Sulcal hyperintensity on FLAIR-MRI in a case of idiopathic intracranial hypertension

Dear Editor:

Neuroimaging has traditionally been used in idiopathic intracranial hypertension (IIH) for the purpose of ruling out other causes of increased intracranial pressure. Nevertheless, in recent years researchers have described radiological signs associated with this entity, such as flattening of the globe, horizontal tortuosity of the optic nerve, and enlarged optic nerve sheath, among others.¹

We present the case of a 15-year-old female who had been treated with isotretinoin during the preceding 7 months. She requested a medical consultation due to experiencing headache, blackouts, and loss of visual acuity during the course of one week. The physical examination found bilateral papilloedema, decreased visual acuity, peripheral visual field constriction, and enlarged blind spot. We performed a cranial CT which showed normal results. Magnetic resonance imaging revealed sulcal hyperintensity on FLAIR images, especially in the bilateral frontal and occipital convexities (Fig. 1). We observed no significant alterations in the gradient echo sequence and no signs of venous thrombosis after injection of contrast. We then performed a lumbar puncture. Cerebrospinal fluid (CSF) opening pressure was 56 cm of water, with a red blood cell count of 1/μL, leukocytes 2/μL, glucose 56 mg/dL and proteins 21 mg/dL, with no xanthochromia. The patient was diagnosed with IIH² according to current diagnostic criteria, and treated with acetazolamide. Clinical progress was good.

Figure 1.

Magnetic resonance image (FLAIR) showing sulcal hyperintensity of the convexity in the frontal and occipital parasagittal regions.

Sulcal hyperintensity on FLAIR (fluid-attenuated inversion recovery) magnetic resonance images is mainly associated with subarachnoid haemorrhage, meningitis, and meningeal carcinomatosis. Focal sulcal hyperintensity has also been described in mass effect lesions and diffuse sulcal hyperintensity in vascular lesions.³ The phenomenon has also been reported in association with high doses of propofol and oxygen.⁴ Likewise, the increase of venous pressure in cases of venous thrombosis may explain the presence of this radiological sign. However, our search of the literature revealed no links between sulcal hyperintensity on FLAIR images and IIH which might be relevant to the differential diagnosis. IIH may be another cause of this radiological sign, possibly because of an alteration in vascular dynamics, including slower CSF flow and a small amount of localised protein leakage, according to the most widely accepted current pathogenic theory about IIH.² These alterations could also cause a failure to suppress CSF signal on FLAIR imaging.