CLINICAL CASE CONFERENCE
Year : 2014 | Volume
: 19 | Issue : 2 | Page : 87--90
Psychosis in an elderly patient with parkinson's disease: issues and considerations
Arghya Pal1, Raman Deep Pattanayak1, Rajesh Sagar1, Vinay Goyal2,
1 Department of Psychiatry, A.I.I.M.S., New Delhi, India
2 Department of Neurology, Neurosciences centre, A.I.I.M.S., New Delhi, India
Department of Psychiatry, A.I.I.M.S., New Delhi
Psychosis in Parkinson«SQ»s disease (PD) is a frequently documented clinical phenomenon, whicj poses several clinical and management issues. The antagonistic nature of medications makes the treatment more challenging. The advanced age and medical co morbidities call for a more cautious monitoring. The goal should be to make the patient optimally functional as far as motor and psychotic symptoms are concerned. The case discussed here demonstrates a case of psychosis occurring in the context of PD, and highlights the complex issues involved in the management, and discuss them in light of recent research.
|How to cite this article:|
Pal A, Pattanayak RD, Sagar R, Goyal V. Psychosis in an elderly patient with parkinson's disease: issues and considerations.J Mental Health Hum Behav 2014;19:87-90
|How to cite this URL:|
Pal A, Pattanayak RD, Sagar R, Goyal V. Psychosis in an elderly patient with parkinson's disease: issues and considerations. J Mental Health Hum Behav [serial online] 2014 [cited 2020 Apr 9 ];19:87-90
Available from: http://www.jmhhb.org/text.asp?2014/19/2/87/153718
Parkinson's disease (PD) is a chronic and debilitating disease, classically presenting with motor symptoms. It is no longer considered as a pure motor disorder, because of an increasingly recognition that nonmotor symptoms such as cognitive dysfunction and dementia, autonomic dysfunction, and sleep-wake cycle dysregulation, among others may form a prominent part of clinical presentation. In addition, affective, psychotic or other psychiatric manifestations may also occur.  The emotional and behavioral symptoms are more prevalent and obvious over the long-term course of the illness and are a major determinant of quality of life, progression of overall disability, and caregiver burden. , Presence of debilitating neuropsychiatric symptoms may be a predictor of adverse outcomes. Further, the psychiatric symptoms may make the treatment more challenging, creating a dilemma about realistic treatment goals. ,
The case discussed below, highlights the several complex issues involved in the management of psychosis in PD, discussed in light of recent research.
Mrs. A was 71-year-old female; a doctor by profession had the neurological illness for 14 years and psychiatric symptoms for nearly 1-year, which were continuous and progressive in the course. Besides self, informants included son and daughter-in-law who were also caregivers for the patient.
Patient was asymptomatic about 14 years back when she started having an asymmetrical tremor of the right hand, which became bilateral in next year, rigidity of limbs, slowness of the gait and motor movements. She was diagnosed as PD and initiated on anti-parkinsonian medications. Gradually over coming years, she left her job due to slowness and had to resort to use of a walker for support. The activities of daily living and self-care were intact, but she would take more time. She continued to be functional, interacted with others in the family and participated in the kitchen and house-related works.
Her husband passed away 1-year and 2 months back, after which the depressive symptoms and repeated remembrances of husband were experienced for about a month, and slowly, she started recovering from grief over next 1 to 2 months. She shifted to her daughter's place thereafter where her mood was euthymic, and no apparent behavioral problems were present.
She continued with her anti-parkinsonian medications (levodopa 1000 mg/day and pramipexole) as previous with no change in the dose during this time. About 2 months later, the patient started to complain that she was being surrounded by ants and would make gestures to kill the ants by rubbing against the floor. On being asked, she would report seeing black ants, which were moving in a line. She would point to the floor, but family members were not able to see anything. During this time, patient was apparently in touch with her surroundings in clear consciousness and awake state. Gradually, these complaints increased in frequency to several times in a day. Over next few weeks, she started to complain that the ants were probably biting her when she was asleep. She would show scratch marks and redness over forearms though was not able to appreciate the biting sensation. This continued for about 3 months, after which she came to stay with her son and daughter-in-law.
