Delusional Disorder Leading to Precipitous Weight Loss

In 1817, James Parkinson first described Parkinson’s disease as the “shaking palsy.”¹ Today, PD affects more than 1 million people in North America, or roughly 150 of every 100,000 persons older than 60 years.¹ The incidence increases with age, and the mean age at diagnosis is 70 years.¹ Within the next 20 years, the number of persons with PD is expected to double as baby boomers continue to age.¹ Given these statistics, nursing home staff are likely to see more patients with PD in their facilities and should be familiar with this condition.

Although PD is commonly known to be one of the most prevalent motor diseases among elders, a significant number of patients with PD also develop concomitant psychiatric and cognitive disturbances, including psychosis and delusions. It is imperative for healthcare providers to promptly recognize and manage these disturbances, as a failure to do so can reduce patients’ quality of life and increase their risk of harm. When psychosis occurs, it is often perceived as debilitating and at least as distressing to patients as the motor complications of PD.² Anti-PD agents, particularly dopamine receptor agonists, have been reported to pose the greatest risk of psychosis, with this condition observed in as many as 40% of PD patients receiving dopaminergic treatment.^3,4 In patients with PD, psychosis most commonly manifests as visual hallucinations,^4,5 but patients can also have auditory, tactile, olfactory, or gustatory hallucinations.^6,7 Other symptoms of psychosis may include delusions, paranoid beliefs, agitation, and florid psychosis, but these are reported less commonly.⁶ Regardless of how they manifest, neuropsychiatric symptoms are a major source of distress to patients and their families, and they are thought to be one of the major precipitating events causing transition from home or assisted living facilities to a long-term care (LTC) facility.^2,8 

Monothematic delusional syndromes in PD have been documented, and some researchers suggest that they are not such a rare occurrence.⁵ We report the case of a patient with PD who presented with a monothematic delusion, which led to self-induced starvation and isolation over an 11-month period. After initiation of an antipsychotic successfully remitted the delusion, the patient no longer isolated herself and she regained much of the weight she had lost. This case serves to illustrate why delusions should be assessed for when encountering behavioral challenges in patients with PD.

Case Presentation 

An 86-year-old white woman who resided at an assisted living facility was subsequently hospitalized for weakness and falls. During the hospitalization, she received a diagnosis of Parkinson’s disease and was then transitioned to an LTC facility. Her other pertinent history includes weakness, fatigue, gastroesophogeal reflux disease, and a recent 22-lb weight loss, which started after her admission to the assisted living facility. Upon admission to the LTC facility, the patient’s height was 5 foot 2 inches and her weight was 167 lb, but at her current presentation she weighed 145 lb. At the time of her nursing home admission, she scored 7 on the Patient Health Questionnaire-9, indicating mild depressive symptoms, and 28 out of 30 on the Folstein Mini-Mental State Examination, indicating minimal cognitive impairment. She had also just been started on a low-dose anti-PD medication, carbidopa-levodopa 25/250 mg by mouth three times daily. She did not report or show any signs of visual or any other hallucinations. She did acknowledge that the new diagnosis of PD caused her considerable emotional stress and that she had anxiety over her relocation to the LTC facility, but she denied depression. 

During her current hospitalization for her weight loss, she received numerous visits from the admitting physician, nurse practitioner, social worker, and nutritionist, all of whom noted that she was refusing to eat meals in the LTC dining room for fear of becoming flatulent and passing gas. It was further reported that the patient did not have a known history of flatulence, yet she consistently expressed anxiety over passing gas in public areas, an event she stated would cause her to be embarrassed. She was treated with simethicone, fiber, and probiotics, and was placed on a nondairy, lactose-free diet. Her primary care provider also saw her and initiated sertraline for depression; this agent was titrated to 100 mg by mouth daily. 

Over the 8 months that followed the patient’s hospitalization, she became increasingly reclusive at the LTC facility and her weight dropped to 128 lb. Efforts to enable the patient to eat meals in her room were unsuccessful. She continued to have fear about passing gas and became increasingly verbally agitated and demonstrated mood lability when this topic was raised. The patient was started on valproic acid for the labile mood, but this treatment was discontinued after it lacked efficacy. Repeated physical examinations continued to show no abnormalities or abdominal issues, such as hyperactive abdominal sounds or abdominal pain or tenderness. Laboratory studies, including a complete blood count and a comprehensive metabolic panel, were noncontributory. The patient continued receiving low-dose anti-PD medications for a significant tremor, and efforts concentrated on counseling her regarding the absence of any clinical findings regarding the perceived flatulence. Despite these efforts, she retained her delusion and continued to state that she was “scared to death” of eating in the dining area and of being publically humiliated about passing gas there.  In addition, the patient refused to consider reduction of the anti-PD medications because of the disturbing tremor.

