Measurement of optic nerve sheath diameter using ultrasound: the optic nerve sheath is demonstrated as a thin bilateral hyperechogenic line surrounding the hypoechogenic optic nerve. The diameter is calculated by the distance of the two cursors named “2”. Normal values range from 5,7-6,0 mm with a definitely pathologic diameter in this patient 

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... Schlachetzki and colleagues (Schlachetzki et al. 2010) (Fig. 5a). This finding is accompanied by absent flow in the CRA, whereas flow in the CRV is still detectable (Fig. 5b). The incidence of this phenomenon was first investigated by Foroozan et al. (Foroozan et al. 2002). In their retrospective study a “spot sign” occurred in 31% of cases of sudden ocular blindness. However, in an ongoing prospective study we found an incidence of up to 90% in patients with CRAO (Ertl et al., submitted). In patients with TA, either reduced (Fig. 6a) or absent flow in CRA (Fig. 6c) was evident. The diagnosis of TA can by firmly supported by hypoechoic vasculitic vessel wall changes in the temporal arteries (so called “halo”-sign) (Arida et al. 2010), but the negative predictive value is only 68% and thus far not sufficient to rule out that disease. In patients with sudden retinal blindness and borderline symptoms for TA (only 2-3 positive ACR-criteria), a visible “spot sign” could be very helpful to rule out vasculitis, as could be demonstrated in the above-mentioned prospective study (Ertl et al., submitted). Quick and sound differentiation of both etiologies is important for the initiation of specific treatments: thrombo-embolic occlusions need to be treated with platelet-inhibitors and high doses of cholesterol-lowering drugs, among control of additional cerebrovascular risk factors, whereas TA requires a sufficient and long-lasting steroid therapy to prevent secondary blindness of the unaffected eye. Absent or reduced flow in the central retinal artery should lead to detailed workup looking for sources of cardiac emboli (ECG, cardiac echo, long term ECG, holter monitoring) and artherosclerosis (IMT using carotid ultrasound, presence of hemodynamically relevant carotid stenoses, etc.). Muller et al. found that in the majority of patients with ocular syndromes and ICA-stenosis greater than 50% (according to the NASCET-classification (Arning et al. 2010)), the ICA-stenosis was located on the ipsilateral side (Muller et al. 1993). Reversely, other studies could show a significant flow reduction in the ophthalmic artery and the central retinal artery in patients with ICA- stenosis of 70% or more (NASCET-classification) (Paivansalo et al. 1999). Consequently peak systolic velocity in the CRA and the posterior ciliary artery improved after carotid endarterectomy (Mawn et al. 1997). A major advantage of OCCS is the visualization of structures lying behind the retina. Indirect fundoscopy and photodocumentation, common tools for ophthalmic investigations, are excellent methods to display pathologies up to the level of the retina or the choroid. Unfortunately, these techniques lack sensitivity or depth penetration beyond the choroid, and thus cannot elicitate the underlying cause of CRAO. Conventional A- and B-mode ultrasound systems for visualization of the globe and orbit used in opthmalmology have transmit frequencies between 10 to 20MHz. The last mentioned very high frequency has difficulties to penetrate beyond the choroid, and often these equipment lack Doppler or color-coded Doppler capabilities. Elevation of intracranial pressure (ICP) is a common phenomenon caused by a variety of neurological disorders as brain tumors, intracranial bleedings, or head trauma. Elevated ICP can be associated with life threatening conditions, e. g. brainstem herniation. Therefore these critically ill patients need to be monitored regularly to an extend of several times a day. Neuroimaging techniques as computed tomography (CT) and magnet resonance imaging (MRI) can help to assess raised ICP but have their diagnostic limitations as well (Hiler et al. 2006; Winkler et al. 2002) and require a potentially harmful patient transport. The gold standard for ICP measurement remain to be invasive intracranial devices: in addition to the need for neurosurgical operation and contraindications (e.g. thrombocytopenia) these methods are associated with certain complications as hemmorhage, infections and shunt malfunction (Brain Trauma Foundation 2000). OCCS might be an interesting bedside alternative for follow-up examination of these critically ill patients. Several studies investigated the utility of measurements of the optic nerve sheath diameter (ONSD) as an indicator for ICP measurement and management (Antonelli et al. 2009; Galetta et al. 1989; Hansen and Helmke 1997). The optic nerve as part of the central nervous system (CNS) is surrounded by cerebrospinal fluid (CSF), and thus communicates with the inner and outer subarachnoid space. Therefore, elevation of ICP can be assessed by measuring the ONSD, but also the intraocular prominence of the papilla. The transducer is positioned as described in the technical segment, the beam is focused on the