1.Hyponatremia Induced Coma during Risperidone Treatment in 2 Cases of Schizophrenia.
Sung Whoi KONG ; Min Ok KIM ; Tae Min KIM ; Chang Hwa LEE ; Kyeong Sook CHOI
Korean Journal of Psychopharmacology 2011;22(1):57-61
Antipyschotics have been frequently reported being associated with hyponatremia. We have experienced two cases of severe hyponatremia with neurological symptoms in patients with acute schizophrenia who were treated with risperidone. Case 1 was a 33-year-old female who developed hyponatremia (Na+114 mEq/L) at 17 days after initiation of treatment with risperidone. Case 2 was a 41-year-old female who developed hyponatremia (Na+107 mEq/L) 5 months after treatment with risperidone. In both cases, polydipsia was not obvious. The exact cause of hyponatremia was uncertain, but we suggest that syndrome of inappropriate secretion of antidiuretic hormone due to risperidone may be the mechanism of hyponatremia in both cases. Although there have been many recent studies about the pathophysiology of hyponatremia among psychiatric patients, the exact mechanism remains unclear. There have been many case reports in the literature of hyponatremia associated with antipsychotics. We suggest that risperidone may be a potential drug that can cause hyponatremia and lead to life-threatening neurological symptoms in the early stage treatment, and that clinicians should monitor patients on a regular basis.
Adult
;
Antipsychotic Agents
;
Coma
;
Female
;
Humans
;
Hyponatremia
;
Morphinans
;
Organothiophosphorus Compounds
;
Polydipsia
;
Risperidone
;
Schizophrenia
2.A Case of Amisulpride Induced Tardive Blepharospasm in Schizophrenia.
Wu Ri PARK ; Sung Whoi KONG ; Je Chun YU ; Chang Hwa LEE ; Kyeong Sook CHOI
Korean Journal of Psychopharmacology 2012;23(3):122-125
Tardive blepharospam is characterized by repetitive, forceful, and sustained involuntary contractions of the orbicularis oculi. We report here one case of neuroleptic-induced tardive blepharospasm that developed during high-dose amisulpride treatment and was treated with clozapine. The patient was a 29-year-old man with a 6-year history of schizophrenia. After 33 months of amisulpride treatment (1200 mg/day), involuntary eye-blinking had developed. Following exclusion of all other possible etiopathological causes of the blepharospasm, we decided to switch the drug treatment from amisulpride to clozapine. On the fourteenth day of clozapine (250 mg/day) treatment, we observed significant improvements in eye-blinking and psychotic symptoms. Four months later, the eye-blinking had remitted completely. We suggest that amisulpride may cause blepharospasm and lead to an impaired ability to perform daily activities. Therefore, we recommend that clinicians regularly monitor involuntary movements in patients receiving antipsychotic treatment, especially when high doses of amisulpride are involved.
Adult
;
Blepharospasm
;
Clozapine
;
Contracts
;
Dyskinesias
;
Humans
;
Organothiophosphorus Compounds
;
Schizophrenia
;
Sulpiride