By Renate Unsöld, Wolfgang Seeger (auth.)
This accomplished monograph opens up sensational new diagnostic and healing views. The topographic info is gifted with very good anatomic arrangements. The vast spectrum of indicators is taken from large scientific event; they're severely analysed and in comparison to the ophthalmological, neurosurgical, and neuroradiological literature. The monograph is a wonderful resource for the ophthalmologic and neurologic clinician who's the 1st to be faced with signs of optic nerve lesions. For the radiologist, it deals a transparent, didactic evaluate of standard pathological alterations of crucial lesions. For the neurosurgeon, the dialogue of optimum strategy and intraoperative findings issues to the potential of early microsurgical intervention that keeps as a lot functionality as attainable.
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Additional info for Compressive Optic Nerve Lesions at the Optic Canal: Pathogenesis — Diagnosis — Treatment
From the optics of the eye up to the primary visual cortex. Diagnostic criteria are based on latency and amplitude of the VEP, sometimes its shape is also taken into account. Pathophysiological Model A simple model explains many of the pathological effects apparent in the VEP: Inflammatory lesions, causing demyelination of the optic nerve fibers, primarily lead to prolongation of the conduction time appearing as latency increase (Halliday 1976). Compression, causing partial blockade of conduction, primarily leads to amplitude reduction but may also be accompanied by increase in latency (Halliday et al.
1968) and others. We observed a young man who experienced only a few episodes of blurred vision, after which he had no symptoms. Computerized tomography showed a marked unilateral pneumatization of the lesser wing of the sphenoid bone, the aerocele reaching far up into the suprasellar cistern. This pneumosinus caused intermittent optic nerve compression for a short time only and - probably by further expansion - was spontaneously" decompressing" the optic nerve (Fig. 44). In rare cases, compression of the pituitary gland by the pneumatocele may cause endocrine disturbances such as galactorrhea or mild hypopituitarism (Lombardi et al.
Compared to the flash-evoked ERG it is of much lower amplitude (5 11Y) and probably results from the activity of the retinal ganglion cells. It decreases with ganglion cell atrophy while the luminance-ERG remains. In acute blockage, the YEP is lost but the pattern-ERG remains until atrophy occurs (up to 3 months; Maffei and Fiorentini 1981). In acute optic neuritis, the YEP may be extinguished but the pattern-ERG is often not affected (Persson and Wanger 1984). The pattern-ERG is less dominated by central retina than the YEP.