Background and Purpose Low pulsatility signals (LPS) on transcranial Doppler ultrasonography are detected (1) with arteriovenous malformations, (2) distal to hemodynamically significant stenosis, and (3) in venous structures. We describe focal LPS in the territory of the internal carotid artery siphon that do not represent any of the above conditions.
Methods We performed retrospective and prospective reviews of transcranial Doppler studies on 3225 patients over 5 years. Clinical and radiological data of all patients with focal LPS were extracted. LPS was defined as a focal signal identified through the orbital windows with a low pulsatility index (<0.6).
Results Sixteen LPS (mean flow velocity [mean±SD], 62±11 cm/s; pulsatility index [mean±SD], 0.41±0.08; depth range, 46 to 72 mm) from 15 patients (mean±SD age, 45±15 years; 4 men, 11 women) were identified. LPS flow direction was away from the probe in 13 cases and toward it in 3. Presenting symptoms included headache, focal neurological deficits, dizziness, and pulsatile tinnitus. All patients had cranial MRI (MRI and MR angiography in 11). Three patients underwent conventional cerebral angiography. Arteriovenous malformations or significant arterial stenoses were not detected on any study.
Conclusions A focal signal from the internal carotid artery siphon region with low pulsatility index and normal mean flow velocity, identified in the absence of other transcranial Doppler abnormalities, is not related to an arteriovenous malformation or proximal arterial stenosis. LPS, as defined, are not of venous origin since mean flow velocity was in the arterial range. LPS are likely related to prominent venous flow in the cavernous sinus secondary to unusually strong pulsation of the intracavernous internal carotid artery.
Aaslid et al1 first clinically introduced TCD; it has since gained wide acceptance as a diagnostic tool in the setting of various cerebrovascular diseases.2 Alterations in flow velocities and PIs formed the basis of diagnostic criteria for extracranial and intracranial arterial stenoses, vasospasm related to subarachnoid hemorrhage, AVMs, brain death, and more recently, the detection of embolic signals and evaluation of cerebral hemodynamics.3 4 5 Diminished PIs are encountered distal to a hemodynamically significant stenosis, in AVM feeding vessels, and in conditions associated with arteriolar vasodilatation (eg, hypercapnia or states of decreased vascular resistance downstream).6 7 8 We describe LPS in the territory of the ICA siphon that do not represent any of the aforementioned conditions.
Subjects and Methods
Between September 1, 1989, and December 31, 1994, 3225 patients underwent TCD studies in our cerebrovascular laboratory. The studies were performed by conventional methods as described earlier,1 9 10 with the use of EME Transcan and the Medasonics Transpect equipment. Data gathered included SFV, DFV, MFV, and Gosling’s PIs of the anterior (MCA, ACA, and ICA) and posterior (posterior cerebral, vertebral, and basilar arteries) circulation. MFVs and PIs were recorded from the TCD screen and confirmed by manual calculation with the use of the following formulas: MFV=(SFV+2DFV)/3; PI=(SFV−DFV)/MFV. We also recorded flow directions and depths at which the signals from the various vascular structures were obtained. Studies were performed at rest with the patients breathing room air. No Valsalva maneuvers were attempted during any study. Hematocrit was measured in all patients. Simultaneous Pco2 recordings were not obtained on any patient.
LPS were defined as (1) focal TCD signals (2) with a PI less than 0.6 (normal=0.65 to 1.2) (3) identified through the orbital windows in the ICA siphon regions (cavernous-parasellar, supraclinoid, or both). Clinical and radiological data of all patients with focal LPS were extracted. Patients whose radiological studies did not include either cranial MRI/MRA or cerebral angiography were excluded from the study. The clinical charts and the radiological studies were reviewed blinded to the side of the LPS by one of the authors (C.G.). Since this study is a descriptive one, no formal statistical analysis was performed.
Twenty-one LPS from 20 patients were identified. Two were excluded because radiological studies were not available. We excluded 3 additional patients with recent subarachnoid hemorrhage and aneurysmal clipping in whom LPS were identified through transtemporal insonation. Of the remaining 15 (mean±SD age, 45±15 years; 4 men, 11 women), 7 presented with headache, 3 had dizziness, 1 complained of pulsatile tinnitus, and 5 had cerebral ischemia-related acute focal neurological deficits. None reported a history of head trauma. Flow direction of the LPS was away from the probe in 13 patients and toward the probe in 3. In 1 patient two signals were demonstrated, one toward and one away from the probe. The spectral power of LPS did not differ from that of other intracranial arteries (Figure⇓). Unlike normal intracranial arteries, however, the LPS waveforms had no envelope, ie, the spectral display of the waveform’s baseline was as intense as its peak. Other ultrasonic characteristics of LPS (depths of insonation, PIs, and MFVs) are described in the Table⇓. All other insonated cerebral arteries exhibited normal flow velocity characteristics. All studies were negative for intracranial stenosis as defined by Rorick et al.11 Cranial CT and MRI before and after gadolinium diethylenetriamine penta-acetic acid enhancement were performed on all patients. Eleven underwent three-dimensional time-of-flight MRA, and 3 were studied by intra-arterial digital subtraction four-vessel angiography. An MR venogram was not performed on any patient. Ischemic infarcts were demonstrated in 5 patients (small [<1.5 cm] in 4, large frontoparietal in the distribution of the MCA and ACA territories in 1). There was no evidence of occlusive cerebrovascular disease by MRA, either intracranial or extracranial. An AVM was not detected by angiography (conventional or MRA). Clinical follow-up data were recorded on 10 of the 15 patients. At an average of 22 months (range, 14 to 28 months) after the initial presentation and TCD study, 5 patients continued to complain of headaches, while the other 5 were neurologically asymptomatic. No follow-up TCD studies were performed.
