Roosy Aulakh¹*, and Harbir Sekhon²

¹ Professor in Department of Pediatrics at Government Medical College and Hospital, Chandigarh, India
² Child and Adolescent Psychiatry Specialist in Clearwater, Florida

*Corresponding Author: Roosy Aulakh, Professor in Department of Pediatrics at Government Medical College and Hospital, Chandigarh, India.

Received: October 4, 2021; Published: May 26, 2022

Citation: Roosy Aulakh and Harbir Sekhon. “Diagnostic Dilemma of Pseudodementia: A Case Report”. Acta Scientific Paediatrics 5.6 (2022): 03-06.

Abstract

The term “pseudodementia” has attracted much controversy. Some neurologists are of the opinion that no such condition exists, while others seem to disagree. There is evidence that older patients suffering from depression may be at risk for subsequent dementia. Some studies have indicated that “pseudodementia” may well lead to an irreversible dementia. The present case illustrates a different and more favorable outcome. An elderly man with major depressive disorder, single episode, was misdiagnosed with dementia and subsequently Parkinson’s disease due to symptoms of significant cognitive impairment and classical symptoms of Parkinson’s disease. These diagnoses were made due to limited or no response to inadequate antidepressant treatment, memory enhancing agents and side effects induced by standard treatment for Parkinson’s disease. After discontinuation of all prior medications, which included L-dopa, amantadine, ropinirole, donepezil, memantine, paliperidone, sertraline, a trial of high-dose selegiline at 60 mg per day produced substantial improvement with complete resolution of cognitive impairment and disappearance of signs of “Parkinson’s disease”. Clinicians should rely on careful history taking, physical and mental status examination and response to previous treatments before making a tentative diagnosis of “dementia”, “Parkinson’s disease” or “pseudodementia”. The outcome, as this case illustrates is markedly affected, sometimes to the detriment of the patient.

Keywords: Dementia; Parkinson’s Disease; Major Depressive Disorder; Pseudodementia; Selegiline.

Introduction

The term “pseudodementia” has attracted much controversy amongst clinicians. There is belief that this may be a separate clinical entity mimicking dementia and characterized by cognitive problems. On the other hand, there is postulation that “pseudodementia” is not an illness but a purely descriptive entity without any diagnostic implications. In this report we will discuss our findings in the case of an elderly Caucasian male who presented at our clinic with symptoms of progressive dementia, as well as possibly Parkinson’s disease. It appears that he was initially misdiagnosed with dementia, due to his cognitive limitations, compounded by poor response to sertraline 50 mg daily, followed by a trial of donepezil 20 mg daily and memantine 20 mg daily. Behavioral problems induced by these medications resulted in a clinician adding paliperidone to his treatment. Side effects induced by paliperidone further caused another diagnostic error, resulting in the diagnosis of Parkinson’s disease. Treatment with a combination of L-dopa, amantadine and ropinirole produced further deterioration of the patient’s symptoms, possibly due to further side effects. Discontinuation of all the medications, followed by initiation of selegiline, titrated to high-dose selegiline therapy at 60 mg per day produced marked cessation of all symptoms, and restoration of cognition. The patient has been stable on selegiline at 40 mg per day for the past year.

Case Report

The patient, a 72-year-old Caucasian male presented at our clinic with complaints of poor motivation, memory problems, insomnia, restlessness, tremor and difficulty with walking. At the time his medications included L-dopa, amantadine, memantine and paliperidone. He was a widower and lived alone. He did not endorse any prior history of neurological problems, strokes, psychiatric disorders or medical ailments. He did have a history of alcohol abuse but stopped drinking completely approximately one year prior to his visit, at the recommendation of his primary care physician.

He initially presented to his primary care physician with heightened concerns about his difficulties with his memory. He also endorsed poor motivation and inability to “carry on with life”. He lived alone, having lost his wife 6 years earlier. He did not have much contact with his extended family, and no longer enjoyed leisure activities including his daily game of golf. A Mini-Mental Status exam administered at the time indicated mild to moderate cognitive impairment. He was given a trial of sertraline 25 mg daily for 2 months with no improvement. This was subsequently increased to 50 mg daily for another month, at which he reported further deterioration in his memory and increased restlessness. Paliperidone 3 mg at night along with donepezil 10 mg daily was then added to his medication regimen. At follow-up he was found to have increased problems with recent and remote memory, motivation, with anhedonia, poor sleep, tremor, mild cogwheel rigidity and a festinate shuffling gait. Lab testing done on the patient including a CBC, CMP, thyroid profile, liver profile, serum folate, B12, vitamin D 3, RPR levels and urine toxicology were all normal. The patient was then referred by his primary care physician to a neurologist for further evaluation and treatment. He was subsequently diagnosed with Parkinson’s disease and placed on L-dopa 300 mg daily increased over 2 months to 600 mg daily. No improvement was noted, at which time donepezil was discontinued. Amantadine 200 mg daily was added to his medication regimen, along with memantine 20 mg daily. Surprisingly he was continued on paliperidone increased to 6 mg daily. He was noted to be markedly confused, with further deterioration in his memory, mood, motivation and sleep. Further testing done included repeat liver functions and Serum copper/ceruloplasmin levels which were normal. An MRI of the brain showed mild generalized atrophy, and an EEG which was normal.