Patient now started reporting that she was able to see larvae, small in size, grey in color, with multiple legs, which could be seen distinctly against her clothing. She had not seen a similar larva previously and was not able to identify the type or species. She denied of any crawling sensation over the skin. Seeing these larvae on her clothes would leave her disgusted and distressed. Over next 6 months, she continued to complain of seeing both ants and larvae on separate occasions, multiple times, almost every day. This would always occur in an awake, nondrowsy state, and there is no history of misrecognition or misidentification. Till this time, she was able to carry out her activities of daily living with minimal support. Her predominant mood was euthymic though occasionally she would be irritable. The sleep and appetite remained normal throughout these initial 8-9 months of illness.
Thereafter, the symptoms progressed and the patient started to see silhouettes of some persons passing across their verandah. Though family members would not see anyone, but the patient would describe silhouettes of adult males of average size wearing shirts and trousers. She reported seeing the silhouettes through curtains, after which she would become scared and come out of her room to be with other family members.
Within a month, patient started reporting that she could see some persons inside her room, who were middle-aged men and wore black shawls to cover their faces. The patient would point to certain directions in her room, complaining about their presence. She would later elaborate that these persons are keeping an eye on her and have come with an evil intention to harm her. Patient did not report hearing their voices at any time and would say that she could see them communsicating to each other by means of gestures.
When the family members denied seeing anybody in the room, she would explain that that those persons are very 'shrewd' and were able to 'mesmerize' the family members so that they were unable to see them. Alternately, she would report that those persons have started hiding at various places in her room, e.g., cupboard or over the fan by changing their size to a smaller size. However, she never reported seeing them in the process of transforming their size/shape. She was convinced that those people were trying to harm her by drawing her blood. She would attribute various minor abrasions on her body to be the places from where they have drawn blood. Although the patient did not see them in action but was sure that they were doing it. She also reported that those persons have fixed cameras all around her room to take her photographs. She would express that her blood and photographs would be used for some research/experimental purpose, and those people are actually trying to kill her. She would start crying or ask her son to lodge a police complaint.
These complaints would persist for several minutes to an hour, occur multiple times in a day, during which a caregiver had to stay by her side. By now, her predominant mood was fearful. The sleep and appetite had decreased considerably. The patient started to resist coming out of her bed, and more assistance was required to help her with activities of daily living.
Over the next few days, patient started to report that those persons were harassing her by touching her private parts and could feel the touch of a number of hands over her back, groin, thighs, and breasts. She could not see any men around her during that time but could distinctly make out the touch sensation. The patient would become very distressed and would start cursing those invisible persons.
During this time, patient's interaction with the family members also decreased. She would request them to stay beside her and not go to work. Her self-care also deteriorated. During evening, she occasionally sat with the family to watch television but she would not be as engaged as previously and would easily be distracted and complain about seeing the persons. Over this period, the mood of the patient would remain irritable. Often she would be found weeping and sometimes cursing. The involuntary movements would continue at the increased intensity, and she would prefer to keep lying down instead of walking. Her sleep and appetite were decreased by about 50%.
Since it was gradually difficult to manage her at home, she was brought to the neurology Out Patient Department for consultation, where pramipexole was tapered off, and levodopa continued as previous. However, psychotic symptoms continued to worsen. The patient started to complain that the persons were emitting some sort of gas. She would tell that whenever she would get up in the morning, she could feel a strange smell. She felt that they were actually anesthetic gases as she remembered the smell from her past experience as a doctor. She also started to complain that the persons were holding her legs, not allowing her to move the limbs. She urged her family to get her admitted or else, feared that the persons may cause grave danger to her safety. She felt that those people visible in her room were quite powerful and capable of harming her, and perhaps doctors may be more powerful persons than them. Hence, she viewed the hospital as a safer place to be compared with her home. Her food intake decreased significantly, and she virtually stopped coming out of her bed.
