of negative symptoms in a clinically stable patient with ... Syndrome Scale (PANSS) negative symptoms score ... âfiredâ it at a neighbor after a brief altercation.
LETTERS symptom is seen. Therefore, models will not be able to simulate this range. For example our previous modeling on Parkinson’s disease was able to evaluate the behavior of the disease only after initiation of symptoms like tremor.5 Since this novel modeling method will simulate a range from normal gait to severe Parkinson’s disease, and it will consider the global features of chaotic system, it seems to be more successful in this regard. Modeling the gap between healthy and initiation of disease state could be important in diagnosis, prediction, and treatment of Parkinson’s disease. This is the main difference between this novel model and previously presented ones. Based on above-mentioned abilities, this novel modeling approach will be able to classify different states of the disease, even those from which we did not have a proper recording. Yashar Sarbaz Farzad Towhidkhah Shahriar Gharibzadeh Biomedical Engineering, Amirkabir University of Technology References
1. Goldberger AL, Amaral LA, Hausdorff JM, et al: Fractal dynamics in physiology: alterations with disease and aging. Proc Natl Acad Sci U S A 2002; 99(suppl 1):2466–2472 2. Hausdorff JM, Mitchell SL, Firtion R, et al: Altered fractal dynamics of gait: reduced stride-interval correlations with aging and Huntington’s disease. J Appl Physiol 1997; 82:262–269 3. Sarbaz Y, Banae M, Gharibzadeh SA: Computational model for the Huntington disease. Med Hypotheses 2007; 68:1154–1158 4. Toro MG, Ruiz JS, Talavera JA, et al: Chaos theories and therapeutic commonalities among depression, Parkinson’s disease, and cardiac arrhythmias. Compr Psychiatry 1999; 40:238–244 5. Haeri M, Sarbaz Y, Gharibzadeh S: Modeling the Parkinson’s tremor and its treatments. J Theor Biol 2005; 236:311– 322
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Successful Smoking Cessation and Improvement of Negative Symptoms With Varenicline in a Stable Schizophrenia Patient To the Editor: The selective nicotinic partial agonist varenicline is approved for smoking cessation1 in more than 30 countries. Freedman2 has reported a case of a patient with a schizophrenic exacerbation after initiation of varenicline for smoking cessation. Here we present a case of successful smoking cessation and substantial improvement of negative symptoms in a clinically stable patient with schizophrenia. Case Report Mr. A is a 27-year-old former student with the diagnosis of schizophrenia, paranoid subtype for 4 years. His last admission as an inpatient took place 2 years ago and was due to delusions, visual and tactile hallucinations, and ideas of reference. He had no insight into his disorder and ideas of grandiosity (“the creator and guardian of the light”). By then he had also been a cannabis user (on average 0.5 g per day). No somatic disorders had been reported. He was then put on depot medication which he received every 14 days (risperidone, 37.5 mg). He smoked cigarettes for 5 years, increasing to 30 cigarettes a day over the last 6 months. His Positive and Negative Syndrome Scale (PANSS) negative symptoms score fluctuated between 42 and 45 over this period of time, with a PANSS positive symptoms score of only 8 points. Quitting smoking strategies like group counseling and nicotine replacement therapy via patch were altogether unsuccessful. Therefore, a trial with varenicline added to risperidone was started. The drug was titrated
to 2 mg per day over a period of 1 week. It was tolerated well, and he experienced no nausea. After 2 weeks, complete abstinence was achieved (that was confirmed via CO measurement in the expiration air) and maintained for 6 months. Moreover, his PANSS negative score decreased from the second week on varenicline to 22 points. Risperidone and 9-hydroxy-risperidone concentrations remained unchanged. Discussion We report for the first time a successful trial of smoking cessation in a patient with very mild positive but marked negative symptoms which substantially improved during the treatment with varenicline without exacerbation of psychotic symptoms. We interpret this clinical observation by the indirect dopamine releasing properties of varenicline.3 Schizophrenia patients seem to have altered nicotinic acetylcholine receptors and stimulation by nicotine has a positive effect on cognition and other symptoms of schizophrenia, which is thought a transient effect.4 Nicotine as a full agonist on nicotinic acetylcholine receptors has a very high affinity for these receptors and a tolerance inducing effect that has not been described for varenicline yet. Since the patient still received risperidone he was probably sufficiently protected from the development of new positive symptoms. Systematic controlled studies of schizophrenia patients with different predominant symptoms treated with varenicline seem warranted to evaluate its possible risks and advantages in this population. Ion Anghelescu, M.D. Department of Psychiatry and Psychotherapy, Charite´, University Medicine Berlin, Germany, Campus Benjamin Franklin, Germany
J Neuropsychiatry Clin Neurosci 21:1, Winter 2009
