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Editor,—It is generally accepted that ectatic or even normal intracranial blood vessels can cause dysfunction of cranial nerves when situated in an aberrant location.1-3Although the occurrence of such compression damage to the optic nerve is poorly recognised, several studies have shown the optic nerves can in fact be damaged by vascular compression.4-8 Recently, optic nerve compression by normal internal carotid arteries (ICA) has been suggested as a possible cause of visual field defects in patients with optic neuropathy4-6 and normal tension glaucoma (NTG).7 8 Various mechanisms have been proposed to explain the aetiology of NTG; however, the exact cause of NTG remains to be elucidated.9
The present study was designed to determine whether optic nerve compression by the ICA can play a role in the visual field defects in patients with NTG.
Sixteen Japanese patients with NTG (average 65.3 (SD 11.9) years) and 16 age matched patients with high tension glaucoma (HTG) (average 65.6 (12.7) years) were included in this study. Magnetic resonance imaging was performed on a 1.5 T system (Signa Advantage, General Electric, Milwaukee, WI, USA). To determine the spatial relations between the optic nerves and the adjacent ICA, coronal and sagittal T1weighted images of these structures were taken with the spoiled gradient recalled acquisition in the steady state, one of the magnetic resonance angiography methods. Radiological diagnosis was made by two or three experienced radiologists who were informed of the age and sex but masked to the type of glaucoma of the patients. The relation between the optic nerve and the adjacent ICA was designated as either “with compression” or “without compression” (Fig 1).
In this series, none of the patients had intracranial abnormalities such as tumours, aneurysms, or significant atherosclerotic changes of the ICA. In the NTG group, compression by ICA was found in 24 (75%) of 32 optic nerves. Bilateral compression was observed in 12 NTG patients. In the HTG patients, compression by ICA was found in 12 (37.5%) of 32 optic nerves. Bilateral compression occurred in only three patients. Statistical analysis showed that the occurrence of optic nerve compression was significantly higher in NTG group than in the HTG group (p = 0.002, χ2 test).
Clinical characteristics of the NTG and HTG patients with compression were compared with those without compression. No statistically significant differences were found in the patients’ age, visual acuity, cup to disc ratio, and visual field variables of the Humphrey 30-2 program (Table 1).
Compressive optic neuropathy is usually caused by intracranial lesions, such as brain tumours and aneurysms, and not by normal vessels.10 However, neuropathy of the trigeminal, facial, and abducens nerves caused from compression by normal blood vessels has been described.1-3 Furthermore, Nishiokaet al reported cases in which impaired visual function was improved by surgical release of compression from normal brain vessels.4 These finding may support the idea that even the optic nerves can be damaged by the compression of normal appearing ICAs that do not show atherosclerotic or aneurysmal changes.
In spite of the high correlation between the presence of vascular compression in patients with NTG, our data do not prove that vascular compression is a major cause of the field defects in NTG. In fact, 25% of our NTG patients did not show vascular compression, and almost half of the control HTG patients also had vascular compression. Moreover, there was no statistically significant difference in the clinical characteristics of the eyes with optic nerve compression compared with those without. However, we did find a significantly higher percentage of patients who showed compression of the optic nerves by the ICA in the NTG than in the HTG patients. This difference suggests the possibility that vascular compression by normal ICA may play a role in the visual field defects in some cases of NTG.