Optic nerve trauma: Clinical, electrophysiological and histological remarks

Abstract

18 patients with post-traumatic visual disease of the optic nerve are presented. In the post-traumatic stage, visual evoked potentials were monitored. In amaurosis there was a high incidence of midface or frontobasal fractures. The severity of the trauma is not correlated with the severity of visual deficits. Flash evoked potential (FEP) findings were different: In most cases there was a correlation of clinical and FEP findings. In some we found false positive potentials in the acute stage. In smaller visual field deficits the alterations of FEP could not be correlated with the clinical disorders. FEP alterations depended on time. The pathophysiological mechanisms are discussed in regard to the pathological findings in 51 unselected autopsies with an investigation of the visual pathway from the intraorbital optic nerve to the visual cortex. Because of the different morphological alterations the clinical, neurological and ophthalmological examination should be followed by standard CT scanning to evaluate intracranial haematomas and by CT scanning with thin slices of the optic nerves and the soft tissue of the orbit. Visual evoked potentials (VEP) and in the unconscious patient, flash evoked potentials (FEP) do not give much more security for therapeutic decisions in comparison with former times. The histological findings do not support the hypothesis that operative decompression is successful.

Surveillance of traumatic optic neuropathy in the UK

“…25,26 Previous epidemiological data derived from multiple retrospective case series and the IONTS have indicated male preponderance, young age, and leading causes from RTAs, falls, and assaults in both adult 27 and paediatric 28,29 cohorts. Despite our study utilizing an effective active surveillance methodology that received high levels of support from the UK ophthalmologists, 30,31 there remained a certain level of underascertainment and consequently we are reporting minimum estimates of incidence rates.…”

Ultrastructural Findings and SOD Levels in Experimental Optic Nerve Injury: Effect of Thyroid-Releasing Hormone on the Degenerative and Regenerative Processes

“…Trauma can lead to interfascicular hemorrhage, edema, perivascular contu sion, and necrosis [29,32], Mucocele, tumor, granuloma, infection, edema, and hematoma are among the causes of indirect optic nerve trauma [19,22,29,32], According to our observations, degenerative changes increased progressively in the first 2 weeks tending to decrease in 1 month. This ob servation is in concordance with previous studies [5,6,10,11,13,24,26,33], One o f the causes of degeneration can be direct pressure on the optic nerve.…”

“…This ob servation is in concordance with previous studies [5,6,10,11,13,24,26,33], One o f the causes of degeneration can be direct pressure on the optic nerve. When the circulation of the retinal artery ceases, the pupil becomes fixed and dilated and central reti nal artery pulsation is observed [32]. Gillium demonstrated retinovascular occlusion by means of flourescein an iographies performed after retrobulbar hematomas.…”

“…actions, visual-evoked response (VER), ophthalmoscopic, neuroradiologic, and histochemical examinations are being used for the evaluation of optic nerve lesions [8,9,32], In contrary to the previous studies, recent experiments revealed that optic nerve fibers are to some extent capable of regeneration [18,26,28].…”

“…Early diagnosis and treatment o f optic nerve injury is important. However, determining the site and the extent of the lesion may be quiet difficult in an unconscious patient [22,29,32]. The most affected site o f the nerve in cranial trauma is the intracanalicular segment [8,34], The nerve is less likely to be injured in the orbita because of some protective factors such as the surrounding orbital fat,…”