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Intracranial hypertension secondary to giant arachnoid granulations
  1. A Arjona1,
  2. F Delgado2,
  3. E Fernandez-Romero3
  1. 1Seccion de Neurologia, Hospital Torrecardenas, Almeria, Spain
  2. 2Servicio de Radiologia, Hospital Universitario Reina Sofia, Cordoba, Spain
  3. 3Servicio de Urgencias, Hospital Alto Guadalquivir, Andujar, Jaen, Spain
  1. For correspondence: A Arjona, C/Violeta 70, E-04720 Aguadulce, Almería, Spain; aarjonap{at}

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We present a case of intracranial hypertension in a non-obese male in whom the only finding resulting from additional tests was the presence of giant arachnoid granulations in lateral sinuses.

A 51 year old man presented episodes of transient obscurations of vision in the left eye lasting a few seconds. On general physical examination, the patient was not obese (170 cm height, 70 kg weight) and no relevant findings were detected. During neurologic examination a complete left papilledema was detected. In the right optic disc a nasal effacement with peripapillary hemorrhages was observed. Campimetry was normal in the right eye; in the left eye an enlargement of the blind spot was observed. Visual acuity was normal. A lumbar puncture in lateral decubitus showed an opening pressure of 27 cm of water. Laboratory studies, cranial magnetic resonance imaging (MRI) and visual evoked potentials were normal or negative. A magnetic resonance venography showed a dominance of the right transverse sinus and filling defect in lateral sinuses. A cerebral digital substraction angiography disclosed bilateral focal areas of nonflow signal protruding into the lumen of both sinuses at the transverse sinus-sigmoid sinus junction compatible with giant arachnoid granulations, and left transverse sinus hypoplasia.

Arachnoid granulations are present in a variable percentage of the population (0.3 B 24%) and very rarely do they produce any symptoms.1–4 Their function is not wholly understood, although cerebrospinal fluid resorption seems the most likely.4 They increase with age so that the granulations may protrude into the lumen of the venous sinus and, in theory at least , dilate it4 and obstruct venous flow.5 If this ocurred it could result in intracranial hypertension,5 as we suggest in our case.

Embedded Image

Venous phase from cerebral angiography, anteroposterior projection, shows left transverse sinus hypoplasia and two focal areas of nonflow signal protruding into sinus lumen in the right transverse sinus–sigmoid sinus junction (arrows). The two defects are round and have a diameter of 8 and 9 mm, respectively. RTS: right lateral sinus, transverse portion; RSS: right lateral sinus, sigmoid portion.