Trigeminal trophic syndrome: A systematic review.

OBJECTIVES: To systematically report and document Trigeminal Trophic Syndrome (TTS), characterize its clinical presentation, diagnostic tests performed, outline management strategies, outcomes; and highlight the role of otolaryngologists in the tissue diagnosis of this rare syndrome. DATA SOURCES: PubMed/Medline, Scopus, and Cochrane databases. REVIEW METHODS: PubMed/Medline, Scopus, and Cochrane databases were systematically reviewed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines to identify all cases of TTS published with an English translation from inception to December 2020. RESULTS: A total of 142 articles describing 214 patients with TTS were included in the analysis. There was a female predominance (62.9 %) and a median age of 57 (range 1-93) years at presentation. A trigeminal neurological insult was identified in 200 (93.5 %) cases. The most common triggers for TTS were treatment for trigeminal neuralgia (35.7 %) and cerebrovascular accident (21.6 %). Self-inflicted trauma occurred in 137 (64 %) patients. Biopsy was done in 123 (57.5 %) patients. Patient education, barrier devices, and medications to address parasthesias were the most common treatment strategies. The majority of patients (72.5 %) received multimodal therapy. Surgery was performed in 35 (22.7 %) patients. Treatment outcomes were discussed in 120 (56.1 %) patients. CONCLUSIONS: TTS is a rare condition with poorly understood pathophysiology. It should be suspected in a patient with non-healing facial ulceration and altered sensation within the trigeminal nerve distribution. Biopsy of the ulcer is important to confirm the diagnosis and exclude malignancy. Treatment options include conservative and pharmacologic measures, and less frequently surgery.

[Features of olfactory impairment connected with trigeminal nerve system]. / Osobennosti narusheniya obonyaniya v aspekte sistemy troinichnogo nerva.

Data on the state of sense of smell in patients who had a new coronavirus infection caused by the SARS-CoV-2 virus are currently reduced because of the impairment of the olfactory nerve system. There are practically no results in studies of disorders in the trigeminal nerve system. OBJECTIVE: Qualitative assessment of olfactory disorders after COVID-19 according to the system of olfactory and trigeminal nerves with a targeted assessment of the functional component of olfactory disorders. MATERIAL AND METHODS: We examined 40 patients aged 19 to 66 who had a coronavirus infection. All patients underwent neurological, otorhinolaryngological examinations, olfactometry, filled out the hospital anxiety and depression scale. RESULTS: Anosmia was diagnosed in 5 (12.5%) patients, hyposmia in 21 (52.5%) patients, and normosmia in 14 (35%) patients. Formed: the 1st group - 14 patients (35%) with normogram according to olfactometry; the 2nd group - 26 patients (65%) with anosmia/hyposmia. In the 1st group, disorders of the anxiety-depressive spectrum were significantly more common. In the 2nd group, a low identification of odors was found, lying in the spectrum of fresh, sharp, unpleasant, irritating, compared with sweet and pleasant or neutral, which indicates a predominant lesion of the trigeminal system. CONCLUSION: In patients with complaints of impaired sense of smell after undergoing COVID-19, the possible functional nature of anosmia/hyposmia should be taken into account, which requires the referral of such patients to psychotherapeutic specialists, and the possible entry of olfactory disorders into the 'trigeminal' spectrum.

Bilateral corneal perforation caused by neurotrophic keratopathy associated with leprosy: a case report.

BACKGROUND: Neurotrophic keratopathy (NK) is a rare degenerative corneal disease caused by damage to the trigeminal nerve. We hereby describe a severe case with bilateral corneal perforation due to leprosy (Hansen's disease)-associated NK. CASE PRESENTATION: An 89-year-old man with a history of leprosy treated 40 years previously in our sanatorium developed bilateral corneal perforation due to NK. He had a history of bilateral persistent epithelial defects and bacterial keratitis. Although epithelialization was obtained with the use of autologous serum eye drops, progressive corneal thinning concomitant with stromalysis led to bilateral perforation. Over one month treatment with topical antibiotics, anti-inflammatory and lubricants resulted in healing of the epithelial defects and corneal perforations. A Cochet-Bonnet esthesiometer demonstrated a total absence of corneal sensation in both eyes. CONCLUSIONS: The present case indicated the irreversible nerve damage due to leprosy that had been cured 23 years ago, which can progress over the years and cause bilateral corneal perforations.