area behind the papilla and the optic nerve should be depicted in the axial plane. The optic nerve sheath is demonstrated as a thin bilateral hyperechogenic line surrounding the hypoechogenic optic nerve (Fig. 7). Due to trabecular structures in this compartment the optic nerve sheat (ONS) reflects a high fraction of ultrasonic energy, while the optic nerve runs in line with the ultrasound beam without reflection. The ONSD is measured 3 mm behind the optic disc by measuring the distance between the hyperechogenic borders of the ONS (Fig. 7). Most authors suggest normal values < 5,0 mm for patients > 1 year (Ballantyne et al. 2002; Blaivas et al. 2003; Girisgin et al. 2007; Helmke and Hansen 1996; Newman et al. 2002; Tayal et al. 2007; Tsung et al. 2005). A reliable cut-off value to predict an ICP > 20cmH 2 O seems to be 5,7-6,0 mm with a sensitivity of 87-95% and a specificity of 79-100% (Geeraerts et al. 2007; Geeraerts et al. 2008; Soldatos et al. 2008; Watanabe et al. 2008). A meta-analysis of six studies having compared the reliability ONSD-measurements with classical invasive ICP monitoring in patients with intracranial hemorrhage and traumatic brain injury also showed a good accuracy of the ultrasound technique. The pooled sensitivity for the detection of raised ICP was 90% (Dubourg et al. 2011). In the hands of experienced sonographers and standardized examination procedures several studies demonstrated a high intra- and interoberserver reliability (Ballantyne et al. 2002; Helmke and Hansen 1996). Apart from the above mentioned symptomatic causes of raised ICP in idiopathic intracranial hypertension (IIH), also often referred to as pseudotumor cerebri, the mechanism of ICP increase are still not well understood. Classically patients, often obese women during childbearing age, present with headache and loss of visual acuity or visual field deficits (Degnan and Levy 2011). Though not being a life threatening condition it is still associated with permanent, and partly severe, visual deficits (Friedman 2001; Lueck and McIlwaine 2002; Rowe and Sarkies 1998; Wall 2010). Visual symptoms are thought to be due to transient or permanent ischemic damage to the optic nerve caused by pressure (Jaggi et al. 2010; Wall 2010). Regular ophthalmologic follow-up examinations with visual acuity tests and fundoscopy are recommended, and patients often need to reduce weight and need to be treated with diuretic drugs (esp. acetazolamide), regular lumbar punctures or even operative shunt techniques. Bäuerle et al. performed a prospective study to evaluate the immediate correlation of optic nerve diameter (OND), ONSD and papilledema with CSF-pressure reduction caused by therapeutic lumbar puncture in patients with IIH. Patients with IIH showed a significantly enlarged ONSD (6.4 ± 0.6 mm bilaterally) compared with healthy individuals (5.4 ± 0.5 mm) and a significant decrease in ONSD (right ONSD 5.8 ± 0.7 mm, p < 0.004; left ONSD 5.9 ± 0.7 mm, p < 0.043) 24 hours after lumbar puncture (Bauerle and Nedelmann 2011). In some patients with IIH, though, the ONSD did not change at all after lumbar puncture. This could be an effect of a postulated optic nerve compartment syndrome, an idea which first came up with persistent papilledema and visual disturbance in IIH-patients despite a functioning lumbo-peritoneal shunt (Kelman et al. 1991). Pathologic changes in trabecular structures of the ONS might interfere with the physiologic bidirectional flow of the CSF to the basal cisterns leading to persistent optic disc swelling (Killer et al. 2007). Years ago, Ossoinig suggested the use of the stretch-test (originally called the "30 degrees-test"): in widened optic nerve patterns due to fluid around the optic nerve parenchyma, a decreased optic nerve thickness was observed after performing the stretch-test (positive test result), whereas in solid lesions of the optic nerve no change of optic nerve thickness was found (negative test result) (Haritoglou et al. 2002). In patients with increased ICP due to any cause, either ophthalmoscopic evaluation or bilateral retrobulbar ultrasound is mandatory, as asymmetric and unilateral papilledemae in patients with IIH are well described (Seggia and De Menezes 1993). In addition, Bäuerle et al. did not find any correlation of papilledema and OND with CSF reduction in the short-term follow-up. Due to anatomic reasons the anterior segment of the ONSD responds quickly to changes of CSF pressure. This is a particular advantage of retrobulbar ultrasound compared to funduscopic re-evaluations, as changes behind the level of the optic disc cannot be visualized by the latter technique. Although papilledema does not quickly respond to changes in CSF-pressure it is a manifestation of chronic ICP-increase (Villa et al. 1997) and other diseases as optic neuritis (Ashurst et al. 2010) for example. To find a proper scanning plane, the probe is set as described above, with a good view on the optic nerve in the axial plane. The plane with the maximum disc elevation or excavation is selected, the measurements are performed in the “freeze” mode: disc elevation is quantified by putting the first caliper on the ...