He opted to seek a second opinion on the recommendation of his primary care physician and presented to our clinic with significant complaints of confusion, memory impairment, loss of interest in life, restlessness, difficulties with performing daily activities of living, insomnia and problems with his gait. Upon first examination he was noted to be mildly sedated, a little confused with a monotonous voice. He was fairly well oriented but with significant disturbance in immediate, recent and remote memory. He showed little interest in cognitive testing and a Mini-Mental Status exam indicated 16 out of 30 points. His affect was flat and expressionless and his mood was apathetic and depressed and congruent with his affect. His thought processes were somewhat disorganized and tangential. He was not delusional. He did not exhibit any hallucinations. His insight and judgment appear to be compromised.

Neurological examination revealed no clear deficits in his cranial nerves II through XII. His muscle tone short symmetrical mild cogwheel rigidity. His reflexes were bilaterally depressed. Babinski was negative.

He exhibited a mild pin-rolling tremor. He walked with slow shuffling steps and had some difficulty with his balance. Romberg test was negative and there was no evidence of cerebellar dysfunction.

With his full informed consent his medications were tapered off and discontinued over 2 weeks. After careful deliberation regarding a robust SSRI retrial vs Selegiline, he opted for treatment with Selegiline. He was placed on a tyramine free diet and advised to maintain complete sobriety with his use of alcohol, which he had stopped completely approximately 6 months prior to his visit with us. He was then placed on selegiline 20 mg daily and followed up in 2 weeks with no significant improvement in his cognition or mood. It was noted that his affect was more appropriate, and his rigidity and tremor had decreased. Selegiline was increased to 40 mg daily and further follow up visit arranged in 2 weeks with no significant changes. Subsequently he was placed on selegiline at 60 mg daily and seen in another 2 weeks. At that time, he was noted to be quite alert and active and cheerful. His cognitive functioning seemed to have returned to normal with a score of 28 out of 30 on the MiniMental status examination.

Cogwheeling rigidity, tremor and shuffling gait had disappeared. He was sleeping much better and showed good motivation. He continued to maintain sobriety, was able to perform all activities of daily living, and develop a more social lifestyle including returning to his leisure activities, especially golf.

In follow up at 1-month intervals for the next 1 year he continued to be stable on selegiline, reduced to 40 mg daily with complete sobriety from alcohol and no other medications.

Discussion

This case illustrates the difficulties faced by clinicians with stereotyping older patients with a recognizable neurological disease. The patient’s major depressive disorder was misdiagnosed with dementia due to inadequate trial of sertraline, followed by side effects induced by paliperidone and donepezil. Unfortunately, his symptoms then appeared to be more consistent with Parkinson’s disease due to adverse side effects of his medications. Treatment with L-dopa, amantadine, memantine produced no benefit. Discontinuation of all the medications followed by the judicious use of high-dose selegiline with a precaution of tyramine free diet produced significant resolution of all his symptoms and an ability to return to “normal functioning” and enjoyment of daily life. Clinicians should be very aware of the need to do a thorough medical examination and history taking to make a proper diagnosis in our ever-increasing geriatric population. Inadequate trial of a medication, in this case sertraline, can lead to a wrong diagnosis of dementia, further compounded by another wrong diagnosis of Parkinson’s disease due to iatrogenic side effects of medications. The term “pseudodementia” may not adequately describe a medical illness but is clearly a syndrome or condition encountered by us, the proper diagnoses and treatment of which, can rapidly restorative patient to normalcy and reduce overall morbidity [115].

Conclusion

Clinicians should rely on careful history taking, physical and mental status examination and response to previous treatments before making a tentative diagnosis of “dementia”, “Parkinson’s disease” or “pseudodementia”. The outcome, as this case illustrates is markedly affected, sometimes to the detriment of the patient.

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Copyright: © 2022 Roosy Aulakh and Harbir Sekhon. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.