Downbeat nystagmus due to anticonvulsant toxicity

Alpert, Jack N.

doi:10.1002/ana.410040516

Cited by 54 publications

(6 citation statements)

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“…The most common associated abnormality is gaze evoked nystagmus, which occurs at extremes of gaze at low serum concentrations and in the primary position at higher concentrations (Kutt et al 1964). Other reported disturbances of ocular motility include downbeat nystagmus (Alpert 1978) and total external ophthalmoplegia (Speltor et al 1976), the latter occurring when concentrations exceed 36 mg/L.…”

Section: Phenytoinmentioning

confidence: 98%

Clinically Important Ocular Reactions to Systemic Drug Therapy

Rennie

1993

Drug Safety

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Many systemically administered drugs produce ocular adverse effects. Fortunately, relatively few are capable of causing significant, irreversible visual impairment. It is the responsibility of every clinician when prescribing systemic therapeutic agents to be aware of potential adverse ocular reactions, to appreciate their significance, and to inform the patient of the potential risks of treatment. In instances where serious adverse reactions relate to the cumulative effects of prolonged treatment, it is the responsibility of the prescribing physician to institute appropriate methods of visual screening. In this respect, it is most important to obtain the necessary individual baseline measurements before treatment is commenced. Chloroquine retinopathy is probably the most feared of all adverse ocular reactions to systemic drug therapy. However, it occurs only rarely if the daily dosage of chloroquine does not exceed 250mg. Regular screening using automated perimetry is mandatory if prolonged therapy is contemplated. Amiodarone almost inevitably produces corneal deposits. These rarely produce symptoms, and resolve upon withdrawal of the drug. Optic neuropathy has recently been described with amiodarone. Systemic anticoagulant therapy may be associated with intraocular hemorrhage in patients with pre-existing disciform macular degeneration, and such agents should be used with caution in affected individuals. Systemic corticosteroids produce posterior subcapsular cataracts in susceptible individuals which may profoundly affect visual acuity. Although elevated intraocular pressure may also result from systemic therapy, the relationship between the pressure rise and development of glaucomatous changes remains unclear. Ethambutol may produce optic neuropathy if the daily dosage exceeds 15 mg/kg. The changes are usually reversible within a few weeks of stopping treatment. High doses of tamoxifen may produce a maculopathy with loss of visual acuity, if given for prolonged periods. The risk must be weighed against the benefits of treatment. Patients receiving more than 800 mg/day of thioridazine have developed retinopathy, which is usually reversible if detected early enough. Tricyclic antidepressants and other agents with anticholinergic properties may cause disturbances of accommodation and pupillary dilatation. The latter may rarely precipitate acute angle closure glaucoma in susceptible individuals.

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Section: Phenytoinmentioning

confidence: 98%

Clinically Important Ocular Reactions to Systemic Drug Therapy

Rennie

1993

Drug Safety

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“…The recent report of down beat nystagmus occurring as a manifestation of anticonvulsant toxicity is noteworthy. 13 Down beat nystagmus has rarely been described as a component of hereditary cerebellar ataxia. Zee et al'4 reported a family with late onset, dominantly inherited, cerebellar ataxia with a variety of oculomotor abnormalities, down beat nystagmus being but one manifestation.…”

Section: Discussionmentioning

confidence: 99%

Familial cerebellar ataxia presenting with down beat nystagmus.

Schott¹

1980

Journal of Medical Genetics

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The proband (1112) first attended the National Hospital, Queen Square at the age of 42, complaining of 5 years' intermittent difficulty in focusing. Occasional vertical oscillopsia and transient diplopia had occurred over the same period, and an optician had detected nystagmus. His brother, 7 years younger, has a similar disorder. The pedigree is illustrated in the figure. The brothers' unaffected parents, who were unrelated, died in their seventies. Received for publication 22 June 1979 Examination at this time was unremarkable except for the finding of second degree down beat nystagmus, which increased in velocity on gaze to the left and right; the nystagmus was unaltered on changes of posture. Eye movements were full but, while voluntary saccadic movements were normal, following movements were markedly broken up by the nystagmus. Optokinetic responses were present on rotation of the drum to the left and right, producing nystagmus in an oblique, downward direction which was attributable to the superimposed down beat vertical nystagmus. No optokinetic nystagmus was produced in the vertical direction. Electronystagmography confirmed spontaneous down beat vertical nystagmus, vestibular in character, which was inhibited by eye closure and darkness, and was consistent with a central disturbance of the vestibular system or its connections.' Caloric responses were absent. The pure tone audiogram was normal.Six years later at the age of 48 he was admitted for assessment of a 4-year history of progressive imbalance of gait. His walking had become unsteady, particularly on turning, and for 2 years he had noticed slight slurring of speech and dificulty in swallowing. He managed a clerical job and was able to use public transport without difficulty.On examination his slight slurring dysarthria was confirmed. His gait was ataxic, he walked with a wide base, and had difficulty in turning without losing balance. Tongue movements were slightly slow. The tendon reflexes were unusually brisk but there were no pathological reflexes. Nystagmus, similar to that noted earlier, was again found; pursuit eye movements were found to be grossly broken up by nystagmus though voluntary movements were normal. Ocular dysmetria was detected on occasions. Neither intellectual deficit nor 115 on 4 April 2019 by guest. Protected by copyright.

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“…The most common of these disturbances is gaze-evoked nystagmus, and although it may only be noted in extremes of eccentric gaze with low concentrations of phenytoin, nystagmus in the primary position may occur with higher concentrations (Kutt et al 1964). Other disturbances of ocular motility including upbeat and downbeat nystagmus (Alpert 1978) and complete ophthalmoplegia, the latter occurring with doses in excess of 36 ~g/ml, have been reported with phenytoin therapy (Speltor et al 1976). …”

Section: Phenytoinmentioning

confidence: 99%