was even present in patients without clinical evidence of optic nerve atrophy.
BACKGROUND: Since papilledema in idiopathic intracranial hypertension is a passive event not primarily affecting the visual tract, resolution with restitution ad integrum is expected if intracranial pressure is rebalanced. Retinal nerve fiber swelling due to papilledema in the acute phase and possible axon loss after long-lasting elevated intracranial pressure was investigated in a controlled cross-sectional study by scanning laser polarimetry. METHODS: A cohort of 23 patients with idiopathic intracranial hypertension according to the modified Dandy diagnostic criteria, and 23 controls matched for age and gender were investigated. All patients received neurological and ophthalmologic examination including scanning laser polarimetry (GDx VCC). Patients were divided into groups depending on the presence of a papilledema (group 1) or the regression of the papilledema after initiation of therapy (group 2). Therapy was based on recommendations of the German Society of Neurology. RESULTS: Scanning laser polarimetry showed an increase of nerve fiber thickness in group 1, and a decrease of the nerve fiber thickness in group 2 compared to controls. Ten of 13 patients showed signs of a regional axon loss in the deviation map of the GDx report, and six had a Nerve Fiber Index above 30. All patients with regressive papilledema and coincidence of visual field damage and pale optic disc appearance had a pathologic result in the GDx examination, but only four of ten patients with a pathologic GDx examination showed coincidence of pale optic disc appearance and visual field damage as sign of underlying optic disc atrophy. CONCLUSION: In patients with apparently effective treatment of clinical symptoms and a regression of papilledema in idiopathic intracranial hypertension, a retinal axon loss was detected by scanning laser polarimetry. Axon loss was even present in patients without clinical evidence of optic nerve atrophy.