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Recurrent Catatonia in Parkinson Disease Letters to the Editors Journal of Clinical Psychopharmacology • Volume 36, Number 1, February 2016 6. Keating GM. Nalmefene: a review of its use She had a medical history significant symptoms and a deferred ECT due to clin- in the treatment of alcohol dependence. for hypertension, coronary artery disease, ical instability, memantine at 5 mg daily CNS Drugs. 2013;27:761–772. asthma, and hypothyroidism. Further in- dose was initiated by enteral route. At the 7. Spanagel R. Alcoholism: a systems formation revealed a history of hospitaliza- 16th to 18th days, her negativism and im- approach from molecular physiology to tion at another center 1 and a half years mobility resolved markedly, and she be- addictive behavior. Physiol Rev. 2009;89: ago, because of a similar episode of immo- gan oral intake of food and fluids. At this 649–705. bility and mutism preceded by a short pe- stage, her mental examination revealed a 8. Nealey KA, Smith AW, Davis SM, et al. riod of agitation and visual hallucinations. general mental confusion and incoherence, κ-opioid receptors are implicated in the She had been continuously treated with ser- but no active psychotic symptoms. At the increased potency of intra-accumbens traline 50 mg and quetiapine 50 mg once 21st day, with near complete resolution of nalmefene in ethanol-dependent rats. daily afterward. the initial symptoms, she was discharged. Neuropharmacology.2011;61:35–42. At our initial examination, patient's On an outpatient visit a month later, she 9. Katsuura Y, Heckmann JA, Taha SA. eyes and mouth were firmly closed and was better off with memantine 10 mg mu-Opioid receptor stimulation in the she had gegenhalten rigidity at her neck BID. Her mental examination revealed mod- nucleus accumbens elevates fatty tastant and extremities. She had no focal neurolog- erate dementia with a mini–mental state ex- intake by increasing palatability and ical signs or meningeal irritation and was amination score of 18/30. suppressing satiety signals. Am J Physiol afebrile with normal vital signs. A physical Five months later, the family reported Regul Integr Comp Physiol. 2011;301: examination revealed findings of dehydra- that the patient had suspiciousness and in- 244–254. tion. An initial complete blood count and somnia and also exhibited a waxing and 10. Gosnell BA, Levine AS. Reward systems blood chemistry including a serum creati- waning overactivity, which involved some and food intake: role of opioids. Int J Obes nine phosphokinase level were in the normal home activities such as cleaning and tidy- (Lond). 2009;33:S54–S58. range, except for moderate hypernatremia ing. The patient was then on a stable antiparkinson regimen arranged at another 11. Soyka M. Nalmefene a treatment of (150 mEq/L) and hypoglycemia (45 mg/dL). alcohol dependence: a current update. Further laboratory analyses revealed a nor- center 3 months earlier, and it consisted of Int J Neuropsychopharmacol. mal thyroid profile, serum vitamin B12/ levodopa/benserazide 50/12.5 mg BID, sus- 2013;18:1–10. folic acid levels, and negative serum tained release levodopa/benserazide 100/ VDRL/rapid plasma reagin tests. A cranial 25 mg BID, levodopa/carbidopa/entacapone magnetic resonance imaging showed a 100/25/200 mg and 150/37.5/200 mg BID, moderately severe global cortical atrophy and pramipexol 2 mg BID. She also received Recurrent Catatonia in and several small periventricular T2 hy- memantine 10 mg BID. Soon afterward, perintensities. After admission, patient's she had a loss of interest in daily activities Parkinson Disease dehydration and hypoglycemia were man- for a period of 3 weeks and became preoc- aged with intravenous fluids. Afterward, a cupied with vague abdominal complaints To the Editors: therapeutic trial of diazepam 5 mg intra- and constipation. According to the family, atatonia is a motor dysregulation syn- muscularly followed by lorazepam 1 mg she was irritable and paranoid and was re- C drome that occurs in various medical orally was given. This brought about a luctant to take her medications. At the in- 1 conditions. However, few reports have de- marked response within2to3hours;thepa- terview, she was unwilling to respond to scribed catatonia in patients with Parkinson 2,3 tient could walk, albeit slowly, sat on a chair, questions and had little eye contact. She also disease (PD). We present an elderly pa- and asked whether the police were after her. demonstrated psychomotor retardation with tient with PD, who developed recurrent ep- However, the response did not persist, and frequent thought blocking. Her mental ex- isodes of catatonia for a period of 3 years, consequently, the dose of lorazepam was amination revealed some depressed mood and discuss the challenges of managing