Blink Reflex in Neurotrophic Keratopathy: An Electrophysiological Evaluation.

PURPOSE: Neurotrophic keratitis (NK) is a rare condition which may result in visual loss. This case review investigates if there may be an association between NK and the blink reflex in the absence of facial nerve palsy and lagophthalmos. METHODS: This is a retrospective case review of 5 patients with trigeminal nerve damage referred to the oculoplastic department with suspected anesthetic corneae. Information on etiology, symptoms, duration, associated medical conditions, medications, examination findings including Mackie stage of keratopathy, management of keratopathy, and blink electrophysiology results was obtained. RESULTS: All 5 patients demonstrated absence of corneal sensation. All patients had preserved facial nerve function with no evidence of lagophthalmos. Keratopathy ranged from Mackie stage 0-2. Management ranged from ocular lubricants to Botulinum-toxin-induced ptosis. Blink studies demonstrated reduction in amplitude as well as increased latency in 2 patients, conferring reduced blink strength. Two patients demonstrated an absent blink reflex on the affected side. One patient had blink latency within the normative range; this patient recovered corneal sensation and was discharged. CONCLUSIONS: Our finding of reduced amplitude in blink studies offers both a factor in pathogenesis of NK and a potential therapeutic target. Additionally, blink studies may provide prognostic information for recovery and therefore guide management. We suggest performing blink electrophysiology in patients with trigeminal nerve damage to assess nerve function.

Neurotrophic Keratitis in a Pediatric Patient With Goldenhar Syndrome and Trigeminal Aplasia Successfully Treated by Corneal Neurotization.

Herein, the authors report an unusual case of a 6-year-old boy with right-sided Goldenhar syndrome and trigeminal nerve aplasia who developed neurotrophic keratopathy (NK). Despite the use of therapeutic contact lenses and multiple temporary tarsorrhaphy, NK worsened showing a central corneal scar, neovascularization, and significant stromal thinning, with risk of corneal perforation. Cochet-Bonnet esthesiometry revealed complete corneal anesthesia. To minimize additional corneal complications, the patient underwent indirect corneal neurotization by a sural nerve autograft anastomosed to the contralateral supratrochlear nerve. At 24-month follow up, no epithelial defects, complications, or recurrence were observed. Significant improvements in corneal sensitivity with esthesiometry score of 20 mm and reflex blinking were achieved. This case highlights corneal anesthesia should be suspected among Goldenhar syndrome ophthalmologic abnormalities and monitored before corneal changes become irreversible. Since corneal neurotization can successfully improve corneal sensation, it could be considered as an early therapeutic option to avoid refractory NK.

[Treatment of neurotrophic keratopathy in combined lesions of the trigeminal and facial nerves]. / Lechenie neirotroficheskoi keratopatii pri sochetannom porazhenii troinichnogo i litsevogo nervov.

Ocular symptomatology in lesions of the facial nerve is associated with disturbed innervation of the circular muscle of the eye that leads to disruption of the protective function of the eyelids and the development of exposure symptoms, and is accompanied by a breach in corneal tear film integrity. The main clinical manifestation of the trigeminal nerve damage is the loss of sensory innervation of the cornea and disruption of the supply of neurotransmitters to its cells, manifesting as corneal hypo- or anesthesia. This triggers a cascade of pathological processes that lead to the development of neurotrophic keratopathy. In combined pathology of the facial and trigeminal nerves, a number of interrelated and mutually aggravating problems arise that require correction of lagophthalmos and functional restoration of the trigeminal nerve, since there is an interaction between the corneal epithelium and trigeminal neurons through trophic neuromodulators, which normally contribute to the proliferation of epithelial cells, their differentiation, migration and adhesion, and are essential for vital functions, metabolism and healing of surface lesions of the eye. Classical methods of treating neurotrophic keratopathy aim to protect the ocular surface, and are palliative or auxiliary, do not provide radical relief of the symptoms of neurotrophic keratopathy. Modern surgical technique of neurotization of the cornea allows restoring the structural growth of the nerve, which provides nerve trophism and corneal sensitivity, and is the only pathogenetically substantiated method of effective treatment of neurotrophic keratopathy. At the same time, direct neurotization has undeniable advantages over methods involving intercalary donor nerves, since neuropeptides from nerve fibers are immediately released into the recipient tissue and start reparative processes. Taking into account the accumulated positive experience of neurotization surgeries, scientific and clinical research should be continued in order to improve the most effective methods of corneal neurotization and promote their wider implementation into clinical practice.