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References
1. Cahill K, Stead LF, Lancaster T: Nicotine receptor partial agonists for smoking cessation. Cochrane Database Syst Rev 2007; CD00103 2. Freedman R: Exacerbation of schizophrenia by varenicline. Am J Psychiatry 2007; 164:1269 3. Rollema H, Coe JW, Chambers LK, et al: Rationale, pharmacology and clinical efficacy of partial agonists of alpha4beta2 nACh receptors for smoking cessation. Trends Pharmacol Sci 2007; 28:316–325 4. Adams CE, Stevens KE: Evidence for a role of nicotinic acetylcholine receptors in schizophrenia. Front Biosci 2007; 12:4755–4772
Frontotemporal Dementia Presenting With Psychotic Symptoms To the Editor: Frontotemporal dementia is a progressive neurodegenerative disorder that affects the frontal lobes, the anterior temporal lobes, or both, and it commonly afflicts people in middle age.1 The initial presentation of frontotemporal dementia is usually dominated by behavioral and personality changes, and psychosis is an unusual early feature.2 We describe a patient with probable frontotemporal dementia who presented with psychotic symptoms along with personality changes. Case Report Mr. A, a 43-year-old white man, was brought to the emergency department by the police after he pulled out an unloaded gun and “fired” it at a neighbor after a brief altercation. When admitted to the psychiatric unit, the patient chuckled that it was a “joke” and tried to underplay the incident. He was not forthcoming during his initial psychiatric evaluation and more information was obtained from his wife. According to her, Mr. A was fired
from his job a couple of years ago following an altercation with a colleague. He was noted to get irritable easily and had also become reclusive. He would spend hours sitting in the dark and listening to rock music and would do nothing around the house. Mr. A was also expelled from his golf club after he made sexual overtures toward a woman. He explained this behavior was a “practical joke” and endorsed that people sometimes would not appreciate his sense of humor. Over the last 2 years, he also developed some psychotic symptoms. He felt that people were staring at him and he would in turn stare back at them. While watching TV, he felt that the characters were “looking” at him. He also believed that his family was plotting against him. On the inpatient unit, he was observed to be hyperphagic with a predilection for ice cream. On mental status examination, Mr. A was disheveled, appeared disinterested in the interview, and had an air of indifference about him. He would chuckle and sometimes would laugh out loud for no apparent reason. Although he endorsed a depressed mood, he was unable to elaborate any more symptoms of depression. His speech was interspersed with the stock phrase “no problem,” but mostly he displayed a poverty of content of speech. He elaborated referential and persecutory delusions as mentioned above and had grandiose ideas of becoming a rock star. He denied any hallucinations and had no insight into his illness. The patient had no family history of psychiatric or neurologic illness. There was no history of drug and alcohol use. His blood work, including electrolytes, liver/renal function tests, thyroid-stimulating hormone (TSH), rapid plasma reagin, B12, folic acid, and blood counts were noncontributory. His head CT, done as a part
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of first-episode psychosis work up, showed prominent bifrontal atrophy and minimal bilateral anterior temporal lobe atrophy. His EEG was normal. Mr. A scored 29/30 on Montreal Cognitive Assessment (he lost a point on abstraction).3 On the Frontal Assessment Battery, he scored 15/17, losing a point again on abstraction and lexical fluency.4 Neurologic examination was unremarkable. Based on the typical clinical presentation meeting the consensus criteria for frontotemporal dementia,5 neuroimaging finding and cognitive testing, Mr. A was diagnosed with frontotemporal dementia. Although a single photon emission computerized tomography (SPECT) study was planned, the patient refused further testing. He was treated with quetiapine, 400 mg b.i.d, and divalproex sodium extended release, 1000 mg b.i.d, (valproate level 79 mg/liter). His psychotic symptoms remitted completely on this combination, but he continued to display the facetious affect, indifference, and lack of insight. Comment The patient in the index case met the core diagnostic features of the consensus guidelines for frontotemporal dementia.5 These include insidious onset and gradual progression, early decline in social interpersonal conduct, early impairment in regulation of personal conduct, early emotional blunting, and early loss of insight. Some of these qualifiers also apply to schizophrenia, and if psychotic features along with negative symptoms dominate the presenting picture, frontotemporal dementia is likely to be misdiagnosed as schizophrenia. Indeed, the literature is dotted with reports of frontotemporal dementia being misdiagnosed as schizophrenia or schizophrenia-like psychosis in the early years of its presentation.2,6–8
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