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... of cases of sudden ocular blindness. However, in an ongoing prospective study we found an incidence of up to 90% in patients with CRAO (Ertl et al., submitted). In patients with TA, either reduced (Fig. 6a) or absent flow in CRA (Fig. 6c) was evident. The diagnosis of TA can by firmly supported by hypoechoic vasculitic vessel wall changes in the temporal arteries (so called “halo”-sign) (Arida et al. 2010), but the negative predictive value is only 68% and thus far not sufficient to rule out that disease. In patients with sudden retinal blindness and borderline symptoms for TA (only 2-3 positive ACR-criteria), a visible “spot sign” could be very helpful to rule out vasculitis, as could be demonstrated in the above-mentioned prospective study (Ertl et al., submitted). Quick and sound differentiation of both etiologies is important for the initiation of specific treatments: thrombo-embolic occlusions need to be treated with platelet-inhibitors and high doses of cholesterol-lowering drugs, among control of additional cerebrovascular risk factors, whereas TA requires a sufficient and long-lasting steroid therapy to prevent secondary blindness of the unaffected eye. Absent or reduced flow in the central retinal artery should lead to detailed workup looking for sources of cardiac emboli (ECG, cardiac echo, long term ECG, holter monitoring) and artherosclerosis (IMT using carotid ultrasound, presence of hemodynamically relevant carotid stenoses, etc.). Muller et al. found that in the majority of patients with ocular syndromes and ICA-stenosis greater than 50% (according to the NASCET-classification (Arning et al. 2010)), the ICA-stenosis was located on the ipsilateral side (Muller et al. 1993). Reversely, other studies could show a significant flow reduction in the ophthalmic artery and the central retinal artery in patients with ICA- stenosis of 70% or more (NASCET-classification) (Paivansalo et al. 1999). Consequently peak systolic velocity in the CRA and the posterior ciliary artery improved after carotid endarterectomy (Mawn et al. 1997). A major advantage of OCCS is the visualization of structures lying behind the retina. Indirect fundoscopy and photodocumentation, common tools for ophthalmic investigations, are excellent methods to display pathologies up to the level of the retina or the choroid. Unfortunately, these techniques lack sensitivity or depth penetration beyond the choroid, and thus cannot elicitate the underlying cause of CRAO. Conventional A- and B-mode ultrasound systems for visualization of the globe and orbit used in opthmalmology have transmit frequencies between 10 to 20MHz. The last mentioned very high frequency has difficulties to penetrate beyond the choroid, and often these equipment lack Doppler or color-coded Doppler capabilities. Elevation of intracranial pressure (ICP) is a common phenomenon caused by a variety of neurological disorders as brain tumors, intracranial bleedings, or head trauma. Elevated ICP can be associated with life threatening conditions, e. g. brainstem herniation. Therefore these critically ill patients need to be monitored regularly to an extend of several times a day. Neuroimaging techniques as computed tomography (CT) and magnet resonance imaging (MRI) can help to assess raised ICP but have their diagnostic limitations as well (Hiler et al. 2006; Winkler et al. 2002) and require a potentially harmful patient transport. The gold standard for ICP measurement remain to be invasive intracranial devices: in addition to the need for neurosurgical operation and contraindications (e.g. thrombocytopenia) these methods are associated with certain complications as hemmorhage, infections and shunt malfunction (Brain Trauma Foundation 2000). OCCS might be an interesting bedside alternative for follow-up examination of these critically ill patients. Several studies investigated the utility of measurements of the optic nerve sheath diameter (ONSD) as an indicator for ICP measurement and management (Antonelli et al. 2009; Galetta et al. 1989; Hansen and Helmke 1997). The optic nerve as part of the central nervous system (CNS) is surrounded by cerebrospinal fluid (CSF), and thus communicates with the inner and outer subarachnoid space. Therefore, elevation of ICP can be assessed by measuring the ONSD, but also the intraocular prominence of the papilla. The transducer is positioned as described in the technical segment, the beam is focused on the area behind the papilla and the optic nerve should be depicted in the axial plane. The optic nerve sheath is demonstrated as a thin bilateral hyperechogenic line surrounding the hypoechogenic optic nerve (Fig. 7). Due to trabecular structures in this compartment the optic nerve sheat (ONS) reflects a high fraction of ultrasonic energy, while the optic nerve runs in line with the ultrasound beam without reflection. The ONSD is measured 3 mm behind the optic disc by measuring the distance between the