A case of senile depression diagnosed by N-isopropyl-P-[123I]-iodoamphetamine single photon emission computed tomography and 18F-fluorodeoxyglucose positron emission tomography

Authors


Dr Norihito Oshima MD, National Hospital Organization Hanamaki Hospital, 500 Suwa, Hanamaki City, Iwate 025-0033, Japan. Email: rxg01737@nifty.ne.jp

Abstract

It is sometimes difficult to distinguish between dementia with depressive mood and depressive pseudodementia (DPD). However, it is important that a differential diagnosis between them is made because cognition and memory disorder in DPD patients are treatable. Herein, we describe a case of senile depression in a woman with memory and cognition problems. Her diagnosis was based on low blood flow and low metabolism in her frontal lobe, detected by N-isopropyl-P-[123I]-iodoamphetamine single photon emission computed tomography (SPECT) and 18F-fluorodeoxyglucose positron emission tomography (PET). After antidepressant therapy, the patient's depressive mood diminished and blood flow and metabolism in the frontal lobe recovered. These findings suggest that SPECT and PET can be used to make a differential diagnosis between senile depression and dementia, as well as for following recovery from a depressive mood.

INTRODUCTION

Most elderly patients have a depressive mood and it is sometimes difficult to distinguish between dementia with depressive mood and depression with cognitive impairment, so-called depressive pseudodementia (DPD). However, it is important to make a differential diagnosis between the two, because cognition and memory disorder in DPD patients are treatable.1 Recently, a few studies have demonstrated the effectiveness of single photon emission computed tomography (SPECT)2 and positron emission tomography (PET)3 in distinguishing between dementia with depressive episodes and DPD. Few reports, however, describe parallel improvements in clinical symptoms and SPECT and PET findings during treatment of DPD. Herein, we report on a case of DPD, illustrating improvements in cerebral blood flow (CBF) on SPECT imaging and in brain metabolism on PET in response to clinical treatment.

CASE REPORT

A 56-year-old woman was diagnosed with depression 7 years ago. She was taking amoxapine 125 mg/day to stabilize her symptoms and paroxetine 20 mg/day for her recurrent depressive mood. However, the depressive mood did not remit completely. The patient entered a substuporous state, which improved immediately, but she then developed apraxia and stereotypic behavior. On the basis of scores on the Revised Hasegawa's Dementia Scale (HDS-R; a brief dementia scale like the Mini-Mental State Examination) and Wechsler Adult Intelligence Scale-Revised (WAIS-R) of 25 and 77.5, respectively, a diagnosis of dementia was made. The patient's family requested another opinion, so she was transferred to our hospital. She was severely agitated, used stereotypic language, showed anxiety, and admitted to having feelings of guilt. Differential diagnosis included dementia and depression with agitation. On admission, serum hemoglobin was 9.2 g/dL, but other laboratory data were within normal ranges. Scores on the Hamilton Depression Rating Scale (HAM-D) and HDS-R were each 18 points (<20, dementia suspected), but the patient was fully oriented. Brain computed tomography was normal. Brain single photon emission computed tomography (SPECT) with N-isopropyl-P-[123I]-iodoamphetamine (123I-IMP) and brain positron emission tomography (PET) with 18F-fluorodeoxyglucose (18F-FDG) on admission showed hypoperfusion in the bilateral frontal lobes (Fig. 1a) and hypometabolism in the bilateral medial frontal lobes (Fig. 1b), respectively. Depression was diagnosed and treatment started. Maprotiline 50 mg/day was administered at first but discontinued because of anuria. Modified electroconvulsive therapy (mECT) with the THYMATRON SYSTEM IV (Somaticks, LCC, USA) was performed six times to treat the patient's persistant depressive mood. As a result, depressive mood, anxiety, and agitation decreased, the HAM-D score decreased to 0, the HDS-R score increased to 29, the WAIS-R score increased to 99, and cognitive impairment improved. One month after mECT, brain SPECT showed improvement of hypoperfusion in the bilateral frontal lobes (Fig. 1c) and brain PET showed improvement of the hypometabolism in the bilateral frontal lobes (Fig. 1d). The patient was discharged and returned to normal activities.

Figure 1.

(a,b) Before treatment, hypoperfusion in the bilateral frontal lobes (a) is shown using N-isopropyl-P-[123I]-iodoamphetamine single photon emission computed tomography (SPECT) and hypometabolism in the bilateral medial frontal lobes (b) is shown using 18F-fluorodeoxyglucose positron emission tomography (PET). (c,d) After treatment for depression, an improvement in the hypoperfusion and hypometabolism in the bilateral frontal lobes is detected with SPECT (c) and PET (d).

DISCUSSION

In this case report, we examined SPECT and PET as supportive tools in making a differential diagnosis between dementia with depressive mood and DPD. Distinguishing between dementia with depressive mood and DPD is difficult. In most patients, DPD progresses to Alzheimer's disease (AD).4,5 In one study, 39 of 44 elderly patients (89%) suffering from DPD developed AD,4 suggesting depressive dementia may be a risk factor for degenerative dementia. Depression, cognitive impairment, and degenerative dementia are on a pathophysiological continuum.6,7 However, regional CBF patterns differ between AD with depressive episodes and DPD in SPECT images. Although reports differ, one study found that DPD patients have significant decreases in CBF in the lateral frontal, left thalamus, and bilateral medial frontal regions in SPECT images.3 Alzheimer's disease patients with depressive episode have significant hypometabolism in the dorsolateral prefrontal lobes in PET images.8 The PET images show that glucose metabolism in the right superior frontal gyrus is lower in AD patients with a depressive mood than in those without a depressive mood.9 These patterns are different from those of AD patients, especially in the early stage, who have hypoperfusion or hypometabolism in the parietal and temporal lobes. In addition, treatment for depression improved frontal and temporal hypoperfusion in SPECT images.10,11 In the present case, SPECT imaging showed hypoperfusion in the bilateral frontal lobes and PET imaging showed hypometabolism in the bilateral medial frontal lobes on admission. Thus, depression was diagnosed not only on the basis of clinical findings, but also from SPECT and PET images. After mECT, depressive symptoms resolved and brain SPECT and PET images showed improvement. In the present case, cognitive impairment also improved (increased WAIS-R score with resolution of depression). Further investigation is required to determine whether DPD progresses to AD. However, the depressive mood should be treated regardless of cognitive impairment. Few reports have used SPECT or PET images to demonstrate improvement after treatment10,11 and few reports have used these imaging modalities to make a differential diagnosis between dementia and DPD.

In our case of senile dementia with cognition and memory loss, the diagnosis was made with the aid of brain SPECT and PET. As the antidepressant treatment decreased clinical symptoms, it also improved hypoperfusion and hypometabolism in the frontal lobe. These findings suggest that SPECT and PET are useful tools to distinguish between senile depression and dementia, as well as for following recovery from a depressive episode. Results of these studies are variable, and thus more are needed.

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