Retinal Vein Changes as a Biomarker to Guide Diagnosis and Management of Elevated Intracranial Pressure

Retinal vein changes, which can be observed on clinical exam or ophthalmic imaging, are promising non-invasive biomarkers for elevated intracranial pressure (ICP) as a complement to other markers of high ICP including optic nerve head swelling. Animal and human studies have demonstrated increase in retinal vein pressure associated with elevated ICP mediated by increase in cerebral venous pressure, compression of venous outflow by elevated cerebral spinal fluid pressure in the optic nerve sheath, and compression of venous outflow by optic nerve head swelling. Retinal vein pressure can be estimated using ophthalmodynamometry. Correlates of retinal vein pressure include spontaneous retinal venous pulsations, retinal vein diameter, and retinal vein tortuosity. All of these have potential for clinical use to diagnose and monitor elevated ICP. Challenges include diagnostic prediction based on single clinical measurements and accurate assessment of retinal vein parameters in cases where optic nerve head swelling limits visualization of the retinal veins.

A Comparison Between Pressure Wire and Microcatheter Measurements for Evaluating the Cerebral Venous Pressure Gradient

Introduction: A pressure gradient of over 8 mm Hg across the stenosis (usually located in the transverse-sigmoid junction) is one of the criteria for cerebral venous stenting in idiopathic intracranial hypertension (IIH) patients. The possible inaccuracy of the traditional microcatheter-based pressure measurements has been discussed in previous studies. In the cardiology field, a dual-sensor pressure wire is routinely used for the evaluation of stenotic lesions. Using a pressure wire for cerebral vasculature was previously discussed in a small case series and case reports. In this study, we compared venous pressure measurements obtained using both a microcatheter and a pressure wire in patients who were candidates for stenting.Methods: A retrospective study was conducted, comparing the two methods of pressure measurements in 26 patients with venous stenosis. Altogether, 120 measurements were performed using both methods. Demographic characteristics, medical history, procedural details, medications, indications for the procedure, and complications were collected from the patient charts.Results: Based on an 8-mm Hg pressure gradient cutoff indication, 19 patients were found eligible to go through unilateral venous stenting based on catheter measurements alone. The wire results corroborated the catheter results in detecting all cases indicated for a stent. This finding implies a sensitivity equal to 100% for the wire measurements. There were no wire-related complications, demonstrating its safety.Conclusions: We conclude that the pressure wire is as safe as the microcatheter and can identify cases requiring intervention. A larger-scale study is needed to assess the measurement accuracy of the pressure wire in brain vasculature.

Tricompartmental, Remote Intracerebral Hemorrhages Following Drainage of a Unilateral Chronic Subdural Hematoma: An Appraisal of the Pathogenesis

Intracerebral hemorrhage is a rare and unanticipated complication after burr hole drainage of a chronic subdural hematoma and usually occurs on the same side as the hematoma. In the absence of bleeding diathesis, iatrogenic injury or hypertension, it is commonly attributed to sudden expansion of the compressed brain, following rapid and uncontrolled removal of the subdural hematoma. Other factors like differential expansion of the various intracranial contents, abrupt changes in hemispheric balance, precipitous increase in focal cerebral blood flow, and unforeseen increase in cerebral venous pressure consequent to faulty positioning may also contribute to the pathogenesis of this complication.

Endovascular treatment of idiopathic intracranial hypertension caused by multiple venous sinus stenoses

Background: Idiopathic intracranial hypertension (IIH) shows symptoms by elevating intracranial pressure. Although sinus stenosis has been detected in many patients with IIH, the role of sinus stenosis in IIH remains obscure. Endovascular treatment for IIH due to transverse sinus stenosis has been frequently documented; however, IIH due to multiple sinus stenoses including the superior sagittal sinus (SSS) is rare. Here, we report a case of IIH due to multiple sinus stenoses treated by sinus stenting. Case Presentation: A 47-year-old woman suffered from intractable headache with IIH presented with stenosis of the right transverse and SSS. Stent placement was carried out since intracranial hypertension and trans-stenotic cerebral venous pressure gradient (CVPG) were presented, and her intractable headache disappeared. Conclusion: IIH can be caused by venous sinus stenoses and stent placement could be an appropriate treatment in patients who demonstrated a CVPG.

