Educationals

Depression is the commonest emotional disorder to follow a stroke. Anxiety reactions occur in 14 to 27% of patients following a stroke, while 30 to 50% of patients develop depression within 6 months of 2 years after a stroke.

There is some acceptance of the idea that mood disturbances represent a psychological response of the individual to severe stress. Patients with a self sufficient pre-morbid personality react more adversely than those with dependency needs. Those who have previously experienced anxiety and depression and those with unsatisfactory family relationships also react adversely.

Among the incriminating factors are included physical handicap, uncertainty about the future, enforced dependency, imposition of an invalid role, loss of job, loss of status, financial problems and a sense of uselessness.

Physical handicap however does not cause depression. But once it occurs it remains thereby creating a vicious circle.

It is common in patients with nonfluent aphasia than in those with global aphasia. But this aphasia does not produce the depression nor can it be accounted for by age or impaired social functioning.

Both the size and site of the lesion correlate independently with the degree of intellectual impairment.

Increased ventricle brain ratio reflection subcortical atrophy existing before the stroke may be an important predisposing factor.

The depression can be either major or minor. Major depression is associated with frontal or basal ganglia injury and may produce depressive pseudodementia. Minor depression is not associated with congnitive disturbances. Major depression after stroke may remit in a year's time, while the minor depression may linger on.

In 54% of the cases the lesion is in the region of the middle cerebral artery, while 24% are associated with lesions in the brain stem or cerebellum.

Left hemispheric lesions have been consistently shown to give a much higher incidence of both catastrophic anxiety reactions and depression . These lesions produce depression with cognitive impairment especially when anteriorly placed.

Right hemispheric lesions are not usually associated with congnitive impairment. If the right hemispheric lesion is anteriorly placed, it can be associated with cheerfulness or euphoria rather than depression.

Major depression following right hemispheric lesion may have a different aetiology than major depression following left hemispheric lesion. A significantly higher frequency of family history of depression has been observed in these patients.

Anterior left sided lesions produce depression by disrupting biogenic amine pathways. The noradrenergic and serotoninergic pathways around the brain stem, hypothalamus and basal ganglia and the frontal cortex are involved. Significant depletion of brain serotonin and noradrenaline have been demonstrated in these cases which may be casual.

Right hemispheric lesions may produce depression as the expression and organisation of emotion are located in the right hemisphere.

Treatment

Nortriptyline is the drug which has been most frequently reported to be useful in post-stroke depression. The dose ranges from 25 mg to 150 mg per day.

Cerebral Tumors and Depression

Depressive changes rarely occur by themselves in tumors. They often accompany other mental manifestations. Irritability in the early stages is later succeeded by anxiety and depression. Impulsive suicidal attempts may be made during paroxysms of headache.

Frontal and temporal locations of tumour are associated with the greatest frequency of both depression and personality disturbances. The frontal location is characterized by irritability, depression or euphoria, and apathy. Irritability is a frequent presenting symptom.

Euphoria is as common in temporal lobe tumours as in frontal lobe tumours. It can be associated with intellectual impairment, anxiety, anger, hypomania. Manic symptoms have also been report- ed. The mental changes are commonly seen with dominant hemisphere lesion associated with dysphasia.

Parietal lobe tumours are less likely to produce mental changes than frontal or temporal lobe lesions. Parietal lobe lesions produce early neurological sings and are less likely to be missed or mistaken for a psychiatric disorder. Depression may occur. This may be associated with congnitive disturbances like dysphasia and apraxia acalcutia (gerstman's syndrome finger agnosia, dyscalculia, dysgraphia, right/left disorientation) when the dominant lobe is affected: Tumours of the non dominant lobe are often associated with visuospatial difficulties, typographical disorientation, dressing apraxia or body image disturbances.