In medical history, patient was diagnosed with hypertension a few years back, which was well-controlled on medication. She also was diagnosed as having age-related macular degeneration in the right eye and immature cataract in left eye over past 2 years. Family history was positive for PD in patient's father. The birth, development or childhood history was unavailable. Physical examination revealed a short-stepping festinating gait with a forward stoop, tremors, and cog wheel rigidity and increased tome in all limbs. Right, eye had diminished vision (6/60) as tested on snellen's chart.
In the mental state examination (MSE), patient was lying on the bed and had a fearful affect. Her speech productivity was markedly reduced, and tone/volume was low. Thought content revealed delusion of persecution and perceptual abnormalities in the form of multi-modal hallucinations (visual, tactile and olfactory) were present. Her attention was aroused but ill sustained. She was not cooperative for higher mental functions. Judgment was impaired, and insight was absent.
The International Classification of Diseases-10 diagnosis  was organic hallucinosis (F06.0), PD (G20), age-related macular degeneration (H35.3) in the right eye, immature cataract (H25) in the left eye and essential hypertension (I10).
In subsequent course, patient's physical status deteriorated in course of treatment due to fever, (total leukocyte count 11,000/cumm and serum sodium 129 mEq/L) after which she became drowsy and nonresponsive to vocal or physical stimuli, and had to be admitted and started on parenteral antibiotics. She was started on tablet levodopa 1000 mg/day in four divided doses along with oral salt replacement and parenteral antibiotics. The patient became afebrile over next 1-2 days.
For psychiatric symptoms, Quetiapine was started at 50 mg/day, and increased to 100 mg/day after 5 days. At this dose, the patient was sedated and was difficult to arouse throughout the day. In the subsequent ward rounds, the dose of quetiapine was reduced to 75 mg, and as levodopa has propensity to exacerbate psychosis, another change was made to slightly decrease the dose of tablet levodopa from 1000 mg to 750 mg. Subsequently, it led to worsening of the motor symptoms of PD. Tablet levodopa was again increased to 1000 mg, and tablet quetiapine was resumed at 100 mg/day (sustained release preparation; single night time dose). Over the next weeks, there was an improvement in the psychotic symptoms of the patient. Her self-care had improved, and she started taking food by herself with support. The patient was discharged with partial improvement, with a reduction in duration and frequency of hallucinations.
Psychotic symptoms occurring in association with PD need special attention in terms of diagnosis, evaluation, and management. Psychosis has a prevalence of about 15-40% over the long-term course of PD. , In the early stages, 1-year prevalence of psychosis is 3%, which increase to 7.7% in 2 years.  Correlates or risk factors for PD psychosis include exposure to PD medications; older age; increasing severity of executive/cognitive impairment or a diagnosis of dementia; increasing severity and duration of PD; comorbid depression; comorbid sleep disorder, including rapid eye movement sleep behavior disorder; visual impairment; and polypharmacy. ,, This patient had some of risk factors described above, such as older age, long duration, cataract, etc., which may have predisposed to onset of psychotic symptoms.
The understanding of the pathophysiology of psychosis in PD has expanded in recent times. Initial interpretation was that the psychotic symptoms occur only as a result of dopaminergic drug adverse effects. Current understanding is that the psychosis is more likely to be a result of a complex interplay extrinsic as well as disease-related factors.  In this patient too, psychotic symptoms made their onset later in the course and do not have a temporal relation with start of anti-parkinsonian medication.