Incidence and predictors of dural venous sinus pressure gradient in idiopathic intracranial hypertension and non-idiopathic intracranial hypertension headache patients: results from 164 cerebral venograms

OBJECTIVE Cerebral venous pressure gradient (CVPG) from dural venous sinus stenosis is implicated in headache syndromes such as idiopathic intracranial hypertension (IIH). The incidence of CVPG in headache patients has not been reported. METHODS The authors reviewed all cerebral venograms with manometry performed for headache between January 2008 and May 2015. Patient demographics, headache etiology, intracranial pressure (ICP) measurements, and radiographic and manometric results were recorded. CVPG was defined as a difference ≥ 8 mm Hg by venographic manometry. RESULTS One hundred sixty-four venograms were performed in 155 patients. There were no procedural complications. Ninety-six procedures (58.5%) were for patients with IIH. The overall incidence of CVPG was 25.6% (42 of 164 procedures): 35.4% (34 of 96 procedures) in IIH patients and 11.8% (8 of 68 procedures) in non-IIH patients. Sixty procedures (36.6%) were performed in patients with preexisting shunts. Seventy-seven patients (49.7%) had procedures preceded by an ICP measurement within 4 weeks of venography, and in 66 (85.7%) of these patients, the ICP had been found to be elevated. CVPG was seen in 8.3% (n = 5) of the procedures in the 60 patients with a preexisting shunt and in 0% (n = 0) of the 11 procedures in the 77 patients with normal ICP (p < 0.001 for both). Noninvasive imaging (MR venography, CT venography) was assessed prior to venography in 112 (68.3%) of 164 cases, and dural venous sinus abnormalities were demonstrated in 73 (65.2%) of these cases; there was a trend toward CVPG (p = 0.07). Multivariate analysis demonstrated an increased likelihood of CVPG in patients with IIH (OR 4.97, 95% CI 1.71–14.47) and a decreased likelihood in patients with a preexisting shunt (OR 0.09, 95% CI 0.02–0.44). CONCLUSIONS CVPG is uncommon in IIH patients, rare in those with preexisting shunts, and absent in those with normal ICP.

Abstract 17967: Systemic Hypertension in Children After Superior Cavo-pulmonary Shunt is Associated With Cerebrovascular Dysautoregulation

Introduction: Hypertension is frequently seen after superior cavo-pulmonary shunt. It is unknown if hypertension is necessary to maintain cerebral blood flow due to increased cerebral venous pressure. We sought to determine the range of arterial blood pressures (ABP) associated with intact and impaired autoregulation after superior cavo-pulmonary shunt. Hypothesis: Hypertension (mean ABP>60 mmHg) is associated with cerebrovascular dysautoregulation after superior cavo-pulmonary shunt. Methods: All patients < 12 months undergoing superior cavo-pulmonary shunt from 10/2014 were eligible. Subjects underwent continuous 100 Hz monitoring of ABP, pulmonary arterial pressure (PAP), and near-infrared spectroscopy measurements of cerebral oximetry (rSO 2 ) and cerebral blood volume (CBV). Cerebrovascular autoregulation was measured by the hemoglobin volume index (HVx). ABP and CBV were low-pass filtered as 10 sec average values. Pearson’s correlation coefficient was performed over 300 sec windows. The associations between HVx changes relative to ABP and PAP were tested using linear regression with generalized estimation of equations. Optimal ABP and PAP defined by lowest HVx was determined using a curve-fit algorithm. The relationship between PAP and ABP was tested by piecewise regression. Results: Ten patients were enrolled. Median age and weight were 6.5 months and 6.2 kg. Optimal ABP and PAP were obtained in 7/10. HVx became impaired with increased ABP (top panel) and increased PAP (middle panel), indicating worse cerebrovascular dysautoregulation. PAP increased with increasing ABP (r = 0.55, p<0.0001) with an intercept of 72 mmHg above which ΔPAP/ΔABP doubled from 0.23 [0.22- 0.24] to 0.46 [0.43 - 0.49] (bottom panel). Elevations of ABP above optimal for HVx did not improve rSO2 (p>0.05). Conclusion: Hypertension after superior cavo-pulmonary shunt is associated with elevated PAP, no improvement in rSO 2 , and cerebrovascular dysautoregulation.

