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This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.
The optic canal, in particular its intracranial end, represents a locus minoris resistentiae for optic nerve compression in a variety of pathologic conditions. The intracranial optic nerve shares the limited space within this narrow passage with the carotid and ophthalmic artery, all being surrounded by bone and rigid dura. Any pathological condition going along with an increase of soft tissue volume, such as in optic nerve sheath tumors, parasellar neoplasms, dolichoectasia of the carotid and/ or ophthalmic artery, hematomas, etc. , or reduction of the lumen of the bony optic canal by hyperpneumatization of the sphenoid sinus, hyperostosis or developmental abnormalities must act as a space-occupying lesion causing optic nerve compression either by pressing the nerve against the vessel or the neighboring dura or bone. The spectrum of clinical signs and symptoms of optic nerve compression in this area is rather wide and includes acute as well as slowly progressive visual loss and all kinds of visual field defects in the presence of a normal disk, papilledema, pri- mary optic atrophy or cavernous optic atrophy mimicking var- ious clinical disease entities such as retrobulbar optic neuritis, anterior and posterior ischemic optic neuropathy, soft glaucoma and others. Some of the lesions causing optic nerve compression in this area are rather small and need to be visualized or excluded by thin section CT such as pneumosinus dilatans of the sphenoid bone, dolichoectasia of the internal carotid artery, small men- ingiomas around the optic foramen and others.
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This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.
The optic canal, in particular its intracranial end, represents a locus minoris resistentiae for optic nerve compression in a variety of pathologic conditions. The intracranial optic nerve shares the limited space within this narrow passage with the carotid and ophthalmic artery, all being surrounded by bone and rigid dura. Any pathological condition going along with an increase of soft tissue volume, such as in optic nerve sheath tumors, parasellar neoplasms, dolichoectasia of the carotid and/ or ophthalmic artery, hematomas, etc. , or reduction of the lumen of the bony optic canal by hyperpneumatization of the sphenoid sinus, hyperostosis or developmental abnormalities must act as a space-occupying lesion causing optic nerve compression either by pressing the nerve against the vessel or the neighboring dura or bone. The spectrum of clinical signs and symptoms of optic nerve compression in this area is rather wide and includes acute as well as slowly progressive visual loss and all kinds of visual field defects in the presence of a normal disk, papilledema, pri- mary optic atrophy or cavernous optic atrophy mimicking var- ious clinical disease entities such as retrobulbar optic neuritis, anterior and posterior ischemic optic neuropathy, soft glaucoma and others. Some of the lesions causing optic nerve compression in this area are rather small and need to be visualized or excluded by thin section CT such as pneumosinus dilatans of the sphenoid bone, dolichoectasia of the internal carotid artery, small men- ingiomas around the optic foramen and others.