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We read with great interest the article by Arjona et al1 concerning a patient with intracranial hypertension (ICH) and giant arachnoid granulations (GAG). The patient was a non-obese male without known risk factors for ICH apart from left transverse sinus hypoplasia and several GAGs in both transverse sinuses. The authors suggested that arachnoid granulations (AGs) might be responsible for ICH by obstructing the sinusal venous flow.
We would like to underline another point of view concerning such a physiological role for AGs. According to Clark,2 the AGs are absent at birth and develop in infants at the time of closure of the fontanelles. They increase in number and size with age and are commonly found in the vicinity of cortical venous entry sites into the sinuses, where there could be weaknesses in the dura mater. Thus they could be regarded as arachnoid herniations developing from intracranial CSF pulsation at higher pressure through dural defects into sinuses at lower pressure.
The role of AGs as the principal site of CSF absorption has been seriously questioned by many researchers. Greitz et al3 proposed that AGs may act as “Starling resistors” to prevent cortical venous collapse during variations in the intracranial pressure. Krisch4 proposed a volume buffering function of the intracranial CSF compartment: AGs replace the fontanelle as a rapid volume buffering structure after its closure. According to these theories, a GAG could be the result of intracranial hypertension as well as the cause of it.
Dilated AGs in the case reported by Arjona et al1 could be considered a compensatory cerebral vascular mechanism for increasing intracranial compliance in response to increased intracranial pressure. The fact that the patient had multiple GAGs bilaterally in both transverse sinuses could point to secondary enlargement of these structures due to ICH. We believe that “idiopathic intracranial hypertension” (IIH) should be the first diagnosis in this case, although this is less common in non-obese males.
King et al5 have demonstrated raised pressures in the superior sagittal sinus, with a pressure drop in the distal transverse sinuses, in the majority of patients with IIH. Interestingly, CSF removal resulted in the abolition of the functional obstruction of the distal transverse sinuses.5 They concluded that elevated venous sinus pressure is not the primary event in the patients with IIH.
The case studied by Arjona et al1 is unique because, as far as we know, there are no previous reports documenting GAGs in a patient with ICH. It illustrates the likely volume buffering and “starling resistor” functions of AGs in such individuals. Whether the GAGs are the cause or effect of ICH is not known, and further studies are required to improve our understanding of the possible roles of AGs in pathological conditions.