gradually increased up to 5 mg/d by the and anhedonia; thus, duloxetine 30 mg/d catatonia in this clinical setting. third day. In the following days, she was and lamotrigine 25 mg/d were prescribed. persistently stuporous, negativistic, and Two weeks later, however, she had to be CASE REPORT uncooperative and had no oral intake. hospitalized for recurrence of catatonic stu- An 80-year-old woman, who had been di- Electroconvulsive therapy (ECT) was then por with fairly similar symptoms at previ- agnosed with idiopathic PD 12 years ago, considered; however, it was deferred be- ous hospitalizations. presented to our emergency department cause of an acute exacerbation of patient's On admission, her physical neurologi- with stupor, mutism, and immobility with asthma and concurrent clinical findings of cal examination was unremarkable except minimal response to painful stimuli. Ac- aspiration pneumonia with a moderate de- for a generalized rigidity, and an extensive cording to her family, during the previous gree of hypoxia, which required treatment biochemical workup of plasma and urine week, she had been severely agitated and with a parenteral antibiotic, inhaled bron- revealed normal results. A standard para- had visual hallucinations. She also became chodilators, and nasal oxygen. At the tenth neoplastic panel and a test for anti-N-methyl- suspicious of her children and believed day, while the patient was still stuporous, D-aspartate receptor antibodies were also that her food was poisoned. Therefore, they an electroencephalogram revealed gener- negative. Because of the anticipated medi- sought help in an emergency unit of a alized low-amplitude theta activity, vertex cal risks related to immobility and lack of psychiatric hospital. However, she became waves, and positive occipital sharp tran- oral intake, modified ECT treatment was increasingly unresponsive afterward and sients of sleep. Hence, an iatrogenic toxic started promptly with family's consent on refused food and fluids for the last few encephalopathy secondary to lorazepam hospital day 3. Electroconvulsive therapy days. The patient had been on stable doses was suspected, and this agent was dis- was repeated on the 2 consecutive days of levodopa/benserazide 200/50 mg 4 times continued. In the following days, the pa- and continued biweekly thereafter. Mean- daily and pramipexol 2 mg twice daily tient was slightly more responsive; she while, levodopa/benserazide 100/25 mg (BID) in the preceding year, with fairly well could open her eyes shortly and occasion- 6 times a day, pramipexol 1 mg BID, and controlled motor symptoms. Her daughter ally follow simple commands. At the 15th memantine 10 mg BID were administered also had PD with age of onset at 40 years. day, on the grounds of resistant catatonic by nasogastric tubing. A mild to moderate 104 www.psychopharmacology.com © 2015 Wolters Kluwer Health, Inc. All rights reserved. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. Journal of Clinical Psychopharmacology • Volume 36, Number 1, February 2016 Letters to the Editors response to ECT appeared after the fourth was treated with parenteral followed by oral lorazepam-resistant catatonic symptoms, session (on day 10) as demonstrated by olanzapine several days before the second ECT unresponsive catatonia, and apathy – spontaneous opening of eyes, after some episode, and an unknown parenteral seda- associated with neurological insults.8,10 12 simple commands and the rare “yes/no” an- tive agent was administered before the Our final observation was that loraz- swers. During this period, on several occa- first. On these 2 occasions, a neuroleptic epam should be administered cautiously sions, she had horrifying complex visual malignant-like syndrome or acute akinesia for catatonia in the elderly patients with and auditory hallucinations, which were in Parkinson disease was an important diag- neurodegenerative diseases such as PD, accompanied by persecutory delusions nostic alternative. However, this could be because higher doses might result in a se- (“thieves coming up” and “bombs ex- effectively ruled out by the absence of hyper- vere encephalopathy or deep sedation, ploding outside”). Therefore, quetiapine termia, severe rigidity, autonomic symp- and it might be particularly challenging 25 mg at bedtime was started, whereas pra- toms, and serum creatinine phosphokinase to distinguish this complication in pres- mipexol was gradually discontinued and elevation. In the last catatonic episode, ence of catatonic stupor. It should be total daily dose of L-dopa was increased where the patient was for a long time under recognized that a general recommenda- up to 900 mg in 5 days. A significantly our follow-up; symptoms emerged gradu- tion of benzodiazepines for the treatment greater
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