We found 16 LPS in 15 patients whose radiological studies did not demonstrate AVMs or carotid stenotic disease. The PI is a dimensionless measure for the arithmetic description of blood flow velocity waveform.12 13 Pulsatility analysis provides hemodynamic information, proximal and distal to the point of observation/insonation. For the cerebral circulation in particular, PIs reflect the resistance to flow impeded mainly by the distal “resistance” arteriolar bed.
Low PI signals by TCD are demonstrated in severe carotid disease.6 14 As mentioned above, no carotid stenosis was demonstrated in our patients by either MRA or conventional angiography. In addition, the MCAs and ACAs homolateral to the LPS had normal blood flow velocities and PIs. Furthermore, there was no significant side-to-side asymmetry in the velocities recorded from the MCAs. Therefore, a hemodynamically significant proximal ICA stenosis does not explain the signal characteristics in the siphon region that we defined as LPS.
Diminished PIs along with bruits and increased MFVs have been consistent findings in AVM feeding arteries. We were unable to radiologically demonstrate an AVM in any patient with LPS. Furthermore, the MFVs of the obtained signals were significantly lower than the ones usually recorded from arteries feeding AVMs (≥100 cm/s).7 15 It is possible that small vascular malformations could have been missed by the MRI/MRA and the obtained signals represented flow in the carotid siphon feeding this malformation; however, we believe that this was unlikely since such small lesions would not alter the flow patterns in a large vessel such as the carotid artery.
The focal character of the observed LPS excludes any systemic changes such as hypercapnia or hypoxia that would result in PI alterations diffusely, ie, in all insonated arteries and bilaterally.8
In 1991, Aaslid et al16 reported insonation of the straight sinus through an occipital window in 9 normal subjects. The mean MFV was 23±3 cm/s, and the PIs varied from 25% to 80% of those in the arterial signals. More recently, Valdueza et al17 described their findings from transtemporal insonation of the basal vein of Rosenthal and the deep middle cerebral vein in 10 healthy subjects. Mean blood flow velocities ranged from 9 to 20 cm/s (mean±SD, 12.1±3.5 cm/s), and the signals were characterized by a low-amplitude pulsatile flow. These cited reports indicate that venous blood flow velocities range between 10 and 25 cm/s, values that are significantly lower than those observed in our patients. Thus, LPS do not represent normal venous flow. This conclusion, however, is weakened by the fact that we did not perform Valsalva maneuvers to confirm or disprove that LPS was of venous origin.
Finally, we believe that our patients did not have carotid-cavernous fistulas since the clinical presentations were not consistent with such diagnosis. Additionally, the reported TCD findings of carotid-cavernous fistulas are completely different from LPS and mainly consist of arterialization and reversal of flow in the superior ophthalmic vein.18 19
The cavernous and supraclinoid segments of the ICA form the carotid siphon, which is accommodated in the small, compact, rigid, trabeculated cavernous sinus.20 Secondary to its anatomic location, the cavernous sinus should be accessible to insonation through the orbits. The ICA in its intracavernous portion lies unsupported but is firmly anchored at the points of its entry and exit from the cavernous sinus. The pulsation of the ICA indirectly influences the flow in the sinus and may help propagation of the venous flow.21 We believe that LPS represent recordings of flow velocities in the cavernous sinus when flow is prominent as a result of unusually strong pulsations in the ICA. This could explain the mixed pattern of these waveforms, ie, pulsatilities in the “venous range” and velocities in the arterial range. However, we have no plausible explanation for the prominence of the carotid artery pulsation in these patients. Review of the cerebral angiograms (MR and conventional) did not show any unusual course of the ICA in the cavernous sinus.
We identified LPS in 0.55% of patients studied in our laboratory. This low frequency of LPS may be due to the fact that the insonation angle of the cavernous sinus is only rarely an optimal one to allow adequate signals to be obtained.
In conclusion, we have described an unusual focal low pulsatility TCD signal obtained through transorbital insonation. Radiological studies failed to reveal any underlying vascular pathology that could account for this finding. A focal TCD signal identified through the transorbital window with a PI less than 0.6 and an MFV in the normal arterial range represents unusually prominent but nonpathological blood flow in the cavernous sinus that is likely related to pronounced pulsation of the intracavernous segment of the ICA. When found in isolation and in the absence of other TCD abnormalities, an LPS may not warrant a neuroradiological evaluation.
Selected Abbreviations and Acronyms
|ACA||=||anterior cerebral artery|
|DFV||=||diastolic flow velocity|
|ICA||=||internal carotid artery|
|LPS||=||low pulsatility signals|
|MCA||=||middle cerebral artery|
|MFV||=||mean flow velocity|
|SFV||=||systolic flow velocity|
|TCD||=||transcranial Doppler ultrasonography|
- Received August 21, 1995.
- Revision received October 24, 1995.
- Accepted October 24, 1995.
- Copyright © 1996 by American Heart Association
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