Expert consensus on the identification, diagnosis, and treatment of neurotrophic keratopathy.

BACKGROUND: Neurotrophic keratopathy (NK) is a relatively uncommon, underdiagnosed degenerative corneal disease that is caused by damage to the ophthalmic branch of the trigeminal nerve by conditions such as herpes simplex or zoster keratitis, intracranial space-occupying lesions, diabetes, or neurosurgical procedures. Over time, epithelial breakdown, corneal ulceration, corneal melting (thinning), perforation, and loss of vision may occur. The best opportunity to reverse ocular surface damage is in the earliest stage of NK. However, patients typically experience few symptoms and diagnosis is often delayed. Increased awareness of the causes of NK, consensus on when and how to screen for NK, and recommendations for how to treat NK are needed. METHODS: An 11-member expert panel used a validated methodology (a RAND/UCLA modified Delphi panel) to develop consensus on when to screen for and how best to diagnose and treat NK. Clinicians reviewed literature on the diagnosis and management of NK then rated a detailed set of 735 scenarios. In 646 scenarios, panelists rated whether a test of corneal sensitivity was warranted; in 20 scenarios, they considered the adequacy of specific tests and examinations to diagnose and stage NK; and in 69 scenarios, they rated the appropriateness of treatments for NK. Panelist ratings were used to develop clinical recommendations. RESULTS: There was agreement on 94% of scenarios. Based on this consensus, we present distinct circumstances when we strongly recommend or may consider a test for corneal sensitivity. We also present recommendations on the diagnostic tests to be performed in patients in whom NK is suspected and treatment options for NK. CONCLUSIONS: These expert recommendations should be validated with clinical data. The recommendations represent the consensus of experts, are informed by published literature and experience, and may improve outcomes by helping improve diagnosis and treatment of patients with NK.

Acute Unilateral Masseter Muscle Paralysis Caused by Pontine Infarction.

In the present report, we discussed the case of a 57-year-old man with unilateral masticatory muscle weakness, nystagmus, skew deviation and facial hypesthesia due to pontine tegmental infarction. Trigeminal motor neuropathy attributed to brain infarction is very rare. Brain magnetic resonance imaging revealed a small dot-like infarction lesion in the pontine tegmentum. Masticatory muscle weakness was confirmed by an electrophysiological study performed on the day after admission in which there was an incomplete interference pattern without spontaneous denervation activity, suggesting that the patient's masseter muscle weakness was caused by an infarction of the trigeminal motor nucleus proper or trigeminal motor nerve fascicles rather than Wallerian degeneration of the trigeminal nerve or the progression of masseter muscle degeneration.

Trigeminal trophic syndrome: an important simulator of discoid cutaneous lupus erythematosus - a case series.

Trigeminal trophic syndrome occurs secondary to trigeminal nerve injury, leading to anaesthesia and paraesthesia, with consequent vigorous facial skin manipulation and lesion production, simulating other facial diseases such as ulcerative discoid lupus erythematosus, tumours and other artificially produced lesions. Ulceration and destruction of the ala nasi is a typical feature besides scratching end excoriations in the cutaneous segment affected. In this series, we present the features of five patients with trigeminal trophic syndrome, highlighting possible confusion with cutaneous lupus. Differential diagnoses, including discoid lupus erythematosus, are discussed, as well as possible treatment modalities.

Case Report: Ocular Tilt Reaction with Internuclear Ophthalmoplegia and Multiple Cranial Nerve Palsies.

