effects side ocular induced-Drug • 7 t Pa r

Laties AM. Ocular toxicology of haloperidol. In: Symposium on Ocular Therapy, Vol. 9, Leopold IH, Burns RP (eds), John Wiley & Sons, New York, pp 87–95, 1976.

Mendelis PS. Haldol (haloperidol) hyponatremia. ADR Highlights January 12, 1981.

Nishida K, Ohashi Y, Kinoshita S, et al. Endothelial decompensation in a schizophrenic patient receiving long-term treatment with tranquilizers. Cornea 11(5): 475–478, 1992.

Patton CM Jr. Rapid induction of acute dyskinesia by droperidol. Anesthesiology 43: 126, 1975.

Selman FB, McClure RF, Helwig H. Loxapine succinate: a double-blind comparison with haloperidol and placebo in schizophrenics. Curr Ther Res 19: 645–652, 1976.

Shapiro AK. More on drug-induced blurred vision. Am J Psychiatry 134: 1449, 1977.

Uchida H, Suzuki T, Watanabe K, et al. Antipsychotic-induced paroxysmal perceptual alteration. Am J Psychiatr 160: 2243–2244, 2003.

Generic name: Lithium carbonate.

Proprietary names: Eskalith, Eskalith CR.

Primary use

This lithium salt is used in the management of the manic phase of manic depressive psychosis.

Ocular side effects

Systemic administration

Certain

1.Decreased vision

2.Nystagmus

a.Horizontal

b.Vertical

c.Downbeat

3.Extraocular muscles

a.Oculogyric crises

b.Decreased spontaneous movements

c.Lateral conjugate deviations

d.Jerky pursuit movements

e.Oscillopsia

4.Eyelids or conjunctiva

a.Conjunctivitis – non-specific

b.Edema

c.Loss of eyelashes or eyebrows

5.Non-specific ocular irritation

a.Lacrimation

b.Photophobia

c.Burning sensation

d.Decreased lacrimation

6.Decreased accommodation

7.Visual hallucinations

8.Exophthalmos – thyroid eye disease

9.Intracranial hypertension

a.Papilledema

b.Visual field defect

10. Abnormal EOG or VEP

11. Decreased dark adaptation

Probable

1.Myasthenia gravis

a.Diplopia

b.Ptosis

c.Paresis of extraocular muscles

2.Aggravates ocular sicca

Possible 

1. Subconjunctival or retinal hemorrhages secondary to druginduced anemia

2. Cornea and conjunctiva – fine lithium deposits

Clinical significance

Lithium salts have been widely used for decades and lithium intoxication is common since therapeutic blood levels have a narrow range before toxicity occurs. Lithium therapy is mainly prophylactic, with therapy lasting years to decades. The review article by Fraunfelder et al (1992) is probably the definitive work on the effects of lithium on the visual system.

Lithium affects many areas of the visual system, including direct effects on the central nervous system and on endocrine glands, which lead to ocular effects. In general, the ocular side ­effects of lithium are reversible on withdrawal of the drug or lowering of the dosage. However, other side effects, such as downbeat nystagmus, can be permanent. Blurred vision is probably the most common side effect experienced by patients taking lithium, but is seldom significant enough to require the cessation of therapy. Usually with time, even while keeping the same dosage, blurred vision will disappear. Blurred vision, however, can be a signal of pending problems, such as intracranial hypertension. In most cases, patients who develop intracranial hypertension have been taking lithium for many years.

Lithium can cause various forms of nystagmus, the most characteristic being downbeat. This can occur at therapeutic dosage ranges of lithium and may be the only adverse drug effect. While some patients have a full recovery after stopping or reducing the dosage of lithium, it may develop into irreversible downbeat nystagmus. If downbeat nystagmus occurs, one needs to reevaluate the risk-benefit ratio of lithium therapy. Lithium can also cause extraocular muscle abnormalities, especially vertical or lateral far-gaze diplopia. In therapeutic dosages, Gooding et al have shown no effect of lithium on smooth pursuit eyetracking performance. Diplopia in any patient taking lithium may require a work-up for myasthenia gravis, especially if associated with ptosis. Ptosis can occur alone. Oculogyric crises have been reported primarily in patients also taking haloperidol.

Thyroid-related eye disease in various forms secondary to hypoor hyperthyroidism has been seen in patients receiving lithium therapy. While this is uncommon, exophthalmos has occurred. Lithium is secreted in the tears and may cause an irritative forum of conjunctivitis, causing epiphoria. However, with time many patients complain of a dry mouth and about the same time ocular dryness. Lithium has been reported to cause cornea and the conjunctiva deposits, but the documentation for this is limited. Lithium can cause a decrease in accommodation, which may occur in up to 10% of patients. However, this primarily occurs in young patients and is rare in older patients. In general, this side effect is minimal and usually resolves after a few months, even while taking the drug. Etminan et al (2004), in a case control study, showed that in the elderly lithium increased the risk of injurious motor vehicle accidents.

References and Further Reading

Brenner R, et al. Measurement of lithium concentrations in human tears. Am J Psychiatry 139: 678–679, 1982.

Corbett J, et al. Downbeat nystagmus and other ocular motor defects caused by lithium toxicity. Neurology 39: 481–487, 1989.

Deleu D, Ebinger G. Lithium-induced internuclear ophthalmoplegia. Clin Neuropharmacol 12: 224–226, 1989.

Dry J, Aron-Rosa A, Pradalier A. Onset of exophthalmos during treatment with lithium carbonate. Biological hyperthyroidism. Therapie 29: 701–708, 1974.