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With the aging of the population, the number of elderly patients referred to our hospital under a diagnosis of depression has been increasing. However, such patients often have other disorders, such as paranoid disorder, dementia and frontal lobe syndrome, and have undergone inappropriate treatment under a different diagnosis. On the other hand, elderly patients diagnosed as having geriatric depression who show slight improvements are often treated with excessive antidepressants, which presents a problem.

In recent years, attention has been directed to the differentiation between depression and dementia. Not only their differentiation, but also the influence of organic factors on the nature and manifestation of depression is an important issue. Pseudodementia in patients with depression is generally understood, but little attention has been paid to pseudodepression in those with organic disorders. Evaluation based on organic changes in the cerebral degeneration process is necessary in patients with pseudodementia, those who show histopathological changes with frontal lobe atrophy and those with a pathological condition immediately before dementia. For such evaluation, interviews with patients are important.

This schema (Fig. 1) represents an outline spectrum of disorders showing decreased volition and is useful for evaluating the condition of patients being examined due to their position in this spectrum. For example, the following patient was located at about involutional depression.

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Figure 1. This schema represents an outline spectrum of disorders showing decreased volition and is useful for evaluating the condition of patients being examined due to their position in this spectrum. For example, the patient of case 1 was located at about major depression and involutional depression, and case 2 was progressing from involutional depression to frontal lobe syndrome.

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CASE 1

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  2. CASE 1
  3. CASE 2
  4. REFERENCES

A 56-year-old male developed insomnia and palpitation as the first symptoms during busy days. These symptoms improved after treatment with hypnotics. In the following year, he experienced difficulty in falling asleep again and visited the psychiatric department of a local hospital. He complained of vague anxiety, a bothersome feeling and depressive mood, but showed improvement after treatment with an antidepressant and a minor tranquilizer. In the subsequent year, a melancholic feeling, anxiety and irritability developed again, but administration of selective serotonin reuptake inhibitor and serotonin noradrenalin reuptake inhibitor for approximately 1 month did not result in improvement. His wife noticed his forgetfulness. He remembered happenings on the previous day well, but often forgot to take drugs. His actions became slow and his cognitive ability seemed to decrease. He was absent-minded, and became lethargic.

At the first consultation, he complained of a feeling of guilt and a melancholic mood, but these complaints were superficial. He had no suicidal idea, avoided eye contact with others, greeted perfunctorily and had a hardened and stiffened face. He was admitted for close examination.

As psychological tests, mini-mental state examination (MMSE), Miyake’s recent memory scale and Rey complex figure test suggested the presence of ‘general impairment in the memory and reproduction of more complex information’. Imaging techniques showed bilateral sylvian fissure dilation and parietal lobe atrophy (Fig. 2), which were consistent with the early characteristics of Alzheimer’s disease.

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Figure 2. MRI of Case 1 showed bilateral sylvian fissure dilation and parietal lobe atrophy, which were consistent with the early characteristics of Alzheimer’s disease.

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After admission, he wandered in the ward, talked incoherently and complained of anxiety and especially marked anxiety in the evening. He often complained of insomnia and constipation and frequently confirmed answers. His tension decreased soon after admission. He appeared to forget the contents of meals, suggesting impaired recent memory. Even after adjustment of antidepressants, the symptoms did not improve. He repeatedly said the same things, without broadening his conversation, but had no sad mood. He tended to forget the details of happenings on the previous day. Based on slowing of the basic rhythm on electroencephalogram and atrophy shown by magnetic resonance imaging, a diagnosis of Alzheimer’s disease was made, and donepezil was administered.

He was followed up for the subsequent 3 years and the decreased volition gradually improved. Recently, he has been living free from worldly cares, painting pictures and taking walks and has maintained a condition allowing the exclusion of both Alzheimer’s disease and depression. This case demonstrates depressive pseudodementia.