SIGNIFICANCE: Ocular tilt reaction (OTR) is an abnormal eye-head postural reaction that consists of skew deviation, head tilt, and bilateral ocular torsion. Understanding of the pathway of the vestibulo-ocular reflex (VOR) is essential because this will help to localize the pathology. PURPOSE: The aim of this study was to report a case of OTR with contralateral internuclear ophthalmoplegia (INO) and fifth and seventh cranial nerve palsies. CASE REPORT: A 51-year-old gentleman with underlying diabetes mellitus presented with sudden onset of diplopia for 3 days. On examination, his visual acuity was 20/30 bilaterally without a relative afferent pupillary defect. He had a right OTR consisting of a right head tilt, a skew deviation with a left eye hypertropia, and bilateral ocular torsion (right excyclotorsion and left incyclotorsion) with nystagmus. He also had a left adduction deficit and right abduction nystagmus consistent with a left INO. Ocular examination revealed evidence of proliferative diabetic retinopathy bilaterally. Two days after the initial presentation, the patient developed left seventh and fifth cranial nerve palsies. MRI showed left pontine infarction and multiple chronic lacunar infarctions. There was an incidental finding of a vascular loop compression on cisternal portions of the left trigeminal, facial, and vestibulocochlear nerves. Antiplatelet treatment was started on top of a better diabetic control. The diplopia was gradually resolved with improved clinical signs. In this case, the left pontine infarction had likely affected the terminal decussated part of the vestibulocochlear nerve from the right VOR pathway, medial longitudinal fasciculus, and cranial nerve nuclei in the left pons. CONCLUSIONS: The OTR can be ipsilateral to the lesion if the lesion is before the decussation of the VOR pathway in the pons, or it can be contralateral to the lesion if the lesion is after the decussation. In case of an OTR that is associated with contralateral INO and other contralateral cranial nerves palsy, a pathology in the pons that is contralateral to the OTR should be considered. Neuroimaging study can hence be targeted to identify the possible cause.

Quantitative and qualitative sensory testing results are associated with numbness rather than neuropathic pain in patients with post-implant trigeminal neuropathy: a cross-sectional pilot study.

Purpose: This study aimed to characterize the sensory profile of patients with post-implant trigeminal neuropathy and identify the association between subjective symptoms and objective signs including psychophysical testing and radiographic imaging. This study further evaluated to the association between quantitative sensory testing (QST)/qualitative sensory testing (QualST) and the severity of nerve injury graded by radiographic imaging. Materials and methods: This retrospective study included 34 patients diagnosed with post-implant trigeminal neuropathy. Data on the neuropathic pain symptom inventory (NPSI), thermal and electric QST, bedside QualST, and cone beam computed tomography (CBCT) was collected and the association between these variables were analysed. Results: Numbness was the most common subjective symptom and evoked pain was the most frequent neuropathic pain. There was no significant correlation between negative and positive symptoms. Spearman's rank correlation analyses indicated that objective findings including QST/QualST correlated with a sensory loss profile rather than a gain of function profile. Moderate positive correlations between some positive symptoms and the score of QualST were observed. The Mann-Whitney U test showed that subjective symptoms did not differ according to the severity of nerve damage according to CBCT, but the electric QST and QualST was discriminative. Conclusions: This study suggests that QST/QualST associated with the severity of nerve damage according to CBCT might be useful in assessing numbness in patients with negative and positive symptoms after implant surgery, but may be of marginal utility in the evaluation of neuropathic pain within the limitation of this cross-sectional study with small sample size.

Trigeminal Neuropathy After Mandibular Fractures: Epidemiology and Neurophysiologic Diagnosis.

OBJECTIVES: To study the trigeminal nerve neuropathy prevalence after mandibular fractures and follow nerve recovery and to examine associations with clinical features. SUBJECTS: The files of 304 patients treated for 424 mandibular fractures in Hadassah Medical Center between 2001 and 2008 were analyzed. Twenty-five patients with paresthesia were examined by electro-diagnostic conduction test (quantitative sensory testing). RESULTS: The most common fracture sites were the symphysis (28.5%) and condyle (21.4%). A strong correlation between fracture severity and treatment modality was found. Nerve damage occurred in 13.4% of nondisplaced fractures and in 65.3% of >5 mm displaced fractures. Patients who were treated by open reduction internal fixation demonstrated the biggest difference in quantitative sensory testing values between the affected and nonaffected sides. C nerve fibers were the most damaged and least regenerated. There was correlation between damage perception and objective test results. CONCLUSIONS: There is a correlation between fracture type and displacement severity on neurologic deficit and prognosis. The objective neurosensory damage was manifested by higher nerve excitation threshold on the injured side. Patients should be informed on the prognosis of neurologic deficit according to fracture type.

Magnetic Resonance Neurography of Traumatic and Nontraumatic Peripheral Trigeminal Neuropathies.