Visual hallucinations are most frequent type of hallucinations in PD patients, occurring in as many as one-fourth of patients.  Visual hallucinations in PD patients are (a) minor e.g., 'presence' hallucinations, or 'passage' hallucinations (brief visions of a person or an animal passing by the visual field); or (b) 'formed' visual hallucinations, which are kinetic, without any relation with the drug administration schedule. The psychotic symptoms in this patient initially started as brief visual hallucinations, which later on progressed to formed hallucinations. Later on, the patient also developed multi-modal hallucinations.
The precise etiology of visual hallucinations in PD is unknown, but some interesting insights emerge from recent literature. Pathology in the visual pathway (reduced acuity, color discrimination, contrast sensitivity or co-existing ophthalmological pathology) has been associated with visual hallucinations.  Overall proposition is that an impairment in the visual pathway along with dysfunctional visuoperceptual processing result in the visual hallucinations with cognitive impairment and disrupted sleep-wake cycle contributing to abnormal filtering of these external and internal perceptions. ,,
During assessment, the presence of severe limb rigidity made it difficult to establish the nature of phenomenological aspects in repeated MSEs. Patient would complain that some persons were 'torturing' her by holding her legs, which was probably a delusional misinterpretation. In other MSEs, she would verbalize 'touch sensations' over the limbs, attributed to an external agency/people, leading us to explore for any somatic passivity phenomenon. Latter could not be established definitively. For clinical monitoring, specific rating scales, such as the Parkinson Psychosis Rating Scale are available. The scale for the assessment of positive symptoms has also proved useful for scoring psychotic symptomatology in PD. 
It is important to rule out secondary causes of parkinsonism prior to initiation of medication.  PD has been over diagnosed at the expense of other Parkinson's plus syndromes such as progressive supranuclear palsy or multisystem atrophy, where psychosis is less common. Another important point is to rule out delirium, which is frequently encountered in the geriatric population, often presenting with psychotic symptoms along with agitation. This patient had been experiencing psychotic symptoms in clear consciousness over past year.
The management of co-occurring psychosis and parkinsonism is challenging, considering the antagonistic nature of the medications used in both conditions. ,,, Antipsychotic medication may worsen parkinsonism, and dopaminergic medication may worsen psychosis. Psychotic symptoms, which are infrequent and not bothersome, need not be managed by medications. There is no Food and Drug Administration approved medication for psychosis in PD, and all uses are 'off-label' as of now. For treating PD psychosis, a first step would be eliminating confounding variables such as delirium, infections or toxic-metabolic imbalances, followed by simplifying parkinsonian medications as tolerated. The drugs may be removed/reduced step-wise in the following order: First the adjunctive drugs (anticholinergics, amantadine and selegiline), second dopamine agonists (bromocriptine, pergolide, talipexole and cabergoline), and finally levodopa/carbidopa.
If additional treatment is warranted, clozapine or quetiapine can be implemented at the low doses. ,, Quetiapine is easy-to-use in clinical settings, does not require blood count monitoring like clozapine, and is shown to be beneficial in open-label reports. Cholinesterase inhibitors such as rivastigmine and donepezil have been considered in the treatment of chronic, mild to moderate psychotic symptoms in PD, but evidence is mixed and not firmly established in case of PD. Though not currently available, the novel 5-HT2a inverse agonist, pimavanserin has shown promise in the treatment of PD psychosis. 
In spite of their relative safety, the atypical antipsychotics should be used in a judicious manner due to their association with a higher risk of mortality when used in elderly patients with dementia.  Management of psychosis and its behavioral and emotional consequences may also be supplemented through nonpharmacological methods. In a study of nondemented PD patients, 36 out of 46 hallucinating patients used self-driven coping strategies such as cognitive, interactive, and visual techniques, to manage their symptoms.  Most of such strategies have been extrapolated from schizophrenia literature and effectiveness is not yet firmly established in PD. The natural course of psychosis in PD is not well understood, so there is little empirical evidence to guide clinicians on the appropriate length of treatment for PD psychosis. ,
To conclude, psychosis in PD is a frequently documented clinical phenomenon, which needs specialized care and management. The etiology of psychosis in PD is still not clear and remains an area open to future research studies. The treatment of psychosis in PD may pose a challenge to the treating team, and the goal should be to make the patient optimally functional as far as motor and psychotic symptoms are concerned.
