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Keywords:

  • delusion;
  • dementia with Lewy bodies;
  • major depressive disorder;
  • Parkinson's disease;
  • stupor;
  • visual hallucination

Abstract

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. CASE REPORT
  5. DISCUSSION
  6. REFERENCES

Dementia with Lewy bodies (DLB) is diagnosed clinically according to the diagnostic criteria in the Third Report of the DLB Consortium. However, psychotic symptoms, such as visual hallucinations, delusions, and stupor, may complicate the clinical diagnosis of DLB. The present study reports on a patient with Parkinson's disease that was difficult to distinguish from DLB because of the presence of various psychotic symptoms. In making a diagnosis of DLB, it is important to assess essential psychiatric features and to observe patients for any changes in these features.


INTRODUCTION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. CASE REPORT
  5. DISCUSSION
  6. REFERENCES

Dementia with Lewy bodies (DLB) is the second most frequent type of degenerative dementia after Alzheimer's disease. However, a number of studies assessing clinical diagnostic accuracy by comparing clinical diagnoses with neuropathologic findings have indicated that the validity of clinical diagnoses is questionable.1–3 Although in 2005 the DLB Consortium incorporated new information on the clinical features of DLB to establish revised clinical diagnostic criteria for the condition,4 it may be particularly difficult to arrive at a correct clinical diagnosis when psychotic symptoms, such as visual hallucinations, delusions, and stupor, are also present. In the present study, we report on a patient in whom it was difficult to distinguish Parkinson's disease (PD) from DLB because of the presence of various psychotic symptoms.

CASE REPORT

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. CASE REPORT
  5. DISCUSSION
  6. REFERENCES

A 64-year-old man was admitted to Shinshu University Hospital with severe depression. Six months prior to admission, he had visited a mental health clinic because of depressive mood, dizziness, nausea, and loss of appetite, for which he had been prescribed amoxapine 10 mg/day, trazodone 150 mg/day, and sulpiride 300 mg/day. However, his depressive symptoms worsened and he was referred to our hospital for inpatient care.

Upon admission, the patient exhibited delusions of guilt and suicidal ideation. Neurological examination revealed mild resting tremor and bradykinesia and rigidity in the neck and upper extremities. The patient was diagnosed with major depressive disorder (MDD) with psychotic features according to the Diagnostic and Statistical Manual of Mental Disorders, 4th edn, Text Revision (DSM-IV-TR).5 He had no motor difficulties prior to the commencement of antipsychotic medication at the previous clinic. Resting tremor was observed symmetrically, but a pill-rolling movement was not seen. Therefore, we could not exclude the possibility that the patient's concurrent parkinsonism was drug induced. The patient's depressive symptoms worsened gradually after admission and his refusal to eat or take medication, which resulted from his delusions, aggravated his mental and physical condition. After we obtained informed consent from his wife, the patient was given modified-electroconvulsive therapy (m-ECT) 10 times and he responded well to this treatment. Amitriptyline 150 mg/day was prescribed to maintain remission. However, after 3 weeks, the patient relapsed and developed stupor, so nine more sessions of m-ECT were administered. This resulted in remission, which was maintained with fluvoxamine 150 mg/day and olanzapine 10 mg/day.

Although the patient remained in remission for 1.5 years on this medication regimen, the olanzapine had to be discontinued because of worsening parkinsonism. Resting tremor worsened and rigidity spread to the lower extremities. In addition, gait disturbance developed and the patient sometimes fell while walking. Although quetiapine 75 mg/day was prescribed as an alternative, the parkinsonism persisted. Around the same time, the patient's wife noticed that he was asking the same questions repeatedly. The patient's Mini-Mental State Examination (MMSE) score was 23, characterized by disturbances of short delayed recall, and brain magnetic resonance imaging revealed mild atrophy of the bilateral hippocampi (Fig. 1). On the basis of these findings, DLB or Alzheimer's disease were suspected and donepezil 5 mg/day was started. However, the patient's activity gradually declined, and depressive mood, anxiety, agitation, insomnia, and appetite loss were observed. Despite several trials with antidepressant medication, delusions of guilt and suicidal ideation appeared again. Four months after commencing donepezil, the patient's condition deteriorated to stupor and he was readmitted to the psychiatric ward at Shinshu University Hospital.

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Figure 1. Magnetic resonance imaging of the head revealing mild atrophy of the cerebral cortex and bilateral hippocampi.

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Upon admission, quetiapine was discontinued because parkinsonism persisted and the patient had an increased risk of aspiration pneumonia. Pill-rolling movement was observed and rigidity was more obvious on the right upper extremity. The patient refused to eat or take medication because of stupor or delusions of guilt, and his physical condition worsened immediately to a level requiring acute treatment with fifteen sessions of m-ECT and sertraline 100 mg/day. However, the patient's mental condition fluctuated between clear consciousness and stupor. In addition, visual hallucinations occurred, in which the patient reported seeing small people, insects, and colorful smoke. Eventually, the patient was diagnosed with probable DLB on the basis of clinical diagnostic criteria.