PURPOSE: The clinical neurosensory testing (NST) is currently the reference standard for the diagnosis of traumatic and nontraumatic peripheral trigeminal neuropathies (PTNs), but exhibits both false-positive and false-negative results compared with surgical findings and frequently results in treatment decision delays. We tested the hypothesis that magnetic resonance neurography (MRN) of PTNs can serve as a diagnostic modality by correlating the NST, MRN, and surgical findings. MATERIALS AND METHODS: Sixty patients with traumatic and nontraumatic PTN of varying etiologies and Sunderland classifications underwent NST, followed by MRN using 1.5T and 3.0T scanners. The protocol included 2-dimensional and 3-dimensional (3D) imaging, including diffusion imaging and isotropic 3D PSIF. The MRN findings were read by 2 readers in consensus with the clinical findings but without knowing the side of abnormality. The MRN results were summarized using the Sunderland classification. In 26 patients, surgery was performed, and the Sunderland classification was assigned using the surgical photographs. Agreement between the MRN findings and NST/surgical classification was evaluated using kappa statistics. Pearson's correlation coefficient was used to assess the correlation between continuous measurements of MRN/NST and surgical classification. RESULTS: Of the 60 patients, 19 males and 41 females, mean age 41 years (range 12 to 75), with 54 complaints of altered sensation of the lip, chin, or tongue, including 16 with neuropathic pain and 4 with no neurosensory complaint, were included. Third molar surgery (n = 29) represented the most common cause of traumatic PTN. Assuming 1 nerve abnormality per patient, the lower class was accepted, a kappa of 0.57 was observed between the MRN and NST classification. A kappa of 0.5 was found between MRN and surgical findings with a Pearson correlation coefficient of 0.67. CONCLUSIONS: MRN anatomically maps PTNs and stratifies the nerve injury and neuropathies with moderate to good agreement with NST and surgical findings for clinical use.

Periocular manifestations of trigeminal trophic syndrome: A case series and literature review.

Trigeminal trophic syndrome (TTS) is a condition whereby persistent facial ulceration presents consequent to central or peripheral insult to the trigeminal nerve. Lesions are created by repetitive self-inflicted manipulation and trauma of dysaesthetic skin within the trigeminal dermatome. We discuss four cases with aetiologies varied from presumed microvascular compromise to resection of cerebral meningioma, cerebrovascular accident, and herpes zoster ophthalmicus. We discuss the management of the under-recognised associated periocular skin ulcerations that result from physical manipulation of dysesthic skin and prove to be persistent and challenging to treat. Patient education and counselling are crucial in understanding and preventing the detrimental effect of physical manipulation of the skin. Occlusive dressings can reduce recurrent trauma. Topical lubricants, antibiotics, or autologous serum may be needed in cases with corneal involvement or exposure. Surgical interventions may be used, but frequently fail if the underlying neurological pathology and skin manipulation has not been adequately addressed. TTS should be suspected in persistent or recurrent facial ulceration with concomitant anaesthesia and paraesthesia in the trigeminal distribution, with alar nasi involvement being a key feature.

The Role of Electromyographic Blink Reflex in the Evaluation of Headache Incidence

Migraine and tension type headache are the most common disabling primary headache disorders. Epidemiological studies have documented their high prevalence and high socioeconomic and personal impacts. According to recent data, migraine ranks as the third most prevalent disorder and seventh-highest specific cause of disability worldwide. Tension-type headache has lifetime prevalence in the general population ranging between 30% and 78% in different studies. According to the International Classification of Headache Disorders, 3rd edition, there also are many other headaches but their incidence in general population is lower than the previously mentioned headaches. Trigeminal nerve and upper cervical segments (C1-C3) are included in pain control of the head region and often evaluated in headache studies in order to improve differential diagnosis and headache treatment. In our study, we evaluated the potential role of electromyographic (EMG) blink reflex in establishing diagnosis of headache and evaluation of trigeminal nerve dysfunction as the possible underlying pathomorphological headache mechanism. Our study included 60 patients with different types of primary headaches and 30 control subjects. Statistical analysis was performed by use of χ2-test and statistical significance was set at p<0.001. Study results showed that patients with trigeminal dysfunction in EMG blink reflex had a 5.6-fold higher risk of developing headache in comparison to subjects with normal EMG blink reflex finding.

Magnetic resonance neurography in the management of peripheral trigeminal neuropathy: experience in a tertiary care centre.

