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The Interaction Between Intracranial Pressure, Intraocular Pressure and Lamina Cribrosal Compression in Glaucoma

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The Interaction Between Intracranial Pressure, Intraocular Pressure and Lamina Cribrosal Compression in Glaucoma CLINICAL AND EXPERIMENTAL OPTOMETRY REVIEW The interaction between intracranial pressure, intraocular pressure and lamina cribrosal compression in glaucoma Clin Exp Optom 2016; 99: 219–226 DOI:10.1111/cxo.12333 Charles W McMonnies DSc This review examines some of the biomechanical consequences associated with the opposing School of Optometry and Vision Science, University of intraocular and intracranial forces. These forces compress the lamina cribrosa and are a poten- New South Wales, Kensington, Australia tial source of glaucomatous pathology. A difference between them creates a displacement E-mail: [email protected] force on the lamina cribrosa. Increasing intraocular pressure and/or decreasing intracranial pressure will increase the trans-lamina cribrosa pressure difference and the risk of its posterior displacement, canal expansion and the formation of pathological cupping. Both intraocular pressure and intracranial pressure can be elevated during a Valsalva manoeuvre with associ- ated increases in both anterior and posterior lamina cribrosa loading as well as its compression. Any resulting thinning of or damage to the lamina cribrosa and/or retinal ganglion cell axons and/or astrocyte and glial cells attached to the matrix of the lamina cribrosa and/or reduction in blood flow to the lamina cribrosa may contribute to glaucomatous neuropathy. Thinning of the lamina cribrosa reduces its stiffness and increases the risk of its posterior displacement. Optic nerve head posterior displacement warrants medical or surgical lowering of intraocular pressure; however, compared to intraocular pressure, the trans-lamina cribrosa pressure difference may be more important in pressure-related pathology of the optic nerve head region. Similarly important could be increased compression loading of the lamina cribrosa. Submitted: 15 April 2015 Reducing participation in activities which elevate intraocular and intracranial pressure will Revised: 30 May 2015 decrease lamina cribrosa compression exposure and may contribute to glaucoma management Accepted for publication: 23 June 2015 and may have prognostic significance for glaucoma suspects. Key words: glaucoma, intracranial pressure, intraocular pressure, lamina cribrosa The glaucomas are multifactorial diseases, increased during a horizontal body position. to glaucomatous pathology rather than al- which result in a progressive loss of retinal It has been suggested that, as an alternative ways being concerned with the absolute ganglion cells (RGCs) and for which the to frequent lumbar punctures, non-invasive values for IOP, cerebrospinal fluid pressure aetiology remains unclear.1 For example, tonometry may be a useful measure for and intracranial pressure. The pattern of neurotrophic factor deprivation, hypoperfu- identifying changes in intracranial pres- axonal abnormality within individual fibre sion or ischaemia, glial cell activation, gluta- sure.10 Notwithstanding a highly significant bundles at the optic nerve head (ONH) mate excitotoxicity and abnormal immune correlation between IOP and intracranial provides support for mechanical compres- response may all contribute to the path- pressure within patients, a significant variabil- sion as a more likely cause of induced neural ogenesis of primary open angle glaucoma ity in the value of this relationship between damage.14 For all finite element models of (POAG).2 A role for adverse biomechanical patients has been demonstrated.11 For glaucoma, the largest strain magnitudes were responses is suggested with elevated intraocu- example, normal IOP was recorded in two found to occur in compression, followed by lar pressure (IOP) being identified as a signif- case series of patients with a diagnosis of shear and then by extension.15 The promi- icant stress factor in the eyes of patients with idiopathic intracranial hypertension.12,13 nence of compressive responses appears, in – glaucoma.3 5 However, the optic nerve is ex- For the purposes of this review and unless part, to be a consequence of IOP and intra- posed to not only IOP but also to intracranial otherwise indicated, any distinction between cranial pressure acting in opposite directions pressure (ICP), as it is surrounded by cerebro- cerebrospinal fluid pressure and intracranial on the lamina cribrosa (LC). It may be possi- spinal fluid in the subarachnoid space.6 The pressure is disregarded and the two terms ble for both IOP and intracranial pressure cerebrospinal fluid pressure (CSFP) is a good are used as specified in the sources cited. to be elevated with associated increased com- surrogate for the retrolaminar tissue intracra- In addition, this