|1||Seppi K, Weintraub D, Coelho M, Perez-Lloret S, Fox SH, Katzenschlager R, et al. The movement disorder society evidence-based medicine review update: Treatments for the non-motor symptoms of Parkinson's disease. Mov Disord 2011;26 Suppl 3:S42-80.|
|2||Zahodne LB, Fernandez HH. Pathophysiology and treatment of psychosis in Parkinson's disease: A review. Drugs Aging 2008;25:665-82.|
|3||Quelhas R. Psychiatric care in Parkinson's disease. J Psychiatr Pract 2013;19:118-41.|
|4||World Health Organization. The International Classification of Mental and Behavioral Disorders: Clinical Description and Diagnostic Guidelines. 10 th ed. Geneva: WHO; 1992.|
|5||Weintraub D, Hurtig HI. Presentation and management of psychosis in Parkinson's disease and dementia with Lewy bodies. Am J Psychiatry 2007;164:1491-8.|
|6||Morgante L, Colosimo C, Antonini A, Marconi R, Meco G, Pederzoli M, et al. Psychosis associated to Parkinson's disease in the early stages: Relevance of cognitive decline and depression. J Neurol Neurosurg Psychiatry 2012;83:76-82.|
|7||Fénelon G, Mahieux F, Huon R, Ziégler M. Hallucinations in Parkinson's disease: Prevalence, phenomenology and risk factors. Brain 2000;123:733-45.|
|8||Matsui H, Udaka F, Tamura A, Oda M, Kubori T, Nishinaka K, et al. Impaired visual acuity as a risk factor for visual hallucinations in Parkinson's disease. J Geriatr Psychiatry Neurol 2006;19:36-40.|
|9||Meppelink AM, de Jong BM, Renken R, Leenders KL, Cornelissen FW, van Laar T. Impaired visual processing preceding image recognition in Parkinson's disease patients with visual hallucinations. Brain 2009;132:2980-93.|
|10||Onofrj M, Thomas A, D'Andreamatteo G, Iacono D, Luciano AL, Di Rollo A, et al. Incidence of RBD and hallucination in patients affected by Parkinson's disease: 8-year follow-up. Neurol Sci 2002;23 Suppl 2:S91-4.|
|11||Gallagher DA, Parkkinen L, O'Sullivan SS, Spratt A, Shah A, Davey CC, et al. Testing an aetiological model of visual hallucinations in Parkinson's disease. Brain 2011;134:3299-309.|
|12||Rabey JM. Hallucinations and psychosis in Parkinson's disease. Parkinsonism Relat Disord 2009;15 Suppl 4:S105-10.|
|13||Hasnain M, Vieweg WV, Baron MS, Beatty-Brooks M, Fernandez A, Pandurangi AK. Pharmacological management of psychosis in elderly patients with Parkinsonism. Am J Med 2009;122:6140-622.|
|14||Goldman JG, Holden S. Treatment of psychosis and dementia in Parkinson's disease. Curr Treat Options Neurol 2014;16:281.|
|15||Zahodne LB, Fernandez HH. Course, prognosis, and management of psychosis in Parkinson's disease: Are current treatments really effective? CNS Spectr 2008;13 Suppl 4:26-33.|
|16||Schneider LS, Dagerman KS, Insel P. Risk of death with atypical antipsychotic drug treatment for dementia: Meta-analysis of randomized placebo-controlled trials. JAMA 2005;294:1934-43.|
|17||Diederich NJ, Pieri V, Goetz CG. Coping strategies for visual hallucinations in Parkinson's disease. Mov Disord 2003;18:831-2.|