effects side ocular induced-Drug • 7 t Pa r

2.Pupils

a.Mydriasis

b.Miosis (coma)

c.Decreased reaction to light

d.Hippus

3.Extraocular muscles

a.Decreased convergence

b.Paresis or paralysis

c.Jerky pursuit movements

d.Random ocular movements

e.Vertical gaze palsy

4.Oscillopsia

5.Nystagmus

a.Downbeat, gaze-evoked, horizontal, jerk or vertical

b.Depressed or abolished optokinetic, latent, positional, voluntary or congenital nystagmus

6.Decreased vision

7.Problems with color vision

a.Color vision defect

b.Objects have yellow or green tinge

8.Visual hallucinations

9.Eyelids or conjunctiva

a.Allergic reactions

b.Conjunctivitis – non-specific

c.Edema

d.Photosensitivity

e.Angioneurotic edema

f.Urticaria

10. Decreased accommodation (primidone)

11. Keratoconjunctivitis sicca (primidone)

12. Abnormal ERG, VEP or critical flicker fusion

13. Cortical blindness (thiopental)

Possible

1.Optic nerve disorders (chronic use)

a.Retrobulbar or optic neuritis

b.Papilledema

c.Optic atrophy

2. Visual fields

a.Scotomas

b.Constriction

3. Subconjunctival or retinal hemorrhages secondary to drug-induced anemia

4. Eyelids or conjunctiva

a.Lupoid syndrome

b.Erythema multiforme

c.Stevens-Johnson syndrome

d.Exfoliative dermatitis

e.Lyell’s syndrome

Ocular teratogenic effects (primidone)

Possible

1. Optic atrophy

2. Ptosis

3. Hypertelorism

4. Epicanthus

5. Strabismus

Clinical significance

New classes of drugs are generally replacing these shortand long-acting barbiturates. Numerous adverse ocular side effects have been attributed to barbiturate usage, yet nearly all

significant­ ocular side effects are in acute barbiturate poisoning or habitual users. Few toxic ocular reactions are found due to barbiturate usage at therapeutic dosages or on short-term therapy. The most common ocular abnormalities are disturbances of ocular movement, such as decreased convergence, paresis of extraocular muscles or nystagmus. The pupillary response to barbiturate intake is quite variable, so this sign has questionable clinical value­ . Phenobarbital has the most frequently reported ocular side effects; however, all barbiturates may produce adverse ocular effects. Chronic barbiturate users have a ‘tattle-tale’ ptosis and blepharoclonus. Normally, a tap on the glabella area of the head produces a few eyelid blinks, but in the barbiturate addict the response will be a rapid fluttering of the eyelids (Hamburger 1965). Bilateral blindness or decreased vision after barbiturateinduced coma usually returns to normal vision. There are a few reports, however, of permanent blindness. Optic neuropathy with complete recovery in a 12-year-old boy from chronic phenobarbital medication is a unique case (Homma et al 1989). The barbiturates do not appear to have teratogenic effects, except possibly primidone. Primidone has been shown to be associated with acute attacks of porphyria. Acute onset of severe photophobia and/or lid reactions is an indicator of ocular porphyria.

References and Further Reading

Alpert JN. Downbeat nystagmus due to anticonvulsant toxicity. Ann Neurol 4: 471, 1978.

Amarenco P, Royer I, Guillevin L. Ophthalmoplegia externa in barbiturate poisoning. Presse Med 13: 2453, 1984.

Clarke RSJ, Fee JH, Dundee JW. Hypersensitivity reactions to intravenous anaesthetics. In: Adverse Response to Intravenous Drugs, Watkins

J, Ward A (eds), Grune & Stratton, New York, pp 41–47, 1978. Crosby SS, et al. Management of Stevens-Johnson syndrome. Clin Pharm

5: 682, 1986.

Hamburger E. Identification and treatment of barbiturate abusers. JAMA 193: 143–144, 1965.

Homma K, Wakakura M, Ishikawa S. A case of phenobarbital-induced optic neuropathy. Neuro-Ophthalmol 9(6): 357–359, 1989.

Martin E, Thiel T, Joeri P, et al. Effect of pentobarbital on visual processing in man. Hum Brain Mapp 10: 132–139, 2000.

Müller E, Huk W, Pauli E, et al. Maculo-papillary branch retinal artery occlusions following the Wada test. Graefe’s Arch Clin Exp Ophthalmol 238: 715–718, 2000.

Murphy DF. Anesthesia and intraocular pressure. Anesth Analg 64: 520, 1985. Nakame Y, et al. Multi-institutional study on the teratogenicity and fetal

toxicity of antiepileptic drugs: a report of a collaborative study group in Japan. Epilepsia 21: 663, 1980.

Raitta C, et al. Changes in the electroretinogram and visual evoked potentials during general anesthesia. Graefe’s Arch Clin Exp Ophthalmol 211: 139, 1979.

Tedeschi G, et al. Specific oculomotor deficits after amylobarbitone. ­Psychopharmacology 79: 187, 1983.

Tseng SCG, et al. Topical retinoid treatment for various dry-eye disorders. Ophthalmology 92: 717, 1985.

Wallar PH, Genstler DE, George CC. Multiple systemic and periocular malformations associated with the fetal hydantoin syndrome. Ann Ophthalmol 10: 1568, 1978.

Generic name: Chloral hydrate.

Proprietary name: Aquachloral.

Primary use

This non-barbiturate sedative-hypnotic is effective in the treatment of insomnia.