Purpose To test the agreement of intraocular pressure (IOP) measurements made with Luneau SA applanators and Goldmann applanator. Materials and Methods A single-blind crossover trial. IOPs were measured in both eyes of subjects with both applanators. Type of applanator was alternated to eliminate systematic bias. Multiple observers were used. Observers were blind to the scale while performing measurements but not to the type of applanator used. The appearance of the meniscus was assessed semiquantitatively. All measurements were combined and presented in a Bland-Altman plot. Results A total of 140 eyes of 79 subjects were tested by seven observers. The range of measurements was 6-45 mmHg (mean 17.8 mmHg) for the Goldmann applanator. On average, the Luneau SA applanator (range of measurements 4-36 mmHg) gave a measurement of 2.35 mmHg less than the Goldmann standard. The standard deviation of these differences was 2.13 mmHg, giving an upper 95% confidence limit of 6.53 mmHg and a lower 95% confidence limit of À1.83 mmHg. The measurements agreed in only 24 out of 140 instances. In 28 eyes, the disposable tonometer end point was difficult to assess owing to excessively thick rings. Linear extrapolation suggests an increase in difference with increasing IOP. Conclusion The inter-head inaccuracy, tendency to underestimate IOP, and lack of systematic inaccuracy make a corrective algorithm impossible to formulate. The range of variation between the Luneau SA disposable applanator and the Goldmann standard is sufficiently large to influence clinical management decisions. We speculate that one explanation is the interaction of the tonometer with the tear film, making end point determination difficult. Further research is being undertaken.
This case illustrates that amitriptyline withdrawal may be responsible for the onset of primary position upbeat nystagmus. This is not a recorded side effect of the drug and it has not been previously reported in the literature. CaseA 42-year-old man was seen in the West Suffolk Eye Department complaining of blurred vision for 5 days. His Snellen visual acuity was 6/60 in the primary position, and on down gaze it improved to 6/6. He had no medical history of eye problems; however, he did suffer from asthma and had had a basal skull fracture in 1996. A computerized tomography scan from 1996 showed right posterior temporal and left subfrontal region gliosis.Eye examination revealed a primary position vertical nystagmus, and the fast phase was up. The nystagmus reduced on down gaze. He had no relative afferent pupillary defect; his eye movements were full; his colour vision, measured with Ishihara plates, was intact; and fundal examination showed no abnormalities. An examination of his central nervous system was normal. A magnetic resonance scan of his brain showed no new changes.He had been taking salbutamol and flixotide inhalers for a number of years to control his asthma. At 6 months before the onset of nystagmus, he had started taking amitriptyline 150 mg once daily, for depression. At 2 weeks before the nystagmus commenced, he reduced his amitriptyline dose down to 100 mg. At 2 weeks after the start of the nystagmus he cut the dose to 50 mg, under the guidance of his GP. The dose was reduced to 25 mg a week later, and stopped after a further week. With the reduction of the drug, he found that his nystagmus gradually resolved.The medicines control agency was informed of a possible association between amitriptyline and the induction of nystagmus; the agency reported two previously documented cases. CommentUpbeat nystagmus is a type of central vestibular nystagmus. It can be caused by lesions from the medulla to the midbrain. It usually increases in up gaze, but not on lateral gaze, and fixation does not dampen it. Causes of upbeat nystagmus include: cerebellar degeneration, multiple sclerosis, infarction of the medulla, tumours, Wernicke's encephalopathy, brain stem encephalitis, Behcet's syndrome, meningitis, congenital, middle ear disease, and drugs. This condition is often seen with medullary lesions; these involve the perihypoglossal nuclei, medial vestibular nuclei, nucleus intercalatus, and the ventral tegmentum. It is also reported in lesions of the anterior vermis of the cerebellum, the brachium conjunctivum, and midbrain.Primary position upbeat nystagmus has been reported secondary to organophosphate toxicity 1 and tobacco. 2 We propose that amitriptyline withdrawal may cause upbeat nystagmus by the following mechanism. Acetylcholine and histamine are found in the vestibular system; acetylcholine is a central vestibular agonist. Amitriptyline blocks histamine and muscarinic acetylcholine receptors and is therefore a vestibular suppressant. We suggest that withdrawal of amitriptyline removes this inhibi...
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