Comments

The CS represents a unique venous reservoir that receives and drains blood through multiple connecting veins and sinuses. The intracavernous venous flow is further characterized by major cerebral arteries, the internal carotids, whose pulse waves are transmitted throughout the sinus and thought to be responsible for the transport of venous blood toward the jugular vein. The complexity of this pump system has been experimentally studied in great detail already by Rabischong in 1974. Studies on hemodynamics of CSFs were conducted as early as 1958 by Heyck, who used nitrous oxide to indirectly determine the AV shunt blood flow.

The interest in identifying distinct hemodynamic features of CSFs has lead to a limited number of studies on the subject using either intraarterial angiography (Hayes 1958; Phelps 1982; Brassel 1983), transcranial Doppler ultrasound (Nornes 1972) or extracranial duplex sonography (Lin 1994). As discussed in more detail in Sect. 4.3, these attempts to better understand and classify arteriovenous shunts of the CS remain necessarily insufficient, as collected data are small, mostly focusing on flow velocities and are usually not assessed within the CS itself.

The usefulness of transophthalmic ultrasonic examinations to discriminate low-flow dural shunts from direct high-flow fistulas and other causes of proptosis, such as conjunctivitis or endocrine ophthalmopathy has been reported (de Keizer 1982, 1986). As this modality encompasses only AV shunts with anterior drainage, assessment of hemodynamics in DCSFs based on flow velocities in the SOV will remain limited in its clinical and prognostic value. Flow data on DCSFs with posterior drainage are completely lacking in the medical literature, thus flow velocity as a single parameter is an inaccurate indicator for the severity of ophthalmic symptoms in the individual patient. For example, as long as anterior flow is moderate, normal venous drainage of the ocular and ophthalmic organs may still function well. On the other hand, venous outflow restriction of the AV shunting due to developing stenosis or thrombosis of the SOV will cause immediate elevation of the venous pressure associated with aggravation of a patient’s symptoms. The severity of symptoms is considered related to the flow rate in AV shunts (Barrow et al. 1985). However, depending on the individual angioarchitecture in a DCSF, draining routes and outflow restrictions, this may not be true at all and clinical assessment may be-

come more or less arbitrary (Phelps et al. 1982). For an accurate hemodynamic classification of DCSFs with clinical or therapeutic implication for prognosis, assessment of intracavernous or even retinal vascular pressure and perfusion would be needed. Like in other DAVFs, data on intrasinus pressure are scarce in DCSFs, or non-existing and most assumptions made on CSFs hemodynamics are purely based on flow velocity and IOP measurements.

Different types of pressure associated with different flow conditions need to be considered to understand hemodynamics in fistulas with various degrees of AV shunting flow. A low-flow arteriovenous fistula is intuitively considered a benign fistula because of its frequent association with minor symptoms and spontaneous occlusion. As demonstrated in the cases presented here, this view may be somewhat misleading. Although shunt flow may be very low or even close to zero (not measurable as in Case 1, Table 10.1), even a small arterialized inflow into the CS can cause devastating ophthalmic and ocular symptoms if venous hypertension due to outflow restriction is present. Such elevation of static pressure may also lead to reversal of flow and redistribution into leptomeningeal veins, potentially changing the clinical prognosis.

High-flow fistulas, on the other hand, will cause major symptoms only if venous pressure increase occurs as well; in this case, dynamic pressure. It is also known that fistulas with unrestricted posterior venous drainage into the superior or inferior petrosal sinus may be completely asymptomatic. As explained above, the orbital circulation can compensate to some degree increased pressure with its collateral circulation so that the IOP will remain normal.

Elevations of mostly static pressures, as observed in Cases #1–3 with low-flow conditions, can be expected in many DCSFs with ongoing thrombosis of the SOV, IPS or the CS itself. The inverse relationship of pressure and flow velocity in Case #1 corresponds with the concept of CS outflow restriction causing venous hypertension. Redistribution of blood flow due to pressure changes in the CS and its connecting efferent and afferent veins is a main feature in the natural history of DCSFs. Case #2 emphasizes that venous hypertension in the orbital system may affect also the ocular systems when compensatory mechanisms are exhausted. This can eventually result in a reduction of the perfusion pressure which can lead to hypoxic changes and intraretinal hemorrhages (Chap. 10.5.). Case #3 revealed no measure-

able AV shunt flow while the patient suffered from advanced chemosis, exophthalmos and visual loss. It clearly demonstrates that the assumption that a “low-flow” fistula will have a mild clinical course, and thus does not require any therapeutic intervention, can be erroneous in some cases, leading to serious clinical deterioration.

Whether or not an elevated venous pressure in the CS will increase the intraocular pressure, or the pressure in draining leptomeningeal veins, depends to a large degree on the individual angioarchitecture. Thus, if a CS is anatomically isolated from the anterior venous drainage due to thrombosis, occlusion or anatomic compartmentalization, a CSF may not necessarily lead to orbital venous hypertension and subsequent increased IOP. On the other hand, it can probably be assumed that even in cases where the SOV is thrombosed, and appears “angiographically not involved” in the drainage of the CS AV shunt, some anatomic, hemodynamic or other biomechanic communication may still exist. Therefore, even though not perceivable by imaging information, elevated pressure in the CS may be very well transmitted into the ophthalmic venous system.