Geriatric depression is characterized by: (i) slight psychomotor inhibition and rather marked anxiety, irritability and distress; (ii) infrequent complaints of a depressive or sad mood, but attention paid to hypochondriac symptoms directly felt, thought stagnation, forgetfulness, decreased volition/interest and lack of confidence, rather than a marked depressive mood; (iii) many hypochondriac symptoms and repeated physical complaints such as insomnia, headache, decreased appetite, constipation, abdominal discomfort, palpitation and frequent urination; (iv) high delusion tendency; (v) transient intellectual decrease; and (vi) frequent induction of delirium.

There have been many studies on pseudodementia. In the 20th century, Kiloh and Wells’‘Can’t do, don’t know’ answer is famous.1 The recent basic view of pseudodementia is that patients with pseudodementia develop Alzheimer’s disease in the near future.2 This case was classified as the following condition: ‘major depressive disorder complicated by cognition/memory disorder, but disappearance of both cognition/memory disorder with remission of the major depression disorder’. However, reflection on the examination findings suggests the necessity for the consideration of the next condition: ‘disappearance of cognition/memory disorder associated with major depressive disorder after antidepressant treatment, but manifestation of Alzheimer’s disease after a few years’.

The next patient showed a change from a reactive depressive state to frontal lobe type dementia.

CASE 2

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  2. CASE 1
  3. CASE 2
  4. REFERENCES

A 74-year-old female developed depression due to her mother’s death after caring for her for many years. Her depressive state did not improve until after approximately 1 year. Her depressive state was basically inhibition, but was sometimes accompanied by anxiety and tension. Subsequently, she developed compulsive behavior, such as hand washing, opening/closing curtains and the confirmation of locking up. During the subsequent 2-year period, compulsive symptoms, rather than depressive symptoms, gradually disappeared and her responses became superficial and showed decreased volition. Among neuropsychological examinations recently performed, the MMSE and Hasegawa’s dementia scale-revised showed a decrease in the intellectual level, while the neuropsychological examinations revealed frontal lobe dysfunction such as impairment of inhibition and fluency. Neuroimaging also showed bilateral frontal lobe atrophy and frontal hypoperfusin, which suggested frontotemporal dementia (Fig. 3)

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Figure 3. Neuroimagings of Case 2 showed bilateral frontal lobe atrophy and frontal hypoperfusion, which were suggesting frontotemporal dementia.

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We have also encountered patients who showed depression at onset, followed by a period of mild cognitive impairment (MCI), the development of Alzheimer’s dementia and showed the complete disappearance of the depressive state over time. There are many such patients. The observation of many patients revealed changes in the psychopathology of the depressive state over time in each case. A marked depressive mood, sad mood and awareness of the depressive state, which are original symptoms of depression, gradually decreased and an ‘attitude’ toward these symptoms disappeared. Awareness of the depressive mood/pathology decreased. These decreases in volition represent the inhibition period, which may lead to apathy requiring changes in treatment principles (Fig. 4).

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Figure 4. The observation of many patients revealed changes in the psychopathology of the depressive state over the time course. A marked depressive mood, sad mood, and awareness of the depressive state, which are original symptoms of depression, gradually decreased, and an “attitude” toward these symptoms disappeared. Awareness of the depressive mood/pathology decreased. These decreases in volition represent the inhibition period, which may lead to apathy requiring changes in treatment principles.

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In terms of a decrease in volition, major depression, involutional depression, organic depression (depression associated with Parkinson’s disease, cerebrovascular disease and so on), frontal lobe syndrome and dementia appeared to constitute a continuous spectrum. However, in the evaluation of organic factors, inquiry into the background of the awareness of depressive and sad feelings is very important. With an increase in the degree of organic factors such as aging, degeneration and circulatory impairment, the ‘attitude’ toward the depressive mood decreases and thinning and lack of awareness of depression will appear.

REFERENCES

  1. Top of page
  2. CASE 1
  3. CASE 2
  4. REFERENCES