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[17] Kuppers E, Ivanova T, Karolczak M, Beyer C. Estrogen: a multifunctional messenger to nigrostriatal dopaminergic neurons. J Neurocytol 2000;29:375 – 85. [18] Rettenbacher MA, Mechtcheriakov S, Bergant A, Brugger A, Fleischhacker WW. Improvement of psychosis during treatment with estrogen and progesterone in a patient with hypoestrogenemia. J Clin Psychiatry 2004;65:275 – 7. [19] Kyomen HH, Nobel KW, Wei JY. The use of estrogen to decrease aggressive physical behavior in elderly men with dementia. J Am Geriatr Soc 1991;39:1110 – 2. [20] Kyomen HH, Satlin A, Hennen J, Wei JY. Estrogen therapy and aggressive behavior in elderly patients with moderate-to-severe dementia: results from a short-term, randomized, double-blind trial. Am J Geriatr Psychiatry 1999;7:339 – 48. [21] Shelton PS, Brooks VG. Estrogen for dementia-related aggression in elderly men. Ann Pharmacother 1999;33:808 – 12. [22] Arafat ES, Hargrove JT, Maxson WS, et al. Sedative and hypnotic effects of oral administration of micronized progesterone may be mediated through its metabolites. Am J Obstet Gynecol 1988;159: 1203 – 9. [23] Bitran D, Hilvers RJ, Kellogg CK. Anxiolytic effects of 3 alphahydroxy-5 alpha[beta]-pregnan-20-one: endogenous metabolites of progesterone that are active at the GABAA receptor. Brain Res 1991;561:157 – 61. [24] Soderpalm AH, Lindsey S, Purdy RH, Hauger R, Wit de H. Administration of progesterone produces mild sedative-like effects in men and women. Psychoneuroendocrinology 2004;29: 339 – 54. [25] Stell BM, Brickley SG, Tang CY, Farrant M, Mody I. Neuroactive steroids reduce neuronal excitability by selectively enhancing tonic inhibition mediated by delta subunit-containing GABAA receptors. Proc Natl Acad Sci U S A 2003;100:14439 – 44. [26] Smith MJ, Keel JC, Greenberg BD, et al. Menstrual cycle effects on cortical excitability. Neurology 1999;53:2069 – 72. [27] Smith SS, Gong QH, Hsu FC, et al. GABA(A) receptor alpha4 subunit suppression prevents withdrawal properties of an endogenous steroid. Nature 1998;392:926 – 30.
Pavor nocturnus as a side effect of a single daily risperidone dose To the Editor, Pavor nocturnus is characterized by nocturnal episodes with extreme anxiety and panic with loud screaming, movements and vegetative symptoms such as tachycardia, tachypnea, sweating, mydriasis and muscle tension. Typically, these symptoms occur during the first third of the night, and the patient has amnesia for the episode. There are a few case reports in the literature on the occurrence of pavor nocturnus in patients under treatment with tricyclic antidepressants or classical neuroleptics [1– 4]. We report two cases of patients who developed pavor nocturnus under treatment with risperidone, an atypical neuroleptic. Mrs. E., a 35-year-old patient with no occupational training, was referred by an outpatient clinic neurologist for evaluation of a suspected tic disorder. A diagnosis of Tourette’s syndrome was established. The patient had been treated with sertraline 100 mg, and in addition, was given risperidone 4 mg, as a single daily dose taken at night. One week after starting treatment with risperidone, the patient reported dramatic dream events. The patient’s
husband reported two nightly episodes occurring within the first third of the night during which the patient, while sleeping, suddenly moved violently, breathed rapidly and then got out of bed and ran around. When he spoke to her, she did not respond. Only energetic shaking woke the patient up. She did not remember the episode. Several EEG recordings did not show any evidence of an epileptic genesis of these episodes. Therefore, we made the diagnosis of pavor nocturnus. After dividing the risperidone dose into two daily doses, the episodes did not recur. Mr. S., a 37-year-old former auto mechanic, has been treated in our outpatient clinic for 3 years with olanzapine 15 mg/day for a schizophrenic psychosis. Because of significant weight gain and hyperglycemia, neuroleptic therapy was switched to risperidone. After reducing the olanzapine dosage and discontinuing of the drug, the patient received risperidone 6 mg once daily taken at night. At a routine visit 8 days after starting risperidone monotherapy, the patient reported that since taking risperidone, he had vivid dreams including several dramatic dream events. During the last two nights, his wife had to waken him a few hours after falling asleep, when he suddenly sat up and screamed loudly. At one point, he even jumped out of bed and ran around the room. Both events occurred within the first third of the night. The patient had complete amnesia for these episodes. EEG recordings were unremarkable. Since the patient had no schizophrenic symptoms at this time, we made the diagnosis of pavor nocturnus. As with our other patient, after dividing the daily risperidone dosage into two doses, the symptoms did not recur.
