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Hyperostosis frontalis interna as a potential source of cerebral oximetry signal interference

A case report

Doshi, Tina L.; Kangrga, Ivan; Vannucci, Andrea

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European Journal of Anaesthesiology (EJA): June 2015 - Volume 32 - Issue 6 - p 448-450
doi: 10.1097/EJA.0000000000000270
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Cerebral oximetry is a noninvasive monitoring technique that uses near-infrared spectroscopy (NIRS) to measure tissue oxygenation in the brain (rSO2), providing an estimate of cerebral perfusion. However, variations in oximeter design, use of systemic vasoconstrictors and underlying skin pigmentation have all been cited as factors that may affect the accuracy of cerebral oximetry readings.1–3 A few authors have suggested that deeper anatomical structures, such as the skull and the frontal sinus, may also play a role, but this hypothesis remains speculative. We suggest that the presence of hyperostosis frontalis interna (HFI) may interfere with cerebral oximeter accuracy.

This case report is exempt from institutional review board (IRB) evaluation following an official review from the Washington University Human Resources Protection Office dated 11 February 2015. A 74-year-old woman was scheduled for left carotid pseudo-aneurysm repair. Prior to induction, a Somanetics INVOS 5100C cerebral oximeter (Troy, Michigan, USA) was connected to the patient's forehead. Although she was awake and neurologically intact, initial bilateral rSO2 was 30 to 40% (normal range 60 to 80%), despite multiple adjustments in probe position (Fig. 1). These values improved only slightly after preoxygenation and induction of general anaesthesia, which proceeded uneventfully. Shortly after induction, the mean arterial pressure (MAP) decreased to 55 mmHg, and a phenylephrine infusion was titrated to maintain the MAP between 75 and 115 mmHg (baseline 80 mmHg) for the duration of the operation. Throughout this time, the cerebral oximeter not only continued to show bilateral values below normal but also still well above the preinduction baseline.

Fig. 1
Fig. 1:
Intraoperative cerebral oximetry and mean arterial blood pressure measurements.

Following carotid cross-clamp, there was a 25% decrease in rSO2 on the operative side, prompting immediate insertion of a carotid shunt. The rSO2 then improved to above baseline values, but the readings on the operative side were approximately 10% lower than on the nonoperative side. Oximeter readings on the operative side dropped briefly once more when the first shunt was replaced by a different type of shunt required to facilitate the surgical repair. The readings were again immediately restored to levels below the preclamping values but above the preinduction baseline. Upon removal of the cross-clamp, bilateral readings returned to baseline. After completion of the surgery, the patient emerged from general anaesthesia, followed commands with motor strength intact and was successfully extubated. She was then transferred to the postanaesthesia care unit in a stable condition.

Several hours later, the patient experienced an expressive aphasia. A computed tomographic (CT) scan of the head showed evidence of a new left middle cerebral artery stroke. The patient was admitted to the neurological ICU for postoperative care, where her symptoms gradually improved. She was eventually discharged to a skilled nursing facility and then lost to follow-up. Search of public records show that the patient has since died.

The precise timing and cause of this patient's stroke is unclear, but it is not our goal to explain the patient's ischaemic event. Rather, our primary objective is to review the possible causes of the low intraoperative rSO2 readings observed and to discuss factors that can influence the detection of decreased cerebral oxygenation in this and other patients monitored with cerebral oximetry.

A number of studies have investigated the effect of scalp contamination on oximeter readings. One study found that temporary scalp ischaemia induced by a pneumatic cuff around the forehead decreased the rSO2 by 7 to 17%.1 Thus, it is possible that our low cerebral oximeter readings may have been caused by cutaneous vasoconstriction from the use of phenylephrine. However, the abnormally low rSO2 at baseline preceded the administration of any vasopressors, making cutaneous vasoconstriction an unlikely explanation.

On closer review of the CT scan, it was noted that the patient had a markedly thickened, irregular frontal bone, consistent with the diagnosis of HFI. We propose that this incidental finding may explain the poor rSO2 signal observed. HFI is a benign thickening of the frontal bone commonly observed in healthy, postmenopausal women, but may also be seen in some neurological, metabolic and endocrine disorders.4 Frontal bone thickness greater than 10 mm is considered to be HFI.4 At the level of oximeter probe placement, our patient's frontal bone thickness was measured as 10.7 and 10.4 mm in the right and left lateral aspects, respectively, and 14.5 and 14.4 mm in the right and left medial aspects, respectively (Fig. 2).

Fig. 2
Fig. 2:
Axial view of patient's skull. Note the thickness of the frontal bone bilaterally.

Computer and experimental models of NIRS in cerebral tissues estimate a mean light penetration depth of approximately 1.7 cm.5 At the thickest aspect of our patient's frontal bone, the signal would have needed to pass through 1.95 cm of scalp tissue, frontal bone, frontal sinus and cerebrospinal fluid (CSF) before reaching the cortical surface (Fig. 2), suggesting that sampling of cerebral tissue for NIRS would have been limited in this instance. In addition, because HFI causes thickening of the internal aspect of the frontal bone, the patient develops a relatively superficial frontal sinus. A study examining the effect of frontal sinus depth on the accuracy of NIRS signals found that a frontal sinus located in the shallow region of the skull tends to reduce the sensitivity of the NIRS signal, while a deep frontal sinus increases signal sensitivity.6 Thus, both HFI itself and the resultant shallow frontal sinus may cause unreliable rSO2 readings.

Few studies have examined the effect of deeper bony structures on the accuracy of cerebral oximetry. A literature search yielded only one case report of signal interference due to a large frontal sinus defect.7 To our knowledge, ours is the only report of possible cerebral oximetry signal interference due to a benign anatomical variant of deeper extra-cerebral structures.

When planning intraoperative cerebral oximetry monitoring, clinicians should consider any individual anatomical variation, particularly when skull imaging is available. Low baseline oximetric values are difficult to interpret. We suggest that in certain patients, low baseline values may be attributed to skull thickness, particularly for those in populations prone to HFI. In such cases, clinicians may obtain better signals by placing the oximeter probes in more lateral or cephalad positions, where the skull may not be as thick. If this manoeuvre is ineffective, clinicians should consider the use of additional methods of assessing cerebral perfusion, such as electroencephalography (EEG) or measurement of carotid artery stump pressures. We believe that this approach supports individualised treatment and helps avoid unnecessary and potentially harmful interventions, such as induced hypertension and hypercapnia.

Acknowledgements relating to this article

Assistance with the letter: we would like to thank Dr Brian Rubin, Professor of Vascular Surgery and Radiology, for his comments and feedback on this submission.

Financial support and sponsorship: none.

Conflicts of interest: none.


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