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Editor,—Diabetic neuropathy can present in numerous forms; as symmetrical sensory polyneuropathy, mononeuropathy, or as an autonomic neuropathy. The earliest functional change in diabetic nerves is delayed conduction velocity, the earliest histological change is segmental demyelination due to damage of Schwann cells. We report an uncommon but important presentation, which can easily be overlooked on clinical examination.
A 27 year old woman was referred to Moorfields Eye Hospital complaining of bilaterally red and irritable eyes accompanied by a gradual reduction in vision over the previous 18 months. This had not responded to a wide range of different topical medications. She had been an insulin dependent diabetic since the age of 11. History of control of her diabetes was good, on a regimen of subcutaneous Monotard and Actrapid. She had no other significant medical history.
On examination she was noted to have bilateral corneal erosions. She had a reduced blink rate and peripheral corneal thinning. Her visual acuity was recorded at 6/60 right, 6/24 left unaided. It was also noted that she had complete corneal anaesthesia in both eyes. Basic neurological examination was otherwise normal.
The patient had the typical appearances of a neurotrophic epithelium. She was started on hypromellose 1% eye drops and chloramphenicol 1% eye drops four times daily, both preservative free to stabilise her epithelium, and this improved her symptoms and vision. Further progress was obtained with therapeutic contact lenses, and her visual acuity improved to 6/18 in both eyes. Because of her corneal anaesthesia she was referred for full neurological investigation.
Autonomic function tests were performed which revealed postural hypotension, blunted pressor tests, and a blocked valsalva test. There was much reduced heart rate variability and responses for her age were thought to be consistent with sympathetic and parasympathetic impairment. Her EMG and nerve conduction studies showed a mild sensory motor neuropathy. A sural nerve biopsy was offered but refused by the patient.
She is currently well maintained with scleral contact lenses and no other symptomatic manifestations of diabetic neuropathy.
Corneal anaesthesia can be physiological or pathological. Corneal sensation decreases with age, and is lower in females, especially premenstrually. Contact lens wear, and infection by herpes zoster and simplex, oedema and surgery will also reduce sensation. Congenital causes of corneal anaesthesia include corneal dystrophy and Riley-Day syndrome, and congenital corneal anaesthesia without an associated syndrome, which is presumed to be due to hypoplasia of the ophthalmic division of the trigeminal nerve. Systemic disease such as diabetes, myotonic dystrophy, scleroderma, and vitamin deficiencies are important causes of corneal anaesthesia, which can often be overlooked. Forty five per cent of diabetic patients had a degree of corneal hypoaesthesia when examined in a study of 130 patients published by Osman et al.1 There is little or no relation between the age of a diabetic patient and the observed decrease in corneal sensitivity. However, corneal sensitivity thresholds do rise with increased duration of diabetes.2
It has been suggested that diabetic peripheral neuropathy was due to occlusive vascular disease and nerve infarctions.3 More recent evidence suggests that common symmetrical distal polyneuropathy is due to segmental demyelination with associated or secondary axonal degeneration.4
Recent studies show that there may be a potential to use topical neurotrophic growth factors as a treatment for neurotrophic corneal ulceration.5 In a study of 14 eyes Lambiaseet al treated neurotrophic corneal ulcers with topical nerve growth factor for 2 weeks. Corneal healing began within 2–14 days and all patients had complete healing of their ulcers after 10 days to 6 weeks.
Corneal anaesthesia may often be overlooked unless it is profound. It can be tested with cotton wisps or an anaesthesiometer. It is important to test the corneal sensation subjectively and objectively and also to test all four quadrants of the cornea.
This case raises three important points:
Chronically red irritable eyes should have their corneal sensation tested. Corneal anaesthesia is easily overlooked by non-ophthalmologists and ophthalmologists alike, and the anaesthetic cornea represents a real risk of profound visual loss from trauma and infection.
Reduced corneal sensation can be a presenting feature of diabetic neuropathy. This woman had no other symptoms or signs of neuropathy apart from her corneal anaesthesia. If a diabetic develops a red or irritable eye, corneal sensation should be tested.
There is some promise for the future in that neurotrophic corneal ulceration may potentially be treated by the use of topical neurotrophic growth factors.5 The research into this project continues and is currently not in clinical practice.
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