A treatment team conference was undertaken, and the decision was made to initiate low-dose quetiapine (12.5 mg by mouth daily) for her delusions. Within one month of initiating this antipsychotic, she began eating in the main dining room and her food intake increased. Three months later, her weight increased to 142 lb, and her weight has held stable at 148 lb. She no longer perseverates about becoming flatulent or vocalizes her previous fear of being humiliated about passing gas. 

Discussion

Psychosis, which translates from the Greek into “illness of the soul or mind,” has been documented since the 1700s.⁹ As previously noted, many symptoms can be associated with psychosis, but two of the most common are delusions and hallucinations. Delusions are false, fixed beliefs, whereas hallucinations are false sensory experiences.^2,9 Many neurological conditions have delusion as a symptom, with some of the most widely recognized being schizophrenia, affective disorders, and Alzheimer’s disease.¹⁰ In patients with PD, the presence of delusions as a symptom of psychosis are thought to be far less common, but have been reported in anywhere from 7% to 35% of patients.^2,5,10 The prevalence of delusions is much higher among PD patients with dementia, occurring in 29% to 54% of patients, than among those without dementia, occurring in 7% to 14% of patients.⁹ 

When delusions occur, they can be polythematic or monothematic. Patients with polythematic delusions have a broad range of delusions, whereas those with monothematic delusions experience one very specific delusion, as occurred with our patient. One of the most famous persons of this century with a monothematic delusion was Kurt Gödel, who in his early 20s authored the incompleteness theorem, which revolutionized mathematics.¹¹ Gödel was a lifelong colleague and friend of Albert Einstein at Princeton University. In later life, Gödel became mentally ill and believed his food was being poisoned. As a result, he would only eat food prepared by his wife, Adele, but when she was hospitalized for a 6-month period and could no longer prepare his food, he refused to eat and starved to death. He weighed only 65 lb when he died in 1978.¹¹ Gödel’s case serves to highlight how delusions can lead to harm and why recognizing them and promptly intervening is important.   

Delusions in patients with PD are typically paranoid or persecutory in nature, and common themes include food poisoning, spousal infidelity, intentions of harm by nursing staff, being watched by others, or being under constant surveillance by cameras.^2,5 Research that has focused on identifying delusional themes did not reveal a somatic delusion (ie, that one’s body or bodily function has been altered in some manner), such as our patient’s fear of passing gas or becoming flatulent in public areas. There is a lack of understanding regarding how delusional themes emerge; for example, why one patient exhibits a delusion regarding spousal infidelity and another a delusion about being under constant surveillance.⁹ 

A challenge of properly recognizing and treating delusions is disentangling them from the myriad medical and psychiatric conditions from which they can stem. In addition to PD, some of the many diagnoses that have delusions as a symptom include schizophreniform disorder, schizoaffective disorder, delusional disorder, brief psychotic disorder, psychotic disorder due to a general medical condition, substance-induced psychotic disorder, and some mood disorders. In addition, although many clinicians may think they can recognize a delusion when they encounter one, errors in clinical judgment do occur, causing someone to be labeled as delusional when they are not. For example, Martha Mitchell, the wife of the American attorney general John Mitchell, was dismissed as being delusional when she reported illegal activity by the White House Administration when Richard Nixon was president.⁹ Based on this famous case, when a healthcare provider now mistakes a person’s perceptions of real events to be delusions, this is sometimes referred to as the Martha Mitchell effect.¹² 

Pathophysiology of Delusions in PD 

Understanding the pathophysiology of delusions in PD is challenging, as there is a complex interplay between extrinsic and disease-related factors. It is now known that delusions can result from the PD itself or be an adverse effect of medications, particularly anti-PD agents.^2,5 Although dopamine receptor agonists have been most commonly implicated as a source of medication-induced delusions,³ other anti-PD agents, including levodopa, amantadine, and anticholinergics, have also been reported to cause delusions and other psychotic behaviors.² It is unclear how dopaminergic medications lead to delusions in PD, but because reductions in or discontinuation of these medications have been documented to be at least partly beneficial in remediating the delusions, these agents are thought to play a role in the development of this form of psychosis.^3,5 It has been postulated that schizophreniform disorders, affective disorders, Alzheimer’s disease, and PD have a “final common pathway” involving dopamine, and high presynaptic dopamine synthesis capacity in the ascending midbrain system has been associated with the severity of psychotic symptoms.¹⁰ However, other neurotransmitter abnormalities are also thought to contribute to psychosis, including y-aminobutyric acid, glutamate, and endocannabinoids, but their role in patients with PD is unclear.¹⁰ 

Another factor that confounds our understanding of the pathophysiology of delusions in PD is that patients can experience delusions despite receiving antipsychotics.² Then there are countless other nonpharmacological variables that may be contributing factors, including cognitive impairment, advancing age, duration of the PD, and the presence of major depressive disorder and sleep disturbances.² These disorders, in combination with the aforementioned factors, contribute to the lack of agreement and clarity regarding the etiology of psychosis in patients with PD, particularly with regard to delusions. In addition, while much is known about brain abnormalities and cognitive deficits that lead to delusions in persons with schizophrenia and other psychological conditions, this information does little to further our understanding about the pathophysiology of delusions in patients with PD.¹⁰

