olanzapine and Eye-Diseases

Topics: Acute Disease; Eye Diseases; Glaucoma, Angle-Closure; Humans; Olanzapine

Chlorpromazine is known to cause ocular pigmentary deposits. However, delayed presentation after cessation of chlorpromazine has not been reported. There are also no reports on whether newer generation of anti-psychotic agents contribute to ocular toxicity. We describe a case of ocular toxicity related to anti-psychotic agents. To the best of our knowledge, this is the first reported case of anterior segment pigmentary deposits associated with olanzapine use, 2 years after the cessation of chlorpromazine. We report a case of ocular toxicity in a patient with history of chlorpromazine usage of 100 mg per day for 13 years and subsequently switched to olanzapine 5 mg for 2 years. There were no signs of ocular toxicity while the patient was on chlorpromazine. However, when the patient switched to olanzapine, she developed the ocular side effect as described for chlorpromazine-induced ocular toxicity, with pigmentary depositions on both corneas and the anterior lens surface and decrease in vision. Olanzapine, a newer anti-psychotic agent, may play a role in the ocular pigmentary deposition, either directly causing pigmentary deposition itself or accentuating the effect of chlorpromazine as the 2 drugs act on the same receptors, although further studies are required to support this hypothesis. As patients with psychiatric conditions may not voluntarily complain of visual symptoms, ocular screening could be considered in these patients receiving chronic anti-psychotic treatment, so that any ocular toxicity could be diagnosed in a timely manner.

Topics: Aged; Antipsychotic Agents; Benzodiazepines; Chlorpromazine; Eye Diseases; Female; Humans; Olanzapine; Schizophrenia

Charles Bonnet syndrome (CBS) is characterised by the triad of complex visual hallucinations, ocular pathology causing visual deterioration and preserved cognitive status. We report a case of a 62-year-old man with a brief history of visual hallucinations. The patient complained of amaurosis with optic nerve atrophy in his left eye and a severe impairment of visual acuity in the right and suddenly experienced complex, vivid, elaborate and coloured visual hallucinations persisting long after eye closure and stopping during sleep. The patient maintained his insight, criticising these visions as unreal and felt distressed by them. Hallucination onset was 3 days before hospital admission. No cognitive impairment and no diseases apart from prostatic adenoma treated with alpha-lythic therapy were reported. Neurological examination and neuroimaging data were normal. Therapy with olanzapine (OLZ) 5 mg/day led to a progressive clearance of visual hallucinations in seven days and was gradually reduced and withdrawn. Three months later the visions reappeared and OLZ 5 mg/day yielded a persisting remission so that at the follow-up examination after 1 year on therapy the patient is still asymptomatic. To date, no established treatment for CBS is stated and in some patients the hallucinations fade spontaneously; in our case an antipsychotic therapy with OLZ was effective while generally anticonvulsant drugs with different mechanism of action such as carbamazepine, valproate and gabapentin are proposed.

Topics: Antipsychotic Agents; Benzodiazepines; Eye Diseases; Hallucinations; Humans; Male; Middle Aged; Olanzapine; Sensory Deprivation; Syndrome; Treatment Outcome; Vision Disorders

Topics: Adult; Antipsychotic Agents; Benzodiazepines; Eye Diseases; Humans; Male; Mucus; Olanzapine; Pirenzepine; Salivary Gland Diseases; Salivation; Schizophrenia