migraine headache intensity and intracranial pressure

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  • Letters to the EditorMigraine Headache Intensityand Intracranial Pressure

    In their article Migraine Aggravation Caused byCephalic Venous Congestion (Doepp F, SchreiberSJ, Dreier JP, Einhaupl KM, Valdueza JM. Headache.2003;43:96-98), Doepp et al reported that 68% of pa-tients with migraine experienced increased headacheintensity when a Queckenstedt maneuver was per-formed with the patients supine. They concluded thatthe increased headache intensity was caused by in-tracranial venous distension. This conclusion may beincorrect.

    Schumacher and Wolff reported that by increasingintracranial pressure and thereby reducing intracra-nial vascular distension, they were able to reduce theintensity of the pain in histamine-induced headache.1

    Increasing intracranial pressure did not, however, re-duce pain intensity in patients with migraine. Theyconcluded that the pain of migraine was not due todistension of intracranial vessels.

    Doepp et al make the assumption that in the up-right position cerebral blood drainage occurs via theintraspinal and extraspinal venous system. Principaloutflow through the internal jugular veins can indeedbe substituted completely by the large vertebral plexusthrough communications at the cranial base.2 Onewould have to ask why this happens when the patientis upright, but not when the patient is supine. Thereshould be adequate drainage even when the jugularveins are occluded.

    Elliot Shevel, BDS, DIP, MFOS, MB, BChHeadache Clinic International

    Johannesburg BranchSuite 243, P Bag X2600

    Houghton 2041South Africa


    1. Schumacher GA, Wolff HG. Experimental studies onheadache: a contrast of histamine headache with theheadache of migraine and that associated with hyper-

    tension. B. Contrast of vascular mechanisms in pre-headache and in headache phenomena of migraine.Arch Neurol Psychiatry. 1941;45:199-214.

    2. Andeweg J. The anatomy of collateral venous flowfrom the brain and its value in aetiologeal inter-pretation of intracranial pathology. Neuroradiology.1996;38:621-628.

    Response From Doepp

    Dr. Shevel raised 2 objections to our article,Migraine Aggravation Caused by Cephalic VenousCongestion. First, Dr. Shevel cites an experimentalstudy from Schumacher and Wolff published in 1941,wherein an increase of intracranial pressure (ICP) pro-voked by connecting the subarachnoid space with ahigh column of fluid was produced in 7 patients dur-ing a migraine attack.1 The authors assumed that theincrease in ICP reduced vascular distension of thebasal cerebral arteries. No decrease of headache in-tensity was observed. Dr. Shevel proposes that thesefindings argue against the hypothesis that cerebral ve-nous distension is involved in the increase of migraineheadache. Even so, several animal studies have shownthat an increase in cerebrospinal fluid (CSF) pressuredoes not cause compression of intracranial arterial orvenous vessels; elevation of CSF pressure leads to amarked dilatation of pial arteries and a minor dilata-tion of pial veins.2,3 In another study, the caliber of pialveins remained unchanged during ICP changes dueto mannitol infusion in cats with normal and elevatedICP.4 Bridging veins become only slightly smaller with-out compression or collapse.5

    Second, we did not argue that extrajugular venousdrainage in a supine position is impossible. Instead, westated that in physiological circumstances the cerebralvenous blood in a horizontal position drains mainlythrough the internal jugular veins (IJVs).6,7 Indeed, bi-lateral IJV compression in the supine position leads toa sufficient cerebral venous drainage via extrajugularpathways above the intraspinal and extraspinal venous


  • 1014 October 2003

    system.8 This is also easily confirmed by the clinicalobservation that even bilateral radical neck dissectionwith removal of both IJVs is normally well-tolerateddespite a horizontal position.9 Taken together, how-ever, these results do not contradict the assumptionthat bilateral IJV compression causes a brief increasein cerebral venous pressure and consecutive vesseldistension before normalization due to drainage viaalternative venous pathways occurs. The observationthat the increase in migraine headache in our patientsstarted immediately with the Queckenstedt maneuversupports this hypothesis. Furthermore, it is well-knownthat a complete venous drainage adaptation follow-ing bilateral IJV removal may require up to severalmonths.10-12 Finally, 32% of our patients did not ex-perience headache worsening during a Queckenstedtmaneuver. This correlates well with our recent findingsthat in approximately 25% of all humans extrajugu-lar drainage pathways are also relevant in the supineposition.13 Prolonged compression maneuver with thepotential for eventual return to baseline headache in-tensity was not performed in our study.

    Florian Doepp, MDDepartment of Neurology

    University Hospital ChariteHumboldt University

    Schumannstrabe 20/2110117 Berlin



    1. Schumacher GA, Wolff HG. Experimental studies onheadache: A. Contrast of histamine headache withthe headache of migraine and that associated withhypertension. B. Contrast of vascular mechanisms inpre-headache and in headache phenomena of mi-graine. Arch Neurol Psychiatry. 1941;45:199-214.

    2. Auer LM, Ishiyama N, Pucher R. Cerebrovascular re-sponse to intracranial hypertension. Acta Neurochir.1987;84:124-128.

    3. Kato Y, Auer LM. Cerebrovascular response toelevation of ventricular pressure. Acta Neurochir.1989;98:184-188.

    4. Auer LM, Haselsberger K. Effect of intravenousmannitol on cat pial arteries and veins during nor-mal and elevated intracranial pressure. Neurosurgery.1987;21:142-146.

    5. Auer LM, Ishiyama N, Hodde KC, Kleinert R, PucherR. Effect of intracranial pressure on bridging veins inrats. J Neurosurg. 1987;67:263-268.

    6. Mueller HR, Hinn G, Buser MW. Internal jugular ve-nous flow measurement by means of a Duplex scan-ner. J Ultrasound Med. 1990;9:261-265.

    7. Valdueza JM, von Munster T, Hoffmann O, SchreiberS, Einhaupl KM. Postural dependency of the cerebralvenous outflow. Lancet. 2000;355:200-201.

    8. Schreiber S, Lurtzing F, Gotze R, Doepp F,Klingebiel R, Valdueza JM. Extrajugular pathwaysof human cerebral venous blood drainageassessedby duplex ultrasound. J Appl Physiol. 2003;94:1802-1805.

    9. Gius JA, Grier DH. Venous adaptation following bi-lateral radical neck dissection with excision of thejugular vein. Surgery. 1950;28:305-321.

    10. Royster HP. The relation between internal jugularvein pressure and cerebrospinal fluid pressure inthe operation of radical neck dissection. Ann Surg.1953;137:826-832.

    11. Corgill DA. Complications of neck dissection. In:Cancer of the Head and Neck. London: Butterworth& Co Ltd; 1967:191-201.

    12. Weissler MC, Pillsbury III HC. Complications ofHead and Neck Surgery. Stuttgart: Thieme Verlag;1995.

    13. Valdueza JM, Doepp F, von Munster T, RademacherJ, Schreiber SJ. Anatomical variability of humancerebral venous outflow. Cerebrovasc Dis. 2003;16(suppl 2):39.


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