Acute subdural hematoma from bridging vein rupture: a potential mechanism for growth

Most acute subdural hematomas (ASDHs) develop after rupture of a bridging vein or veins. The anatomy of the bridging vein predisposes to its tearing within the border cell layer of the dura mater. Thus, the subdural hematoma actually forms within the dura. The hematoma grows by continued bleeding into the border cell layer. However, the venous pressure would not be expected to cause a large hematoma. Therefore, some type of mechanism must account for the hematoma's expansion. Cerebral venous pressure (CVP) has been demonstrated in animal models to be slightly higher than intracranial pressure (ICP), and CVP tracks the ICP as pressure variations occur. The elevation of CVP as the ICP increases is thought to result from an increase in outflow resistance of the terminal portion of the bridging veins. This probably results from a Starling resistor model or, less likely, from a muscular sphincter. A hypothesis is derived to explain the mechanism of ASDH enlargement. Tearing of one or more bridging veins causes these vessels to bleed into the dural border cell layer. Subsequent ICP elevation from the ASDH, cerebral swelling, or other cause results in elevation of the CVP by increased outflow resistance in the intact bridging veins. The increased ICP causes further bleeding into the hematoma cavity via the torn bridging veins. Thus, the ASDH enlarges via a positive feedback mechanism. Enlargement of an ASDH would cease as blood within the hematoma cavity coagulates. This would stop the dissection of the dural border cell layer, and pressure within the hematoma cavity would equalize with that in the torn bridging vein or veins.

Idiopathic intracranial hypertension

Case History—A 40 yr old man presenting with headache and visual disturbance. Idiopathic intracranial hypertension is a syndrome of raised intracranial pressure in the absence of an intracranial mass lesion, enlargement of the cerebral ventricles due to hydrocephalus, or venous thrombosis in the dural sinuses. Impaired cerebrospinal fluid absorption and raised cerebral venous pressure have both been implicated. Obese females of childbearing age are predominantly affected. Rarely, provocative factors include tetracycline, vitamin A derivatives, hypervitaminosis A, and vitamin A excess....

Cephalic Venous Congestion Aggravates only Migraine-Type Headaches

We performed the Queckenstedt's (Q)-test (compression over bilateral internal jugular veins) and a sham test on 33 patients with migraine attacks (coded as 1.1 based on headache classification proposed by International Headache Society (IHS)), 15 with migrainous attacks (IHS code 1.7), and 15 with tension-type headache (IHS code 2.1) in both supine and sitting positions. ‘Migrainous headache‘ (code 1.7) was defined if the headache characteristics fulfilled all but one criteria for ‘migraine without aura’. Migraine sufferers reported a marked increase in headache intensity after a 30-second Q-test in both supine and sitting positions. Aggravation was greater in the supine position. The intensity increase was not demonstrated in the sham test, or in patients with migrainous attacks or tensiontype headaches after the Q-test. Patients with acute migraine thus appear more sensitive to increased cerebral venous pressure or intracranial pressure. The discrepancy of intensity changes between supine and sitting positions may reflect different amount of venous return through the internal jugular veins.