The occurrence of dream events and pavor nocturnus under treatment with classical neuroleptics and tricyclic antidepressants, particularly when given at a single daily dose, has been described in the literature [1– 4]. To our knowledge, pavor nocturnus under treatment with atypical neuroleptics such as risperidone has not been reported. After exclusion of other possible causes, and based on the fact that the symptoms occurred in the first third of the night and in clear association with the initiation of treatment with risperidone at a single daily dose taken at night, we believe that the pavor nocturnus was induced by risperidone. In addition, symptoms disappeared after switching to two daily doses, as described in the literature for classical neuroleptics [1]. There is one report of a sleep-related eating disorder (SRED) induced in a patient with psychotic disorder due to vascular dementia treated with risperidone 2 mg/day [5]. After dose reduction to 1 mg/day, the episodes disappeared completely. The authors conclude that the occurrence of SRED induced by risperidone might be due to risperidone’s potent antagonism at the D2- and 5-HT2-receptors resulting in an increase of slow-wave sleep periods. Up to the present, the mechanisms for inducing these side effects on sleep are unknown. In recent published reviews about the effects of antipsychotic drugs on sleep [6,7], evidence was presented that atypical antipsychotics like olanzapine, risperidone and clozapine increase total sleep time and
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stage 2 sleep in schizophrenic patients. Additionally, olanzapine and risperidone enhanced slow-wave sleep, the period of sleep usually associated with pavor nocturnus. It can be assumed that this enhancement of slow-wave sleep might be responsible for the induction of pavor nocturnus by risperidone in our patients. The disappearance of the symptoms after splitting to two daily doses of risperidone might be due to lower peak plasma levels. We think that further studies on the effects of antipsychotic treatment on sleep are necessary. Christian Prueter, M.D. Department of Psychiatry and Psychotherapy University Hospital, Technical University 52074 Aachen, Germany Hospital for Psychiatry, Psychotherapy and Neurology Hospital Maria Hilf, D-52538 Gangelt, Germany E-mail address:
[email protected] Frank G. Luecke, M.D. Department of Psychiatry and Psychotherapy University Hospital, Technical University 52074 Aachen, Germany Paul Hoff, M.D., Ph.D. Department of Psychiatry and Psychotherapy University Hospital, Technical University 52074 Aachen, Germany Department of Psychiatry and Psychotherapy University Hospital, 8029 Zuerich, Switzerland doi: 10.1016/j.genhosppsych.2005.02.007
References [1] Flemenbaum A. Pavor nocturnus: a complication of single daily tricyclic or neuroleptic dosage. Am J Psychiatry 1976;133:570 – 2. [2] McLeod MN, Fisher P. Pavor nocturnus in a schizophrenic patient: a review and case study. Am J Psychiatry 1978;135:235 – 6. [3] Pilette WL. Phenothiazines and night terrors. Am J Psychiatry 1978; 135:869. [4] Allen RM. Attenuation of drug-induced anxiety dreams and pavor nocturnus by benzodiazepines. J Clin Psychiatry 1983;44:106 – 8. [5] Lu ML, Shen WW. Sleep-related eating disorder induced by risperidone. J Clin Psychiatry 2004;65(2):273 – 4. [6] Monti JM, Monti D. Sleep in schizophrenia and the effects of antipsychotic drugs. Sleep Med Rev 2004;8:133 – 48. [7] Sharpley AL, Vasallo CM, Cowen PJ. Olanzapine increases slow wave sleep: evidence for blockade of central 5-HT(2C) receptors in vivo. Biol Psychiatry 2000;47(5):468 – 70.
Cryptococcal meningitis mimicking primary mania in a young female To the Editor, Cryptococcal meningitis is a rare cause of secondary mania. Having conducted an extensive search of MEDLINE, EMBASE and PsycINFO, supplemented with crossreferencing, we could only locate 4 reported cases [1–3].
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Three of those cases were Caucasian males and one was a Melanesian male, all aged above 30. We would like to report a case of cryptococcal meningitis that presented as a manic episode in a young Chinese female. Ms. M, a 25-year-old woman, who used to enjoy good physical and mental health and had no known family history of psychiatric illness, attended the emergency room (ER) on August 23, 2003 (Day 1), after the insidious onset of a fever that had lasted for 1 month. She also experienced significant weight loss, chills, rigor, bone pain, insomnia and poor appetite. Two days before the consultation at the ER, she had displayed marked changes in behavior that were characterized by irritability, an elated mood and grandiose ideas. The examination at the ER revealed that the patient had a temperature of 37.28C and that she was disorientated as to time and place. Manic symptoms, such as her elated mood, irritability, excessive logorrhea, grandiose ideas and flight of ideas were clearly present. A neurological examination showed neither neck rigidity nor photophobia, her pupils were equal and were reactive to light, her cranial nerves were intact, the muscle tone of all four limbs was normal with full-power, normal tendon jerks and flexor plantar response. Fundoscopy revealed normal optic discs. She was admitted to a medical ward where her CBC and a computer tomogram of brain were normal. A lumbar puncture (LP) was not performed. Ms. M was transferred to an acute psychiatric unit of a university-affiliated general hospital on Day 3. An examination of her mental state revealed that she was fully orientated as to time, place and person but exhibited classical manic features, including an elated mood, labile affect, an overfriendly attitude, excessive logorrhea, flight of ideas, grandiose delusions and distractibility. The diagnosis at that juncture was a manic episode. Olanzapine 5 mg/day, clonazepam 3 mg/day and sodium valproate 400 mg/day were commenced. Gradually, her mood came under partial control. However, the fever persisted and even rose to 398C, together with chills and rigor by Day 9. Ms. M was transferred back to the medical ward on the same day. An LP performed on Day 10 showed an opening pressure of 125 mm CSF. The fluid was clear and colorless and contained 7 WBC/ml. The protein content was 1.05 g/l, sugar, 1.4 mmol/l. Bacterial and viral cultures were all negative, as were her VDRL blood and HIV tests. No India ink stain or cryptococcal antigen titer was performed, and no pathogen was identified. The dosage of olanzapine was increased to 10 mg/day. Blood tests for lupus erythematosus were all negative. An EEG examination found prominent and reactive 10-Hz alpha in the posterior regions without seizure activity, focal slowing or periodicity. The medical diagnosis was aseptic meningitis. The fever persisted, despite intravenous injection of cefotaxime 2 g 4 hourly from Days 9 to 13. An LP was performed for a second time and showed an opening pressure of 90 mm CSF. The fluid was clear and
