Space Obstructive Syndrome: Intracranial Hypertension, Intraocular Pressure, and Papilledema in Space

Address correspondence and reprint requests to: Thomas C. Wiener, M.D., 2323 Clear Lake City Blvd., #152, Houston, TX 77062; [email protected].

Wiener TC. Space obstructive syndrome: intracranial hypertension, intraocular pressure, and papilledema in space. Aviat Space Environ Med 2012; 83:64–6.

Humans undergo several consistent and measurable changes of fluid distribution and regulation in the course of adapting to microgravity. Recently, a syndrome of objective findings has been described by Mader et al. associated with long-duration missions, including hyperopic shifts, mildly elevated intracranial pressure, papilledema, globe flattening, choroidal folds, and other anatomic findings. Experience with venous obstructive lesions leads the author to propose a primary obstructive process, unique to or exacerbated by microgravity, acting at the level of the proximal internal jugular veins, termed Space Obstructive Syndrome (SOS). Literature, anatomy, and ultrasound observations revealed four major potential compression zones of the internal jugular vein, with Zone I between the sternocleidomastoid muscle and the carotid artery as the primary area of compression, both in 1 G in an upright position and in microgravity. Internal jugular vein compression, along with loss of gravitationally induced cranial outflow of blood in the vertebral veins and collaterals, may lead to intracranial venous hypertension with resultant facial/head and upper airway swelling, increased intraocular pressure, intracranial hypertension, and papilledema. Further study and proof of concept will necessitate ultrasound, Doppler flow study, and internal jugular vein pressure measurements on orbit in the International Space Station. If proven, SOS will give researchers opportunity for study and development of mitigation strategies such as artificial gravity systems.


HUMANS UNDERGO several consistent and measurable changes of fluid distribution and regulation in the course of adapting to microgravity. The shift of fluids from the lower extremities to the thorax and head has been well described, manifesting in visible facial swelling and crew sensations of head fullness and stuffiness (2,11). Although central venous pressure (CVP) paradoxically decreases upon arrival into microgravity (1), jugular venous distension is a consistent and well-described finding (5,11). Less consistently, vision changes have been reported anecdotally by crewmembers for many years. A postflight survey of nearly 300 astronauts found subjective visual degradation in 23% of respondents after short-duration flight (less than 2 wk) and in 48% after long-duration flight (typically 6 mo), with crewmembers typically noting decreases in near visual acuity (8).

Recently, a syndrome of objective findings has been described associated with long-duration missions, including hyperopic shifts, mildly elevated intracranial pressure, papilledema, globe flattening, choroidal folds, and other anatomic findings (8,9). Several potential contributing factors exist in the spaceflight environment. These include the headward fluid shift itself, altered venous pressure dynamics, high cabin carbon dioxide concentrations influencing cerebral blood flow, and local organ effects in the optic nerve and retinal structure; however, at this time, the causal mechanism remains unknown. Experience with surgical lesions causing venous obstruction leads the author to propose a primary obstructive process, unique to or exacerbated by microgravity, acting at the level of the proximal internal jugular (IJ) veins. Termed Space Obstructive Syndrome (SOS), this phenomenon may account for the majority of the findings noted above.

Valdueza showed that IJ blood flow decreased with increased vertebral venous flow during head elevation from 0° to 90° (12), perhaps due to IJ collapse caused by external pressure when standing. The IJ veins are the major cerebral outflow path when supine and the vertebral veins are the major path when upright (4). As the upright posture has essentially no meaning in microgravity due to loss of the hydrostatic gradient, it may be that vertebral venous outflow is inherently impaired in this environment. This would render the cerebral circulation more dependent on IJ drainage for venous return and, thus, more susceptible to IJ obstruction.