Quetiapine 100 mg/day and Yi-Gan-San (a traditional oriental medicine) 7.5 g/day were added with the aim of improving the visual hallucinations,6 delusions of guilt, and stupor; however, the quetiapine dose needed to be reduced to 25 mg/day because of the exacerbation of parkinsonism. The patient could not apply eye lotion and use chopsticks correctly. Hypophonia was observed and the swallowing function deteriorated. Although an additional 20 sessions of m-ECT were conducted, visual hallucinations and delusions continued. Gabapentin 600 mg/day and zonisamide 200 mg/day were started as antiparkinsonian agents, and the dose of quetiapine was increased successfully to 100 mg/day without exacerbation of parkinsonism. This resulted in the disappearance of the hallucinations and delusions and complete remission. Single photon emission computed tomography (SPECT) demonstrated left occipital hypoperfusion (Fig. 2). In addition, cardiac [123I]-meta-iodobenzylguanidine (MIBG) scintigraphy revealed impaired cardiac uptake, with a reduction in the heart : mediastinum ratio to 1.31 in the early image and 1.5 in the delayed image (Fig. 3). This suggested that the patient's parkinsonism was not drug induced, but idiopathic. After the patient had been referred to a neurologist, levodopa 100 mg/day was prescribed initially, which was increased gradually to 400 mg/day, resulting in a marked improvement in the parkinsonism, including tremor, rigidity, bradykinesia, and gait disturbance. The Hoehn-Yahr stage was reduced from Stage IV to Stage III.

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Figure 2. Single photon emission computed tomography demonstrating left occipital hypoperfusion.

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Figure 3. [123I]-Meta-iodobenzylguanidine (MIBG) scintigraphy of the patient demonstrating impaired cardiac uptake.

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Although parkinsonism persisted, no psychotic symptoms were observed after the remission and the patient's MMSE score improved to 30. On recovery from his severe depressive state, the patient's diagnosis was revised from DLB to PD and comorbid MDD with psychotic features. The patient has shown no relapse of major depression and no cognitive impairment over a period of 1.5 years on sertraline 100 mg/day and quetiapine 100 mg/day.

DISCUSSION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. CASE REPORT
  5. DISCUSSION
  6. REFERENCES

Psychotic symptoms, such as visual hallucinations and delusions, are often observed in PD, particularly during treatment with antiparkinsonian agents.7–9 However, visual hallucinations are more specific to DLB than to PD.10 Although stupor and delusions of guilt are rarely observed in DLB, they frequently occur in major depressive disorder with psychotic features.

When psychotic symptoms are present, it is difficult to assess the essential and core features of DLB according to the clinical diagnostic criteria because stupor or delusions themselves may cause cognitive impairment and clinical fluctuations. Furthermore, the visual hallucinations observed in PD are difficult to distinguish from those in DLB, particularly during treatment with antiparkinsonian agents. In addition, the use of antipsychotic drugs that cause parkinsonism complicates the assessment as to whether the parkinsonism is idiopathic or drug induced. In situations like this, DLB may be wrongly diagnosed.

In the present case, we diagnosed probable DLB according to clinical diagnostic criteria while the psychotic symptoms were active. That is, stupor and delusions caused cognitive impairment and clinical fluctuations, and then vivid visual hallucinations occurred and parkinsonism persisted throughout the clinical course (Fig. 4). Moreover, SPECT demonstrated left occipital hypoperfusion that suggested a diagnosis of DLB. However, the diagnosis was revised from DLB to PD and comorbid MDD with psychotic features after complete remission, because the patient was not demented.

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Figure 4. Clinical and therapeutic course of the patient. ECT, electroconvulsive therapy.

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In conclusion, to make a correct diagnosis, it is important to assess the essential psychiatric features and to observe patients for any changes in these features.

REFERENCES

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. CASE REPORT
  5. DISCUSSION
  6. REFERENCES
  • 1
    Litvan I, MacIntyre A, Goetz CG et al. Accuracy of the clinical diagnoses of Lewy Body Disease, Parkinson's disease, and Dementia with Lewy Bodies: A clinicopathologic study. Arch Neurol 1998; 55: 969978.
  • 2
    Lopez OL, Litvan I, Catt KE et al. Accuracy of four clinical diagnostic criteria for the diagnosis of neurodegenerative dementias. Neurology 1999; 53: 12921299.
  • 3
    Hohl U, Tiraboschi P, Hansen LA, Thal LJ, Corey-Bloom J. Diagnostic accuracy of Dementia with Lewy Bodies. Arch Neurol 2000; 57: 347351.
  • 4
    McKeith IG, Dickson DW, Lowe J et al. Diagnosis and management of Dementia with Lewy Bodies: Third report of the DLB consortium. Neurology 2005; 65: 18631872.
  • 5
    American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorder, 4th edn. Text Revision. Washington, DC: American Psychiatric Association, 2000.
  • 6
    Iwasaki K, Maruyama M, Tomita N et al. Effects of the traditional Chinese herbal medicine Yi-Gan San for cholinesterase inhibitor-resistant visual hallucinations and neuropsychiatric symptoms in patients with dementia with Lewy Bodies. J Clin Psychiatry 2005; 66: 16121613.
  • 7
    Aarsland D, Larsen JP, Cummings JL, Laake K. Prevalence and clinical correlates of psychotic symptoms in Parkinson disease: A community-based study. Arch Neurol 1999; 56: 595601.
  • 8
    Goetz CG, Leurgans S, Pappert EJ, Raman R, Stemer AB. Prospective longitudinal assessment of hallucinations in Parkinson's disease. Neurology 2001; 57: 20782082.
  • 9
    Papapetropoulos S, Mash DC. Psychotic symptoms in Parkinson's disease: From description to etiology. J Neurol 2005; 252: 753764.
  • 10
    Aarsland D, Ballard C, Larsen JP, McKeith I. A comparative study of psychiatric symptoms in dementia with Lewy bodies and Parkinson's disease with and without dementia. Int J Geriatr Psychiatry 2001; 16: 528536.