Management  

Managing delusions in patients with PD requires a multifactorial approach, as there are many considerations. First, it is important to ascertain whether the delusions represent an advancement of PD or whether they have been precipitated by the use of anti-PD medications.⁴ Second, stressful psychosocial factors (eg, relocation to a new living environment, death of a spouse or grown child, reduced financial security) should be taken into consideration, as such factors have been speculated to contribute to the onset and maintenance of delusional beliefs.² Finally, with regard to the LTC patient, the psychosocial environment of the facility should be considered, as this can also influence how neuropsychiatric symptoms manifest.⁸ 

LTC staff should understand that delusions are both distressing and debilitating to patients due to the emotional experiences that this particular form of psychosis provides. During their small qualitative study of delusions in eight patients with PD, Todd and colleagues² identified the following four emotional themes when they conducted a phenomenological analysis of their patients’ accounts: fear (“I got very frightened.”); uncertainty and losing control (“Why is this happening?”); loss of identify and sense of self (“I feel like I’m disintegrating.”); and acceptance (“I’ve just tried to make the best of things.”). Our case patient may be conceptualized as experiencing two of these themes: losing control (ie, feeling that she could not prevent herself from passing gas) and fear (ie, feeling that she would be publically humiliated for inadvertently doing so). 

Since delusions are thought to be part of a disease process or an adverse event of its treatment, the prevailing view of managing psychotic symptoms in PD is largely based on the medical model. Reduction or discontinuation of dopamine receptor agonists (levodopa), amantadine, and anticholinergics is thought to be one approach.^1,4 There is some concern, however, with discontinuing dopamine receptor agonists because motoric symptoms will inevitably recur.⁴ Clinicians are recommended to consider reducing the use of anti-PD drugs in the presence of psychotic symptoms, but they also need to weigh the risks and benefits of doing so and individualize treatment to care for patients with PD as their illness progresses.¹ 

Because options for treating psychosis in PD patients are limited, antipsychotics can be used despite their limited efficacy in ameliorating symptoms and their inherent safety risks, which include stroke and all-cause mortality.¹³ Clinicians should keep in mind that safety risks with these agents are increased among elders who also have dementia.¹³ When prescribing an antipsychotic, the atypical neuroleptic agents quetiapine and clozapine are recommended, as they are least likely to worsen motoric symptoms in PD patients. Although the atypical neuroleptics risperidone and olanzapine can ameliorate psychosis, they have been shown to worsen motoric symptoms, making them less attractive therapeutic options.⁴ Also, cholinesterase inhibitors (ie, donepezil, rivastigmine) have shown efficacy in attenuating psychotic symptoms in PD, yet without reducing the benefit of dopaminergic treatment for the bothersome motoric symptoms of the illness.⁴ Before prescribing any antipsychotics to PD patients, nonpharmacological approaches should be attempted to minimize safety risks in this vulnerable patient population. For example, some research has shown that increased socialization can ameliorate visual hallucinations in patients with PD.^2,14 Whether psychosocial interventions, such as day programs, therapeutic outings, or other community activities, would be effective in also attenuating delusions remains unclear. 

Conclusion 

Neuropsychiatric symptoms are frequently encountered in patients with PD. Visual hallucinations are the most common symptom, but delusions can also occur. Dysregulation of dopamine is thought to play a role in the manifestation of delusions, but it is not known whether the delusions are a component of the PD, precipitated by the initiation of anti-PD medications, or both. Delusions experienced by patients with PD typically encompass paranoia or persecution, but it is not known how or why specific themes manifest. We speculate that the emergence of the case patient’s delusion was the result of many factors, including her PD diagnosis (PD is known to have neuropsychiatric symptoms), initiation of anti-Parkinson medications (these are known to contribute to psychosis), and the presence of several psychosocial stressors (these are known to be contributing factors), most notably her recent PD diagnosis and the loss of her independence after having to relocate to an LTC facility. The underlying theme of these experiences points to loss of control over her body, due to her PD, and over her immediate environment, due to being forced to relocate to an LTC facility. Not being able to control her meals at the facility might have led her to develop a monothematic delusion about food. After various interventions failed to resolve her delusion, a low-dose, atypical antipsychotic was initiated. Although antipsychotics are associated with many safety risks, particularly in elders, when used cautiously and patients are carefully monitored, they can represent an important therapeutic intervention when all other interventions have failed. Use of an antipsychotic resolved our patient’s delusion, and she continues to take this agent under close supervision. Since the agent was initiated, we have observed no abnormal involuntary movements, her weight has remained steady, and she now participates in various activities at the facility. She even recently astounded her family by attending a holiday dinner, and prior to this, she had not left the LTC facility in more than 2 years.