OBJECTIVE: This tertiary care experience examines the utility of magnetic resonance neurography (MRN) in the management of peripheral trigeminal neuropathies. MATERIALS AND METHODS: Seventeen patients with clinically suspected peripheral trigeminal neuropathies (inferior alveolar nerve and lingual nerve) were imaged uniformly with 1.5-T examinations. MRN results were correlated with clinical and surgical findings in operated patients and the impact on clinical management was assessed. RESULTS: Clinical findings included pain (14/17), sensory changes (15/17), motor changes (2/17) and palpable masses (3/17). Inciting events included prior dental surgery (12/17), trauma (1/17) and idiopathic incidents (4/17). Non-affected side nerves and trigeminal nerves in the intracranial and skull base course were normal in all cases. Final diagnoses on affected sides were nerve inflammation (4/17), neuroma in continuity (2/17), LN transection (1/17), scar entrapment (3/17), infectious granuloma (1/17), low-grade injuries (3/17) and no abnormality (3/17). Associated submandibular gland and sublingual gland oedema-like changes were seen in 3/17 cases because of parasympathetic effects. Moderate-to-excellent MRN-surgical correlation was seen in operated (8/17) patients, and neuroma and nerve transection were prospectively identified in all cases. CONCLUSION: MRN is useful for the diagnostic work-up of suspected peripheral trigeminal neuropathy patients with significant impact on clinical management and moderate-to-excellent correlation with intra-operative findings. KEY POINTS: • MRN substantially impacts diagnostic thinking and management in peripheral trigeminal neuropathy. • MRN has moderate-to-excellent correlation with intra-operative findings. • MRN should be considered in pre-surgical planning of peripheral trigeminal neuropathy subjects.

Thirteen-And-A-Half Syndrome.

We describe a 50-year-old man who developed eight-and-a-half syndrome associated with an ipsilateral trigeminal nerve palsy because of a post-transplant lymphoproliferative disorder. This case widens the spectrum of eight-and-a-half syndrome to include a thirteen-and-a-half syndrome.

[Chondroma adjacent to Meckel's cave mimicking a fifth cranial nerve neurinoma. A case report]. / Condroma adyacente al cavum de Meckel simulando un neurinoma del quinto par craneal. A propósito de un caso.

Cranial chondromas are tumours arising from chondrocyte embryonic remnants cells that usually appear in the skull base synchondrosis. In contrast to the rest of the organism, where chondroid tumours are the most common primary bone tumour just behind the haematopoietic lineage ones, they are a rarity at cranial level, with an incidence of less than 1% of intracranial tumours. The case is reported on a 42 year-old male referred to our clinic due to the finding of an extra-axial lesion located close to the Meckel's cave region, with extension to the posterior fossa and brainstem compression after progressive paraparesis of 6 months onset. With the diagnosis of trigeminal schwannoma, a subtotal tumour resection was performed using a combined supra-infratentorial pre-sigmoidal approach. The postoperative histopathology report confirmed the diagnosis of cranial chondroma.

How Blink Anomalies Can Contribute to Post-LASIK Neurotrophic Epitheliopathy.

: Post-LASIK (laser in situ keratomileusis) symptoms and signs of dry eye have multiple causes. For example, tear osmolarity and the concentration of inflammatory mediators can increase because of reduced aqueous production and increased evaporative loss as a result of lower blink rates and increased interblink intervals. The tear concentration of inflammatory mediators can also increase because of surgical trauma, wound healing, comorbid systemic and ocular diseases, and the use of punctal plugs. Studies that examine only mechanical sensitivity of the cornea cannot detect changes in chemical sensitivity, which can persist longer. Symptoms may be partly attributed to sensitization of the traumatized corneal or lid wiper sensory nerves by inflammatory mediators. Increased lid wiper sensitivity could increase awareness of blinks, especially if ocular surface lubricity is reduced. Incomplete blinks have been found to represent 10 to 22% of the total number of blinks. Loss of neural stimuli and lower blink rates increase the significance of incomplete blinks that approximately double related interblink intervals and tear evaporation. The most common location of post-LASIK epitheliopathy is the inferior area of the cornea, which is overexposed by incomplete blinks. The relevance of incomplete blinking to post-LASIK epitheliopathy is supported by the relative absence of this complication in the similarly neurotrophically disadvantaged upper corneal areas for which blink rates and other tear functions usually appear to be adequate to prevent epitheliopathy, which stains. Occupational or leisure-time activities such as computer use and reading, which have been found to reduce blink rates and blink completeness, appear to be significant risk factors for symptoms and signs of dry eye. Apart from reducing symptoms and signs of dry eye, prophylactic and post-LASIK blink exercises to reduce incomplete blink rates and associated overexposure of the ocular surface may also contribute to more accurate refractive outcomes through faster wound healing.