discussion is concerned in pression of the lamina cribrosa but without nial pressure,5 which can be a major determi- part with conditions under which changes significant extension and shear responses. nant of the biomechanical significance of in and differences between IOP and intra- Compression of the lamina cribrosa may variations in IOP varies with body position7,8 cranial pressure (the trans-lamina cribrosa damage the retinal ganglion cell axons, astro- as does intracranial pressure,9 with both pressure difference, TLCPD) can be relevant cyte and glial cells attached to the matrix of © 2016 The Authors Clinical and Experimental Optometry 99.3 May 2016 Clinical and Experimental Optometry © 2016 Optometry Australia 219 Compression of the lamina cribrosa McMonnies the lamina cribrosa as well as result in hypo- lamina cribrosa and suggests an explanation may occur sporadically or routinely from day perfusion or ischaemia, with associated for increasing glaucoma prevalence with to day (Table 18). Significant differences in increased risks of glaucomatous progression. age, which can be exacerbated by associated intracranial pressure between patients with The aim of this review is to examine some of age-related IOP increases.1 glaucoma and non-glaucomatous controls the biomechanical features associated with The trans-lamina cribrosa pressure differ- suggest that fluctuations in the intracranial the trans-lamina cribrosa pressure difference ence is not the same as the trans-lamina pressure and the trans-lamina cribrosa pres- with particular consideration of compression cribrosa pressure gradient (TLCPG) because sure gradient may also be important factors of the lamina cribrosa, damage and thinning, the latter is partly determined by the thick- in the pathogenesis of glaucoma.21 as contributors to glaucomatous pathology. ness of the lamina cribrosa (the trans-lamina Whether lamina cribrosal thinning in ad- PubMed searches for ‘intraocular pressure cribrosa pressure gradient is equal to IOP- vanced glaucoma is cause or effect is unclear and intracranial pressure’ and for ‘lamina ICP divided by the thickness of the lamina but the thinning acts to increase the magni- cribrosal compression’ yielded 320 and 68 cribrosa).24 Risk for glaucoma appears likely tude of the trans-lamina cribrosa pressure publications respectively. A representative to increase in association with an increased gradient.47 For example, it is possible that sample of these and related publications trans-lamina cribrosa pressure gradient reduced thickness of the lamina cribrosa is a were used as the basis for this review accord- resulting from a reduced thickness of the consequence of compressive stress due to ing to their relevance to the biomechanical lamina cribrosa and/or an increased trans- opposing intracranial pressure and IOP characteristics of the lamina cribrosa and lamina cribrosa pressure difference.24 Nor- loading. Consequently, a lamina cribrosa the significance of the forces to which it is mal thickness of the lamina cribrosa is which becomes thinner due to glaucomatous exposed. around 458 μm16 and normal trans-lamina changes might progressively become more cribrosa pressure difference around 5.4 susceptible to IOP-related mechanical dam- 22 TRANS-LAMINA CRIBROSA PRESSURE mmHg, so that the normal trans-lamina age because of increasing compliance and DIFFERENCE AND GRADIENT cribrosa pressure gradient is about 1.0 reduced resistance to IOP and intracranial mmHg per 85 μm of lamina cribrosal thick- pressure due to associated reduced stiffness Intraocular pressure appears to be a misno- ness. The trans-lamina cribrosa pressure of the lamina cribrosa.5 Neither IOP nor mer for what really is a trans-corneal pressure gradient is higher in POAG than in normal cerebrospinal fluid pressure alone and only difference16,17 between atmospheric and in- tension glaucoma.22 The trans-lamina the trans-lamina cribrosa pressure gradient traocular pressures. In a similar fashion to cribrosa pressure gradient increases as the is significantly associated with perimetric the cornea, the lamina cribrosa functions as lamina cribrosa thins in glaucoma, as well loss.48 For example, the lack of glaucomatous a barrier between the posterior force of IOP as when the trans-lamina cribrosa pressure damage in some ocular hypertensive patients and the anterior force of intracranial pres- gradient increases due to an IOP elevation might be explained by higher IOP being sure,1 resulting in the trans-lamina cribrosa and/or a lowering of intracranial pressure.6 associated with elevated intracranial pressure, pressure difference. Sustained elevation of Compared with a normal value of 458 μm,16 so that the trans-lamina cribrosa pressure intracranial pressure can develop with an in- a mean thickness of the lamina cribrosa of gradient is within normal limits.6 In contrast, crease in cerebrospinal fluid formation, an
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