To explore this further, the author has identified four potential IJ compression points (Table I). Zone I is along the sternocleidomastoid muscle in the mid-neck and is suspected to be the main area of compression in SOS. The IJ vein is located in most individuals between or somewhat lateral to the carotid artery and the sternocleidomastoid muscle (during standing). Note that Zone IV compression only involves the left brachiocephalic vein; the right brachiocephalic vein is not similarly compressed (6). Pilot observations by the author of ultrasound imaging in a standing position showed the IJ vein in Zone I. When supine, Zone I showed an IJ with increased diameter, as expected. Analysis of the images reveals that when supine, the IJ, due to the weight of the contained blood, falls laterally out of Zone I compression, allowing the dramatic size increase (Fig. 1). This weight driven displacement would not occur in microgravity; the IJ veins remain in Zone I compression, yet vertebral vein flow is still relatively stagnant. Venous outflow of the head now has minimum outflow and maximum obstruction. As Gisolf noted (3), “The outflow pathway will affect the blood flow through the brain (unfavorably) only when the resistance in the outflow pathway is of the same magnitude as total cerebral vascular resistance. Theoretically, this will occur in patients after bilateral internal jugular vein resection or other obstruction of the jugular veins with a coexisting obstruction of the vertebral venous pathway.” This is speculated to occur in microgravity with SOS and there may be IJ compression and relative vertebral venous system obstruction (loss of gravitationally induced blood outflow).

Fig. 1.

Left internal jugular vein, A) upright relaxed, B) upright Valsalva, and C) supine comparison. Note in A) the internal jugular vein is not visible due to collapse and, in the supine position, the internal jugular vein has fallen laterally out of Zone I compression. Double arrow: sternocleidomastoid muscle, left arrow: carotid artery, star: internal jugular vein.


The thickest area of the sternocleidomastoid muscle perpendicular to the carotid artery may be compared to the muscle thickness at the same level just lateral to the carotid artery, which has the largest diameter of the muscle. A ratio of these two measurements suggests a relationship between a larger ratio and SOS. As a thicker muscle is normally seen in men, this might support the observation that thus far all chronically symptomatic astronauts are men.

Thus, in microgravity, lessened outflow of blood from the head along with IJ compression causes venous hypertension. The resulting cerebral venous hypertension may lead to decreased outflow of cerebrospinal fluid (CSF) with resultant CSF hypertension, papilledema, possible optic disc damage, and intracranial hypertension. Hence, SOS may be the result of a cascade from a primary causative factor (Fig. 2). Long-term postflight changes such as continued intracranial hypertension and visual problems may stem from the chronic venous and CSF hypertension leading to local fibrotic changes in target organs (10).

Fig. 2.

Space Obstructive Syndrome cascade phenomenon. IOP = intraocular pressure. ICH = intracranial hypertension.


Head-down tilt studies are not useful in elucidating this mechanism because the internal jugular vein falls out of Zone I compression. The important dynamic is the longer-term steady-state change in those destined to develop SOS after circulating plasma volume and red blood cell changes have occurred after at least 14 d in microgravity (7). Testing of the SOS hypothesis will most likely involve the use of diagnostic equipment such as onboard ultrasound on the International Space Station.

Ultrasound imaging, Doppler flow studies, and invasive pressure measurements with intravenous catheters and pressure transducers on orbit would be optimal to further evaluate the SOS hypothesis. Measurements cranial to the level of obstruction will show elevated intravenous pressure, in comparison to pressures below the level of obstruction in Zone I, unless there is obstruction in Zones II–IV. To address potential compression in Zones II–IV, the best tool would be transesophageal ultrasound and flow Doppler, to avoid obscuration by the skeletal system. Measurements of central venous pressure should reflect caudal internal jugular vein pressure to the obstruction level in Zone I unless there is Zone II–IV compression.

Ultimately, the long-term solution for SOS and other concerns of microgravity may be space structures involving artificial gravity, and research platforms to define the amount of artificial gravity needed would be valuable. As space tourism increases, there will be spaceflight participants that are less healthy and less screened than NASA astronauts. SOS may become more concerning in someone who has a predilection, or underlying disease process that, combined with SOS, could cause in-flight or postflight problems.

Testing the SOS hypothesis will give researchers opportunities for study and proof of concept. Strategies for mitigation of symptoms and identification of those predisposed will occur. A study of the problems of SOS in the environment of the International Space Station may lead to greater safety as space exploration lengthens in duration and as more of the general public begins travel into space.


Presented at the 82nd Annual Scientific Meeting of the Aerospace Medical Association, May 9, 2011, Anchorage, AK. Additional information is available at

No conflict of interest to disclose and no funding was received for this work.

Author and affiliation: Thomas C. Wiener, B.S., M.D., FACS, private practice, Houston, TX.

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