In Case #2, the left CS was exposed to higher pressure values than the right, whereas the patient’s ophthalmic symptoms were dominant on the right side. On the contrary, in Case #3 the patient’s symptoms were clearly caused by the elevated CS pressure evidencing that her SOV, although thrombosed and to a large degree angiographically occluded, transmitted significant pressure. The compromised ocular and orbital venous circulation due to thrombotic outflow restriction will be further aggravated by a residual AV shunt, even when very small and almost undetectable by angiography.

Some authors may classify Cases #2 and #3 as “restrictive” or “late restrictive” types, representing the final stage in the natural history that will undergo complete spontaneous occlusion and healing (Suh et al. 2005). However, as this classification is purely based on angiographic patterns, associated and potentially deleterious effects of hemodynamic parameters are not being considered. Only indirect conclusions with regard to impairment of cerebellar hemodynamics in cases with posterior drainage can be made (Fujita et al. 2002). Lack of realistic data on flow and pressure and their changes during the natural course of these fistulas is the reason that questions, such as why DCSFs with leptomeningeal venous drainage tend to bleed less frequently than DAVFs with the same type of drainage, remain un-

answered to date. Full understanding of pathophysiology and assessment of prognosis and associated risks will become possible only if the forces inherent to the shunting flow can be measured accurately and interpreted properly in the context of individual anatomy. As the increased intraocular pressure is responsible for ophthalmological symptoms, venous hypertension in DCSFs is likely playing a more important role than flow velocity or shunt volume per se, especially in patients with partial or complete occlusion of draining veins. With regard to orbital symptoms, except for the pulsating exophthalmos, an elevated static pressure under low-flow conditions may have similar deleterious effects on the intraorbital pressure in patients with DCSFs as has a high dynamic pressure under high-flow conditions.

Although more data, including that of patients with high-flow shunts, are necessary to fully understand these relationships, it seems justified to suggest including venous pressure in hemodynamic classifications. “Low-flow” fistulas exhibiting venous hypertension might be more properly identified as “high-pressure” fistulas.

To the author’s knowledge, the study of Aihara et al. (1999) is the only one published that provides some venous pressure measurements in the CS before and after TVO. The authors reported three patients, observing a significant increase from 43 mmHg to 75 mm Hg in one “high-flow” fistula, and discuss a possible causal relationship with a diplopia that developed after treatment and resolved within 4 months. In another patient with a “high-flow” fistula, a fall in intrasinus pressure from 93 mm Hg to 48 mm Hg was documented. This patient complained of temporary worsening of her symptoms. Flow measurements were not performed and the figures do not allow a clear judgment about the flow conditions. Assuming a high-flow situation with unrestricted venous outflow in these cases, the elevated pressure most likely is dynamic pressure caused by increased flow velocities.

Increase of intrasinus pressure occurring during coil packing and at the end of the coil occlusion was observed in two of my cases, with no clinical correlation such as CN deficits. As it has been suggested, increased local (mechanical) pressure due to the densely packed platinum coils may be an explanation (Aihara et al. 1999). Such pressure elevation caused by mechanical stress may be difficult to differentiate from increased pressure due to rerouting of venous drainage or premature occlusion of venous exits such as the SOV. It may, however, explain the

development of new CN deficits after overpacking the CS in cases of complete shunt occlusions (Roy and Raymond 1997). The influence of coil overpacking with CN deficits has recently been studied by Nishino et al. (2008), who found that the cumulative volume and specific location of coils correlate with CN deficits induced by TVO.

The small number of cases available and the lack of continuous and truly simultaneous assessment of both parameters, flow and pressure, is a limiting factor of the presented invasive studies of hemodynamics in DCSFs. It should also be noted that for invasive measurements, the type of measured pressure depends on the orientation of the probe relative to the local flow direction. If the probe is perpendicular to the flow, static pressure will be measured. If the probe is pointing upstream, dynamic pressure will also be assessed. Systematic collection of such data that may be facilitated using currently available devices with sensors for both pressure and flow are needed to gain sufficient insights into the hemodynamics of cavernous sinus arteriovenous shunts and their correlation with clinical presentations of DCSFs patients.

In summary, rather little is known about hemodynamics in DCSFs, except for flow in the SOV in cases with anterior drainage, and the flow in supplying carotid arteries. Sufficient data on flow and pressure within the CS itself, or its efferent and afferent veins, are lacking due to inaccessibility with clinical imaging modalities such as ultrasound and MRI. Invasive tools for measurements, such as improved sensor-tipped guidewires, currently remain the only reliable source for studying hemodynamics in vivo and may play an increasing role during endovascular treatment of these lesions. Hemodynamic classifications based on angiographic contrast filling pattern or ultrasound measurements remain inaccurate and incomplete. This is demonstrated by invasively recorded pressure and flow data revealing that some “low-flow fistulas” might be more properly named “high-pressure fistulas”. Further studies of in vivo hemodynamics are needed for a complete understanding of the complex pathophysiology, clinical presentation, and natural course of DCSFs.

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