Research Reports - Visual performance and the ocular surface in traumatic brain injury

Ocul Surf. 2013 Jan;11(1):25-34

Cockerham GC, Lemke S, Glynn-Milley C, Zumhagen L, Cockerham KP

The pathophysiology of neurotrauma is reviewed and an original study
investigating the prevalence of dry eye disease in a sample of veterans with
traumatic brain injury (TBI) is presented. Fifty-three veterans with TBI were
evaluated by history of injury, past ocular history, and medication use. Ocular
Disease Surface Index (OSDI), ocular examination, cranial nerve evaluation, tear
osmolarity, tear film break-up time (TFBUT), ocular surface staining and tear
production testing were performed. A matched comparison group underwent similar
testing. TBI causes were blast (44) or non-blast (9). TBI subjects scored
significantly worse on the OSDI (P<.001), and ocular surface staining by Oxford
scale (P<.001) than non-TBI subjects. Scores for tear film breakup (P=.6), basal
tear production less than 3 mm (P=.13), and tear osmolarity greater than 314
mOsm/L (P=.15) were all higher in TBI subjects; significantly more TBI subjects
had at least one abnormal dry eye measure than comparisons (P<.001). The OSDI
related to presence of dry eye symptoms (P<.01). These effects were present in
both blast and non-blast TBI. Seventy percent of TBI subjects were taking at
least one medication in the following classes: antidepressant, atypical
antipsychotic, anticonvulsant, or h1-antihistamine. There was no association
between any medication class and the OSDI or dry eye measures. Reduced corneal
sensation in 21 TBI subjects was not associated with OSDI, tear production, or
TFBUT, but did correlate with reduced tear osmolarity (P=.05). History of
refractive surgery, previous contact lens wear, facial nerve weakness, or
meibomian gland dysfunction was not associated with DED. In summary, we found a
higher prevalence of DED in subjects with TBI, both subjectively and objectively.
This effect is unrelated to medication use, and it may persist for months to
years. We recommend that patients with TBI from any cause be evaluated for DED
using a battery of standard testing methods described in a protocol presented in
this article. Further research into the pathophysiology and outcomes of DED in
neurotrauma is needed.

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