hyperechogenic borders of the ONS (Fig. 7). Most authors suggest normal values < 5,0 mm for patients > 1 year (Ballantyne et al. 2002; Blaivas et al. 2003; Girisgin et al. 2007; Helmke and Hansen 1996; Newman et al. 2002; Tayal et al. 2007; Tsung et al. 2005). A reliable cut-off value to predict an ICP > 20cmH 2 O seems to be 5,7-6,0 mm with a sensitivity of 87-95% and a specificity of 79-100% (Geeraerts et al. 2007; Geeraerts et al. 2008; Soldatos et al. 2008; Watanabe et al. 2008). A meta-analysis of six studies having compared the reliability ONSD-measurements with classical invasive ICP monitoring in patients with intracranial hemorrhage and traumatic brain injury also showed a good accuracy of the ultrasound technique. The pooled sensitivity for the detection of raised ICP was 90% (Dubourg et al. 2011). In the hands of experienced sonographers and standardized examination procedures several studies demonstrated a high intra- and interoberserver reliability (Ballantyne et al. 2002; Helmke and Hansen 1996). Apart from the above mentioned symptomatic causes of raised ICP in idiopathic intracranial hypertension (IIH), also often referred to as pseudotumor cerebri, the mechanism of ICP increase are still not well understood. Classically patients, often obese women during childbearing age, present with headache and loss of visual acuity or visual field deficits (Degnan and Levy 2011). Though not being a life threatening condition it is still associated with permanent, and partly severe, visual deficits (Friedman 2001; Lueck and McIlwaine 2002; Rowe and Sarkies 1998; Wall 2010). Visual symptoms are thought to be due to transient or permanent ischemic damage to the optic nerve caused by pressure (Jaggi et al. 2010; Wall 2010). Regular ophthalmologic follow-up examinations with visual acuity tests and fundoscopy are recommended, and patients often need to reduce weight and need to be treated with diuretic drugs (esp. acetazolamide), regular lumbar punctures or even operative shunt techniques. Bäuerle et al. performed a prospective study to evaluate the immediate correlation of optic nerve diameter (OND), ONSD and papilledema with CSF-pressure reduction caused by therapeutic lumbar puncture in patients with IIH. Patients with IIH showed a significantly enlarged ONSD (6.4 ± 0.6 mm bilaterally) compared with healthy individuals (5.4 ± 0.5 mm) and a significant decrease in ONSD (right ONSD 5.8 ± 0.7 mm, p < 0.004; left ONSD 5.9 ± 0.7 mm, p < 0.043) 24 hours after lumbar puncture (Bauerle and Nedelmann 2011). In some patients with IIH, though, the ONSD did not change at all after lumbar puncture. This could be an effect of a postulated optic nerve compartment syndrome, an idea which first came up with persistent papilledema and visual disturbance in IIH-patients despite a functioning lumbo-peritoneal shunt (Kelman et al. 1991). Pathologic changes in trabecular structures of the ONS might interfere with the physiologic bidirectional flow of the CSF to the basal cisterns leading to persistent optic disc swelling (Killer et al. 2007). Years ago, Ossoinig suggested the use of the stretch-test (originally called the "30 degrees-test"): in widened optic nerve patterns due to fluid around the optic nerve parenchyma, a decreased optic nerve thickness was observed after performing the stretch-test (positive test result), whereas in solid lesions of the optic nerve no change of optic nerve thickness was found (negative test result) (Haritoglou et al. 2002). In patients with increased ICP due to any cause, either ophthalmoscopic evaluation or bilateral retrobulbar ultrasound is mandatory, as asymmetric and unilateral papilledemae in patients with IIH are well described (Seggia and De Menezes 1993). In addition, Bäuerle et al. did not find any correlation of papilledema and OND with CSF reduction in the short-term follow-up. Due to anatomic reasons the anterior segment of the ONSD responds quickly to changes of CSF pressure. This is a particular advantage of retrobulbar ultrasound compared to funduscopic re-evaluations, as changes behind the level of the optic disc cannot be visualized by the latter technique. Although papilledema does not quickly respond to changes in CSF-pressure it is a manifestation of chronic ICP-increase (Villa et al. 1997) and other diseases as optic neuritis (Ashurst et al. 2010) for example. To find a proper scanning plane, the probe is set as described above, with a good view on the optic nerve in the axial plane. The plane with the maximum disc elevation or excavation is selected, the measurements are performed in the “freeze” mode: disc elevation is quantified by putting the first caliper on the uppermost part of the swollen disc, the second caliper is positioned on the strongly reflecting line representing the lamina cribrosa (Fig. 8). In patients with IIH the severity of disc swelling seems to have prognostic implications as well: in a combined retrospective and prospective study Wall et al. found a significant correlation of ...