• Jan Hannerz and Kaj Ericson.
• Department of Neurology, Karolinska Hospital, Stockholm, Sweden.
• Headache. 2009 Feb 1; 49 (2): 178-84.

ObjectiveIdiopathic intracranial hypertension (IIH) is usually considered to result from deficient intracranial absorption of cerebrospinal fluid, but has also been suggested to be caused by decreased cranial venous flow because of increased intrathoracic pressure resulting from intra-abdominal obesity. To test this hypothesis, cerebrospinal fluid pressure (Pcsf), extracranial venous pressure (Pvf), intracranial venous pressure, and body mass index (BMI) were studied in patients with IIH with papilledema compared with patients with chronic tension-type headache (CTTH).Design And SubjectsThe Pcsf and the pressures in frontal veins without (Pvf) and with bilateral compression of the supraorbital branch of the frontal veins and the superficial facial veins (Pvfc), the latter considered to be about equal to Pvfc, were studied in 10 consecutive patients with IIH with papilledema. Ten consecutive CTTH patients were used for controls. Orbital phlebography was performed to confirm that the compression of facial veins other than the frontal veins resulted in adequate communication between the frontal vein used for the studies and the cavernous sinus.ResultsCerebrospinal fluid pressure was between 200 and 250 mm water in 5 of the CTTH patients and above 350 mm water in all IIH patients. Body mass index was >25 in all CTTH patients and similar in the 2 groups. Cerebrospinal fluid pressure was similar to Pvfc in all 10 CTTH patients but significantly greater in 6 of the 10 IIH patients. Pvf was similar in the 2 groups and related to BMI.ConclusionsChronic tension-type headache patients may be prone to have Pcsf > 200 mm water and BMI > 25. Papilledema because of intracranial hypertension occurred in the present study at Pcsf > 350 mm water. The findings of Pvfc and Pcsf being similar in all CTTH patients support the suggestion that the techniques used for measuring intracranial venous pressure are adequate. The findings of similar BMI in the CTTH and the IIH patients who differed significantly as to Pcsf refute the hypothesis that obesity precedes, and is the cause of, intracranial hypertension in IIH. The difference between Pcsf and Pvfc in 6 of the IIH patients also does not support such a hypothesis but may indicate that IIH is due to deficient intracranial cerebrospinal fluid absorption. Since a relationship between intracranial hypertension and obesity is established and obesity is not found to cause intracranial hypertension in IIH, intracranial hypertension may be suggested to be the primary cause of weight increase in IIH. Obesity, however, may secondarily increase the preexistent IIH.

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