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Letters to the Editor
August 2004

Treatment of Traumatic Optic Neuropathy Remains Controversial—Reply

Arch Otolaryngol Head Neck Surg. 2004;130(8):1000-1001. doi:10.1001/archotol.130.8.1000-b

In reply

We appreciate Dr Perry's keen interest in our study. The IONTS was transformed into an observational study because of insufficient eligible patients. The authors observed that their study lacks standardization of visual acuity testing, has a bias of timing of initial visual examination, and includes the patients who were not seen immediately after injury.1

Although the role of steroids in the management of traumatic optic neuropathy is controversial, clinical studies to validate the role of steroids or to prove their harmful effects in such cases are not available.2 The steroids are known to help in maintenance of tissue blood flow, aerobic energy metabolism, improvement of reversal of extracellular calcium, reduction of neurofilament degradation, and enhancement of neuronal excitability and synaptic transmission.3 So some form of treatment is better than no treatment.

In our series, 40% of cases had optic nerve compression by the fractured bone fragments without disruption of nerve sheath, which may have caused neuropraxia resulting in damming of the flow of axoplasm. Because the optic nerve is enclosed in a bony canal, it has a limited compensatory space. The mean volume of intracanalicular subarachanoid space is reported to be 21.16 mm3 and hence a small amount of blood or swelling can cause optic nerve compression, which warrants surgical decompression.4

In light of the mentioned facts, it is pertinent to mention that each case should be managed on its own merits, keeping in mind the advantages and disadvantages of steroid therapy and optic nerve decompression. We believe that patients should receive a detailed consultation regarding the available modalities before giving consent. We found that the combined therapy protocol gives better results in cases with traumatic optic neuropathy. In cases with poor prognostic factors such as total blindness, canalicular fracture, and late presentation, the risk-benefit ratio must be analyzed before any treatment is offered. The incidence of carotid artery bleeding during optic nerve decompression is very rare and can be managed endoscopically.

A randomized, controlled, double-blind study will definitely be a better proposal but has its own limitations in clinical practice.

Correspondence: Dr Gupta, Department of Otorhinolaryngology, Head and Neck Surgery, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India (akgpgi@hotmail.com).

References
1.
Levin  LABeck  RWJoseph  MP  et al The treatment of traumatic optic neuropathy: the International Optic Neuropathy Trauma Study.  Ophthalmology.1999;106:1268-1277.PubMedGoogle Scholar
2.
Steinsapir  KDGoldberg  RA Traumatic optic neuropathies.  In:  Walsh and Hoyt's Clinical Neuro-ophthalmology.5th ed. Baltimore, Md: Williams & Wilkins; 1997:715-739. Google Scholar
3.
Hall  ED The neuroprotective pharmacology of methylprednisolone.  J Neurosurg.1992;76:13-22.PubMedGoogle Scholar
4.
Tao  HMa  ZDai  PJiang  L Computer-aided three dimensional reconstruction and measurement of the optic canal and intracanalicular structures.  Laryngoscope.1999;109:1499-1502.PubMedGoogle Scholar
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