Late Life Depression and Mania

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Carl Gerhard Gottfries1

Estimates of prevalence of late life depression vary widely according to the population studied, sample size, definition of depression and method of diagnosis. The prevalence of depression among people 65 years of age and older is usually estimated to 15% if all depressive disorders with clinically significant symptoms requiring intervention are included [1]. Major depressive disorders and bipolar affective disease occur somewhat less frequently

1 Institute of Clinical Neuroscience, Department of Psychiatry and Neurochemistry, SU/Molndal, Sweden among the elderly when compared to younger adults. There are few studies on the prevalence of mania in the elderly. Retrospective studies generally have found that the number of new cases of mania and the prevalence of mania in the population decrease, although there is evidence to contradict this belief [2]. The diagnosis of mania in the elderly is confounded by the overlap of manic symptoms with other syndromes that occur in the elderly, as dementia, confusional states, and delirium. Pure mania as a part of a bipolar disorder is rather rare. This may be the result of premature death of patients with bipolar disorders due to suicide or cardiovascular disease. It may, however, also reflect age-related differences in symptom presentation of both depression and mania in the elderly.

The symptomatology of late life depression is more heterogeneous than that of younger patients. The most common symptoms are somatic complaints, irritability, insomnia, fatigue, and comorbid anxiety. Compared to younger adults, elderly patients tend to somatize depressive symptoms. When mania is present, this is most often in the form of mixed mania with dysphoria and concomitant confusional states. Sometimes the syndrome is named disinhibition as uncontrolled emotional behaviour may dominate the picture.

Also the aetiology of late life depression is more heterogeneous than that of depression in younger adults. Women are more depressed than men are; the difference between the sexes, however, is less pronounced than in younger adults. Patients with a family history of depression are also more likely to be depressed than those with no family history of depression, but genetic factors seem to have less importance in old age depression.

In the elderly it is obvious that the ageing process and neurodegenerative disorders are important risk factors for syndromes of depression and mania. In patients with Alzheimer's dementia (AD) 25% also fulfil the criteria for major depressive disorders and in patients with vascular dementia (VAD) the frequency of depression is similarly high. In stroke patients the frequency of depression is almost 50% the year after the stroke attack. If not only depression but also behavioural and psychological symptoms in dementia (BPSD) are investigated, the frequency of these symptoms is around 85%. BPSD are often subdivided into subgroups. There are syndromes where overactivity is dominating, others where agitation and psychotic symptoms are dominating. Depression and insomnia are also frequent symptoms in BPSD. The prevalence of mania in demented patients is not well studied, and assumed to be low. However, if mixed mania, disinhibition syndromes and BPSD were investigated, the frequency of these syndromes might well be high.

As Shulman et al point out in their review, there is an association between cerebrovascular disease and bipolar disorders. Cognitive impairment is a prominent feature of old age mania. A clinical impression is that mania or disinhibition syndromes are more frequent in VAD and frontal lobe dementia (FLD) than in AD. In fact, both "vascular depression" and "vascular mania" are discussed [3]. Depression with onset in old age is associated with white matter lesion [4]. This may indicate that vascular disturbances may be present and these changes do not only cause cognitive impairment but also depression and BPSD.

In post-mortem human brain material from aged people and patients with AD and VAD, reduced levels of serotonin are reported [5]. This may well explain an increased risk for manic symptoms or disinhibited behaviour. However, white matter damage may also cause a disconnection between the frontal lobes and basal ganglia and brainstem, thus increasing the risk for disinhibited behaviour. This may also explain why patients with vascular depression appear to have more psychomotor retardation, greater lack of insight, and less agitation and guilt than elderly patients with early-onset depression without vascular risk factors.

The study of the one carbon metabolism has created interest lately. This metabolism is of importance for many metabolic processes in the body and in the brain. It is dependent on the access to folic acid, vitamin B12 and pyridoxine (vitamin B6). A marker for the one carbon metabolism is serum homocysteine, which increases if the metabolic process is disturbed. In elderly patients with depression, mania, cognitive impairment and elderly with heart-vessel disorders a disturbance of the one carbon metabolism has been observed [6-8]. Of still greater interest is that Coppen et al. [9] have shown that patients with affective disorders who are on long-term treatment with lithium have less morbidity if the treatment is combined with folic acid. Patients with low serum folate respond less favourably to treatment with selective serotonin reuptake inhibitors (SSRIs) and there is a correlation between the response to treatment with sertraline, an SSRI, and serum folate levels, although the levels are within the normal distribution [10]. A disturbed one carbon metabolism may thus be a common risk factor for depression, mania, cognitive impairment and vascular disorders in the elderly that should be considered in the treatment.

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